Back Clinic Physical Rehabilitation Team. Physical medicine and rehabilitation, which is also known as physiatry or rehabilitation medicine. Its goals are to enhance, restore functional ability and quality of life to those with physical impairments or disabilities affecting the brain, spinal cord, nerves, bones, joints, ligaments, muscles, and tendons. A physician that has completed training is referred to as a physiatrist.
Unlike other medical specialties that focus on a medical cure, the goals of the physiatrist are to maximize the patient’s independence in activities of daily living and improve quality of life. Rehabilitation can help with many body functions. Physiatrists are experts in creating a comprehensive, patient-centered treatment plan. Physiatrists are integral members of the team. They utilize modern, as well as, tried and true treatments to bring optimal function and quality of life to their patients. And patients can range from infants to octogenarians. For answers to any questions you may have please call Dr. Jimenez at 915-850-0900
Concussion, also known as mild traumatic brain injury (MTBI), has been a poorly understood condition known to the majority of healthcare providers as difficult to objectify and manage.
Historically, there has been no testing available to conclude an accurate diagnosis. In the absence of objective imaging findings of bleeding in the brain, a diagnosis of “mild traumatic brain injury” has been affixed to the condition, whereas if there’s evidence of traumatic bleeding then the diagnosis “traumatic brain injury” is applied.
Although Hartvigsen, Boyle, Cassidy and Carroll (2014) reported that 600 out of 100,000 Americans are affected every year by concussion, Jeter et al, (2012) reported that close to 40 percent of people experiencing a mild brain injury do not report it to their doctor, making accurate statistics very tricky to conclude. Despite potential under reporting in the people, we realize concussion is an issue that has consequences that are important from the perspective of a clinical result and we cannot afford to ignore this condition.
Mechanism of Injury: Mild Traumatic Brain Injury
Mild traumatic brain injury or concussion results from transfer of mechanical energy from the outside environment to the brain due to traumatic events where there’s a sudden acceleration and then a sudden deceleration of the mind and brain, such as in a Coup/Contrecoup injury during a whiplash scenario. As the brain is freely moving to a degree because it’s only surrounded by cerebral spinal fluid, it continues moving in the original direction and as the head “whips” rapidly in the opposite direction, the brain bounces off parts of the inner skull, which in turn rebounds shortly after the head changes direction. This is one easily defined mechanism of MTBI that doesn’t cause gross bleeding, yet leaves the brain injured through direct compression or overstretching (axonal shearing) of central nervous system components.
Although this has been examined extensively in the military, it’s been recently investigated in professional sports, where after several lawsuits and lives at risk, there are now definitive “concussion protocols” in place. Part of the protocols as reported from the British Journal of Sports Medicine (2016) is the Sports Concussion Assessment Tool 2 or SCAT2 that’s been adopted by numerous professional sports leagues. However, the majority of concussion victims are not active participants in the military or a professional sports team and many find their way into chiropractic practices as a consequence of sports injuries, car accidents, slip and falls and every other sort of head trauma etiology. Even though the mechanisms might vary, the induced end results are the same.
For generalized patient intake protocols, according to both Medicare and academia standards, a questionnaire outlining a summary of body systems is mandated, and part of those questions center on brain function. As reported by Jeter et al behavioral and cognitive symptoms, signs and symptoms are reported on standard patient intake questionnaires and require consideration of a diagnosis of concussion.
Prominent symptoms of concussion include: balance issues, vomiting, nausea, headache, drowsiness, dizziness, fatigue, vision, light or noise sensitivity and sleep disturbances. Cognitive symptoms include deficits in attention, concentration, memory, mental processing speed, and working memory or decision making. Behavioral symptoms include anxiety, depression, irritability, depression and aggression. The researchers went on to report that approximately 25 percent of the cases can have these symptoms persist.
Diagnosis and Treatment for MTBI
As a profession, chiropractic is a important part of the rehabilitation for the concussion population as the post-traumatic patient typically presents to the average chiropractic practice. As chiropractors (along with all healthcare providers), even if you mix the history with the above symptoms inclusive of neurological, behavioral and cognitive traits, you then have the direction or “triage road map” of the way to conclusively differentially diagnose your individual, including what tests to consider conducting in order to do so. The first line of testing is to consider imaging to rule out bleeding and ensure the patient does not require an immediate consultation. Treating blindly can place your patient in risk that is possible.
Imaging of the brain requires either MRI or CAT scans, MRI being the more sensitive, and in the absence of bleeding, the diagnosis is limited to MTBI or concussion (used interchangeably). More recently, diffusion tensor imaging (DTI) has been a tool available to picture mTBI victims that uses tissue water diffusion speeds to determine bleeding at a very small level giving demonstrable evidence to brain injury. As reported by Soares, Marques, Alves, and Sousa, (2013), DTI has several issues to overcome to certify accuracy including, but not limited to, tissue type, integrity, barriers and quantitative diffusion rates that are required to infer molecular diffusion prices. DTI is a model based upon assumption with a outlook as a tool.
Historically, MTBI was exclusively diagnosed by an omission of advanced imaging findings and the presence and persistence of the neurology, cognitive and behavioral signs and symptoms. Today, brain-derived neurotrophic factors (BDNF) offer responses about carpal brain pathology that is both conclusive and reproducible. Based on Korley et al. (2015), brain-derived neurotrophic factors is a secreted autocrine (compound hormone or messenger in blood) which promotes the development, maintenance, survival, differentiation and regeneration of neurons. BDNF also is important for synaptic plasticity (strengthening of synapses over time) and memory processing. Germane to MTBI and concussion, BDNF has been implicated in decreasing brain injury, with elevations and restoring traumatic brain injury.
Korley went on to report that BDNF levels were the highest in the normal group with lower values in mTBI and even lower in traumatic brain injury (TBI) subjects. In addition BDNF values were associated with incomplete recovery of patients that were MTBI compared to moderate or severe TBI patients. Because of this, it has been ascertained that BDNF has for identifying associated sequelae at 6 23, a prognostic value.
Korley stated that BDNF is the most abundantly secreted brain neurotrophin and as a secreted protein and can be readily measured using well-established immune-assay methods, identifying it as a non-necrosis brain injury biomarker. This distinguishes BDNF from other biomarkers which are components of neurons and myelin based proteins among other structures. In order for structural fibers to be found in high abundance in circulation, adequate cellular necrosis and damage to the blood barrier membrane must be observed, however BDNF does not require cellular damage or necrosis to be observed in circulation enabling DDNF to be more plentiful in flow than structural proteins.
Following a traumatic brain event, BDNF supports synaptic reorganization and recovery during the brain circuitry “reconnection” phase. Therefore, a better prognosis is indicated by lowered values. In patients with a co-morbidity of BDNF of anxiety, depressive disorders and schizophrenia BDNF values on the day of injury predispose this population to incomplete recovery as a risk element. Korley et al.. Concluded that serum BDNF discriminates between MTBI and TBI cases. Also, diminished BDNF values are associated with recovery in identifying and useful symptoms 6-months post-trauma.
Conclusion
Simply put, a blood test could assist providers in concluding the existence and/or severity of traumatic brain injury or mild traumatic brain injury. An early diagnosis is afforded by the results so you can devise a treatment plan inclusive of changing activities of everyday living to prevent additional damage and optimize the repair procedure with minimizing further chemical, physical or emotional stressors.
Based upon interviews with leading neurologists and neurosurgeons who understand and have first-hand expertise of both receiving chiropractic care and handling and treating MTBI patients, it is strongly recommended that until the signs and symptoms of the neurologic, cognitive and behavioral abate that high-velocity rotational cervical adjustments be avoided to enable the brain to “repair and rewire” the connections without additional possibilities of and Coup/ Contrecoup energy to the mind. This is a recommendation which we agree while recognizing that chiropractic care should not be avoided adapted to allow the brain to heal.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
References:
1. Hartvigsen, J., Boyle, E., Cassidy, J. D., & Carroll, L. J. (2014). Mild traumatic brain injury after motor vehicle collision: What are the symptoms and who treats them? A population-based 1-year inception cohort study. Archives of Physical Medicine and Rehabilitation, 95(Suppl. 3), S286-S294.
2. Jeter, C. B., Hergenroeder, G. W., Hylin, M. J., Redell, J. B., Moore, A. N., & Dash, P. K. (2013). Biomarkers for the diagnosis and prognosis of mild traumatic brain injury/concussion. Journal of Neurotrauma, 30(8), 657-670.
3. British Journal of Sports Medicine. (2016). Sport concussion assessment tool 2. Retrieved from bjsm.bmj.com/content/43/Suppl_1/i85.full.pdf
4. Soares, J. M., Marques, P., Alves, V., & Sousa, N. (2013). A hitchhiker�s guide to diffusion tensor imaging. Frontiers in Neuroscience, 7(31), 1-14.
5. Korley, F. K., Diaz-Arrastia, R., Wu, A. H. B., Yue, J. K., Manley, G. T., Sair, H. I., Van Eyk, J., Everett, A. D., Okonkwo, D. O., Valadka, A. B., Gordon, W. A., Maas, A. I., Mukherjee, P., Yuh, E. L., Lingsma, H. F., Puccio, A. M., & Schnyer, D. M., (2015). Circulating brain-derived neurotrophic factor has diagnostic and prognostic value in traumatic brain injury. Journal of Neurotrauma, 32, 1-11.
Additional Topics: Weakened Ligaments After Whiplash
Whiplash is a commonly reported injury after an individual has been involved in an automobile accident. During an auto accident, the sheer force of the impact often causes the head and neck of the victim to jerk abruptly, back-and-forth, causing damage to the complex structures surrounding the cervical spine. Chiropractic care is a safe and effective, alternative treatment option utilized to help decrease the symptoms of whiplash.
Chiropractor, Dr. Alex Jimenez looks at lumbar spine disc herniation. What are the Likely signs and symptoms associated with disc herniation, and what would be the selection criteria for micro-discectomy operation in athletes? Complaint in the young college age athlete and professional athlete, and it’s been estimated that over 30% of athletes complain of back pain at least once in the profession(1).
Lumbar spinal disc herniation is one kind Of lumbar injury that can’t just cause painful low back pain, but can also compress nerve roots and create radicular referral of pain into the lower leg with related sensation changes and muscle contraction. This injury will not only influence the short-term opponent ability of the athlete, but might also reoccur and eventually become persistent possibly causing a career ending injury.
Managing disc herniation from the athlete Usually begins with conservative therapy and if this fails, surgical solutions are considered. But often elite athletes will request a quicker resolution to their symptoms to minimize time away from competitors. Therefore, providing the criteria for lumbar spine surgery are suggested, the conservative period will often be compressed, and surgery will be sought earlier. The favored surgical process for the athlete with a disc herniation is that the lumbar disc micro-discectomy.
Anatomy & Biomechanics
A significant biomechanical role in the spine, allowing for motion between the spinal segments while spreading compressive, shear, and torsional forces(2). These discs include a thick outer ring of fibrous cartilage termed the annulus fibrosis (akin to the onion rings enclosing the center of the onion), which encompasses a more gelatinous core called the nucleus pulposus, which is included within the cartilage end plates inferiorly and superiorly.
The intervertebral disc consists of Cells and substances such as collagen, proteoglycans, and thin fibrochondrocytic tissues, which enable transmission and absorption of forces arising from body weight and muscle activity. To do so, the disc depends mainly on the structural condition of the nucleus pulposus, annulus fibrosis and the vertebra lend plate. If the disc is normal and is functioning optimally, then forces are spread across the disc evenly(3).
But disc degeneration (mobile Degradation, lack of hydration( disc failure) may decrease the capacity of the disc to withstand extrinsic forces, as forces are no longer distributed and spread evenly. Tears and fissures from the annulus can lead, and with adequate external forces, the disc material may herniate. Alternatively, a sizable biomechanical force set on a healthy, ordinary disc may cause extrusion of disc material as a result of crushing failure of this annular fibers — illustrations include a hefty compression type mechanism because of a fall on the tailbone, or strong muscle contraction such as heavy weight lifting(4).
Herniations represent protrusions of Disc material beyond the confines of this annular lining and in the spinal canal (see Figure 1)(5). If the protrusion does not invade the canal or undermine nerve roots then back pain may be the only symptom.
Endoscopic Discectomy 3D Simulation
The pain associated with lumbar Radiculopathy happens due to a mix of nerve root ischemia (due to compression) and inflammation (because of neurochemical inflammatory mediators released from the disc). Throughout a herniation, the nucleus pulposus puts pressure on weakened regions of the annulus, and proceeds through the diminished websites in the annulus in which it ultimately forms a herniation(6 ft). It follows from this that some kind of disc degeneration may exist prior to the disc may really herniated(7).
In contrast to other respiratory Tissues, discs have a inclination to degenerate earlier in life, with some studies demonstrating adolescents presenting signs of degeneration between the ages of 11 to 16(8). With increasing age, there’s further degeneration of the intervertebral discs.
While the disc might be in danger of harm in All fundamental planes of motion, it’s particularly susceptible during repetitive flexion, or hyper-flexion, combined with lateral bending or rotation(10). Traumatic events such as excessive axial compression may also damage the inner structure of the disc. This can occur as a result of a fall or powerful muscular forces developed during tasks such as heavy lifting.
Athletes are generally exposed to high loading conditions. Examples of this include:
1. World-class power lifters, in which the calculated compressive loads on the backbone are involving 18800 Newtons (N) and also 36400N acting in the L3-4 motion segment(11).
2. Elite level football linesmen who have Been proven to present time-related hypertrophy of this disc and changes in vertebrae endplate in response to this repetitive high loading and axial pressure(12).
3. Long distance runners have been Shown to undergo significant strain into the intervertebral disc, indicated by a reduction in disc height(13).
Herniations could be classified depending on Ultimately, herniations are also identified based on level, with most herniations happening at the L4/5 and L5/S1 intervertebral disc level; these can then in turn affect the L5 and S1 nerve roots resulting in clinical sciatica(15). Upper level herniations are less common, and when they do occur with radiculopathy, they will affect the femoral nerve. Finally, the prevalence of disc injury rises increasingly caudally, with the best numbers at the L5/S1 degrees(16).
Herniation In Athletes
The offending movements implicated in The 20-35 age group are the most common group to herniate a disc, most likely because of the fluid nature of the nucleus pulposis and due to behavior(18). This age group are more likely to participate in sports which need high lots of flexion and spinning or are reckless with their positions and positions during loading.
The sports most at risk of disc herniation are:
Hockey
Wrestling
Soccer
Swimming
Basketball
Golf
Tennis
Weightlifting
Rowing
Throwing events
These are the sports that involve either significant Furthermore, those who take part in more and more severe training regimes seem to be at higher risk of spinal pathologies, as do people involved in sports.
Signs & Symptoms Indicating Discectomy
The efficacy of management programs for lumbar spine disc herniation — in terms of the decision to operate or treat conservatively — will be discussed in greater depth in part 2 of this series. However, the decision to operate within an athlete is generally driven by the motivation and approaching goals the athlete has put themselves. They may in fact favor a comparatively simple micro-discectomy instead of waiting for symptoms to abate through an extended period of rehabilitation.
This conservative period of Management may involve medicine therapy, epidural injections, relative back and back muscle recovery, acupuncture, osteo/chiropractic interventions. On the other hand, the normal presenting symptoms and signs that suggest a substantial disc herniation that will require surgical intervention in the athlete comprise:
Low back pain with pain radiating down one or both legs
Positive straight leg raise test
Radicular pain and neurological signs consistent with the nerve root level affected
Mild weakness of distal muscles such as extensor hallucis longus, peroneals, tibialis anterior and soleus. These would fit with the myotome relevant for the disc level
MRI confirming a disc herniation
Possible bladder and bowel symptoms
Failed conservative rehabilitation
Time span in which to enable conservative rehabilitation to be effective. In the overall population, medical practitioners will most likely prescribe a minimal 6-week traditional period of treatment with an overview at 6 weeks as to whether to expand the rehabilitation a further 6 weeks or to seek a specialist opinion. The expert may then attempt more medically orientated interventions such as epidural injections.
The athlete nevertheless will have these They might be more inclined to experience an epidural very early in the conservative period to assess the effectiveness of this procedure. If no signs of progress are evident in a couple of weeks then they may choose to get an immediate lumbar spine micro- discectomy.
Endoscopic Lumbar Discectomy
Local Doctor performs lumbar discectomy using minimally invasive techniques. From the El Paso, TX. Spine Center.
Imaging
MRI remains the favored system of Identifying lumbar spine disc herniation, since it’s also very sensitive to detecting nerve root impingements(23). However, abnormal MRI scans can occur in otherwise asymptomatic patients(25); hence, clinical correlation is always essential before any surgical thought. What’s more, patients can present with clinical signs and symptoms which suggest the diagnosis of acute herniated disc, and yet lack evidence of sufficient pathology on MRI to warrant operation.
Therefore it has been proposed that a Volumetric analysis of a herniated disc on MRI may be potentially beneficial in checking the suitability for operation. Several writers have previously mentioned the possible value of volumetric evaluation of herniated disc on MRI as part of their selection criteria for lumbar surgery(26).
In a survey conducted in Michigan State University, it was found that the size and positioning of the herniated disc determined that the likelihood for operation with what researchers called ‘types 2-B’ and ‘types 2-AB’ being the most likely candidates for surgery(27).
The MRI protocol to your lumbar spine consists of (see Figure 2)
1.Sagittal plane echo T1- weighted sequence
2. Sagittal fast spin echo proton density sequence
3. Sagittal fast spin echo inversion recovery sequence
4.Axial spin echo T1- weighted sequence
Summary
Disc herniations are not a common Complaint in athletes, but they do happen in sports which involve high loads or repetitive flexion and rotation movements. Sufferers of a disc herniation will normally feel focused low-back pain, maybe with referral in the lower limb with associated neurological symptoms if the nerve root was compressed.
Managing a disc herniation within an General population as frequently the risk of a Protracted failed rehabilitation period is Bypassed for the protected and low risk Micro-discectomy procedure. In the Discuss the exact surgical alternatives involved Observing a lumbar spine micro-discectomy.
References
1. Sports Med. 1996;21(4):313�20
2. Radiology. Oct 2007;245(1):62-77
3. Arthritis Research & Therapy. 2003;5(3):120-30
4. The Journal of Bone and Joint Surgery. American volume. Feb 2004;86-A(2):382 � 96
5. Radiology. Oct 2007;245(1):43-61
6. Spine. Sep 15 1996;21(18):2149-55
7. Spine. May-Jun 1982;7(3):184-91
8. Spine. Dec 1 2002;27(23):2631-44
9. Lancet 1986;2:1366�7
10. Disease-A-Month:DM. Dec 2004;50(12):636-69
11. Spine. Mar 1987;12(2):146-9
12. The American Journal of Sports Medicine. Sep 2004;32(6):1434-9
13. The Journal of International Medical Research. 2011;39(2):569-79
14. Spine. 2001;26:E93-113
15. Spine. 1990;15:679-82
16. British Journal of Sports Medicine. Jun 2003;37(3):263-6
17. Prim Care. 2005;32(1):201�29
18. McGill, S.M. Low back disorders: Evidence based prevention and rehabilitation, Human Kinetics Publishers, Champaign, IL, U.S.A., 2002. Second Edition, 2007
19. Spine. Apr 1991;16(4):437-43
20. Skeletal radiology. Jul 2006;35(7):503-9
21. British Journal of Sports Medicine. Nov 2007;41(11):836-41
22. The American Journal of Sports Medicine. Jun 2009;37(6):1208-13
23. Spine. Mar 15 1995;20(6):699-709
24. Phys Sportsmed. 2005;33(4):21�7
25. J Bone Joint Surg Am 1990 . 2:403�408
26. J Orthop Surg (Hong Kong) 2001. 9:1�7
27. Eur Spine J (2010) 19:1087�1093
A good read to understanding alteration of motion segment integrity (AOMSI) is the article �Biomechanical Analysis of clinical instability in the cervical spine� White, et al., Clin Ortho Relat Res, 1975;(109):85-96.
AOMSI is a biomechanical analysis. It�s all about numbers that have clinical meaning and significance. Threshold values have been determined that quantify without a doubt the patient has serious injury. It is a test of structural integrity of the ligaments interconnecting the motion segments. In this case, structural integrity has to do with the material properties of ligament tissue. Those properties include strength and flexibility. When a material is both strong and flexible, it�s called a semi-rigid material. Strength is related to the composition of the material. Strength might be thought of as load carrying capacity before failure.
Mechanism of Injury: Ligaments
Ligament tissue has previously been bench tested to describe its physical characteristics of stress/strain. That is, given so much load (stress) how much elongation will occur (strain). During normal physiologic loads the ligament remains intact and recoils to its original length when the load is removed. If the load becomes too large the materials (ligaments) begin to yield. They go past their elastic limit. When this happens the (strained) ligament fibers will not return to their original shape. The ligament loses its restraining capacity to hold the joint in normal stabilization and hypermobility occurs.
The ligaments, if sufficiently strained or avulsed results in AOMSI. The following paragraphs illustrates that if AOMSI is found there must be gross destruction or yielding of multiple ligaments. We need to build a BIG motion segment with Velcro ligaments. When you tear them off, they make a really nice ripping noise. That drives home the point.
In the White et al work, they found that the motion segment stayed intact i.e., less than 11 degrees� rotation (angualr mtion) and less than 3.5 mm translation, until they transected over 50% of the ligaments from an anterior or posterior approach. And when they transected from either approach the loss of stability was not linear but suddenly catastrophic. And they meant that suddenly the two vertebra totally separated in rotation or translation.
Suddenly Separated: pulled apart, head off of body, all neural components compromised, paralysis. Keeping that in mind, what are the injuries of someone just under the threshold? Severe to very severe. They stand the possibility of a serious event with much less force.
Prevalence of Ligament Injury: AOMSI
If AOMSI is detected, think about more than 50% of ligaments transected. That will start to explain the seriousness of the finding. In a patient/child that demonstrates hypermobility everywhere, then you take a statistical average of all segments, and look at the aberrant statistical finding if it exists. There are clues to injury everywhere when you understand what the numbers mean in reference to stability and function.
To diagnose ligament laxity, it is imperative that imaging be performed and a basic flexion-extension x-ray is all that is required. In today�s medical economy, advanced imaging of MRI or CT Scan, although accurate becomes an unnecessary expenditure and an x-ray renders very accurate demonstrative images to conclude a definitive diagnosis. In determining if there is an impairment, it is necessary to follow the AMA Guides to the Evaluation of Permanent Impairment as the 4th, 5th and 6th editions all render an impairment for AOMSI as sequella to ligament laxity, which is damage to the ligament from trauma.
This document is intended to serve as a simple explanation as to the severity of ligament damage and how to demonstrably diagnose the injury. It is also critical to remember that ligament do �wound repair.� In normal physiology, ligaments grow during puberty from cells within the ligaments called fibroblasts. They produce both collagen (white) and elastin (yellow) tissue, which gives the ligaments both tensile and elastic strength. Upon puberty the cells stop producing tissue and remains dormant. Upon injury, the fibroblast reactivates, but can only produce collage leaving the joint wound repaired in an aberrant juxtaposition (place) with poor movement abilities due to the lack of the requisite elastin. In turn, according to Hauser et. Al (2013) this leads to permanent loss of function of the ligament and arthritis of the joint. This is not a speculative statement; it is based upon Wolff�s that dates back to the late 1800�s and has been a guiding principle in healthcare for more than a century.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
References:
White, et al., Clin Ortho Relat Res, 1975;(109):85-96
Hauser, Dolan,Phillips, Newlin, Moore Woldin, B.A.(2013) Ligament injury and healing: A review of current clinical diagnostics and therapeutics.The Open Rehabilitation Journal, 6,1-20.
Additional Topics: Weakened Ligaments After Whiplash
Whiplash is a commonly reported injury after an individual has been involved in an automobile accident. During an auto accident, the sheer force of the impact often causes the head and neck of the victim to jerk abruptly, back-and-forth, causing damage to the complex structures surrounding the cervical spine. Chiropractic care is a safe and effective, alternative treatment option utilized to help decrease the symptoms of whiplash.
According to the American Academy of Orthopedic Surgery �The most common soft tissues injured are muscles, tendons, and ligaments.
Acute injuries are caused by a sudden trauma, such as a fall, twist, or blow to the body. Examples of an acute injury include sprains, strains, and contusions.�� (orthoinfo.aaos.org/topic.cfm?topic=A00111) We must also not forget that there are other soft tissues that can get injured and the true definition of soft tissue, which is anything not bone is soft tissue.
This includes the brain, lungs, heart and any other organ in the body. However, in medicine soft tissue injuries are commonly known to be limited to the muscles, ligaments and tendons.
Soft Tissue Injury Classification
When we look at the type of structures that muscles, tendons and ligament are composed of, we will realize that they are connective tissue. According to the National Institute of Health �Connective tissue is the material inside your body that supports many of its parts. It is the “cellular glue” that gives your tissues their shape and helps keep them strong. It also helps some of your tissues do their work (www.nlm.nih.gov/medlineplus/connectivetissuedisorders.html). Unlike fracture repair where the bone is replaced and usually heals properly if aligned and rested, connective tissue disorders undergo a different type of wound repair that has aberrant tissue replacement as sequella to bodily injury and has subsequent abnormal permanent function.
If we focus on sprains or ligamentous injuries, according to the American Academy of Orthopedic Surgery there are three types of sprains:
Sprains are classified by severity:1
Grade 1 sprain (mild):�Slight stretching and some damage to the fibers (fibrils) of the ligament.
Grade 2 sprain (moderate):�Partial tearing of the ligament. There is abnormal looseness (laxity) in the joint when it is moved in certain ways.
Grade 3 sprain (severe):�Complete tear of the ligament. This causes significant instability and makes the joint nonfunctional.
Regardless of the severity of the sprain, there is tissue damage or bodily injury and the next step is to determine if there is healing or wound repair. According to Woo, Hildebrand, Watanabe, Fenwick, Papageorgiou and Wang (1999) ��as a result the combination of cell therapy with growth factor therapy may offer new avenues to improve the healing of ligament and tendon. Of course, specific recommendations regarding growth factor selection, and timing and method of application cannot be made at this time.
Previous attempts at determining optimal doses of growth factors have provided contradictory results. Although growth factor treatment has been shown to improve the properties of healing ligaments and tendons, these properties do not reach the level of the uninjured tissue.� (p. s320)
�No treatment currently exists to restore an injured tendon or ligament to its normal condition.�, stated Dozer and Dupree (2005). (pg. 231).
Soft Tissue Recovery Process
According to Hauser, Dolan, Phillips, Newlin, Moore and Woldin (2013) �injured ligament structure is replaced with tissue that is grossly, histologically, biochemically and biomechanically similar to scar tissue. Fully remodeled scar tissue remains grossly, microscopically and functionally different from normal tissues� (p. 6) �the persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue.
Since remodel ligament tissue is morphologically and mechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joints and predisposing other soft tissues in and around the joints further damage.� (p.7) �studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that didn�t feel, do so characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament undergo injury during a single traumatic event.� (p.8) �osteoarthritis for joint degeneration is one of the most common consequences of ligament laxity.
Traditionally, the pathophysiology of osteoarthritis was thought to be due of aging and wear and tear on the joint, but more recent studies have shown that ligaments play a critical role in the development of osteoarthritis. Osteoarthritis begins when one or more of ligaments become unstable or lax, and the bones began to track improperly and put pressure on different areas, resulting in the rubbing the bone on cartilage. This causes breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joints mechanics. Hypomobility and ligament laxity have become clear risk factors for the prevalence of osteoarthritis.� (p.9)
Looking globally at the research over the last 16 years, in 1999 it was concluded that the most current treatments to repair or heal the injured ligament do not reach the level of the uninjured tissue. In in 2005 it was concluded that no treatment currently exists to restore an injured tendons or ligaments to its normal condition. In addition the current standard of ligament research in 2013 concluded that that ligaments do not feel independently, but damage ligaments are a direct cause of osteoarthritis and biomechanical dysfunction (abnormality of joint mechanics). The latest research has also concluded that ligament damage or sprains is the key element in osteoarthritis and not simply aging or wear and tear on the joint.
As a result it is now clear based upon the scientific evidence that a soft tissue injury is a connective tissue disorder that has permanent negative sequela and is the cause of future arthritis. This is no longer a debatable issue and those in the medical legal forum who are still arguing �transient soft tissue injuries� are simply rendering rhetoric out of ignorance and a possible ulterior motive because the facts clearly delineate the negative sequella based upon decades of multiple scientific conclusions.
The caveat to this argument is that although there is irrefutable bodily injury with clear permanent sequella, does it also cause permanent functional loss in every scenario? Those are two separate issues and as a result of the function of ligaments, which is to connect bones to bones the arbiter for normal vs. abnormal function is ranges of motion of the joint. That can be accomplished by either a two-piece inclinometer for the spine, which according to the American Medical Association Guides to the Evaluation of Permanent Impairment, 5th Edition (p. 400) is the standard (and is still the medical standard as the 6th Edition refers to the 5th for Ranges of motion).
The other diagnostic demonstrable evidence to conclude aberrant function is to conclude laxity of ligaments through x-ray digitizing. Both diagnostic tools confirm demonstrably loss of function of the spinal joints. ��
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
Woo S, Hildebrand K., Watanabe N., Fenwick J., Papageorgiou C., Wang J. (1999) Tissue Engineering of Ligament and Tendon Healing, Clinical Orthopedics and Related Research 367S pgs. S312-S323
Tozer S., Duprez D. (2005) Tendon and Ligament: Development, Repair and Disease, Birth Defects Research (part C) 75:226-236
Hauser R., Dolan E., Phillips H., Newlin A., Moore R. and B. Woldin (2013) �Ligament Injury and Healing: A Review of Current Clinical Diagnostics and Therapeutics, The Open Rehabilitation Journal (6) 1-20
Cocchiarella L., Anderson G., (2001) Guides to the Evaluation of Permanent Impairment, 5th Edition, Chicago IL, AMA Press
Additional Topics: Preventing Spinal Degeneration
Spinal degeneration can occur naturally over time as a result of age and the constant wear-and-tear of the vertebrae and other complex structures of the spine, generally developing in people over the ages of 40. On occasion, spinal degeneration can also occur due to spinal damage or injury, which may result in further complications if left untreated. Chiropractic care can help strengthen the structures of the spine, helping to prevent spinal degeneration.
According to the National Institute of Health�s, National Institute of Arthritis and Musculoskeletal and Skin Disorders:
A sprain is an injury to a ligament (tissue that connects two or more bones at a joint). In a sprain, one or more ligaments is stretched or torn. A strain is an injury to a muscle or a tendon (tissue that connects muscle to bone). In a strain, a muscle or tendon is stretched or torn.
Historically, doctors of all disciplines in the clinical setting and lawyers in the medical-legal arena have erroneously attempted to separate them into 2 distinct injuries allowing a false conclusion to be derived in either prognosis or legal arguments when considering connective tissue pathology as sequella to trauma.
Anatomy of Sprains and Strains
Solomonow (2009) wrote:
There are several ligaments in every joint in the human skeleton and they are considered as the primary restraints of the bones constituting the joint. Ligaments are also sensory organs and have significant input to sensation and reflexive/synergistic activation of muscles. The muscles associated with any given joint, therefore, also have a significant role as restraints. In some joints, such as the intervertebral joints of the spine, the role of the muscles as restraints is amplified. The role of ligaments as joint restraints is rather complex when considering the multitude of physical activities performed by individuals in routine daily functions, work and sports, the complexity of the anatomy of the different joints and the wide range of magnitude and velocity of the external loads. As joints go through their range of motion, with or without external load, the ligaments ensure that the bones associated with the joint travel in their prescribed anatomical tracks, keep full and even contact pressure of the articular surfaces, prevent separation of the bones from each other by increasing their tension, as may be necessary, and ensuring stable motion. Joint stability, therefore, is the general role of ligaments without which the joint may subluxate, cause damage to the capsule, cartilage, tendons, nearby nerves and blood vessels, discs (if considering spinal joints) and to the ligaments themselves. Such injury may debilitate the individual by preventing or limiting his/her use of the joint and the loss of function. Pgs. 136-137
While ligaments are primarily known as mechanical or supportive structures responsible for joint stability, they have equally important neurological functions. Anatomical studies have shown that ligaments in the extremities and the spine are endowed with nerves called mechanoreceptors. The presence of such that sense and send neurological information to the spine and brain in the ligaments confirms that they contribute to proprioception (feeling and analyzes one�s physical positon in space and time) and kinesthesia (similar to proprioception but can maintain feeling in these nerves even with aberrant neurological imput elsewhere) and also has a distinct role in reflex activation or inhibition of muscular activities.
Simply put, the nerves in ligaments attempts to alter muscle activity to prevent further biomechanical failure and pathology (bodily injury), which effects one�s ability to move in a balanced homeostatic manner leading to further functional loss in a short amount of time. The presence of such nerves in the ligaments confirms that they contribute to proprioception and kinesthesia and have a distinct role in reflex activation or inhibition of muscular activities. Therefore, the muscles and tendons (which are inherent in muscular activity), are responsive and dependent upon ligament activity in function with both normal and pathological (inclusive of trauma) activities.
Solomonow (2009) also reported that as far back as the turn of the last century, that a reflex may exist from sensory receptors in the ligaments to muscles that may directly or indirectly modify the load imposed on the ligament. A clear demonstration of a reflex activation of muscles finally provided in 1987 and reconfirmed several times since then. It was further shown that such a ligamento-muscular reflex exists in most extremity joints and in the spine.
Mechanism of Injury
A Single trauma according to Panjabi (2006) can cause either a tear in the ligament called laxity or a subfailure injury of the spinal ligaments and injury to the mechanoreceptors embedded in the ligaments and the following cascade of events occur: pgs. 669-670
NOTE: The subfailure injury of the spinal ligament is defined as an injury caused by stretching of the tissue beyond its physiological limit, but less than its failure point.
When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors are corrupted.
Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.
The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors, further corrupting the muscle response pattern.
The corrupted muscle response pattern produces high stresses and strains in spinal components leading to further subfailure injury of the spinal ligaments, mechanoreceptors and muscles, and overload of facet joints.
The abnormal stresses and strains produce inflammation of spinal tissues, which have abundant supply of nociceptive sensors and neural structures.
Consequently, over time, chronic biomechanical failure develops leading to premature degeneration and long-term pain.
Simply explained, when there is a ligament injury or sprain, the nerves in the ligament fire signals that go to the central nervous system and causes the muscles to react as compensation to bodily injury to stabilize the structure. That in turn sets up another cascade of problems if not compensated for or repaired as the muscle spasticity cannot maintain itself for long periods of time and goes into a posture of tetanus, or perpetual spasm until the lactic acid builds. This is followed by the muscle failing and putting the entire structure in a chronic biomechanically unstable position and causing the bone to remodel or become arthritic.
According to Hauser ET. Al (2013) ligament instability in either subfailures or laxity are a clear cause of osteoarthritis. This is not speculative as the inured will develop arthritis in 100% of the time and is consistent with Wolff�s Law that has been, and continues to be accepted since the late 18th century.
Therefore, as per the above scenario, strain-sprain is an intertwined syndrome that cannot either mechanically or neurologically be separated and will cause arthritis in 100% of the post-trauma instance. How much arthritis and how quickly it will develop is dependent upon how much ligamentous damage there is.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
Solomonow, M. (2009). Ligaments: a source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
Panjabi, M. M. (2006). A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.
Hauser R., Dolan E., Phillips H., Newlin A., Moore R., Woldin B., Ligament & Healing Injuries: A Review of Current Clinical Diagnostics and Therapeutics, The Open Rehabilitation Journal, 2013, 6, 1-20
Additional Topics: Preventing Spinal Degeneration
Spinal degeneration can occur naturally over time as a result of age and the constant wear-and-tear of the vertebrae and other complex structures of the spine, generally developing in people over the ages of 40. On occasion, spinal degeneration can also occur due to spinal damage or injury, which may result in further complications if left untreated. Chiropractic care can help strengthen the structures of the spine, helping to prevent spinal degeneration.
Thomas M Kosloff1*�, David Elton1�, Jiang Tao2� and Wade M Bannister2�
CHIROPRACTIC & MANUAL THERAPIES
Abstract
Background: There is controversy surrounding the risk of manipulation, which is often used by chiropractors, with respect to its association with vertebrobasilar artery system (VBA) stroke. The objective of this study was to compare the associations between chiropractic care and VBA stroke with recent primary care physician (PCP) care and VBA stroke.
Methods: The study design was a case�control study of commercially insured and Medicare Advantage (MA) health plan members in the U.S. population between January 1, 2011 and December 31, 2013. Administrative data were used to identify exposures to chiropractic and PCP care. Separate analyses using conditional logistic regression were conducted for the commercially insured and the MA populations. The analysis of the commercial population was further stratified by age (<45 years; ?45 years). Odds ratios were calculated to measure associations for different hazard periods. A secondary descriptive analysis was conducted to determine the relevance of using chiropractic visits as a proxy for exposure to manipulative treatment.
Results: There were a total of 1,829 VBA stroke cases (1,159 � commercial; 670 � MA). The findings showed no significant association between chiropractic visits and VBA stroke for either population or for samples stratified by age. In both commercial and MA populations, there was a significant association between PCP visits and VBA stroke incidence regardless of length of hazard period. The results were similar for age-stratified samples. The findings of the secondary analysis showed that chiropractic visits did not report the inclusion of manipulation in almost one third of stroke cases in the commercial population and in only 1 of 2 cases of the MA cohort.
Conclusions: We found no significant association between exposure to chiropractic care and the risk of VBA stroke. We conclude that manipulation is an unlikely cause of VBA stroke. The positive association between PCP visits and VBA stroke is most likely due to patient decisions to seek care for the symptoms (headache and neck pain) of arterial dissection. We further conclude that using chiropractic visits as a measure of exposure to manipulation may result in unreliable estimates of the strength of association with the occurrence of VBA stroke.
Keywords: Chiropractic, Primary care, Cervical manipulation, Vertebrobasilar stroke, Adverse events
Background
The burden of neck pain and headache or migraine among adults in the United States is significant. Survey data indicate 13% of adults reported neck pain in the past 3 months [1]. In any given year, neck pain affects 30% to 50% of adults in the general population [2]. Prevalence rates were reportedly greater in more eco- nomically advantaged countries, such as the USA, with a higher incidence of neck pain noted in office and com- puter workers [3]. Similar to neck pain, the prevalence of headache is substantial. During any 3-month time- frame, severe headaches or migraines reportedly affect one in eight adults [1].
Neck pain is a very common reason for seeking health care services. �In 2004, 16.4 million patient visits or 1.5% of all health care visits to hospitals and physician offices, were for neck pain� [4]. Eighty percent (80%) of visits occurred as outpatient care in a physician�s office [4]. The utilization of health care resources for the treatment of headache is also significant. �In 2006, adults made nearly 11 million physician visits with a headache diagno- sis, over 1 million outpatient hospital visits, 3.3 million emergency department visits, and 445 thousand inpatient hospitalizations� [1].
In the United States, chiropractic care is frequently utilized by individuals with neck and/or headache com- plaints. A national survey of chiropractors in 2003 re- ported that neck conditions and headache/facial pain accounted respectively for 18.7% and 12% of the patient chief complaints [5]. Chiropractors routinely employ spinal manipulative treatment (SMT) in the management of patients presenting with neck and/or headache [6], either alone or combined with other treatment approaches [7-10].
While evidence syntheses suggest the benefits of SMT for neck pain [7-9,11-13] and various types of headaches [10,12,14-16], the potential for rare but serious adverse events (AE) following cervical SMT is a concern for researchers [17,18], practitioners [19,20], professional organizations [21-23], policymakers [24,25] and the public [26,27]. In particular, the occurrence of stroke affecting the vertebrobasilar artery system (VBA stroke) has been associated with cervical manipulation. A recent publication [28] assessing the safety of chiropractic care reported, �…the frequency of serious adverse events varied between 5 strokes/ 100,000 manipulations to 1.46 serious adverse events/ 10,000,000 manipulations and 2.68 deaths/10,000,000 manipulations�. These estimates were, however, derived from retrospective anecdotal reports and liability claims data, and do not permit confident conclusions about the actual frequency of neurological complications following spinal manipulation.
Several systematic reviews investigating the association between stroke and chiropractic cervical manipulation�have reported the data are insufficient to produce definitive conclusions about its safety [28-31]. Two case�control studies [32,33] used visits to a chiropractor as a proxy for SMT in their analyses of standardized health system databases for the population of Ontario (Canada). The more recent of these studies [32] also included a case-crossover methodology, which reduced the risk of bias from confounding variables. Both case�control studies reported an increased risk of VBA stroke in association with chiropractic visits for the population under age 45 years old. Cassidy, et al. [32] found, how- ever, the association was similar to visits to a primary care physician (PCP). Consequently, the results of this study suggested the association between chiropractic care and stroke was non-causal. In contrast to these studies, which found a significant association between chiropractic visits and VBA stroke in younger patients (<45 yrs.), the analysis of a population-based case-series suggested that VBA stroke patients who consulted a chiropractor the year before their stroke were older (mean age 57.6 yrs.) than previously documented [34].
The work by Cassidy, et al. [32] has been qualitatively appraised as one of the most robustly designed investigations of the association between chiropractic manipulative treatment and VBA stroke [31]. To the best of our knowledge, this work has not been reproduced in the U.S. population. Thus, the main purpose of this study is to replicate the case�control epidemiological design published by Cassidy, et al. [32] to investigate the association between chiropractic care and VBA stroke; and compare it to the association between recent PCP care and VBA stroke in samples of the U.S. commercial and Medicare Advantage (MA) populations. A secondary aim of this study is to assess the utility of employing chiropractic visits as a proxy measure for exposure to spinal manipulation.
Methods
Study design and population
We developed a case�control study based on the experience of commercially insured and MA health plan members between January 1, 2011 and December 31, 2013. General criteria for membership in a commercial or MA health plan included either residing or working in a region where health care coverage was offered by the in- surer. Individuals must have Medicare Part A and Part B to join a MA plan. The data set included health plan members located in 49 of 50 states. North Dakota was the only State not represented.
Both case and control data were extracted from the same source population, which encompassed national health plan data for 35,726,224 unique commercial and 3,188,825 unique MA members. Since members might be enrolled for more than one year, the average�annual commercial membership was 14.7 million members and the average annual MA membership was 1.4 million members over the three year study period, which is comparable to ~5% of the total US population based on the data available from US Census Bureau [35]. Administrative claims data were used to identify cases, as well as patient characteristics and health service utilization.
The stroke cases included all patients admitted to an acute care hospital with vertebrobasilar (VBA) occlusion and stenosis strokes as defined by ICD-9 codes of 433.0, 433.01, 433.20, and 433.21 during the study period. Pa- tients with more than one admission for a VBA stroke were excluded from the study. For each stroke case, four age and gender matched controls were randomly se- lected from sampled qualified members. Both cases and controls were randomly sorted prior to the matching using a greedy matching algorithm [36].
Exposures
The index date was defined as the date of admission for the VBA stroke. Any encounters with a chiropractor or a primary care physician (PCP) prior to the index date were considered as exposures. To evaluate the impact of chiropractic and PCP treatment, the designated hazard period in this study was zero to 30 days prior to the index date. For the PCP analysis, the index date was excluded from the hazard period since patients might consult PCPs after having a stroke. The standard health plan coverage included a limit of 20 chiropractic visits. In rare circumstances a small employer may have selected a 12-visit limit. An internal analysis (data not shown) revealed that 5% of the combined (commercial and MA) populations reached their chiropractic visit limits. Instances of an employer not covering chiropractic care were estimated to be so rare that it would have had no measurable impact on the analysis. There were no limits on the number of reimbursed PCP visits per year.
Analyses
Two sets of similar analyses were performed, one for the commercially insured population and one for the MA population. In each set of analyses, conditional logistic regression models were used to examine the association between the exposures and VBA strokes. To measure the association, we estimated the odds ratio of having the VBA stroke and the effect of total number of chiropractic visits and PCP visits within the hazard period. The analyses were applied to different hazard periods, including one day, three days, seven days, 14 days and 30 days for both chiropractic and PCP visits. The results of the chiropractic and PCP visit analyses were then compared to find evidence of excess risk of having stroke for patients with chiropractic visits during the
hazard period. Previous research has indicated that most patients who experience a vertebral artery dissection are under the age of 45. Therefore, in order to investigate the impact of exposure on the population at different ages, separate analyses were performed on patients stratified by age (under 45 years and 45 years and up) for the study of the commercial population. The number of visits within the hazard period was entered as a con- tinuous variable in the logistic model. The chi square test was used to analyze the proportion of co-morbidities in cases as compared to controls.
A secondary analysis was performed to evaluate the relevance of using chiropractic visits as a proxy for spinal manipulation. The commercial and MA databases were queried to identify the proportions of cases of VBA stroke and matched controls for which at least one chiropractic spinal manipulative treatment procedural code (CPT 98940 � 98942) was or was not recorded. The analysis also calculated the use of another manual therapy code (CPT 97140), which may be employed by chiropractors as an alternative means of reporting spinal manipulation.
Ethics
The New England Institutional Review Board (NEIRB) determined that this study was exempt from ethics review.
Results
The commercial study sample included 1,159 VBA stroke cases over the three year period and 4,633 age and gender matched controls. The average age of the patients was 65.1 years and 64.8% of the patients were male (Table 1). The prevalence rate of VBA stroke in the commercial population was 0.0032%.
There were a total of 670 stroke cases and 2,680 matched controls included in the MA study. The aver- age patient age was 76.1 years and 58.6% of the patients were male (Table 2). For the MA population, the prevalence rate of VBA stroke was 0.021%.
Claims during a one year period prior to the index date were extracted to identify comorbid disorders. Both the commercial and MA cases had a high percentage of comorbidities, with 71.5% of cases in the commercial study and 88.5% of the cases in the MA study reporting at least one of the comorbid conditions (Table 3). Six comorbid conditions of particular interest were identified, including hypertensive disease (ICD-9 401�404), ischemic�heart disease (ICD-9 410�414), disease of pulmonary circulation (ICD-9 415�417), other forms of heart disease (ICD-9 420�429), pure hypercholesterolemia (ICD-9 272.0) and diseases of other endocrine glands (ICD-9 249�250). There were statistically significant differences (p = <0.05) between groups for most comorbidities. Greater proportions of comorbid disorders (p = <0.0001) were reported in the commercial and MA cases for hyper- tensive disease, heart disease and endocrine disorders (Table 3). The commercial cases also showed a larger proportion of diseases of pulmonary circulation, which was statistically significant (p = 0.0008). There were no significance differences in pure hypercholesterolemia for either the commercial or MA populations. Overall, cases in both the commercial and MA populations were more likely (p = <0.0001) to have at least one co- morbid condition.
Among the commercially insured, 1.6% of stroke cases had visited chiropractors within 30 days of being admit- ted to the hospital, as compared to 1.3% of controls visit- ing chiropractors within 30 days prior to their index date. Of the stroke cases, 18.9% had visited a PCP within 30 days prior to their index date, while only 6.8% of controls had visited a PCP (Table 4). The proportion of exposures for chiropractic visits was lower in the MA sample within the 30-day hazard period (cases = 0.3%; controls = 0.9%). However, the proportion of exposures for PCP visits was higher, with 21.3% of cases having PCP visits as compared to12.9% for controls (Table 5).
The results from the analyses of both the commercial population and the MA population were similar (Tables 6, 7 and 8). There was no association between chiropractic visits and VBA stroke found for the�overall sample, or for samples stratified by age. No estimated odds ratio was significant at the 95% confidence level. MA data were insufficient to calculate statistical measures of association for hazard periods less than 0�14 days for chiropractic visits. When stratified by age, the data were too sparse to calculate measures of association for hazard periods less than 0�30 days in the commercial population. The data were too few to analyze associative risk by headache and/or neck pain diagnoses (data not shown).
These results showed there is an association existing between PCP visits and VBA stroke incidence regardless of age or length of hazard period. A strong association was found for those visits close to the index date (OR 11.56; 95% CI 6.32-21.21) for all patients with a PCP visit within 0�1 day hazard period in the commercial sample. There was an increased risk of VBA stroke associated with each PCP visit within 30-days prior to the index date for MA patients (OR 1.51; 95% CI 1.32-1.73) and commercial patients (OR 2.01; 95% CI 1.77-2.29).
The findings of the secondary analysis showed � that of 1159 stroke cases from commercial population � there were a total of 19 stroke cases associated with chiropractic visits for which 13 (68%) had claims documentation indicating chiropractic SMT was performed. For the control group of the commercial cohort, 62 of 4633 controls had claims of any kind of chiropractic visits and 47 of 4633 controls had claims of SMT. In the commercial control group, 47 of 62 DC visits (76%) included SMT in the claims data. Only 1 of 2 stroke cases in the MA population included SMT in the claims data. For the MA cohort, 21 of 24 control chiropractic visits (88%) included SMT in the claims data (Table 9).
None of the stroke cases in either population included CPT 97140 as a substitute for the more conventionally re- ported chiropractic manipulative treatment procedural codes (98940 � 98942). For the control groups, there were three instances where CPT 97140 was reported without CPT 98940 � 98942 in the commercial population. The CPT code 97140 was not reported in MA control cohort.
Discussion
The primary aim of the present study was to investigate the association between chiropractic manipulative treatment and VBA stroke in a sample of the U.S. population. This study was modeled after a case�control design previously conducted for a Canadian population [32]. Administrative data for enrollees in a large national health care insurer were analyzed to explore the occurrence of VBA stroke across different time periods of exposure to chiropractic care in comparison with PCP care.
Unlike Cassidy et al. [32] and most other case�control studies [33,37,38], our results showed there was no significant association between VBA stroke and chiropractic visits. This was the case for both the commercial and MA populations. In contrast to two earlier case�control studies [32,33], this lack of association was found to be irrespective of age. Although, our results (Table 8) did lend credence to previous reports that VBA stroke occurs more frequently in patients under the age of 45 years. Additionally, the results from the present study did not identify a relevant temporal impact. There was no significant association, when the data were sufficient to calculate estimates, between chiropractic visits and stroke regardless of the hazard period (timing of most recent visit to a chiropractor and the occurrence of stroke).
There are several possible reasons for the variation in results with previous similar case�control studies. The younger (<45 yrs.) commercial cohort that received chiropractic care in our study had noticeably fewer cases. The 0�30 days hazard period included only 2 VBA stroke cases. There were no stroke cases for other hazard periods in this population. In contrast, earlier studies reported sufficient cases to calculate risk estimates for most hazard periods [32,33].
Another factor that potentially influenced the difference in results concerns the accuracy of hospital claims data in the U.S. vs. Ontario, Canada. The source population in the Province of Ontario was identified, in part, from the Discharge Abstract Database (DAD). The DAD includes hospital discharge and emergency visit diagnoses that have undergone a standardized assessment by a medical records coder [39]. To the best of our know- ledge, similar quality management practices were not routinely applied to hospital claims data used in sourcing the population for our study.
An additional reason for the disparity in results may be due to differences in the proportions of chiropractic visits where SMT was reportedly performed. Our study showed that SMT was not reported by chiropractors in more than 30% of commercial cases. It is plausible that a number of the cases in earlier studies also did not�include SMT as an intervention. Differences between studies in the proportion of cases reporting SMT may have affected the calculation of risk estimates.
Also, there were an insufficient number of cases having cervical and/or headache diagnoses in our study. Therefore, our sample population may have included proportionally less cases where cervical manipulation was performed.
Our results were consistent with previous findings [32,33] in showing a significant association between PCP visits and VBA stroke. The odds ratios for any PCP visit increase dramatically from 1�30 days to 1�1 day (Tables 6 and 7). This finding is consistent with the hypothesis that patients are more likely to see a PCP for symptoms related to vertebral artery dissection closer to the index date of their actual stroke. Since it is unlikely that the services provided by PCPs cause VBA strokes, the association�between recent PCP visits and VBA stroke is more likely attributable to the background risk related to the natural history of the condition [32].
A secondary goal of our study was to assess the utility of employing chiropractic visits as a surrogate for SMT. Our findings indicate there is a high risk of bias associated with using this approach, which likely overestimated the strength of association. Less than 70% of stroke cases (commercial and MA) associated with chiropractic care included SMT. A somewhat higher proportion of chiropractic visits included SMT for the control groups (commercial = 76%; MA = 88%).
There are plausible reasons that support these findings. Internal analyses of claims data (not shown) consistently demonstrate that one visit is the most common number associated with a chiropractic episode of care. The single visit may consist of an evaluation without treatment such as SMT. Further; SMT may have been viewed as contraindicated due to signs and symptoms of vertebral artery dissection (VAD) and/or stroke. This might explain the greater proportion of SMT provided to control groups in both the commercial and MA populations.
Overall, our results increase confidence in the findings of a previous study [32], which concluded there was no excess risk of VBA stroke associated chiropractic care compared to primary care. Further, our results indicate there is no significant risk of VBA stroke associated with chiropractic care. Additionally, our findings highlight the potential flaws in using a surrogate variable (chiropractic visits) to estimate the risk of VBA stroke in association with a specific intervention (manipulation).
Our study had a number of strengths and limitations. Both case and control data were extracted from the same source population, which encompassed national health plan data for approximately 36 million�commercial and 3 million MA members. A total of 1,829 cases were identified, making this the largest case� control study to investigate the association between chiropractic manipulation and VBA stroke. Due to the nationwide setting and large sample size, our study likely reduced the risk of bias related to geographic factors. However, there was a risk of selection bias � owing to the data set being from a single health insurer � including income status, workforce participation, and links to health care providers and hospitals.
Our study closely followed a methodological approach that had previously been described [32], thus allowing for more confident comparisons.
The current investigation analyzed data for a number of comorbid conditions that have been identified as potentially modifiable risk factors for a first ischemic stroke [40]. The differences between groups were statistically significant for most comorbidities. Information was not obtainable about behavioral comorbid factors e.g., smoking and body mass. With the exception of hypertensive disease, there are reasons to question the clinical significance of these conditions in the occurrence of ischemic stroke due to vertebral artery dissection. A large multinational case-referent study investigated the association between vascular risk factors (history of vascular disease, hypertension, smoking, hypercholesterolemia, diabetes mellitus, and obesity/overweight) for ischemic stroke and the occurrence of cervical artery dissection [41]. Only hypertension had a positive association (odds ratio 1.67; 95% confidence interval, 1.32 to 2.1; P <0.0001) with cervical artery dissection.
While the effect of other unmeasured confounders cannot be discounted, there is reason to suspect the absence of these data was not deleterious to the results. Cassidy, et al. found no significant differences in the results their case-crossover design, which affords better control of unknown confounding variables, and the findings of their case�control study [32].
Our results highlight just how unusual VBA stroke is in the MA cohort (prevalence = 0.021%) and � even more so � for the commercial population (prevalence = 0.0032%). As a result, some limitations of this study re- lated to the rarity of reporting VBA stroke events. Despite the larger number of cases, data were insufficient to calculate estimates and confidence intervals for seven measures of exposure (4 commercial and 3 MA) for chiropractic visits. Additionally, we were not able to compute estimates specifically for headache and neck pain diagnoses due to small numbers. Confidence intervals associated with estimates tended to be wide making the results imprecise [42].
There were limitations related to the use of administrative claims data. �Disadvantages of using secondary data for research purposes include: variations in coding from hospital to hospital or from department to department, errors in coding and incomplete coding, for example in the presence of comorbidities. Random errors in coding and registration of discharge diagnoses may dilute and attenuate estimates of statistical association� [43]. The recordings of unvalidated hospital discharge diagnostic codes for stroke have been shown to be less precise when compared to chart review [44,45] and validated patient registries�[43,46]. Cassidy, et al. [32] conducted a sensitivity analysis to determine the effect of diagnostic misclassification bias. Their conclusions did not change when the effects of misclassification were assumed to be similarly distributed between chiropractic and PCP cases.
A particular limitation in using administrative claims data is the paucity of contextual information surround- ing the clinical encounters between chiropractors/PCPs and their patients. Historical elements describing the occurrence/absence of recent trauma or activities reported in case studies [47-51] as potential risk factors for VBA stroke were not available in claims data. Confidence was low concerning the ability of claims data to provide accurate and complete reporting of other health disorders, which have been described in case�control designs as being associated with the occurrence of VBA stroke e.g., migraine [52] or recent infection [53]. Symptoms and physical examination findings that would have permitted further stratification of cases were not reported in the claims data.
The reporting of clinical procedures using current pro- cedural terminology (CPT) codes presented additional shortcomings concerning the accuracy and interpretation of administrative data. One inherent constraint was the lack of anatomic specificity associated with the use of standardized procedural codes in claims data. Chiropractic manipulative treatment codes (CPT 98940 � 98942) have been formatted to describe the number of spinal regions receiving manipulation. They do not identify the particular spinal regions manipulated.
Also, treatment information describing the type(s) of manipulation was not available. When SMT was re- ported, claims data could not discriminate among the range of techniques including thrust or rotational manipulation, various non-thrust interventions e.g., mechanical instruments, soft tissue mobilizations, muscle energy techniques, manual cervical traction, etc. Many of these techniques do not incorporate the same bio- mechanical stressors associated with the type of manipulation (high velocity low amplitude) that has been investigated as a putative risk factor for VBA stroke [54-56]. It seems plausible that the utility of future VBA stroke research would benefit from explicit descriptions of the particular type of manipulation performed.
Moreover, patient responses to care � including any adverse events suggestive of vertebral artery dissection or stroke-like symptoms � were not obtainable in the data set used for the current study.
In the absence of performing comprehensive clinical chart audits, it is not possible to know from claims data what actually transpired in the clinical encounter. Further, chart notes may themselves be incomplete or otherwise fail to precisely describe the nature of interventions [57]. Therefore, manipulation codes represent surrogate
measures, albeit more direct surrogate measures, than simply using the exposure to chiropractic visits.
Our study was also limited to replication of the case� control design described by Cassidy, et al. [32]. For pragmatic reasons, we did not attempt to conduct a case-crossover design. While the addition of a case- crossover design would have provided better control of confounding variables, Cassidy, et al. [32] showed the results were similar for both the case control and case crossover studies.
The findings of this case�control study and previous retrospective research underscore the need to rethink how to better conduct future investigations. Researchers should seek to avoid the use of surrogate measures or use the least indirect measures available. Instead, the focus should be on capturing data about the types of services and not the type of health care provider.
In alignment with this approach, it is also important for investigators to access contextual data (e.g., from electronic health records), which can be enabled by qualitative data analysis computer programs [58]. The acquisition of the elements of clinical encounters � including history, diagnosis, intervention, and adverse events � can provide the infrastructure for more action- able research. Because of the rarity of VBA stroke, large data sets (e.g., registries) containing these elements will be necessary to achieve adequate statistical power for making confident conclusions.
Until research efforts produce more definitive results, health care policy and clinical practice judgments are best informed by the evidence about the effectiveness of manipulation, plausible treatment options (including non-thrust manual techniques) and individual patient values [20].
Conclusions
Our findings should be viewed in the context of the body of knowledge concerning the risk of VBA stroke. In contrast to several other case�control studies, we found no significant association between exposure to chiropractic care and the risk of VBA stroke. Our secondary analysis clearly showed that manipulation may or may not have been reported at every chiropractic visit. Therefore, the use of chiropractic visits as a proxy for manipulation may not be reliable. Our results add weight to the view that chiropractic care is an unlikely cause of VBA strokes. However, the current study does not exclude cervical manipulation as a possible cause or contributory factor in the occurrence of VBA stroke.
Authors’ Contributions
DE conceived of the study, and participated in its design and coordination. JT participated in the design of the study, performed the statistical analysis and helped to draft the manuscript. TMK participated in the design and coordination of the study, and wrote the initial draft and revisions of the manuscript. WMB participated in the coordination of the study and the statistical analysis, and helped to draft the manuscript. All authors contributed to the interpretation of the data. All authors read and approved the final manuscript.
Author Details
1Optum Health � Clinical Programs at United Health Group, 11000 Optum Circle, Eden Prairie MN 55344, USA. 2Optum Health � Clinical Analytics at United Health Group, 11000 Optum Circle, Eden Prairie MN 55344, USA.
Received: 14 October 2014 Accepted: 28 April 2015
Published Online: 16 June 2015
References
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Results Of A Population-Based Case-Control & Case-Crossover Study
J. David Cassidy, DC, PhD, DrMedSc,*�� Eleanor Boyle, PhD,* Pierre Co�te ?, DC, PhD,*��� Yaohua He, MD, PhD,* Sheilah Hogg-Johnson, PhD,�� Frank L. Silver, MD, FRCPC, and Susan J. Bondy, PhD�
SPINE Volume 33, Number 4S, pp S176 �S183 �2008, Lippincott Williams & Wilkins
Neck pain is a common problem associated with consid- erable comorbidity, disability, and cost to society.1�5 In North America, the clinical management of back pain is provided mainly by medical physicians, physi- cal therapists and chiropractors.6 Approximately 12% of American and Canadian adults seek chiropractic care annually and 80% of these visits result in spinal manipulation.7,8 When compared to those seeking medical care for back pain, Canadian chiropractic pa- tients tend to be younger and have higher socioeco- nomic status and fewer health problems.6,8 In On- tario, the average number of chiropractic visits per episode of care was 10 (median 6) in 1985 through 1991.7 Several systematic reviews and our best- evidence synthesis suggest that manual therapy can benefit neck pain, but the trials are too small to eval- uate the risk of rare complications.9 �13
Two deaths in Canada from vertebral artery dissection and stroke following chiropractic care in the 1990s attracted much media attention and a call by some neurologists to avoid neck manipulation for acute neck pain.14 There have been many published case reports linking neck manipulation to vertebral artery dissection15�and stroke.�The prevailing theory is that extension�and/or rotation of the neck can damage the vertebral artery, particularly within the foramen transversarium at the C1�C2 level. Activities leading to sudden or sustained rotation and extension of the neck have been implicated, included motor vehicle collision, shoulder checking while driving, sports, lifting, working over- head, falls, sneezing, and coughing.16 However, most cases of extracranial vertebral arterial dissection are thought to occur spontaneously, and other factors such as connective tissue disorders, migraine, hyper- tension, infection, levels of plasma homocysteine, vessel abnormalities, atherosclerosis, central venous�catherization, cervical spine surgery, cervical percutaneous nerve blocks, radiation therapy and diagnostic cerebral angiography have been identified as possible risk factors.17�21
The true incidence of vertebrobasilar dissection is un- known, since many cases are probably asymptomatic, or the dissection produces mild symptoms.22 Confirming the diagnosis requires a high index of suspicion and good vascular imaging. The cases that are most likely to be diagnosed are those that result in stroke.19,22 Ischemic stroke occurs when a thrombus develops intraluminally and embolizes to more distal arteries, or less commonly, when the dissection extends distally into the intracranial vertebral artery, obliterating branching vessels.22 The best incidence estimate comes from Olmstead county, where vertebral artery dissection causing stroke affected 0.97 residents per 100,000 population between 1987 and 2003.23
To date there have been two case-control studies of stroke following neck manipulation. Rothwell et al used Ontario health data to compare 582 cases of VBA stroke to 2328 age and sex-matched controls.24 For those aged 45 years, cases were five times more likely than con- trols to have visited a chiropractor within 1 week of VBA stroke. Smith et al studied 51 patients with cervical ar- tery dissection and ischemic stroke or transient ischemic attack (TIA) and compared them to 100 control patients suffering from other strokes not caused by dissections.25 Cases and controls came from two academic stroke cen- ters in the United States and were matched on age and sex. They found no significant association between neck manipulation and ischemic stroke or TIA. However, a subgroup analysis showed that the 25 cases with verte- bral artery dissection were six times more likely to have consulted a chiropractor within 30 days before their stroke than the controls.
Finally, because patients with vertebrobasilar artery dissection commonly present with headache and neck pain,23 it is possible that patients seek chiropractic care for these symptoms and that the subsequent VBA stroke occurs spontaneously, implying that the associ- ation between chiropractic care and VBA stroke is not causal.23,26 Since patients also seek medical care for headache and neck pain, any association between pri- mary care physician (PCP) visits and VBA stroke could be attributed to seeking care for the symptoms of verte- bral artery dissection.
The purpose of this study is to investigate the association between chiropractic care and VBA stroke and compare it to the association between recent PCP care and VBA stroke using two epidemiological designs. Evidence that chiropractic care increases the risk of VBA stroke would be present if the measured association between chiropractic visits and VBA stroke exceeds the association between PCP visits and VBA strokes.
Study Design
We undertook population-based case-control and case- crossover studies. Both designs use the same cases. In the case- control design, we sampled independent control subjects from the same source population as the cases. In the case-crossover design, cases served as their own controls, by sampling control periods before the study exposures.27 This design is most appropriate when a brief exposure (e.g., chiropractic care) causes a transient change in risk (i.e., hazard period) of a rare-onset disease (e.g., VBA stroke). It is well suited to our research questions, since within person comparisons control for unmeasured risk factors by design, rather than by statistical modeling.28 �30 Thus the advantage over the case control design is better control of confounding.
Source Population
The source population included all residents of Ontario (109,020,875 person-years of observation over 9 years) covered by the publicly funded Ontario Health Insurance Plan (OHIP). Available utilization data included hospitalizations with diagnostic coding, and practitioner (physician and chiropractic) utilization as documented by fee-for-service billings accompanied by diagnostic coding. We used two data sources: (1) the Discharge Abstract Database (DAD) from the Canadian Institute for Health Information, which captures hospital separations and ICD codes, and (2) the OHIP Databases for services provided by physicians and chiropractors. These data- bases can be linked from April 1992 onward.
Cases
We included all incident vertebrobasilar occlusion and stenosis strokes (ICD-9433.0 and 433.2) resulting in an acute care hospital admission from April 1, 1993 to March 31, 2002. Codes were chosen in consultation with stroke experts and an epidemiologist who participated in a similar past study (SB).24 Cases that had an acute care hospital admission for any type of stroke (ICD-9433.0, 433.2, 434, 436, 433.1, 433.3, 433.8, 433.9, 430, 431, 432, and 437.1), transient cerebral ischemia (ICD- 9435) or late effects of cerebrovascular diseases (ICD-9438) before their VBA stroke admission or since April 1, 1991 were excluded. Cases residing in long-term care facilities were also excluded. The index date was defined as the hospital admission date for the VBA stroke.
Controls
For the case-control study, four age and sex-matched controls were randomly selected from the Registered Persons Database, which contains a listing of all health card numbers for Ontario. Controls were excluded if they previously had a stroke or were residing in a long-term care facility.
For the case crossover study, four control periods were randomly chosen from the year before the VBA stroke date, using a time-stratified approach.31 The year was divided into disjoint strata with 2 week periods between the strata. For the 1 month hazard period, the disjoint strata were separated by 1 month periods and the five remaining control periods were used in the analyses. We randomly sampled disjoint strata because chiropractic care is often delivered in episodes, and this strategy eliminates overlap bias and bias associated with time trends in the exposure.32
Exposures
All reimbursed ambulatory encounters with chiropractors and PCPs were extracted for the one-year period before the index date from the OHIP database. Neck-related chiropractic visits were identified using diagnostic codes: C01�C06, cervical and cervicothoracic subluxation; C13�C15, multiple site subluxation; C30, cervical sprain/strain; C40, cervical neuritis/ neuralgia; C44, arm neuritis/neuralgia; C50, brachial radiculitis; C51, cervical radiculitis; and C60, headache. For PCP visits, we included community medicine physicians if they submitted ambulatory fee codes to OHIP. Fee codes for group therapy and signing forms were excluded. Headache or neck pain- related PCP visits were identified using the diagnostic codes: ICD-9307, tension headaches; 346, migraine headaches; 722, intervertebral disc disorders; 780, headache, except tension headache and migraine; 729, fibrositis, myositis and muscular rheumatism; and 847, whiplash, sprain/strain and other traumas associated with neck (These codes include other diagnoses, and we list only those relevant to neck pain or headache). There is no limit on the number of reimbursed PCP visits per year. However, there are limits chiropractors, but less than 15% of patients surpass them.24
Statistical Analysis
Conditional logistic regression was used to estimate the asso- ciation between VBA stroke after chiropractor and PCP visits. Separate models were built using different a priori specified hazard periods, stratified by age ( 45 years and 45 years) and by visits with or without head and neck pain related diag- nostic codes. For the chiropractic analysis, the index date was included in the hazard period, since chiropractic treatment might cause immediate stroke and patients would not normally consult a chiropractor after having a stroke. However, the in- dex day was excluded from the PCP analysis, since patients might consult these physicians after experiencing a stroke. We tested different hazard periods, including 1 day, 3 days, 1 week, 2 weeks, and 1 month before the index date. Exposure occurred if any chiropractic or PCP visits were recorded during the des- ignated hazard periods.
We also measured the effect of cumulative numbers of chiropractic and PCP visits in the month before the index date by computing the odds ratio for each incremental visit. These estimates were similarly stratified by age and by diagnostic codes related to headache and/or neck pain. Finally, we conducted analyses to determine if our results were sensitive to chiropractic and PCP visits related to neck complaints and headaches. We report our results as odds ratios (OR) and 95% confidence intervals. Confidence intervals were estimated by accelerated bias corrected bootstraps with 2000 replications using the variance co-variance method.33 All statistical analyses were per- formed using STATA/SE version 9.2.34
Results
A total of 818 VBA strokes met our inclusion/exclusion criteria over the 9 year inception period. Of the 3272 matched control subjects, 31 were excluded because of prior stroke, one had died before the index date and 76 were receiving long-term care. Thus, 3164 control subjects were matched to the cases. The mean age of cases and controls was 63 years at the index date and 63% were male. Cases had a higher proportion of comorbid conditions (Table 1). Of the 818 stroke cases, 337�(41.2%) were coded as basilar occlusion and stenosis, 443 (54.2%) as vertebral occlusion and stenosis and 38 (4.7%) had both codes.
Overall, 4% of cases and controls had visited a chiropractor within 30 days of the index date, while 53% of cases and 30% of controls had visited a PCP within that time (Table 2). For those under 45 years of age, 8 cases (7.8%) had consulted a chiropractor within 7 days of the index date, compared to 14 (3.4%) of controls. For PCPs, 25 cases (24.5%) under 45 years of age had a consultation within 7 days of the index date, com- pared to 27 (6.6%) of controls. With respect to the number of visits within 1 month of the index date, 7.8% of cases under the age of 45 years had three or more chiropractic visits, whereas 5.9% had three or more PCP visits (Table 2).
The case control and case crossover analyses gave similar results. (Tables 3�7) Age modified the effect of chiropractic visits on the risk of VBA stroke. For those under 45 years of age, there was an increased association between chiropractic visits and VBA stroke regardless of the hazard period. For those 45 years of age and older, there was no association. Each chiropractic visit in the month before the index date was associated with an in- creased risk of VBA stroke in those under 45 years of age (OR 1.37; 95% CI 1.04�1.91 from the case crossover analysis) (Table 7). We were not able to estimate boot- strap confidence intervals in some cases because of sparse data.
Similarly, we found that visiting a PCP in the month before the index date was associated with an increased risk of VBA stroke regardless of the hazard period, or the age of the subject. Each PCP visit in the month before the stroke was associated with an increased risk of VBA stroke both in those under 45 years of age (OR 1.34; 95% CI 0.94 �1.87 from the case crossover analysis) and 45 years and older (OR 1.52; 95% CI 1.36�1.67 from the case crossover analysis) (Table 7).
Our results were sensitive to chiropractic and PCP visits related to neck complaints and headaches, and we observed sharp increases in the associations when restricting the analyses to these visits (Tables 3�7). Overall,�these associations were more pronounced in the PCP analyses. However, the data are sparse, and we were unable to compute bootstrap confidence intervals in many cases.
Discussion
Our study advances knowledge about the association between chiropractic care and VBA stroke in two respects. First, our case control results agree with past case control studies that found an association between chiropractic care and vertebral artery dissection and VBA stroke.24,25 Second, our case crossover results confirm these findings using a stronger research design with better control of confounding variables. The case-crossover design controls for time independent confounding factors, both known and unknown, which could affect the risk of VBA stroke. This is important since smoking, obesity, undiagnosed hypertension, some connective tis- sue disorders and other important risk factors for dissection and VBA stroke are unlikely to be recorded in ad- ministrative databases.
We also found strong associations between PCP visits and subsequent VBA stroke. A plausible explanation for this is that patients with head and neck pain due to vertebral artery dissection seek care for these symptoms, which precede more than 80% of VBA strokes.23 Since it�is unlikely that PCPs cause stroke while caring for these patients, we can assume that the observed association between recent PCP care and VBA stroke represents the background risk associated with patients seeking care for dissection-related symptoms leading to VBA stroke. Be- cause the association between chiropractic visits and VBA stroke is not greater than the association between PCP visits and VBA stroke, there is no excess risk of VBA stroke from chiropractic care.
Our study has several strengths and limitations. The study base includes an entire population over a 9-year period representing 109,020,875 person-years of observation. Despite this, we found only 818 VBA strokes, which limited our ability to compute some estimates and bootstrap confidence intervals. In particular, our age stratified analyses are based on small numbers of ex- posed cases and controls (Table 2). Further stratification by diagnostic codes for headache and neck pain related visits imposed even greater difficulty with these estimates. However, there are few databases that can link�incident VBA strokes with chiropractic and PCP visits in a large enough population to undertake a study of such a rare event.
A major limitation of using health administrative data are misclassification bias, and the possibility of bias in assignment of VBA-related diagnoses, which has previously been raised in this context.24 Liu et al have shown that ICD-9 hospital discharge codes for stroke have a poor positive predictive value when compared to chart review.35 Furthermore, not all VBA strokes are secondary to vertebral artery dissection and administrative databases do not provide the clinical detail to determine the specific cause. To investigate this bias, we did a sensitivity analysis using different positive predictive values for stroke diagnosis (ranging from 0.2 to 0.8). Assuming non differential misclassification of chiropractic and PCP cases, our analysis showed attenuation of the estimates towards the null with lower positive predictive values, but the conclusions did not change (i.e., associations remained positive and significant�data not shown). The�reliability and validity of the codes to classify headache and cervical visits to chiropractors and PCPs is not known.
It is also possible that patients presenting to hospital with neurologic symptoms who have recently seen a chiropractor might be subjected to a more vigorous diagnostic workup focused on VBA stroke (i.e., differential misclassification).36 In this case, the predictive values of the stroke codes would be greater for cases that had seen a chiropractor and our results would underestimate the association between PCP care and VBA stroke.
A major strength of our study is that exposures were measured independently of case definition and handled identically across cases and controls. However, there was some overlap between chiropractic care and PCP care. In the month before their stroke, only 16 (2.0%) of our cases had seen only a chiropractor, while 20 (2.4%) had seen both a chiropractor and PCP, and 417 (51.0%) had�just seen only a PCP. We were not able to run a subgroup analysis on the small number of cases that just saw a chiropractor. However, subgroup analysis on the PCP cases (n 782) that did not visit a chiropractors during the 1 month before their stroke did not change the conclusions (data not shown).
Our results should be interpreted cautiously and placed into clinical perspective. We have not ruled out neck manipulation as a potential cause of some VBA strokes. On the other hand, it is unlikely to be a major cause of these rare events. Our results suggest that the association between chiropractic care and VBA stroke found in previous studies is likely explained by present- ing symptoms attributable to vertebral artery dissection. It might also be possible that chiropractic manipulation, or even simple range of motion examination by any practitioner, could result in a thromboembolic event in a patient with a pre-existing vertebral dissection. Unfortunately, there is no acceptable screening procedure to identify patients with neck pain at risk of VBA stroke.37 These events are so rare and difficult to diagnose that future studies would need to be multi-centered and have unbiased ascertainment of all potential exposures. Given our current state of knowledge, the decision of how to treat patients with neck pain and/or headache should be driven by effectiveness and patient preference.38
Conclusion
Our population-based case-control and case-crossover study shows an association between chiropractic visits and VBA strokes. However, we found a similar association between primary care physician visits and VBA stroke. This suggests that patients with undiagnosed vertebral artery dissection are seeking clinical care for head- ache and neck pain before having a VBA stroke.
Acknowledgments
The authors acknowledge the members of the Decade of the Bone and Joint 2000 �2010 Task Force on Neck Pain and its Associate Disorders for advice about de- signing this study. In particular, they acknowledge the help of Drs. Hal Morgenstern, Eric Hurwitz, Scott Haldeman, Linda Carroll, Gabrielle van der Velde, Lena Holm, Paul Peloso, Margareta Nordin, Jaime Guzman, Eugene Carragee, Rachid Salmi, Alexander Grier, and Mr. Jon Schubert.
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From the *Centre of Research Expertise for Improved Disability Outcomes (CREIDO), University Health Network Rehabilitation Solutions, Toronto Western Hospital, and the Division of Heath Care and Outcomes Research, Toronto Western Research Institute, Toronto, ON, Canada; �Department of Public Health Sciences, Management and Evaluation, University of Toronto, Toronto, ON, Canada; �Department of Health Policy, Management and Evalua- tion, University of Toronto, Toronto, ON, Canada; �Institute for Work & Health, Toronto, ON, Canada; �University Health Net- work Stroke Program, Toronto Western Hospital, Toronto, ON, Canada; and Division of Neurology, Department of Medicine, Fac- ulty of Medicine, University of Toronto, Toronto, ON, Canada. Supported by Ontario Ministry of Health and Long-term Care. P.C. is supported by the Canadian Institute of Health Research through a New Investigator Award. S.H.-J. is supported by the Institute for Work & Health and the Workplace Safety and Insurance Board of Ontario. The opinions, results, and conclusions are those of the authors and no endorsement by the Ministry is intended or should be inferred.
The manuscript submitted does not contain information about medical device(s)/drug(s).
University Health Network Research Ethics Board Approval number 05-0533-AE.
Address correspondence and reprint requests to J. David Cassidy, DC, PhD, DrMedSc, Toronto Western Hospital, Fell 4-114, 399 Bathurst Street, Toronto, ON, Canada M5T 2S8; E-mail: dcassidy@uhnresearch.ca
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