ClickCease
+1-915-850-0900 spinedoctors@gmail.com
Select Page

Neck Pain

Back Clinic Neck Treatment Team. Dr. Alex Jimenezs collection of neck pain articles contain a selection of medical conditions and/or injuries regarding symptoms surrounding the cervical spine. The neck is made up of various complex structures; bones, muscles, tendons, ligaments, nerves, and other types of tissues. When these structures are damaged or injured as a result of improper posture, osteoarthritis, or even whiplash, among other complications, the pain and discomfort an individual experiences can be impairing. Through chiropractic care, Dr. Jimenez explains how the use of spinal adjustments and manual manipulations focuses on the cervical spine can greatly help relieve the painful symptoms associated with neck issues. For more information, please feel free to contact us at (915) 850-0900 or text to call Dr. Jimenez personally at (915) 540-8444.


Whiplash Treatment Guidelines in El Paso, TX

Whiplash Treatment Guidelines in El Paso, TX

Whiplash is one of the most prevalent types of injuries resulting from an automobile accident, most commonly during rear-end auto collisions. However, whiplash-associated disorders can develop due to a variety of other circumstances, including sports injuries, amusement park rides or physical abuse. Whiplash occurs when the soft tissues of the neck, such as the muscles, tendons and ligaments, extend beyond their natural range of motion because of a sudden back-and-forth movement of the head. Furthermore, the sheer force of an impact can stretch and even tear the complex structures surrounding the cervical spine.

 

The symptoms of whiplash-associated disorders may take days, weeks or even months to manifest, which is why it’s important for individuals who’ve been involved in an automobile accident to seek immediate medical attention. There are many different types of treatment options which can safely and effectively help treat whiplash. The purpose of the following article is to demonstrate the treatment guidelines of neck pain-associated disorders and whiplash-associated disorders.

 

The Treatment of Neck Pain-Associated Disorders and Whiplash-Associated Disorders: A Clinical Practice Guideline

 

Abstract

 

  • Objective: The objective was to develop a clinical practice guideline on the management of neck pain�associated disorders (NADs) and whiplash-associated disorders (WADs). This guideline replaces 2 prior chiropractic guidelines on NADs and WADs.
  • Methods: Pertinent systematic reviews on 6 topic areas (education, multimodal care, exercise, work disability, manual therapy, passive modalities) were assessed using A Measurement Tool to Assess Systematic Reviews (AMSTAR) and data extracted from admissible randomized controlled trials. We incorporated risk of bias scores in the Grading of Recommendations Assessment, Development, and Evaluation. Evidence profiles were used to summarize judgments of the evidence quality, detail relative and absolute effects, and link recommendations to the supporting evidence. The guideline panel considered the balance of desirable and undesirable consequences. Consensus was achieved using a modified Delphi. The guideline was peer reviewed by a 10-member multidisciplinary (medical and chiropractic) external committee.
  • Results: For recent-onset (0-3 months) neck pain, we suggest offering multimodal care; manipulation or mobilization; range-of-motion home exercise, or multimodal manual therapy (for grades I-II NAD); supervised graded strengthening exercise (grade III NAD); and multimodal care (grade III WAD). For persistent (N3 months) neck pain, we suggest offering multimodal care or stress self-management; manipulation with soft tissue therapy; high-dose massage; supervised group exercise; supervised yoga; supervised strengthening exercises or home exercises (grades I-II NAD); multimodal care or practitioner�s advice (grades I-III NAD); and supervised exercise with advice or advice alone (grades I-II WAD). For workers with persistent neck and shoulder pain, evidence supports mixed supervised and unsupervised high-intensity strength training or advice alone (grades I-III NAD).
  • Conclusions: A multimodal approach including manual therapy, self-management advice, and exercise is an effective treatment strategy for both recent-onset and persistent neck pain. (J Manipulative Physiol Ther 2016;39:523-44.e20) Key
  • Indexing Terms: Practice Guideline; Neck Pain; Whiplash Injuries; Chiropractic; Therapeutic Intervention; Disease Management; Musculoskeletal Disorders

 

Dr. Alex Jimenez’s Insight

Whiplash occurs when the sheer force of an impact causes the head and neck to jolt abruptly back-and-forth in any direction, stretching the complex structures surrounding the cervical spine beyond their normal range. Neck pain, headache and radiating pain resulting from whiplash are common complaints frequently reported by individuals after being involved in an automobile accident. However, whiplash can also result from a variety of other circumstances. Whiplash-associated disorders are a prevalent source of disability and a common reason many auto accident victims seek medical attention from chiropractors, physical therapists and primary care physicians. Fortunately, many treatment guidelines exist to safely and effectively improve as well as manage the symptoms of whiplash. Chiropractic care is a well-known alternative treatment option for whiplash-associated disorders. Spinal adjustments and manual manipulations can safely and effectively restore the original alignment of the spine, reducing symptoms and alleviating whiplash complications.

 

Introduction

 

Neck pain and its associated disorders (NAD), including headache and radiating pain into the arm and upper back, are common and result in significant social, psychological, and economic burden.1-4 Neck pain, whether attributed to work, injury, or other activities,5 is a prevalent source of disability and a common reason for consulting primary health care providers, including chiropractors, physical therapists, and primary care physicians.6 The estimated annual incidence of neck pain measured in 4 studies ranged between 10.4% and 21.3%, with a higher incidence noted in office and computer workers.7 Although some studies report that between 33% and 65% of people have recovered from an episode of neck pain at 1 year, most cases follow an episodic course over a person�s lifetime, and thus, relapses are common.7 Neck pain is a leading cause of morbidity and chronic disability worldwide.5,8 In 2008 the Bone and Joint Decade Task Force on Neck Pain and Its Associated Disorders reported that 50% to 75% of individuals with neck pain also report pain 1 to 5 years later.4 Several modifiable and nonmodifiable environmental and personal factors influence the course of neck pain, including age, previous neck injury, high pain intensity, self-perceived poor general health, and fear avoidance.7

 

Neck pain related to whiplash-associated disorders (WADs) most commonly results from motor vehicle accidents.9,10�Whiplash-associated disorders disrupt the daily lives of adults around the world and are associated with considerable pain, suffering, disability, and costs.3,11 Whiplash-associated disorders are defined as an injury to the neck that occurs with sudden acceleration or deceler- ation of the head and neck relative to other parts of the body, typically occurring during motor vehicle collisions.10,12 The majority of adults with traffic injuries report pain in the neck and upper limb pain. Other common symptoms of WADs include headache, stiffness, shoulder and back pain, numbness, dizziness, sleeping difficulties, fatigue, and cognitive deficits.9,10 The global yearly incidence rate of emergency department visits as a result of acute whiplash injuries after road traffic crashes is between 235 and 300 per 100,000.3,13,14 In 2010, there were 3.9 million nonfatal traffic injuries in the United States.11 The economic costs of motor vehicle crashes that year totaled USD$242 billion, including $23.4 billion in medical costs and $77.4 billion in lost productivity (both market and household).11 In Ontario, traffic collisions are a leading cause of disability and health care use and�expenditures, resulting in the automobile insurance system paying nearly CND$4.5 billion in accident benefits in 2010.15

 

Diagram showing the process of whiplash resulting from an automobile accident.

 

More than 85% of patients experience neck pain after a motor vehicle accident, often associated with sprains and strains to the back and extremities, headache, psychological symptomatology, and mild traumatic brain injury.10 Whiplash injuries have an effect on general health, with recovery in the short term reported by 29% to 40% of individuals with WAD in Western countries that have compensation schemes for whiplash injuries. 16,17 The median time to first reported recovery is estimated at 101 days (95% confidence interval: 99-104) and about 23% are still not recovered after 1 year.13

 

Image displaying X-rays before and after whiplash.

 

Image demonstrating an X-ray of the neck during flexion and extension.

 

 

The 2000-2010 Bone and Joint Decade Task Force on Neck Pain and its Associated Disorders recommended that all types of neck pain, including WADs,18 be included under the classification of NAD.19 NAD can be classified into 4 grades, distinguished by the severity of symptoms, signs, and impact on activities of daily life (Table 1).

 

The clinical management of musculoskeletal disorders, and neck pain in particular, can be complex and often involves combining multiple interventions (multimodal care) to address its symptoms and consequences.19�In this guideline, multimodal care refers to treatment involving at least 2 distinct therapeutic methods, provided by 1 or more health care disciplines.20 Manual therapy (including spinal manipulation), medication, and home exercise with advice are commonly used multimodal treatments for recent- onset and persistent neck pain.21,22 Thus, there is a need to determine which treatments or combinations of treatments are more effective for managing NAD and WAD.

 

Rationale for Developing This Guideline

 

The Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration20 recently updated the systematic reviews from the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders (Neck Pain Task Force).23 Consequently, it was deemed timely to update the recommendations of 2 chiropractic guidelines on NAD (2014)24 and WAD (2010)25 produced by the Canadian Chiropractic Association and the Canadian Federation of Chiropractic Regulatory and Educational Accrediting Boards (the �Federation�) into a single guideline.

 

Table 1 Classification of Neck Pain-Associated Disorders and Whiplash-Associated Disorders

 

Scope and Purpose

 

The aim of this clinical practice guideline (CPG) was to synthesize and disseminate the best available evidence on the management of adults and elderly patients with recent onset (0-3 months) and persistent (N3 months) neck pain and its associated disorders, with the goal of improving clinical decision making and the delivery of care for patients with NAD and WAD grades I to III. Guidelines are �Statements that include recommendations intended to optimize patient care that are informed by a systematic review of evidence and an assessment of the benefits and harms of alternative care options.�26

 

The target users of this guideline are chiropractors and other primary care health care providers delivering conservative care to patients with NADs and WADs, as well as policymakers. We define conservative care as treatment designed to avoid invasive medical therapeutic measures or operative procedures.

 

OPTIMa published a closely related guideline in the European Spine Journal.27 Although we reached similar results, OPTIMa developed recommendations using the modified Ontario Health Technology Advisory Committee (OHTAC) framework.28 In contrast, our guideline used the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. GRADE provides a common, sensible, and transparent approach to grading quality (or certainty) of evidence and strength of recom- mendations (www.gradeworkinggroup.org). GRADE was the highest scoring instrument among 60 evidence grading systems29 and has been determined to be reproducible among trained raters.30 GRADE is now considered a standard in guideline development and has been adopted by many international guideline organizations and journals.31 The Canadian Chiropractic Guideline Initiative (CCGI) guideline panel considered available high-quality systematic reviews, updated the search of the peer-reviewed published reports up to December 2015, and then used the GRADE approach to formulate recommen- dations for the management of neck pain and associated disorders.

 

Framework

 

To inform its work, the CCGI considered recent advances in methods to conduct knowledge synthesis,32 derive evidence-based recommendations, 31,33 adapt high- quality guidelines, 34 and develop 35 and increase the uptake of CPGs.36,37 An overview of CCGI structure and methods is provided in Appendix 1.

 

Methods

 

Ethics

 

Because no novel human participant intervention was required and secondary analyses were considered, the research presented in this guideline is exempt from institutional ethics review board approval.

 

Selection of Guideline Development Panelists

 

The CCGI project lead (A.B.) appointed 2 co-chairs (J.O. and G.S.) for the guideline development group and nominated the project executive committee and the remaining guideline panelists. J.O. served as the lead methodologist on the guideline panel. G.S. helped ensure geographic representation of the panel and advised on specific duties of panel members, time commitment, and decision-making process for reaching consensus (develop- ment of key questions and of recommendations). To ensure a broad representation, the guideline panel included clinicians (P.D., J.W.), clinician researchers (F.A., M.D., C.H., S.P., I.P., J.S.) methodologists (J.O., A.B., M.S., J.H.), a professional leader/decision maker (G.S.), and 1 patient advocate (B.H.) to ensure that patient values and preferences were considered. One observer (J.R.) moni- tored the 3 face-to-face meetings of the guideline panel held in Toronto (June and September 2015 and April 2016).

 

All CCGI members, including guideline panelists and peer reviewers, were required to disclose any potential conflict of interest by topic before participation and during the guideline development process. There was no self- declaration of conflicts of interest among the panel or the reviewers.

 

Key Question Development

 

Six topic areas (exercise, multimodal care, education, work disability, manual therapy, passive modalities) on the conservative management of NAD and WAD grades I to III were covered in 5 recent systematic reviews by the OPTIMa Collaboration,38-42 among a total of 40 reviews on the management of musculoskeletal disorders.20 The panel met over 2 days in June 2015 to brainstorm about potential key questions.

 

Table 2 Topics and Key Questions Addressed by the Guideline Development Group

 

Table 2 Continued

 

Table 2 Continued (last)

 

Search Update and Study Selection

 

The panel assessed the quality of eligible systematic reviews using the AMSTAR tool43 and its 11 criteria (amstar.ca/Amstar_Checklist.php).

 

Because the last search dates of included systematic reviews were 2012,40,41 2013,38,39,42 and 2014,42 the panel updated the literature searches in Medline and Cochrane Central databases on December 24, 2015 using the published search strategies. We used a 2-phase screening process to select additional eligible studies. In phase 1, 2 independent reviewers screened titles and abstracts to determine the relevance and eligibility of studies. In phase 2, the same pairs of independent reviewers screened full-text articles to make a final determination of eligibility. Reviewers met to resolve disagreements and reach consensus on the eligibility of studies in both phases, with arbitration by a third reviewer if needed. Studies were included if they1 met the PICO (population, intervention, comparator, outcome) criteria and2 were randomized controlled trials (RCTs) with an inception cohort of at least 30 participants per treatment arm with the specified condition, because this sample size is considered the minimum needed for non-normal distributions to approx- imate the normal distribution.44

 

Data Abstraction and Quality Assessment

 

Data were extracted from the included studies identified in each systematic review, including study design, participants, intervention, control, outcomes, and funding.

 

The internal validity of included studies was assessed by the OPTIMa collaboration using the Scottish Intercollegiate Guidelines Network (SIGN) criteria.45

 

For articles retrieved from the updated search, pairs of independent reviewers critically appraised the internal validity of eligible studies using the SIGN criteria,46 similar to the OPTIMa collaboration reviews. Reviewers reached consensus through discussion. A third reviewer was used to resolve disagreements if consensus could not be reached. A quantitative score or a cutoff point to determine the internal validity of studies was not used. Instead, the SIGN criteria were used to assist reviewers in making an informed overall judgment on the risk of bias of included studies. 47

 

Synthesis of Results

 

J.O. extracted data from scientifically admissible studies into evidence tables. A second reviewer (A.B.) indepen- dently checked the extracted data. We performed a qualitative synthesis of findings and stratified results based on the type and duration of the disorder (ie, recent [symptoms lasting b3 months] vs persistent [symptoms lasting N3 months]).

 

Recommendation Development

 

We used the Guideline Development Tool (http:// www.guidelinedevelopment.org), and assessed the quality of the body of evidence for our outcomes of interest by�applying the GRADE approach.48 We used the evidence profiles to summarize the evidence.49 The quality of evidence rating (high, moderate, low, or very low) reflects our confidence in the estimate of the effect to support a recommendation and considers the strengths and limitations of the body of evidence stemming from risk of bias, imprecision, inconsistency, indirectness of results, and publication bias.50 Assessment of quality of evidence was carried out in the context of its relevance to the primary care setting.

 

Figure 1 PRISMA Flow Diagram

 

Using the Evidence to Decisions (EtD) Framework (www.decide-collaboration.eu/etd-evidence- decision-framework), the panel formally met in September 2015 and April 2016 to consider the balance of desirable and undesirable consequences to determine the strength of each recommendation, using informed judgment on the quality of evidence and effect sizes, resource use, equity, acceptability, and feasibility. To make a recommendation, the panel needed to express an average judgment that was beyond neutral with respect to the balance between desirable and undesirable consequences of an intervention, as outlined in the EtD. We defined the strength rating of a recommendation (strong or weak) as the extent to which the desirable consequences of an intervention outweigh its undesirable consequences. A strong recommendation can be made when the desirable consequences clearly outweigh the undesirable consequences. In contrast, a weak recommendation is made when, on the balance of probabilities, the desirable consequences likely outweigh the undesirable consequences. 49,51

 

Figure 2 PRISMA Flow Diagram

 

The panel provided recommendations based on the evidence if statistically and clinically significant differ- ences were found. The panel followed a 2-step process in making a recommendation. We first agreed that there should be evidence of clinically meaningful changes occurring over time in the study population and that a single consensus threshold of clinical effectiveness should be applied consistently. We reached a consensus decision that a 20% change in the outcome of interest within any study group was required to make a recommendation. The decision to use a 20% threshold was informed by current published reports and relevant available minimal clinically important differences (MCIDs).52-55

 

However, MCIDs can vary across populations, settings, and conditions and depending on whether within-group or between-group differences are being assessed. Therefore, the panel considered MCID values for the most relevant outcomes (ie, 10% for visual analog scale [VAS] or Neck Disability Index [NDI; 5/50 on the NDI], 20% for numerical rating scale [NRS]) and chose the more conservative of these values as the threshold when evaluating between group differences.52,54

 

Second, the results from relevant studies were used to formulate a recommendation where appropriate. A treat- ment determined to be effective (with statistically significant differences between baseline and follow-up scores and�clinical significance based on the MCID applied in the study) was recommended by our panel. If a study found 2 or more treatments to be equally effective based on our threshold, then the panel recommended all equivalently effective treatments.

 

Figure 3 PRISMA Flow Diagram

 

The EtD Frameworks were completed and recommen- dations were drafted over a series of conference calls with panel members after making judgments about 4 decision domains: quality of evidence (confidence in estimates of effect); balance of desirable (eg, reduced pain and disability) and undesirable outcomes (eg, adverse reactions); confidence about the values and preferences for the target population; and resource implications (costs).56,57 A synthe- sis of our judgments about the domains determined the direction (ie, for or against a management approach) and the strength of recommendations (the extent to which one can be confident that the desirable conse- quences of an intervention outweigh the undesirable consequences). A specific format was followed to formulate recommendations using patient description and the treatment comparator.56 Remarks were added for clarification if needed. If the desirable and undesirable consequences were judged to be evenly balanced and the evidence was not compelling, the panel decided not to write any recommendation.

 

A modified Delphi technique was used at an in-person meeting to achieve consensus on each recommendation.58 Using an online tool (www.polleverywhere.com), panelists�voted their level of agreement with each recommendation (including quality of evidence and strength of recom- mendation) based on a 3-point scale (yes, no, neutral). Before voting, panelists were encouraged to discuss and provide feedback on each recommendation in terms of suggested wording edits or general remarks. To achieve consensus and be included in the final manuscript, each recommendation had to have at least 80% agreement with a response rate of at least 75% of eligible panel members. All recommendations achieved consensus in the first round.

 

Figure 4 PRISMA Flow Diagram

 

Peer Review

 

A 10-member external committee composed of stake- holders, end-users, and researchers from Canada, the United States, and Lebanon (Appendix 2) independently reviewed the draft manuscript, recommendations, and supporting evidence. The AGREE II instrument was used to assess the methodological quality of the guideline.35 Feedback received was collected and considered in a revised draft for a second round of review. Chairs of the guideline panel provided a detailed response to reviewers� comments. For a glossary of terms, please see Appendix 3.

 

Figure 5 PRISMA Flow Diagram

 

Results

 

Key Question Development

 

Thirty-two standardized key questions were developed in line with the PICO (population, intervention, comparator, outcome) format. The panel recognized overlap in content and relevance among some key questions. After combining 3 questions, we ultimately addressed a total of 29 key questions (Table 2).

 

Study Selection and Quality Assessment: OPTIMa Reviews

 

OPTIMa searches yield 26 335 articles screened.38-42 After removal of duplicates and screening, 26 273 articles did not meet selection criteria, leaving 109 articles eligible for critical appraisal. Fifty-nine studies (62 articles) published from 2007 to 2013 were deemed scientifically admissible and included in the synthesis (Appendix 4). Each review used was rated as either moderate or high quality (AMSTAR score 8-11).59

 

Search Update and Study Selection

 

Our updated search yielded 7784 articles. We removed 1411 duplicates and screened 6373 articles for eligibility (Figs. 1-5). After screening, 6321 articles did not meet our selection criteria (phase 1), leaving 52 articles for full-text review (phase 2) and critical appraisal (studies on the topic of multimodal care (n = 12), structured patient education (n = 3),�exercise (n = 8), work disability interventions (n = 13), manual therapy (n = 4), soft tissues (n = 2), and passive modalities (n = 6). Of the 52 RCTs, 4 scientifically admissible studies were included in our synthesis. The remaining articles failed to address the key question (n = 1); selected population (n = 2), outcomes (n = 13), or intervention (n = 11); had no between estimates (n = 19); or were duplicates (n = 1) or a secondary analysis of an included study (n = 1) (Appendix 5).

 

Table 3 Neck Manipulation vs Neck Mobilization

 

Table 4 Multimodal Care vs Home Exercises vs Medication

 

Table 5 Strengthening Exercises vs Advice

 

Quality Assessment and Synthesis of Results

 

The GRADE evidence profile and risk of bias within included studies are presented in Tables 3-15 and Appendix 6, respectively.

 

Recommendations

 

We present recommendations as follows:

  • Recent-onset (0-3 months) grades I to III NAD
  • Recent-onset (0-3 months) grades I to III WAD
  • Persistent (N3 months) grades I to III NAD
  • Persistent (N3 months) grades I to III WAD

 

Recommendations for Recent-Onset (0-3 Months) Grades I to III NAD

 

Manual Therapy

 

Key Question 1: Should neck manipulation vs neck mobilization be used for recent-onset (0-3 months) grades I to II NAD?

 

Summary of Evidence. One RCT by Leaver et al. 60 evaluated the effectiveness of neck manipulation or neck mobilization delivered by physiotherapists, chiropractors, or osteopaths for recent-onset grades I to II neck pain (?2 NRS). All patients received advice, reassurance, or a continued exercise program as indicated for 4 treatments over 2 weeks unless recovery was achieved or a serious adverse event occurred. There was no statistically significant difference in Kaplan-Meier recovery curves between groups for recovery from neck pain and recovery of normal activity, and no statistically significant differences between groups for pain, disability, or other outcomes (function, global perceived effect, or health-related quality of life) at any follow-up point (Table 3).

 

One other RCT by Dunning et al.61 evaluated the effectiveness of a single high-velocity, low-amplitude (thrust) manipulation (n = 56) directed to the upper cervical spine (C1-C2) and upper thoracic spine (T1-T2) compared with a (nonthrust) mobilization (n = 51) directed to the same anatomical regions for 30 seconds for patients with neck pain. Findings indicated a greater reduction in pain (NPRS) and disability (NDI) in the thrust manipulation group compared with the mobilization at 48 hours. No serious adverse events were reported. Minor adverse events were not collected. This study did not inform our recommendation because1 patient complaints were not recent onset (mean�duration N337 days in both groups), and2 outcomes were measured at 48 hours only. The Guideline Development Group (GDG) considered this an important study limitation because one cannot assume these benefits would have carried on for a longer period. The panel acknowledged, however, that some patients may value obtaining fast pain relief even if temporary.

 

The panel determined that the overall certainty in the evidence was low, with large desirable relative to undesirable effects. The relative small cost of providing the option would make it more acceptable to stakeholders and feasible to implement. Although the panel decided the desirable and undesirable consequences were closely balanced, the following statement was provided:

 

Recommendation: For patients with recent (0-3 months) grades I to II NAD, we suggest manipulation or mobilization based on patient preference. (Weak recommendation, low-quality evidence)

 

Table 6 Multimodal Care vs Education

 

Table 7 Exercise vs No Treatment

 

Table 8 Yoga vs Education

 

Exercise

 

Key Question 2: Should integrated neuromuscular inhibition technique be used for recent-onset (0-3 months) grades I to II NAD?

 

Summary of Evidence. Nagrale et al.62 reported non� clinically significant differences for neck pain and disability outcomes at 4 weeks. This study suggested that a soft tissue therapy intervention to the upper trapezius, combining ischemic compression, strain-counterstrain, and muscle energy technique, provides similar clinical benefit compared with muscle energy technique alone. Participants were required to have neck pain of less than 3 months� duration.

 

The panel determined moderate certainty in the evidence, with small desirable and undesirable effects and no serious adverse events. Low costs are required for the intervention and no specific equipment is needed, with the exception of training to provide the technique. Because the intervention is widely practiced and taught, it is acceptable and feasible to implement. However, its effects on health equities cannot be determined. Overall, the panel decided the balance between the desirable and undesirable consequences was uncertain, and more evidence is needed before a recommendation can be made.

 

Multimodal Care

 

Key Question 3: Should multimodal care vs intramuscular ketorolac be used for recent (0-3 months) grades I to III NAD?

 

Summary of Evidence. McReynolds et al. 63 presented short-term outcomes of pain intensity and concluded that sessions of multimodal care (manipulation, soft tissue techniques) provided equivalent outcomes to an intramuscular injection of ketorolac. However, the follow-up time of 1 hour is generally atypical and the dosing was determined to be incomplete for multimodal care as reported. Furthermore, the study was limited to an emergency setting only.

 

The panel determined low certainty in the clinical evidence, with small desirable and undesirable effects. There is relatively low risk for multimodal care, considering the reported outcomes were equal. From a clinician standpoint, resources required are small assuming no additional staff are needed. However, one practitioner gave most multimodal therapies. Expenses may vary depending on the definition of multimodal care. This option should not create health inequities, except for those who cannot access clinicians or choose to pay out of pocket, and would be feasible to implement. Professional associ- ations would generally support the option, yet extended multimodal therapies can incur additional costs, which can be unfavorable to both payors and patients. Overall, the balance between the desirable and undesirable conse- quences is uncertain and more research is needed in this area before any recommendation can be made.

 

Table 9 Exercises vs Home Range or Motion or Stretching Exercises

 

Table 10 Multimodal Care vs Self-Management

 

Exercise

 

Key Question 4: Should multimodal care vs home exercises vs medication be used for recent-onset (0-3 months) grades I to II NAD?

 

Summary of Evidence. One RCT by Bronfort et al.22 evaluated the efficacy of multimodal care over 12 weeks compared with a 12-week home exercise and advice program or medication on neck pain (11-box NRS) and disability (NDI) in 181 adult patients with acute and subacute neck pain (2-12 weeks� duration and a score of ?3 on a 10-point scale). Multimodal care by a chiropractor (mean of 15.3 visits, range 2-23) included manipulation and mobilization, soft tissue massage, assisted stretching, hot and cold packs, and advice to stay active or modify activity as needed. Daily home exercise was to be done up to 6 to 8 times per day (individualized program including self- mobilization exercise of the neck and shoulder joints) with advice by a physical therapist (two 1-hour sessions, 1-2 weeks apart on posture and activity of daily living). Medication prescribed by a physician included nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, opioid analgesic, or muscle relaxants (dosage was not reported). The results displayed in Table 4 indicated that multimodal care and home exercises and advice were as effective as medication in reducing pain and disability at short term (26 weeks). However, medication was associated with a higher risk for adverse events (mostly gastrointestinal symptoms and drowsiness in 60% of participants) than home exercises. The choice of medications was based on the participant�s history and response to treatment. Clinicians and patients should be aware that current evidence is insufficient to determine the effectiveness of long-term opioid therapy for improving chronic pain and function. Importantly, evidence supports a dose-dependent risk for serious harms, including increased risk for overdose, dependence, and myocardial infarction.64

 

Recommendation: For patients with recent (0-3 months) neck pain grades I to II, we suggest either range-of-motion home exercises, medication, or multimodal manual therapy for reduction in pain and disability. (Weak recommendation, moderate- quality evidence)

 

Remark: Home exercises included education self-care advice, exercises, and instruction on activities of daily living. Medication included NSAIDs, acetaminophen, muscle relaxant, or a combination of these. Multimodal manual therapy included manipulation and mobilization with limited light soft tissue massage, assisted stretching, hot and cold packs, and advice to stay active or modify activity as needed.

 

Key Question 5: Should supervised graded strengthening exercises vs advice be used for recent-onset (0-3 months) grade III NAD?

 

Summary of Evidence. One RCT by Kuijper et al.65 evaluated the effectiveness of supervised strengthening exercises compared with advice to stay active for recent-onset grade III neck pain. This RCT reported that strengthening exercises (n = 70) were more effective than advice to stay active (n = 66).65 Trial participants were followed at 3 weeks, 6 weeks, and 6 months. Based on panel consensus, outcomes determined to be important in the assessment of effectiveness in this RCT included neck and arm pain (VAS) and disability (NDI). These outcomes were both statistically and clinically significant (Table 5).

 

In this RCT, the strengthening exercise program was delivered by physiotherapists 2 times per week for 6 weeks.65 It included supervised graded strengthening exercises for the shoulder and daily home exercises to strengthen the superficial and deep neck muscles (mobility, stability, and muscle strengthening). Participants in the comparison group were advised to continue daily activities. Both groups were allowed to use painkillers. See Key Question 6 for a recommendation on cervical collar.

 

Recommendation: For patients with recent (0-3 months) grade III neck and arm pain, we suggest supervised graded strengthening exercises* rather than advice alone.� (Weak recommendation, moderate-quality evidence)

 

Remark: *Supervised graded strengthening exercises con- sisted of strengthening and stability exercises twice a week for 6 weeks with daily home exercises (which included mobility, stability, and muscle strengthening). �Advice alone consisted of maintaining activity of daily living without specific treatment.

 

Table 11 Manipulation vs No Manipulation

 

Table 12 Massage vs No Treatment

 

Table 13 Multimodal Care vs Continued Practitioner Care

 

Table 14 Group Exercise vs Education or Advice

 

Table 15 General Exercise and Advice vs Advice Alone

 

Passive Physical Modalities

 

Key Question 6: Should cervical collar vs graded strengthening exercise program be used for recent-onset (0-3 months) grade III NAD?

 

Summary of Evidence. One RCT by Kuijper et al.65 randomly assigned 205 patients with recent-onset neck�cervical radiculopathy (NAD grade III) to 1 of 3 groups 1 : Rest and semi-hard cervical collar for 3 weeks, then weaned off during weeks 3-6 2 ; physiotherapy (mobilizing and stabilizing the cervical spine, standardized graded neck strengthening exercises twice per week for 6 weeks, and education to do daily home exercises); or3 a control group (wait and see with advice to continue daily activities). All patients received written and oral reassurance about the usually benign course of the symptoms and were allowed painkillers.

 

Wearing a semi-hard cervical collar or receiving standardized graded strengthening exercise program and home exercises for 6 weeks provided similar improvements in arm pain (VAS), neck pain (VAS), or disability (NDI) compared with a wait-and-see policy at 6 weeks. There were no between-group differences at 6 months.

 

Because of uncertainty about potential for iatrogenic disability associated with the prolonged use of cervical collar,27,42 one recommendation made in the current guideline favoring strengthening exercise programs over advice, and the lack of consensus among the guideline panel, the GDG decided not to make a recommendation against the use of cervical collar (first vote on the proposed recommendation with direct results from the study [11% agree, 11% neutral, 78% disagree, 1 abstained]). A second vote favored also removing the remark from the recommendation (27% agree, 9% neutral, 64% disagree, 1 did not vote). Choice should be based on patient�s preference and management changed if recovery is slow.66

 

Key Question 7: Should low-level laser therapy be used for recent-onset (0-3 months) grade III NAD?

 

Summary of Evidence. One RCT by Konstantinovic et al.67 evaluated the effectiveness of low-level laser therapy (LLLT) delivered 5 times per week for 3 weeks compared with placebo (inactive laser treatment) for recent-onset grade III neck pain. LLLT leads to statistically but not clinically significant improvements in neck pain and disability at 3 weeks compared with placebo. Transitional worsening in pain (20%) and persistent nausea (3.33%) were observed in the LLLT group, whereas no adverse events were reported in the placebo group.

 

The panel determined the overall certainty of the evidence was moderate, with small desirable effects and minor adverse events. LLLT can be expensive. If practitioners choose not to purchase, it may negatively affect health equities. However, the option is acceptable to stakeholders and is relatively easy to implement. The panel was uncertain about the balance between desirable and undesirable consequences and voted against making a recommendation because of a lack of clear evidence (LLLT was no better than placebo but both groups demonstrated within-group change over time).

 

Work Disability Prevention Interventions

 

Key Questions 8 and 9: Should work disability prevention interventions vs fitness and strengthening exercise program be used for recent-onset nonspecific work-related upper limb disorders?�Should work disability prevention interventions be used for recent-onset work-related neck and upper limb complaints?

 

In reviewing the evidence on work disability prevention interventions,41 the GDG concluded that the balance between desirable and undesirable consequences was �closely balanced or uncertain.� As a result, the guideline panel was unable to formulate recommendations for these key questions, yet future research is very likely to either positively or negatively support the various types of work disability prevention interventions.

 

Although some benefits were reported favoring computer-prompted and instructed exercise interventions,68 the incremental self-reported improvement was insufficient to formulate a recommendation considering1 a follow-up period of 8 weeks in reviewed studies is too short to estimate long-term sustained benefits; and2 the potential costs related to programming and worker instruction may be significant.

 

Overall, it appears that adding computer-prompted exercises (with workplace breaks), or workplace breaks alone, to a program of ergonomic modification and education improves self-perceived recovery and symptomatic benefits in computer workers with neck and upper back complaints.41 However, it is unclear whether the addition of computer- prompted exercises to the various established workplace interventions alters perceived or objective health outcomes. Future research may identify added benefits in order for stakeholders to consider the extra cost as being surmountable.

 

Recommendations for Recent-Onset (0-3 Months) Grades I to III WAD

 

Multimodal Care

 

Key Question 10: Should multimodal care vs education be used for recent (0-3 months) grades I to III WAD?

 

Summary of Evidence. A 2-part RCT by Lamb et al.69 evaluated the effectiveness of oral advice compared with written material for improving pain (self-rated neck pain) and disability (NDI) in patients with recent-onset grades I to III WAD. Lamb et al.69 included a total of 3851 participants with a history of WAD grades I to III of less than 6 weeks� duration who sought treatment at an emergency department. A total of 2253 participants received active management advice in the emergency department incorporating oral advice and the Whiplash Book, which included reassurance, exercises, encouragement to return to normal activities, and advice against using a collar;�1598 participants received usual care advice, including verbal and written advice along with anti-inflammatory medication, physiotherapy, and analgesics. No between-group difference was observed in self-rated neck pain and disability at 12-month follow-up and no difference in workdays lost was observed at 4-month follow-up (Table 6).

 

Lamb et al.69 included 599 participants with WAD grades I to III that persisted for 3 weeks after attending emergency departments. Three hundred participants were treated by a physiotherapist (maximum 6 sessions over 8 weeks) including psychological strategies (goal setting or pacing, coping, reassurance, relaxation, pain and recov- ery), self-management advice (posture and positioning), exercises (shoulder complex mobilization and range of motion [ROM]; cervical and scapular stability and proprioception), and cervical and thoracic spine Maitland mobilization and manipulation; a total of 299 received single-session reinforcement advice from a physiothera- pist during their previous visit to emergency department. No difference in self-rated disability was identified at 4-month follow-up; however, greater reductions in workdays lost after 8-month follow-up were determined with self-management advice over single-session rein- forcement. Similar findings were found in an earlier study.70

 

Recommendation: For adult patients with recent (0-3 months) WAD grades I to III, we suggest multimodal care over education alone. (Weak recommendation, moderate-quality evidence)

 

Remark: Multimodal care may consist of manual therapy (joint mobilization, other soft tissue techniques), education, and exercises.

 

Structured Education

 

Key Question 11: Should structured patient education vs education reinforcement be used for recent-onset (0-3 months) WAD?

 

Summary of Evidence. Lamb et al.69 reported outcomes at 4 months for self-rated disability, identifying no clinically significant differences between groups. The study sug- gested that oral advice and an educational pamphlet provide similar benefits.

 

The panel determined moderate quality in the clinical evidence, yet uncertain desirable effects with small, minor, and transient adverse events. Relatively few resources would be required for the intervention, and wide dissemination of educational materials through electronic tools can help reduce inequities. The option is acceptable to stakeholders and feasible to implement. Overall, the desirable consequences probably outweigh the undesirable consequences. The panel determined this topic and its evidence has substantial overlap with Key Question 10. Therefore, one recommendation was made, addressing both topics.

 

Recommendations for Persistent (N3 Months) Grades I to III NAD

 

Exercise

 

Key Question 12: Should supervised exercise (ie, qigong exercise) vs no treatment (wait listing) be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. Two RCTs (Table 7) evaluated the effectiveness of supervised qigong compared with super- vised exercise therapy and no treatment on neck pain (101-point VAS), disability (NDI), and Neck Pain and Disability Scale in a total of 240 patients with chronic neck pain (N6 months). 71,72 Rendant et al. 72 reported that, in adults with chronic neck pain, supervised qigong is more effective than no treatment and as effective as exercise therapy in reducing neck pain and disability at 3 and 6 months. Conclusions regarding the effectiveness of these 2 interventions compared with no treatment in patients aged older than 55 years cannot be drawn from the included studies.

 

In their study of these interventions for neck pain in elderly patients, von Trott et al.71 observed a reduction in pain and disability in both intervention groups at 3 and 6 months (although not statistically significant). The quality of the evidence was downgraded to low based on the SIGN criteria (concealment method not reported). In the von Trott et al. study, the interventions consisted of two 45-minute sessions per week for 3 months (a total of 24 sessions),71 whereas in the Rendant et al. study, interventions consisted of 12 treatments in the first 3 months and 6 treatments in the following 3 months (total of 18 sessions).72 Exercise therapy in both studies included repeated active cervical rotations and strengthening and flexibility exercises in the form of Dantian qigong71 or Neiyanggong qigong.72 Similar minor transient side effects were reported in both the intervention and comparison groups.

 

Recommendation: For adult patients with persistent (N6 months) neck pain grades I to II, we suggest supervised group exercises* to reduce neck pain and disability. (Weak recommendation, moderate-quality evidence)

 

Remark: Patients received 18 to 24 group sessions during a period of 4 to 6 months. Patients considered had a rating of 40/100 on a pain scale (VAS). The intervention group reached suggested MCID level of 10% difference for pain and functional outcomes. *Exercises included qigong or ROM, flexibility, and strengthening exercises. No evidence of significant effect in the elderly population.

 

Key Question 13: Should supervised yoga vs education be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. Yoga is an ancient Indian practice involving postural exercises, breathing control, and med-
itation. 20 One RCT by Michalsen et al. 73 evaluated the effectiveness of Iyengar yoga compared with a self-care/exercise program on neck pain (VAS) and disability (NDI) in 76 patients with chronic neck pain (pain for at least 3 months and a score of more than 40 mm on a 100-mm VAS). Yoga consisted of a weekly 90-minute session for 9 weeks of a wide range of postures aimed to enhance flexibility, alignment, stability, and mobility. The self-care/ exercise group had to practice for 10 to 15 minutes at least 3 times a week a series of 12 exercises focusing on muscle stretching and strengthening and joint mobility. The results indicated that yoga is more effective for reducing neck pain and disability at short term (4 and 10 weeks) than self-care/ exercise (Table 8). No serious adverse events were reported in either group. In this study, the quality of evidence was downgraded to low because blinding was �poorly ad- dressed.�45

 

One RCT by Jeitler et al.74 evaluated the effectiveness of Jyoti meditation compared with exercise on neck pain (VAS). The results showed that Jyoti meditation (sitting motionless, repeating a mantra, and visual concentration while keeping the eyes closed) is more effective than exercise (established and previously used self-care manual for specific exercise and education for chronic neck pain).74 Because Jyoti meditation only includes 1 of the 3 components of yoga (ie, meditation), Jeitler et al.74 was not considered in developing the following recommendation.

 

Recommendation: For patients with persistent (N3 months) grades I to II neck pain and disability, we suggest supervised yoga over education and home exercises for short- term improvement in neck pain and disability. (Weak recommendation, low-quality evidence)

 

Remark: Baseline intensity of pain was more than 40/100 and duration was at least 3 months. Yoga was specific to the Iyengar type, with a maximum of 9 sessions over 9 weeks.

 

Key Question 14: Should supervised strengthening exercises vs home ROM or stretching exercises be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. Three RCTs evaluated the effectiveness of supervised strengthening exercises compared with home exercises for grades I to II neck pain and disability.38 Two RCTs (Hakkinen et al.75 and Salo et al.76) reported no significant between group differences at 1 year for primary or secondary outcomes. One RCT (N = 170) reported that supervised strengthening exercises were more effective than home ROM exercises.77 Two smaller RCTs (N = 107) found that both treatments are equally effective.75,76 All 3 trials had a follow-up of 1 year. Based on our panel�s consensus, outcomes determined to be important in the assessment of effectiveness for these RCTs included pain (NRS) and disability (NDI).

 

In the RCT by Evans et al.77 the strengthening exercise program (delivered by exercise therapists) was determined to be more effective than home exercises. The program�included 20 supervised sessions over a period of 12 weeks and consisted of neck and upper body dynamic resistance strengthening program with and without spinal manipula- tive therapy.77 Conversely, the home exercises included an individualized program of neck and shoulder self- mobilization with initial advice regarding posture and daily activities (Table 9). In the 2 RCTs demonstrating equivalence, the strengthening program included 10 supervised sessions over 6 weeks of isometric exercises for the neck flexors and extensors, dynamic shoulder and upper extremity exercises, abdominal and back exercises, and squats.43,44

 

A fourth RCT by Maiers et al.78 assessed the effectiveness of supervised rehabilitative exercises in combination with and compared with home exercises alone for persistent neck pain in individuals aged 65 years or older. All participants in the study received 12 weeks of care. One group received 20 supervised 1-hour exercise sessions in addition to home exercises. Home exercises consisted of four 45- to 60-minute sessions to improve flexibility, balance, and coordination and enhance trunk strength and endurance. Participants also received instruc- tions on pain management, practical demonstrations of body mechanics (lifting, pushing, pulling, and rising from a lying position), and massaging to stay active. Results favored supervised rehabilitative exercises combined with home exercises over home exercise for pain (NRS) and disability (NDI) at 12 weeks. However, between-group differences did not reach statistical significance.

 

Recommendation: For patients with persistent (N3 months) grades I to II neck pain, we suggest supervised strengthening exercises or home exercises. (Weak recommendation, low-quality evidence)

 

Remark: For reduction in pain, supervised strength- ening exercises, provided along with ROM exercises and advice, were evaluated at 12 weeks within 20 sessions. Home exercises include stretching or self-mobilization.

 

Key Question 15: Should strengthening exercises vs general strengthening exercises be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. Griffiths et al.79 presented non� clinically significant outcomes for neck pain and disability among patients with persistent neck pain and concluded there is no added benefit of incorporating specific isometric exercise to a general exercise program. Dosages were up to 4 sessions per 6-week period, with advice for 5 to 10 times at home. The general exercise program consisted of postural exercise, active ROM, 5 to 10 times daily with reinforcement.

 

The panel determined there is low certainty in the clinical evidence and uncertainty in the desirable effects of the intervention. Isometric exercises have little anticipated adverse effects, require minimal resources, and are generally acceptable to stakeholders and feasible to�implement. Yet uncertainty remains regarding their effects on health equity and the overall balance between desirable and undesirable consequences. More research is needed in this area before a recommendation can be made.

 

Key Question 16: Should combined supervised strengthening, ROM, and flexibility exercises vs no treatment (wait listing) be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. von Trott et al. 71 and Rendant et al. 72 presented significant outcomes for reduction in neck pain and disability that favor combined strengthening, ROM, and flexibility exercises. Both studies address different popula- tions and lead to similar outcomes (von Trott et al.71 addressed elderly populations).

 

The panel determined there was moderate certainty in the clinical evidence, with large desirable and small undesirable anticipated effects. Yet there may be differences in adverse events for strengthening vs ROM and flexibility exercises, along with the chal- lenges of such adverse events being self-reported. For example, strengthening exercises likely coincide with short-term pain after the intervention. Further, signifi- cant space may be required for exercises, which may incur large costs that need to be considered up front. As a result, there is uncertainty about the feasibility to implement and whether this could widely affect health inequalities. However, the option would be acceptable to stakeholders. Overall, the desirable consequences would probably outweigh the undesirable consequences. The panel determined this topic and its evidence has substantial overlap with Key Question 12 (qigong was considered exercise). Therefore, 1 recommendation was made, addressing both topics.

 

Manual Therapy

 

Key Question 17: Should multimodal care vs self-management be used for persistent (N3 months) grades I-II NAD?

 

Summary of Evidence. One RCT by Gustavsson et al.80 evaluated the effectiveness of self-management of persis- tent musculoskeletal tension type neck pain for grades I to II neck pain. They compared treatment effects of a multicom- ponent pain and stress self-management group intervention (n = 77) to individually administered multimodal physical therapy (n = 79). Measures of pain (NRS) and disability (NDI) were collected at baseline and at 10 and 20 weeks. Both groups had within-group differences for decreased pain intensity and disability. At the 20-week follow-up after an average of 7 sessions, based on the measures used, the multicomponent pain and stress self-management group intervention had a greater treatment effect on coping with pain and patients� self-reported pain control and disability than the multimodal care group. The initial treatment effects were largely maintained over a 2-year follow-up period (Table 10).81

 

Recommendation: For patients with persistent (N3 months) neck pain and associated disorders grades I to II, we suggest multimodal care* or stress self-management� based on patient preference, prior response to care, and resources available. (Weak recommendation, low-quality evidence)

 

Remark: *Individualized multimodal care may include manual therapy (manipulation, mobilization, massage, trac- tion), acupuncture, heat, transcutaneous electrical nerve stimulation, exercise, and/or ultrasound. �Stress self-manage- ment may include relaxation, balance and body awareness exercises, pain and stress self-management lectures, and discussion. The multimodal care group received an average of 7 (range 4-8) sessions, compared with 11 (range 1-52) sessions for the stress self-management group over 20 weeks.

 

Education

 

Key Question 18: Should structured patient education vs massage therapy be used for persistent (N3 months) NAD?

 

Summary of Evidence. Sherman et al.82 reported non� clinically significant outcomes at 4 weeks for disability. This study suggests a mailed self-care book and a course in massage therapy provide similar clinical benefits for
patients with persistent neck pain.

 

The panel determined the overall certainty of the evidence was low, with relatively large anticipated effects and no serious adverse events noted from intervention (some headaches possibly). There is uncertainty in the costs required, including necessary staff, equipment, and mate- rials. Yet this option is feasible to implement in most settings and has strong implications for reducing health inequities. As a preventive strategy, the intervention is acceptable to stakeholders, including the chiropractic practitioners, patients, and policymakers. The panel was uncertain about the balance between the desirable and undesirable consequences. Additional high-quality studies are needed in this area before any recommendation can be made.

 

Manual Therapy

 

Key Question 19: Should manipulation be used for persistent grades I to II NAD?

 

Summary of Evidence. Evans et al.77 compared spinal manipulation in addition to 20 weeks of supervised exercise therapy (20 sessions) to supervised exercise therapy alone in adults with persistent grades I to II neck pain, whereas Maiers et al.78 compared spinal manipulation in addition to home exercises (20 sessions maximum) to home exercise alone in seniors with persistent grades I to II neck pain. Pain and disability outcomes at 12 and 52 weeks did not reach statistical significance in between-group differences, except for pain level at 12 weeks in the Maiers study.78 A third RCT by Lin et al.83 allocated 63 persistent neck pain patients (NAD I-II) to the experimental group (n = 33) treated with�cervical spine manipulation and traditional Chinese massage (TCM) compared with TCM alone (n = 30) over 3 weeks. Results favored cervical manipulation with TCM over TCM alone for pain (NPS) and disability (Northwick Park Neck Disability Questionnaire) at 3 months (Table 11).

 

The panel concluded low certainty in the evidence, with small desirable and undesirable effects of the intervention. Few resources are required for the intervention, and it is probably acceptable to stakeholders and feasible to implement. Although the panel decided the desirable and undesirable consequences were closely balanced, the following statement was provided.

 

Recommendation: For patients with persistent grades I to II NAD, we suggest manipulation in conjunction with soft tissue therapy. (Weak recommendation, low-quality evidence)

 

Remark: Evaluated after eight 20-minute sessions (over a 3-week period). Does not include manipulation as a standalone treatment.

 

Manual Therapy

 

Key Question 20: Should massage vs no treatment (wait listing) be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. Sherman et al.82 and Lauche et al.84 reported non�clinically significant differences in outcomes for disability at 4 and 12 weeks, respectively. Sherman et al.82 suggested Swedish and/or clinical massage with verbal self- care advice provides similar clinical benefit to a self-care book for disability outcomes. Lauche et al.84 suggested cupping massage and progressive muscle relaxation lead to similar changes in disability. Sherman et al.85 reported outcomes for neck pain and disability at 4 weeks and suggested that higher doses of massage provide superior clinical benefit (Table 12).

 

The panel determined low certainty in the evidence, with small desirable and undesirable effects. Additional costs may be needed to get clinical benefit. Sherman et al.85 suggested a minimum of 14 hours of staff time needed. Because of the costs associated with high-dose massage, it may not be entirely acceptable to patients or payors. However, this option is feasible and relatively easy to implement in educated and affluent populations similar to subjects primarily studied.85 Overall, the panel decided the desired consequences probably outweigh the undesirable consequences and suggest offering this option.

 

Recommendation: For patients with persistent (N3 months) grades I to II NAD, we suggest high-dose massage over no treatment (wait listing) based on patient preferences and resources available. (Weak recommendation, low-quality evidence)

 

Remark: Interventions were given 3 times for 60 minutes a week for 4 weeks. Lower dosages and duration did not have therapeutic benefit, and we cannot suggest offering as an option.

 

Passive Physical Modalities

 

Key Question 21: Should LLLT be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. After full-text screening and review, no studies addressing between-group differences among outcomes of pain or disability were included to inform this key question. The lack of evidence and uncertainty in the overall balance between desirable and undesirable consequences led the panel to decide not to write a recommendation for this topic at this time. More high-quality studies are needed in this area before certainty in judgments or recommendations can be made.

 

Key Question 22: Should transcutaneous electrical nerve stimulation vs multimodal soft tissue therapy program be used for persistent (N3 months) grades I to II NAD?

 

Summary of Evidence. After full-text screening and review, no studies addressing between-group differences among outcomes of pain or disability were included to inform this key question. The lack of evidence and uncertainty in the overall balance between desirable and undesirable consequences led the panel to decide not to write a recommendation for this topic at this time. More high quality studies are needed in this area before certainty in judgments or recommendations can be made.

 

Key Question 23: Should cervical traction be used for grade III NAD (variable duration)?

 

Summary of Evidence. After full-text screening and review, no studies addressing between-group differences among outcomes of pain or disability were included to inform this key question. The lack of evidence and uncertainty in the overall balance between desirable and undesirable consequences led the panel to decide not to write a recommendation for this topic at this time. More high-quality studies are needed in this area before certainty in judgments or recommendations can be made.

 

Multimodal Care

 

Key Question 24: Should multimodal care vs continued practitioner care be used for persistent grades I to III NAD?

 

Summary of Evidence. One RCT by Walker et al.86 evaluated the effectiveness of multimodal care for neck pain with or without unilateral upper extremity symptoms (grades I-III). They compared treatment effects of combined multimodal care and home exercises (n = 47) to multimodal minimal intervention (n = 47). Both intervention groups received on average of 2 sessions per week for 3 weeks. No interventions were rendered after 6 weeks. Baseline self- reported questionnaires included neck and arm pain (VAS) and disability (NDI). All measures were repeated at 3, 6, and 52 weeks. Patients in the multimodal care and home exercise group had significantly greater reduction in short-term neck pain and in short-term and long-term disability compared with the multimodal minimal interven- tion group (Table 13). A secondary analysis of the Walker et al. study87 determined that patients receiving both�cervical thrust and nonthrust manipulations did no better than the group receiving cervical nonthrust manipulations only. This underpowered secondary analysis prohibits any definitive statement regarding the presence or absence of a treatment advantage of one approach over the other. The reduction in pain reported by Walker�s multimodal care and exercise group compared favorably to the change scores reported by other studies, including Hoving et al.88,89

 

In an RCT, Monticone et al.90 evaluated the effective- ness of multimodal care for persistent neck pain. They compared treatment effect of multimodal care alone (n = 40) to multimodal care in conjunction with cognitive behavioral treatment (n = 40). Both groups had a reduction in pain (NRS) and disability (NPDS), but there were no clinically significant differences between the groups at 52 weeks. The addition of a cognitive behavioral treatment did not provide greater outcomes than multimodal care alone.

 

Recommendation: For patients presenting with persistent neck pain grades I to III, we suggest clinicians offer multimodal care* and/ or practitioner advice based on patient preference. (Weak recommendation, low-quality evidence)

 

Remark: *Multimodal care and exercises may consist of thrust/nonthrust joint manipulation, muscle energy, stretching, and home exercises (cervical retraction, deep neck flexor strengthening, cervical rotation ROM). �Multimodal minimal intervention may consist of postural advice, encouragement to maintain neck motion and daily activities, cervical rotation ROM exercise, instructions to continue prescribed medication, and therapeutic pulsed (10%) ultrasound at 0.1 W/cm2 for 10 minutes applied to the neck and cervical ROM exercises.

 

Exercise

 

Key Question 25: Should group exercises vs education or advice be used for workers with persistent neck and shoulder pain?

 

Summary of Evidence. We have combined the key questions for �Should structured patient education vs exercise programs be used for persistent neck pain and associated disorders in workers?� and �Should workplace-based exercises vs advice be used for neck pain in workers?� One large cluster RCT (n = 537) by Zebis et al.91 evaluated the effectiveness of strength training in the workplace compared with receiving advice to stay physically active on nonspecific neck and shoulder pain intensity. The findings indicated a similar reduction in neck and shoulder pain intensity at 20 weeks for the exercise program compared with advice (Table 14). The intervention consisted of 3 sessions per week, each lasting 20 minutes, for up to 20 weeks (total of 60 sessions).

 

The workplace exercise program consisted of high- intensity strength training relying on principles of progres- sive overload and involved local neck and shoulder muscles strengthening with 4 different dumbbell exercises and 1 exercise for the wrist extensor muscles. More than 15% of�workers assigned to the workplace exercise group reported minor and transient complaints. The comparison group reported no adverse events.

 

A subgroup analysis92 of the primary Zebis et al. study91 included 131 women with a baseline neck pain rating of at least 30 mm VAS from the 537 male and female participants. Results favored specific resistance training over advice to stay active for pain (VAS) at 4 weeks. This study was not included because findings were already considered in the primary study.

 

Recommendation: For workers with persistent neck and shoulder pain, we suggest mixed supervised and unsupervised high- intensity strength training or advice alone. (Weak recommendation, moderate-quality evidence)

 

Remark: For reduction in pain intensity, 3 sessions per week, each lasting 20 minutes, over a 20-week period. Exercise includes strengthening. Extra resources are likely required for complete exercise intervention implementation.

 

Structured Patient Education

 

Key Question 26: Should structured patient education vs exercise programs be used for persistent (N3 months) NAD in workers?

 

Summary of Evidence. Andersen et al.93 reported non� clinically significant outcomes at 10 weeks for neck and shoulder pain, suggesting weekly e-mailed information on general health behaviors and shoulder abduction exercise programs provide similar clinical benefit. Yet implementa- tion of high-intensity strength training exercises in industrial workplaces (implementation of exercise into day-to-day life and to increase active leisure time) is generally supported.94,95 In another RCT, pain reduction was significantly greater than in the group receiving advice alone. 91 Findings from Zebis et al. 91 are also included in the exercise intervention section of this guideline.

 

The panel determined moderate certainty in the clinical evidence, with small desirable and undesirable effects of the intervention. The resources required are relatively small, assuming the practitioner presents the education to the patient. Health inequities would be positively affected, and the intervention would be acceptable to stakeholders and feasible to implement. The panel decided not to repeat these findings in the current section. The panel felt that the benefits of increasing the frequency and intensity of exercise regimes was not restricted to those working in an industrial environment or to any specific population subgroup with the exception of older adults.

 

Work Disability Prevention Interventions

 

Key Questions 27-29: Should work-based hardening vs clinic-based hardening be used for persistent (N3 months) work-related rotator cuff tendinitis? Should work disability prevention interventions be used for persistent neck and shoulder pain?�Should work disability prevention interventions be used for persistent (N3 months) upper extremity symptoms?

 

Table 16 Treatment Interventions Not to be Offered for NAD

 

Summary of Evidence. In reviewing the evidence on work disability prevention interventions,41 the GDG concluded that the balance between desirable and undesirable consequences was �closely balanced or uncertain� for Key Questions 27-29. As a result, the guideline panel was unable to formulate recommendations for these key questions, yet future research is very likely to either positively or negatively support the various types of work disability prevention interventions.

 

Recommendations for Persistent (N3 Months) Grades I to III WAD Exercise

 

Key Question 30: Should supervised general exercise and advice vs advice alone be used for persistent (N3 months) grades I to II WAD?

 

Summary of Evidence. In an RCT, Stewart et al. (2007)96 evaluated the effectiveness of 3 advice sessions alone compared with 3 advice sessions combined with 12 exercise sessions over 6 weeks on neck pain (NRS) and disability�(NDI) among 134 patients with persistent grades I to II WAD. The results, presented in Table 15, indicated that supervised exercises with advice are as effective as advice alone at long term (12 months). Advice included standardized education, reassurance, and encouragement to resume light activity and consisted of 1 consultation and 2 follow-up phone contacts. However, the quality of the evidence was downgraded to low based on SIGN criteria (randomization and outcome measurement were �poorly addressed�) and the low number of participants and events.45

 

A pragmatic trial assigned 172 patients with persistent WAD grades I to II to receive a comprehensive 12-week exercise program (20 sessions including manual therapy technique the first week [no manipulation] and cognitive behavioral therapy delivered by physiotherapists) or advice (1 session and telephone support).97 The comprehensive exercise program was not more effective than advice alone for pain reduction or disability, although findings favored a comprehensive physiotherapy exercise program over advice.

 

The panel determined low certainty in the evidence, with small desirable and undesirable effects and no serious adverse events (5 patients who received the comprehensive exercise program and 4 who received advice had minor transient adverse events). Overall, the panel decided the balance between the desirable and undesirable conse- quences such as costs was uncertain, and more evidence is needed before a recommendation can be made.

 

In a 20-week cluster RCT, Gram et al. (2014)98 randomly assigned 351 office workers to 2 training groups receiving the same total amount of planned exercises 3 times per week, with 1 group supervised throughout the intervention period and the other receiving minimal supervision only initially, and a reference group (without exercise). Although results indicated that supervised training at the workplace reduced neck pain, results were not clinically significant and both training groups improved independently of the extent of supervision. The panel decided not to consider this study in formulating a recommendation because exercise was not directly com- pared with advice and an important loss to follow-up occurred across groups. Although supervised exercise appears to be beneficial, costs can be high. This could possibly be mitigated, however, by offering group treat- ment, which may increase compliance and accountability with a supervised group.

 

Recommendation: For patients with persistent (N3 months) grades I to II WAD, we suggest supervised exercises with advice or advice alone based on patient preference and resources available. (Weak recommendation, low-quality evidence)

 

Remark: Extra resources may be required for supervised exercises.

 

Multimodal Care

 

Key Question 31: Should multimodal care vs self- management program be used for persistent (N3 months) grade II WAD?

 

Summary of Evidence. Jull et al.99 reported no clinically or statistically significant outcomes for pain and disability at 10 weeks. They suggested that multimodal care (exercises, mobilization, education, and ergonomic advice) provided similar outcomes to a self-management program based on an educational booklet (mechanism of whiplash, reassur- ance of recovery, stay active, ergonomic advice, exercise). Care did not include high-velocity manipulation. Although this study is specific to physiotherapists, it is well within the scope of chiropractors (manual therapists).

 

One other RCT by Jull et al.100 evaluated the effectiveness of multidisciplinary individualized treat- ments for patients with acute whiplash (b4 weeks postinjury). Patients randomly assigned to pragmatic intervention (n = 49) could receive medication including opioid analgesia, multimodal physiotherapy, and psy- chology for post-traumatic stress over 10 weeks. No significant differences in frequency of recovery (NDI ? 8%) between pragmatic and usual care groups was found at 6 or 12 months. There was no improvement in current nonrecovery rates at 6 months (63.6%, pragmatic care; 48.8%, usual care), indicating no advantage of the early multiprofessional intervention.

 

The panel determined low certainty in the clinical evidence, with small desirable and undesirable effects reported. Yet there were relatively small costs and resources required to implement the intervention. Electronic dissem- ination of the educational component of multimodal care may reduce health inequities. The option may be acceptable to clinicians (assuming collaborative care approaches), policymakers, and patients and is likely feasible to implement in usual care settings. Overall, the balance between the desirable and undesirable consequences is uncertain, and no recommendation is given at this time. Further studies need to be conducted in this area and should involve multimodal care including high-velocity proce- dures or manipulation.

 

Education

 

Key Question 32: Should structured patient education vs advice be used for persistent (N3 months) WAD?

 

Summary of Evidence. Stewart et al. (2007)96 reported non�clinically significant between differences for pain and disability outcomes at 6 weeks. This study suggested that adding a physiotherapy-based graded exercise program to a structured advice intervention provided similar clinical benefit as structured education alone.

 

The panel determined low certainty of the evidence, with low desirable and undesirable anticipated effects. The main complaints were muscle pain, knee pain, and spinal pain with mild headaches.96 The small resources required for the intervention may reduce health inequities, and the option is acceptable to stakeholders and feasible to implement in most settings.

 

The panel determined that this key question had substantial overlap with Key Question 5 and decided to make 1 recommendation addressing both topics.

 

Discussion

 

This evidence-based guideline establishes the best practice for the management of NAD and WAD resulting from or aggravated by a motor vehicle collision and updates 2 previous guidelines on similar topics.24,25 This guideline covers recent-onset (0-3 months) and persistent (N3 months) NADs and WADs grades I to III. It does not cover the management of musculoskeletal thoracic spine or chest wall pain.

 

The primary outcomes reported in the selected studies were neck pain intensity and disability. Although all recommendations included in this guideline are based on low risk of bias RCTs, the overall quality of evidence is generally low considering other factors considered by GRADE such as imprecision, and thus the strength of recommendations is weak at this time. Weak recommen- dations mean that clinicians need to devote more time to the process of shared decision making and ensure that the informed choice reflects patient values and preferences.56 Interventions not described in this guideline cannot be recommended for the management of patients with NAD or WAD because of a lack of evidence about their effective- ness and safety (Table 16).

 

A recent systematic review and meta-analysis by Wiangkham (2015)101 on the effectiveness of conservative management for acute WAD grade II included 15 RCTs, all assessed as high risk of bias (n = 1676 participants), across 9 countries. Authors concluded that conservative interven- tions (noninvasive treatment), including active mobilization exercises, manual techniques, physical agents, multimodal therapy, behavioral approaches, and education, are gener- ally effective for recent-onset WAD grade II to reduce pain in the medium and long term and to improve cervical ROM in the short term compared with standard or control intervention.101 Although findings from the Wiangkham review are generally in line with those from the systematic reviews we included in this guideline,24,25 the pooling of high risk of bias and of clinically heterogeneous trials seriously challenges the validity of this more recent review.

 

Similarities and Differences With Recommendations by the OPTIMa Collaboration

 

First, the recommendations for the management of minor injuries of the neck were recently released by the Ministry�of Finance of Ontario in collaboration with the OPTIMa Collaboration 20 and published as a separate guideline. 27 They considered the risks of bias of included RCTs using the SIGN criteria45 and the guideline recommendations developed using the modified OHTAC framework,28 based on 3 decision determinants1: overall clinical benefit (evidence of effectiveness and safety) 2 ; value for money (evidence of cost-effectiveness where available); and3 consistency with expected societal and ethical values. In the current guideline, we used the GRADE approach, which, in addition to considering risk of bias of included RCTs, takes into account 4 other factors (imprecision, inconsistency, indirectness, publication bias) to rate the confidence in effect estimates (quality of evidence) for each outcome.102 As a result of imprecision of estimates in several RCTs, the overall quality of admissible studies was deemed low. GRADE considers similar decision determi- nants as the modified OHTAC to develop recommendations when subsequently making an overall rating of confidence in effect estimates across all outcomes based on those outcomes considered critical to a particular recommenda- tion.56 Accordingly, the guideline panel was asked to consider this low quality of evidence when judging the �desirable� consequences. When the benefits of important outcomes slightly outweighed undesirable effects of the intervention, a weak recommendation was made (ie, suggestions for care). This is likely to involve ensuring patients understand the implications of the choices they are making, possibly using a formal decision aid.56 However, if the judgment was �closely balanced or uncertain,� no recommendation could be made.

 

Second, OPTIMa 20 recommended that interventions should only be provided in accordance with published evidence for effectiveness, including parameters of dosage, duration, and frequency, and within the most appropriate phase. The emphasis during the early phase (0-3 months) should be on education, advice, reassurance, activity, and encouragement. Health care professionals should be encouraged to consider watchful waiting and clinical monitoring as evidence-based therapeutic options during the acute phase. For injured persons requiring therapy, time-limited and evidence-based interventions should be implemented on a shared decision-making basis, an approach that equally applies to patients in the persistent phase (4-6 months). Despite using slightly different methods to derive recommendations, the 2 processes generally led to similar guidance.

 

Third, OPTIMa20 reported that the following interven- tions are not recommended for recent-onset NAD: struc- tured patient education alone (either verbal or written); strain-counterstrain or relaxation massage; cervical collar; electroacupuncture (electrical stimulation of acupuncture points with acupuncture needles or electrotherapy applied to the skin), a topic not covered in our guideline; electric muscle stimulation; heat (clinic based). Similarly for�persistent NAD, programs solely of clinic-based supervised high-dose strengthening exercises, strain-counterstrain or relaxation massage, relaxation therapy for pain or disability outcomes, transcutaneous electrical nerve stimulation (TENS), electric muscle stimulation, pulsed shortwave diathermy, heat (clinic based), electroacupuncture, and botulinum toxin injec- tions are not recommended. In contrast, based on the RCT by Zebis et al.91 the current guideline suggests offering multimodal care and/or patient education for industrial workers presenting with neck pain grades I to III. Although structured patient education used alone cannot be expected to yield large benefits for patients with neck pain, this strategy may be of benefit during the recovery of patients with persistent WAD when used as an adjunct therapy.40 For persistent neck pain (grades I-II), Gustavsson et al.80 reported that multimodal care combining manual therapy (spinal manipulation, mobilization, massage, traction) and passive modalities (heat, TENS, exercise, and/or ultrasound) reduced neck disability. It should be noted, however, that past reviews were unable to make any definitive conclusions about the effectiveness of TENS as an isolated treatment for acute pain 103 or chronic pain 104 in adults, nor about the effectiveness of heat therapy.105,106

 

A comparison of the recommendations with 2 previous chiropractic guidelines 24,25 reveals that a multimodal approach including manual therapy, advice, and exercise remains the overall recommended strategy of choice for the treatment of neck pain. However, treatment modalities included in recommended multimodal care differed accord- ing to the quality of the evidence available at the time. The 2010 guideline on the management of WAD developed treatment recommendations based on low-quality evidence from 8 available RCTs and 3 cohort studies.25 Overall, recommendations for recent and persistent WAD are similar (multimodal care, and supervised exercise and multidisciplinary care, respectively). The 2014 guideline on neck pain24 developed 11 treatment recommendations from 41 RCTs. The current guideline developed 13 recommenda- tions from 26 low risk of bias RCTs. In line with the 2014 guideline24 for recent-onset neck pain, the current recom- mendations suggest offering multimodal care including mobilization, advice, and exercises. The current guideline recommendations also suggest offering supervised graded strengthening and stability exercises. Similar to the 2014 guideline for persistent neck pain (grades I-II),24 the current recommendations suggest offering multimodal care consisting of manual therapy (spinal manipulation therapy or mobilization) and exercises. Details on specific exercise modalities are now provided, including suggestions for supervised and unsuper- vised exercises, strength training, and supervised group exercises such as workplace exercise programs and supervised yoga.

 

Adverse Events

 

This guideline did not specifically review the evidence on adverse events from treatments. However, in the review�by Wong et al.42 on manual therapy and passive modalities, 22 of the low risk of bias RCTs addressed the risk of harm from conservative care. Most adverse events were mild to moderate and transient (mostly increased stiffness and pain at the site of treatment, with a mean rate of about 30%). No serious neurovascular adverse events were reported. Another review of published RCTs and prospective cohort studies confirmed that around half of people treated with manual therapy can expect minor to moderate adverse events after treatment, but that the risk of major adverse events is small.107 The pooling of data from RCTs of manual therapy on the incidence of adverse events indicated that the relative risk of minor or moderate adverse events was similar for manual therapy and exercise treatments, and for sham/passive/control interventions.

 

A patient-centered holistic and collaborative view of the needs of the patient with pain and disability is encouraged. 108,109 Although chiropractors are not responsible for pharmacologic management, they should have sufficient knowledge about pharmacologic agents and their adverse events. One eligible RCT22 found home exercises and advice to be as effective as medication (acetaminophen, NSAIDs, muscle relaxant, and opioid analgesic) in reducing pain and disability at short term for patients with acute or subacute neck pain grades I to II. However, medication was associated with a higher risk for adverse events. Of interest, recent evidence suggests that acetaminophen is not effective for managing low back pain,110,111 and the effectiveness of long-term opioid therapy for improving chronic pain and function is uncertain.64 However, a dose-dependent risk for serious harms is associated with long-term use of opioid (increased risk for overdose, opioid abuse and dependence, fractures, myocardial infarction, and use of medications to treat sexual dysfunction).64 Risk of unintentional opioid overdose injury appears to be particularly important in the first 2 weeks after initiation of long-acting agents.112,113

 

Recommendations

 

I. Stakeholders

 

Choosing a Care Provider. A range of health care providers (chiropractors, general medical practitioners, physiothera- pists, registered massage therapists, and osteopaths) deliver care for NADs and WADs.108,114 Considering the level of skills required to deliver manual therapy, including spinal manipulative therapy and other forms of therapies (eg, prescription of specific exercise) and based on individual patient preference, cervical spine manipulation as part of multimodal care should be delivered by properly trained licensed professionals. 115

 

II. Practitioners

 

Best Practice Recommendations-Initial Assessment and Monitoring.

 

This guideline specifically addresses the treatment of NAD and WAD grades I to III. Importantly, our panel supports�the following 5 best practice recommendations on patients care outlined in the OPTIMa guideline27: Clinicians should1 rule out major structural or other pathologic conditions as the cause of neck pain�associated disorders before classifying as grade I, II, or III2; assess prognostic factors for delayed recovery3; educate and reassure patients about the benign and self-limited nature of the typical course of NAD grades I to III and the importance of maintaining�activity and movement4; refer patients with worsening symptoms and those who develop new physical or psychological symptoms for further evaluation at any time during their care; and5 reassess the patient at every visit to determine whether additional care is necessary, the condition is worsening, or the patient has recovered. Patients reporting significant recovery should be discharged. Similar recommendations were formulated by the Neck Pain Task Force116 and in prior practitioner guides on the management of WAD and NAD by chiropractors.24,25

 

Benefits of Physical Activity and Self-management. Educating patients about the benefits of being physically active and participating in their care has become the standard of care internationally. Despite the benefits of therapeutic exercise for managing chronic neck pain and the strong evidence favoring regular physical activity to reduce related comorbidities, care providers fail to routinely prescribe these to patients.117-120 When prescribed, the amount of supervision and types of exercises do not follow practice guidelines and are not linked to the degree of patient impairment.118,121 On the patient side, adherence to prescribed exercise programs is often low. 122

 

The promotion of physical activity, including exercise, is a first-line treatment considered important in the prevention and treatment of musculoskeletal pain and its related comorbidities (eg, coronary heart disease, type 2 diabetes, and depression).123-126 For a minority of patients with chronic spine pain, clinician-delivered interventions and pharmacologic treatments are appropriate; and in fewer cases, multidisciplinary pain management or surgery may be indicated. 118

 

People with musculoskeletal pain will often adopt an inactive lifestyle. Unfortunately, physical inactivity is associated with important adverse health effects, including increased risks of coronary heart disease, type 2 diabetes, and breast and colon cancers, and shorter life expectancy in general.127 The World Health Organization128 provided clear guidance on physical activity for health for children, adults, and elders. In addition, recent research suggests that WAD patients with high levels of passive coping�strategies have slower pain and disability recovery.129 Self-management support (SMS) strategies aimed at increasing physical activity and active coping strategies are key to effectively managing spinal pain and related comorbidities. 124,125,130-134 The CCGI developed a theory-based knowledge translation (KT) intervention targeting identified barriers to professional behavior change to increase the uptake of SMS strategies among Canadian chiropractors.135 Interviews of clinicians identified 9 theoretical domains as likely relevant (ie, factors perceived to influence the use of multimodal care to manage nonspecific neck pain).135 The intervention, comprising a webinar and a learning module on Brief Action Planning, is a highly structured SMS strategy that allows patient- centered goals136 and is being pilot-tested among Canadian chiropractors (ongoing pilot trial).137 Care providers are encouraged to perform periodic clinical revaluations and to monitor patient progression of self-management strategies while discouraging dependence on passive treatment.

 

Figure 6 Algorithm of Recommendations for Managing NAD

 

Figure 7 Algorithm of CCGI Recommendations for WAD

 

Figure 8 CCGI Patient Information Sheet

 

III. Research

 

Overall, the quality of the research on conservative management of NADs and WADs remains low, partly explaining that only weak recommendations could be formulated for clinical practice. Further, the reporting of RCTs remains suboptimal. 138 Past recommendations for improving the quality of the research still apply.24,25 Future research should aim to clarify the role of spinal manipulation therapy alone or as part of multimodal care for the management of recent neck pain and have adequate frequency and length of follow-up. For instance, a large number of patient visits to the emergency departments each year are for acute neck and arm pain resulting from WADs.14,139 A small RCT suggested that cervical spine manipulation is a reasonable alternative to intramuscular NSAID for immediate pain relief in these patients.63 However, the small sample size, comparison of a single session of spinal manipulation to an NSAID injection, and a 1-day follow-up was not representative of clinical practice.

 

Few recent adequately controlled high-quality research studies of chiropractic care for NADs have been published. In addition, studies included in the reviews did not estimate the maximum therapeutic benefits (ie, best dosage for treatment under evaluation). Well-designed clinical trials with sufficient numbers of participants, longer-term treatments, and follow-up periods are needed to increase the confidence in the recommendations and to advance our understanding of effective and cost-effective conservative care, and spinal manipulation, for the management of patients with NADs and WADs.

 

Dissemination and Implementation Plan. Evidence-based practice aims to improve clinical decision making and patient care.140,141 When followed, CPGs have the potential to improve health outcomes and the efficiency of the health care system.142-144 However, low adherence to CPGs has been noted across health care sectors145 and in the management of musculoskeletal conditions, including NADs and WADs.77,101,102 Such gaps contribute to wide geographic variations in the use and quality of health care services. 146

 

Efforts to bridge the �research-practice gap� have led to a growing interest in KT.145,147 Knowledge translation is defined as the exchange, synthesis, and ethically sound application of knowledge to improve health and provide more effective health services. 148 Knowledge translation aims to bridge the research-practice gap and improve patient outcomes by promoting the integration and exchange of research and evidence-based knowledge into clinical practice.

 

To prepare for guideline implementation, we considered the Guideline Implementation Planning Checklist 149 and�available strategies and supporting evidence141,150 to increase guideline uptake. Although effects of KT inter- ventions tend to be modest, they are likely important at a population health level.37

 

To raise awareness, chiropractic professional organiza- tions are encouraged to inform their members of new CCGI guidelines and tools easily accessible on our website (www. chiroguidelines.org). The guideline implementation tools framework was used to clarify the objectives of the tools; identify end users and the context and setting where tools will be used; provide instructions for use; and describe methods to develop the tools and related evidence and to evaluate the tools.151 Implementation tools designed to increase guideline uptake include practitioner and patients� handouts (Fig. 8, Appendix 7); algorithms (Figs. 6 and 7), webinars, videos, and learning modules (www.cmcc. ca/CE); point-of-care checklists; and health status reminders.152-154 The CCGI has established a network of opinion leaders across Canada (www.chiroguidelines.org). Based on successful efforts to implement a WAD guideline in Australia using opinion leaders among regulated physiotherapists, chiropractors, and osteopaths, 155 the CCGI is planning a series of implementation studies among Canadian chiropractors.137 We will also pilot within chiropractic practice-based research networks.156 Monitor- ing guideline use in chiropractic is challenging because the use of electronic health records to routinely collect clinical practice information is not common in Canada and those using electronic health records often collect different indicators. 157 Nonetheless, the frequency of downloads (posting of the open access guideline on the CCGI website) and number of registering participants and completion of educational online material (webinar, video, and learning module) will be monitored monthly as proxy measures of guideline uptake.

 

Guideline Update

 

The methods for updating the guideline will be as follows: 1) Monitoring changes in evidence, available interventions, importance and value of outcomes, resources available or relevance of the recommendations to clinicians (limited systematic literature searches each year for 3-5 years and survey to experts in the field annually): 2) assessing the need to update (relevance of the new evidence or other changes, type and scope of the update); and 3) communi- cating the process, resources, and timeline to the Guideline Advisory Committee of the CCGI, who will submit a recommendation to the Guideline Steering Committee to make a decision to update and schedule the process.158-163

 

Strengths and Limitations

 

Shortcomings for this guideline include the low quantity and quality of supporting evidence found during the searches. Most of the downgrading of evidence supporting the outcomes occurred because of imprecision. In addition, our updated search of the published reports included 2 databases (Medline and Cochrane Central Register of Controlled Trials) but was limited to the English published reports, which possibly excluded some relevant studies. This, however, is an unlikely source of bias.164,165 Qualitative studies that explored the lived experience of patients were not included. Thus, this review cannot comment on how patients valued and experi- enced their exposure to manual therapies or passive physical modalities. Although the composition of the guideline panel was diverse, with experienced methodologists, expert clini- cians, and stakeholder and patient representatives, only 1 member was from another health discipline (physiotherapist). The scope of this guideline focused on selected outcomes such as pain and disability, although included studies assessed several additional outcomes.

 

Conclusion

 

This CPG supersedes the original (2005) and revised (2014) neck pain guideline as well as the 2010 whiplash-associated guidelines produced by the Canadian Chiropractic Association (CCA); Canadian Federation of Chiropractic Regulatory and Educational Accrediting Boards (CFCREAB).

 

People should receive care based on evidence-based therapeutic options. Based on patient preference and resources available, a mixed multimodal approach includ- ing manual therapy and advice about self-management and exercise (supervised/unsupervised or at home) may be an effective treatment strategy for recent-onset and persistent NAD and WAD grades I to III. Progress should be regularly monitored for evidence of benefit, in particular on the basis of pain alleviation and reduction of disability.

 

Funding Sources and Conflicts of Interest

 

Funds provided by the Canadian Chiropractic Research Foundation. The views of the funding body have not influenced the content of the guideline. No conflicts of interest were reported for this study.

 

Guideline Disclaimer

 

The evidence-based practice guidelines published by the CCGI include recommendations intended to optimize patient care that are informed by a systematic review of evidence and an assessment of the benefits and harms of alternative care options.21 Guidelines are intended to inform clinical decision making, are not prescriptive in nature, and do not replace professional chiropractic care or advice, which always should be sought for any specific condition. Furthermore, guidelines may not be complete or�accurate because new studies that have been published too late in the process of guideline development or after publication are not incorporated into any particular guideline before it is disseminated. CCGI and its working group members, executive committee, and stakeholders (the �CCGI Parties�) disclaim all liability for the accuracy or completeness of a guideline, and disclaim all warranties, expressed or implied. Guideline users are urged to seek out newer information that might impact the diagnostic and/or treatment recommendations contained within a guideline. The CCGI Parties further disclaim all liability for any damages whatsoever (including, without limitation, direct, indirect, incidental, punitive, or consequential damages) arising out of the use, inability to use, or the results of use of a guideline, any references used in a guideline, or the materials, information, or procedures contained in a guideline, based on any legal theory whatsoever and whether or not there was advice of the possibility of such damages.

 

Through a comprehensive and systematic literature review, CCGI evidence-based CPGs incorporate data from the existing peer-reviewed literature. This literature meets the prespecified inclusion criteria for the clinical research question, which CCGI considers, at the time of publication, to be the best evidence available for general clinical information purposes. This evidence is of varying quality from original studies of varying methodological rigor. CCGI recommends that performance measures for quality improvement, performance-based reimbursement, and public reporting purposes should be based on rigorously developed guideline recommendations.

 

Contributorship Information

 

Ncbi.nlm.nih.gov/pubmed/27836071

 

Practical Applications

 

  • A multimodal approach including manual therapy, self-management advice, and exercise can be an effective treatment strategy for recent-onset and persistent neck pain and whiplash-associated disorders.

 

Acknowledgements

 

We thank the following people for their contributions to this paper: Dr. John Riva, DC, observer; Heather Owens, Research Coordinator, proofreading; Cameron McAlpine (Director of Communication & Marketing, Ontario Chiro- practic Association), for assistance in producing the companion document intended for patients with NAD; members of the guideline panel who served on the Delphi consensus panel, who made this project possible by generously donating their expertise and clinical judgment.

 

Appendixes and Other Information

 

Ncbi.nlm.nih.gov/pubmed/27836071

 

In conclusion, whiplash-associated disorders can cause damage to the complex structures of the cervical spine, or neck, because the sheer force of an impact can extend the soft tissues beyond their natural range of motion. Many healthcare professionals can safely and effectively treat whiplash as well as other automobile accident injuries. The results of the article above demonstrate that a multimodal approach, including manual therapy, self-management advice and exercise can be an efficient treatment strategy for both recent-onset and persistent neck pain caused by whiplash-associated disorders.�Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Back Pain

 

According to statistics, approximately 80% of people will experience symptoms of back pain at least once throughout their lifetimes. Back pain is a common complaint which can result due to a variety of injuries and/or conditions. Often times, the natural degeneration of the spine with age can cause back pain. Herniated discs occur when the soft, gel-like center of an intervertebral disc pushes through a tear in its surrounding, outer ring of cartilage, compressing and irritating the nerve roots. Disc herniations most commonly occur along the lower back, or lumbar spine, but they may also occur along the cervical spine, or neck. The impingement of the nerves found in the low back due to injury and/or an aggravated condition can lead to symptoms of sciatica.

 

blog picture of cartoon paperboy big news

 

EXTRA IMPORTANT TOPIC:�Neck Pain Treatment El Paso, TX Chiropractor

 

 

MORE TOPICS: EXTRA EXTRA: El Paso, Tx | Athletes

 

Blank
References

1. Ferrari R, Russell A. Regional musculoskeletal conditions: neck pain. Best Pract Res Clin Rheumatol. 2003;17(1):57-70.
2. Hogg-Johnson S, van der Velde G, Carroll LJ, et al. The burden and determinants of neck pain in the general population: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine.
2008;33(4 Suppl):S39-S51.
3. Holm L, Carroll L, Cassidy JD, et al. The burden and
determinants of neck pain in whiplash-associated disorders after traffic collisions: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;33(4 Suppl):S52-S59.
4. Co?te? P, van der Velde G, Cassidy JD, et al. The burden and determinants of neck pain in workers: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;33(4 Suppl): S60-S74.
5. Vos T, Flaxman A, Naghavi M, et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380(9859): 2163-2196.
6. Co?te? P, Cassidy JD, Carroll L. The treatment of neck and low back pain: who seeks care? Who goes where? Med Care. 2001;39(9):956-967.
7. Hoy DG, Protani M, De R, Buchbinder R. The epidemi- ology of neck pain. Best Pract Res Clin Rheumatol. 2010; 24(6):783-792.
8. Murray C, Abraham J, Ali M, et al. The state of us health, 1990-2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310(6):591-606.
9. Manchikanti L, Singh V, Datta S, Cohen S, Hirsch J. Physicians. ASoIP. Comprehensive review of epidemiolo- gy, scope, and impact of spinal pain. Pain Physician. 2009; 12(4):E35-E70.
10. Hincapie? C, Cassidy J, Co?te? P, Carroll L, Guzma?n J. Whiplash injury is more than neck pain: a population-based study of pain localization after traffic injury. J Occup Environ Med. 2010;52(4):434-440.
11. Blincoe L, Miller T, Zaloshnja E, Lawrence B. The Economic and Societal Impact of Motor Vehicle Crashes, 2010. (Revised) (Report No. DOT HS 812 013). Washington, DC: National Highway Traffic Safety Administration; 2015.
12. Bannister G, Amirfeyz R, Kelley S, Gargan M. Whiplash injury. J Bone Joint Surg. 2009;91-B(7):845-850.
13. Johansson M, Boyle E, Hartvigsen J, Carroll L, Cassidy J. A population-based, incidence cohort study of mid-back pain after traffic collisions: factors associated with global recovery. EuroJ Pain. 2015;19(10):186-195.
14. Styrke J, Stalnacke B, Bylund P, Sojka P. A 10-year incidence of acute whiplash injuries after road traffic crashes in a defined population in northern Sweden. PM R. 2012;4(10):739-747.
15. Ontario MoFo. Ontario Auto Insurance Anti-Fraud Task Force Interim Report. Available at: www.fin.gov.on. ca/en/autoinsurance/interim-report.pdf Accessed May 7, 2016.
16. Karlsborg M, Smed A, Jespersen H, et al. A prospective study of 39 patients with whiplash injury. Acta Neurol Scand. 1997;95(2):65-72.
17. Sterling M, Jull G, Vicenzino B, Kenardy J, Darnell R. Development of motor system dysfunction following whiplash injury. Pain. 2003;103(1-2):65-73.
18. Guzman J, Hurwitz EL, Carroll LJ, et al. A new conceptual model of neck pain: linking onset, course, and care: the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;33(4 Suppl): S14-S23.
19. Leaver A, Maher C, McAuley J, Jull G, Refshauge K. Characteristics of a new episode of neck pain. Man Ther. 2013;18(3):254-257.
20. Co?te? P, Shearer H, Ameis A, et al. Enabling recovery from common traffic injuries: a focus on the injured person. UOIT-CMCC Centre for the Study of Disability Prevention and Rehabilitation; 2015.
21. Clar C, Tsertsvadze A, Court R, Hundt G, Clarke A, Sutcliffe P. Clinical effectiveness of manual therapy for the management of musculoskeletal and non-musculoskeletal conditions: systematic review and update of UK evidence report. Chiropract Man Ther. 2014;22(1):12.
22. Bronfort G, Evans R, Anderson A, Svendsen K, Bracha Y, Grimm R. Spinal manipulation, medication, or home exercise with advice for acute and subacute neck pain. Ann Intern Med. 2012;156(1 Part 1):1-10.
23. Hurwitz EL, Carragee EJ, van der Velde G, et al. Treatment of neck pain: noninvasive interventions. Results of the Bone and Joint Decade 2000�2010 Task Force on Neck Pain and its Associated Disorders. Spine. 2008;33(4S):S123-S152.
24. Bryans R, Decina P, Descarreaux M, et al. Evidence-based guidelines for the chiropractic treatment of adults with neck pain. J Manip Physiol Therap. 2014;37(1):42-63.
25. Shaw L, Descarreaux M, Bryans R, et al. A systematic review of chiropractic management of adults with whiplash- associated disorders: recommendations for advancing evidence-based practice and research. Work. 2010;35(3): 369-394.
26. Graham G, Mancher M, Miller Wolman D, Greenfield S, Steinberg E, editors. Clinical Practice Guidelines We Can Trust. Institute of Medicine, Shaping the Future for Health.
Washington, DC: National Academies Press; 2011.
27. Co?te? P, Wong JJ, Sutton D, et al. Management of neck pain and associated disorders: a clinical practice guideline from the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. Euro Spine J. 2016;25(7): 2000-2022.
28. Johnson AP, Sikich NJ, Evans G, et al. Health technology assessment: a comprehensive framework for evidence- based recommendations in ontario. Int J Technol Assess Health Care. 2009;25(2):141-150.
29. Shukla V, Bai A, Milne S, Wells G. Systematic review of the evidence grading system for grading level of evidence. German J Evid Qual Health Care. 2008; 102:43.
30. Mustafa RA, Santesso N, Brozek J, et al. The GRADE approach is reproducible in assessing the quality of evidence of quantitative evidence syntheses. J Clin Epidemiol. 2013;66(7):736-742.e5.
31. Woolf S, Schunemann H, Eccles M, Grimshaw J, Shekelle P. Developing clinical practice guidelines: types of evidence and outcomes; values and economics, synthesis, grading, and presentation and deriving recommendations. lImplementation Sci. 2012;7(1):61.
32. Tricco A, Tetzlaff J, Moher D. The art and science of knowledge synthesis. J Clin Epidemiol. 2011;64(1):11-20.
33. Guyatt G, Eikelboom JW, Akl EA, et al. A guide to GRADE
guidelines for the readers of JTH. J Thromb Haemost. 2013;
11(8):1603-1608.
34. Adaptation. The ADAPTE Manual and Resource
Toolkit V2. G-I-N Adaptation Working Group. Available at: www.g-i-n.net/working-groups/adaptation Accessed May 16, 2016.
35. Brouwers M, Kho M, Browman G, et al. AGREE II: advancing guideline development, reporting and evalua- tion in health care. J Clin Epidemiol. 2010;63(12): 1308-1311.
36. Flottorp S, Oxman AD, Cooper JG, Hjortdahl P, Sandberg S, Vorland LH. Retningslinjer for diagnostikk og behand- ling av sar hals. Tidsskr Nor Laegeforen. 2000;120: 1754-1760.
37. Grimshaw J, Eccles M, Lavis J, Hill S, Squires J. Knowledge translation of research findings. Implementation Sci. 2012;7(1):50.
38. Southerst D, Nordin M, Co?te? P, et al. Is exercise effective for the management of neck pain and associated disorders or whiplash-associated disorders? A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. Spine J. 2014;S1529-1530(14): 00210-1.
39. Sutton D, Cote P, Wong J, et al. Is multimodal care effective for the management of patients with whiplash-associated disorders or neck pain and associated disorders? A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. Spine J. 2014 [S1529-9430(14):00650-0].
40. Yu H, Co?te? P, Southerst D, Wong J, et al. Does structured patient education improve the recovery and clinical outcomes of patients with neck pain? A systematic review from the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. Spine J. 2014;pii: S1529- 9430(14).
41. Varatharajan S, Co?te? P, Shearer H, et al. Are work disability prevention interventions effective for the management of neck pain or upper extremity disorders? A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. J Occup Rehabil. 2014;24(4): 692-708.
42. Wong JJ, Shearer HM, Mior S, et al. Are manual therapies, passive physical modalities, or acupuncture effective for the management of patients with whiplash-associated disorders or neck pain and associated disorders? An update of the Bone and Joint Decade Task Force on Neck Pain and Its Associated Disorders by the Optima Collaboration. Spine J. 2015;20(8 Suppl).
43. Shea B, Grimshaw J, Wells G, Boers M, Andersson N, Hamel C. Development of AMSTAR: a measurement tool to assess the methodological quality of systematic reviews. BMC Med Res Methodol. 2007;7:10.
44. Norman G, Streiner D. Biostatistics: The Bare Essentials. 3rd ed. Hamilton, ON: BC Decker; 2008.
45. Ricci S, Celani M, Righetti E. Development of clinical guidelines: methodological and practical issues. Neurol Sci. 2006;27(Suppl 3):S228-S230.
46. van der Velde G, van Tulder M, Co?te? P, et al. The sensitivity of review results to methods used to appraise and incorporate trial quality into data synthesis. Spine. 2007; 32(7):796-806.
47. Slavin R. Best evidence synthesis: an intelligent alternative to meta-analysis. J Clin Epidemiol. 1995;48(1):9-18.
48. Network GI, GRADE Working Group. Resources. Available at: www.g-i-n.net/working-groups/updating-guidelines/re- sources. Accessed May 5, 2016.
49. Guyatt G, Oxman A, Vist G, et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ. 2008;336(7650):924-926.
50. Guyatt G, Oxman A, Akl E, Kunz R, Vist G, Brozek J, et al. GRADE guidelines 1. Introduction: GRADE evidence profiles and summary of findings tables. J Clin Epidemiol. 2011;64(4):38-94.
51. Treweek S, Oxman A, Alderson P, et al. Developing and evaluating communication strategies to support informed decisions and practice based on evidence (DECIDE): protocol and preliminary results. Implementation Sci. 2013; 8(1):6.
52. McCarthy M, Grevitt M, Silcocks P, Hobbs G. The reliability of the Vernon and Mior neck disability index, and its validity compared with the short form-36 health survey questionnaire. Eur Spine J. 2007;16(12):2111-2117.
53. Stauffer M, Taylor S, Watson D, Peloso P, Morrison A. Definition of nonresponse to analgesic treatment of arthritic pain: an analytical literature review of the smallest detectable difference, the minimal detectable change, and the minimal clinically important difference on the pain visual analog scale. Int J Inflam. 2011;2011:231926.
54. Hawker GA, Mian S, Kendzerska T, French M. Measures of adult pain: visual analog scale for pain (VAS Pain), numeric rating scale for pain (NRS Pain), McGill Pain Questionnaire (MPQ), Short-Form McGill Pain Questionnaire (SF-MPQ), Chronic Pain Grade Scale (CPGS), Short Form-36 Bodily Pain Scale (SF-36 BPS), and Measure of Intermittent and Constant Osteoarthritis Pain (ICOAP. Arthritis Care Res. 2011;63(S11):S240-S252.
55. Blozik E, Himmel W, Kochen MM, Herrmann-Lingen C, Scherer M. Sensitivity to change of the Neck Pain and Disability Scale. Euro Spine J. 2011;20(6):882-889.
56. Andrews J, Guyatt G, Oxman AD, et al. GRADE guidelines: 14. Going from evidence to recommendations: the signifi- cance and presentation of recommendations. J Clin Epidemiol. 2013;66(7):719-725.
57. Andrews JC, Schu?nemann HJ, Oxman AD, et al. GRADE guidelines: Going from evidence to recommendation� determinants of a recommendation’s direction and strength. J Clinl Epidemiol. 2013;66(7):726-735.
58. Black N, Murphy M, Lamping D, McKee M, Sanderson C, Askham J. Consensus development methods: a review of best practice in creating clinical guidelines. J Health Serv Res Policy. 1999;4(4):236-248.
59. Seo H-J, Kim KU. Quality assessment of systematic reviews or meta-analyses of nursing interventions conducted by Korean reviewers. BMC Med Res Methodol. 2012;12:129.
60. Leaver A, Maher C, Herbert R, et al. A randomized controlled trial comparing manipulation with mobilization for recent onset neck pain. Arch Phys Med Rehabil. 2010;91(9):1313-1318.
61. Dunning J, Cleland J, Waldrop M, et al. Upper cervical and upper thoracic thrust manipulation versus nonthrust mobiliza- tion in patients with mechanical neck pain: a multicenter randomized clinical trial. J Orthop Sports Phys Ther. 2012; 42(1):5-18.
62. Nagrale A, Glynn P, Joshi A, Ramteke G. The efficacy of an integrated neuromuscular inhibition technique on upper trapezius trigger points in subjects with non-specific neck pain: a randomized controlled trial. J Man Manip Ther. 2010; 18(1):37-43.
63. McReynolds T, Sheridan B. Intramuscular ketorolac versus osteopathic manipulative treatment in the management of acute neck pain in the emergency department: a randomized clinical trial. JAOA. 2005;105(2):57-68.
64. Chou R, Turner JA, Devine EB, et al. The effectiveness and risks of long-term opioid therapy for chronic pain: a systematic review for a National Institutes of Health Pathways to Prevention Workshop Effectiveness and Risks of Long-Term Opioid Therapy for Chronic Pain. Ann Inter Med. 2015;162(4):276-286.
65. Kuijper B, Tans J, Beelen A, Nollet F, de Visser M. Cervical collar or physiotherapy versus wait and see policy for recent onset cervical radiculopathy: randomised trial. BMJ. 2009;339:b3883.
66. Cassidy J. Mobilisation or immobilisation for cervical radiculo- pathy? BMJ. 2009;339(b):3952.
67. Konstantinovic L, Cutovic M, Milovanovic A, et al. Low-level laser therapy for acute neck pain with radiculopathy: a double- blind placebo-controlled randomized study. Pain Med. 2010; 11(8):1169-1178.
68. van den Heuvel S, de Looze M, Hildebrandt V, The? K. Effects of software programs stimulating regular breaks and exercises on work-related neck and upper-limb disorders. Scand J Work Environ Health. 2003;29(2):106-116.
69. Lamb S, Gates S, Williams M, et al. Emergency department treatments and physiotherapy for acute whiplash: a pragmatic, two-step, randomised controlled trial. Lancet. 2013;381(9866): 546-556.
70. Ferrari R, Rowe BH, Majumdar SR, et al. Simple educational intervention to improve the recovery from acute whiplash: results of a randomized, controlled trial. Acad Emerg Med. 2005;12(8): 699-706.
71. von Trott P, Wiedemann A, Lu?dtke R, Rei�hauer A, Willich S, Witt C. Qigong and exercise therapy for elderly patients with chronic neck pain (QIBANE): a randomized controlled study. J Pain. 2009;10(5):501-508.
72. Rendant D, Pach D, Ludtke R, et al. Qigong versus exercise versus no therapy for patients with chronic neck pain: a randomized controlled trial. Spine. 2011;36(6):419-427.
73. Michalsen A, Traitteur H, Lu?dtke R, et al. Yoga for chronic neck pain: a pilot randomized controlled clinical trial. J Pain. 2012; 13(11):1122-1130.
74. Jeitler M, Brunnhuber S, Meier L, et al. Effectiveness of jyoti meditation for patients with chronic neck pain and psychological distress-a randomized controlled clinical trial. J Pain. 2015;16(1): 77-86.
75. Hakkinen A, Kautiainen H, Hannonen P, Ylinen J. Strength training and stretching versus stretching only in the treatment of patients with chronic neck pain: a randomized one-year follow-up
study. Clin Rehabil. 2008;22(7):593-600.
76. Salo P, Ylonen-Kayra N, Hakkinen A, Kautiainen H, Malkia E,
Ylinen J. Effects of long-term home-based exercise on health- related quality of life in patients with chronic neck pain: a randomized study with a 1-year follow-up. Disabil Rehabil. 2012; 34(23):1971-1977.
77. Evans R, Bronfort G, Schulz G, et al. Supervised exercise with and without spinal manipulation performs similarly and better than home exercise for chronic neck pain: a randomized controlled trial. Spine. 2012;37(11):903-914.
78. Maiers M, Bronfort G, Evans R, et al. Spinal manipulative therapy and exercise for seniors with chronic neck pain. Spine J. 2014;14(9):1879-1889.
79. Griffiths C, Dziedzic K, Waterfield J, Sim J. Effectiveness of specific neck stabilization exercises or a general neck exercise program for chronic neck disorders: a randomized controlled trial. J Rheumatol. 2009;36(2):390-397.
80. Gustavsson C, Denison E, von Koch L. Self-management of persistent neck pain: a randomized controlled trial of a multi- component group intervention in primary health care. Eur J Pain. 2010;14(6):630.e1-11.
81. Gustavsson C, Denison E, von Koch L. Self-management of persistent neck pain: two-year follow-up of a randomized controlled trial of a multicomponent group intervention in primary health care. Spine. 2011;36(25):2105-2115.
82. Sherman K, Cherkin D, Hawkes R, Miglioretti D, Deyo R. Randomized trial of therapeutic massage for chronic neck pain. Clin J Pain. 2009;25(3):233-238.
83. Lin J, Shen T, Chung R, Chiu T. The effectiveness of Long’s manipulation on patients with chronic mechanical neck pain: a randomized controlled trial. Manual Ther. 2013;18(4):308-315.
84. Lauche R, Materdey S, Cramer H, et al. Effectiveness of home- based cupping massage compared to progressive muscle relaxation in patients with chronic neck pain�a randomized controlled trial. PLoS One. 2013;8(6):e65378.
85. Sherman K, Cook A, Wellman R, et al. Five-week outcomes from a dosing trial of therapeutic massage for chronic neck pain. Ann Fam Med. 2014;12(2):112-120.
86. Walker MJ, Boyles RE, Young BA, et al. The effectiveness of manual physical therapy and exercise for mechanical neck pain: a randomized clinical trial. Spine (Phila Pa 1976). 2008;33(22): 2371-2378.
87. Boyles R, Walker M, Young B, Strunce J, Wainner R. The addition of cervical thrust manipulations to a manual physical therapy approach in patients treated for mechanical neck pain: a secondary analysis. J Orthop Sports Phys Ther. 2010;40(3): 133-140.
88. Hoving JL, de Vet HC, Koes BW, et al. Manual therapy, physical therapy, or continued care by the general practitioner for patients with neck pain: long-term results from a pragmatic randomized clinical trial. Clin J Pain. 2006;22(4):370-377.
89. Hoving JL, Koes BW, de Vet HCW, et al. Manual Therapy, physical therapy, or continued care by a general practitioner for patients with neck pain: a randomized, controlled trial. Ann Intern Med. 2002;136(10):713-722.
90. Monticone M, Baiardi P, Vanti C, et al. Chronic neck pain and treatment of cognitive and behavioural factors: results of a randomised controlled clinical trial. Euro Spine J. 2012;21(8): 1558-1566.
91. Zebis M, Andersen L, Pedersen M, et al. Implementation of neck/shoulder exercises for pain relief among industrial workers: a randomized controlled trial. BMC Musculoskelet Disord. 2011;12:205.
92. Zebis MK, Andersen CH, Sundstrup E, Pedersen MT, Sj�gaard G, Andersen LL. Time-wise change in neck pain in response to rehabilitation with specific resistance training: implications for
exercise prescription. PLoS One. 2014;9(4):e93867.
93. Andersen C, Andersen L, Gram B, et al. Influence of frequency and duration of strength training for effective management of neck and shoulder pain: a randomised controlled trial. Br J
Sports Med. 2012;46(14):1004-1010.
94. Andersen L, Jorgensen M, Blangsted A, Pedersen M, Hansen E,
Sjogaard GA. randomized controlled intervention trial to relieve and prevent neck/shoulder pain. Med Sci Sports Exerc. 2008; 40(6):983-990.
95. Sjogren T, Nissinen K, Jarvenpaa S, Ojanen M, Vanharanta H, Malkia E. Effects of a workplace physical exercise intervention on the intensity of headache and neck and shoulder symptoms and upper extremity muscular strength of office workers: a cluster randomized controlled cross-over trial. Pain. 2005;116(1-2):119-128.
96. Stewart M, Maher C, Refshauge K, Herbert R, Bogduk N, Nicholas M. Randomized controlled trial of exercise for chronic whiplash-associated disorders. Pain. 2007;128(1-2):59-68.
97. Michaleff Z, Maher C. Lin C-WC, et al. Comprehensive physiotherapy exercise programme or advice for chronic whiplash (PROMISE): a pragmatic randomised controlled trial. Lancet. 2014;384(9938):133-141.
98. Gram B, Andersen C, Zebis MK, et al. Effect of training supervision on effectiveness of strength training for reducing neck/shoulder pain and headache in office workers: cluster randomized controlled trial. BioMed Ress Int. 2014;2014:9.
99. Jull G, Sterling M, Kenardy J, Beller E. Does the presence of sensory hypersensitivity influence outcomes of physical reha- bilitation for chronic whiplash? A preliminary RCT. Pain. 2007; 129(1-2):28-34.
100. Jull G, Kenardy J, Hendrikz J, Cohen M, Sterling M. Management of acute whiplash: a randomized controlled trial of multidisciplin- ary stratified treatments. Pain. 2013;154(9):1798-1806.
101. Wiangkham T, Duda J, Haque S, Madi M, Rushton A. The effectiveness of conservative management for acute whiplash associated disorder (WAD) II: a systematic review and meta- analysis of randomised controlled trials. PLoS One. 2015;10(7): e0133415.
102. Guyatt G, Oxman AD, Sultan S, et al. GRADE guidelines: 11. Making an overall rating of confidence in effect estimates for a single outcome and for all outcomes. J Clin Epidemiol. 2013; 66(2):151-157.
103. Walsh D, Howe T, Johnson M, Sluka K. Transcutaneous electrical nerve stimulation for acute pain. Cochrane Database Syst Rev. 2009(2)CD006142.
104. Nnoaham K, Kumbang J. Transcutaneous electrical nerve stimulation (TENS) for chronic pain. Cochrane Database Syst Rev. 2008(3)CD003222.
105. French S, Cameron M, Walker B, Reggars J, Esterman A. Superficial heat or cold for low back pain. Cochrane Database Syst Rev. 2006(1)CD004750.
106. Malanga GA, Yan N, Stark J. Mechanisms and efficacy of heat and cold therapies for musculoskeletal injury. Postgrad Med. 2015;127(1):57-65.
107. Carnes D, Mullinger B, Underwood M. Defining adverse events in manual therapies: a modified Delphi consensus study. lManual Ther. 2010;15(1):2-6.
108. Haldeman S, Carroll LJ, Cassidy JD. The empowerment of people with neck pain: introduction: the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;33(4 Suppl):S8-S13.
109. Maiers M, Vihstadt C, Hanson L, Evans R. Perceived value of spinal manipulative therapy and exercise among seniors with chronic neck pain: a mixed methods study. J Rehabil Med. 2014;46(10):1022-1028.
110. Chou R, Deyo R, Friedly J, et al. Noninvasive treatments for low back pain. Comparative Effectiveness Review No. 169. (Prepared by the Pacific Northwest Evidence-based Practice Center under Contract No. 290-2012-00014-I.). AHRQ Publication No. 16-EHC004-EF. Rockville, MD. Available at: www.effectivehealthcare.ahrq.gov/reports/final.cfm. Accessed May 15, 2016.
111. Machado G, Maher C, Ferreira P, et al. Efficacy and safety of paracetamol for spinal pain and osteoarthritis: systematic review and meta-analysis of randomised placebo controlled trials. BMJ. 2015;350:h1225.
112. Miller M, Barber CW, Leatherman S, et al. Prescription opioid duration of action and the risk of unintentional overdose among patients receiving opioid therapy. JAMA Intern Med. 2015; 175(4):608-615.
113. Volkow N, McLellan A. Opioid abuse in chronic pain� misconceptions and mitigation strategies. N Engl J Med. 2016; 374(13):1253-1263.
114. Foster N, Hartvigsen J, Croft P. Taking responsibility for the early assessment and treatment of patients with musculoskeletal pain: a review and critical analysis. Arthritis Res Ther. 2012;14(1):205.
115. World Health Organization. WHO Guidelines on Basic Training and Safety in Chiropractic. Geneva, Switzerland: World Health Organization; 2005.
116. Guzman J, Haldeman S, Carroll L, et al. Clinical practice implications of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders: from concepts and findings to recommendations. Spine. 2008;33(4 Suppl):S199-S213.
117. Dietl M, Korczak D. Over-, under- and misuse of pain treatment in Germany. GMS Health Technol Assess. 2011; 7:Doc03. dx.doi.org/10.3205/hta000094.
118. Freburger J, Carey T, Holmes G, Wallace A, Castel L, Darter J. Exercise prescription for chronic back or neck pain: who prescribes it? Who gets it? What is prescribed? lArthritis Care Res. 2009;61:192-200.
119. Goode A, Freburger J, Carey T. Prevalence, practice patterns, and evidence for chronic neck pain. Arthritis Care Res. 2010;62(11):1594-1601.
120. Kamaleri Y, Natvig B, Ihlebaek CM, Bruusgaard D. Localized or widespread musculoskeletal pain: does it matter? Pain. 2008;138(1):41-46.
121. MacDermid J, Miller J, Gross A. Knowledge translation tools are emerging to move neck pain research into practice. lOpen Orthop J. 2013;20(7):582-593.
122. Medina-Mirapeix F, Escolar-Reina P, Gascon-Canovas J, Montilla-Herrador J, Jimeno-Serrano F, Collins S. Predictive factors of adherence to frequency and duration components in home exercise programs for neck and low back pain: an observational study. BMC Musculoskelet Disord. 2009;10(1):155.
123. Kay T, Gross A, Goldsmith C, et al. Exercises for mechanical neck disorders. Cochrane Database Syst Rev. 2012;8:CD004250.
124. Bertozzi L, Gardenghi I, Turoni F, et al. Effect of
therapeutic exercise on pain and disability in the manage- ment of chronic nonspecific neck pain: systematic review and meta-analysis of randomized trials. Phys Ther. 2013; 93(8):1026-1036.
125. Hartvigsen J, Natvig B, Ferreira M. Is it all about a pain in the back? Best Pract Res Clin Rheumatol. 2013;27(5):613-623.
126. Ambrose K, Golightly Y. Physical exercise as non-pharmaco- logical treatment of chronic pain: why and when. Best Pract Res Clin Rheumatol. 2015;29(1):120-130.
127. Lee I, Shiroma E, Lobelo F, Puska P, Blair S, Katzmarzyk P. Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy. Lancet. 2012;380(9838):219-229.
128. World Health Organization. Global Recommendations on Physical Activity for Health. Geneva, Switzerland: World Health Organization; 2010.
129. Carroll LJ, Ferrari R, Cassidy JD, Cote P. Coping and recovery in whiplash-associated disorders: early use of passive coping strategies is associated with slower recovery of neck pain and pain-related disability. Clin J Pain. 2014;30(1):1-8.
130. Gore M, Sadosky A, Stacey B, Tai K, Leslie D. The burden of chronic low back pain: clinical comorbidities, treatment patterns, and health care costs in usual care settings. Spine. 2012;37(11):E668-E677.
131. Bodenheimer T, MacGregor K, Charifi C. Helping patients manage their chronic conditions. Oakland, CA: California HealthCare Foundation; 2005.
132. Ritzwoller D, Crounse L, Shetterly S, Rublee D. The association of comorbidities, utilization and costs for patients identified with low back pain. BMC Musculoskelet Disord. 2006;7(1):72.
133. Sallis R, Franklin B, Joy L, Ross R, Sabgir D, Stone J. Strategies for promoting physical activity in clinical practice. Prog Cardiovasc Dis. 2015;57(4):375-386.
134. Von Korff M, Crane P, Lane M, et al. Chronic spinal pain and physical-mental comorbidity in the United States: results from the national comorbidity survey replication. Pain. 2005;113(3): 331-339.
135. Bussie?res A, Al Zoubi F, Quon J, et al. Fast tracking the design of theory-based KT interventions through a consensus process. Implementation Sci. 2015;10(1):18.
136. Gutnick D, Reims K, Davis C, Gainforth H, Jay M, Cole S. Brief action planning to facilitate behavior change and support patient self-management. J Clin Outcomes Manag. 2014;21: 17-29.
137. Dhopte P, Ahmed S, Mayo N, French S, Quon JA, Bussie?res A. Testing the feasibility of a knowledge translation intervention designed to improve chiropractic care for adults with neck pain disorders: study protocol for a pilot cluster-randomized controlled trial. Pilot and Feasibility Studies. 2016;2(1):1-11.
138. Turner L, Shamseer L, Altman D, et al. Consolidated standards of reporting trials (CONSORT) and the complete- ness of reporting of randomised controlled trials (RCTs) published in medical journals. Cochrane Database Syst Rev. 2012;11:MR000030.
139. Quinlan K, Annest J, Myers B, Ryan G, Hill H. Neck strains and sprains among motor vehicle occupants�United States, 2000. Accid Anal Prev. 2004;36(1):21-27.
140. Titler M. The evidence for evidence-based practice imple- mentation. Patient Safety and Quality: An Evidence-Based Handbook for Nurses, vol. 1. Rockville, MD: AHRQ; 2008. p. 113-161.
141. The Canadian Agency for Drugs and Technologies in Health. Rx for Change database. Available at: www.cadth.ca/rx-change. Accessed May 6, 2016.
142. Grimshaw J, Thomas R, MacLennan G, Fraser C, Ramsay C, Vale L. Effectiveness and efficiency of guideline dissemina- tion and implementation strategies. Health Technol Assess. 2004;8(6):1-72.
143. Bishop PB, Quon JA, Fisher CG, Dvorak MFS. The Chiropractic Hospital-based Interventions Research Outcomes (CHIRO) Study: a randomized controlled trial on the effectiveness of clinical practice guidelines in the medical and chiropractic management of patients with acute mechanical low back pain. Spine J. 2010;10(12):1055-1064.
144. Grimshaw J, Schunemann H, Burgers J, Cruz A, Heffner J, Metersky M. Disseminating and implementing guidelines. Article 13 in integrating and coordinating efforts in COPD guideline development. Proc Am Thorac Soc. 2012;9(5): 298-303.
145. Pronovost P. Enhancing physicians’ use of clinical guide- lines. JAMA. 2013;310(23):2501-2502.
146. Schuster, MA, Elizabeth A, McGlynn R, Brook H. How good is the quality of health care in the United States? Milbank. 2005;83(4):843-895.
147. Greenhalgh T, Howick J, Maskrey N. Evidence based medicine: a movement in crisis? BMJ. 2014;348:g3725. 148. Canadian Institutes of Health Research. Knowledge translation�
definition. 2008 Available at: www.cihr-irsc.gc.ca/e/29529.html.
Accessed May 6, 2016.
149. Gagliardi A, Marshall C, Huckson S, James R, Moore V.
Developing a checklist for guideline implementation planning: review and synthesis of guideline development and implemen- tation advice. Implementation Sci. 2015;10(1):19.
150. Cochrane-Effective Practice and Organisation of Care (EPOC). Available at: epoc.cochrane.org/our-reviews. Accessed May 6, 2016.
151. Gagliardi A, Brouwers M, Bhattacharyya O. A framework of the desirable features of guideline implementation tools (GItools): Delphi survey and assessment of GItools. Implementation Sci. 2014;9(1):98.
152. Okelo S, Butz A, Sharma R, et al. Interventions to modify health care provider adherence to asthma guidelines: a systematic review. Pediatrics. 2013;132(3):517-534.
153. Murthy L, Shepperd S, Clarke M, et al. Interventions to improve the use of systematic reviews in decision-making by health system managers, policy makers and clinicians. Cochrane Database Syst Rev. 2012;9CD009401.
154. Garg A, Adhikari N, McDonald H, et al. Effects of computerized clinical decision support systems on practitioner performance and patient outcomes: a systematic review. JAMA. 2005; 293(10):1223-1238.
155. Rebbeck T, Macedo L, Maher C. Compliance with clinical guidelines for whiplash improved with a targeted implemen- tation strategy: a prospective cohort study. BMC Health Serv Res. 2013;13(1):213.
156. Bussie?res A, Co?te? P, French S, et al. Creating a chiropractic practice-based research network (PBRN): enhancing the management of musculoskeletal care. J Can Chiropr Assoc. 2014;58(1):8-15.
157. Canadian Chiropractic Research Database (CCRD). National Report. The Canadian Chiropractic Association: A Compre- hensive Inventory of Practical Information About Canada�s Licensed Chiropractors; 2011.
158. Becker M, Neugebauer E, Eikermann M. Partial updating of clinical practice guidelines often makes more sense than full updating: a systematic review on methods and the development of an updating procedure. J Clin Epidemiol. 2014;67(1):33-45.
159. Alonso-Coello P, Marti?nez Garci?a L, Carrasco JM, Sola? I, Qureshi S, Burgers JS. The updating of clinical practice guidelines: insights from an international survey. Implementation Sci. 2011;6(1):1-8.
160. Marti?nez Garci?a L, Are?valo-Rodri?guez I, Sola? I, Haynes R, Vandvik P, Alonso-Coello P. Strategies for monitoring and updating clinical practice guidelines: a systematic review. Implementation Sci. 2012;7(1):1-10.
161. Moher D, Tsertsvadze A, Tricco A, et al. A systematic review identified few methods and strategies describing when and how to update systematic reviews. J Clin Epidemiol. 2007;60(11):1095. e1-11.
162. Shekelle P, Eccles M, Grimshaw J, Woolf S. When should clinical guidelines be updated? BMJ. 2001;323(7305):155-157.
163. Vernooij R, Sanabria A, Sola I, Alonso-Coello P, Martinez Garcia L. Guidance for updating clinical practice guidelines: a systematic review of methodological handbooks. Implement Sci. 2014;9:3.
164. Moher D, Pham B, Lawson M, Klassen T. The inclusion of reports of randomised trials published in languages other than English in systematic reviews. Health Technol Assess. 2003; 7(41):1-90.
165. Morrison A, Polisena J, Husereau D, et al. The effect of English-
language restriction on systematic review-based meta-analyses: a
systematic review of empirical studies. Int J Technol Assess
Health Care. 2012;28(20120426):138-144.
166. Harbour R, Miller JA. new system for grading recommen- dations in evidence based guidelines. BMJ. 2001;323(7308): 334-336.
167. Cleland J, Mintken P, Carpenter K, et al. Examination of a clinical prediction rule to identify patients with neck pain likely to benefit from thoracic spine thrust manipulation and a general cervical range of motion exercise: multi-center randomized clinical trial. Phys Ther. 2010;90(9):1239-1250.
168. Escortell-Mayor E, Riesgo-Fuertes R, Garrido-Elustondo S, et al. Primary care randomized clinical trial: Manual therapy effectiveness in comparison with TENS in patients with neck pain. Man Ther. 2011;16(1):66-73.
169. Lamb S, Williams M, Williamson E, et al. Managing Injuries of the Neck Trial (MINT): a randomised controlled trial of treatments for whiplash injuries. Health Technol Assess. 2012; 16(49:iii-iv):1-141.
170. Pool J, Ostelo R, Knol D, Vlaeyen J, Bouter L, de Vet HI. a behavioral graded activity program more effective than manual therapy in patients with subacute neck pain?: results of a randomized clinical trial. Spine. 2010;35(10): 1017-1024.
171. Skillgate E, Bohman T, Holm L, Vinga?rd E, Alfredsson L. The long-term effects of naprapathic manual therapy on back and neck pain. Results from a pragmatic randomized controlled trial. BMC Musculoskelet Disord. 2010;11(1): 1-11.
172. Kongsted A, Qerama E, Kasch H, et al. Education of patients after whiplash injury: is oral advice any better than a pamphlet? Spine. 2008;33(22):E843-E848.
173. Andersen L, Saervoll C, Mortensen O, Poulsen O, Hannerz H, Zebis M. Effectiveness of small daily amounts of progressive resistance training for frequent neck/shoulder pain: Rando- mised controlled trial. Pain. 2011;152(2):440-446.
174. Cheng A, Hung L. Randomized controlled trial of workplace- based rehabilitation for work-related rotator cuff disorder. lJ Occup Rehab. 2007;17(3):487-503.
175. Feuerstein M, Nicholas R, Huang G, Dimberg L, Ali D, Rogers H. Job stress management and ergonomic interven- tion for work-related upper extremity symptoms. Appl Ergon. 2004;35(6):565-574.
176. van Eijsden-Besseling M, Bart Staal J, van Attekum A, de Bie RA, van den Heuvel W. No difference between postural exercises and strength and fitness exercises for early, non- specific, work-related upper limb disorders in visual display unit workers: a randomised trial. Aust J Physiother. 2008; 54(2):95-101.
177. Cameron I, Wang E, Sindhusake DA. randomized trial comparing acupuncture and simulated acupuncture for subacute and chronic whiplash. Spine. 2011;36(26):E1659-E1665.
178. Cleland JA, Glynn PE, Whitman JM, et al. Short-term response of thoracic spine thrust versus non-thrust manipulation in patients with mechanical neck pain: preliminary analysis of a randomized clinical trial. J Manual Manipulat Ther. 2007;14: 172
179. Dundar U, Evcik D, Samli F, Pusak H, Kavuncu V. The effect of gallium arsenide aluminum laser therapy in the management of cervical myofascial pain syndrome: a double blind, placebo- controlled study. Clin Rheumatol. 2007;26(6):930-934.
180. Fu W, Zhu X, Yu P, Zhang J. Analysis on the effect of acupuncture in treating 5 cervical spondylosis with different syndrome types. Chin J Integr Med. 2009;15(6):426-430.
181. Kanlayanaphotporn R, Chiradejnant A, Vachalathiti R. The immediate effects of mobilization technique on pain and range of motion in patients presenting with unilateral neck pain: a randomized controlled trial. Arch Phys Med Rehabil. 2009; 90(2):187-192.
182. Kanlayanaphotporn R, Chiradejnant A, Vachalathiti R. Immediate effects of the central posteroanterior mobiliza- tion technique on pain and range of motion in patients with mechanical neck pain. Dis Rehab. 2010;32(8): 622-628.
183. Klein R, Bareis A, Schneider A, Linde K. Strain-counter- strain to treat restrictions of the mobility of the cervical spine in patients with neck pain: a sham-controlled randomized trial. Complement Ther Med. 2013;21(1):1-7.
184. Liang Z, Zhu X, Yang X, Fu W, Lu A. Assessment of a traditional acupuncture therapy for chronic neck pain: a pilot randomised controlled study. Complementary Ther Med. 2011; 19(Suppl 1):S26-S32.
185. Masaracchio M, Cleland JA, Hellman M, Hagins M. Short-term combined effects of thoracic spine thrust manipulation and cervical spine nonthrust manipulation in individuals with mechanical neck pain: a randomized clinical trial. J Orthop Sports Phys. 2013;43(3):118-127.
186. Saavedra-Hernandez M, Castro-Sanchez A, Arroyo-Morales M, et al. Short term effects of kinesio taping versus cervical thrust manipulation in patients with mechanical neck pain: a randomized clinical trial. J Orthop Sports Phys Ther. 2012;42: 724-730.
187. Sillevis R, Hellman M, Beekhuizen K. Immediate effects of a thoracic spine thrust manipulation on the autonomic nervous system: a randomized clinical trial. J Manual Manipulat Ther. 2010;18:181-190.
188. White P, Lewith G, Prescott P, Conway J. Acupuncture versus placebo for the treatment of chronic mechanical neck pain: a randomized, controlled trial. Ann Inter Med. 2004;141(12): 911-919.
189. Young I, Cleland J, Aguilera A, et al. Manual therapy, exercise, and traction for patients with cervical radiculopathy: a randomized clinical trial. Phys Ther. 2009;89:632-642.

Close Accordion
Spinal Manipulation vs. Mobilization for Cervicogenic Headache in El Paso, TX

Spinal Manipulation vs. Mobilization for Cervicogenic Headache in El Paso, TX

A primary headache is characterized as head pain caused by a headache disorder itself. The three types of primary headache disorders include, migraine, tension-type headaches and cluster headaches. Head pain is a painful and debilitating symptom that can also occur as a result of another underlying cause. A secondary headache is characterized as head pain which occurs due to an injury and/or condition. A spinal misalignment, or subluxation, along the cervical spine, or neck, is commonly associated with a variety of headache symptoms.

 

Cervicogenic headache is a secondary headache caused by an injury and/or condition affecting the surrounding structures of the cervical spine, or neck. Many healthcare professionals will recommend the use of drugs/medications to help improve headache, however, several alternative treatment options can be safely and effectively used to treat secondary headaches. The purpose of the following article is to demonstrate the impact of upper cervical and upper thoracic manipulation versus mobilization and exercise in patients with cervicogenic headache.

 

Upper Cervical and Upper Thoracic Manipulation Versus Mobilization and Exercise in Patients with Cervicogenic Headache: a Multi-Center Randomized Clinical Trial

 

Abstract

 

  • Background: Although commonly utilized interventions, no studies have directly compared the effectiveness of cervical and thoracic manipulation to mobilization and exercise in individuals with cervicogenic headache (CH). The purpose of this study was to compare the effects of manipulation to mobilization and exercise in individuals with CH.
  • Methods: One hundred and ten participants (n?=?110) with CH were randomized to receive both cervical and thoracic manipulation (n?=?58) or mobilization and exercise (n?=?52). The primary outcome was headache intensity as measured by the Numeric Pain Rating Scale (NPRS). Secondary outcomes included headache frequency, headache duration, disability as measured by the Neck Disability Index (NDI), medication intake, and the Global Rating of Change (GRC). The treatment period was 4 weeks with follow-up assessment at 1 week, 4 weeks, and 3 months after initial treatment session. The primary aim was examined with a 2-way mixed-model analysis of variance (ANOVA), with treatment group (manipulation versus mobilization and exercise) as the between subjects variable and time (baseline, 1 week, 4 weeks and 3 months) as the within subjects variable.
  • Results: The 2X4 ANOVA demonstrated that individuals with CH who received both cervical and thoracic manipulation experienced significantly greater reductions in headache intensity (p?<?0.001) and disability (p?<?0.001) than those who received mobilization and exercise at a 3-month follow-up. Individuals in the upper cervical and upper thoracic manipulation group also experienced less frequent headaches and shorter duration of headaches at each follow-up period (p?<?0.001 for all). Additionally, patient perceived improvement was significantly greater at 1 and 4-week follow-up periods in favor of the manipulation group (p?<?0.001).
  • Conclusions: Six to eight sessions of upper cervical and upper thoracic manipulation were shown to be more effective than mobilization and exercise in patients with CH, and the effects were maintained at 3 months.
  • Trial registration: NCT01580280 April 16, 2012.
  • Keywords: Cervicogenic headache, Spinal manipulation, Mobilization, High velocity low amplitude thrust

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

In comparison to primary headache, such as migraine, cluster headache and tension-type headache, secondary headache is characterized as head pain caused by another illness or physical issue. In the case of cervicogenic headache, the cause of head pain is due to an injury and/or condition along the cervical spine and its surrounding structures, including the vertebrae, intervertebral discs and soft tissues. In addition, many healthcare professionals believe that primary headache can be associated with health issues in the cervical spine, or neck. Cervicogenic headache treatment should target the source of the symptoms and it can vary depending on the patient. Chiropractic care utilizes spinal adjustments and manual manipulations to carefully restore the original structure and function of the spine, helping to reduce stress and pressure in order to improve cervicogenic headache symptoms, among other type of headache. Chiropractic care can also be utilized to help treat primary headaches, such as migraines.

 

Background

 

The International Classification of Headache Disorders defines cervicogenic headache (CH) as, �headache caused by a disorder of the cervical spine and its component bony, disc, and/or soft tissue elements, usually but not invariably accompanied by neck pain.� [1] (p.760) The prevalence of CH has been reported to be between 0.4 and 20 % of the headache population [2, 3], and as high as 53 % in patients with headache after whiplash injury [4]. The dominant features of CH usually include: unilaterality of head pain without side-shift, elicitation of pain with external pressure over the ipsilateral upper neck, limited cervical range of motion, and the triggering of attacks by various awkward or sustained neck movements [4, 5].

 

Individuals with CH are frequently treated with spinal manipulative therapy including both mobilization and manipulation [6]. Spinal mobilization consists of slow, rhythmical, oscillating techniques whereas manipulation consists of high-velocity low-amplitude thrust techniques. [7] In a recent systematic review, Bronfort and colleagues reported that spinal manipulative therapy (both mobilization and manipulation) were effective in the management of adults with CH [8]. However, they did not report if manipulation resulted in superior outcomes compared to mobilization for the management of this population.

 

Several studies have investigated the effect of spinal manipulation in the management of CH [9�13]. Haas et al. [10] investigated the effectiveness of cervical manipulation in subjects with CH. Jull et al. [11] demonstrated treatment efficacy for manipulative therapy and/or exercise in the management of CH. However the manipulative therapy group included manipulation and mobilization therefore it cannot be determined if the beneficial effect was a result of the manipulation, mobilization or the combination.

 

A few studies have examined the benefits of manipulation versus mobilization for the management of mechanical neck pain with or without exercise [14�16]. However, no studies have directly compared the effects of manipulation versus mobilization and exercise in patients with CH. Considering the purported risks of manipulation [17], it is essential to determine if manipulation results in improved outcomes compared to mobilization for the management of patients with CH. Therefore, the purpose of this randomized clinical trial was to compare the effects of manipulation versus mobilization and exercise in patients with CH. We hypothesized that patients receiving manipulation over a 4-week treatment period would experience greater reductions in headache intensity, headache frequency, headache duration, disability, and medication intake at a 3-month follow-up than patients receiving cervical and thoracic mobilization combined with exercise.

 

Methods

 

Participants

 

In this multi-center randomized clinical trial, consecutive patients with CH presenting to 1 of 8 outpatient physical therapy clinics from a variety of geographical locations (Arizona, Georgia, New York, Ohio, Pennsylvania, South Carolina) were recruited over a 29-month period (from April 2012 to August 2014). For patients to be eligible, they had to present with a diagnosis of CH according to the revised diagnostic criteria [5] developed by the Cervicogenic Headache International Study Group (CHISG) [5, 18, 19]. CH was classified according to the �major criteria� (not including confirmatory evidence by diagnostic anesthetic blockades) and �head pain characteristics� of the CHISG. Therefore, in order to be included in the study, patients had to exhibit all of the following criteria: (1) unilaterality of the head pain without sideshift, starting in the upper posterior neck or occipital region, eventually spreading to the oculofrontotemporal area on the symptomatic side, (2) pain triggered by neck movement and/or sustained awkward positions, (3) reduced range of motion in the cervical spine [20] (i.e., less than or equal to 32 � of right or left passive rotation on the Flexion-Rotation Test [21�23], (4) pain elicited by external pressure over at least one of the upper cervical joints (C0-3), and (5) moderate to severe, non-throbbing and non-lancinating pain. In addition, participants had to have a headache frequency of at least 1 per week for a minimum of 3 months, a minimum headache intensity pain score of two points (0�10 on the NPRS scale), a minimum disability score of 20 % or greater (i.e., 10 points or greater on the 0�50 NDI scale), and be between 18 and 65 years of age.

 

Patients were excluded if they exhibited other primary headaches (i.e., migraine, TTH), suffered from bilateral headaches, or exhibited any red flags (i.e., tumor, fracture, metabolic diseases, rheumatoid arthritis, osteoporosis, resting blood pressure greater than 140/90 mmHg, prolonged history of steroid use, etc.), presented with two or more positive neurologic signs consistent with nerve root compression (muscle weakness involving a major muscle group of the upper extremity, diminished upper extremity deep tendon reflex, or diminished or absent sensation to pinprick in any upper extremity dermatome), presented with a diagnosis of cervical spinal stenosis, exhibited bilateral upper extremity symptoms, had evidence of central nervous system involvement (hyperreflexia, sensory disturbances in the hand, intrinsic muscle wasting of the hands, unsteadiness during walking, nystagmus, loss of visual acuity, impaired sensation of the face, altered taste, the presence of pathological reflexes), had a history of whiplash injury within the previous 6 weeks, had prior surgery to the head or neck, had received treatment for head or neck pain from any practitioner within the previous month, had received physical therapy or chiropractic treatment for head or neck pain within the previous 3 months, or had pending legal action regarding their head or neck pain.

 

The most recent literature suggests that pre-manipulative cervical artery testing is unable to identify those individuals at risk of vascular complications from cervical manipulation [24, 25], and any symptoms detected during pre-manipulative testing may be unrelated to changes in blood flow in the vertebral artery [26, 27]. Hence, pre-manipulative cervical artery testing was not performed in this study; however, screening questions for cervical artery disease had to be negative [24, 28, 29]. This study was approved by the Institutional Review Board at Long Island University, Brooklyn, NY. The study was registered at www.clinicaltrials.gov with trial identifier NCT01580280. All patients were informed that they would receive either manipulation or mobilization and exercise and then provided informed consent before their enrollment in the study.

 

Treating Therapists

 

Twelve physical therapists (mean age 36.6 years, SD 5.62) participated in the delivery of treatment for patients in this study. They had an average of 10.3 (SD 5.66, range 3�20 years) years of clinical experience, and all had completed a 60 h post-graduate certification program that included practical training in manual techniques including the use of cervical and thoracic manipulation. To ensure all examination, outcome assessments, and treatment procedures were standardized, all participating physical therapists were required to study a manual of standard operating procedures and participate in a 4 h training session with the principal investigator.

 

Examination Procedures

 

All patients provided demographic information, completed the Neck Pain Medical Screening Questionnaire, and completed a number of self-report measures, followed by a standardized history and physical examination at baseline. Self-report measures included headache intensity as measured by the NPRS (0�10), the NDI (0�50), headache frequency (number of days with headache in the last week), headache duration (total hours of headache in the last week), and medication intake (number of times the patient had taken narcotic or over-the-counter pain medication in the past week).

 

The standardized physical examination was not limited to, but included measurements of C1-2 (atlanto-axial joint) passive right and left rotation ROM using the Flexion-Rotation Test (FRT). The inter-rater reliability for the FRT has been found to be excellent (ICC: 0.93; 95 % CI: 0.87, 0.96) [30].

 

Outcome Measures

 

The primary outcome measure used in this study was the patient�s headache intensity as measured by the NPRS. Patients were asked to indicate the average intensity of headache pain over the past week using an 11-point scale ranging from 0 (�no pain�) to 10 (�worst pain imaginable�) at baseline, 1-week, 1-month, and 3-months following the initial treatment session [31]. The NPRS is a reliable and valid instrument to assess pain intensity [32�34]. Although no data exists in patients with CH, the MCID for the NPRS has been shown to be 1.3 in patients with mechanical neck pain [32] and 1.74 in patients with a variety of chronic pain conditions [34]. Therefore, we chose to only include patients with an NPRS score of 2 points (20 %) or greater.

 

Secondary outcome measures included the NDI, the Global Rating of Change (GRC), headache frequency, headache duration, and medication intake. The NDI is the most widely used instrument for assessing self-rated disability in patients with neck pain [35�37]. The NDI is a self-report questionnaire with 10-items rated from 0 (no disability) to five (complete disability) [38]. The numeric responses for each item are summed for a total score ranging between 0 and 50; however, some evaluators have chosen to multiply the raw score by two, and then report the NDI on a 0�100 % scale [36, 39]. Higher scores represent increased levels of disability. The NDI has been found to possess excellent test-retest reliability, strong construct validity, strong internal consistency and good responsiveness in assessing disability in patients with mechanical neck pain [36], cervical radiculopathy [33, 40], whiplash associated disorder [38, 41, 42], and mixed non-specific neck pain [43, 44]. Although no studies have examined the psychometric properties of the NDI in patients with CH, we chose to only include patients with an NDI score of ten points (20 %) or greater, because this cut-off score captures the MCID for the NDI, which has been reported to approximate four, eight, and nine points (0�50) in patients with mixed non-specific neck pain [44], mechanical neck pain [45], and cervical radiculopathy [33], respectively. Headache frequency was measured as the number of days with headache in the last week, ranging from 0 to 7 days. Headache duration was measured as the total hours of headache in the last week, with six possible ranges: (1) 0�5 h, (2) 6�10 h, (3) 11�15 h, (4) 16�20 h, (5) 21�25 h, or (6) 26 or more hours. Medication intake was measured as the number of times the patient had taken prescription or over-the-counter analgesic or anti-inflammatory medication in the past week for their headaches, with five options: (1) not at all, (2) once a week, (3) once every couple of days, (4) once or twice a day, or (5) three or more times a day.

 

Patients returned for 1-week, 4-weeks, and 3-months follow-ups where the aforementioned outcome measures were again collected. In addition, at the 1-week, 4-weeks and 3-months follow-ups, patients completed a 15-point GRC question based on a scale described by Jaeschke et al. [46] to rate their own perception of improved function. The scale ranges from -7 (a very great deal worse) to zero (about the same) to +7 (a very great deal better). Intermittent descriptors of worsening or improving are assigned values from -1 to -6 and +1 to +6, respectively. The MCID for the GRC has not been specifically reported but scores of +4 and +5 have typically been indicative of moderate changes in patient status [46]. However, it should be noted that recently Schmitt and Abbott reported that the GRC might not correlate with changes in function in a population with hip and ankle injuries [47]. All outcome measures were collected by an assessor blind to group assignment.

 

On the initial visit patients completed all outcome measures then received the first treatment session. Patients completed 6�8 treatment sessions of either manipulation or mobilization combined with exercise over 4 weeks. Additionally, subjects were asked if they had experienced any �major� adverse events [48, 49] (stroke or permanent neurological deficits) at each follow-up period.

 

Randomization

 

Following the baseline examination, patients were randomly assigned to receive either manipulation or mobilization and exercise. Concealed allocation was performed by using a computer-generated randomized table of numbers created by an individual not involved with recruiting patients prior to the beginning of the study. Individual, sequentially numbered index cards with the random assignment were prepared for each of 8 data collection sites. The index cards were folded and placed in sealed opaque envelopes. Blinded to the baseline examination, the treating therapist opened the envelope and proceeded with treatment according to the group assignment. Patients were instructed not to discuss the particular treatment procedure received with the examining therapist. The examining therapist remained blind to the patient�s treatment group assignment at all times; however, based on the nature of the interventions it was not possible to blind patients or treating therapists.

 

Manipulation Group

 

Manipulations targeting the right and left C1-2 articulations and bilateral T1-2 articulations were performed on at least one of the 6�8 treatment sessions (Figs. 1 and ?and2).2). On other treatment sessions, therapists either repeated the C1-2 and/or T1-2 manipulations or targeted other spinal articulations (i.e., C0-1, C2-3, C3-7, T2-9, ribs 1�9) using manipulation. The selection of the spinal segments to target was left to the discretion of the treating therapist and it was based on the combination of patient reports and manual examination. For both the upper cervical and upper thoracic manipulations, if no popping or cracking sound was heard on the first attempt, the therapist repositioned the patient and performed a second manipulation. A maximum of 2 attempts were performed on each patient similar to other studies [14, 50�53]. The clinicians were instructed that the manipulations are likely to be accompanied by multiple audible popping sounds [54�58]. Patients were encouraged to maintain usual activity within the limits of pain; however, mobilization and the prescription of exercises, or any use of other modalities, were not provided to this group.

 

Figure 1 HVLA Thrust Manipulation Directed to the right C1-2 Articulation | El Paso, TX Chiropractor

 

Figure 2 HVLA Thrust Manipulation Directed Bilaterally to the Upper Thoracic Spine | El Paso, TX Chiropractor

 

The manipulation targeting C1-2 was performed with the patient in supine. For this technique, the patient�s left posterior arch of the atlas was contacted with the lateral aspect of the proximal phalanx of the therapist�s left second finger using a �cradle hold�. To localize the forces to the left C1-2 articulation, the patient was positioned using extension, a posterior-anterior (PA) shift, ipsilateral side-bend and contralateral side-shift. While maintaining this position, the therapist performed a single high-velocity, low-amplitude thrust manipulation to the left atlanto-axial joint using right rotation in an arc toward the underside eye and translation toward the table (Fig. 1). This was repeated using the same procedure but directed to the right C1-2 articulation.

 

The manipulation targeting T1-2 was performed with the patient in supine. For this technique, the patient held her/his arms and forearms across the chest with the elbows aligned in a superoinferior direction. The therapist contacted the transverse processes of the lower vertebrae of the target motion segment with the thenar eminence and middle phalanx of the third digit. The upper lever was localized to the target motion segment by adding rotation away and side-bend towards the therapist while the underside hand used pronation and radial deviation to achieve rotation toward and side-bend away moments, respectively. The space inferior to the xiphoid process and costochondral margin of the therapist was used as the contact point against the patient�s elbows to deliver a manipulation in an anterior to posterior direction targeting T1-2 bilaterally (Fig. 2).

 

Mobilization and Exercise Group

 

Mobilizations targeting the right and left C1-2 articulations and bilateral T1-2 articulations were performed on at least one of the 6�8 treatment sessions. On other treatment sessions, therapists either repeated the C1-2 and/or T1-2 mobilizations or targeted other spinal articulations (i.e., C0-1, C2/3, C3-7, T2-9, ribs 1�9) using mobilization. The selection of the spinal segments to target was left to the discretion of the treating therapist and it was based on the combination of patient reports and manual examination. However, in order to avoid a �contact� or �attention effect� when compared with the manipulation group, therapists were instructed to mobilize one cervical segment (i.e., right and left) and one thoracic segment or rib articulation on each treatment session.

 

The mobilization targeting the C1-2 articulation was performed in prone. For this technique, the therapist performed one 30 s bout of left-sided unilateral grade IV PA mobilizations to the C1-2 motion segment as described by Maitland [7]. This same procedure was repeated for one 30 s bout to the right atlanto-axial joint. In addition, and on at least one session, mobilization directed to the upper thoracic (T1-2) spine with the patient prone was performed. For this technique, the therapist performed one 30 s bout of central grade IV PA mobilizations to the T1-2 motion segment as described by Maitland [7]. Therefore, we used 180 (i.e., three 30 s bouts at approximately 2 Hz) end-range oscillations in total on each subject for the mobilization treatment. Notably, there is no high quality evidence to date to suggest that longer durations of mobilization result in greater pain reduction than shorter durations or dosages of mobilization [59, 60].

 

Cranio-cervical flexion exercises [11, 61�63] were performed with the patient in supine, with the knees bent and the position of the head standardized by placing the craniocervical and cervical spines in a mid-position, such that a line between the subject�s forehead and chin was horizontal, and a horizontal line from the tragus of the ear bisected the neck longitudinally. An air-filled pressure biofeedback unit (Chattanooga Group, Inc., Hixson, TN) was placed suboccipitally behind the patient�s neck and preinflated to a baseline of 20 mmHg [63]. For the staged exercises, patients were required to perform the craniocervical flexion action (�a nod of the head, similar to indicating yes�) [63] and attempt to visually target pressures of 22, 24, 26, 28, and 30 mmHg from a resting baseline of 20 mmHg and to hold the position steady for 10 s [61, 62]. The action of nodding was performed in a gentle and slow manner. A 10 s rest was allowed between trials. If the pressure deviated below the target pressure, the pressure was not held steady, substitution with the superficial flexors (sternocleidomastoid or anterior scalene) occurred, or neck retraction was noticed before the completion of the 10 s isometric hold, it was regarded as a failure [63]. The last successful target pressure was used to determine each patient�s exercise level wherein 3 sets of 10 repetitions with a 10 s isometric hold were performed. In addition to mobilizations and cranio-cervical flexion exercises, patients were required to perform 10 min of progressive resistance exercises (i.e., using Therabands� or free weights) to the muscles of the shoulder girdle during each treatment session, within their own tolerance, and specifically focusing on the lower trapezius and serratus anterior [11].

 

Sample Size

 

The sample size and power calculations were performed using online software from the MGH Biostatistics Center (Boston, MA). The calculations were based on detecting a 2-point (or 20 %) difference in the NPRS (headache intensity) at the 3 months follow-up, assuming a standard deviation of three points, a 2-tailed test, and an alpha level equal to 0.05. This generated a sample size of 49 patients per group. Allowing for a conservative dropout rate of 10 %, we planned to recruit at least 108 patients into the study. This sample size yielded greater than 90 % power to detect a statistically significant change in the NPRS scores.

 

Data Analysis

 

Descriptive statistics, including frequency counts for categorical variables and measures of central tendency and dispersion for continuous variables were calculated to summarize the data. The effects of treatment on headache intensity and disability were each examined with a 2-by-4 mixed-model analysis of variance (ANOVA), with treatment group (manipulation versus mobilization and exercise) as the between-subjects variable and time (baseline, 1 week, 4 weeks, and 3 months follow-up) as the within-subjects variable. Separate ANOVAs were performed with the NPRS (headache intensity) and NDI (disability) as the dependent variable. For each ANOVA, the hypothesis of interest was the 2-way interaction (group by time).

 

An independent t-test was used to determine the between group differences for the percentage change from baseline to 3-month follow-up in both headache intensity and disability. Separate Mann�Whitney U tests were performed with the headache frequency, GRC, headache duration and medication intake as the dependent variable. We performed Little�s Missing Completely at Random (MCAR) test [64] to determine if missing data points associated with dropouts were missing at random or missing for systematic reasons. Intention-to-treat analysis was performed by using Expectation-Maximization whereby missing data are computed using regression equations. Planned pairwise comparisons were performed examining the difference between baseline and follow-up periods between-groups using the Bonferroni correction at an alpha level of .05.

 

We dichotomized patients as responders at the 3-month follow-up using a cut score of 2 points improvement for headache intensity as measured by the NPRS. Numbers needed to treat (NNT) and 95 % confidence intervals (CI) were also calculated at the 3 months follow-up period using each of these definitions for a successful outcome. Data analysis was performed using SPSS 21.0.

 

Results

 

Two hundred and fifty-one patients with a primary complaint of headaches were screened for possible eligibility. The reasons for ineligibility can be found in Fig. 3, the flow diagram of patient recruitment and retention. Of the 251 patients screened, 110 patients, with a mean age of 35.16 years (SD 11.48) and a mean duration of symptoms of 4.56 years (SD 6.27), satisfied the eligibility criteria, agreed to participate, and were randomized into manipulation (n?=?58) and mobilization and exercise (n?=?52) groups. Baseline variables for each group can be found in Table 1. Twelve therapists from 8 outpatient physical therapy clinics each treated 25, 23, 20, 14, 13, 7, 6 or 2 patients, respectively; furthermore, each of the 12 therapists treated approximately an equal proportion of patients in each group. There was no significant difference (p?=?0.227) between the mean number of completed treatment sessions for the manipulation group (7.17, SD 0.96) and the mobilization and exercise group (6.90, SD 1.35). In addition, the mean number of treatment sessions that targeted the C1-2 articulation was 6.41 (SD 1.63) for the manipulation group and 6.52 (SD 2.01) for the mobilization and exercise group, and this was not significantly different (p?=?0.762). One hundred seven of the 110 patients completed all outcome measures through 3 months (97 % follow-up). Little�s Missing Completely at Random (MCAR) test was not statistically significant (p?=?0.281); therefore, we used the Expectation-Maximization imputation technique to replace missing values with predicted values for the missing 3-month outcomes.

 

Figure 3 Flow Diagram of Patient Recruitment and Retention | El Paso, TX Chiropractor

 

Table 1 Baseline Variables, Demographics and Outcome Measures | El Paso, TX Chiropractor

 

The overall group by time interaction for the primary outcome of headache intensity was statistically significant for the NPRS (F(3,106)?=?11.196; p?<?0.001; partial eta squared?=?0.24). Between-group differences revealed that the manipulation group experienced statistically significant greater improvement in the NPRS at both the 1-week (2.1, 95 % CI: 1.2, 2.9), 4-week (2.3, 95 % CI: 1.5, 3.1) and 3-month (2.1, 95 % CI: 1.2, 3.0) follow-up periods (Table 2). In addition, an independent samples t-test revealed the between-group difference in percentage change in headache intensity (36.58 %, 95 % CI: 22.52, 50.64) from baseline to 3-month follow-up was statistically significant (t(108)?=?5.156; p?<?0.001) in favor of manipulation. See Table 3 for the percentage of subjects gaining 50, 75, and 100 % reduction in headache intensity at 3 months.

 

Table 2 Changes in Headache Intensity and Disability | El Paso, TX Chiropractor

 

Table 3 Percentage of Subjects Gaining 50, 75, and 100 Percent Reduction | El Paso, TX Chiropractor

 

For secondary outcomes a significant group by time interaction existed for the NDI (F(3,106)?=?8.57; p?<?0.001; partial eta squared?=?0.20). At each follow-up period the manipulation group had superior outcomes in disability reduction as compared to the mobilization and exercise group. An independent samples t- test revealed the between-group mean percentage change in disability (35.56 %, 95 % CI: 24.95, 46.17) from baseline to 3 months follow-up was statistically significant (t(108)?=?6.646, p?<?0.001); indicating the manipulation group experienced a significantly greater percentage in disability reduction (Table 3).

 

Mann�Whitney U tests revealed that patients in the upper cervical and upper thoracic manipulation group experienced less frequent headaches at 1 week (p?<?0.001; median 2.0 versus 3.0), 4 weeks (p?<?0.001; median 1.0 versus 3.0) and 3 months (p?<?0.001; median 1.0 versus 2.5) than patients in the mobilization and exercise group. Headache duration was significantly lower at 1 week (p?=?0.005; median 2.0 versus 3.0, 4 weeks (p?<?0.001; median 1.0 versus 2.0) and 3 months (p?<?0.001; median 1.0 versus 2.0) in the manipulation group. Additionally, patient perceived improvement as measured by the GRC was significantly greater at 1 week (p?<?0.001, 4.0 versus 1.0), 4 weeks (p?<?0.001, 6.0 versus 3.0) and 3 months (p?<?0.001, 6.0 versus 3.0) than patients in the mobilization and exercise group. At 3 months, patients receiving upper cervical and upper thoracic manipulation experienced significantly (p?<?0.001) greater reductions in medication intake as compared to the mobilization and exercise group. Based on the cutoff score of 2 points on the NPRS, the NNT was 4.0 (95 % CI: 2.3, 7.7) in favor of the manipulation group at 3-month follow-up.

 

We did not collect any data on the occurrence of �minor� adverse events [48, 49] (transient neurological symptoms, increased stiffness, radiating pain, fatigue or other); however, no �major� adverse events [48, 49] (stroke or permanent neurological deficits) were reported for either group.

 

Discussion

 

Statement of Principal Findings

 

To our knowledge, this study is the first randomized clinical trial to directly compare the effectiveness of both cervical and thoracic manipulation to mobilization and exercise in patients with CH. The results suggest 6�8 sessions of manipulation over 4 weeks, directed mainly to both the upper cervical (C1-2) and upper thoracic (T1-2) spines, resulted in greater improvements in headache intensity, disability, headache frequency, headache duration, and medication intake than mobilization combined with exercises. The point estimates for between-group changes in headache intensity (2.1 points) and disability (6.0 points or 12.0 %) exceeded the reported MCIDs for both measures. Although the MCID for the NDI in patients with CH has not yet been investigated, it should however be noted that the lower bound estimate of the 95 % CI for disability (3.5 points) was slightly below (or approximated in two cases) the MCID that has been found to be 3.5 [65], 5 [66], and 7.5 [45] points in patients with mechanical neck pain, 8.5 [33] points in patients with cervical radiculopathy, and 3.5 [44] points in patients with mixed, non-specific neck pain. However, it should be recognized that both groups made clinical improvement. In addition, the NNT suggests for every four patients treated with manipulation, rather than mobilization, one additional patient achieves clinically important pain reduction at 3 months follow-up.

 

Strengths and Weaknesses of the Study

 

The inclusion of 12 treating physical therapists from 8 private clinics in 6 different geographical states enhances the overall generalizability of our findings. Although significant differences were recognized up to 3 months, it is not known if these benefits would have been sustained at long-term. In addition, we used high-velocity, low-amplitude manipulation techniques that employed bidirectional thrusts into rotation and translation simultaneously and Maitland based grade IV PA mobilization techniques; thus, we cannot be certain that these results are generalizable to other kinds of manual therapy techniques. Some might argue that the comparison group might have not received adequate intervention. We sought to balance internal and external validity so standardized treatment for both groups and provided a very explicit description of the techniques used which will also allow for replication. Furthermore, we did not measure minor adverse events and only asked about two potential major adverse events. Another limitation is that we included multiple secondary outcomes. Therapist preferences as to which technique they thought would be superior was not collected and potentially could impact the results.

 

Strengths and Weaknesses in Relation to Other Studies: Important Differences in Results

 

Jull et al. [11] demonstrated treatment efficacy for manipulative therapy and exercise in the management of CH; however, this treatment package included both mobilization and manipulation. The current study may provide evidence that the management of patients with CH should include some form of manipulation despite the fact it is often suggested that cervical manipulation should be avoided because of the risk of serious adverse events [67, 68]. Furthermore, it has been shown that individuals receiving spinal manipulation for neck pain and headaches are no more likely to experience a vertebrobasilar stroke than if they received treatment by their medical physician [69]. Additionally, after reviewing 134 case reports, Puentedura et al. concluded that with appropriate selection of patients by careful screening of red flags and contraindications, the majority of adverse events associated with cervical manipulation could have been prevented [70].

 

Meaning of the Study: Possible Explanations and Implications for Clinicians and Policymakers

 

Based on the results of the current study clinicians should consider incorporating spinal manipulation for individuals with CH. A recent systematic review found both mobilization and manipulation to be effective for the management of patients with CH but was unable to determine which technique was superior [8]. Additionally, clinical guidelines reported that manipulation, mobilization and exercise were all effective for the management of patients with CH; however, the guideline made no suggestions regarding the superiority of either technique. [71] The current results may assist authors of future systematic reviews and clinical guidelines in providing more specific recommendations about the use of spinal manipulation in this population.

 

Unanswered Questions and Future Research

 

The underlying mechanisms as to why manipulation may have resulted in greater improvements remains to be elucidated. It has been suggested that high-velocity displacement of vertebrae with impulse durations of less than 200 ms may alter afferent discharge rates [72] by stimulating mechanoreceptors and proprioceptors, thereby changing alpha motorneuron excitability levels and subsequent muscle activity [72�74]. Manipulation might also stimulate receptors in the deep paraspinal musculature, and mobilization might be more likely to facilitate receptors in the superficial muscles [75]. Biomechanical [76, 77], spinal or segmental [78, 79] and central descending inhibitory pain pathway [80�83] models are plausible explanations for the hypoalgesic effects observed following manipulation. Recently, the biomechanical effects of manipulation have been under scientific scrutiny [84], and it is plausible that the clinical benefits found in our study are associated with a neurophysiological response involving temporal sensory summation at the dorsal horn of the spinal cord [78]; however, this proposed model is currently supported only on findings from transient, experimentally induced pain in healthy subjects [85, 86], not patients with CH. Future studies should examine different manual therapy techniques with varying dosages and include a 1-year follow-up. Furthermore, future studies examining the neurophysiological effects of both manipulation and mobilization will be important for determining why there may or may not be a difference in clinical effects between these two treatments.

 

Conclusion

 

The results of the current study demonstrated that patients with CH who received cervical and thoracic manipulation experienced significantly greater reductions in headache intensity, disability, headache frequency, headache duration, and medication intake as compared to the group that received mobilization and exercise; furthermore, the effects were maintained at 3 months follow-up. Future studies should examine the effectiveness of different types and dosages of manipulation and include a long-term follow-up.

 

Acknowledgements

 

None of the authors received any funding for this study. The authors wish to thank all the participants of the study.

 

Footnotes

 

  • Competing interests: Dr. James Dunning is the President of the American Academy of Manipulative Therapy (AAMT). AAMT provides postgraduate training programs in spinal manipulation, spinal mobilization, dry needling, extremity manipulation, extremity mobilization, instrument-assisted soft-tissue mobilization and therapeutic exercise to licensed physical therapists, osteopaths and medical doctors. Drs. James Dunning, Raymond Butts, Thomas Perreault, and Firas Mourad are senior instructors for AAMT. The other authors declare that they have no competing interests.
  • Authors� contributions: JRD participated in the conception, design, data acquisition, statistical analyses and drafting of the manuscript. RB and IY participated in the design, data collection, statistical analyses and revision of the manuscript. FM participated in the design, statistical analyses, data interpretation and revision of the manuscript. MH participated in the conception, design and revision of the manuscript. CF and JC were involved in the statistical analyses, interpretation of data, and critical revision of the manuscript for important intellectual content. TS, JD, DB, and TH were involved in data collection and revision of the manuscript. All authors read and approved the final manuscript.

 

Contributor Information

 

Ncbi.nlm.nih.gov/pmc/articles/PMC4744384/

 

In conclusion,�head pain caused by secondary headache due to a health issue along the surrounding structures of the cervical spine, or neck, can cause painful and debilitating symptoms which can affect the patient’s quality of life. Spinal manipulation and mobilization can be safely and effectively utilized to help improve cervicogenic headache symptoms. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Back Pain

 

According to statistics, approximately 80% of people will experience symptoms of back pain at least once throughout their lifetimes. Back pain is a common complaint which can result due to a variety of injuries and/or conditions. Often times, the natural degeneration of the spine with age can cause back pain. Herniated discs occur when the soft, gel-like center of an intervertebral disc pushes through a tear in its surrounding, outer ring of cartilage, compressing and irritating the nerve roots. Disc herniations most commonly occur along the lower back, or lumbar spine, but they may also occur along the cervical spine, or neck. The impingement of the nerves found in the low back due to injury and/or an aggravated condition can lead to symptoms of sciatica.

 

blog picture of cartoon paperboy big news

 

EXTRA IMPORTANT TOPIC: Migraine Pain Treatment

 

 

MORE TOPICS: EXTRA EXTRA: El Paso, Tx | Athletes

 

Blank
References
1.�The International Classifcation of Headache Disorders: 3rd Edition. Cephalalgia. 2013;33(9):629-808.[PubMed]
2.�Anthony M. Cervicogenic headache: prevalence and response to local steroid therapy.�Clin Exp Rheumatol.�2000;18(2 Suppl 19):S59�64.�[PubMed]
3.�Nilsson N. The prevalence of cervicogenic headache in a random population sample of 20-59 year olds.�Spine (Phila Pa 1976)�1995;20(17):1884�8. doi: 10.1097/00007632-199509000-00008.�[PubMed][Cross Ref]
4.�Bogduk N, Govind J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment.�Lancet Neurol.�2009;8(10):959�68. doi: 10.1016/S1474-4422(09)70209-1.[PubMed][Cross Ref]
5.�Sjaastad O, Fredriksen TA, Pfaffenrath V. Cervicogenic headache: diagnostic criteria. The Cervicogenic Headache International Study Group.�Headache.�1998;38(6):442�5. doi: 10.1046/j.1526-4610.1998.3806442.x.�[PubMed][Cross Ref]
6.�Fernandez-de-Las-Penas C, Alonso-Blanco C, Cuadrado ML, Pareja JA. Spinal manipulative therapy in the management of cervicogenic headache.�Headache.�2005;45(9):1260�3. doi: 10.1111/j.1526-4610.2005.00253_1.x.�[PubMed][Cross Ref]
7.�Maitland GD.�Vertebral Manipulation.�5. Oxford: Butterworth-Heinemann; 1986.
8.�Bronfort G, Haas M, Evans R, Leininger B, Triano J. Effectiveness of manual therapies: the UK evidence report.�Chiropr Osteopat.�2010;18:3. doi: 10.1186/1746-1340-18-3.�[PMC free article][PubMed][Cross Ref]
9.�Haas M, Groupp E, Aickin M, Fairweather A, Ganger B, Attwood M, et al. Dose response for chiropractic care of chronic cervicogenic headache and associated neck pain: a randomized pilot study.�J Manipulative Physiol Ther.�2004;27(9):547�53. doi: 10.1016/j.jmpt.2004.10.007.�[PubMed][Cross Ref]
10.�Haas M, Spegman A, Peterson D, Aickin M, Vavrek D. Dose response and efficacy of spinal manipulation for chronic cervicogenic headache: a pilot randomized controlled trial.�Spine J.�2010;10(2):117�28. doi: 10.1016/j.spinee.2009.09.002.�[PMC free article][PubMed][Cross Ref]
11.�Jull G, Trott P, Potter H, Zito G, Niere K, Shirley D, et al. A randomized controlled trial of exercise and manipulative therapy for cervicogenic headache.�Spine (Phila Pa 1976)�2002;27(17):1835�43. doi: 10.1097/00007632-200209010-00004.�[PubMed][Cross Ref]
12.�Nilsson N. A randomized controlled trial of the effect of spinal manipulation in the treatment of cervicogenic headache.�J Manipulative Physiol Ther.�1995;18(7):435�40.�[PubMed]
13.�Nilsson N, Christensen HW, Hartvigsen J. The effect of spinal manipulation in the treatment of cervicogenic headache.�J Manipulative Physiol Ther.�1997;20(5):326�30.�[PubMed]
14.�Dunning JR, Cleland JA, Waldrop MA, Arnot CF, Young IA, Turner M, et al. Upper cervical and upper thoracic thrust manipulation versus nonthrust mobilization in patients with mechanical neck pain: a multicenter randomized clinical trial.�J Orthop Sports Phys Ther.�2012;42(1):5�18. doi: 10.2519/jospt.2012.3894.�[PubMed][Cross Ref]
15.�Hurwitz EL, Morgenstern H, Harber P, Kominski GF, Yu F, Adams AH. A randomized trial of chiropractic manipulation and mobilization for patients with neck pain: clinical outcomes from the UCLA neck-pain study.�Am J Public Health.�2002;92(10):1634�41. doi: 10.2105/AJPH.92.10.1634.[PMC free article][PubMed][Cross Ref]
16.�Leaver AM, Maher CG, Herbert RD, Latimer J, McAuley JH, Jull G, et al. A randomized controlled trial comparing manipulation with mobilization for recent onset neck pain.�Arch Phys Med Rehabil.�2010;91(9):1313�8. doi: 10.1016/j.apmr.2010.06.006.�[PubMed][Cross Ref]
17.�Wand BM, Heine PJ, O’Connell NE. Should we abandon cervical spine manipulation for mechanical neck pain? Yes.�BMJ.�2012;344:e3679. doi: 10.1136/bmj.e3679.�[PubMed][Cross Ref]
18.�Sjaastad O, Fredriksen TA. Cervicogenic headache: criteria, classification and epidemiology.�Clin Exp Rheumatol.�2000;18(2 Suppl 19):S3�6.�[PubMed]
19.�Vincent MB, Luna RA. Cervicogenic headache: a comparison with migraine and tension-type headache.�Cephalalgia.�1999;19(Suppl 25):11�6. doi: 10.1177/0333102499019S2503.�[PubMed][Cross Ref]
20.�Zwart JA. Neck mobility in different headache disorders.�Headache.�1997;37(1):6�11. doi: 10.1046/j.1526-4610.1997.3701006.x.�[PubMed][Cross Ref]
21.�Hall T, Robinson K. The flexion-rotation test and active cervical mobility–a comparative measurement study in cervicogenic headache.�Man Ther.�2004;9(4):197�202. doi: 10.1016/j.math.2004.04.004.[PubMed][Cross Ref]
22.�Hall TM, Briffa K, Hopper D, Robinson KW. The relationship between cervicogenic headache and impairment determined by the flexion-rotation test.�J Manipulative Physiol Ther.�2010;33(9):666�71. doi: 10.1016/j.jmpt.2010.09.002.�[PubMed][Cross Ref]
23.�Ogince M, Hall T, Robinson K, Blackmore AM. The diagnostic validity of the cervical flexion-rotation test in C1/2-related cervicogenic headache.�Man Ther.�2007;12(3):256�62. doi: 10.1016/j.math.2006.06.016.�[PubMed][Cross Ref]
24.�Hutting N, Verhagen AP, Vijverman V, Keesenberg MD, Dixon G, Scholten-Peeters GG. Diagnostic accuracy of premanipulative vertebrobasilar insufficiency tests: a systematic review.�Man Ther.�2013;18(3):177�82. doi: 10.1016/j.math.2012.09.009.�[PubMed][Cross Ref]
25.�Kerry R, Taylor AJ, Mitchell J, McCarthy C. Cervical arterial dysfunction and manual therapy: a critical literature review to inform professional practice.�Man Ther.�2008;13(4):278�88. doi: 10.1016/j.math.2007.10.006.�[PubMed][Cross Ref]
26.�Thomas LC, Rivett DA, Bateman G, Stanwell P, Levi CR. Effect of selected manual therapy interventions for mechanical neck pain on vertebral and internal carotid arterial blood flow and cerebral inflow.�Phys Ther.�2013;93(11):1563�74. doi: 10.2522/ptj.20120477.�[PubMed][Cross Ref]
27.�Quesnele JJ, Triano JJ, Noseworthy MD, Wells GD. Changes in vertebral artery blood flow following various head positions and cervical spine manipulation.�J Manipulative Physiol Ther.�2014;37(1):22�31. doi: 10.1016/j.jmpt.2013.07.008.�[PubMed][Cross Ref]
28.�Taylor AJ, Kerry R. The ‘vertebral artery test’.�Man Ther.�2005;10(4):297. doi: 10.1016/j.math.2005.02.005.�[PubMed][Cross Ref]
29.�Kerry R, Taylor AJ, Mitchell J, McCarthy C, Brew J. Manual therapy and cervical arterial dysfunction, directions for the future: a clinical perspective.�J Man Manip Ther.�2008;16(1):39�48. doi: 10.1179/106698108790818620.�[PMC free article][PubMed][Cross Ref]
30.�Hall TM, Robinson KW, Fujinawa O, Akasaka K, Pyne EA. Intertester reliability and diagnostic validity of the cervical flexion-rotation test.�J Manipulative Physiol Ther.�2008;31(4):293�300. doi: 10.1016/j.jmpt.2008.03.012.�[PubMed][Cross Ref]
31.�Jensen MP, Karoly P, Braver S. The measurement of clinical pain intensity: a comparison of six methods.�Pain.�1986;27(1):117�26. doi: 10.1016/0304-3959(86)90228-9.�[PubMed][Cross Ref]
32.�Cleland JA, Childs JD, Whitman JM. Psychometric properties of the Neck Disability Index and numeric pain rating scale in patients with mechanical neck pain.�Arch Phys Med Rehabil.�2008;89(1):69�74. doi: 10.1016/j.apmr.2007.08.126.�[PubMed][Cross Ref]
33.�Young IA, Cleland JA, Michener LA, Brown C. Reliability, construct validity, and responsiveness of the Neck Disability Index, patient-specific functional scale, and numeric pain rating scale in patients with cervical radiculopathy.�Am J Phys Med Rehabil.�2010;89(10):831�9. doi: 10.1097/PHM.0b013e3181ec98e6.�[PubMed][Cross Ref]
34.�Farrar JT, Young JP, Jr, LaMoreaux L, Werth JL, Poole RM. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale.�Pain.�2001;94(2):149�58. doi: 10.1016/S0304-3959(01)00349-9.�[PubMed][Cross Ref]
35.�Vernon H. The Neck Disability Index: state-of-the-art, 1991-2008.�J Manipulative Physiol Ther.�2008;31(7):491�502. doi: 10.1016/j.jmpt.2008.08.006.�[PubMed][Cross Ref]
36.�MacDermid JC, Walton DM, Avery S, Blanchard A, Etruw E, McAlpine C, et al. Measurement properties of the Neck Disability Index: a systematic review.�J Orthop Sports Phys Ther.�2009;39(5):400�17. doi: 10.2519/jospt.2009.2930.�[PubMed][Cross Ref]
37.�Pietrobon R, Coeytaux RR, Carey TS, Richardson WJ, DeVellis RF. Standard scales for measurement of functional outcome for cervical pain or dysfunction: a systematic review.�Spine (Phila Pa 1976)�2002;27(5):515�22. doi: 10.1097/00007632-200203010-00012.�[PubMed][Cross Ref]
38.�Vernon H, Mior S. The Neck Disability Index: a study of reliability and validity.�J Manipulative Physiol Ther.�1991;14(7):409�15.�[PubMed]
39.�Vernon H. The psychometric properties of the Neck Disability Index.�Arch Phys Med Rehabil.�2008;89(7):1414�5. doi: 10.1016/j.apmr.2008.05.003.�[PubMed][Cross Ref]
40.�Cleland JA, Fritz JM, Whitman JM, Palmer JA. The reliability and construct validity of the Neck Disability Index and patient specific functional scale in patients with cervical radiculopathy.�Spine (Phila Pa 1976)�2006;31(5):598�602. doi: 10.1097/01.brs.0000201241.90914.22.�[PubMed][Cross Ref]
41.�Hoving JL, O’Leary EF, Niere KR, Green S, Buchbinder R. Validity of the neck disability index, Northwick Park neck pain questionnaire, and problem elicitation technique for measuring disability associated with whiplash-associated disorders.�Pain.�2003;102(3):273�81. doi: 10.1016/S0304-3959(02)00406-2.�[PubMed][Cross Ref]
42.�Miettinen T, Leino E, Airaksinen O, Lindgren KA. The possibility to use simple validated questionnaires to predict long-term health problems after whiplash injury.�Spine (Phila Pa 1976)�2004;29(3):E47�51. doi: 10.1097/01.BRS.0000106496.23202.60.�[PubMed][Cross Ref]
43.�McCarthy MJ, Grevitt MP, Silcocks P, Hobbs G. The reliability of the Vernon and Mior neck disability index, and its validity compared with the short form-36 health survey questionnaire.�Eur Spine J.�2007;16(12):2111�7. doi: 10.1007/s00586-007-0503-y.�[PMC free article][PubMed][Cross Ref]
44.�Pool JJ, Ostelo RW, Hoving JL, Bouter LM, de Vet HC. Minimal clinically important change of the Neck Disability Index and the Numerical Rating Scale for patients with neck pain.�Spine (Phila Pa 1976)�2007;32(26):3047�51. doi: 10.1097/BRS.0b013e31815cf75b.�[PubMed][Cross Ref]
45.�Young BA, Walker MJ, Strunce JB, Boyles RE, Whitman JM, Childs JD. Responsiveness of the Neck Disability Index in patients with mechanical neck disorders.�Spine J.�2009;9(10):802�8. doi: 10.1016/j.spinee.2009.06.002.�[PubMed][Cross Ref]
46.�Jaeschke R, Singer J, Guyatt GH. Measurement of health status. Ascertaining the minimal clinically important difference.�Control Clin Trials.�1989;10(4):407�15. doi: 10.1016/0197-2456(89)90005-6.[PubMed][Cross Ref]
47.�Schmitt J, Abbott JH. Global ratings of change do not accurately reflect functional change over time in clinical practice.�J Orthop Sports Phys Ther.�2015;45(2):106�11. doi: 10.2519/jospt.2015.5247.�[PubMed][Cross Ref]
48.�Carlesso L, Macdermid JC, Santaguida L. Standardization of adverse event terminology and reporting in orthopaedic physical therapy – applications to the cervical spine.�J Orthop Sports Phys Ther.�2010;40:455�63. doi: 10.2519/jospt.2010.3229.�[PubMed][Cross Ref]
49.�Carlesso LC, Gross AR, Santaguida PL, Burnie S, Voth S, Sadi J. Adverse events associated with the use of cervical manipulation and mobilization for the treatment of neck pain in adults: a systematic review.�Man Ther.�2010;15(5):434�44. doi: 10.1016/j.math.2010.02.006.�[PubMed][Cross Ref]
50.�Cleland JA, Glynn P, Whitman JM, Eberhart SL, MacDonald C, Childs JD. Short-term effects of thrust versus nonthrust mobilization/manipulation directed at the thoracic spine in patients with neck pain: a randomized clinical trial.�Phys Ther.�2007;87(4):431�40. doi: 10.2522/ptj.20060217.�[PubMed][Cross Ref]
51.�Gonzalez-Iglesias J, Fernandez-de-las-Penas C, Cleland JA, Alburquerque-Sendin F, Palomeque-del-Cerro L, Mendez-Sanchez R. Inclusion of thoracic spine thrust manipulation into an electro-therapy/thermal program for the management of patients with acute mechanical neck pain: a randomized clinical trial.�Man Ther.�2009;14(3):306�13. doi: 10.1016/j.math.2008.04.006.�[PubMed][Cross Ref]
52.�Gonzalez-Iglesias J, Fernandez-de-las-Penas C, Cleland JA, Gutierrez-Vega MR. Thoracic spine manipulation for the management of patients with neck pain: a randomized clinical trial.�J Orthop Sports Phys Ther.�2009;39(1):20�7. doi: 10.2519/jospt.2009.2914.�[PubMed][Cross Ref]
53.�Lau HM, Wing Chiu TT, Lam TH. The effectiveness of thoracic manipulation on patients with chronic mechanical neck pain – a randomized controlled trial.�Man Ther.�2011;16(2):141�7. doi: 10.1016/j.math.2010.08.003.�[PubMed][Cross Ref]
54.�Beffa R, Mathews R. Does the adjustment cavitate the targeted joint? An investigation into the location of cavitation sounds.�J Manipulative Physiol Ther.�2004;27(2):e2. doi: 10.1016/j.jmpt.2003.12.014.[PubMed][Cross Ref]
55.�Dunning J, Mourad F, Barbero M, Leoni D, Cescon C, Butts R. Bilateral and multiple cavitation sounds during upper cervical thrust manipulation.�BMC Musculoskelet Disord.�2013;14:24. doi: 10.1186/1471-2474-14-24.�[PMC free article][PubMed][Cross Ref]
56.�Reggars JW. The manipulative crack. Frequency analysis.�Australas Chiropr Osteopathy.�1996;5(2):39�44.�[PMC free article][PubMed]
57.�Ross JK, Bereznick DE, McGill SM. Determining cavitation location during lumbar and thoracic spinal manipulation: is spinal manipulation accurate and specific?�Spine (Phila Pa 1976)�2004;29(13):1452�7. doi: 10.1097/01.BRS.0000129024.95630.57.�[PubMed][Cross Ref]
58.�Evans DW, Lucas N. What is ‘manipulation’? A reappraisal.�Man Ther.�2010;15(3):286�91. doi: 10.1016/j.math.2009.12.009.�[PubMed][Cross Ref]
59.�Gross A, Miller J, D’Sylva J, Burnie SJ, Goldsmith CH, Graham N, et al. Manipulation or mobilisation for neck pain: a cochrane review.�Man Ther.�2010;15(4):315�33. doi: 10.1016/j.math.2010.04.002.[PubMed][Cross Ref]
60.�Moss P, Sluka K, Wright A. The initial effects of knee joint mobilization on osteoarthritic hyperalgesia.�Man Ther.�2007;12(2):109�18. doi: 10.1016/j.math.2006.02.009.�[PubMed][Cross Ref]
61.�Falla D, Bilenkij G, Jull G. Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task.�Spine (Phila Pa 1976)�2004;29(13):1436�40. doi: 10.1097/01.BRS.0000128759.02487.BF.�[PubMed][Cross Ref]
62.�Falla D, Jull G, Dall’Alba P, Rainoldi A, Merletti R. An electromyographic analysis of the deep cervical flexor muscles in performance of craniocervical flexion.�Phys Ther.�2003;83(10):899�906.�[PubMed]
63.�Jull G. Deep cervical flexor muscle dysfunction in whiplash.�Journal of Musculoskeletal Pain.�2000;8:143�54. doi: 10.1300/J094v08n01_12.�[Cross Ref]
64.�Rubin LH, Witkiewitz K, Andre JS, Reilly S. Methods for handling missing data in the behavioral neurosciences: Don’t throw the baby Rat out with the bath water.�J Undergrad Neurosci Educ.�2007;5(2):A71�7.�[PMC free article][PubMed]
65.�Jorritsma W, Dijkstra PU, de Vries GE, Geertzen JH, Reneman MF. Detecting relevant changes and responsiveness of neck pain and disability scale and Neck Disability Index.�Eur Spine J.�2012;21(12):2550�7. doi: 10.1007/s00586-012-2407-8.�[PMC free article][PubMed][Cross Ref]
66.�Stratford PW, Riddle DL, Binkley JM, Spadoni G, Westaway MD, Padfield B. Using the Neck Disability Index to make decisions concerning individual patients.�Physiother Can.�1999;51:107�12.
67.�Ernst E. Manipulation of the cervical spine: a systematic review of case reports of serious adverse events, 1995-2001.�Med J Aust.�2002;176(8):376�80.�[PubMed]
68.�Oppenheim JS, Spitzer DE, Segal DH. Nonvascular complications following spinal manipulation.�Spine J.�2005;5(6):660�6. doi: 10.1016/j.spinee.2005.08.006.�[PubMed][Cross Ref]
69.�Cassidy JD, Boyle E, Cote P, He Y, Hogg-Johnson S, Silver FL, et al. Risk of vertebrobasilar stroke and chiropractic care: results of a population-based case-control and case-crossover study.�Spine (Phila Pa 1976)�2008;33(4 Suppl):S176�83. doi: 10.1097/BRS.0b013e3181644600.�[PubMed][Cross Ref]
70.�Puentedura EJ, March J, Anders J, Perez A, Landers MR, Wallmann HW, et al. Safety of cervical spine manipulation: are adverse events preventable and are manipulations being performed appropriately? A review of 134 case reports.�J Man Manip Ther.�2012;20(2):66�74. doi: 10.1179/2042618611Y.0000000022.[PMC free article][PubMed][Cross Ref]
71.�Childs JD, Cleland JA, Elliott JM, Teyhen DS, Wainner RS, Whitman JM, et al. Neck pain: clinical practice guidelines linked to the international classification of functioning, disability, and health from the orthopedic section of the American Physical Therapy Association.�J Orthop Sports Phys Ther.�2008;38(9):A1�A34. doi: 10.2519/jospt.2008.0303.�[PubMed][Cross Ref]
72.�Pickar JG, Kang YM. Paraspinal muscle spindle responses to the duration of a spinal manipulation under force control.�J Manipulative Physiol Ther.�2006;29(1):22�31. doi: 10.1016/j.jmpt.2005.11.014.[PubMed][Cross Ref]
73.�Herzog W, Scheele D, Conway PJ. Electromyographic responses of back and limb muscles associated with spinal manipulative therapy.�Spine (Phila Pa 1976)�1999;24(2):146�52. doi: 10.1097/00007632-199901150-00012.�[PubMed][Cross Ref]
74.�Indahl A, Kaigle AM, Reikeras O, Holm SH. Interaction between the porcine lumbar intervertebral disc, zygapophysial joints, and paraspinal muscles.�Spine (Phila Pa 1976)�1997;22(24):2834�40. doi: 10.1097/00007632-199712150-00006.�[PubMed][Cross Ref]
75.�Bolton PS, Budgell BS. Spinal manipulation and spinal mobilization influence different axial sensory beds.�Med Hypotheses.�2006;66(2):258�62. doi: 10.1016/j.mehy.2005.08.054.�[PubMed][Cross Ref]
76.�Cassidy JD, Lopes AA, Yong-Hing K. The immediate effect of manipulation versus mobilization on pain and range of motion in the cervical spine: a randomized controlled trial.�J Manipulative Physiol Ther.�1992;15(9):570�5.�[PubMed]
77.�Martinez-Segura R, Fernandez-de-las-Penas C, Ruiz-Saez M, Lopez-Jimenez C, Rodriguez-Blanco C. Immediate effects on neck pain and active range of motion after a single cervical high-velocity low-amplitude manipulation in subjects presenting with mechanical neck pain: a randomized controlled trial.�J Manipulative Physiol Ther.�2006;29(7):511�7. doi: 10.1016/j.jmpt.2006.06.022.�[PubMed][Cross Ref]
78.�Bialosky JE, Bishop MD, Price DD, Robinson ME, George SZ. The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model.�Man Ther.�2009;14(5):531�8. doi: 10.1016/j.math.2008.09.001.�[PMC free article][PubMed][Cross Ref]
79.�Dunning J, Rushton A. The effects of cervical high-velocity low-amplitude thrust manipulation on resting electromyographic activity of the biceps brachii muscle.�Man Ther.�2009;14(5):508�13. doi: 10.1016/j.math.2008.09.003.�[PubMed][Cross Ref]
80.�Haavik-Taylor H, Murphy B. Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study.�Clin Neurophysiol.�2007;118(2):391�402. doi: 10.1016/j.clinph.2006.09.014.�[PubMed][Cross Ref]
81.�Millan M. Descending control of pain.�Prog Neurobiology.�2002;66:355�74. doi: 10.1016/S0301-0082(02)00009-6.�[PubMed][Cross Ref]
82.�Skyba D, Radhakrishnan R, Rohlwing J, Wright A, Sluka K. Joint manipulation reduces hyperalgesia by activation of monoamine receptors but not opioid or GABA receptors in the spinal cord.�Pain.�2003;106:159�68. doi: 10.1016/S0304-3959(03)00320-8.�[PMC free article][PubMed][Cross Ref]
83.�Zusman M. Forebrain-mediated sensitization of central pain pathways: “non-specific” pain and a new image for manual therapy.�Man Ther.�2002;7:80�8. doi: 10.1054/math.2002.0442.�[PubMed][Cross Ref]
84.�Bialosky JE, George SZ, Bishop MD. How spinal manipulative therapy works: why ask why?�J Orthop Sports Phys Ther.�2008;38(6):293�5. doi: 10.2519/jospt.2008.0118.�[PubMed][Cross Ref]
85.�Bishop MD, Beneciuk JM, George SZ. Immediate reduction in temporal sensory summation after thoracic spinal manipulation.�Spine J.�2011;11(5):440�6. doi: 10.1016/j.spinee.2011.03.001.[PMC free article][PubMed][Cross Ref]
86.�George SZ, Bishop MD, Bialosky JE, Zeppieri G, Jr, Robinson ME. Immediate effects of spinal manipulation on thermal pain sensitivity: an experimental study.�BMC Musculoskelet Disord.�2006;7:68. doi: 10.1186/1471-2474-7-68.�[PMC free article][PubMed][Cross Ref]
Close Accordion
Psychological Therapy for Chronic Pain Management in El Paso, TX

Psychological Therapy for Chronic Pain Management in El Paso, TX

Psychological therapy, also known as psychotherapy, refers to the use of psychological methods to help change an individual’s way of thinking as well as improve their coping skills in order for them to learn how to best deal with stress. Psychological therapies have widely been utilized as a part of the multidisciplinary management of chronic pain. Common psychotherapies include, cognitive-behavioral therapy, mindfulness-based stress reduction and even chiropractic care. The connection between the mind and the body in relation to disease and illness have long been discussed in many research studies.

 

Evidence-based research studies have demonstrated that proper stress management through the use of psychological therapy as well as mindfulness interventions can effectively benefit patients with chronic pain. By way of instance, chiropractic care can safely and effectively help reduce stress, anxiety and depression by correcting spinal misalignments, or subluxation. A balanced spine can improve mood and mental health. Chiropractic care can include lifestyle modifications, such as nutritional advice, physical activity and exercise recommendations, and promote better sleeping habits, to further enhance the benefits of the treatment. The purpose of the following article is to demonstrate how psychological therapies impact the management of chronic pain.

 

Dr.-Jimenez-works-on-patients-back.jpg

 

Psychological Therapies for the Management of Chronic Pain

 

Abstract

 

Pain is a complex stressor that presents a significant challenge to most aspects of functioning and contributes to substantial physical, psychological, occupational, and financial cost, particularly in its chronic form. As medical intervention frequently cannot resolve pain completely, there is a need for management approaches to chronic pain, including psychological intervention. Psychotherapy for chronic pain primarily targets improvements in physical, emotional, social, and occupational functioning rather than focusing on resolution of pain itself. However, psychological therapies for chronic pain differ in their scope, duration, and goals, and thus show distinct patterns of treatment efficacy. These therapies fall into four categories: operant-behavioral therapy, cognitive-behavioral therapy, mindfulness-based therapy, and acceptance and commitment therapy. The current article explores the theoretical distinctiveness, therapeutic targets, and effectiveness of these approaches as well as mechanisms and individual differences that factor into treatment response and pain-related dysfunction and distress. Implications for future research, dissemination of treatment, and the integration of psychological principles with other treatment modalities are also discussed.

 

Keywords: pain management, multidisciplinary pain treatment, psychological therapy

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

Chiropractic care is an alternative treatment option which utilizes spinal adjustments and manual manipulations to treat injuries and/or conditions associated with the musculoskeletal and nervous system. Chiropractic treatment primarily focuses on spinal health, however, because the spine is the root of the nervous system, chiropractic care can also be effectively used to treat a variety of mental health issues. As a chiropractor, I make sure to focus on the body as a whole, rather than treating the symptoms of a single injury and/or condition. The truth of the matter is, chiropractic treatment must also deal with the emotional component of each health issue in order to provide overall relief. Psychosomatic disorders, refers to a physical illness caused or aggravated by a mental factor, such as stress. Chiropractic care can be utilized as a psychological therapy, in which, a chiropractor may recommend a series of lifestyle modifications to help reduce stress, anxiety and depression, together with spinal adjustments and manual manipulations to reduce symptoms associated with mental health issues. Furthermore, the understanding of the connection between the mind and body is essential in chiropractic treatment towards overall health and wellness.

 

Introduction to the Non-Pharmacological Treatment of Pain

 

Pain is an essential biological function that signals disturbance or damage in the body, prevents further harm through overuse of the afflicted area, and promotes physiological homeostasis.[1] Whether through abnormal healing, additional bodily damage, or failed medical intervention, pain may become chronic. Chronic pain no longer signals damage to the body and is instead a detriment to the physical and psychological well-being of the sufferer. Unfortunately, medical intervention frequently cannot resolve chronic pain, resulting in increased need for management approaches to pain, as is the approach to other chronic medical conditions.[2] In recent years, the biopsychosocial model has informed research and intervention in pain psychology, wherein physical, cognitive, affective, and interpersonal factors are used to inform treatment.[2] Currently, psychological interventions for chronic pain target a variety of domains, including physical functioning, pain medication use, mood, cognitive patterns, and quality of life, while changes in pain intensity may be secondary.[3] As such, psychological interventions for pain are ideally suited as complementary treatments to medical treatment.[4] In order to articulate the distinct philosophies and effects of each psychological intervention, it is important to first consider the variety of ways that pain affects psychological functioning.

 

Psychological Reactions to Pain

 

Recurrent pain may contribute to development of maladaptive cognitions and behavior that worsen daily functioning, increase psychiatric distress, or prolong the experience of pain.[5] Individuals suffering from chronic pain tend to show increased vulnerability to a variety of psychiatric conditions, including depressive disorders,[6] anxiety disorders,[7] and posttraumatic stress disorder.[7] However, the relationship between depression and pain is likely bidirectional, as the presence of a major depressive disorder has been identified as a key risk factor in the transition from acute pain to chronic pain.[8] Additionally, individuals with pain may suffer from significant anxiety and depressive symptomatology that does not reach the severity of a clinical diagnosis.[9] Further, chronic pain negatively impacts quality of life[10] and contributes to higher levels of disability.[10] Individuals with chronic pain are also vulnerable to higher rates of obesity,[11] sleep disturbance,[12] and fatigue,[13] show greater rates of medical utilization,[10] and are vulnerable to problematic pain medication use.[14] Given the negative psychological consequences of chronic pain, it is worthwhile to consider three psychological mechanisms related to pain-related distress that have proven to be suitable targets for intervention: pain catastrophizing, fear of pain, and pain acceptance.

 

Pain catastrophizing is defined as a negative cognitive and affective mental set related to expected or actual pain experience.[15] Pain catastrophizing is characterized by magnification of the negative effects of pain, rumination about pain, and feelings of helplessness in coping with pain.[16] Pain catastrophizing has been associated with various forms of dysfunction, including increased rates of depression[17] and anxiety,[16] greater functional impairment and disability due to pain,[17] and lower overall quality of life.[18] Individuals who catastrophize about their pain report lower levels of perceived control over pain,[19] poorer emotional and social functioning,[20] and poorer responses to medical intervention.[21] Pain catastrophizing also contributes to poorer pain coping and overall functioning, making pain catastrophizing a viable target for psychological intervention. Addressing catastrophic thoughts about pain improves physical and psychological functioning in the short term[22] and improves the likelihood of returning to work despite the presence of persistent pain.[23]

 

Pain-related fear is another psychological mechanism that has significant implications for physical and psychological functioning in chronic pain. Pain-related fear reflects a fear of injury or worsening of one�s physical condition through activities that may trigger pain.[24] Pain-related fear is associated with increased pain intensity[25] and increased disability.[26] Pain-related fear contributes to disability by fostering passive or avoidant pain-coping behaviors that contribute to physical deconditioning and pain.[27] If left unaddressed, fear of pain can impair gains in physical rehabilitation settings.[28] Evidence suggests that pain catastrophizing precedes pain-related fear,[24] but both of these mechanisms uniquely contribute to pain and physical disability.[5,29]

 

Recently, there has been increased attention to the psychological flexibility model, which extends the fear-avoidance model of chronic pain and proposes to improve treatment outcomes through fostering of accepting attitudes towards pain.[30] Psychological flexibility has been defined as an ability to engage in the present moment in a way that allows the individual to either maintain or adjust his or her behavior in the way that is most consistent with internally held goals and values;[31] this idea is especially important in times of greater pain, given the narrowing of focus that is common during times of pain.[32] Similar to psychological acceptance, which fosters a nonjudgmental approach to distressing thoughts and emotions, pain acceptance is defined as a process of nonjudgmentally acknowledging pain, stopping maladaptive attempts to control pain, and learning to live a richer life in spite of pain.[33] Pain acceptance influences emotional functioning through two distinct mechanisms: a willingness to experience pain, which buffers against negative emotional reactions to pain, and continued engagement in valued activities despite the presence of pain, which bolsters positive emotions.[34] Acceptance of pain is theorized to uncouple the occurrence of catastrophic thoughts about pain from subsequent emotional suffering[35] and reduces reliance on control- or avoidance-based coping,[36] thereby freeing cognitive and emotional resources for more meaningful pursuits.[33] Pain acceptance has demonstrated positive associations with cognitive, emotional, social, and occupational functioning in chronic pain populations.[36] Acceptance of pain predicts lower levels of pain catastrophizing[37] and greater levels of positive affect, which in turn reduce the association between pain intensity and negative emotions.[38] Pain acceptance is a particularly salient target for intervention in mindfulness- and acceptance-based therapies for chronic pain, which will be discussed later (see Table 1).

 

Table 1 Descriptions of Psychological Therapies for Pain

Table 1: Descriptions of psychological therapies for pain.

 

Psychological Intervention as an Approach to Pain Management

 

Operant Behavioral Approaches

 

Fordyce[39] proposed a behavioral model of pain adaptation in which maladaptive behavioral responses to pain develop through contingent relief from pain or pain-related fear. According to this theory, a behavioral drive to avoid pain leads individuals to avoid behaviors that are painful but maintain their physical and emotional health; this avoidance contributes to the development and maintenance of pain chronicity, deconditioning, and depression.[40] Operant therapy for chronic pain utilizes reinforcement and punishment contingencies to reduce pain-related behaviors and foster more adaptive behaviors, including graded patterns of activity, activity pacing, and time-contingent medication management.[40] Behavioral therapy for pain has shown positive effects on a variety of domains, including pain experience, mood, negative cognitive appraisals, and functioning in social roles.[3]

 

A recent application of learning theory to chronic pain involves in vivo exposure treatment for pain-related fear, which focuses on decreasing the perceived harmfulness of physical activity.[41] Learning theory posits that the aversive signal of pain may be passed to neutral stimuli (like physical movement behaviors), which contributes to avoidant behavior. In vivo exposure therapy extinguishes threat, fear, and behavioral avoidance through progressively increasing engagement in painful behaviors in the absence of catastrophic outcomes; when these behaviors are performed without serious negative consequences, patients may realize that their expectations about the consequences of physical movement and pain are unrealistic.[24,42] Consistent with exposure treatments for phobias and other anxiety disorders, in vivo exposure treatment for fear of pain involves development of a personalized, graded hierarchy of activities that elicit a fearful response, psychoeducation related to pain, fear, and behavior, and ultimately slow and systematic exposure to activities related to the individual�s fear hierarchy.[41] In vivo exposure treatment for pain-related fear has demonstrated efficacy in improving pain, pain catastrophizing, and functional disability,[41] and in decreasing pain-related fear and anxiety, depression, and anxiety.[43] Exclusively behavioral approaches to pain have been less prevalent in recent years but have demonstrated efficacy in lower back pain samples, among others (see Table 2). The effects of in vivo exposure on functional disability appear to be mediated by decreased catastrophizing and perceived harmfulness of activity[41] but may be differentially effective for patients of differing baseline levels of functionality.[40]

 

Table 2 Demonstrated Efficacy of Psychological Interventions

Table 2: Demonstrated efficacy of psychological interventions by pain population.

 

Cognitive-Behavioral Therapy

 

Cognitive-behavioral therapy (CBT) adopts a biopsychosocial approach to the treatment of chronic pain by targeting maladaptive behavioral and cognitive responses to pain and social and environmental contingencies that modify reactions to pain.[44] CBT principles have demonstrated efficacy for a variety of psychiatric disorders and physical illnesses, in addition to pain.[45] CBT for pain develops coping skills intended to manage pain and improve psychological functioning, including structured relaxation, behavioral activation and scheduling of pleasurable events, assertive communication, and pacing of behavior in order to avoid prolongation or exacerbation of pain flares. Unlike operant-behavioral approaches, CBT for pain also addresses maladaptive beliefs about pain and pain catastrophizing through formal use of cognitive restructuring: identification and replacement of unrealistic or unhelpful thoughts about pain with thoughts that are oriented towards adaptive behavior and positive functioning.[44] CBT for pain has been widely implemented as a standard treatment for pain and constitutes the current �gold standard� for psychological intervention for pain.[44]

 

According to recent meta-analytic studies,[45] CBT for pain demonstrates small-to-medium effect sizes in a variety of domains and shows effects on pain and functioning comparable to standard medical care for pain.[3] CBT significantly improves disability and pain catastrophizing after treatment and yields longer-term improvements in disability, above and beyond the effects of usual medical care,[3] as well as smaller effects on pain, catastrophizing, and mood when compared to no treatment.[3] CBT-related changes in helplessness and catastrophizing are uniquely predictive of later changes in pain intensity and pain-related interference in daily functioning.[22] CBT is also a valuable adjunct treatment in physical rehabilitation programs.[46] The benefits of CBT for pain have been noted in many chronic pain populations (see Table 2) but may not be as robust in some populations, including fibromyalgia.[47] Further, some have suggested that the effects of CBT are at best moderately sized and not maintained long-term.[30] The intractable nature of chronic pain may make adaptation difficult as attempts to control pain may prove ineffectual, ultimately contributing to greater psychological distress.[36] Recent efforts have thus expanded the cognitive-behavioral model of pain intervention to address these issues, which has yielded two newer treatment modalities: mindfulness-based stress reduction (MBSR) and acceptance and commitment therapy (ACT). Unlike CBT, these approaches focus on fostering acceptance of chronic pain rather than emphasizing strategies for controlling pain, thereby improving emotional well-being and greater engagement in nonpain-related pursuits. Though these interventions both target acceptance of pain, they differ in their therapeutic implementation and approach to meditation and daily practice.

 

Mindfulness-Based Stress Reduction

 

Mindfulness-based interventions approach seeks to uncouple the sensory aspects of pain from the evaluative and emotional aspects of pain,[48] and promote detached awareness of the somatic and psychological sensations within the body.[48] As the chronic pain signal often cannot be extinguished, this detachment may enhance individual responses to chronic pain.[48] Through mindful awareness and meditation, thoughts about pain can be viewed as discrete events rather than an indication of an underlying problem that necessitates immediate and possibly maladaptive responses.[49] An individual may then recognize these sensations or thoughts as something familiar, which may serve to ameliorate emotional or maladaptive behavioral responses to pain.

 

MBSR is a form of meditation developed in Eastern philosophy and later adapted to Western intervention that enhances awareness and acceptance of physical, cognitive, and emotional states and disconnects psychological reactions from the uncontrollable experience of pain flares.[44] MBSR interventions have traditionally been structured as 2-hour sessions occurring weekly over 10 weeks that develop awareness of the body and proprioceptive signals, awareness of the breath and physical sensations, and development of mindful activities (such as eating, walking, and standing).[48] MBSR promotes mindfulness through daily meditation, which is a requisite component of the treatment.[50] The mechanisms underlying effective MBSR intervention may be similar to desensitization to pain, as meditations involve motionless sitting practices that expose participants to painful sensations in the absence of catastrophic consequences.[48,50] In this way, MBSR interventions may function similarly to in vivo exposure for pain but serve the additional purpose of increasing tolerance for negative emotions, thereby fostering more adaptive responses to pain.[50] MBSR also reduces rumination[51] and interoception of distressing physical signals[52] and increases mindful awareness[51] and acceptance of pain.[53] MBSR necessitates cultivation of daily mindfulness practices,[48] yet compliance rates of MBSR have been found to compare favorably to behavioral pain management techniques.[54] However, evidence on the importance of daily practice is mixed; the amount of time devoted to these mindful activities correlates with symptom improvement in some studies,[55] yet compliance rates appear to correlate only modestly with improvement in others.[54] Unlike CBT, which identifies thoughts as distorted and in need of change, practitioners of mindfulness adopt a nonjudgmental approach to thoughts as �discrete events� that encourage emotional distance from thoughts.[44,50] Further, CBT is a goal-oriented treatment modality, targeting an increased relaxation response or an altered behavioral or thought response, whereas mindfulness does not prescribe specific goals, relying instead on nonjudgmental observation.[50] Further, mindfulness instructors are expected to engage in their own daily mindfulness practices, whereas CBT practitioners do not necessarily need daily practice in CBT to teach it effectively.[50]

 

MBSR has demonstrated efficacy in addressing the severity of medical symptoms and psychological symptoms,[48] pain intensity,[56] and coping with stress and pain;[54] these treatment gains may last up to 4 years after intervention in many domains.[54] MBSR has been effective in diverse pain samples,[48,54,56] and in individuals with irritable bowel syndrome,[52] neck pain,[57] migraine,[57] fibromyalgia,[58] and chronic musculoskeletal pain.[59] Additionally, MBSR addresses co-occurring symptoms of depression in individuals with some chronic pain conditions like fibromyalgia[60] and enhances the effects of multidisciplinary treatment on disability, anxiety, depression, and catastrophizing.[61] Meta-analytic studies of MBSR in chronic pain have shown small to moderate effects of MBSR on anxiety, depression, and psychological distress in patients with chronic illnesses including pain,[62] and these benefits tend to be robust across studies.[63] However, as with CBT, MBSR may be differentially effective across populations; a recent longitudinal study noted greater improvements in pain, health-related quality of life, and psychological well-being for back or neck pain than in fibromyalgia, chronic migraine, or headache.[57]

 

Acceptance and Commitment Therapy

 

ACT adopts a theoretical approach that thoughts do not need to be targeted or changed; instead, responses to thoughts may be altered so that their negative consequences are minimized.[31] ACT interventions improve well-being through nonjudgmental and purposeful acknowledgment of mental events (ie, thoughts and emotions), fostering acceptance of these events, and increasing the ability of the individual to remain present and aware of personally relevant psychological and environmental factors; in doing so, individuals are able to adjust their behavior in a way that is consistent with their goals or values, rather than focusing on immediate relief from thoughts and emotions.[31] In the treatment of pain, ACT fosters purposeful awareness and acceptance of pain, thereby minimizing the focus on reducing pain or thought content and instead directing efforts towards fulfilling behavioral functioning.[44] ACT shares conceptual similarity with MBSR due to shared goals of promoting mindfulness and acceptance of pain but, unlike MBSR, ACT does not utilize daily mindful meditation and instead focuses on identification of the values and goals of the individual, which serve to direct behavior.[64] ACT-based interventions have demonstrated benefits on various aspects of mental health in chronic pain populations, including mental health quality of life, self-efficacy, depression, and anxiety.[65] Some studies of ACT interventions for chronic pain have reported medium or larger effect sizes for improvements in pain-related anxiety and distress, disability, number of medical visits, current work status, and physical performance,[66,67] with smaller effects of this intervention noted on pain and depression.[64] However, meta-analytic studies of acceptance-based therapies for pain have revealed that ACT does not show incrementally greater efficacy in comparison to other established psychological treatments for chronic pain.[64]

 

Future Directions and Remaining Questions

 

The extant literature suggests that each of the previously reviewed psychological interventions has retained value for the treatment of chronic pain. At present, there is little evidence of the superiority of any treatment approach, with one exception: CBT has demonstrated incrementally greater benefit in many areas than the effects of behavioral therapy.[3] As previously noted, however, operant-behavioral principles have been adopted for newer treatment approaches like in vivo exposure for fear of pain, which has demonstrated good benefit in multidisciplinary treatment with some pain populations.[41] Recent reviews have concluded that MBSR and ACT are promising but yield generally comparable effects to CBT, despite their distinct intervention methods.[64] The ability to draw conclusions regarding treatment superiority is further limited by the smaller number of high-quality studies of ACT or MBSR compared to the more robust CBT literature.[64]

 

Some critical questions remain regarding the comparative effectiveness of these interventions. First, the effects of CBT are significant in the short term but are not consistently maintained across time, possibly due to decreased adherence.[3] It is conceivable that acceptance-based approaches, which are predicated less on mechanistic coping strategies and instead foster accepting attitudes towards pain, may show greater rates of long-term adherence and longer-term benefits than CBT, though future study of this question is needed. Further, some pain disorders (such as fibromyalgia) have shown comparatively poorer treatment response to CBT than other pain disorders in some studies, which highlights the possible benefit of alternative interventions in such populations. Indeed, ACT and MBSR have also shown efficacy in fibromyalgia populations, though there remains a need to identify predictors of differential treatment response.[65]

 

Safety and Tolerability of Psychological Therapies

 

Psychological therapies for pain are presumed to be at low risk for adverse effects to the recipient; as a result, there is a dearth of empirical evidence regarding the risks of psychological interventions.[68] Some have suggested that patients who enter psychological treatment face risks of incorrect psychological diagnosis, psychological dependence, undermining of a patient�s ability to make their own decisions, or manipulation by the therapist to achieve nontherapeutic goals.[69,70] However, these concerns are alleviated through proper clinical and ethical training of practitioners and are not typically considered salient risks of psychological therapies when they are properly administered.[70] Recently, there has been a call for additional research to address the possibility of adverse psychotherapeutic effects[71] as well as a more systematic method of monitoring and identifying adverse events related to psychotherapy.[68] Though the rates of adverse effects of psychotherapy are still largely unknown, it is encouraging that recent studies have begun to specifically report the incidence of adverse events directly.[72]

 

Factors Affecting the Outcomes of Psychological Intervention

 

Practitioners should be cautioned against the assumption of homogeneity among patients with pain disorders, as a variety of factors may predict treatment response.[69,71] Turk[73] proposed that individuals coping with comparable levels of pain show distinct patterns of response that could be clustered into recognizable subclasses: �dysfunctional� patients, who report high levels of pain-related interference and distress; �interpersonally distressed� patients, who report lacking the support of loved ones in coping with their pain; and �adaptive copers,� who report notably higher levels of function and perceived social support and lower levels of pain-related dysfunction. Turk proposed that these patient subgroups respond differently to psychological intervention, and subsequent findings have supported this idea: �dysfunctional� patients have demonstrated greater response to interdisciplinary treatment involving psychological care than �interpersonally distressed� patients.[74] Identification of patient subgroups may be accomplished using instruments like the Multidisciplinary Pain Inventory[75] and through detailed assessment of chronic pain intensity and disability.[76] Additionally, patients� readiness to adopt a self-management approach to their own chronic pain appears to have significant implications for treatment response;[77] patients who are in the precontemplation stage of treatment readiness may benefit more from insight-focused therapy, versus those in an action stage, who may benefit more from establishing relaxation-based and other active coping strategies.[77] Patient readiness to self-manage pain may be assessed using the Pain Stages of Change Questionnaire.[77] Additionally, treatment response may be subject to patient beliefs about the importance of intervention-specific behaviors and about one�s own ability to perform these actions.[78]

 

Additionally, there may be demographic, psychological, and medical differences among patients that are relevant to treatment response, including the etiology of pain conditions, socioeconomic status, and cultural and ethnic background; these factors require further empirical research in order to optimize clinical outcomes but have not yet received adequate attention in the clinical literature.[79] For example, baseline levels of physical functioning appear to predict response to certain psychological treatment modalities like in vivo exposure for fear of pain.[40] Further, baseline levels of pain, depression, and anxiety have been found to predict dropout rates in some samples,[80,81] though these effects are not apparent in all samples.[3] In addition to being an important mechanism of treatment, there is evidence that baseline levels of fear of pain may also predict differential treatment response; individuals more fearful of pain at the outset of a multidisciplinary pain treatment program showed greater responsiveness to in vivo exposure for this problem.[28] The presence of medical comorbidities that are likely to impact future functioning is also important to consider; recently, psychological interventions have been developed that address comorbid symptoms of sleep,[82] obesity,[29] and fatigue[83] that may accompany chronic pain. Hybrid treatments may be more important in independent clinical practice, where comorbidity is more common.[82] Notably, there is little evidence that personality variables factor significantly into treatment response; most of the connections between personality traits and variables relevant to psychological intervention for pain are theoretical and have not consistently emerged in empirical research.[84,85]

 

Patient age is also an important consideration in examining responses to interventions for pain. Older adults have increased risks of various ailments related to pain, including arthritis and osteoporosis, but may have poor tolerance to medications for these conditions.[86] Further, age may alter psychological reactions to pain; the emotional aspects of pain are more strongly correlated with pain catastrophizing in younger adults than older adults while sensory aspects of pain appear more strongly related to pain catastrophizing in older adults.[87] Additionally, treatment protocols may require accommodation for elderly populations; addressing an elderly patient�s fear of movement may be complicated by a fear of falling that is absent in younger populations.[88] As memory concerns are more common in older adulthood, treatment protocols may be improved if they minimize the demand for memorized tasks.[89] Unfortunately, research is lacking for specific psychological interventions in elderly populations.[86] In general, psychological interventions are presumed to be of low risk for older adults,[90] and CBT for pain has received comparatively greater empirical support for older adults.[88] Overall, the efficacy of psychological intervention for pain in older adults is an area that warrants additional study in the future.

 

Treatment availability is a key consideration for psychological intervention, especially for patients in poverty or living in remote geographical locations. Though it is beyond the scope of this paper to review ethnic and socioeconomic contributors to health, low socioeconomic status is a significant risk factor for the development of chronic pain and factors heavily into racial disparities in health outcomes.[91] As financial challenges may restrict access to traditional psychological interventions, the importance of alternative modalities for provision of mental health interventions for chronic pain is paramount. Teleinterventions[92] and Internet-based interventions[93] may be viable for psychological treatment of chronic pain; Internet-based programs delivering ACT,[94] CBT,[46] and mindfulness interventions[95] have demonstrated benefits in psychosocial functioning, mood, and pain coping. However, methodologically rigorous clinical trials and evidence for maximally effective and efficient implementation of these programs are needed, as many interventions have shown modest effects and comparatively high dropout rates.[96]

 

Combining psychological treatment modalities with one another and with other medical interventions may constitute the next logical step in enhancing treatment outcomes. Institution of a flexible, goal-oriented approach, akin to ACT, may enhance engagement and adherence in CBT.[97] Additionally, a combination of graded in vivo exposure and ACT may show incremental benefit in addressing pain-related fear and anxiety.[98] Effects of CBT may also be enhanced in conjunction with treatments like biofeedback[99] and hypnosis.[100] A word of caution: presentation of psychological treatment by nontraditional practitioners may show variable effectiveness unless treatment approaches are adjusted appropriately.[101] If trained properly, however, appropriately-designed cognitive-behavioral interventions can be effectively administered by physiotherapists,[102] physical therapists,[103] nurses, and occupational therapists.[104]

 

Conclusion

 

Psychotherapy constitutes a valuable modality for addressing the behavioral, cognitive, emotional, and social factors that both result from and contribute to pain-related dysfunction and distress through enhancement of self-management strategies. There are several distinct psychological interventions that differ in their theoretical approaches, therapeutic targets, and areas of efficacy, but CBT, ACT, MBSR, and operant behavioral approaches to pain may all play important roles for enhancing the self-management abilities of individuals with chronic pain. However, there remains a need to identify predictors of differential treatment response and salient patient subgroups to optimize treatment outcomes, as well as additional and alternative means to provision of psychological services for those who are unwilling or unable to engage in traditional psychotherapy. More empirical research into contributing factors of differential treatment response and the dissemination of psychological treatment for pain may result in significant savings to the physical, emotional, and financial costs of chronic pain.

 

Footnotes

 

Disclosure:�The author reports no conflicts of interest in this work.

 

In conclusion, psychological therapies, such as cognitive-behavioral therapy, mindfulness-based stress reduction and even chiropractic care, have been demonstrated to effective help treat chronic pain, according to research studies. The connection between the mind and body has previously been referenced as a cause for a variety of health issues, including chronic pain. Finally, the article above demonstrated the effects of psychological therapy for chronic pain management. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Back Pain

 

According to statistics, approximately 80% of people will experience symptoms of back pain at least once throughout their lifetimes. Back pain is a common complaint which can result due to a variety of injuries and/or conditions. Often times, the natural degeneration of the spine with age can cause back pain. Herniated discs occur when the soft, gel-like center of an intervertebral disc pushes through a tear in its surrounding, outer ring of cartilage, compressing and irritating the nerve roots. Disc herniations most commonly occur along the lower back, or lumbar spine, but they may also occur along the cervical spine, or neck. The impingement of the nerves found in the low back due to injury and/or an aggravated condition can lead to symptoms of sciatica.

 

blog picture of cartoon paperboy big news

 

EXTRA IMPORTANT TOPIC: Managing Workplace Stress

 

 

MORE IMPORTANT TOPICS: EXTRA EXTRA: Car Accident Injury Treatment El Paso, TX Chiropractor

 

Blank
References
1.�Craig AD. A new view of pain as a homeostatic emotion.�Trends Neurosci.�2003;26(6):303�307.[PubMed]
2.�Gatchel RJ. Comorbidity of chronic pain and mental health disorders: the biopsychosocial perspective.�Am Psychol.�2004;59(8):795�805.�[PubMed]
3.�Williams AC, Eccleston C, Morley S. Psychological therapies for the management of chronic pain (excluding headache) in adults.�Cochrane Database Syst Rev.�2012;11:CD007407.�[PubMed]
4.�Turk DC, Audette J, Levy RM, Mackey SC, Stanos S. Assessment and treatment of psychosocial comorbidities in patients with neuropathic pain.�Mayo Clin Proc.�2010;85(Suppl 3):S42�S50.[PMC free article][PubMed]
5.�Thibault P, Loisel P, Durand MJ, Catchlove R, Sullivan MJ. Psychological predictors of pain expression and activity intolerance in chronic pain patients.�Pain.�2008;139(1):47�54.�[PubMed]
6.�Bair MJ, Robinson RL, Katon W, Kroenke K. Depression and pain comorbidity: a literature review.�Arch Intern Med.�2003;163(20):2433�2445.�[PubMed]
7.�McWilliams LA, Cox BJ, Enns MW. Mood and anxiety disorders associated with chronic pain: an examination in a nationally representative sample.�Pain.�2003;106(1�2):127�133.�[PubMed]
8.�Young Casey C, Greenberg MA, Nicassio PM, Harpin RE, Hubbard D. Transition from acute to chronic pain and disability: a model including cognitive, affective, and trauma factors.�Pain.�2008;134(1�2):69�79.[PubMed]
9.�Geenen R, Newman S, Bossema ER, Vriezekolk JE, Boelen PA. Psychological interventions for patients with rheumatic diseases and anxiety or depression.�Best Pract Res Clin Rheumatol.�2012;26(3):305�319.[PubMed]
10.�Winkelmann A, Perrot S, Schaefer C, et al. Impact of fibromyalgia severity on health economic costs: results from a European cross- sectional study.�Appl Health Econ Health Policy.�2011;9(2):125�136.[PubMed]
11.�Wright LJ, Schur E, Noonan C, Ahumada S, Buchwald D, Afari N. Chronic pain, overweight, and obesity: findings from a community-based twin registry.�J Pain.�2010;11(7):628�635.�[PMC free article][PubMed]
12.�Smith MT, Haythornthwaite JA. How do sleep disturbance and chronic pain inter-relate? Insights from the longitudinal and cognitive- behavioral clinical trials literature.�Sleep Med Rev.�2004;8(2):119�132.[PubMed]
13.�Kato K, Sullivan PF, Eveng�rd B, Pedersen NL. Chronic widespread pain and its comorbidities: a population-based study.�Arch Intern Med.�2006;166(15):1649�1654.�[PubMed]
14.�Richardson LP, Russo JE, Katon W, et al. Mental health disorders and long-term opioid use among adolescents and young adults with chronic pain.�J Adolesc Health.�2012;50(6):553�558.�[PMC free article][PubMed]
15.�Sullivan MJ, Thorn B, Haythornthwaite JA, et al. Theoretical perspectives on the relation between catastrophizing and pain.�Clin J Pain.�2001;17(1):52�64.�[PubMed]
16.�Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing scale: development and validation.�Psychol Assess.�1995;7(4):524�532.
17.�Keefe FJ, Brown GK, Wallston KA, Caldwell DS. Coping with rheumatoid arthritis pain: catastrophizing as a maladaptive strategy.�Pain.�1989;37(1):51�56.�[PubMed]
18.�Wollaars MM, Post MW, van Asbeck FW, Brand N. Spinal cord injury pain: the influence of psychologic factors and impact on quality of life.�Clin J Pain.�2007;23(5):383�391.�[PubMed]
19.�Crisson JE, Keefe FJ. The relationship of locus of control to pain coping strategies and psychological distress in chronic pain patients.�Pain.�1988;35(2):147�154.�[PubMed]
20.�Hamilton NA, Karoly P, Zautra AJ. Health goal cognition and adjustment in women with fibromyalgia.�J Behav Med.�2005;28(5):455�466.�[PubMed]
21.�Mankovsky T, Lynch M, Clark A, Sawynok J, Sullivan MJ. Pain catastrophizing predicts poor response to topical analgesics in patients with neuropathic pain.�Pain Res Manag.�2012;17(1):10�14.[PMC free article][PubMed]
22.�Burns JW, Glenn B, Bruehl S, Harden RN, Lofland K. Cognitive factors influence outcome following multidisciplinary chronic pain treatment: a replication and extension of a cross-lagged panel analysis.�Behav Res Ther.�2003;41(10):1163�1182.�[PubMed]
23.�Sullivan MJL, Adams H, Ellis T. Targeting catastrophic thinking to promote return to work in individuals with fibromyalgia.�J Cogn Psychother.�2012;26(2):130�142.
24.�Leeuw M, Goossens ME, Linton SJ, Crombez G, Boersma K, Vlaeyen JW. The fear-avoidance model of musculoskeletal pain: current state of scientific evidence.�J Behav Med.�2007;30(1):77�94.�[PubMed]
25.�Demmelmaier I, Asenl�f P, Lindberg P, Denison E. Biopsychosocial predictors of pain, disability, health care consumption, and sick leave in first-episode and long-term back pain: a longitudinal study in the general population.�Int J Behav Med.�2010;17(2):79�89.�[PubMed]
26.�Zale EL, Lange KL, Fields SA, Ditre JW. The relation between pain-related fear and disability: a meta-analysis.�J Pain.�2013;14(10):1019�1030.�[PMC free article][PubMed]
27.�Samwel HJ, Evers AW, Crul BJ, Kraaimaat FW. The role of helplessness, fear of pain, and passive pain-coping in chronic pain patients.�Clin J Pain.�2006;22(3):245�251.�[PubMed]
28.�Werneke MW, Hart DL, George SZ, Stratford PW, Matheson JW, Reyes A. Clinical outcomes for patients classified by fear-avoidance beliefs and centralization phenomenon.�Arch Phys Med Rehabil.�2009;90(5):768�777.�[PubMed]
29.�Somers TJ, Keefe FJ, Pells JJ, et al. Pain catastrophizing and pain-related fear in osteoarthritis patients: relationships to pain and disability.�J Pain Symptom Manage.�2009;37(5):863�872.�[PMC free article][PubMed]
30.�Pincus T, McCracken LM. Psychological factors and treatment opportunities in low back pain.�Best Pract Res Clin Rheumatol.�2013;27(5):625�635.�[PubMed]
31.�Hayes SC, Luoma JB, Bond FW, Masuda A, Lillis J. Acceptance and commitment therapy: model, processes and outcomes.�Behav Res Ther.�2006;44(1):1�25.�[PubMed]
32.�Eccleston C, Crombez G, Aldrich S, Stannard C. Worry and chronic pain patients: a description and analysis of individual differences.�Eur J Pain.�2001;5(3):309�318.�[PubMed]
33.�McCracken LM. Learning to live with the pain: acceptance of pain predicts adjustment in persons with chronic pain.�Pain.�1998;74(1):21�27.�[PubMed]
34.�Kranz D, Bollinger A, Nilges P. Chronic pain acceptance and affective well-being: a coping perspective.�Eur J Pain.�2010;14(10):1021�1025.�[PubMed]
35.�Vowles KE, McCracken LM, Eccleston C. Patient functioning and catastrophizing in chronic pain: the mediating effects of acceptance.�Health Psychol.�2008;27(Suppl 2):S136�S143.�[PubMed]
36.�McCracken LM, Eccleston C. A prospective study of acceptance of pain and patient functioning with chronic pain.�Pain.�2005;118(1�2):164�169.�[PubMed]
37.�Vowles KE, McCracken LM, Eccleston C. Processes of change in treatment for chronic pain: the contributions of pain, acceptance, and catastrophizing.�Eur J Pain.�2007;11(7):779�787.�[PubMed]
38.�Kratz AL, Davis MC, Zautra AJ. Pain acceptance moderates the relation between pain and negative affect in female osteoarthritis and fibromyalgia patients.�Ann Behav Med.�2007;33(3):291�301.[PMC free article][PubMed]
39.�Fordyce WE.�Behavioral Methods for Chronic Pain and Illness.�St Louis, MO: Mosby; 1976. p. 1.
40.�Gatzounis R, Schrooten MG, Crombez G, Vlaeyen JW. Operant learning theory in pain and chronic pain rehabilitation.�Curr Pain Headache Rep.�2012;16(2):117�126.�[PubMed]
41.�Leeuw M, Goossens ME, van Breukelen GJ, et al. Exposure in vivo versus operant graded activity in chronic low back pain patients: results of a randomized controlled trial.�Pain.�2008;138(1):192�207.[PubMed]
42.�den Hollander M, de Jong JR, Volders S, Goossens ME, Smeets RJ, Vlaeyen JW. Fear reduction in patients with chronic pain: a learning theory perspective.�Expert Rev Neurother.�2010;10(11):1733�1745.[PubMed]
43.�Woods MP, Asmundson GJ. Evaluating the efficacy of graded in vivo exposure for the treatment of fear in patients with chronic back pain: a randomized controlled clinical trial.�Pain.�2008;136(3):271�280.[PubMed]
44.�Day MA, Thorn BE, Burns JW. The continuing evolution of biopsychosocial interventions for chronic pain.�J Cogn Psychother.�2012;26(2):114�129.
45.�Hofmann SG, Asnaani A, Vonk IJ, Sawyer AT, Fang A. The efficacy of cognitive behavioral therapy: a review of meta-analyses.�Cognit Ther Res.�2012;36(5):427�440.�[PMC free article][PubMed]
46.�Buhrman M, Fredriksson A, Edstr�m G, et al. Guided Internet-delivered cognitive behavioural therapy for chronic pain patients who have residual symptoms after rehabilitation treatment: randomized controlled trial.�Eur J Pain.�2013;17(5):753�765.�[PubMed]
47.�Bennett R, Nelson D. Cognitive behavioral therapy for fibromyalgia.�Nat Clin Pract Rheumatol.�2006;2(8):416�424.�[PubMed]
48.�Kabat-Zinn J. An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: theoretical considerations and preliminary results.�Gen Hosp Psychiatry.�1982;4(1):33�47.�[PubMed]
49.�Lauwerier E, Van Damme S, Goubert L, Paemeleire K, Devulder J, Crombez G. To control or not? A motivational perspective on coping with pain.�Acta Neurol Belg.�2012;112(1):3�7.�[PubMed]
50.�Baer RA. Mindfulness training as a clinical intervention: a conceptual and empirical review.�Clin Psychol: Sci Pract.�2003;10(2):125�143.
51.�Campbell TS, Labelle LE, Bacon SL, Faris P, Carlson LE. Impact of Mindfulness-Based Stress Reduction (MBSR) on attention, rumination and resting blood pressure in women with cancer: a waitlist-controlled study.�J Behav Med.�2012;35(3):262�271.�[PubMed]
52.�Garland EL, Gaylord SA, Palsson O, Faurot K, Douglas Mann J, Whitehead WE. Therapeutic mechanisms of a mindfulness-based treatment for IBS: effects on visceral sensitivity, catastrophizing, and affective processing of pain sensations.�J Behav Med.�2012;35(6):591�602.�[PMC free article][PubMed]
53.�Kabat-Zinn J.�Full Catastrophe Living: The Program of the Stress Reduction Clinic at the University of Massachusetts Medical Center.�New York, NY: Delta; 1990.
54.�Kabat-Zinn J, Lipworth L, Burney R, Sellers W. Four-year follow-up of a meditation-based program for the self-regulation of chronic pain: treatment outcomes and compliance.�Clin J Pain.�1986;2(3):159�173.
55.�Carmody J, Baer RA. Relationships between mindfulness practice and levels of mindfulness, medical and psychological symptoms and well-being in a mindfulness-based stress reduction program.�J Behav Med.�2008;31(1):23�33.�[PubMed]
56.�Randolph P, Caldera YM, Tacone AM, Greak BL. The long-term combined effects of medical treatment and a mindfulness-based behavioral program for the multidisciplinary management of chronic pain in West Texas.�Pain Digest.�1999;9:103�112.
57.�Rosenzweig S, Greeson JM, Reibel DK, Green JS, Jasser SA, Beasley D. Mindfulness-based stress reduction for chronic pain conditions: variation in treatment outcomes and role of home meditation practice.�J Psychosom Res.�2010;68(1):29�36.�[PubMed]
58.�Grossman P, Tiefenthaler-Gilmer U, Raysz A, Kesper U. Mindfulness training as an intervention for fibromyalgia: evidence of postintervention and 3-year follow-up benefits in well-being.�Psychother Psychosom.�2007;76(4):226�233.�[PubMed]
59.�Plews-Ogan M, Owens JE, Goodman M, Wolfe P, Schorling J. A pilot study evaluating mindfulness-based stress reduction and massage for the management of chronic pain.�J Gen Intern Med.�2005;20(12):1136�1138.�[PMC free article][PubMed]
60.�Sephton SE, Salmon P, Weissbecker I, et al. Mindfulness meditation alleviates depressive symptoms in women with fibromyalgia: results of a randomized clinical trial.�Arthritis Rheum.�2007;57(1):77�85.[PubMed]
61.�Cassidy EL, Atherton RJ, Robertson N, Walsh DA, Gillett R. Mindfulness, functioning and catastrophizing after multidisciplinary pain management for chronic low back pain.�Pain.�2012;153(3):644�650.�[PubMed]
62.�Bohlmeijer E, Prenger R, Taal E, Cuijpers P. The effects of mindfulness-based stress reduction therapy on mental health of adults with a chronic medical disease: a meta-analysis.�J Psychosom Res.�2010;68(6):539�544.�[PubMed]
63.�Merkes M. Mindfulness-based stress reduction for people with chronic diseases.�Aust J Prim Health.�2010;16(3):200�210.�[PubMed]
64.�Veehof MM, Oskam MJ, Schreurs KM, Bohlmeijer ET. Acceptance-based interventions for the treatment of chronic pain: a systematic review and meta-analysis.�Pain.�2011;152(3):533�542.�[PubMed]
65.�Wicksell RK, Kemani M, Jensen K, et al. Acceptance and commitment therapy for fibromyalgia: a randomized controlled trial.�Eur J Pain.�2013;17(4):599�611.�[PubMed]
66.�McCracken LM, MacKichan F, Eccleston C. Contextual cognitive-behavioral therapy for severely disabled chronic pain sufferers: effectiveness and clinically significant change.�Eur J Pain.�2007;11(3):314�322.�[PubMed]
67.�Vowles KE, McCracken LM. Acceptance and values-based action in chronic pain: a study of treatment effectiveness and process.�J Consult Clin Psychol.�2008;76(3):397�407.�[PubMed]
68.�Dimidjian S, Hollon SD. How would we know if psychotherapy were harmful?�Am Psychol.�2010;65(1):21�33.�[PubMed]
69.�Berk M, Parker G. The elephant on the couch: side-effects of psychotherapy.�Aust N Z J Psychiatry.�2009;43(9):787�794.�[PubMed]
70.�Green B. Adverse effects of psychotherapy.�Advances in Psychiatric Treatment.�2011;17(6):476.
71.�Barlow DH. Negative effects from psychological treatments: a perspective.�Am Psychol.�2010;65(1):13�20.�[PubMed]
72.�Shadick NA, Sowell NF, Frits ML, et al. A randomized controlled trial of an internal family systems-based psychotherapeutic intervention on outcomes in rheumatoid arthritis: a proof-of-concept study.�J Rheumatol.�2013;40(11):1831�1841.�[PubMed]
73.�Turk DC. The potential of treatment matching for subgroups of patients with chronic pain: lumping versus splitting.�Clin J Pain.�2005;21(1):44�55.�discussion 69�72.�[PubMed]
74.�Turk DC, Okifuji A, Sinclair JD, Starz TW. Differential responses by psychosocial subgroups of fibromyalgia syndrome patients to an interdisciplinary treatment.�Arthritis Care Res.�1998;11(5):397�404.[PubMed]
75.�Kerns RD, Turk DC, Rudy TE. The West Haven-Yale multidimensional pain inventory (WHYMPI)�Pain.�1985;23(4):345�356.�[PubMed]
76.�Von Korff M, Ormel J, Keefe FJ, Dworkin SF. Grading the severity of chronic pain.�Pain.�1992;50(2):133�149.�[PubMed]
77.�Kerns RD, Rosenberg R, Jamison RN, Caudill MA, Haythornthwaite J. Readiness to adopt a self-management approach to chronic pain: the Pain Stages of Change Questionnaire (PSOCQ)�Pain.�1997;72(1�2):227�234.�[PubMed]
78.�Kratz AL, Molton IR, Jensen MP, Ehde DM, Nielson WR. Further evaluation of the Motivational Model of Pain Self-Management: coping with chronic pain in multiple sclerosis.�Ann Behav Med.�2011;41(3):391�400.�[PMC free article][PubMed]
79.�Reese C, Mittag O. Psychological interventions in the rehabilitation of patients with chronic low back pain: evidence and recommendations from systematic reviews and guidelines.�Int J Rehabil Res.�2013;36(1):6�12.�[PubMed]
80.�Kraaimaat F, Brons MR, Geenen R, Bijlsma JW. The effect of cognitive behavior therapy in patients with rheumatoid arthritis.�Behav Res Ther.�1995;33(5):487�495.�[PubMed]
81.�Wetherell JL, Afari N, Rutledge T, et al. A randomized, controlled trial of acceptance and commitment therapy and cognitive-behavioral therapy for chronic pain.�Pain.�2011;152(9):2098�2107.�[PubMed]
82.�Tang NK, Goodchild CE, Salkovskis PM. Hybrid cognitive-behaviour therapy for individuals with insomnia and chronic pain: a pilot randomised controlled trial.�Behav Res Ther.�2012;50(12):814�821.[PubMed]
83.�Knoop H, Stulemeijer M, Prins JB, van der Meer JW, Bleijenberg G. Is cognitive behaviour therapy for chronic fatigue syndrome also effective for pain symptoms?�Behav Res Ther.�2007;45(9):2034�2043.[PubMed]
84.�Bishop SR. What do we really know about mindfulness-based stress reduction?�Psychosom Med.�2002;64(1):71�83.�[PubMed]
85.�Turner JA, Holtzman S, Mancl L. Mediators, moderators, and predictors of therapeutic change in cognitive-behavioral therapy for chronic pain.�Pain.�2007;127(3):276�286.�[PubMed]
86.�Park J, Hughes AK. Nonpharmacological approaches to the management of chronic pain in community-dwelling older adults: a review of empirical evidence.�J Am Geriatr Soc.�2012;60(3):555�568.[PubMed]
87.�Kraaij V, Pruymboom E, Garnefski N. Cognitive coping and depressive symptoms in the elderly: a longitudinal study.�Aging Ment Health.�2002;6(3):275�281.�[PubMed]
88.�Keefe FJ, Porter L, Somers T, Shelby R, Wren AV. Psychosocial interventions for managing pain in older adults: outcomes and clinical implications.�Br J Anaesth.�2013;111(1):89�94.�[PMC free article][PubMed]
89.�Nicholson NL, Blanchard EB. A controlled evaluation of behavioral treatment of chronic headache in the elderly.�Behav Ther.�1993;24(3):395�408.
90.�Morone NE, Greco CM. Mind-body interventions for chronic pain in older adults: a structured review.�Pain Med.�2007;8(4):359�375.�[PubMed]
91.�Fuentes M, Hart-Johnson T, Green CR. The association among neighborhood socioeconomic status, race and chronic pain in black and white older adults.�J Natl Med Assoc.�2007;99(10):1160�1169.[PMC free article][PubMed]
92.�Naylor MR, Naud S, Keefe FJ, Helzer JE. Therapeutic Interactive Voice Response (TIVR) to reduce analgesic medication use for chronic pain management.�J Pain.�2010;11(12):1410�1419.�[PMC free article][PubMed]
93.�Hoch DB, Watson AJ, Linton DA, et al. The feasibility and impact of delivering a mind-body intervention in a virtual world.�PLoS One.�2012;7(3):e33843.�[PMC free article][PubMed]
94.�Buhrman M, Skoglund A, Husell J, et al. Guided internet-delivered acceptance and commitment therapy for chronic pain patients: a randomized controlled trial.�Behav Res Ther.�2013;51(6):307�315.[PubMed]
95.�Davis MC, Zautra AJ. An online mindfulness intervention targeting socioemotional regulation in fibromyalgia: results of a randomized controlled trial.�Ann Behav Med.�2013;46(3):273�284.�[PubMed]
96.�Macea DD, Gajos K, Daglia Calil YA, Fregni F. The efficacy of Web-based cognitive behavioral interventions for chronic pain: a systematic review and meta-analysis.�J Pain.�2010;11(10):917�929.[PubMed]
97.�Schrooten MG, Vlaeyen JW, Morley S. Psychological interventions for chronic pain: reviewed within the context of goal pursuit.�Pain Management.�2012;2(2):141�150.�[PubMed]
98.�Bailey KM, Carleton RN, Vlaeyen JW, Asmundson GJ. Treatments addressing pain-related fear and anxiety in patients with chronic musculoskeletal pain: a preliminary review.�Cogn Behav Ther.�2010;39(1):46�63.�[PubMed]
99.�Glombiewski JA, Sawyer AT, Gutermann J, Koenig K, Rief W, Hofmann SG. Psychological treatments for fibromyalgia: a meta-analysis.�Pain.�2010;151(2):280�295.�[PubMed]
100.�Castel A, Casc�n R, Padrol A, Sala J, Rull M. Multicomponent cognitive-behavioral group therapy with hypnosis for the treatment of fibromyalgia: long-term outcome.�J Pain.�2012;13(3):255�265.[PubMed]
101.�Gross AR, Kaplan F, Huang S, et al. Psychological care, patient education, orthotics, ergonomics and prevention strategies for neck pain: a systematic overview update as part of the ICON Project.�Open Orthop J.�2013;7:530�561.�[PMC free article][PubMed]
102.�Hunt MA, Keefe FJ, Bryant C, et al. A physiotherapist-delivered, combined exercise and pain coping skills training intervention for individuals with knee osteoarthritis: a pilot study.�Knee.�2013;20(2):106�112.�[PubMed]
103.�Bruflat AK, Balter JE, McGuire D, Fethke NB, Maluf KS. Stress management as an adjunct to physical therapy for chronic neck pain.�Phys Ther.�2012;92(10):1348�1359.�[PMC free article][PubMed]
104.�Lamb SE, Mistry D, Lall R, et al. Back Skills Training Trial Group Group cognitive behavioural interventions for low back pain in primary care: extended follow-up of the Back Skills Training Trial (ISRCTN54717854)�Pain.�2012;153(2):494�501.�[PubMed]
Close Accordion
Cognitive-Behavioral Therapy for Auto Accident Injuries in El Paso, TX

Cognitive-Behavioral Therapy for Auto Accident Injuries in El Paso, TX

Being involved in an automobile accident is an undesirable situation which can result in a variety of physical trauma or injury as well as lead to the development of a number of aggravating conditions. Auto accident injuries, such as whiplash, can be characterized by painful symptoms, including chronic neck pain, however, recent research studies have found that emotional distress resulting from an auto collision could manifest into physical symptoms. Stress, anxiety, depression and post traumatic stress disorder, or PTSD, are common psychological issues which may occur as a result of an automobile accident.

 

The researchers of the research studies also determined that cognitive-behavioral therapy may be an effective treatment for emotional distress and psychological issues which may have developed as a result of the auto accident injuries. Additionally, auto accident injuries may also cause stress, anxiety, depression and even PTSD if left untreated for an extended amount of time. The purpose of the article below is to demonstrate the effects of cognitive-behavioral therapy, together with alternative treatment options like chiropractic care and physical therapy. for auto accident injuries, such as whiplash.

 

Neck Exercises, Physical and Cognitive Behavioural-Graded Activity as a Treatment for Adult Whiplash Patients with Chronic Neck Pain: Design of a Randomised Controlled Trial

 

Abstract

 

Background

 

Many patients suffer from chronic neck pain following a whiplash injury. A combination of cognitive, behavioural therapy with physiotherapy interventions has been indicated to be effective in the management of patients with chronic whiplash-associated disorders. The objective is to present the design of a randomised controlled trial (RCT) aimed at evaluating the effectiveness of a combined individual physical and cognitive behavioural-graded activity program on self-reported general physical function, in addition to neck function, pain, disability and quality of life in patients with chronic neck pain following whiplash injury compared with a matched control group measured at baseline and 4 and 12 months after baseline.

 

Methods/Design

 

The design is a two-centre, RCT-study with a parallel group design. Included are whiplash patients with chronic neck pain for more than 6 months, recruited from physiotherapy clinics and an out-patient hospital department in Denmark. Patients will be randomised to either a pain management (control) group or a combined pain management and training (intervention)group. The control group will receive four educational sessions on pain management, whereas the intervention group will receive the same educational sessions on pain management plus 8 individual training sessions for 4 months, including guidance in specific neck exercises and an aerobic training programme. Patients and physiotherapists are aware of the allocation and the treatment, while outcome assessors and data analysts are blinded. The primary outcome measures will be Medical Outcomes Study Short Form 36 (SF36), Physical Component Summary (PCS). Secondary outcomes will be Global Perceived Effect (-5 to +5), Neck Disability Index (0-50), Patient Specific Functioning Scale (0-10), numeric rating scale for pain bothersomeness (0-10), SF-36 Mental Component Summary (MCS), TAMPA scale of Kinesiophobia (17-68), Impact of Event Scale (0-45), EuroQol (0-1), craniocervical flexion test (22 mmHg – 30 mmHg), joint position error test and cervical range of movement. The SF36 scales are scored using norm-based methods with PCS and MCS having a mean score of 50 with a standard deviation of 10.

 

Discussion

 

The perspectives of this study are discussed, in addition to the strengths and weaknesses.

 

Trial registration

 

The study is registered in www.ClinicalTrials.gov identifier NCT01431261.

 

Background

 

The Danish National Board of Health estimates that 5-6,000 subjects per year in Denmark are involved in a traffic accident evoking whiplash-induced neck pain. About 43% of those will still have physical impairment and symptoms 6 months after the accident [1]. For Swedish society, including Swedish insurance companies, the economic burden is approximately 320 million Euros [2], and this burden is likely to be comparable to that of Denmark. Most studies suggest that patients with Whiplash-Associated Disorders (WAD) report chronic neck symptoms one year after the injury [3]. The main problems in whiplash patients with chronic neck pain are cervical dysfunction and abnormal sensory processing, reduced neck mobility and stability, impaired cervicocephalic kinaesthetic sense, in addition to local and possibly generalised pain [4,5]. Cervical dysfunction is characterised by reduced function of the deep stabilising muscles of the neck.

 

Besides chronic neck pain, patients with WAD may suffer from physical inactivity as a consequence of prolonged pain [6,7]. This influences physical function and general health and can result in a poor quality of life. In addition, WAD patients may develop chronic pain followed by sensitisation of the nervous system [8,9], a lowering of the threshold for different sensory inputs (pressure, cold, warm, vibration and electrical impulses) [10]. This can be caused by an impaired central pain inhibition [11] – a cortical reorganisation [12]. Besides central sensitisation, the group with WAD may have poorer coping strategies and cognitive functions, compared with patients with chronic neck pain in general [13-15].

 

Studies have shown that physical training, including specific exercises targeting the deep postural muscles of the cervical spine, is effective in reducing neck pain [16-18] for patients with chronic neck pain, albeit there is a variability in the response to training with not every patient showing a major change. Physical behavioural-graded activity is a treatment approach with a focus on increasing general physical fitness, reducing fear of movement and increasing psychological function [19,20]. There is insufficient evidence for the long-term effect of treatment of physical and cognitive behavioural-graded activity, especially in chronic neck pain patients. Educational sessions, where the focus is on understanding complex chronic pain mechanisms and development of appropriate pain coping and/or cognitive behavioural strategies, have shown reduced general pain [6,21-26]. A review indicated that interventions with a combination of cognitive, behavioural therapy with physiotherapy including neck exercises is effective in the management of WAD patients with chronic neck pain [27], as also recommended by the Dutch clinical guidelines for WAD [28]. However, the conclusions regarding the guidelines are largely based on studies performed on patients with either acute or sub-acute WAD [29]. A more strict conclusion was drawn for WAD patients with chronic pain in the Bone and Joint Decade 2000-2010 Task Force, stating, that ‘because of conflicting evidence and few high-quality studies, no firm conclusions could be drawn about the most effective non-invasive interventions for patients with chronic WAD” [29,30]. The concept of combined treatment for WAD patients with chronic pain has been used in a former randomised controlled trial [31]. The results indicated that a combination of non-specific aerobic exercises and advice containing standardised pain education and reassurance and encouragement to resume light activity, produced better outcomes than advice alone for patients with WAD 3 months after the accident. The patients showed improvements in pain intensity, pain bothersomeness and functions in daily activities in the group receiving exercise and advice, compared with advice alone. However, the improvements were small and only apparent in the short term.

 

This project is formulated on the expectation that rehabilitation of WAD patients with chronic neck pain must target cervical dysfunctions, training of physical function and the understanding and management of chronic pain in a combined therapy approach. Each single intervention is based upon former studies that have shown effectiveness [6,18,20,32]. This study is the first to also include the long-term effect of the combined approach in patients with chronic neck pain after whiplash trauma. As illustrated in Figure ?Figure1,1, the conceptual model in this study is based upon the hypothesis that training (including both individually-guided specific neck exercises and graded aerobic training) and education in pain management (based on a cognitive behavioural approach) is better for increasing the patients’ physical quality of life, compared with education in pain management alone. Increasing the physical quality of life includes increasing the general physical function and level of physical activity, decreasing fear of movement, reducing post-traumatic stress symptoms, reducing neck pain and increasing neck function. The effect is anticipated to be found immediately after the treatment (i.e. 4 months; short-term effect) as well as after one year (long-term effect).

 

Figure 1 Hypothesis of the Intervention Effect

Figure 1: Hypothesis of the intervention effect for patients with chronic neck pain after a whiplash accident.

 

Using a randomised controlled trial (RCT) design, the aim of this study is to evaluate the effectiveness of: graded physical training, including specific neck exercises and general aerobic training, combined with education in pain management (based on a cognitive behavioural approach) versus education in pain management (based on a cognitive behavioural approach), measured on physical quality of life’, physical function, neck pain and neck functions, fear of movement, post-traumatic symptoms and mental quality of life, in patients with chronic neck pain after whiplash injury.

 

Methods/Design

 

Trial Design

 

The study is conducted in Denmark as an RCT with a parallel group design. It will be a two-centre study, stratified by recruitment location. Patients will be randomised to either the Pain Management group (control) or the Pain Management and Training group (intervention). As illustrated in Figure ?Figure2,2, the study is designed to include a secondary data assessment 12 months after baseline; the primary outcome assessment will be performed immediately after the intervention program 4 months after baseline. The study utilises an allocation concealment process, ensuring that the group to which the patient is allocated is not known before the patient is entered into the study. The outcome assessors and data analysts will be kept blinded to the allocation to intervention or control group.

 

Figure 2 Flowchart of the Patients in the Study

Figure 2: Flowchart of the patients in the study.

 

Settings

 

The participants will be recruited from physiotherapy clinics in Denmark and from The Spine Centre of Southern Denmark, Hospital Lilleb�lt via an announcement at the clinics and the Hospital. Using physiotherapy clinics spread across Denmark, the patients will receive the intervention locally. The physiotherapy clinics in Denmark receive patients via referral from their general practitioners. The Spine Centre, a unit specialising in treating patients with musculoskeletal dysfunctions and only treating out-patients, receives patients referred from general practitioners and/or chiropractors.

 

Study Population

 

Two hundred adults with a minimum age of 18 years, receiving physiotherapy treatment or having been referred for physiotherapy treatment will be recruited. For patients to be eligible, they must have: chronic neck pain for at least 6 months following a whiplash injury, reduced physical neck function (Neck Disability Index score, NDI, of a minimum of 10), pain primarily in the neck region, finished any medical /radiological examinations, the ability to read and understand Danish and the ability to participate in the exercise program. The exclusion criteria include: neuropathies/ radiculopathies (clinically tested by: positive Spurling, cervical traction and plexus brachialis tests) [33], neurological deficits (tested as in normal clinical practice through a process of examining for unknown pathology), engagement in experimental medical treatment, being in an unstable social and/or working situation, pregnancy, known fractures, depression according to the Beck Depression Index (score > 29) [18,34,35], or other known coexisting medical conditions which could severely restrict participation in the exercise program. The participants will be asked not to seek other physiotherapy or cognitive treatment during the study period.

 

Intervention

 

Control

 

The Pain Management (control) group will receive education in pain management strategies. There will be 4 sessions of 11/2 hours, covering topics regarding pain mechanisms, acceptance of pain, coping strategies, and goal-setting, based upon pain management and cognitive therapy concepts [21,26,36].

 

Intervention

 

The Pain Management plus Training (intervention) group will receive the same education in pain management as those in the control group plus 8 treatment sessions (instruction in neck exercises and aerobic training) with the same period of 4 months length. If the treating physiotherapist estimates additional treatments are needed, the treatment can be extended with 2 more sessions. Neck training: The treatment of neck-specific exercises will be progressed through different phases, which are defined by set levels of neck function. At the first treatment session, patients are tested for cervical neuromuscular function to identify the specific level at which to start neck training. A specific individually tailored exercise program will be used to target the neck flexor and extensor muscles. The ability to activate the deep cervical neck flexor muscles of the upper cervical region to increase their strength, endurance and stability function is trained progressively via the craniocervical training method using a biopressure feedback transducer [18,37]. Exercises for neck-eye coordination, neck joint positioning, balance and endurance training of the neck muscles will be included as well, since it has been shown to reduce pain and improve sensorimotor control in patients with insidious neck pain [17,38]. Aerobic training: The large trunk and leg muscles will be trained with a gradually increasing physical training program. Patients will be allowed to select activities such as walking, cycling, stick walking, swimming, and jogging. The baseline for training duration is set by exercising 3 times at a comfortable level, that does not exacerbate pain and aims at a rated perceived exertion (RPE) level of between 11 and 14 on a Borg scale [39]. The initial duration of training is set 20% below the average time of the three trials. Training sessions are carried out every second day with a prerequisite that pain is not worsened, and that RPE is between 9 and 14. A training diary is used. If patients do not experience a relapse, and report an average RPE value of 14 or less, the exercise duration for the following period (1 or 2 weeks) is increased by 2-5 minutes, up to a maximum of 30 minutes. If the RPE level is 15 or higher, the exercise duration will be reduced to an average RPE score of 11 to 14 every fortnight [20,40]. By using these pacing principles, the training will be graded individually by the patient, with a focus on perceived exertion – with the aim of increasing the patient’ s general physical activity level and fitness.

 

Patients’ compliance will be administered by registration of their participation in the control and intervention group. The patients in the control group will be considered to have completed the pain management if they have attended 3 out of 4 sessions. The patiesnts in the intervention group will be considered to have completed if the patient has attended a minimum of 3 out of 4 pain management sessions and a minimum of 5 out of 8 trainings sessions. Each patient’s home training with neck exercises and aerobic training will be registered by him/her in a logbook. Compliance with 75% of the planned home training will be considered as having completed the intervention.

 

Physiotherapists

 

The participating physiotherapists will be recruited via an announcement in the Danish Physiotherapy Journal. The inclusion criteria consist of: being a qualified physiotherapist, working at a clinic and having at least two years of working experience as a physiotherapist, having attended a course in the described intervention and passed the related exam.

 

Outcome Measures

 

At baseline the participants’ information on age, gender, height and weight, type of accident, medication, development of symptoms over the last two months (status quo, improving, worsening), expectation of treatment, employment and educational status will be registered. As a primary outcome measure, Medical Outcomes Study Short Form 36 (SF36) – Physical Component Summary (PCS) will be used [41,42]. The PCS scales are scored using norm-based methods [43,44] with a mean score of 50 with a standard deviation of 10. The primary outcome with respect to having an effect, will be calculated as a change from baseline [45]. Secondary outcomes contain data on both clinical tests and patient-reported outcomes. Table ?Table11 presents clinical tests for measuring the intervention effect on neuromuscular control of the cervical muscles, cervical function and mechanical allodynia. Table ?Table22 presents the patient-related outcomes from questionnaires used to test for perceived effect of the treatment, neck pain and function, pain bothersomeness, fear of movement, post-traumatic stress and quality of life and potential treatment modifiers.

 

Table 1 Clinical Outcomes Used for Measurement of Treatment Effect

Table 1: Clinical outcomes used for measurement of treatment effect on muscle strategy, function and treatment modifiers.

 

Table 2 Patient Reported Outcomes Used for Measured of Treatment Effect

Table 2: Patient reported outcomes used for measured of treatment effect on pain and function.

 

Patients will be tested at baseline, 4 and 12 months after baseline, except for GPE, which will only be measured 4 and 12 months after baseline.

 

Power and Sample Size Estimation

 

The power and sample size calculation is based on the primary outcome, being SF36-PCS 4 months after baseline. For a two-sample pooled t-test of a normal mean difference with a two-sided significance level of 0.05, assuming a common SD of 10, a sample size of 86 per group is required to obtain a power of at least 90% to detect a group mean difference of 5 PCS points [45]; the actual power is 90.3%, and the fractional sample size that achieves a power of exactly 90% is 85.03 per group. In order to adjust for an estimated 15% withdrawal during the study period of 4 months, we will include 100 patients in each group. For sensitivity, three scenarios were applied: firstly, anticipating that all 2 � 100 patients complete the trial, we will have sufficient power (> 80%) to detect a group mean difference as low as 4 PCS points; secondly, we will be able to detect a statistically significant group mean difference of 5 PCS points with sufficient power (> 80%) even with a pooled SD of 12 PCS points. Thirdly and finally, if we aim for a group mean difference of 5 PCS points, with a pooled SD of 10, we will have sufficient power (> 80%) with only 64 patients in each group. However, for logistical reasons, new patients will no longer be included in the study 24 months after the first patient has been included.

 

Randomisation, Allocation and Blinding Procedures

 

After the baseline assessment, the participants are randomly assigned to either the control group or the intervention group. The randomisation sequence is created using SAS (SAS 9.2 TS level 1 M0) statistical software and is stratified by centre with a 1:1 allocation using random block sizes of 2, 4, and 6. The allocation sequence will be concealed from the researcher enrolling and assessing participants in sequentially numbered, opaque, sealed and stapled envelopes. Aluminium foil inside the envelope will be used to render the envelope impermeable to intense light. After revealing the content of the envelope, both patients and physiotherapists are aware of the allocation and the corresponding treatment. Outcome assessors and data analysts are however kept blinded. Prior to the outcome assessments, the patients will be asked by the research assistant not to mention the treatment to which they have been allocated.

 

Statistical Analysis

 

All the primary data analyses will be carried out according to a pre-established analysis plan; all analyses will be done applying SAS software (v. 9.2 Service Pack 4; SAS Institute Inc., Cary, NC, USA). All descriptive statistics and tests are reported in accordance with the recommendations of the ‘Enhancing the QUAlity and Transparency Of health Research’ (EQUATOR) network; i.e., various forms of the CONSORT statement [46]. Data will be analysed using a two-factor Analysis of Covariance (ANCOVA), with a factor for Group and a factor for Gender, using the baseline value as covariate to reduce the random variation, and increase the statistical power. Unless stated otherwise, results will be expressed as the difference between the group means with 95% confidence intervals (CIs) and associated p-values, based on a General Linear Model (GLM) procedure. All the analyses will be performed using the Statistical Package for Social Sciences (version 19.0.0, IBM, USA) as well as the SAS system (v. 9.2; SAS Institute Inc., Cary, NC, USA). A two-way analysis of variance (ANOVA) with repeated measures (Mixed model) will be performed to test the difference over time between the intervention and the control groups; interaction: Group � Time. An alpha-level of 0.05 will be considered as being statistically significant (p < 0.05, two- sided). The data analysts will be blinded to the allocated interventions for primary analyses.

 

The baseline scores for the primary and secondary outcomes will be used to compare the control and intervention groups. The statistical analyses will be performed on the basis of the intention-to-treat principle, i.e. patients will be analysed in the treatment group to which they were randomly allocated. In the primary analyses, missing data will be replaced with the feasible and transparent ‘Baseline Observation Carried Forward’ (BOCF) technique, and for sensitivity also a multiple imputation technique will apply.

 

Secondarily, to relate the results to compliance, a ‘per protocol’ analysis will be used as well. The ‘per protocol’ population he patients who have ‘completed’ the intervention to which they were allocated, according to the principles described in the intervention section above.

 

Ethical Considerations

 

The Regional Scientific Ethical Committee of Southern Denmark approved the study (S-20100069). The study conformed to The Declaration of Helsinki 2008 [47] by fulfilling all general ethical recommendations.

 

All subjects will receive information about the purpose and content of the project and give their oral and written consent to participate, with the possibility to drop out of the project at any time.

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

Managing stress, anxiety, depression and symptoms of post traumatic stress disorder, or PTSD, after being involved in an automobile accident can be difficult, especially if the incident caused physical trauma and injuries or aggravated a previously existing condition. In many cases, the emotional distress and the psychological issues caused by the incident may be the source of the painful symptoms. In El Paso, TX, many veterans with PTSD visit my clinic after manifesting worsening symptoms from a previous auto accident injury. Chiropractic care can provide patients the proper stress management environment they need to improve their physical and emotional symptoms. Chiropractic care can also treat a variety of auto accident injuries, including whiplash, head and neck injuries, herniated disc and back injuries.

 

Discussion

 

This study will contribute to a better understanding of treating patients with chronic neck pain following a whiplash accident. The knowledge from this study can be implemented into clinical practice, as the study is based on a multimodal approach, mirroring the approach, which in spite of the current lack of evidence, is often used in a clinical physiotherapy setting. The study may also be included in systematic reviews thereby contributing to updating the knowledge about this population and to enhancing evidence-based treatment.

 

Publishing the design of a study before the study is performed and the results obtained has several advantages. It allows the design to be finalised without its being influenced by the outcomes. This can assist in preventing bias as deviations from the original design can be identified. Other research projects will have the opportunity to follow a similar approach with respect to population, interventions, controls and outcome measurements. The challenges of this study are related to standardising the interventions, treating a non-homogeneous population, defining and standardising relevant outcome measures on a population with long-lasting symptoms and having a population from two different clinical settings. Standardisation of the interventions is obtained by teaching the involved physiotherapists in an instructional course. Population homogeneity will be handled by strict inclusion and exclusion criteria and by monitoring the baseline characteristics of the patients, and differences between groups based on other influences than the intervention/control will be possible to analyse statistically. This research design is composed as an ‘add-on’ design: both groups receive pain education; the intervention group receives additional physical training, including specific neck exercises and general training. Today there is insufficient evidence for the effect of treatment for patients with chronic neck pain following a whiplash accident. All participating patients will be referred for a treatment (control or intervention), as we consider it unethical not to offer some form of treatment, i.e. randomising the control group to a waiting list. The add-on design is chosen as a pragmatic workable solution in such a situation [48].

 

For whiplash patients with chronic pain, the most responsive disability measures (for the individual patient, not for the group as a whole) are considered to be the Patient Specific Functional Scale and the numerical rating scale of pain bothersomeness [49]. By using these and NDI (the most often used neck disability measure) as secondary outcome measures, it is anticipated that patient-relevant changes in pain and disability can be evaluated. The population will be recruited from and treated at two different clinical settings: the out-patient clinic of The Spine Centre, Hospital Lilleb�lt and several private physiotherapy clinics. To avoid any influence of the different settings on the outcome measures, the population will be block randomised related to the settings, securing equal distribution of participants from each setting to the two intervention groups.

 

Competing Interests

 

The authors declare that they have no competing interests.

 

Authors’ Contributions

 

IRH drafted the manuscript. IRH, BJK and KS participated in the design of the study. All contributed to the design. RC, IRH; BJK and KS participated in the power and sample size calculation and in describing the statistical analysis as well as the allocation and randomization procedure. All authors read and approved the final manuscript. Suzanne Capell provided writing assistance and linguistic corrections.

 

Pre-Publication History

 

The pre-publication history for this paper can be accessed here: www.biomedcentral.com/1471-2474/12/274/prepub

 

Acknowledgements

 

This study has received funding from the Research Fund for the Region of Southern Denmark, the Danish Rheumatism Association, the Research Foundation of the Danish Association of Physiotherapy, the Fund for Physiotherapy in Private Practice, and the Danish Society of Polio and Accident Victims (PTU). The Musculoskeletal Statistics Unit at the Parker Institute is supported by grants from the Oak Foundation. Suzanne Capell provided writing assistance and linguistic correction.

 

The trial is registered in www.ClinicalTrials.gov identifier NCT01431261.

 

A Randomized Controlled Trial of Cognitive-Behavioral Therapy for the Treatment of PTSD in the context of Chronic Whiplash

 

Abstract

 

Objectives

 

Whiplash-associated disorders (WAD) are common and involve both physical and psychological impairments. Research has shown that persistent posttraumatic stress symptoms are associated with poorer functional recovery and physical therapy outcomes. Trauma-focused cognitive-behavioral therapy (TF-CBT) has shown moderate effectiveness in chronic pain samples. However, to date, there have been no clinical trials within WAD. Thus, this study will report on the effectiveness of TF-CBT in individuals meeting the criteria for current chronic WAD and posttraumatic stress disorder (PTSD).

 

Method

 

Twenty-six participants were randomly assigned to either TF-CBT or a waitlist control, and treatment effects were evaluated at posttreatment and 6-month follow-up using a structured clinical interview, self-report questionnaires, and measures of physiological arousal and sensory pain thresholds.

 

Results

 

Clinically significant reductions in PTSD symptoms were found in the TF-CBT group compared with the waitlist at postassessment, with further gains noted at the follow-up. The treatment of PTSD was also associated with clinically significant improvements in neck disability, physical, emotional, and social functioning and physiological reactivity to trauma cues, whereas limited changes were found in sensory pain thresholds.

 

Discussion

 

This study provides support for the effectiveness of TF-CBT to target PTSD symptoms within chronic WAD. The finding that treatment of PTSD resulted in improvements in neck disability and quality of life and changes in cold pain thresholds highlights the complex and interrelating mechanisms that underlie both WAD and PTSD. Clinical implications of the findings and future research directions are discussed.

 

In conclusion, being involved in an automobile accident is an undesirable situation which can result in a variety of physical trauma or injury as well as lead to the development of a number of aggravating conditions. However, stress, anxiety, depression and post traumatic stress disorder, or PTSD, are common psychological issues which may occur as a result of an automobile accident. According to research studies, physical symptoms and emotional distress may be closely connected and treating both physical and emotional injuries could help patients achieve overall health and wellness. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Back Pain

 

According to statistics, approximately 80% of people will experience symptoms of back pain at least once throughout their lifetimes. Back pain is a common complaint which can result due to a variety of injuries and/or conditions. Often times, the natural degeneration of the spine with age can cause back pain. Herniated discs occur when the soft, gel-like center of an intervertebral disc pushes through a tear in its surrounding, outer ring of cartilage, compressing and irritating the nerve roots. Disc herniations most commonly occur along the lower back, or lumbar spine, but they may also occur along the cervical spine, or neck. The impingement of the nerves found in the low back due to injury and/or an aggravated condition can lead to symptoms of sciatica.

 

blog picture of cartoon paperboy big news

 

EXTRA IMPORTANT TOPIC: Managing Workplace Stress

 

 

MORE IMPORTANT TOPICS: EXTRA EXTRA: Car Accident Injury Treatment El Paso, TX Chiropractor

 

Blank
References

1. The National Institute of Public H. Folkesundhedsrapporten, 2007 (engl: Public Health Report, Denmark, 2007) 2007. p. s.112.
2. Whiplash kommisionen och Svenska Lkl. Diagnostik och tidigt omh�ndertagande av whiplashskador (engl: Diagnostics and early treatment of Whiplash Injuries) Sandviken: Sandvikens tryckeri; 2005.
3. Carroll LJ, Hogg-Johnson S, van dV, Haldeman S, Holm LW, Carragee EJ, Hurwitz EL, Cote P, Nordin M, Peloso PM. et al. Course and prognostic factors for neck pain in the general population: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;12(4 Suppl):S75�S82. [PubMed]
4. Nijs J, Oosterwijck van J, Hertogh de W. Rehabilitation of chronic whiplash: treatment of cervical dysfunctions or chronic pain syndrome? ClinRheumatol. 2009;12(3):243�251. [PubMed]
5. Falla D. Unravelling the complexity of muscle impairment in chronic neck pain. ManTher. 2004;12(3):125�133. [PubMed]
6. Mannerkorpi K, Henriksson C. Non-pharmacological treatment of chronic widespread musculoskeletal pain. BestPractResClinRheumatol. 2007;12(3):513�534. [PubMed]
7. Kay TM, Gross A, Goldsmith C, Santaguida PL, Hoving J, Bronfort G. Exercises for mechanical neck disorders. CochraneDatabaseSystRev. 2005. p. CD004250. [PubMed]
8. Kasch H, Qerama E, Kongsted A, Bendix T, Jensen TS, Bach FW. Clinical assessment of prognostic factors for long-term pain and handicap after whiplash injury: a 1-year prospective study. EurJNeurol. 2008;12(11):1222�1230. [PubMed]
9. Curatolo M, Arendt-Nielsen L, Petersen-Felix S. Central hypersensitivity in chronic pain: mechanisms and clinical implications. PhysMedRehabilClinNAm. 2006;12(2):287�302. [PubMed]
10. Jull G, Sterling M, Kenardy J, Beller E. Does the presence of sensory hypersensitivity influence outcomes of physical rehabilitation for chronic whiplash?–A preliminary RCT. Pain. 2007;12(1-2):28�34. doi: 10.1016/j.pain.2006.09.030. [PubMed] [Cross Ref]
11. Davis C. Chronic pain/dysfunction in whiplash-associated disorders95. JManipulative Physiol Ther. 2001;12(1):44�51. doi: 10.1067/mmt.2001.112012. [PubMed] [Cross Ref]
12. Flor H. Cortical reorganisation and chronic pain: implications for rehabilitation. JRehabilMed. 2003. pp. 66�72. [PubMed]
13. Bosma FK, Kessels RP. Cognitive impairments, psychological dysfunction, and coping styles in patients with chronic whiplash syndrome14. Neuropsychiatry NeuropsycholBehavNeurol. 2002;12(1):56�65. [PubMed]
14. Guez M. Chronic neck pain. An epidemiological, psychological and SPECT study with emphasis on whiplash-associated disorders9. Acta OrthopSuppl. 2006;12(320):receding-33. [PubMed]
15. Kessels RP, Aleman A, Verhagen WI, van Luijtelaar EL. Cognitive functioning after whiplash injury: a meta-analysis5. JIntNeuropsycholSoc. 2000;12(3):271�278. [PubMed]
16. O’Sullivan PB. Lumbar segmental ‘instability’: clinical presentation and specific stabilizing exercise management. ManTher. 2000;12(1):2�12. [PubMed]
17. Jull G, Falla D, Treleaven J, Hodges P, Vicenzino B. Retraining cervical joint position sense: the effect of two exercise regimes. JOrthopRes. 2007;12(3):404�412. [PubMed]
18. Falla D, Jull G, Hodges P, Vicenzino B. An endurance-strength training regime is effective in reducing myoelectric manifestations of cervical flexor muscle fatigue in females with chronic neck pain. ClinNeurophysiol. 2006;12(4):828�837. [PubMed]
19. Gill JR, Brown CA. A structured review of the evidence for pacing as a chronic pain intervention. EurJPain. 2009;12(2):214�216. [PubMed]
20. Wallman KE, Morton AR, Goodman C, Grove R, Guilfoyle AM. Randomised controlled trial of graded exercise in chronic fatigue syndrome. MedJAust. 2004;12(9):444�448. [PubMed]
21. Hayes SC, Luoma JB, Bond FW, Masuda A, Lillis J. Acceptance and commitment therapy: model, processes and outcomes. BehavResTher. 2006;12(1):1�25. [PubMed]
22. Lappalainen R, Lehtonen T, Skarp E, Taubert E, Ojanen M, Hayes SC. The impact of CBT and ACT models using psychology trainee therapists: a preliminary controlled effectiveness trial. BehavModif. 2007;12(4):488�511. [PubMed]
23. Linton SJ, Andersson T. Can chronic disability be prevented? A randomized trial of a cognitive-behavior intervention and two forms of information for patients with spinal pain. Spine (Phila Pa 1976) 2000;12(21):2825�2831. doi: 10.1097/00007632-200011010-00017. [PubMed] [Cross Ref]
24. Moseley L. Combined physiotherapy and education is efficacious for chronic low back pain. AustJPhysiother. 2002;12(4):297�302. [PubMed]
25. Soderlund A, Lindberg P. Cognitive behavioural components in physiotherapy management of chronic whiplash associated disorders (WAD)–a randomised group study6. GItalMedLavErgon. 2007;12(1 Suppl A):A5�11. [PubMed]
26. Wicksell RK. Exposure and acceptance in patients with chronic debilitating pain – a behavior therapy model to improve functioning and quality of life. Karolinska Institutet; 2009.
27. Seferiadis A, Rosenfeld M, Gunnarsson R. A review of treatment interventions in whiplash-associated disorders70. EurSpine J. 2004;12(5):387�397. [PMC free article] [PubMed]
28. van der Wees PJ, Jamtvedt G, Rebbeck T, de Bie RA, Dekker J, Hendriks EJ. Multifaceted strategies may increase implementation of physiotherapy clinical guidelines: a systematic review. AustJPhysiother. 2008;12(4):233�241. [PubMed]
29. Verhagen AP, Scholten-Peeters GG, van WS, de Bie RA, Bierma-Zeinstra SM. Conservative treatments for whiplash34. CochraneDatabaseSystRev. 2009. p. CD003338.
30. Hurwitz EL, Carragee EJ, van dV, Carroll LJ, Nordin M, Guzman J, Peloso PM, Holm LW, Cote P, Hogg-Johnson S. et al. Treatment of neck pain: noninvasive interventions: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;12(4 Suppl):S123�S152. [PubMed]
31. Stewart MJ, Maher CG, Refshauge KM, Herbert RD, Bogduk N, Nicholas M. Randomized controlled trial of exercise for chronic whiplash-associated disorders. Pain. 2007;12(1-2):59�68. doi: 10.1016/j.pain.2006.08.030. [PubMed] [Cross Ref]
32. Ask T, Strand LI, Sture SJ. The effect of two exercise regimes; motor control versus endurance/strength training for patients with whiplash-associated disorders: a randomized controlled pilot study. ClinRehabil. 2009;12(9):812�823. [PubMed]
33. Rubinstein SM, Pool JJ, van Tulder MW, Riphagen II, de Vet HC. A systematic review of the diagnostic accuracy of provocative tests of the neck for diagnosing cervical radiculopathy. EurSpine J. 2007;12(3):307�319. [PMC free article] [PubMed]
34. Peolsson M, Borsbo B, Gerdle B. Generalized pain is associated with more negative consequences than local or regional pain: a study of chronic whiplash-associated disorders7. JRehabilMed. 2007;12(3):260�268. [PubMed]
35. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. ArchGenPsychiatry. 1961;12:561�571. [PubMed]
36. Wicksell RK, Ahlqvist J, Bring A, Melin L, Olsson GL. Can exposure and acceptance strategies improve functioning and life satisfaction in people with chronic pain and whiplash-associated disorders (WAD)? A randomized controlled trial. Cogn BehavTher. 2008;12(3):169�182. [PubMed]
37. Falla D, Jull G, Dall’Alba P, Rainoldi A, Merletti R. An electromyographic analysis of the deep cervical flexor muscles in performance of craniocervical flexion. PhysTher. 2003;12(10):899�906. [PubMed]
38. Palmgren PJ, Sandstrom PJ, Lundqvist FJ, Heikkila H. Improvement after chiropractic care in cervicocephalic kinesthetic sensibility and subjective pain intensity in patients with nontraumatic chronic neck pain. JManipulative Physiol Ther. 2006;12(2):100�106. doi: 10.1016/j.jmpt.2005.12.002. [PubMed] [Cross Ref]
39. Borg G. Psychophysical scaling with applications in physical work and the perception of exertion. ScandJWork EnvironHealth. 1990;12(Suppl 1):55�58. [PubMed]
40. Wallman KE, Morton AR, Goodman C, Grove R. Exercise prescription for individuals with chronic fatigue syndrome. MedJAust. 2005;12(3):142�143. [PubMed]
41. McCarthy MJ, Grevitt MP, Silcocks P, Hobbs G. The reliability of the Vernon and Mior neck disability index, and its validity compared with the short form-36 health survey questionnaire. EurSpine J. 2007;12(12):2111�2117. [PMC free article] [PubMed]
42. Bjorner JB, Damsgaard MT, Watt T, Groenvold M. Tests of data quality, scaling assumptions, and reliability of the Danish SF-36. JClinEpidemiol. 1998;12(11):1001�1011. [PubMed]
43. Ware JE Jr, Kosinski M, Bayliss MS, McHorney CA, Rogers WH, Raczek A. Comparison of methods for the scoring and statistical analysis of SF-36 health profile and summary measures: summary of results from the Medical Outcomes Study. MedCare. 1995;12(4 Suppl):AS264�AS279. [PubMed]
44. Ware JE Jr. SF-36 health survey update. Spine (Phila Pa 1976) 2000;12(24):3130�3139. doi: 10.1097/00007632-200012150-00008. [PubMed] [Cross Ref]
45. Carreon LY, Glassman SD, Campbell MJ, Anderson PA. Neck Disability Index, short form-36 physical component summary, and pain scales for neck and arm pain: the minimum clinically important difference and substantial clinical benefit after cervical spine fusion. Spine J. 2010;12(6):469�474. doi: 10.1016/j.spinee.2010.02.007. [PubMed] [Cross Ref]
46. Moher D, Hopewell S, Schulz KF, Montori V, Gotzsche PC, Devereaux PJ, Elbourne D, Egger M, Altman DG. CONSORT 2010 Explanation and Elaboration: Updated guidelines for reporting parallel group randomised trials. JClinEpidemiol. 2010;12(8):e1�37. [PubMed]
47. Subjects WDoH-EPfMRIH. WORLD MEDICAL ASSOCIATION DECLARATION OF HELSINKI. WMA Declaration of Helsinki – Ethical Principles for Medical Research Involving Human Subjects. 2008.
48. Dworkin RH, Turk DC, Peirce-Sandner S, Baron R, Bellamy N, Burke LB, Chappell A, Chartier K, Cleeland CS, Costello A. et al. Research design considerations for confirmatory chronic pain clinical trials: IMMPACT recommendations. Pain. 2010;12(2):177�193. doi: 10.1016/j.pain.2010.02.018. [PubMed] [Cross Ref]
49. Stewart M, Maher CG, Refshauge KM, Bogduk N, Nicholas M. Responsiveness of pain and disability measures for chronic whiplash. Spine (Phila Pa 1976) 2007;12(5):580�585. doi: 10.1097/01.brs.0000256380.71056.6d. [PubMed] [Cross Ref]
50. Jull GA, O’Leary SP, Falla DL. Clinical assessment of the deep cervical flexor muscles: the craniocervical flexion test. JManipulative Physiol Ther. 2008;12(7):525�533. doi: 10.1016/j.jmpt.2008.08.003. [PubMed] [Cross Ref]
51. Revel M, Minguet M, Gregoy P, Vaillant J, Manuel JL. Changes in cervicocephalic kinesthesia after a proprioceptive rehabilitation program in patients with neck pain: a randomized controlled study. ArchPhysMedRehabil. 1994;12(8):895�899. [PubMed]
52. Heikkila HV, Wenngren BI. Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. ArchPhysMedRehabil. 1998;12(9):1089�1094. [PubMed]
53. Treleaven J, Jull G, Grip H. Head eye co-ordination and gaze stability in subjects with persistent whiplash associated disorders. Man Ther. 2010. [PubMed]
54. Williams MA, McCarthy CJ, Chorti A, Cooke MW, Gates S. A systematic review of reliability and validity studies of methods for measuring active and passive cervical range of motion. JManipulative Physiol Ther. 2010;12(2):138�155. doi: 10.1016/j.jmpt.2009.12.009. [PubMed] [Cross Ref]
55. Kasch H, Qerama E, Kongsted A, Bach FW, Bendix T, Jensen TS. Deep muscle pain, tender points and recovery in acute whiplash patients: a 1-year follow-up study. Pain. 2008;12(1):65�73. doi: 10.1016/j.pain.2008.07.008. [PubMed] [Cross Ref]
56. Sterling M. Testing for sensory hypersensitivity or central hyperexcitability associated with cervical spine pain. JManipulative Physiol Ther. 2008;12(7):534�539. doi: 10.1016/j.jmpt.2008.08.002. [PubMed] [Cross Ref]
57. Ettlin T, Schuster C, Stoffel R, Bruderlin A, Kischka U. A distinct pattern of myofascial findings in patients after whiplash injury. ArchPhysMedRehabil. 2008;12(7):1290�1293. [PubMed]
58. Vernon H, Mior S. The Neck Disability Index: a study of reliability and validity. JManipulative Physiol Ther. 1991;12(7):409�415. [PubMed]
59. Vernon H. The Neck Disability Index: state-of-the-art, 1991-2008. JManipulative Physiol Ther. 2008;12(7):491�502. doi: 10.1016/j.jmpt.2008.08.006. [PubMed] [Cross Ref]
60. Vernon H, Guerriero R, Kavanaugh S, Soave D, Moreton J. Psychological factors in the use of the neck disability index in chronic whiplash patients. Spine (Phila Pa 1976) 2010;12(1):E16�E21. doi: 10.1097/BRS.0b013e3181b135aa. [PubMed] [Cross Ref]
61. Sterling M, Kenardy J, Jull G, Vicenzino B. The development of psychological changes following whiplash injury. Pain. 2003;12(3):481�489. doi: 10.1016/j.pain.2003.09.013. [PubMed] [Cross Ref]
62. Stalnacke BM. Relationship between symptoms and psychological factors five years after whiplash injury. JRehabilMed. 2009;12(5):353�359. [PubMed]
63. Rabin R, de CF. EQ-5D: a measure of health status from the EuroQol Group. AnnMed. 2001;12(5):337�343. [PubMed]
64. Borsbo B, Peolsson M, Gerdle B. Catastrophizing, depression, and pain: correlation with and influence on quality of life and health – a study of chronic whiplash-associated disorders4. JRehabilMed. 2008;12(7):562�569. [PubMed]

Close Accordion
Mindfulness Interventions for Auto Accident Injuries in El Paso, TX

Mindfulness Interventions for Auto Accident Injuries in El Paso, TX

When you’ve been involved in a car crash, the auto accident injuries resulting from the incident may not always have a physical cause. The emotional distress due to trauma or injury from the impact of an automobile accident may often be so immense, it can lead to a variety of painful symptoms. If such stress is not treated immediately, it could result in the development of psychological conditions. Stress, anxiety, depression and in severe cases, PTSD, or post traumatic stress disorder, are some of the most common psychological issues you may end up encountering after a traumatic auto accident.

 

Anxiety and Irrational Fears

 

In several cases, the victim of an automobile accident may develop irrational fears as a result of the incident. As a matter of fact, many of these individuals report experiencing anxiety about getting behind the wheel again. For them, the fear of being in another accident may ultimately cause them to avoid driving altogether. For many other individuals still, the irrational fear of suffering a panic attack while on the road may be the cause for them to avert driving entirely. If the anxiety and irrational fears caused by the emotional distress of an auto accident worsen, it may permanently�discourage a person from driving again.

 

Depression

 

It is also possible for people who’ve been involved in an auto accident to develop depression following the incident. In the end, you wind up experiencing psychological trauma as a result of physical trauma. There are numerous symptoms of depression which you might readily recognize. These include problems with sleep, losing your appetite, and headaches. As it becomes worse, however, you might end up feeling sad or hopeless all of the time, which could lead to worsening symptoms.

 

Post Traumatic Stress Disorder (PTSD)

 

It’s highly possible for individuals involved in an automobile accident to suffer from post traumatic stress disorder, or PTSD. According to the National Center For PTSD, as much as 9 percent of people who experience auto accident injuries end up suffering from PTSD. Moreover, at least 14 percent of car crash survivors who seek mental health care are experiencing PTSD.

 

A new research study demonstrated that mindfulness interventions might be just as essential to your health as traditional treatment, especially if you’ve got post traumatic stress disorder, or PTSD. Researchers have demonstrated that chiropractic care can lead to a substantial advancement in the mind-body stress component of a patient’s overall health and wellness.

 

 

Chiropractic Care for Auto Accident Injuries

 

Addressing automobile accident injuries, such as whiplash, which also result in anxiety and irrational fears, depression and especially PTSD, demands a multi-disciplinary strategy. Chiropractic is an alternative treatment option which focuses on injuries and/or conditions of the musculoskeletal and nervous system. A chiropractor commonly utilizes spinal adjustments and manual manipulations to carefully correct spinal misalignments, or subluxations, which could be causing pain and discomfort. By releasing pressure and muscle tension, a doctor of chiropractic, or chiropractor, can help reduce stress and emotional distress which could be causing the individual’s anxiety, irrational fears, depression and PTSD. If further help is required, the chiropractor can recommend patients to the best healthcare specialist to help them with their symptoms. The purpose of the following article is to demonstrate the prevalence of PTSD on individuals involved in a traffic collision as well as to show how mindfulness interventions can ultimately help improve as well as manage the stress symptoms people may experience after a car crash.

 

Prediction of Post Traumatic Stress Disorder by Immediate Reactions to Trauma: a Prospective Study in Road Traffic Accident Victims

 

Abstract

 

Road traffic accidents often cause serious physical and psychological sequelae. Specialists of various medical faculties are involved in the treatment of accident victims. Little is known about the factors which might predict psychiatric disorders, e.g. Posttraumatic Stress Disorder (PTSD) after accidents and how psychological problems influence physical treatment. In a prospective study 179 unselected, consecutively admitted road traffic accident victims were assessed a few days after the accident for psychiatric diagnoses, severity of injury and psychopathology. All were inpatients and had to be treated for bone fractures. At 6-months follow-up assessment 152 (85%) of the patients were interviewed again. Of the patients, 18.4% fulfilled the criteria for Posttraumatic Stress Disorder (DSM-III-R) within 6 months after the accident. Patients who developed PTSD were injured more severely and showed more symptoms of anxiety, depression and PTSD a few days after the accident than patients with no psychiatric diagnosis. Patients with PTSD stayed significantly longer in the hospital than the other patients. Multiple regression analysis revealed that the length of hospitalization was due mainly to a diversity of factors such as severity of injury, severity of accident, premorbid personality and psychopathology. Posttraumatic stress disorder is common after road traffic accidents. Patients with PTSD at follow-up can be identified by findings from early assessment. Untreated psychological sequelae such as PTSD cause longer hospitalization and therefore more costs than in non-PTSD patients.

 

 

Trauma-Focused Cognitive Behavior Therapy and Exercise for Chronic Whiplash: Protocol of a Randomized Controlled Trial

 

Abstract

 

  • Introduction:�As a consequence of a road traffic crash, persistent pain and disability following whiplash injury are common and incur substantial personal and economic costs. Up to 50% of people who experience a whiplash injury will never fully recover and up to 30% will remain moderately to severely disabled by the condition. The reason as to why symptoms persist past the acute to sub-acute stage and become chronic is unclear, but likely results from complex interactions between structural injury, physical impairments, and psychological and psychosocial factors. Psychological responses related to the traumatic event itself are becoming an increasingly recognised factor in the whiplash condition. Despite this recognition, there is limited knowledge regarding the effectiveness of psychological interventions, either delivered alone or in combination with physiotherapy, in reducing the physical and pain-related psychological factors of chronic whiplash. Pilot study results have shown positive results for the use of trauma-focused cognitive behaviour therapy to treat psychological factors, pain and disability in individuals with chronic whiplash. The results have indicated that a combined approach could not only reduce psychological symptoms, but also pain and disability.
  • Aims:�The primary aim of this randomised, controlled trial is to investigate the effectiveness of combined trauma-focused cognitive behavioural therapy, delivered by a psychologist, and physiotherapy exercise to decrease pain and disability of individuals with chronic whiplash and post-traumatic stress disorder (PTSD). The trial also aims to investigate the effectiveness of the combined therapy in decreasing post-traumatic stress symptoms, anxiety and depression.
  • Participants and Setting:�A total of 108 participants with chronic whiplash-associated disorder (WAD) grade II of > 3 months and < 5 years duration and PTSD (diagnosed with the Clinician Administered PTSD Scale (CAPS) according to the DSM-5) will be recruited for the study. Participants will be assessed via phone screening and in person at a university research laboratory. Interventions will take place in southeast Queensland, Australia and southern Denmark.
  • Intervention:�Psychological therapy will be delivered once a week over 10 weeks, with participants randomly assigned to either trauma-focused cognitive behavioural therapy or supportive therapy, both delivered by a clinical psychologist. Participants will then receive ten sessions of evidence-based physiotherapy exercise delivered over a 6-week period.
  • Outcome Measures:�The primary outcome measure is neck disability (Neck Disability Index). Secondary outcomes focus on: pain intensity; presence and severity of PTSD (CAPS V and PTSD Checklist 5); psychological distress (Depression, Anxiety Stress Scale 21); patient perceived functionality (SF-12, Tampa Scale of Kinesiophobia, and Patient-Specific Functional Scale); and pain-specific self-efficacy and catastrophising (Pain Self-Efficacy Questionnaire and Pain Catastrophizing Scale). After psychotherapy (10 weeks after randomisation) and physiotherapy (16 weeks after randomisation), as well as at the 6-month and 12-month follow-ups, a blind assessor will measure the outcomes.
  • Analysis:�All analyses will be conducted on an intention-to-treat basis. The primary and secondary outcomes that are measured will be analysed using linear mixed and logistic regression models. Any effect of site (Australia or Denmark) will be evaluated by including a site-by-treatment group-by-time interaction term in the mixed models analyses. Effect modification will only be assessed for the primary outcome of the Neck Disability Index.
  • Discussion:�This study will provide a definitive evaluation of the effects of adding trauma-focused cognitive behaviour therapy to physiotherapy exercise for individuals with chronic WAD and PTSD. This study is likely to influence the clinical management of whiplash injury and will have immediate clinical applicability in Australia, Denmark and the wider international community. The study will also have implications for both health and insurance policy makers in their decision-making regarding treatment options and funding.

 

Introduction

 

Persistent pain and disability following whiplash injury as a consequence of a road traffic crash (RTC) is common and incurs substantial personal and economic costs. Up to 50% of people who experience a whiplash injury will never fully recover and up to 30% will remain moderately to severely disabled by the condition [1-3]. Less recognised are the mental health issues that accompany this condition. The prevalence of psychiatric disorders has been shown to be 25% for PTSD, 31% for Major Depressive Episode and 20% for Generalised Anxiety Disorder [4-6]. Whiplash injury accounts for the vast majority of any submitted claims as well as the greatest incurred costs in Queensland compulsory third party scheme [7]. In Australia, Whiplash injuries comprise approximately 75% of all survivable RTC injuries [8] with total costs of more than $950 M per annum [9], exceeding costs for both spinal cord and traumatic brain injury [7]. In Denmark, whiplash costs an estimated 300 million USD per annum if loss of work is included [10].

 

Neck pain is the cardinal symptom of individuals following whiplash injury. It is now generally accepted that there is an initial peripheral injury of some kind to the neck [11] although the specific injured structure in individual patients is difficult to clinically identify with current imaging techniques. The reason as to why symptoms persist past the acute to sub-acute stage and become chronic is not clear but likely results from complex interactions between structural injury, physical impairments, psychological and psychosocial factors [12]. However it is clear that chronic WAD is a heterogeneous and complex condition involving physical impairments such as movement loss, disturbed movement patterns and sensory disturbances [13] as well as pain related psychological responses such as catastrophizing [14, 15], kinesiophobia [16], activity avoidance and poor self-efficacy for pain control [17]. In addition recent studies have shown that posttraumatic stress symptoms or event related distress is common [18-20]. Thus it would seem logical that interventions targeting both the physical and psychological manifestations of the whiplash condition would be of benefit.

 

In contrast to many common musculoskeletal pain conditions (e.g. low back pain, non-specific neck pain) whiplash related neck pain usually occurs following a traumatic event, namely a motor vehicle crash. Psychological responses related to the traumatic event itself, posttraumatic stress symptoms, are emerging as an important additional psychological factor in the whiplash condition. Recent data indicates that post-traumatic stress symptoms are prevalent in individuals who have sustained whiplash injuries following motor vehicle accidents [18, 20, 21]. The early presence of posttraumatic stress symptoms have been shown to be associated with poor functional recovery from the injury [13, 18]. Recent data from our laboratory have shown that following whiplash injury 17% of individuals will follow a trajectory of initial moderate/severe posttraumatic stress symptoms that persist for at least 12 months and 43% will follow a trajectory of moderate initial symptoms that decrease but remain at mild to moderate (sub-clinical) levels for at least 12 months (the duration of the study) [4]. See Figure 1. These figures are significant as they are similar to the prevalence of PTSD in individuals admitted to hospital following �more severe� motor vehicle injuries [22].

 

Figure 1 Data from Whiplash Injured Participants

Figure 1: Data from 155 whiplash injured participants measured at 1, 3, 6 & 12 months post-accident. The Posttraumatic Stress Diagnostic Scale (PDS) was measured at each time point. Group based trajectory modelling identified 3 distinct clinical pathways (trajectories). 1. Chronic moderate/severe (17%) 2. Recovering: initial moderate levels of posttraumatic stress decreasing to mild/ moderate levels. 3. Resilient: negligible symptoms throughout2. PDS symptom score Cut-offs: 1�10 mild, 11�20 moderate, 21�35.

 

Although chronic WAD is a considerable health problem the number of published randomized controlled trials (RCTs) is very limited [23]. A recent systematic review concluded that there is evidence to suggest that exercise programs are modestly effective in relieving whiplash-related pain, at least over the short term [23]. For example, Stewart et al [24] showed only a 2 point (on a 10 point scale) decrease in pain levels immediately after a 6 week functional exercise management intervention that adhered to pain-related CBT principals but with no significant sustained effects at more long term follow-ups of 6 and 12 months. In a preliminary RCT conducted in our laboratory (published in 2007), a more neck specific exercise approach also delivered only modest effects, in that pain and disability scores decreased by just clinically relevant amounts (8�14% on the Neck disability Index) when compared to a single advice session [25].

 

The systematic review also concluded that there is conflicting evidence regarding the effectiveness of psychological interventions either delivered alone or in combination with physiotherapy [23]. The studies included in the review were of variable quality and mostly utilized CBT in some format to address pain related cognitions and distress [26, 27]. No study specifically targeted PTSD symptoms.

 

Thus the seemingly logical proposal of interventions to target the physical and pain�related psychological factors of chronic WAD is not working as well as would be anticipated. This expectation is based on more favourable outcomes with such approaches for other musculoskeletal pain conditions such as low back [28].

 

In an endeavour to understand why exercise rehabilitation approaches are not very effective for chronic WAD, we undertook a NHMRC (570884) funded randomized controlled trial that included effect modifiers of PTSD symptoms and sensory disturbances. In this larger (n=186) multicentre trial, preliminary analysis indicate that only 30% of patients with chronic WAD and a PTSD diagnosis had a clinically relevant change in Neck Disability Index scores (>10% change) compared to 70% of WAD patients without PTSD following an exercise rehabilitation program. All included participants reported moderate or greater levels of pain and disability indicating that the co-morbid presence of PTSD prevents a good response to physical rehabilitation. We could find no modifying effect of any sensory changes. The results of this study lead us to propose that first treating PTSD and then instituting physical rehabilitation will be a more effective intervention to improve health outcomes for chronic WAD.

 

Trauma-focused CBT is a highly effective treatment for PTSD symptoms [29] and the Australian Guidelines for Treatment of Acute Stress Disorder and PTSD recommend that individually delivered trauma-focused CBT should be provided to people with these conditions [30]. There is data available to indicate that trauma-focused CBT may potentially have an effect not only on PTSD symptoms but also on pain and disability. The results of a recent empirical examination explored directional relationships between PTSD and chronic pain in 323 survivors of accidents [31]. The results indicated a mutual maintenance of pain intensity and posttraumatic stress symptoms at 5 days post injury but by 6 months post injury (chronic stage), PTSD symptoms impacted significantly on pain but not vice versa. Whilst this study did not specifically focus on whiplash injury, it provides indication that addressing PTSD symptoms in the chronic stage of WAD may allow for a decrease in levels of pain thus facilitating the potential effects of more pain/disability focused approaches to management such as exercise and pain-focused CBT.

 

Based on our findings of the co-occurrence of PTSD and WAD, we conducted a small pilot study with the aim being to test the effects of trauma-focused CBT on psychological factors, pain and disability in individuals with chronic WAD [32]. Twenty-six participants with chronic WAD and a diagnosis of PTSD were randomly assigned to treatment (n = 13) or no-Intervention (n = 13) control. The treatment group underwent 10 weekly sessions of trauma-focused CBT for PTSD. Assessments of PTSD diagnosis, psychological symptoms, disability, and pain symptoms were made at baseline and post-assessment (10-12 weeks). Following the treatment intervention, there was not only a significant reduction in psychological symptoms (PTSD symptom severity; numbers meeting the diagnostic criteria for PTSD; depression, anxiety and stress scores) but also a significant decrease in pain and disability and improvements in physical function, bodily pain and role physical items of the SF36 (Table 1).

 

Table 1. Results of pilot randomised control trial

Trauma-focused CBT No-intervention Control
Neck Disability Index (0-100)*
Baseline 43.7 (15) 42.8 (14.3)
Post intervention 38.7 (12.6) 43.9 (12.9)
SF-36 Physical Function �
Baseline 55.8 (25.9) 55.4 (28.2)
Post intervention 61.5 (20.1) 51.1 (26.3)
SF -36 Bodily Pain �
Baseline 31.2 (17.2) 22.6 (15.5)
Post intervention 41.8 (18) 28.2 (15.8)
Posttraumatic Stress Disorder Diagnosis (SCID-IV)
Baseline N= 13 (100%) N= 13 (100%)
Post intervention N= 5 (39.5%) N= 12 (92.3%)

* higher score=worse; �higher scores=better

 

The results of this study indicate that trauma-focused CBT provided to individuals with chronic WAD has positive effects, not only on psychological status but also on pain and disability the cardinal symptoms of this condition. Whilst the mean change of 5% was marginal in terms of a clinical relevance [33], the effect size for change of the NDI was moderate (d=0.4) and shows promise for a greater effect in a larger sample size [34]. Nevertheless our pilot trial findings suggest that trauma-focused CBT alone will not be enough for successful management of chronic WAD and for this reason our proposed trial will combine this approach with exercise. These findings are potentially ground breaking in the area of whiplash management and it is imperative that they are now tested in a full randomised controlled design.

 

In summary, we have already shown that individuals with chronic WAD and moderate PTSD symptoms do not respond as well to a physical rehabilitation based intervention as those without PTSD symptoms [25]. Our recent pilot study indicates that trauma-focused CBT has a beneficial effect on both psychological status and pain and disability. We propose that by pre-treating the PTSD, PTSD symptoms and pain related disability will decrease allowing the exercise intervention to be more effective than has been seen to date [24, 25]. Therefore our proposed research will address this identified gap in knowledge by being the first to evaluate the efficacy of a combined trauma-focused CBT intervention followed by exercise for chronic WAD.

 

The primary aim of this project is to investigate the effectiveness of combined trauma-focused CBT and exercise to decrease pain and disability of individuals with chronic whiplash and PTSD. The secondary aims are to investigate the effectiveness of combined trauma-focused CBT and exercise to decrease posttraumatic stress symptoms, anxiety and depression, and to investigate the effectiveness of trauma-focused CBT alone on posttraumatic stress symptoms and pain/disability.

 

This trial is expected to commence in June 2015 and completed by December 2018.

 

Design

 

This study will be a randomised controlled multi-centre trial evaluating 10 weeks of trauma-focused CBT compared with 10 weeks of supported therapy, each followed by a 6 week exercise program. Outcomes will be measured at 10 weeks, 16 weeks, 6 and 12 months post randomisation. A total of 108 people with chronic whiplash disorder (>3 months, <5 years duration) and PTSD (DSM-5 diagnosed with CAPS) will be enrolled in the study. The assessors measuring outcomes will be blinded to the assigned treatment group allocation. The protocol conforms to CONSORT guidelines.

 

Figure 2 Study Design

 

Methods

 

Participants

 

A total of 108 participants with chronic whiplash associated disorder (WAD) grade II (symptom duration >3 months and <5 years) and PTSD will be recruited from Southeast Queensland and Zealand, Denmark. Participants will be recruited via:

 

  1. Advertisements (the Danish national health register, newspaper, newsletter and internet): potential participants will be invited to make contact with project staff.
  2. Physiotherapy and General Medical Practices: the study will be promoted in physiotherapy and medical clinics where project staff already have a relationship. Patients deemed to be appropriate for inclusion will be given an information sheet about the project and invited to contact project staff directly.

 

There is a two-step process to determining inclusion to this study: initial online/telephone interview followed by a screening clinical examination. The initial interview will identify duration of whiplash injury (inclusion criteria) and moderate pain based on NDI scores, and potential exclusion criteria. Likelihood of PTSD will be based on conservative PCL-5 scores, requiring at least one moderate score per symptom and a minimum score of 30 overall. A description of the project will be provided to all volunteers at the point of initial contact. Volunteers deemed likely to be eligible will be invited to attend a screening clinical examination. If more than four weeks passes between the phone interview and clinical screening than the NDI and PCL-5 measures are to be re-administered.

 

Prior to undertaking the screening clinical examination, volunteers will be provided with participant information and asked to complete informed consent documentation. During the screening examination, participants who have significant co-morbidity such as serious spinal pathology will be identified and excluded from participation. To screen for serious pathology, a diagnostic triage will be conducted following the Motor Accident Authority of NSW Whiplash Guidelines [35]. The screening examination will also include a clinical interview by a research assistant who will administer the Clinician Administered PTSD scale 5 (CAPS 5) to determine the presence and severity of PTSD [36]. The research assistant will also confirm the absence of exclusion criteria such as past history or current presentation of psychosis, bipolar disorder, organic brain disorder and severe depression substance abuse. If participants report a diagnosis of an exclusion criteria the relevant section of SCID-I will be utilised to clarify diagnosis.

 

During the initial screen or during treatment, if a participant is identified as being at high risk of self-harm or suicide, they will be referred to appropriate care in accordance with the professional standards of psychologists. Participants who meet the inclusion criteria (NDI >30% and PTSD diagnosis) will then be evaluated on all outcome measures for baseline results. It is possible that volunteers invited to attend the screening clinical examination will not meet the inclusion criteria (NDI >30% and PTSD diagnosis) and will therefore be excluded from further participation. Volunteers will be informed of this possibility during the telephone interview and also during the informed consent process. The Interview will be recorded and a random selection will be assessed for consistency

 

Inclusion Criteria

 

  • Chronic WAD Grade II (no neurological deficit or fracture) [37] of at least 3 months duration but less than 5 years duration
  • At least moderate pain and disability (>30% on the NDI)
  • A diagnosis of PTSD (DSM-5, APA, 2013) using the CAPS 5
  • Aged between 18 and 70 years old
  • Proficient in written English or Danish (depending on country of participation)

 

Exclusion Criteria

 

  • Known or suspected serious spinal pathology (e.g. metastatic, inflammatory or infective diseases of the spine)
  • Confirmed fracture or dislocation at the time of injury (WAD Grade IV)
  • Nerve root compromise (at least 2 of the following signs: weakness/reflex changes/sensory loss associated with the same spinal nerve)
  • Spinal surgery in the last 12 months
  • A history or current presentation of psychosis, bipolar disorder, organic brain disorder or severe depression.

 

Sample Size

 

We are interested in detecting a clinically important difference between the two interventions, given that baseline values for each group are statistically equivalent as a result of the randomisation. Based on a two-sided t-test a sample of 86 (43 per group) will provide 80% power to detect a significant difference at alpha 0.05 between the group means of 10 points on the 100 point NDI (assuming a SD of 16, based on our pilot data and data from recent trials ). Effects smaller than this are unlikely to be considered clinically worthwhile. Allowing for a 20% loss to follow up by 12 months, we would require 54 participants per treatment group.

 

Intervention

 

Randomisation

 

Participants will be randomly allocated to treatment group. The randomisation schedule will be generated by the study biostatistician. Randomisation will be by random permuted blocks of 4 to 8. Consecutively numbered, sealed, opaque envelopes will be used to conceal randomisation. Group allocation will be performed immediately following completion of baseline measures by an independent (non-blinded) research assistant . This same research assistant will arrange all appointment times with the treating practitioners and the blinded assessor for all outcome measures. Participants will be instructed not to reveal details about their treatment to the examiner in order to assist with blinding. Patients will be scheduled to receive their first treatment within one week of randomisation.

 

Intervention group – Trauma-focused Cognitive-behavioural therapy (CBT)

 

A psychological intervention that targets PTSD symptoms will consist of 10 weekly 60-90 minute sessions of individually delivered trauma-focused CBT based on the Australian Guidelines for the treatment of Adults with Acute Stress Disorder and PTSD [38] (see Table 2). Session one will focus on providing psycho-education regarding the common symptoms of PTSD, maintaining factors and providing a rationale for various treatment components. Sessions two and three will continue to develop patient�s knowledge of PTSD symptoms and teach anxiety management strategies including deep breathing and progressive muscle relaxation. Cognitive restructuring which involves challenging unhelpful and irrational thoughts and beliefs will commence in session three and continue throughout treatment. Participants will start prolonged exposure in session four which will be paired with relaxation and cognitive challenging. Session six will introduce graded in-vivo exposure. Relapse prevention will also be included in the final two sessions [12]. Participants will be asked to complete a home practice over the course of their sessions which will be recorded and brought to the next session. Treatment will be delivered by registered psychologists with postgraduate clinical training and experience delivering trauma-focused CBT interventions.

 

Table 2. Overview of CBT program

Session Overview
1 Introduction and rationale
2 Relaxation training
3 Relaxation training and cognitive challenging
4 and 5 Cognitive challenging and prolonged exposure
6 Prolonged exposure and in vivo exposure
7 and 8 Prolonged exposure and in-vivo exposure
9 Relapse prevention
10 Relapse prevention and end of treatment

 

 

Control group – Supportive Therapy

 

The first session will involve education about trauma and an explanation of the nature of supportive therapy. The following sessions will include discussions of current problems and general problem-solving skills. Home practice will involve diary keeping of current problems and mood states. Supportive therapy will specifically avoid exposure, cognitive restructuring or anxiety management techniques. If the results of the trial are favourable and participants randomised to this intervention still have a PTSD diagnosis at the 12 month follow-up, they will be offered a referral to a clinical psychologist.

 

Exercise Program

 

Following the 10 week psychological therapy sessions (intervention or control), All participants will participate in the same exercise program. The 6-week exercise program will be carried out under supervision from a physiotherapist (2 sessions in each of the first four weeks; and 1 session in week 5 and week 6) and will comprise specific exercises to improve the movement and control of the neck and shoulder girdles as well as proprioceptive and co-ordination exercises (see Table 3). The exercises will be tailored by the physiotherapist for each individual participant.

 

The program begins with a clinical examination of the cervical muscles and the axio-scapular-girdle muscles and includes tests that assess ability to recruit the muscles in a coordinated manner, tests of balance, cervical kinaesthesia and eye movement control and tests of muscle endurance at low levels of maximum voluntary contraction. The specific impairments that are identified are then addressed with an exercise program that is supervised and progressed by the physiotherapist. This specific treatment program has been described in detail [15] and focuses on activating and improving the co-ordination and endurance capacity of the neck flexor, extensor and scapular muscles in specific exercises and functional tasks, and a graded program directed to the postural control system, including balance exercises, head relocation exercises and exercises for eye movement control.

 

Participants will also perform the exercises at home, once a day. A log book will be completed by participants to record compliance with the exercises. At the same time, the physiotherapist will guide the subject�s return to normal activities.

 

Physiotherapists will adhere to cognitive-behavioural principles during training and supervision of all exercises [26]. The cognitive behavioural therapy principles include the encouragement of skill acquisition by modelling, setting progressive goals, self-monitoring of progress, and positive reinforcement of progress. Self-reliance will be fostered by encouraging subjects to engage in problem-solving to deal with difficulties rather than seeking reassurance and advice, by encouraging relevant and realistic activity goals, and by encouraging self-reinforcement. Daily physical activity at home will be encouraged and monitored using a diary. Written and illustrated exercise instructions will be provided.

 

Table 3. Overview of the exercise program

Week Sessions per week Components
1 2 ������� Baseline & follow-up assessments to guide initial prescription & progression of program

������� Exercise to improve cervical and scapular muscle control, kinaesthesia & balance

������� Education and advice

������� Daily home program including exercise & graded increase of physical activities

������� CBT principles such as goal setting, reinforcement used by physiotherapists

������� Discharge session to reinforce progress and plan for continued activity

2 2
3 2
4 2
5 1
6 1

 

 

Outcome Measures

 

At the baseline assessment, personal characteristics such as age, gender, level of education, compensation status, accident date and information about symptoms of whiplash will be collected. The following outcome measures will be assessed by a blind assessor at baseline, 10 weeks, 16 weeks, 6 months and 12 months post randomisation.

 

The Neck Disability Index (NDI) will be the primary outcome measure [21]. The NDI is a valid measure and reliable measure of neck pain related disability [21] and is recommended for use by the Bone and Joint Decade Neck Pain Task Force [7] and at the recent International Whiplash Summit [11, 16].

 

Secondary outcome measures include:

 

  1. Average pain intensity over last week (0-10 scale) [39]
  2. Average pain intensity over last 24 hours (0-10 scale) [39]
  3. Patient�s global impression of recovery (-5 to +5 scale) [39]
  4. Clinician administered PTSD scale 5 (CAPS 5) [40].
  5. The PTSD Checklist (PCL-5) [41]
  6. Depression Anxiety Stress Scale-21 (DASS-21) [42]
  7. Generic measure of health status (SF-12) [43]
  8. Patient-generated measure of disability (Patient-Specific Functional Scale) [44]
  9. Physical measures (cervical range of movement, pressure pain threshold, cold pain threshold)
  10. Pain Catastrophizing Scale (PCS) [45]
  11. Pain Self Efficacy Questionnaire (PSEQ) [46]
  12. Tampa Scale of Kinesiophobia (TSK) [47]

 

Expectations of a beneficial treatment effect will be measured with the Credibility Expectancy Questionnaire (CEQ) [48] at the first and last week of each treatment. Working alliance as reported by the client and the therapist (psych or physio) will also be measured at the first and last week of each treatment using the Working Alliance Inventory (WAI) [49].

 

Monitoring of Treatment Sites

 

Treatment sites will be located in areas easily accessible by public transport. Attempts will be made to have both the psychology and exercise sessions held at the same site. Prior to commencement of the trial, psychologists and physiotherapists at each treatment site will be provided with the appropriate therapist protocol. Psychologists will be trained to implement the CBT program and the supported therapy by senior investigators at a one day workshops. Physiotherapists will be trained by senior investigators to implement the exercise program at a one day workshop.

 

Prior to starting the trial, the different treatment provider sites and therapists will be provided with a copy of the trial and treatment protocols. Both psychological therapies will be conducted according to a procedural manual. Therapists will be required to record each session as well as complete a checklist of adherence to the protocol. A random sample of these recordings and checklists will be evaluated and ongoing supervision provided by a psychologist on the research team. Physiotherapy exercises will be based on a previous exercise trial for chronic WAD [25]. An audit of the physiotherapy sessions will be conducted twice during the intervention by a senior investigator expert in this area. A handover will occur between psychologist and physiotherapist to maintain continuity of care.

 

Adverse Events

 

Apart from the usual ethics committee based provisions for reporting of adverse effects, practitioners will be requested to report any adverse event to the Chief Investigators. Also at the 16 week follow-up, information about adverse effects of treatment will be sought from all subjects using open-ended questioning. At 6 and 12 months follow-up, data relating to the number of recurrences of neck pain, and the number of health care contacts will also be collected.

 

Statistical Analysis

 

The study biostatistician will analyse the data in a blinded manner. All analyses will be conducted on an intention to treat basis. The primary and secondary outcomes measured at 10 weeks, 16 weeks, 6 months, and 12 months will be analysed using linear mixed and logistic regression models that will include their respective baseline scores as a covariate, subjects as a random effect and treatment conditions as fixed factors. Diagnostics will be used to examine assumptions, including homogeneity of variances. Effect sizes will be calculated for all measures with an effect size of 0.2 considered small, 0.5 medium and 0.8 large. Alpha will be set at 0.05. Any effect of site (Qld or Denmark) will be evaluated by including a site-by-treatment group-by-time interaction term to the mixed models analyses. Effect modification will only be assessed for the primary outcome of NDI.

 

Funding

 

  • The trial is funded by a NHMRC Project grant 1059310.
  • The Council of the Danish Victims Fund Project grant 14-910-00013

 

Potential Significance

 

This project addresses a problem of major importance to human health. Whiplash is an enormous health burden for both Australia and all countries where there are motor vehicles. Current conservative approaches to the management of chronic WAD have been shown to be only marginally effective. One reason for this may be due to the lack of attention of current practice to the psychological status of whiplash injured patients. This study will provide a definitive evaluation of the effects of adding trauma-focused CBT to exercise for individuals with chronic WAD and PTSD.

 

This study is likely to influence the clinical management of whiplash injury and will have immediate clinical applicability. Any intervention that may improve health outcomes for individuals with chronic whiplash will have far reaching effects in both Australia and internationally. Our study will also have implications for both health and insurance policy makers in their decision making regarding treatment options and funding. A search of the WHO International Clinical Trials Registry Platform Search Portal on 2/3/13 revealed no planned or completed trial that would duplicate our work.

 

Conflict of Interest Declaration

 

The authors declare no conflict of interest.

 

Role of Psychosocial Stress in Recovery from Common Whiplash

 

Abstract

 

It is widely accepted that psychosocial factors are related to illness behaviour and there is some evidence that they may influence the rate of recovery from post-traumatic disorders. The abilities of psychosocial stress, somatic symptoms, and subjectively assessed cognitive impairment to predict delayed recovery from common whiplash were investigated in a follow-up study. 78 consecutive patients referred 7.2 (SD 4.5) days after they had sustained common whiplash in car accidents were assessed for psychosocial stress, negative affectivity, personality traits, somatic complaints, and cognitive impairment by semistructured interview and by several standardised tests. On examination 6 months later 57 patients were fully recovered and 21 had persisting symptoms. The groups’ scores for the independent variables assessed at the baseline examination were compared. Stepwise regression analysis showed that psychosocial factors, negative affectivity, and personality traits were not significant in predicting the outcome. However, initial neck pain intensity, injury-related cognitive impairment, and age were significant factors predicting illness behaviour. This study, which was based on a random sample and which considered many other possible predictive factors as well as psychosocial status, does not support previous findings that psychosocial factors predict illness behaviour in post-trauma patients.

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

Being involved in an automobile accident can be a traumatic experience for anyone. From physical injuries and financial problems, to emotional distress, an auto accident can place a heavy burden on those individuals who’ve experienced it, especially if the auto accident injuries begin to take a toll on the mind. Many patients visit my chiropractic office with anxiety, irrational fears, depression and PTSD after being involved in an automobile accident. Learning to trust again to receive chiropractic care can be challenging, but through careful and effective spinal adjustments and manual manipulations, our staff can provide patients with the sense of safety they need to continue treatment and achieve overall health and wellness.

 

In conclusion,�automobile accidents can cause a variety of physical injuries and conditions, such as whiplash, back pain and headaches, as well as financial issues, however, auto accident injuries and complications can also lead to emotional distress. According to evidence-based research studies, like the one above, emotional distress has been connected to chronic pain symptoms. Fortunately, researchers have conducted numerous research studies to demonstrate how mindfulness interventions, like chiropractic care, can help reduce emotional distress and improve painful symptoms. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Back Pain

 

According to statistics, approximately 80% of people will experience symptoms of back pain at least once throughout their lifetimes. Back pain is a common complaint which can result due to a variety of injuries and/or conditions. Often times, the natural degeneration of the spine with age can cause back pain. Herniated discs occur when the soft, gel-like center of an intervertebral disc pushes through a tear in its surrounding, outer ring of cartilage, compressing and irritating the nerve roots. Disc herniations most commonly occur along the lower back, or lumbar spine, but they may also occur along the cervical spine, or neck. The impingement of the nerves found in the low back due to injury and/or an aggravated condition can lead to symptoms of sciatica.

 

blog picture of cartoon paperboy big news

 

EXTRA IMPORTANT TOPIC: Managing Workplace Stress

 

 

MORE IMPORTANT TOPICS: EXTRA EXTRA: Car Accident Injury Treatment El Paso, TX Chiropractor

 

 

Blank
References
  1. Sterling, M., G. Jull, and J. Kenardy, Physical and psychological factors maintain long-term predictive capacity post-whiplash injury. Pain, 2006. 122(1-2): p. 102-108.
  2. Carroll, L.J.P., et al., Course and Prognostic Factors for Neck Pain in the General Population: Results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine, 2008. 33(4S)(Supplement): p. S75-S82.
  3. Rebbeck, T., et al., A prospective cohort study of health outcomes following whiplash associated disorders in an Australian population. Injury Prevention, 2006. 12(2): p. 93-98.
  4. Sterling, M., J. Hendrikz, and J. Kenardy, Compensation claim lodgement and health outcome developmental trajectories following whiplash injury: A prospective study. PAIN, 2010. 150(1): p. 22-28.
  5. MAYOU, R. and B. BRYANT, Psychiatry of whiplash neck injury. The British Journal of Psychiatry, 2002. 180(5): p. 441-448.
  6. Kenardy, J., et al., Adults’ adjustment to minor and moderate injuries following road traffic crashes: Wave 1 findings., in Report to MAIC QLD. 2011.
  7. MAIC, Annual Report 2009-2010. 2010: Brisbane.
  8. Connelly, L.B. and R. Supangan, The economic costs of road traffic crashes: Australia, states and territories. Accident Analysis & Prevention, 2006. 38(6): p. 1087-1093.
  9. Littleton, S.M., et al., The association of compensation on longer term health status for people with musculoskeletal injuries following road traffic crashes: Emergency department inception cohort study. Injury, 2011. 42(9): p. 927-933.
  10. Schmidt, D., Whiplash koster kassen. Livtag, 2012. 1.
  11. Siegmund, G.P., et al., The Anatomy and Biomechanics of Acute and Chronic Whiplash Injury. Traffic Injury Prevention, 2009. 10(2): p. 101-112.
  12. B�rsbo, B., M. Peolsson, and B. Gerdle, The complex interplay between pain intensity, depression, anxiety and catastrophising with respect to quality of life and disability. Disability and Rehabilitation, 2009. 31(19): p. 1605-1613.
  13. Sterling, M., et al., Physical and psychological factors predict outcome following whiplash injury. Pain, 2005. 114(1-2): p. 141-148.
  14. Schmitt, M.A.M.M.T., et al., Patients with Chronic Whiplash-Associated Disorders: Relationship Between Clinical and Psychological Factors and Functional Health Status. American Journal of Physical Medicine & Rehabilitation, 2009. 88(3): p. 231-238.
  15. Sullivan, M.J.L., et al., Catastrophizing, pain, and disability in patients with soft-tissue injuries. Pain, 1998. 77(3): p. 253-260.
  16. Nederhand, M.J., et al., Predictive value of fear avoidance in developing chronic neck pain disability: consequences for clinical decision making. Archives of Physical Medicine and Rehabilitation, 2004. 85(3): p. 496-501.
  17. Bunketorp-Kall, L.S., C. Andersson, and B. Asker, The impact of subacute whiplash-associated disorders on functional self-efficacy: a cohort study. International Journal of Rehabilitation Research, 2007. 30(3): p. 221-226.
  18. Buitenhuis, J., et al., Relationship between posttraumatic stress disorder symptoms and the course of whiplash complaints. Journal of Psychosomatic Research, 2006. 61(5): p. 681-689.
  19. Sterling, M. and J. Kenardy, The relationship between sensory and sympathetic nervous system changes and posttraumatic stress reaction following whiplash injury�a prospective study. Journal of Psychosomatic Research, 2006. 60(4): p. 387-393.
  20. Sullivan, M.J.L., et al., Pain, perceived injustice and the persistence of post-traumatic stress symptoms during the course of rehabilitation for whiplash injuries. PAIN, 2009. 145(3): p. 325-331.
  21. Sterling, M., et al., The development of psychological changes following whiplash injury. Pain, 2003. 106(3): p. 481-489.
  22. O’Donnell, M.L., et al., Posttraumatic disorders following injury: an empirical and methodological review. Clinical Psychology Review, 2003. 23(4): p. 587-603.
  23. Teasell, R., et al., A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): Part 4 – noninvasive interventions for chronic WAD. Pain Research & Management, 2010. 15(5): p. 313 – 322.
  24. Stewart, M.J., et al., Randomized controlled trial of exercise for chronic whiplash-associated disorders. Pain, 2007. 128(1�2): p. 59-68.
  25. Jull, G., et al., Does the presence of sensory hypersensitivity influence outcomes of physical rehabilitation for chronic whiplash? � A preliminary RCT. Pain, 2007. 129(1�2): p. 28-34.
  26. S�derlund, A. and P. Lindberg, Cognitive behavioural components in physiotherapy management of chronic whiplash associated disorders (WAD) – a randomised group study. Physiotherapy Theory and Practice, 2001. 17(4): p. 229-238.
  27. Wicksell, R.K., et al., Can Exposure and Acceptance Strategies Improve Functioning and Life Satisfaction in People with Chronic Pain and Whiplash?Associated Disorders (WAD)? A Randomized Controlled Trial. Cognitive Behaviour Therapy, 2008. 37(3): p. 169-182.
  28. Ostelo, R.W., et al., Behavioural treatment for chronic low-back pain. Cochrane Database Syst Rev, 2005. 1(1).
  29. BISSON, J.I., et al., Psychological treatments for chronic post-traumatic stress disorder: Systematic review and meta-analysis. The British Journal of Psychiatry, 2007. 190(2): p. 97-104.
  30. NHMRC, Australian Guidelines for the Treatment of Adults with ASD and PTSD. 2007: Canberra.
  31. Jenewein, J., et al., Mutual influence of posttraumatic stress disorder symptoms and chronic pain among injured accident survivors: A longitudinal study. Journal of Traumatic Stress, 2009. 22(6): p. 540-548.
  32. Dunne, R.L.P., J.P.F. Kenardy, and M.P.M.B.G.D.M.P.F. Sterling, A Randomized Controlled Trial of Cognitive-behavioral Therapy for the Treatment of PTSD in the Context of Chronic Whiplash. Clinical Journal of Pain November/December, 2012. 28(9): p. 755-765.
  33. Macdermid, J., et al., Measurement Properties of the Neck Disability Index: A Systematic Review. Journal of Orthopaedic & Sports Physical Therapy, 2009. 39(5): p. 400-C12.
  34. Arnold, D.M.M.D.M., et al., The design and interpretation of pilot trials in clinical research in critical care. Critical Care Medicine Improving Clinical Trials in the Critically Ill: Proceedings of a Roundtable Conference in Brussels, Belgium, March 2008, 2009. 37(1): p. S69-S74.
  35. MAA. Guidelines for the management of whiplash associated disorders. 2007; Available from: www.maa.nsw.gov.au.
  36. Weathers, F.W., et al. The Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). Interview available from the National Center for PTSD. 2013; Available from: www.ptsd.va.gov.
  37. Spitzer, W., et al., Scientific Monograph of Quebec Task Force on Whiplash Associated Disorders: redefining “Whiplash” and its management. Spine, 1995. 20(8S): p. 1-73.
  38. ACPMH, Australian guidelines for the treatment of adults with acute stress disorder and post-traumatic stress disorder. 2007, Melbourne, VIC: Australian Centre for Posttraumatic Mental Health.
  39. Pengel, L.H.M.M., K.M.P. Refshauge, and C.G.P. Maher, Responsiveness of Pain, Disability, and Physical Impairment Outcomes in Patients With Low Back Pain. Spine, 2004. 29(8): p. 879-883.
  40. Weathers, F.W., T.M. Keane, and J.R.T. Davidson, Clinician-administered PTSD scale: A review of the first ten years of research. Depression and Anxiety, 2001. 13(3): p. 132-156.
  41. Weathers, F., et al., The PTSD Checklist for DSM-5 (PCL-5). Scale available from the National Center for PTSD. www.? ptsd.? va.? gov, 2013.
  42. Lovibond, S. and P. Lovibond, Manual for the Depression Anxiety Stress Scales. 2nd ed. 1995, Sydney: Psychological Foundation.
  43. Ware, J., et al., User�s manual for the SF-12v2� Health Survey with a supplement documenting SF-12� Health Survey. 2002, Lincoln, Rhode Island: QualityMetric Incorporated
  44. Westaway, M., P. Stratford, and J. Binkley, The Patient-Specific Functional Scale: Validation of Its Use in Persons With Neck Dysfunction. Journal of Orthopaedic & Sports Physical Therapy, 1998. 27(5): p. 331-338.
  45. Sullivan, M.J.L., S.R. Bishop, and J. Pivik, The Pain Catastrophizing Scale: Development and validation. Psychological Assessment, 1995. 7(4): p. 524-532.
  46. Nicholas, M.K., The pain self-efficacy questionnaire: Taking pain into account. European Journal of Pain, 2007. 11(2): p. 153-163.
  47. Miller, R., S. Kori, and D. Todd, The Tampa Scale for Kinesiophobia. Tampa, FL. Unpublished report, 1991.
  48. Devilly, G.J. and T.D. Borkovec, Psychometric properties of the credibility/expectancy questionnaire. Journal of Behavior Therapy and Experimental Psychiatry, 2000. 31(2): p. 73-86.
  49. Horvath, A.O. and L.S. Greenberg, Development and validation of the Working Alliance Inventory. Journal of Counseling Psychology, 1989. 36(2): p. 223-233.
Close Accordion
Mobile Devices Are Wrecking Our Spines In El Paso, TX.

Mobile Devices Are Wrecking Our Spines In El Paso, TX.

Nearly everyone has a smartphone or mobile device these days, and while there is some merit to this technology by keeping us more connected � at least virtually � it is wreaking havoc on our bodies. When you look at the posture that people assume when texting, reading email, or browsing social media while on their mobile device or smartphone, you will see their head bent forward and rounded shoulders. They typically hold the device either at chest level or waist level meaning that their hands are together, forming an almost crouch position.

This is very bad for the spine but it creates problems for other parts of the body even beyond the spine. Let�s take a look at some of the common issues that come with bad smartphone posture.

Mobile Device Injuries

Text Neck

The more you tilt your head downward (just as you do when looking at a smartphone), the more pounds of pressure you put on your neck and back. Your spine supports the weight of your head. The more it is thrust forward, looking down, the heavier your head gets. Doctors are seeing many young people with this problem, some even as young as 8 years old.

It is characterized by tightness or tension in the neck and shoulders as well as the upper back. Some patients report pain while others feel pressure, and others feel tightness. Sometimes the pain will spread throughout the body or from the neck to the arms and hands.

Forearm & Wrist Pain

Even the way you hold your phone in your hands can cause problems. Since you keep your hand in one position for long periods of time your muscles never have a chance to relax. You have several muscles engaged to do this: the forearms, the wrist, and the neck.

If you are experiencing pain, sometimes shooting, in your elbow or wrist your smartphone use may be the culprit. So put the phones away or leave them at home.

Sore Upper & Lower Back

As your neck struggles to support your head which is rolled forward, it stands to reason that you will experience back pain. In fact, both upper and lower back pain have been attributed to smartphone use.

Think about the muscles that run along your spine. They help stabilize it and help control and support your head. When you hunch over you strain those muscles in your upper back. What you may not realize is that similar strain is being put on the muscles in your lower back as well.

mobile el paso tx

Blackberry Thumb

The muscles in your hand are very small but they can cause you a great deal of pain if you frequently use a mobile device. As you type on the keyboard of your smart phone, it can cause problems with tendons and ligament as well as the muscles.

This repetitive stress of the body is caused daily by people who stay hunched over their small phone screen. The repetitive movement of your thumb as it manipulates the device can cause inflammation in the thumb and hand.

Headaches From Tension In Neck & Back

One of the most common ailments associated with mobile device usage is headaches. These headaches can come from tension in the neck, strained muscled in the back, or overworked muscles through the hand and arm into the shoulder. It can also come from eyestrain caused by staring at the screen for extended amounts of time, looking at tiny text.

There is no doubt that mobile device usage is becoming a serious problem in our society today. While there are the people who text while driving or while walking, posing a significant threat to their own and others� safety, what they are doing to their own bodies is enough to cause alarm.

Chiropractic care can ease the pain and reverse a good portion of the damage that has been done, but if when people continue with the same bad habits the treatment is only temporary. There needs to be a focused effort made to pull people out of their mobile devices, at least a portion of the time, to minimize the structural spinal damage they are doing to themselves.

Chiropractic Treatment For Proper Posture

Chronic Neck Pain | Understanding Cervical Instability

Chronic Neck Pain | Understanding Cervical Instability

Being involved in an automobile accident can cause damage or injury to the complex structures of the cervical spine which can go unnoticed for months if left untreated. Medically referred to as whiplash-associated disorders, or whiplash, symptoms resulting after an auto accident can often take days to even weeks or months to manifest. Persistent neck pain that lasts for more than 3 months then becomes chronic neck pain, an issue which can be difficult to manage if not treated accordingly. Chronic neck pain may also result due to other underlying issues. The following article demonstrates which types of treatment methods can help relieve chronic neck pain symptoms and its associated complications, including capsular ligament laxity and cervical instability.

 

Chronic Neck Pain: Making the Connection Between Capsular Ligament Laxity and Cervical Instability

 

Abstract

 

The use of conventional modalities for chronic neck pain remains debatable, primarily because most treatments have had limited success. We conducted a review of the literature published up to December 2013 on the diagnostic and treatment modalities of disorders related to chronic neck pain and concluded that, despite providing temporary relief of symptoms, these treatments do not address the specific problems of healing and are not likely to offer long-term cures. The objectives of this narrative review are to provide an overview of chronic neck pain as it relates to cervical instability, to describe the anatomical features of the cervical spine and the impact of capsular ligament laxity, to discuss the disorders causing chronic neck pain and their current treatments, and lastly, to present prolotherapy as a viable treatment option that heals injured ligaments, restores stability to the spine, and resolves chronic neck pain.

 

The capsular ligaments are the main stabilizing structures of the facet joints in the cervical spine and have been implicated as a major source of chronic neck pain. Chronic neck pain often reflects a state of instability in the cervical spine and is a symptom common to a number of conditions described herein, including disc herniation, cervical spondylosis, whiplash injury and whiplash associated disorder, postconcussion syndrome, vertebrobasilar insufficiency, and Barr�-Li�ou syndrome.

 

When the capsular ligaments are injured, they become elongated and exhibit laxity, which causes excessive movement of the cervical vertebrae. In the upper cervical spine (C0-C2), this can cause a number of other symptoms including, but not limited to, nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches. In the lower cervical spine (C3-C7), this can cause muscle spasms, crepitation, and/or paresthesia in addition to chronic neck pain. In either case, the presence of excessive motion between two adjacent cervical vertebrae and these associated symptoms is described as cervical instability.

 

Therefore, we propose that in many cases of chronic neck pain, the cause may be underlying joint instability due to capsular ligament laxity. Currently, curative treatment options for this type of cervical instability are inconclusive and inadequate. Based on clinical studies and experience with patients who have visited our chronic pain clinic with complaints of chronic neck pain, we contend that prolotherapy offers a potentially curative treatment option for chronic neck pain related to capsular ligament laxity and underlying cervical instability.

 

Keywords: Atlanto-axial joint, Barr�- Li�ou syndrome, C1-C2 facet joint, capsular ligament laxity, cervical instability, cervical radiculopathy, chronic neck pain, facet joints, post-concussion syndrome, prolotherapy, spondylosis, vertebrobasilar insufficiency, whiplash.

 

Introduction

 

In the realm of pain management, an ever-growing number of treatment-resistant patients are being left with relatively few conventional treatment options that effectively and permanently relieve their chronic pain symptoms. Chronic cervical spine pain is particularly challenging to treat, and data regarding the long-term efficacy of traditional therapies has been extremely discouraging [1]. The prevalence of neck pain in the general population has been reported to range between 30% and 50%, with women over 50 making up the larger portion [1-3]. Although many of these cases resolve with time and require minimal intervention, the recurrence rate of neck pain is high, and about one-third of people will suffer from chronic neck pain (defined as pain that persists longer than 6 months), and 5% will develop significant disability and reduction in quality of life [2, 4]. For this group of chronic pain patients, modern medicine offers few options for long-term recovery.

 

Treatment protocols for acute and sub-acute neck pain are standard and widely agreed upon [1, 2]. However, conventional treatments for chronic neck pain remain debatable and include interventions such as use of nonsteroidal anti-inflammatory drugs (NSAIDs) and narcotics for pain management, cervical collars, rest, physiotherapy, manual therapy, strengthening exercises, and nerve blocks. Furthermore, the literature on long-term treatment outcomes has been inconclusive at best [5-9]. Chronic neck pain due to whiplash injury or whiplash associated disorder (WAD) is particularly resistant to long-term treatment; conventional treatment for these conditions may give temporary relief but long-term outcomes have been disappointing [10].

 

In light of the poor treatment options and outcomes for chronic neck pain, we propose that in many of these cases, the underlying condition may be related to capsular ligament laxity and subsequent joint instability of the cervical spine. Should this be the case and joint instability is the fundamental problem causing chronic neck pain, a new treatment approach may be warranted.

 

The diagnosis of chronic neck pain due to cervical instability is particularly challenging. In most cases, diagnostic tools for detecting cervical instability have been inconsistent and lack specificity [11-15], and are therefore inadequate. A better understanding of the pathogenesis of cervical instability may better enable practitioners to recognize and treat the condition more effectively. For instance, when cervical instability is related to injury of soft tissue (eg, ligaments) alone and not fracture, the treatment modality should be one that stimulates the involved soft tissue to regenerate and repair itself.

 

Dr Jimenez works on wrestler's neck

 

In that context, comprehensive dextrose prolotherapy offers a promising treatment option for resolving cervical instability and the subsequent pain and disability it causes. The distinct anatomy of the cervical spine and the pathology of cervical instability described herein underlie the rationale for treating the condition with prolotherapy.

 

Anatomy

 

The cervical spine consists of the first seven vertebrae in the spinal column and is divided into two segments, the upper cervical (C0-C2) and lower cervical (C3-C7) regions. Despite having the smallest vertebral bodies, the cervical spine is the most mobile segment of the entire spine and must support a high degree of movement. Consequently, it is highly reliant on ligamentous tissue for stabilizing the neck and spinal column, as well as for controlling normal joint motion; as a result, the cervical spine is highly susceptible to injury.

 

The upper cervical spine consists of C0, called the occiput, and the first two cervical vertebrae, C1 and C2, or atlas and axis, respectively. C1 and C2 are more specialized than the rest of the cervical vertebrae. C1 is ring-shaped and lacks a vertebral body. C2 has a prominent vertebral body called the odontoid process or dens which acts as a pivot point for the C1 ring [16]. This pivoting motion (Fig. ?1), coupled with the lack of intervertebral discs in the upper cervical spine, allows for more movement and rotation of the joint, thus facilitating mobility rather than stability [17]. Collectively, the upper cervical spine is responsible for 50% of total neck flexion and extension at the atlanto-occipital (C0-C1) joint, as well as 50% of total neck rotation that occurs at the atlanto-axial joint (C1-C2) [16]. This motion is possible because the atlas (C1) rotates around the axis (C2) via the dens and the anterior arch of the atlas.

 

Figure 1 Atlanto-Axial Rotational Instability

Figure 1: Atlanto-axial rotational instability. The atlas is shown in the rotated position on the axis. The pivot is the eccentrically placed odontoid process. In rotation, the wall of the vertebral foramen of Cl decreases the opening of the spinal canal between Cl and C2. This can potentially cause migraine headaches, C2 nerve root impingement, dizziness, vertebrobasilar insufficiency, ‘drop attacks; neck-tongue syndrome, Barr�-Li�ou syndrome, severe neck pain, and tinnitus.

 

The intrinsic, passive stability of the spine is provided by the intervertebral discs and surrounding ligamentous structures. The upper cervical spine is stabilized solely by ligaments, including the transverse, alar, and capsular ligaments. The transverse ligament runs behind the dens, originating on a small tubercle on the medial side of a lateral mass of the atlas and inserting onto the identical tubercle on the other side. Thus, the transverse ligament restricts flexion of the head and anterior displacement of the atlas. The left and right alar ligaments originate from the posterior dens and attach to the medial occipital condyles on the ipsilateral sides. They work to limit axial rotation and are under the greatest tension in rotation and flexion. By holding C1 and C2 in proper position, the transverse and alar ligaments help to protect the spinal cord, brain stem, and nervous system from excess movement in the upper cervical spine [18].

 

The lower cervical spine, while less specialized, allows for the remaining 50% of neck flexion, extension, and rotation. Each vertebra in this region (C3-C7) has a vertebral body, in between which lies an intervertebral disc, the largest avascular structure of the body. This disc is a piece of fibrocartilage that helps cushion the joints and allows for more stability and is comprised of an inner gelatinous nucleus pulposus, which is surrounded by an outer, fibrous annulus fibrosus. The nucleus pulposus is designed to sustain compression loads and the annulus fibrosus, to resist tension, shear and torsion [19]. The annulus fibrosus is thought to determine the proper functioning of the entire intervertebral disc [20] and has been described as a lamellar structure consisting of 15-26 distinct concentric fibrocartilage layers that constitute a criss-crossing fiber matrix [19]. However, the form of this structure has been disputed. A microdissection study using cadavers reported that the cervical annulus fibrosus does not consist of concentric laminae of collagen fibers as it does in lumbar discs. Instead, the authors contend that the three-dimensional architecture of the cervical annulus fibrosus is more like that of a crescentic anterior interosseous ligament surrounding the nucleus pulposus [21].

 

In addition to the discs, multiple ligaments and the two synovial joints on each pair of adjacent vertebrae (facet joints) allow for controlled, fully three dimensional motions. Capsular ligaments wrap around each facet joint, which help to maintain stability during neck rotation. Each vertebra in the lower cervical spine (in addition to C2) contains a spinous process that serves as an attachment site for the interspinal ligaments. These tissues connect adjacent spinous processes and limit flexion of the cervical spine. Anteriorly, they meet with the ligamentum flavum.

 

Three other ligaments, the ligamentum flavum, anterior longitudinal ligament (ALL), and posterior longitudinal ligament (PLL), help to stabilize the cervical spine during motion and protect against excess flexion and extension of the cervical vertebrae. From C1-C2 to the sacrum, the ligamentum flava run down the posterior aspect of the spinal canal and join the laminae of adjacent vertebrae while helping to maintain proper neck posture. The ALL and PLL both run alongside the vertebral bodies. The ALL begins at the occiput and runs anteriorly to the anterior sacrum, helping to stabilize the vertebrae and intervertebral discs and limit spinal extension. The PLL also helps to stabilize the vertebrae and intervertebral discs, as well as limit spinal flexion. It extends from the body of the axis to the posterior sacrum and runs within the anterior aspect of the spinal canal across from the ligamentum flava.

 

A spinous process and two transverse processes emanate off the neural arch (or vertebral arch) which lies at the posterior aspect of the cervical vertebral column. The transverse processes are bony prominences that protrude postero-laterally and serve as attachment sites for various muscles and ligaments. With the exception of C7, each of these processes has a foramen which allows for passage of the vertebral artery towards the brain; the C7 transverse process has foramina which allow for passage of the vertebral vein and sympathetic nerves [22]. The transverse processes of the cervical vertebrae are connected via the intertransverse ligaments; each attaches a transverse process to the one below and helps to limit lateral flexion of the cervical spine.

 

Facet Joints

 

The inferior articular process of the superior cervical vertebra, except for C0-C1, and the superior articular process of the inferior cervical vertebra join to form the facet joints of the cervical spine; in the case of C0-C1, the inferior articular process of C1 joins the occipital condyles. Also referred to as zygapophyseal joints (Fig. ?2), the facet joints are diarrthrodial, meaning they function similar to the knee joint in that they contain synovial cells and joint fluid and are surrounded by a capsule. They also contain a meniscus which helps to further cushion the joint, and like the knee, are lined by articular cartilage and surrounded by capsular ligaments, which stabilize the joint. These capsular ligaments hold adjacent vertebrae to one another, and the articular cartilage therein is aligned such that its opposing tissue surfaces provide for a low-friction environment [23].

 

Figure 2 Typical Z Joint

Figure 2: Typical Z (zygapophyseal/ facet) joint. Each facet joint has articular cartilage, the synovium where synovial fluid is produced, and a meniscus.

 

There is some dissimilarity in facet joint anatomy between the upper and lower cervical spine. Even in the upper cervical region, C0-C1 and C1-C2 facet joints differ anatomically. At C0-C1, the convex shape of the occipital condyles enables them to fit into the concave surface of the inferior articular process. The C1-C2 facet joints are oriented cranio-caudally, meaning they run more parallel to their transverse processes. As such, their capsular ligaments are normally relatively lax, and thus, are inherently less stable and meant to facilitate mobility (i.e., rotation) [23, 24].

 

In contrast, the facet joints of the lower cervical spine are positioned at more of an angle. In the transverse plane, the angles of the right and left C2-C3 facet joints are estimated to be 32� to 65� and 32� to 60�, respectively, while those of the C6-C7 facet joints are typically steeper at 45� to 75� and 50� to 78� [25]. As the cervical spine extends downward, the angle of the facet joint becomes bigger such that the joint slopes backwards and downwards. Thus, the facet joints of the lower cervical spine have progressively less rotation than those of the upper cervical spine. Furthermore, the presence of intervertebral discs helps give the lower cervical spine more stability.

 

Nevertheless, injury to any of the facet joints can cause instability to the cervical spine. Researchers have found there is a continuum between the amount of trauma and degree of instability to the cervical facets, with greater trauma causing a higher degree of facet instability [26-28].

 

Cervical Capsular Ligaments

 

The capsular ligaments are extremely strong and serve as the main stabilizing tissue in the spinal column. They lie close to the intervertebral centers of rotation and provide significant stability in the neck, especially during axial rotation [29]; consequently, they serve as essential components for ensuring neck stability with movement. The capsular ligaments have a high peak force and elongation potential, meaning they can withstand large forces before rupturing. This was demonstrated in a dynamic mechanical study in which the capsular ligaments and ligamentum flavum were shown to have the highest average peak force, up to 220 N and 244 N, respectively [30]. This was reported as considerably greater than the force shown in the anterior longitudinal ligament and middle third disc.

 

While much has been reported about the strength of the capsular ligaments as related to cervical stability, when damaged, these ligaments lose their strength and are unable to support the cervical spine properly. For instance, in an animal study, it was shown that sequential removal of sheep capsular ligaments and cervical facets caused an undue increase in range of motion, especially in axial rotation, flexion and extension with caudal progression [31]. Human cadaver studies have also indicated that transection or injury of joint capsular ligaments significantly increases axial rotation and lateral flexion [32, 33]. Specifically, the largest increase in axial rotation with damage to a unilateral facet joint was 294% [33].

 

Capsular ligament laxity can occur instantaneously as a single macrotrauma, such as a whiplash injury, or can develop slowly as cumulative microtraumas, such as those from repetitive forward or bent head postures. In either case, the cause of injury occurs through similar mechanisms, leading to capsular ligament laxity and excess motion of the facet joints, which often results in cervical instability. When ligament laxity develops over time, it is defined as �creep� (Fig. ?3) and refers to the elongation of a ligament under a constant or repetitive stress [34]. While this constitutes low-level subfailure ligament injuries, it may represent the vast majority of cervical instability cases and can potentially incapacitate people due to disabling pain, vertigo, tinnitus or other concomitant symptoms of cervical instability. Such symptoms can be caused by elongation-induced strains of the capsular ligaments; these strains can progress to subsequent subfailure tears in the ligament fibers or to laxity in the capsular ligaments, leading to instability at the level of the cervical facet joints [35]. This is most evident when the neck is rotated (ie, looking to the left or right) and that movement�causes a �cracking� or �popping� sound. Clinical instability indicates that the spine is unable to maintain normal motion and function between vertebrae under normal physiological loads, inducing irritation to nerves, possible structural deformation, and/or incapacitating pain.

 

Figure 3 Ligament Laxity and Creep

Figure 3: Ligament laxity and creep. When ligaments are under a constant stress, they display creep behavior. Creep refers to a time-dependent increase in strain and causes ligaments to “stretch out” over time.

 

Furthermore, the capsular ligaments surrounding the facet joints are highly innervated by mechanoreceptive and nociceptive free nerve endings. Hence, the facet joint has long been considered the primary source of chronic spinal pain [36-38]. Additionally, injury to these nerves has been shown to affect the overall joint function of the facet joints [39]. Therefore, injury to the capsular ligaments and subsequent nerve endings could explain the prevalence of chronic pain and joint instability in the facet joints of the cervical spine.

 

Cervical Instability

 

Clinical instability is not to be confused with hypermobility. In general, instability implies a pathological condition with resultant symptoms, whereas joint hypermobility alone does not (Fig. ?4). Clinical instability refers to a loss of motion stiffness in a particular spinal segment when the application of force to it produces greater displacement(s) than would otherwise be seen in a normal structure. In clinical instability, symptoms such as pain and muscle spasms can thus be experienced within a person�s range of motion, not just at its furthest extension point. These muscle spasms can cause intense pain and are the body�s response to cervical instability in that the ligaments act as sensory organs involved in ligamento-muscular reflexes. The ligamento-muscular reflex is a protective reflex emanating from mechanoreceptors (ie, pacinian corpuscles, golgi tendon organs, and ruffini endings) in the ligaments and transmitted to the muscles. Subsequent activation of these muscles helps to preserve joint stability, either directly by muscles crossing the joint or indirectly by muscles that do not cross the joint but limit joint motion [40].

 

Figure 4 Cervical Spinal Motion Continuum and Role of Prolotherapy

Figure 4: Cervical spinal motion continuum and role of prolotherapy. When minor or moderate spinal instability occurs, treatment with prolotherapy may be of benefit in alleviating symptoms and restoring normal cervical joint function.

 

In a clinically unstable joint where neurologic insult is present, it is presumed that the joint has undergone more severe damage in its stabilizing structures, which may include the vertebrae themselves. In contrast, joints that are hypermobile demonstrate increased segmental mobility but are able to maintain their stability and function normally under physiological loads [41].

 

Clinical instability can be classified as mild, moderate or severe, with the later being associated with catastrophic injury. Minor injuries of the cervical spine are those involving soft tissues alone without evidence of fracture and are the most common causes of cervical instability. Mild or moderate clinical instability is that which is without neurologic (somatic) injury and is typically due to cumulative micro-traumas.

 

Diagnosis of Cervical Instability

 

Cervical instability is a diagnosis based primarily on a patient�s history (ie, symptoms) and physical examination because there is yet to be standardized functional X-rays or imaging able to diagnose cervical instability or detect ruptured ligamentous tissue without the presence of bony lesions [24]. For example, in one autopsy study of cryosection samples of the cervical spine, [42] only one out of ten gross ligamentous disruptions was evident on x-ray. Furthermore, there is often little correlation between the degree of instability or hypermobility shown on radiographic studies and clinical symptoms [43-45]. Even after severe whiplash injuries, plain radiographs are usually normal despite clinical findings indicating the presence of soft tissue damage.

 

However, functional computerized tomography (fCT) and magnetic resonance imaging (fMRI) scans and digital motion x-ray (DMX) are able to adequately depict cervical instability pathology [46, 47]. Studies using fCT for diagnosing soft tissue ligament or post-whiplash injuries have demonstrated the ability of this technique to show excess atlanto-occipital or atlanto-axial movement during axial rotation [48, 49]. This is especially pertinent when patients have signs and symptoms of cervical instability, yet have normal MRIs in a neutral position.

 

Functional imaging technology, as opposed to static standard films, is necessary for adequate radiologic depiction of instability in the cervical spine because they provide dynamic imaging of the neck during movement and are helpful for evaluating the presence and degree of cervical instability (Fig. ?5). There are also specialized physical examination tests specific for upper cervical instability, such as the Sharp-Purser test, upper cervical flexion test, and cervical flexion-rotation test.

 

Figure 5 3D CT Scan of Upper Cervical Spine

Figure 5: 3D CT scan of upper cervical spine. C1-C2 instability can easily be seen in the patient, as 70% of C1 articular facet is subluxed posteriorly (arrow) on C2 facet when the patient rotates his head (turns head to the left then the right).

 

Upper Cervical Pathology and Instability

 

Although not usually apparent radiographically, injury to the ligaments and soft tissues of C0-C2 from head or neck trauma is more likely than are cervical fractures or subluxation of bones [50, 51]. Ligament laxity across the C0-C1-C2 complex is primarily caused by rotational movements, especially those involving lateral bending and axial rotation [52-54]. With severe neck traumas, especially those with rotation, up to 25% of total lesions can be attributed to ligament injuries of C0-C2 alone. Although some ligament injuries in the C0-C2 region can cause severe neurological impairment, the majority involve sub-failure loads to the facet joints and capsular ligaments, which are the primary source of most chronic pain in post-neck trauma [26, 55].

 

Due to its lack of osseous stability, the upper cervical spine is also vulnerable to injury by high velocity manipulation. The capsular ligaments of the atlanto-axial joint are especially susceptible to injury from rotational thrusts, and thus, may be at risk during mechanically mediated manipulation. The capsular ligaments in the occipto-atlantal joint function as joint stabilizers and can also become injured due to excessive or abnormal forces [46].

 

Excessive tension on the capsular ligaments can cause upper cervical instability and related neck pain [56]. Capsular ligament tension is increased during abnormal postures, causing elongation of the capsular ligaments, with magnitudes increased by up to 70% of normal [57]. Such excessive ligament elongation induces laxity to the facet joints, which puts the cervical spine more at risk for further degenerative changes and instability. Therefore, capsular ligament injury appears to cause upper cervical instability because of laxity in the stabilizing structure of the facet joints [58].

 

Cervical Pain Versus Cervical Radiculopathy

 

According to the International Association for the Study of Pain (IASP), cervical spinal pain is pain perceived as anywhere in the posterior region of the cervical spine, defining it further as pain that is �perceived as arising from anywhere within the region bounded superiorly by the superior nuchal line, inferiorly by an imaginary transverse line through the tip of the first thoracic spinous process, and laterally by sagittal planes tangential to the lateral borders of the neck� [59]. Similarly, cervical pain is divided equally by an imaginary transverse plane into upper cervical pain and lower cervical pain. Suboccipital pain is that pain located between superior nuchal line and an imaginary transverse line through the tip of the second cervical spinous process. Likewise, cervico-occipital pain is perceived as arising in the cervical region and extending over the occipital region of the skull. These sources of pain could be a result of underlying cervical instability.

 

The IASP defines radicular pain as that arising in a limb or the trunk wall, caused either by ectopic activation of nociceptive afferent fibers in a spinal nerve or its roots or by other neuropathic mechanisms, and may be episodic, recurrent, or sudden [59]. Clinically, there is a 30% rate of radicular symptoms during axial rotation in those with rotator instabilities [60]. Thus, radicular pain may also be a result of underlying cervical instability.

 

With capsular ligament laxity, hypertrophic facet joint changes occur (including osteophytosis) as cervical degeneration progresses, causing encroachment on cervical nerve roots as they exit the spine through the neural foramina. This condition is called cervical radiculopathy and manifests as stabbing pain, numbness, and/or tingling down the upper extremity in the area of the affected nerve root.

 

The neural foramina lie between the intervertebral disc and the joints of Luschka (uncovertebral joints) anteriorly and the facet joint posteriorly. Their superior and inferior borders are the pedicles of adjacent vertebral bodies. Cervical nerve roots there are vulnerable to compression or injury by the facet joints posteriorly or by the joints of Luschka and the intervertebral disc anteriorly.

 

Cadaver studies have demonstrated that cervical nerve roots take up as much as 72% of the space in the neural foramina [61]. Normally, this provides ample room for the nerves to function optimally. However, if the cervical spine and capsular ligaments are injured, facet joint hypertrophy and degeneration of the cervical discs can occur. Over time, this causes narrowing of the neural foramina (Fig. ?6) and a decrease in space for the nerve root. In the event of another ligament injury, instability of the hypertrophied bones can occur and further reduce the patency of the neural foramen.

 

Figure 6 Digital Motion X-Ray Demonstrating Multi-Level Cervical Instability

Figure 6: Digital motion X-ray demonstrating multi-level cervical instability. Neural foraminal narrowing is shown at two levels during lateral extension versus lateral flexion.

 

Cervical radiculopathy from a capsular ligament injury typically produces intermittent radicular symptoms which become more noticeable when the neck is moved in a certain direction, such as during rotation, flexion or extension. These movements can cause encroachment on cervical nerve roots and subsequent paresthesia along the pathway therein of the affected nerve and may be why evidence of cervical radiculopathy does not show up on standard MRI or CT scans.

 

When disc herniation is the cause of cervical radiculopathy, it typically presents with acute onset of severe neck and arm pain unrelieved by any position and often results in encroachment on a cervical nerve root. While disc herniation can easily be seen on routine (non-functional) MRI or CT scans, evidence of radiculopathy from cervical instability cannot. Most cases of acute radiculopathy due to disc herniation resolve with non-surgical active or passive therapies, but some patients continue to have clinically significant symptoms, in which case surgical treatments such as anterior cervical decompression with fusion or posterior cervical laminoforaminotomy can be performed [62]. Cervical radiculopathy is also strongly associated with spondylosis, a disease generally attributed to aging that involves an overall degeneration of the cervical spine. The disorder is characterized by degenerative changes in the intervertebral disc, osteophytosis of the vertebral bodies, and hypertrophy of the facet joints and laminar arches. Since more than one cervical spine segment is usually affected in spondylosis, the symptoms of radiculopathy are more diffuse than those typical of unilateral soft disc herniation and present as neck, mid-upper back, and arm pain with paresthesia.

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

“I was involved in an automobile accident that left me with chronic neck pain. What could be causing my painful and persistent neck pain symptoms?”�Being involved in an automobile accident can be a traumatic experience, resulting in both mental and physical harm. Whiplash-associated injuries are some of the most common diagnosis behind reported cases of chronic neck pain after an auto accident. During a car crash, the force of the impact can abruptly jerk the head back-and-forth, stretching the complex structures around the cervical spine beyond their natural range, causing damage or injury.The following article provides an overview of chronic neck pain, its mechanism of injury and effective treatment methods for neck pain.

 

Cervical Spondylosis: the Instability Connection

 

Spondylosis has previously been described as occurring in three stages: the dysfunctional stage, the unstable stage, and the stabilization stage (Fig. ?7) [63]. Spondylosis begins with repetitive trauma, such as rotational strains or compressive forces to the spine. This causes injury to the facet joints which can compromise the capsular ligaments. The dysfunctional phase is characterized by capsular ligament injuries and subsequent cartilage degeneration and synovitis, ultimately leading to abnormal motion in the cervical spine. Over time, facet joint dysfunction intensifies as capsular laxity occurs. This stretching response can cause cervical instability, marking the unstable stage. During this progression, ongoing degeneration is occurring in the intervertebral discs, along with other parts of the cervical spine. Ankylosis (stiffening of the joints) can also occur at the unstable cervical spine segment, and rarely, causes entrapment of nearby spinal nerves. The stabilization phase occurs with the formation of marginal osteophytes as the body tries to heal the spine. These bridging bony deposits can lead to a natural fusion of the affected vertebrae [64].

 

Figure 7 Cervical OA The 3 Phases of the Degenerative Cascade

Figure 7: Cervical OA: The 3 phases of the degenerative cascade. Used with permission from: Kramer WC, et al. Pathogenetic mechanisms of posttraumatic osteoarthritis: opportunities for early intervention. Int J Clin Exp Me d. 2011; 4(4): 285-298.

 

The degenerative cascade, however, begins long before symptoms become evident. Initially, spondylosis develops silently and is asymptomatic [65]. When symptoms of cervical spondylosis do develop, they are generally nonspecific and include neck pain and stiffness [66]. Only rarely do neurologic symptoms develop (ie, radiculopathy or myelopathy), and most often they occur in people with congenitally narrowed spinal canals [67]. Physical exam findings are often limited to restricted range of neck motion and poorly localized tenderness. Clinical symptoms commonly manifest when a new cervical ligament injury is superimposed on the underlying degeneration. In patients with spondylosis and underlying capsular ligament laxity, cervical radiculopathy is more likely to occur because the neural foramina may already be narrowed from facet joint hypertrophy and disc degeneration, enabling any new injury to more readily pinch on an exiting nerve root.

 

Thus, there are compelling reasons to believe that facet joint/capsular ligament injuries in the cervical spine may be an etiological basis for the degenerative cascade in cervical spondylosis and may be responsible for the attendant cervical instability. Animal models used for initiating disc degeneration in research studies have shown the induction of spinal instability through injury of the facet joints [68, 69]. In similar models, capsular ligament injuries of the facet joints caused multidirectional instability of the cervical spine, greatly increasing axial rotation motion correlating with cervical disc injuries [31, 28, 70, 71]. Using human specimens, surgical procedures such as discectomy have been shown to cause an immediate increase in motion of the segments involved [72]. Stabilization procedures such as neck fusion have been known to create increased pressure on the adjacent cervical spinal segments; this is referred to as adjacent segment disease. This can develop when the loss of motion from cervical fusion causes greater shearing and increased rotation and traction stress on adjacent vertebrae at the facet joints [73-75]. Thus, instability can �travel� up or down from the fused segment, furthering disc degeneration. These findings support the theory that iatrogenic-introduced stress and instability at adjacent spinal segments contribute to the pathogenesis of cervical spondylosis [74].

 

Whiplash Trauma

 

Damage to cervical ligaments from whiplash trauma has been well studied, yet these injuries are still often difficult to diagnose and treat. Standard x-rays often do not reveal present injury to the cervical spine and as a consequence, these injuries go unreported and patients are left without proper treatment for their condition [76]. Part of the difficulty lies in the fact that major injury to the cervical spine may only produce minor symptoms in some patients, whereas minor injury may produce more severe symptoms in others [77]. These symptoms include acute and/or chronic neck pain, headache, dizziness, vertigo and paresthesia in the upper extremities [78, 79].

 

MRI and autopsy studies have both shown an association between chronic symptoms in whiplash patients and injuries to the cervical discs, ligaments and facet joints [42, 80]. Success in relieving neck pain in whiplash patients has been documented by numerous clinical studies using nerve block and radiofrequency ablation of facet joint afferents, including capsular ligament nerves, such that increased interest has developed regarding the relationships between injury to the facet joints and capsular ligaments and post-whiplash dysfunction and related symptoms [36, 81].

 

Multiple studies have implicated the cervical facet joint and its capsule as a primary anatomical site of injury during whiplash exposure to the neck [55, 57, 82, 83]. Others have shown that injury to the cervical facet joints and capsular ligaments are the most common cause of pain in post-whiplash patients [84-86]. Cinephotographic and cineradiographic studies of both cadavers and human subjects show that under the conditions of whiplash, a resultant high impact force occurs in the cervical facet joints, leading to their injury and the possibility of cervical spine instability [84].

 

In whiplash trauma, up to 10 times more force is absorbed in the capsular ligaments versus the intervertebral disc [30]. Unlike the disc, the facet joint has a much smaller area in which to disperse this force. Ultimately, the capsular ligaments become elongated, resulting in abnormal motions in the spinal segments affected [30, 87]. This sequence has been documented with both in vitro and in vivo studies of segmental motion characteristics after torsional loads and resultant disc degeneration [88-90].

 

Injury to the facet joints and capsular ligaments has been further confirmed during simulated whiplash traumas [91]. Maximum capsular ligament strains occur during shear forces, such as when a force is applied while the head is rotated (axial rotation). While capsular ligament injury in the upper cervical spinal region can occur from compressive forces alone, exertion from a combination of shear, compression and bending forces is more likely and usually involves much lower loads to cause injury [92]. However, if the head is turned during whiplash trauma, the peak strain on the cervical facet joints and capsular ligaments can increase by 34% [93]. In one study reporting on an automobile rear-impact simulation, the magnitude of the joint capsule strain was 47% to 196% higher in instances when the head was rotated 60� during impact, compared with those when the head was forward facing [94]. The impact was greatest in the ipsilateral facet joints, such that head rotation to the left caused higher ligament strain at the left facet joint capsule.

 

In other simulations, whiplash trauma has been shown to reduce cervical ligament strength (ie, failure force and average energy absorption capacity) compared with controls or computational models [30, 87]; this is especially true in the case of capsular ligaments, since such trauma causes capsular ligament laxity. One study conclusively demonstrated that whiplash injury to the capsular ligaments resulted in an 85% to 275% increase in ligament elongation (ie, laxity) compared to that of controls [30]. The study also reported evidence that tension of the capsular ligaments is requisite for producing pain from the facet joint.

 

Post-Concussion Syndrome

 

Each year in the United States, approximately 1.7 million people are diagnosed with traumatic brain injury (TBI), although many more go undiagnosed because they do not seek out medical care [95]. Of these, approximately 75% – 90% are diagnosed as having a concussion. A concussion is considered a mild TBI and is defined as any transient neurologic dysfunction resulting from a biomechanical force, usually a sudden or forceful blow to the head which may or may not cause a loss of consciousness. Concussion induces a barrage of ionic, metabolic, and physiologic events [96] and manifests in a composite of symptoms affecting a patient�s physical, cognitive, and emotional states, and his or her sleep cycle, any one of which can be fleeting or long-term in duration [97]. The diagnosis of concussion is made by the presence of any one of the following: (1) any loss of consciousness; (2) any loss of memory for events immediately before or after the injury; (3) any alteration in mental status at the time of the accident; (4) focal neurological deficits that may or may not be transient [98].

 

While most individuals recover from a single concussion, up to one-third of those will continue to suffer from residual effects such as headache, neck pain, dizziness and memory problems one year after injury [99]. Such symptoms characterize a disorder known as post-concussion syndrome (PCS) and are much like those of WAD; both disorders are likely due to cervical instability. According to the International Classification of Diseases, 10th Revision (ICD-10), the diagnosis of PCS is made when a person has had a head injury sufficient enough to result in loss of consciousness and develops at least three of eight of the following symptoms within four weeks: headache, dizziness, fatigue, irritability, sleep problems, concentration difficulties, memory issues, and problems tolerating stress [100, 101]. Of those treated for PCS who had mild head injury, 80% report having chronic daily headaches; surprisingly, of those with moderate to severe head injury, only 27% reported having chronic daily headaches [102]. The impact of the brain on the skull is believed to be the cause of the symptoms of both concussion and PCS, although the specific mechanisms underlying neural tissue damage are still being investigated.

 

PCS-associated symptoms also overlap with many symptoms common to WAD. This overlap in symptomology may be due to a common etiology of underlying cervical instability that affects the cervical spine near the neck. Data has revealed that over half of patients with damage to the upper cervical spine from whiplash injury had evidence of concurrent head trauma [103]. It was shown that whiplash can cause minor brain injuries similar to that of concussion if it occurs with such rapid neck movement that there is a collision between the brain and skull. Thus, one may conjecture that concussion involves a whiplash-type injury to the neck.

 

Despite unique differences in the biomechanics of concussion and whiplash, both types of trauma involve an acceleration-deceleration of the head and neck. This impact to the head can not only cause injury to the brain and skull, but can also damage surrounding ligaments of the neck since these tissues undergo the same accelerating-decelerating force. The acceleration-deceleration forces which occur during whiplash injury are staggering. Direct head trauma has been shown to produce forces between 10,000 and 15,000 N on the head and between 1,000 and 1,500 N on the neck, depending on the angle at which the object hits the head [104, 105]. Cervical capsular ligaments can become lax with as little as 5 N of force, although most studies report cervical ligament failure at around 100 N [30, 55, 91, 106]. Even low speed rear impact collisions at as little as 7 mph to 8 mph can cause the head to move roughly 18 inches at a force as great as 7 G in less than a quarter of a second [107]. Numerous experimental studies have suggested that certain features of injury mechanisms including direction and degree of acceleration and deceleration, translation and rotation forces, position and posture of head and neck, and even seat construction may be linked to the extent of cervical spine damage and to the actual structures damaged [23, 27, 35, 50, 61].

 

Debate over the veracity of PCS or WAD symptomology has persisted; however, there is no single explanation for the etiology of these disorders, especially since the onset and duration of symptoms can vary greatly among individuals. Many of the symptoms of PCS and WAD tend to increase over time, especially when those affected are engaged in physical or cognitive activity. Chronic neck pain is often described as a long-term result of both concussion and whiplash, indicating that the most likely structures to become injured during these traumas are the capsular ligaments of the cervical facet joints. In light of this, we propose that the best scientific anatomical explanation is cervical instability in the upper cervical spine, resulting from ligament injury (laxity).

 

Vertebrobasilar Insufficiency

 

The occipito-atlanto-axial complex has a unique anatomical relationship with the vertebral arteries. In the lower cervical spine, the vertebral arteries lie in a relatively straight-forward course as they travel through the transverse foramina from C3-C6. However, in the upper cervical spine the arteries assume a more serpentine-like course. The vertebral artery emerges from the transverse process of C2 and sweeps laterally to pass through the transverse foramen of C1 (atlas). From there it passes around the posterior border of the lateral mass of C1, at which point it is farthest from the midline plane at the level of C1 [108, 109]. This pathway creates extra space which allows for normal head rotation without compromising vertebral artery blood flow.

 

Considering the position of the vertebral arteries in the canals of the transverse processes in the cervical vertebrae, it is possible to see how head positioning can alter vertebral arterial flow. Even normal physiological neck movements (ie, neck rotation) have been shown to cause partial occlusion of up to 20% or 30% in at least one vertebral artery [110]. Studies have shown that contralateral neck rotation is associated with vertebral artery blood flow changes, primarily between the atlas and axis; such changes can also occur when osteophytes are present in the cervical spine [111, 112].

 

Proper blood flow in the vertebral arteries is crucial because these arteries travel up to form the basilar artery at the brainstem and provide circulation to the posterior half of the brain. When this blood supply is insufficient, vertebrobasilar insufficiency (VBI) can develop and cause symptoms, such as neck pain, headaches/migraines, dizziness, drop attacks, vertigo, difficulty swallowing and/or speaking, and auditory and visual disturbances. VBI usually occurs in the presence of atherosclerosis or cervical spondylosis, but symptoms can also arise when there is intermittent vertebral artery occlusion induced by extreme rotation or extension of the head [113, 114]. This mechanical compression of the vertebral arteries can occur along with other anomalies, including cervical osteophytes, fibrous bands, and osseous prominences [115, 116] These anomalies were seen in about half of the cases of vertebral artery injury after cervical manipulation, as reported in a recent review [117].

 

Whiplash injury itself has been shown to reduce vertebral artery blood flow and elicit symptoms of VBI [118, 119]. In one study, the authors concluded that patients with persistent vertigo or dizziness after whiplash injury are likely to have VBI if the injury was traumatic enough to cause a circulation disorder in the vertebrobasilar arterial system [118]. Other researchers have surmised that excessive cervical instability, especially of the upper cervical spine, can cause obstruction of the vertebral artery during neck rotation, thus compromising blood flow and triggering symptoms [120-122].

 

Barr�-Li�ou Syndrome

 

A lesser known, yet relatively common, cause of neck pain is Barr�-Li�ou syndrome. In 1925, Jean Alexandre Barr�, and in 1928, Yong Choen Li�ou, each independently described a syndrome presenting with headache, orbital pressure/pain, vertigo, and vasomotor disturbances and proposed that these symptoms were related to alterations in the posterior cervical sympathetic chain and vertebral artery blood flow in patients who had cervical spine arthritis or other arthritic disorders [123, 124]. Barr�-Li�ou syndrome is also referred to as posterior cervical syndrome or posterior cervical sympathetic syndrome because the condition is now presumed to develop more from disruption of the posterior cervical sympathetic nervous system, which consists of the vertebral nerve and the sympathetic nerve network surrounding it. Symptoms include neck pain, headaches, dizziness, vertigo, visual and auditory disturbances, memory and cognitive impairment, and migraines. It has been surmised that cervical arthritis or injury provokes an irritation of both the vertebral and sympathetic nerves. As a result, current treatment now centers on resolution of cervical instability and its effects on the posterior sympathetic nerves [124]. Other research has found an association between the sympathetic symptoms of Barr�-Li�ou and cervical instability and has documented successful outcomes in case reports when the instability was addressed by various means including prolotherapy [125].

 

Symptoms of Barr�-Li�ou syndrome also appear to develop after trauma. In one study, 87% of patients with a diagnosis of Barr�-Li�ou syndrome reported that they began experiencing symptoms after suffering a cervical injury, primarily in the mid-cervical region [126]; in a related study, this same region was found to exhibit more instability than other spinal segments [127] The various symptoms that characterize Barr�-Li�ou syndrome can also mimic symptoms of PCS or WAD, [128] which can pose a challenge for practitioners in making a definitive diagnosis (Fig. ?8). The diagnosis of Barr�-Li�ou syndrome is made on clinical grounds, as there is yet to be a definitive test to document irritation of the sympathetic nervous system.

 

Figure 8 Overlap in Chronic Symptomology

Figure 8: Overlap in chronic symptomology between atlanto-axial instability, whiplash associated disorder, post-concussion syndrome, vertebrobasilar insufficiency, and Barr�-Li�ou syndrome. There is considerable overlap in symptoms amongst these conditions, possibly because they all appear to be due to cervical instability.

 

Other Sources of Cervical Pain

 

Various tensile forces place strains with differing deformations on a variety of viscoelastic spinal structures, including the ligaments, the annulus and nucleus of the intervertebral disc, and the spinal cord. Further to this, cadaver experiments have shown that the spinal cord and the intervertebral disc components carry considerably lower tensile forces than the spinal ligament column [129, 130]. Encapsulated mechanoreceptors and free nerve endings have been identified in the periarticular tissues of all major joints of the body including those in the spine, and in every articular tissue except cartilage [131]. Any innervated structure that has been injured by trauma is a potential chronic pain generator; this includes the intervertebral discs, facet joints, spinal muscles, tendons and ligaments [132-134].

 

The posterior ligamentous structures of the human spine are innervated by four types of nerve endings: pacinian corpuscles, golgi tendon organs, and ruffini and free nerve endings [40]. These receptors monitor joint excursion and capsular tension, and may initiate protective muscular reflexes that prevent joint degeneration and instability, especially when ligaments, such as the anterior and posterior longitudinal, ligamentum flavum, capsular, interspinous and supraspinous, are under too much tension [131, 135]. Collectively, the cervical region of the spinal column is at risk to sustain deformations at all levels and in all components, and when the threshold crosses a particular level at a particular component, injury is imminent owing to the relative increased flexibility or joint laxity.

 

Other Sources of Trauma

 

As described earlier, the nucleus pulposus is designed to sustain compression loads and the annulus fibrosus that surrounds it, to resist tension, shear and torsion. The stress in the annulus fibers is approximately 4-5 times the applied stress in the nucleus [136, 137]. In addition, annulus fibers elongate by up to 9% during torsional loading, but this is still well below the ultimate elongation at failure of over 25% [138]. Pressure within the nucleus is approximately 1.5 times the externally applied load per unit of disc area. As such, the nucleus is relatively incompressible, which causes the intervertebral disc to be susceptible to injury in that it bulges under loads – approximately 1 mm per physiological load [139]. As the disc degenerates on bulging (herniates), it looses elasticity, further compromising its ability to compress. Shock absorption is no longer spread or absorbed evenly by the surrounding annulus, leading to greater shearing, rotation, and traction stress on the disc and adjacent vertebrae. The severity of disc herniation can range from protrusion and bulging of the disc without rupture of the annulus fibrosus to disc extrusion, in which case, the annulus is perforated, leading to tearing of the structure.

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

“What type of treatment methods can provide effective relief from my chronic neck pain symptoms?”�The symptoms of chronic neck pain can be debilitating and can ultimately affect any individual’s ability to carry on with their everyday activities. While neck pain is a common symptom in a variety of injuries and/or conditions affecting the cervical spine, there are also a number of treatment methods available to help improve neck pain. However, some treatments also address stabilizing the cervical spine as well as healing damaged or injured tissues. Chiropractic care is a well-known alternative treatment option which has been demonstrated to help cure symptoms of neck pain at the source, according to several research studies.

 

Treatment Options

 

There are a number of treatment modalities for the management of chronic neck pain and cervical instability, including injection therapy, nerve blocks, mobilization, manipulation, alternative medicine, behavioral therapy, fusion, and pharmacologic agents such as NSAIDS and opiates. However, these treatments do not address stabilizing the cervical spine or healing ligament injuries, and thus, do not offer long-term curative options. In fact, cortisone injections are known to inhibit, rather than promote healing. As mentioned earlier in this paper, most treatments have shown limited evidence in their efficacy or are inconsistent in their results. In a systematic review of the literature from January 2000 to July 2012 on physical modalities for acute to chronic neck pain, acupuncture, laser therapy, and intermittent traction were found to provide moderate benefits [5].

 

The literature contains many reports on injection therapy for the treatment of chronic neck pain. Cervical interlaminar epidural injections with or without steroids may provide significant improvement in pain and function for patients with cervical disc herniation and radiculitis [140]. As a follow-up to its one-year results, a randomized, double-blind controlled trial found that the clinical effectiveness of therapeutic cervical medial branch blocks with or without steroids in managing chronic neck pain of facet joint origin provided significant improvement over a period of 2 years [141].

 

However, many other studies have had more nebulous results. In a systematic review of therapeutic cervical facet joint interventions, the evidence for both cervical radiofrequency neurotomy and cervical medial branch blocks is fair, and for cervical intra-articular injections with local anesthetic and steroids, the evidence is limited [142]. In a later corresponding systematic review, the same group of authors concluded that the strength of evidence for diagnostic facet joint nerve blocks is good (?75% pain relief), but stated the evidence is limited for dual blocks (50% to 74% pain relief), as well as for single blocks (50% to 74% pain relief) and (?75% pain relief.) [6]. In another systematic review evaluating cervical interlaminar epidural injections, the evidence indicated that the injection therapy showed significant effects in relieving chronic intractable pain of cervical origin; specific to long-term relief the indicated level of evidence was Level II-1 [143].

 

In the case of manipulative therapy, the results of a randomized trial disputed the hypothesis that supervised home exercises, combined or not with manual therapy, can be of benefit in treating non-specific chronic neck pain, as compared to no treatment [7]. The study found that there were no differences in primary or secondary outcomes among the three groups and that no significant change in health-related quality of life was associated with the preventive phase. Participants in the combined intervention group did not have less pain or disability and fared no better functionally than participants from the two other groups during the preventive phase of the trial. Another randomized clinical trial comparing the effects of applying joint mobilization at symptomatic and asymptomatic cervical levels in patients with chronic nonspecific neck pain was inconclusive in that there was no significant difference in pain intensity immediately after treatment between groups during resting position, painful active movement, or vertebral palpation [8]. Massage therapy had similar inconclusive results. Evidence was reported as �not strong� [144] in one randomized trial comparing groups receiving massage treatment for neck pain versus those reading a self-care book, while another found that cupping massage was no more effective than progressive muscle relaxation in reducing chronic non-specific neck pain [9]. Acupuncture appears to have better results in relieving neck pain but leaves questions as to the effects on the autonomic nervous system, suggesting that acupuncture points per se have different physical effects according to location [145].

 

Cervical disc herniation is a major source of chronic neck and spinal pain and is generally treated by either surgery or epidural injections, but their effectiveness continues to be debatable. In a randomized, double-blind, controlled clinical trial assigning patients to treatment with epidural injections with lidocaine or lidocaine mixed with betamethasone, 72% of patients in the local anesthetic group and 68% of patients in the local anesthetic with steroid group had at least a 50% improvement in pain and disability at 2 years, indicating that either protocol may be beneficial in alleviating chronic pain from cervical disc herniation [146].

 

In a systematic review of pharmacological interventions for neck pain, Peloso, et al. [147] reported that, aside from evidence in one study of a small immediate benefit for the psychotropic agent eperison hydrochloride (a muscle relaxant), most studies had low to very low quality methodologic evidence. Furthermore, they found evidence against a long-term benefit for medial branch block of facet joints with steroids and against a short-term benefit for botulinum toxin-A compared to saline, concluding that there is a lack of evidence for most pharmacological interventions.

 

Collectively, these interventions for the treatment of chronic neck pain may each offer temporary relief, but many fall short of a cure. Aside from these conventional treatment options, there are pain medications and pain patches, but their use is controversial because they offer little restorative value and often lead to dependence. If joint instability is the fundamental problem causing chronic neck pain and its associated autonomic symptoms, prolotherapy may be a treatment approach that meets this challenge.

 

Prolotherapy for Cervical Instability

 

To date, there is no consensus on the diagnosis of cervical spine instability or on traditional treatments that relieve chronic neck pain. In such cases, patients often seek out alternative treatments for pain and symptom relief. Prolotherapy is one such treatment which is intended for acute and chronic musculoskeletal injuries, including those causing chronic neck pain related to underlying joint instability and ligament laxity (Fig. ?9).

 

Figure 9 Stress-Strain Curve for Ligaments and Tendons

Figure 9: Stress-strain curve for ligaments and tendons. Ligaments can withstand forces and revert back to their original position up to Point C. At this point, prolotherapy treatment may succeed in tightening the tissue. Once the force continues past Point C. the ligament becomes permanently elongated or stressed.

 

Chronic neck pain and cervical instability are particularly difficult to treat when capsular ligament laxity is the cause because ligament cartilage is notoriously slow in healing due to a lack of blood supply. Most treatment options do not address this specific problem, and therefore, have limited success in providing a long-term cure.

 

Whiplash is a prime example because it often results in ligament laxity. In a five-part series evaluating the strength of evidence supporting WAD therapies, Teasell, et al. [10, 148-151] report that there is insufficient evidence to support any treatment for subacute WAD, stating that radiofrequency neurotomy may be the most effective treatment for chronic WAD. Furthermore, they state that immobilization with a soft collar is ineffective to the point of impeding recovery, saying that activation-based therapy is recommended instead, a conclusion similar to that of Hauser et al. [40] For chronic WAD, exercise programs were the most effective noninvasive treatment and radiofrequency neurotomy, the most effective of surgical or injection-based interventions, although evidence was not strong enough to establish the efficacy of any one treatment [10].

 

Prolotherapy is referred to as a regenerative injection technique (RIT) because it is based on the premise that the regenerative/reparative healing process consists of three overlapping phases: inflammatory, proliferative with granulation, and remodeling with contraction (Fig. ?10) [152]. The prolotherapy technique involves injecting an irritating solution (usually a dextrose/sugar solution) at painful ligament and tendon attachment sites to produce a mild inflammatory response. Such a response initiates a healing cascade that duplicates the natural healing process of poorly vascularized tissue (ligaments, tendons, and cartilage) [40, 153]. In doing so, tensile strength, elasticity, mass and load-bearing capacity of collagenous connective tissues become increased [152]. This occurs because the increased glucose concentration causes increases in cell protein synthesis, DNA synthesis, cell volume, and proliferation, all of which stimulate ligament size and mass and ligament-bone junction strength, as well as the production of growth factors, which are essential for ligament repair and growth [154].

 

Figure 10 The Biology of Prolotherapy

Figure 10: The biology of prolotherapy.

 

While the most studied type of prolotherapy is the Hackett-Hemwall procedure which uses dextrose as the proliferant, there are multiple other choices that are suitable, such as polidocanol, manganese, human growth hormone, and zinc. In addition to the Hackett-Hemwall procedure, there is another procedure called cellular prolotherapy, which involves the use of a patient�s own cells from blood, bone marrow, or adipose tissue as the proliferant to generate healing.

 

It is important to note that prolotherapy not only involves the treatment of joints, but also the associated tendon and ligament attachments surrounding them; hence, it is a comprehensive and highly effective means of wound healing and pain resolution. The Hackett-Hemwall prolotherapy technique was developed in the 1950s and is being transitioned into mainstream medicine due to an increasing number of studies reporting positive outcomes [155-158].

 

Prolotherapy has a long history of being used for whiplash-type soft tissue injuries of the neck. In separate studies, Hackett and his colleagues early on had remarkably successful outcomes in treating ligament injuries; more than 85% of patients with cervical ligament injury-related symptoms, including those with headache or WAD, reported they had minor to no residual pain or related symptoms after prolotherapy [125, 159, 160]. Similar favorable outcomes for resolving neck pain were reported recently by Hauser, et al. [161]. Hooper, et al. also reported on a case series [162] in which patients with whiplash received intra-articular injections (prolotherapy) into each zygapophysial (facet)

 

joint and attained consistently improved scores in the Neck Disability Index (NDI) at 2, 6 and 12 months post treatment; average change in Neck Disability Index (NDI) was significant (13.77; p < 0.001) at baseline versus 12 months. Specific to cervical instability, Centeno, et al. [163] performed fluoro-scopically guided prolotherapy and reported that stabilization of the cervical spine with prolotherapy correlated with symptom relief, as depicted in blinded pre and post radiographic readings. Prolotherapy has also been found effective for other ligament injuries, including the lower back, [164-166] knee, [167-169] and other peripheral joints, [170-172] as well as congenital systemic ligament laxity conditions [173].

 

Evidence that prolotherapy induces the repair of ligaments and other soft tissue structures has been reported in both animal and human studies. Animal research conducted by Hackett [174] demonstrated that proliferation and strengthening of tendons occurred, while Liu and associates [175] found that prolotherapy injections to rabbit ligaments increased ligamentous mass (44%), thickness (27%), as well as ligament-bone junction strength (28%) over a six-week period. In a study on human subjects, Klein et al. [176] used electron microscopy and found an average increase in ligament diameter from 0.055 �m to 0.087 �m after prolotherapy, as shown in biopsies of posterior sacroi-liac ligaments. They also found a linear ligament orientation similar to what is found in normal ligaments. In a case study, Auburn, et al. [177] documented a 27% increase in iliolum-bar ligament size after prolotherapy, via ultrasound.

 

Studies have also been published on the use of prolotherapy for resolving chronic pain, [152, 178, 179] as well as for conditions specifically related to joint instability in the cervical spine [163, 180] In our own pain clinic, we have used prolotherapy successfully on patients who had chronic pain in the shoulder, elbow, low back, hip, and knee [181-186].

 

Conclusion

 

The capsular ligaments are the main stabilizing structures of the facet joints in the cervical spine and have been implicated as a major source of chronic neck pain. Such pain often reflects a state of instability in the cervical spine and is a symptom common to a number of conditions such as disc herniation, cervical spondylosis, whiplash injury and whiplash associated disorder, postconcussion syndrome, vertebrobasilar insufficiency, and Barr�-Li�ou syndrome.

 

When the capsular ligaments are injured, they become elongated and exhibit laxity, which causes excessive movement of the cervical vertebrae. In the upper cervical spine (C0-C2), this can cause symptoms such as nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches. In the lower cervical spine (C3-C7), this can cause muscle spasms, crepitation, and/or paresthesia in addition to chronic neck pain. In either case, the presence of excessive motion between two adjacent cervical vertebrae and these associated symptoms is described as cervical instability.

 

Therefore, we propose that in many cases of chronic neck pain, the cause may be underlying joint instability due to capsular ligament laxity. Furthermore, we contend that the use of comprehensive Hackett-Hemwall prolotherapy appears to be an effective treatment for chronic neck pain and cervical instability, especially when due to ligament laxity. The technique is safe and relatively non-invasive as well as efficacious in relieving chronic neck pain and its associated symptoms. Additional randomized clinical trials and more research into its use will be needed to verify its potential to reverse ligament laxity and correct the attendant cervical instability.

 

Dr. Jimenez works on patient's back

 

Acknowledgements

 

Declared none.

 

Conflict of Interest

 

Ms. Woldin and Ms. Sawyer have nothing to declare. Dr. Hauser and Ms. Steilen declare that they perform prolotherapy at Caring Medical Rehabilitation Services.

 

Dr Jimenez White Coat

Dr. Alex Jimenez’s Insight

“I was diagnosed with a whiplash-associated disorder after reporting chronic neck pain symptoms following an automobile accident. What form of care can help me manage the persistent symptoms?”�In order to manage chronic neck pain symptoms, not only is it essential for you to seek immediate medical attention from the proper healthcare professional, its also important to understand the mechanism of injury behind your persistent symptoms. Tendons, ligaments and other structures surrounding the cervical spine, such as the facet joints, can become damaged or injured during an auto accident and their care must be consistent to achieve overall recovery. Many healthcare professionals can provide patients with individualized guidelines on the management of their whiplash-associated disorders and chronic neck pain.

 

Facet Joint Kinematics and Injury Mechanisms During Simulated Whiplash

 

Abstract

 

Study Design: Facet joint kinematics and capsular ligament strains were evaluated during simulated whiplash of whole cervical spine specimens with muscle force replication.

 

Objectives: To describe facet joint kinematics, including facet joint compression and facet joint sliding, and quantify peak capsular ligament strain during simulated whiplash.

 

Summary of Background Data: Clinical studies have implicated the facet joint as a source of chronic neck pain in whiplash patients. Prior in vivo and in vitro biomechanical studies have evaluated facet joint compression and excessive capsular ligament strain as potential injury mechanisms. No study has comprehensively evaluated facet joint compression, facet joint sliding, and capsular ligament strain at all cervical levels during multiple whiplash simulation accelerations.

 

Methods: The whole cervical spine specimens with muscle force replication model and a bench-top trauma sled were used in an incremental trauma protocol to simulate whiplash of increasing severity. Peak facet joint compression (displacement of the upper facet surface towards the lower facet surface), facet joint sliding (displacement of the upper facet surface along the lower facet surface), and capsular ligament strains were calculated and compared to the physiologic limits determined during intact flexibility testing.

 

Results: Peak facet joint compression was greatest at C4-C5, reaching a maximum of 2.6 mm during the 5 g simulation. Increases over physiologic limits (P < 0.05) were initially observed during the 3.5 g simulation. In general, peak facet joint sliding and capsular ligament strains were largest in the lower cervical spine and increased with impact acceleration. Capsular ligament strain reached a maximum of 39.9% at C6-C7 during the 8 g simulation.

 

Conclusions: Facet joint components may be at risk for injury due to facet joint compression during rear-impact accelerations of 3.5 g and above. Capsular ligaments are at risk for injury at higher accelerations.

 

The Treatment of Neck Pain-Associated Disorders and Whiplash-Associated Disorders: A Clinical Practice Guideline

 

Abstract

 

Objective: The objective was to develop a clinical practice guideline on the management of neck pain-associated disorders (NADs) and whiplash-associated disorders (WADs). This guideline replaces 2 prior chiropractic guidelines on NADs and WADs.

 

Methods: Pertinent systematic reviews on 6 topic areas (education, multimodal care, exercise, work disability, manual therapy, passive modalities) were assessed using A Measurement Tool to Assess Systematic Reviews (AMSTAR) and data extracted from admissible randomized controlled trials. We incorporated risk of bias scores in the Grading of Recommendations Assessment, Development, and Evaluation. Evidence profiles were used to summarize judgments of the evidence quality, detail relative and absolute effects, and link recommendations to the supporting evidence. The guideline panel considered the balance of desirable and undesirable consequences. Consensus was achieved using a modified Delphi. The guideline was peer reviewed by a 10-member multidisciplinary (medical and chiropractic) external committee.

 

Results: For recent-onset (0-3 months) neck pain, we suggest offering multimodal care; manipulation or mobilization; range-of-motion home exercise, or multimodal manual therapy (for grades I-II NAD); supervised graded strengthening exercise (grade III NAD); and multimodal care (grade III WAD). For persistent (>3 months) neck pain, we suggest offering multimodal care or stress self-management; manipulation with soft tissue therapy; high-dose massage; supervised group exercise; supervised yoga; supervised strengthening exercises or home exercises (grades I-II NAD); multimodal care or practitioner’s advice (grades I-III NAD); and supervised exercise with advice or advice alone (grades I-II WAD). For workers with persistent neck and shoulder pain, evidence supports mixed supervised and unsupervised high-intensity strength training or advice alone (grades I-III NAD).

 

Conclusions:�A multimodal approach including manual therapy, self-management advice, and exercise is an effective treatment strategy for both recent-onset and persistent neck pain.

 

Copyright � 2016. Published by Elsevier Inc.

 

Keywords: Chiropractic; Disease Management; Musculoskeletal Disorders; Neck Pain; Practice Guideline; Therapeutic Intervention; Whiplash Injuries

 

In conclusion, chronic neck pain, particularly that resulting from whiplash-associated disorders, can be treated using treatment methods which focus on the rehabilitation of the complex structures surrounding the cervical spine. Furthermore, by understanding chronic neck pain as it relates to cervical instability as well as its impact on capsular ligament laxity, patients can seek the proper treatment for their type of chronic neck pain, including whiplash. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Neck Pain

 

Neck pain is a common complaint which can result due to a variety of injuries and/or conditions. According to statistics, automobile accident injuries and whiplash injuries are some of the most prevalent causes for neck pain among the general population. During an auto accident, the sudden impact from the incident can cause the head and neck to jolt abruptly back-and-forth in any direction, damaging the complex structures surrounding the cervical spine. Trauma to the tendons and ligaments, as well as that of other tissues in the neck, can cause neck pain and radiating symptoms throughout the human body.

 

blog picture of cartoon paperboy big news

 

IMPORTANT TOPIC: EXTRA EXTRA: A Healthier You!

 

 

Blank
References
1. Childs J, Cleland J, Elliott J , et al. Neck pain clinical practice guidelines linked to the international classification of functioning, disability, and health from the orthopaedic section of the American Physical Therapy Association. J Orthop Sports Phys Ther. 2008;38(9): A1�34. [PubMed]
2. C�t� P, Cassidy JD, Carroll LJ, Kristman V. The annual incidence and course of neck pain in the general population a population based cohort study. Pain. 2004;112(3): 267�73. [PubMed]
3. Hogg-Johnson S, van der Velde G, Carroll LJ , et al. The burden and determinants of neck pain in the general population. Eur Spine J. 2008;17(Suppl 1 ): 39�51.
4. Childs JD, Fritz JM, Flynn TW , et al. A clinical prediction rule to identify patients with low back pain most likely to benefit from spinal manipulation a validation study. Ann Intern Med. 2004;141(12): 920�8. [PubMed]
5. Graham N, Gross AR, Carlesso LC , et al. ICON. An ICON overview on physical modalities for neck pain and associated disorders. Open Orthop J. 2013;7(Suppl 4 ): 440�60. [PMC free article] [PubMed]
6. Onyewu O, Manchikanti L, Falco FJE , et al. An update of the appraisal of the accuracy and utility of cervical discography in chronic neck pain. Pain Physician. 2012;15: E777�806. [PubMed]
7. Martel J, Dugas C, Dubois JD, Descarreaux M. A randomised controlled trial of preventive spinal manipulation with and without a home exercise program for patients with chronic neck pain. BMC Musculoskelet Disord. 2011;12: 41. [PMC free article] [PubMed]
8. Aquino RL, Caires PM, Furtado FC, Loureiro AV, Ferreira PH, Ferreira ML. Applying joint mobilization at different cervical vertebral levels does not influence immediate pain reduction in patients with chronic neck pain a randomized clinical trial. J Manual Manipulative Ther. 2009;17(2): 95�100. [PMC free article] [PubMed]
9. Lauche R, Materdey S, Cramer H , et al. Effectiveness of home-based cupping massage compared to progressive muscle relaxation in patients with chronic neck pain-a randomized controlled trial. PLoS ONE. 2013;8(6): e65378. [PMC free article] [PubMed]
10. Teasell RW, McClure JA, Walton D , et al. A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): part 1 – overview and summary. Pain Res Manage. 2010;15(5): 287�94. [PMC free article] [PubMed]
11. Murphy DR, Hurwitz EL. Application of a diagnosis-based clinical decision guide in patients with neck pain. Chiropr Manual Ther. 2011;19: 19. [PMC free article] [PubMed]
12. Suzuki F, Fukami T, Tsuji A, Takagi K, Matsuda M. Discrepancies of MRI findings between recumbent and upright positions in atlantoaxial lesion. Report of two cases. Eur Spine J. 2008;17(Suppl 2 ): S304�7. [PMC free article] [PubMed]
13. R�ijezon U, Djupsj�backa M, Bj�rklund M, H�ger-Ross C, Grip H, Liebermann DG. Kinematics of fast cervical rotations in persons with chronic neck pain a cross-sectional and reliability study. BMC Musculoskelet Disord. 2010;11: 22. [PMC free article] [PubMed]
14. Gelalis ID, Christoforou G, Arnaoutoglou CM, Politis AN, Manoudis G, Xenakis TA. Misdiagnosed bilateral C5-C6 dislocation causing cervical spine instability a case report. Cases J. 2009;2: 6149. [PMC free article] [PubMed]
15. Taylor M, Hipp JA, Gertzbein SD, Gopinath S, Reitman CA. Observer agreement in assessing flexion-extension X-rays of the cervical spine, with and without the use of quantitative measurements of intervertebral motion. Spine J. 2007;7(6): 654�8. [PMC free article] [PubMed]
16. Windsor RE. Cervical spine anatomy. http: //emedicine.medscape. com/article/1948797-overview#a30 [Accessed April 14. 2014.
17. Driscoll DR. Anatomical and biomechanical characteristics of upper cervical ligamentous structures a review. J Manipulative and Physiol Ther. 1987;10(3): 107�10. [PubMed]
18. Cusick JF, Yoganandan N. Biomechanics of the cervical spine part 4: major injuries. Clin Biomech. 2002;17(1): 1�20. [PubMed]
19. Nachemson A. The influence of spinal movements of the lumbar intradiscal pressure on the tensile stresses in the annulus fibrosus. Acta Orthop Scan. 1963;33: 183�207. [PubMed]
20. Zak M, Pezowicz C. Spinal sections and regional variations in the mechanical properties of the annulus fibrosus subjected to tensile loading. Acta Bioeng Biomech. 2013;15(1): 51�9. [PubMed]
21. Mercer S, Bogduk N. The ligaments and annulus fibrosus of human adult cervical intervertebral discs. Spine (Phila Pa 1976). 1999;24(7): 619�28. [PubMed]
22. Kuri J, Stapleton E. The spine at trial practical medicolegal concepts about the spine. http: //books.google.com/books?id=Gi6w jdftC7cC&pg=PA12&lpg=PA12&dq=cervical+spine+transverse+processes&source=bl&ots=tboGEQAnuB&sig=Vi4bIDA24bLxGWWEivgAmmlETFo&hl=en&sa=X&ei=YETZUteXHMTAyAGNkICIBQ&ved=0CDYQ6AEwAjgK#v=onepage&q=cervical%20spine%20transverse%20processes&f=false [Accessed April 14. 2014.
23. Jaumard N, Welch WC, Winkelstein BA. Spinal facet joint biomechanics and mechanotransduction in normal, injury, and degenerative conditions. J Biomech Eng. 2011;133(7): 071010. [PMC free article] [PubMed]
24. Volle E. Functional magnetic resonance imaging video diagnosis of soft-tissue trauma to the craniocervical joints and ligaments. Int Tinnitus J. 2000;6(2): 134�9. [PubMed]
25. Pal GP, Routal RV, Saggu KG. The orientation of the articular facets of the zygapophyseal joints at the cervical and upper thoracic region. J Anat. 2001;198(Pt 4): 431�41. [PMC free article] [PubMed]
26. Quinn KP, Lee KE, Ahaghotu CC, Winkelstein BA. Structural changes in the cervical facet capsular ligament potential contributions to pain following subfailure loading. Stapp Car Crash J. 2007;51: 169�87. [PubMed]
27. Panjabi MM, Bibu K, Cholewicki J. Whiplash injuries and the potential for mechanical instability. Eur Spine J. 1998;7: 484�92. [PMC free article] [PubMed]
28. Zdeblick TA, Abitbol JJ, Kunz DN, McCabe RP, Garfin S. Cervical stability after sequential capsule resection. Spine (Phila Pa 1976). 1993;18: 2005�8. [PubMed]
29. Rasoulinejad P, McLachlin SD, Bailey SI, Gurr KR, Bailey CS, Dunning CE. The importance of the posterior osteoligamentous complex to subaxial cervical spine stability in relation to a unilateral facet injury. Spine J. 2012;12(7): 590�5. [PubMed]
30. Ivancic PC, Coe MP, Ndu AB , et al. Dynamic mechanical properties of intact human cervical spine ligaments. Spine J. 2007;7(6): 659�65. [PMC free article] [PubMed]
31. DeVries NA, Gandhi AA, Fredericks DC, Grosland NM, Smucker JD. Biomechanical analysis of the intact and destabilized sheep cervical spine. Spine (Phila Pa 1976). 2012;37(16): E957�63. [PubMed]
32. Crisco JJ, 3rd, Oda T, Panjabi MM, Bueff HU, Dvor�k J, Grob D. Transections of the C1-C2 joint capsular ligaments in the cadaveric spine. Spine (Phila Pa 1976). 1991;16: S474�9. [PubMed]
33. Nadeau M, McLachlin SD, Bailey SI, Gurr KR, Dunning CE, Bailey CS. A biomechanical assessment of soft-tissue damage in the cervical spine following a unilateral facet injury. J Bone Joint Surg. 2012;94(21): e156. [PubMed]
34. Frank CB. Ligament structure, physiology, and function. J Musculoskelet Neuronal Interact. 2004;4(2): 199�201. [PubMed]
35. Chen HB, Yang KH, Wang ZG. Biomechanics of whiplash injury. Chin J Traumatol. 2009;12(5): 305�14. [PubMed]
36. Boswell MV, Colson JD, Sehgal N, Dunbar EE, Epter R. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain Physician. 2007;10(1): 229�53. [PubMed]
37. Aprill C, Bogduk N. The prevalence of cervical zygapophyseal joint pain a first approximation. Spine (Phila Pa 1976). 1992;17: 744�7. [PubMed]
38. Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of cervical zygapophaseal joint pain after whiplash. Spine (Phila Pa 1976). 1995;20: 20�5. [PubMed]
39. McLain RF. Mechanoreceptor endings in human cervical facet joints. Iowa Orthop J. 1993;13: 149�54. [PMC free article] [PubMed]
40. Hauser RA, Dolan EE, Phillips HJ, Newlin AC, Moore RE Woldin BA. Ligament injury and healing a review of current clinical diagnostics and therapeutics. Open Rehabil J. 2013;6: 1�20.
41. Bergmann TF, Peterson DH. Chiropractic technique principles and procedures, 3rd ed. New York Mobby Inc. 1993
42. J�nsson H , Jr, Bring G, Rauschning W, Sahlstedt B. Hidden cervical spine injuries in traffic accident victims with skull fractures. J Spinal Disord. 1991;4(3): 251�63. [PubMed]
43. van Mameren H, Drukker J, Sanches H, Beursgens J. Cervical spine motion in the sagittal plane (I) range of motion of actually performed movements, an x-ray cinematographic study. Eur J Morphol. 1990;28(1): 47�68. [PubMed]
44. van Mameren H, Sanches H, Beursgens J, Drukker J. Cervical spine motion in the sagittal plane II positions of segmental averaged instantaneous centers of rotation-a cineradiographic study. Spine (Phila Pa 1976). 1992;17(5): 467�74. [PubMed]
45. Bogduk N, Mercer S. Biomechanics of the cervical spine 1: normal kinematics. Clin Biomech. 2000;15(9): 633�48. [PubMed]
46. Radcliff K, Kepler C, Reitman C, Harrop J, Vaccaro A. CT and MRI-based diagnosis of craniocervical dislocations the role of the occipitoatlantal ligament. Clin Orthop Rel Res. 2012;70(6): 1602�13. [PMC free article] [PubMed]
47. Hino H, Abumi K, Kanayama M, Kaneda K. Dynamic motion analysis of normal and unstable cervical spines using cineradiography.an in vivo study. Spine (Phila Pa 1976). 1999;24(2): 163�8. [PubMed]
48. Dvorak J, Penning L, Hayek J, Panjabi MM, Grob D, Zehnder R. Functional diagnostics of the cervical spine using computer tomography. Neuroradiology. 1988;30: 132�7. [PubMed]
49. Antinnes J, Dvorak J, Hayek J, Panjabi MM, Grob D. The value of functional computed tomography in the evaluation of soft-tissue injury in the upper cervical spine. Eur Spine J. 1994;3: 98�101. [PubMed]
50. Wilberger JE, Maroon JC. Occult posttraumatic cervical ligamentous instability. J Spinal Disord. 1990;(2): 156�61. [PubMed]
51. Levine A, Edwards CC. Traumatic lesions of the occipitoatlantoaxial complex. Clin Orthop Rel Res. 1989;239: 53�68. [PubMed]
52. Chang H, Gilbertson LG, Goel VK, Winterbottom JM, Clark CR, Patwardhan A. Dynamic response of the occipito-atlanto-axial (C0-C1-C2):complex in right axial rotation. J Orthop Res. 1992;10(3): 446�53. [PubMed]
53. Goel VK, Winterbottom JM, Schulte KR, Chang H , et al. Ligamentous laxity across C0-C1-C2 complex.Axial torque-rotation characteristics until failure. Spine (Phila Pa 1976). 1990;5(10): 990�6. [PubMed]
54. Goel VK, Clark CR, Gallaes K, Liu YK. Moment-rotation relationships of the ligamentous occipito-atlanto-axial complex. J Biomech. 1988;21(8): 673�80. [PubMed]
55. Quinn KP, Winkelstein BA. Cervical facet capsular ligament yield defines the threshold for injury and persistent joint-mediated neck pain. J Biomech. 2007;40(10): 2299�306. [PubMed]
56. Winkelstein BA, Santos DG. An intact facet capsular ligament modulates behavioral sensitivity and spinal glial activation produced by cervical facet joint tension. Spine (Phila Pa 1976). 2008;33(8): 856�62. [PubMed]
57. Stemper BD, Yoganandan N, Pintar FA. Effects of abnormal posture on capsular ligament elongations in a computational model subjected to whiplash loading. J Biomech Eng. 2005;38(6): 1313�23. [PubMed]
58. Ivancic PC, Ito S, Tominaga Y , et al. Whiplash causes increased laxity of cervical capsular ligament. Clin Biomech. 2008;23(2): 159�65. [PMC free article] [PubMed]
59. IASP Spinal pain, section 1: spinal and radicular pain syndromes. http: //www.iasp-pain.org/AM/Template.cfm?Section=Classification _of_Chronic_Pain&Template=/CM/ContentDisplay.cfm&ContentID=16268. Accessed Nov 25. 2013.
60. Argenson C, Lovet J, Sanouiller JL, de Peretti F. Traumatic rotatory displacement of the lower cervical spine. Spine (Phila Pa 1976). 1988;3(7): 767�73. [PubMed]
61. Tominaga Y, Maak TG, Ivancic PC, Panjabi MM, Cunningham BW. Head-turned rear impact causing dynamic cervical intervertebral foraminal narrowing implications for ganglion and nerve root injury. J Neurosurg Spine. 2006;4: 380�7. [PubMed]
62. Caridi JM, Pumberger M, Hughes AP. Cervical radiculopathy a review. HSS J. 2011;7(3): 265�72. [PMC free article] [PubMed]
63. Kirkaldy-Willis HF, Farfan HF. Instability of the lumbar spine. Clin Orthop Rel Res. 1982;(165): 110�23. [PubMed]
64. Voorhies RM. Cervical spondylosis recognition, differential diagnosis, and management. Ochsner J. 2001;3(2): 78�84. [PMC free article] [PubMed]
65. Binder AI. Cervical spondylosis and neck pain. BMJ. 2007;334: 527�31. [PMC free article] [PubMed]
66. Aker PD, Gross AR, Goldsmith CH, Peloso P. Conservative management of mechanical neck pain systematic overview and meta-analysis. BMJ. 1996;313: 1291�6. [PMC free article] [PubMed]
67. McCormack BM, Weinstein PR. Cervical spondylosis an update. West J Med. 1996;165: 43�51. [PMC free article] [PubMed]
68. Peng BG, Hou SX, Shi Q, Jia LS. The relationship between cartilage end-plate calcification and disc degeneration an experimental study. Chin Med J. 2001;114: 308�12. [PubMed]
69. Mauro A, Eisenstein SM, Little C , et al. Are animal models useful for studying human disc disorders/degeneration?. Eur Spine J. 2008;17: 2�19. [PMC free article] [PubMed]
70. Oxland TR, Panjabi MM, Southern EP, Duranceau JS. An anatomic basis for spinal instability a porcine trauma model. J Orthop Res. 1991;9(3): 452�62. [PubMed]
71. Wang JY, Shi Q, Lu WW , et al. Cervical intervertebral disc degeneration induced by unbalanced dynamic and static forces a novel in vivo rat model. Spine (Phila Pa 1976) 2006;Jun 15; 31: 1532�38. [PubMed]
72. Schulte K, Clark CR, Goel VK. Kinematics of the cervical spine following discectomy and stabilization. Spine (Phila Pa 1976). 1989;(10): 1116�21. [PubMed]
73. Kelly MP, Mok JM, Frisch RF, Tay BK. Adjacent segment motion after anterior cervical discectomy and fusion versus prodisc-c cervical total disk arthroplasty analysis from a randomized, controlled trial. Spine (Phila Pa 1976) 2011; 36(15): 1171�9. [PubMed]
74. Bydon M, Xu R, Macki M , et al. Adjacent segment disease after anterior cervical discectomy and fusion in a large series. Neurosurgery. 2014;74: 139�46. [PubMed]
75. Song JS, Choi BW, Song KJ. Risk factors for the development of adjacent segment disease following anterior cervical arthrodesis for degenerative cervical disease comparison between fusion methods. J Clin Neurosci. 2014;21(5): 794�8. [PubMed]
76. Johansson BH. Whiplash injuries can be visible by functional magnetic resonance imaging. Pain Res Manage. 2006;11(3): 197�9. [PMC free article] [PubMed]
77. Swinkels RA, Oostendorp RA. Upper cervical instability fact or fiction. J Manip Physiol Ther. 1996;19(3): 185�94. [PubMed]
78. Barnsley L, Lord S, Bogduk N. Whiplash injury. Pain. 1994;58: 283�307. [PubMed]
79. Spitzer WO, Skovron ML, Salmi LR , et al. Scientific monograph of the Quebec task force on whiplash-associated disorders redefining “whiplash” and its management. Spine (Phila Pa 1976). 1995;20(8) Suppl : 1S�73. [PubMed]
80. Kaale BR, Krakenes J, Albrektsen G, Wester K. Head position and impact direction in whiplash injuries associations with MRI-verified lesions of ligaments and membranes in the upper cervical spine. J Neurotrauma. 2005;22(11): 1294�302. [PubMed]
81. Falco FJ, Erhart S, Wargo BW , et al. Systematic review of diagnostic utility and therapeutic effectiveness of cervical facet joint interventions. Pain Physician. 2009;12(2): 323�44. [PubMed]
82. Winkelstein BA, Nightingale RW, Richardson WJ, Myers BS, editors. Proceedings of the 43rd Stapp Car Crash Conference. Saniego CA.: 1999. Cervical facet joint mechanics its application to whiplash injury.
83. Lee DJ, Winkelstein BA. The failure response of the human cervical facet capsular ligament during facet joint retraction. J Biomech. 2012;45(14): 2325�9. [PubMed]
84. Bogduk N, Yoganandan N. Biomechanics of the cervical spine part 3: minor injuries. Clin Biomech. 2001;16(4): 267�75. [PubMed]
85. Lord SM, Barnsley L, Wallis BJ, Bogduk N. The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine (Phila Pa 1976). 1995;20(1): 20�5. [PubMed]
86. Lee KE, Davis MB, Mejilla RM, Winkelstein BA. In vivo cervical facet capsule distraction mechanical implications for whiplash and neck pain. Stapp Car Crash J. 2004;48: 373�95. [PubMed]
87. Tominaga Y, Ndu AB, Coe MP , et al. Neck ligament strength is decreased following whiplash trauma. BMC Musculoskelet Disord. 2006;7: 103. [PMC free article] [PubMed]
88. Stokes IA, Frymoyer JW. Segmental motion and instability. Spine (Phila Pa 1976). 1987;7: 688�91. [PubMed]
89. Stokes IA, Iatridis JC. Mechanical conditions that accelerate intervertebral disc degeneration overload versus immobilization. Spine (Phila Pa 1976). 2004;29: 2724�32. [PubMed]
90. Veres SP, Robertson PA, Broom ND. The influence of torsion on disc herniation when combined with flexion. Eur Spine J. 2010;19: 1468�78. [PMC free article] [PubMed]
91. Winkelstein BA, Nightingale RW, Richardson WJ, Myers BS. The cervical facet capsule and its role in whiplash injury a biomechanical investigation. Spine (Phila Pa 1976). 2000;25(10): 1238�46. [PubMed]
92. Siegmund GP, Myers BS, Davis MB, Bohnet HF, Winkelstein BA. Mechanical evidence of cervical facet capsule injury during whiplash a cadaveric study using combined shear, compression, and extension loading. Spine (Phila Pa 1976). 2001;26(19): 2095�101. [PubMed]
93. Siegmund GP, Davis MB, Quinn KP , et al. Head-turned postures increase the risk of cervical facet capsule injury during whiplash. Spine (Phila PA 1976). 2008;33(15): 1643�9. [PubMed]
94. Storvik SG, Stemper BD. Axial head rotation increases facet joint capsular ligament strains in automotive rear impact. Med Bio Eng Comput. 2011;49(2): 153�61. [PubMed]
95. Centers for Disease Control Injury prevention & control traumatic brain injury. http: //www.cdc.gov/TraumaticBrainInjury/statistics. html [Accessed March 4. 2014.
96. Centers for Disease Control Concussion.facts for physicians booklet. http: //www.cdc.gov/concussion/HeadsUp/physicians_too l_kit.html [Accessed March 4. 2014.
97. Giza C, Hovda D. The neurometabolic cascade of concussion. J Athl Train. 2001;36: 228�35. [PMC free article] [PubMed]
98. Cuccurullo S, Elovic E, Baerga E, Cuccurullo S, editors. Demos Medical Publishing: New York; 2004. Mild traumatic brain injury and postconcussive syndrome Physical medicine and rehabilitation board review.
99. Leddy J, Sandhu H, Sodhi V, Baker J, Willer B. Rehabilitation of concussion and post-concussion syndrome. Sports Health. 2012;4(2): 147�54. [PMC free article] [PubMed]
100. ICD-10, International statistical classification of diseases and related health problems 10th revision. World Health Organization. [PubMed]
101. Boake C, McCauley SR, Levin HS , et al. Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury. J Neuropsych Clin Neurosci. 2005;17: 350�6. [PubMed]
102. Couch Jr, Bears C. Chronic daily headache in the posttrauma syndrome relation to extent of head injury. Headache. 2001;41: 559�64. [PubMed]
103. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury. Clin Sports Med. 2011;30: 33�48. [PubMed]
104. Saari A, Dennison CR, Zhu Q , et al. Compressive follower load influences cervical spine kinematics and kinetics during simulated head-first impact in an in vitro model. J Biomech Eng. 2013;135(11): 111003. [PubMed]
105. Zhou S-W, Guo L-X, Zhang S-Q, Tang C-Y. Study on cervical spine injuries in vehicle side impact. Open Mech Eng J. 2010;4: 29�35.
106. Yoganandan N, Kumaresan S, Pintar FA. Geometric and mechanical properties of human cervical spine ligaments. J Biomech Invest. 2000;122: 623�9. [PubMed]
107. Radanov BP, Sturzenegger M, Distefano G, Schnidrig A, Aljinovic M. Factors influencing recovery from headache after common whiplash. BMJ. 1993;307: 652�5. [PMC free article] [PubMed]
108. Martins J, Pratesi R, Bezerra A. Anatomical relationship between vertebral arteries and cervical vertebrae a computerized tomography study. Int J Morph. 2003;21: 123�9.
109. Cacciola F, Phalke U, Goel A. Vertebral artery in relationship to C1-C2 vertebrae an anatomical study. Neurology India. 2004;52: 178�84. [PubMed]
110. Mitchell JA. Changes in vertebral artery blood flow following normal rotation of the cervical spine. J Manip Physiol Ther. 2003;26: 347�51. [PubMed]
111. Mitchell J. Vertebral artery blood flow velocity changes associated with cervical spine rotation a meta-analysis of the evidence with implications for professional practice. J Man Manip Ther. 2009;17: 46�57. [PMC free article] [PubMed]
112. Haynes M, Hart R, McGeachie J. Vertebral arteries and neck rotation doppler velocimeter interexaminer reliability. Ultrasound Med Biol. 2000;26: 57�62. [PubMed]
113. Kuether TA, Nesbit GM, Clark VM, Barnwell SL. Rotational vertebral artery occlusion a mechanism of vertebrobasilar insufficiency. Neurosurgery. 1997;41: 427�32. [PubMed]
114. Yang PJ, Latack JT, Gabrielsen TO, Knake JE, Gebarski SS, Chandler WF. Rotational vertebral artery occlusion at C1-C2. Am J Neuroradiol. 1985;6: 96�100. [PubMed]
115. Cape RT, Hogan DB. Vertebral-basilar insufficiency. Can Family Physician. 1983;29: 305�8. [PMC free article] [PubMed]
116. Go G, Soon-Hyun H, Park IS, Park H. Rotational vertebral artery compression bow hunter’s syndrome. J Korean Neurosurg Soc. 2013;54: 243�5. [PMC free article] [PubMed]
117. Gordin K, Hauser R. The case for utilizing prolotherapy as a promising stand-alone or adjunctive treatment for over-manipulation syndrome. J Applied Res. 2013;13: 1�28.
118. Endo K, Ichimaru K, Komagata M, Yamamoto K. Cervical vertigo and dizziness after whiplash injury. Eur Spine J. 2006;15: 886�90. [PMC free article] [PubMed]
119. Creighton D, Kondratek M, Krauss J, Huijbregts P, Qu H. Ultrasound analysis of the vertebral artery during non-thrust cervical translatoric spinal manipulation. J Man Manip Ther. 2011;19: 84�90. [PMC free article] [PubMed]
120. Inamasu J, Nakatsukasa M. Rotational vertebral artery occlusion associated with occipitoatlantal assimilation, atlantoaxial subluxation and basilar impression. Clin Neurol Neurosurg. 2013;115: 1520�3. [PubMed]
121. Kim HA, Yi HA, Lee CY, Lee H. Origin of isolated vertigo in rotational vertebral artery syndrome. Neuro Sci. 2011;32: 1203�7. [PubMed]
122. Yacovino DA1, Hain TC. Clinical characteristics of cervicogenic related dizziness and vertigo. Sem Neurol. 2013;33: 244�55. [PubMed]
123. Limousin CA. Foramen arcuale and syndrome of Barr�-Li�ou. Int Orthop. 1980;4(1): 19�23. [PubMed]
124. Pearce J. Barr�-Li�ou �syndrome�. J Neurol Neurosurg Psychol. 2004;75(2): 319. [PMC free article] [PubMed]
125. Hackett GS, Huang TC, Raferty A. Prolotherapy for headache; pain in the head and neck, and neuritis. Headache. 1962:3�11. [PubMed]
126. Tamura T. Cranial symptoms after cervical injury.Aetiology and treatment of the Barr -Li ou syndrome. J Bone Joint Surg Br. 1989;71B:282�7. [PubMed]
127. Qian J, Tian Y, Qiu GX, Hu JH. Dynamic radiographic analysis of sympathetic cervical spondylosis instability. Chin Med Sci J. 2009;24: 46�9. [PubMed]
128. Humphreys BK, Peterson C. Comparison of outcomes in neck pain patients with and without dizziness undergoing chiropractic treatment a prospective cohort study with 6 month follow-up. Chiropr Man Ther. 2013;21(1): 3. [PMC free article] [PubMed]
129. Pintar FA, Yoganandan N, Myers T, Elhagediab A, Sances A ., Jr Biomechanical properties of human lumbar spine ligaments. J Biomech. 1992;25: 1351�6. [PubMed]
130. Yoganandan N, Pintar D, Maiman J, Cusick JF, Sances A , Jr, Walsh PR. Human head-neck biomechanics under axial tension. Med Eng Phys. 1996;18: 289�94. [PubMed]
131. Mc Lain R. Mechanoreceptors endings in human cervical facet joints. Iowa Orthop J. 1993;13: 149�54. [PMC free article] [PubMed]
132. Steindler A, Luck J. Differential diagnosis of pain low in the back allocation of the source of pain by the procaine hydrochloride method. JAMA. 1938;110: 106�13.
133. Donelson R, Aprill C, Medcalf R, Grant W. A prospective study of centralization of lumbar and referred pain a predictor of symptomatic discs and anular competence. Diagn Ther. 1997;22: 1115�22. [PubMed]
134. Meleger AL, Krivickas LS. Neck and back pain musculoskeletal disorders. Neurol Clin. 2007;25: 419�38. [PubMed]
135. Silver P. Direct observation of changes in tension in the supraspinous and interspinous ligaments during flexion and extension of the vertebral column in man. J Anat. 1954:550�1.
136. Nachemson A. Lumbar intradiscal pressure.Experimental studies on post-mortem material. Acta Orthop Scand. 1960;43S:1�104. [PubMed]
137. Galante J. Tensile properties of the human lumbar annulus fibrosus. Acta Orthop Scand. 1967;100S:1�91. [PubMed]
138. Stokes IA. Surface strain on human intervertebral discs. J Orthop Res. 1987;5: 348�55. [PubMed]
139. Stokes IA. Bulging of the lumbar intervertebral discs non-contacting measurements of anatomical specimens. J Spinal Disord. 1988;1: 189�93. [PubMed]
140. Manchikanti L, Malla Y, Cash KA, McManus CD, Pampati V. Fluoroscopic cervical interlaminar epidural injections in managing chronic pain of cervical postsurgery syndrome preliminary results of a randomized, double-blind, active control trial. Pain Physician. 2012;15: 13�26. [PubMed]
141. Manchikanti L, Singh V, Falco FJE, Cash KA, Fellows B. Comparative outcomes of a 2-year follow-up of cervical medial branch blocks in management of chronic neck pain a randomized, double-blind controlled trial. Pain Physician. 2010;13: 437�50. [PubMed]
142. Falco FJE, Manchikanti L, Datta S , et al. Systematic review of the therapeutic effectiveness of cervical facet joint interventions an update. Pain Physician. 2012;15: E839�68. [PubMed]
143. Benyamin R, Singh V, Parr AT, Conn A, Diwan S, Abdi S. Systematic review of the effectiveness of cervical epidurals in the management of chronic neck pain. Pain Physician. 2009;12: 137�57. [PubMed]
144. Sherman KJ, Cherkin DC, Hawkes RJ, Miglioretti DL, Deyo RA. Randomized trial of therapeutic massage for chronic neck pain. Clin J Pain. 2009;25(3): 233�8. [PMC free article] [PubMed]
145. Matsubara T, Arai Y-CP, Shiro Y , et al. Comparative effects of acupressure at local and distal acupuncture points on pain conditions and autonomic function in females with chronic neck pain. Evidence-Based Complementary Alternative Med. 2011; 2011: 543921. [PMC free article] [PubMed]
146. Manchikanti L, Cash KA, Pampati V, Wargo BW, Malla Y. A randomized, double-blind, active control trial of fluoroscopic cervical interlaminar epidural injections in chronic pain of cervical disc herniation results of a 2-year follow-up. Pain Physician. 2013;16: 465�78. [PubMed]
147. Peloso PM, Khan M, Gross AR , et al. Pharmacological interventions including medical injections for neck pain an overview as part of the ICON project. Open Orthop J. 2013;7(Suppl 4 M8 ): 473�93. [PMC free article] [PubMed]
148. Teasell RW, McClure JA, Walton D, Pretty J , et al. A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): part 2 – interventions for acute WAD. Pain Res Manage. 2010;15(5): 295�304. [PMC free article] [PubMed]
149. Teasell RW, McClure JA, Walton D , et al. A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): part 3 – interventions for subacute WAD. Pain Res Manag. 2010;15(5): 305�12. [PMC free article] [PubMed]
150. Teasell RW, McClure JA, Walton D , et al. A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): part 4 -noninvasive interventions for chronic WAD. Pain Res Manag. 2010;15(5): 313�22. [PMC free article] [PubMed]
151. Teasell RW, McClure JA, Walton D , et al. A research synthesis of therapeutic interventions for whiplash-associated disorder (WAD): part 5 – surgical and injection-based interventions for chronic WAD. Pain Res Manag. 2010;15(5): 323�34. [PMC free article] [PubMed]
152. Linetsky FS, Manchikanti L. Regenerative injection therapy for axial pain. Tech Reg Anaesh Pain Manag. 2005;9: 40�9.
153. Hackett G, editor. Oak Park IL. 5th ed. 1993. Ligament and tendon relaxation treated by prolotherapy ; pp. 94�6.
154. Goswami A. Prolotherapy. J Pain Palliative Care Pharmacother. 2012;26: 376�8. [PubMed]
155. Hauser RA, Maddela HS, Alderman D , et al. Journal of Prolotherapy international medical editorial board consensus statement on the use of prolotherapy for musculoskeletal pain. J Prolotherapy. 2011;3: 744�6.
156. Kim J. The effect of prolotherapy for osteoarthritis of the knee. J Korean Ac Rehab Med. 2002;26: 445�8.
157. Rabago D, Slattengren A, Zgierska A. Prolotherapy in primary care practice. Primary Care. 2010;37: 65�80. [PMC free article] [PubMed]
158. Distel LM, Best TM. Prolotherapy a clinical review of its role in treating chronic musculoskeletal pain. PMR. 2011;3(6) Suppl1 : S78�81. [PubMed]
159. Hackett G. Prolotherapy in whiplash and low back pain. Postgrad Med. 1960:214�9. [PubMed]
160. Kafetz D. Whiplash injury and other ligamentous headache – its management with prolotherapy. Headache. 1963;3: 21�8. [PubMed]
161. Hauser RA, Hauser MA. Dextrose prolotherapy for unresolved neck pain an observational study of patients with unresolved neck pain who were treated with dextrose prolotherapy at an outpatient charity clinic in rural Illinois. Pract Pain Manage. 2007;10: 56�69.
162. Hooper RA, Frizzell JB, Faris P. Case series on chronic whiplash related neck pain treated with intraarticular zygapophysial joint regeneration injection therapy. Pain Physician. 2007;10: 313�8. [PubMed]
163. Centeno CJ, Elliott J, Elkins WL, Freeman M. Fluoroscopically guided cervical prolotherapy for instability with blinded pre and post radiographic reading. Pain Physician. 2005;8(1): 67�72. [PubMed]
164. Lee J, Lee HG, Jeong CW, Kim CM, Yoon MH. Effects of intraarticular prolotherapy on sacroiliac joint pain. Korean J Pain. 2009:229�33.
165. Cusi M, Saunders J, Hungerford B, Wisbey-Roth T, Lucas P, Wilson S. The use of prolotherapy in the sacroiliac joint. Brit J Sports Med. 2010;44: 100�4. [PubMed]
166. Naeim F, Froetscher L, Hirschberg GG. Treatment of chronic iliolumbar syndrome by infiltration of the iliolumbar ligament. West J Med. 1982;136: 372�4. [PMC free article] [PubMed]
167. Kim J. Effects of prolotherapy on knee joint pain due to ligament laxity. J Korean Pain Soc. 2004;17: 47�5.
168. Reeves K, Hassanein KM. Long-term effects of dextrose prolotherapy for anterior cruciate laxity. Alternative Ther. 2003;9: 58�62. [PubMed]
169. Jo D. Effects of prolotherapy on knee joint pain due to ligament laxity. J Korean Pain Soc. 2004;17: 47�50.
170. Kim S. Effects of prolotherapy on chronic musculoskeletal disease. Korean J Pain. 2002;15: 121�5.
171. Wheaton MT, Jensen N. The ligament injury-osteoarthritis connection the role of prolotherapy in ligament repair and the prevention of osteoarthritis. J Prolotherapy. 2011;3: 790�812.
172. Refai H, Altahhan O, Elsharkawy R. The efficacy of dextrose prolotherapy for temporomandibular joint hypermobility a preliminary prospective, randomized double-blind, placebo-controlled clinical trial. J Oral Maxillofac Surg. 2011;69(12): 2962�70. [PubMed]
173. Hauser R, Phillips HJ. Treatment of joint hypermobility syndrome, including Ehlers-Danlos syndrome, with Hackett-Hemwall prolotherapy. J Prolotherapy. 2011;3: 612�29.
174. Hackett G. Joint stabilization an experimental, histologic study with comments on the clinical application in ligament proliferation. Am J Surg. 1955;89: 967�73. [PubMed]
175. Liu Y, Tipton C, Matthes R, Bedford TG, Maynard JA, Walmer HC. An in situ study of the influence of a sclerosing solution in rabbit medial collateral ligaments and its junction strength. Connect Tissue Res. 1983;11: 95�102. [PubMed]
176. Klein R, Dorman T, Johnson C. Proliferant injections for low back pain histologic changes of injected ligaments and objective measurements of lumbar spine mobility before and after treatment. J Neuro Ortho Med Surg. 1989;10: 123�6.
177. Auburn A, Benjamin S, Bechtel R, Matthews S. Increase in cross sectional area of the iliolumbar ligament using prolotherapy agents an ultrasonic case study. J Prolotherapy. 1999;1: 156�62.
178. Linetsky FS, Miguel R, Torres F. Treatment of cervicothoracic pain and cervicogenic headaches with regenerative injection therapy. Curr Pain Headache Rep. 2004;8(1): 41�8. [PubMed]
179. Alderman D. Prolotherapy for knee pain. Pract Pain Manage. 2007;7(6): 70�9.
180. Hooper RA, Yelland M, Fonstad P, Southern D. Prospective case series of litigants and non-litigants with chronic spinal pain treated with dextrose prolotherapy. Int Musculoskelet Med. 2011;33: 15�20.
181. Hauser RA. A retrospective study on Hackett-Hemwall dextrose prolotherapy for chronic shoulder pain at an outpatient charity clinic in rural Illinois. J Prolotherapy. 2009;4: 205�16.
182. Hauser RA, Hauser MA, Holian P. Hackett-Hemwall dextrose prolotherapy for unresolved elbow pain. Pract Pain Manage. 2009:14�26.
183. Hauser RA. Dextrose prolotherapy for unresolved low back pain a retrospective case series study. J Prolotherapy. 2009;3: 145�55.
184. Hauser RA. A retrospective study on Hackett-Hemwall dextrose prolotherapy for chronic hip pain at an outpatient charity clinic in rural Illinois. J Prolotherapy. 2009;(2): 76�88.
185. Hauser RA. A retrospective study on dextrose prolotherapy for unresolved knee pain at an outpatient charity clinic in rural Illinois. J Prolotherapy. 2009;(1): 11�21.
186. Hauser R, Woldin B. Treating osteoarthritic joints using dextrose prolotherapy and direct bone marrow aspirate injection therapy. Open Arthritis J. 2014;7: 1�9.
Close Accordion