Back Clinic Chronic Pain Chiropractic Physical Therapy Team. Everyone feels pain from time to time. Cutting your finger or pulling a muscle, pain is your body’s way of telling you something is wrong. The injury heals, you stop hurting.
Chronic pain works differently. The body keeps hurting weeks, months, or even years after the injury. Doctors define chronic pain as any pain that lasts for 3 to 6 months or more. Chronic pain can affect your day-to-day life and mental health. Pain comes from a series of messages that run through the nervous system. When hurt, the injury turns on pain sensors in that area. They send a message in the form of an electrical signal, which travels from nerve to nerve until it reaches the brain. The brain processes the signal and sends out the message that the body is hurt.
Under normal circumstances, the signal stops when the cause of pain is resolved, the body repairs the wound on the finger or a torn muscle. But with chronic pain, the nerve signals keep firing even after the injury is healed.
Conditions that cause chronic pain can begin without any obvious cause. But for many, it starts after an injury or because of a health condition. Some of the leading causes:
Arthritis
Back problems
Fibromyalgia, a condition in which people feel muscle pain throughout their bodies
Infections
Migraines and other headaches
Nerve damage
Past injuries or surgeries
Symptoms
The pain can range from mild to severe and can continue day after day or come and go. It can feel like:
A dull ache
Burning
Shooting
Soreness
Squeezing
Stiffness
Stinging
Throbbing
For answers to any questions you may have please call Dr. Jimenez at 915-850-0900
You try to stand up from a seated position and feel a stab of pain in your lower back. It may even shoot through your hip, buttock, or down the back of your thigh. The pain may even get worse then you walk uphill or sit for a long period of time. While these symptoms could mean a pinched nerve, lumbar disc herniation, hip bursitis, or degenerative hip disease, it could also be sacroiliac joint dysfunction.
What Is Sacroiliac Joint Dysfunction?
The sacroiliac (SI) joint is located in the pelvis. It is very strong as it is a weight bearing joint connecting the pelvis to the sacrum. It is surrounded by tough ligaments that reinforce it, providing added support.
There is an SI joint located on each side of the sacrum and they work together, moving as a single unit to act as a shock absorber for the spine and for transmitting force of the upper body. Just like any other joint in the body, the SI joint can be injured or diseased, causing it to become unstable and inflamed, causing pain and limited mobility.
What Causes SI Joint Inflammation?
While doctors have not established how the pain is generated, it is believed that it is due to a change in the normal motion of the joint. This could occur due to:
Hypermobility (Instability or Too Much Movement) � This can cause the pain to reside in the lower back. It can also be felt in the hip or both the hip and lower back and may even radiate into the groin.
Hypomobility (Fixation or Too Little Movement) � This can cause the pain to reside in the lower back or buttocks and may radiate down one leg, usually in the back of the thigh. It usually doesn�t reach the knee, but sometimes can even reach the ankle and foot. In this way, the condition mimics sciatica.
Sacroiliac joint dysfunction typically affects women who are young or middle aged. Older women and men are rarely affected although it does happen.
What Are Treatment Options For Sacroiliac Joint Pain?
When SI joint pain is initially diagnosed the treatment is usually fairly conservative. Medication, physical therapy, and injections are used by doctors for pain management.
NSAIDs and other similar medications decrease inflammation and reduce pain, while physical therapy can readjust the SI joint in cases where it is dislocated or immobilized. It also includes exercises that stabilize the joint for pain management over the long term.
Steroid injections directly into the sacroiliac joint can help with the reduction of inflammation and pain while making physical therapy more effective. When steroid injections are effective but the effects are temporary there is another non-surgical treatment that is sometimes used called RFA, or radiofrequency ablation.
In cases where the conservative methods do not achieve the desired results there are surgical options that provide pain reduction and stabilization on a more permanent scale. SI fusion involves fusing the joint, providing relief.
However, there is a treatment option that is non-invasive, doesn�t involve steroids or medications that could have harmful side effects � chiropractic.
Spinal manipulation � This is the traditional chiropractic adjustment that is also known as high-velocity, low-amplitude (HVLA) thrust.
Spinal mobilization � This is a less forceful, gentle chiropractic adjustment also known as low-velocity, low-amplitude thrust.
Chiropractic is proven to be an effective, non-invasive, gentle method for relieving the pain and inflammation of SI joint dysfunction. No medication, no surgery, just relief.
So if you�ve been suffering from sacroiliac joint dysfunction, give us a call! Our Doctor of Chiropractic is here to help!
Injury Medical Clinic: Sciatica Treatments & Recoveries
Biomarkers (short for biological markers) are biological measurements of a biological condition. By definition, a biomarker is “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes or pharmacological responses to a therapeutic intervention” Biomarkers are the measurements utilized to perform a clinical evaluation like blood pressure or cholesterol level and therefore are used to monitor and forecast health conditions in individuals or across populations so that appropriate treatment options could be proposed. Biomarkers may be used by itself or in combination to assess the health or disease state of an individual.
Variety of Biomarkers
A wide selection of biomarkers are used now. Every biological system, such as the cardiovascular system, metabolic system or the immune system, has its own specific biomarkers. Many of these biomarkers are rather easy to quantify and form part of regular medical examinations. By way of instance, a general health check may include assessment of blood pressure, heart rate, cholesterol, triglycerides and fasting glucose levels. Body dimensions such as weight, body mass index, or BMI, and waist-to-hip ratio are routinely used for assessing conditions like obesity and metabolic disorders, among others. These varieties in biomarkers can ultimately be useful in the diagnosis of a variety of health issues.
Attributes of a Perfect Biomarker
An ideal biomarker has particular characteristics that make it suitable for assessing a particular disease or condition. Ideally, an ideal marker should possess the following features, as it should be:
Safe and simple to measure
Cost effective to follow up
Modifiable with treatment
Consistent across gender and cultural groups
Biomarkers as Health and Disease Predictors
Biomarkers are used to predict significant ailments like diabetes and cardiovascular disease, among others. Each individual biomarker indicates whether there’s a disease or health condition and can be combined to offer a thorough demonstration of how healthy an individual is and whether further diagnosis needs to be made. Biomarkers ultimately serve as health and disease predictors, capable of determining a potential onset of disease or illness, such as that of cancer.
Biomarkers in Cancer Detection and Drug Development
The principles of biomarkers in disease have been applied to the discovery, screening, diagnosis, treatment and monitoring of cancer. Traditionally, anti-cancer drugs and/or medications were agents that eliminated both cancer cells and healthy cells. However, more targeted therapies have now been developed that can be instructed to kill cancer cells only, while sparing healthy cells. The evaluation of a typical biomarker in cancer will help in the development of therapies that may target the biomarker. This can minimize the risk of toxicity and reduce the cost of treatment. In cancer research, genetic studies are valuable because genetic abnormalities so often underlie the evolution of cancer. Certain DNA or RNA markers might therefore help in the treatment and detection of specific cancers. The purpose of the following article, however, is to demonstrate the biomarkers involved in low back pain, disc degeneration and other chronic pain health issues, such as neuropathic pain.
Inflammatory Biomarkers of Low Back Pain and Disc Degeneration: a Review
Abstract
Biomarkers are biological characteristics that can be used to indicate health or disease. This paper reviews studies on biomarkers of low back pain (LBP) in human subjects. LBP is the leading cause of disability, caused by various spine-related disorders, including intervertebral disc degeneration, disc herniation, spinal stenosis, and facet arthritis. The focus of these studies is inflammatory mediators, because inflammation contributes to the pathogenesis of disc degeneration and associated pain mechanisms. Increasingly, studies suggest that the presence of inflammatory mediators can be measured systemically in the blood. These biomarkers may serve as novel tools for directing patient care. Currently, patient response to treatment is unpredictable with a significant rate of recurrence, and, while surgical treatments may provide anatomical correction and pain relief, they are invasive and costly. The review covers studies performed on populations with specific diagnoses and undefined origins of LBP. Since the natural history of LBP is progressive, the temporal nature of studies is categorized by duration of symptomology/disease. Related studies on changes in biomarkers with treatment are also reviewed. Ultimately, diagnostic biomarkers of LBP and spinal degeneration have the potential to shepherd an era of individualized spine medicine for personalized therapeutics in the treatment of LBP.
Biomarkers for Chronic Neuropathic Pain and their Potential Application in Spinal Cord Stimulation: a Review
Abstract
This review was focused on understanding which substances inside the human body increase and decrease with increasing neuropathic pain. We reviewed various studies, and saw correlations between neuropathic pain and components of the immune system (this system defends the body against diseases and infections). Our findings will especially be useful for understanding ways to reduce or eliminate the discomfort, chronic neuropathic pain brings with it. Spinal cord stimulation (SCS) procedure is one of the few fairly efficient remedial treatments for pain. A follow-up study will apply our findings from this review to SCS, in order to understand the mechanism, and further optimize efficaciousness.
Chronic neuropathic pain disorders represent a common long-term disability in the United States, as well as, globally. They affect 1 in 4 Americans. Chronic neuropathic pain treatment has limited success because of poor understanding of the mechanisms that lead to the initiation and maintenance. Additionally, the effectiveness of neuropathic pain management regimens and procedures has been difficult to determine in the past, due to the subjectivity related to pain perception, and a lack of standardized assessment of neuropathic pain. However, one of the most effective management strategies in recent times is spinal cord stimulation (SCS). The main goals of spinal cord stimulation are to improve physical function and quality of life in the patients afflicted with chronic neuropathic pain associated with complex regional pain syndrome (CRPS), failed back syndrome, and other chronic neuropathic pain syndromes [1�2]. Despite limited knowledge of how people benefit from SCS, more than 20,000 stimulators are implanted each year, with more than a half-billion dollars in revenue [3]. While it is generally believed that spinal cord stimulation inhibits pain transmission in the dorsal horn, the exact mechanisms by which SCS relieves neuropathic pain is unknown. Chronic neuropathic pain is caused often by inflammation and/or nerve injury. The advances have shown that inflammation and nerve injury produce changes in the expression of cytokines, neurotransmitters, and structural proteins [4]. It is very likely that there are changes in the body�s serum biomarkers of neuropathic pain before SCS and after SCS. Such a study would contribute greatly to the field of neuromodulation, as objective quantifiers of neuropathic pain control before and after SCS have not yet been investigated. Such definitive data regarding the effectiveness of SCS in relieving neuropathic pain and improving function will be important in future use of SCS.
In preparation for the launching of this study, the authors� goal with this transcript is to provide a review of the literature regarding known biomarkers for chronic neuropathic pain, and then prepare a role for biomarker analysis in the prediction of therapy success in SCS.
Data
The expression of certain genes is altered under chronic pain conditions. This alteration has helped provide an insight into the identification of potential biomarkers [5]. Current advanced research suggests that genetic expression of cytokines, positively or negatively, correlates with the experience of chronic pain. This negative or positive correlation primarily depends on the nature of the cytokine. Cytokines are signaling proteins which mediate the activation, differentiation, and proliferation of immune cells. They can be pro-inflammatory or anti-inflammatory. A misaligned balance between pro-inflammatory and anti-inflammatory cytokines has been common in most of the studies conducted (Table 1). Pro-inflammatory cytokines such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, have been found to play significant roles in the amplification of chronic pain states. In studies involving discogenic pain, Complete Freund�s adjuvant (CFA)-induced discogenic pain in animal models has been observed to coincide with a sustained up-regulation of the above named cytokines [6]. In a more recent study, chronic constriction injury (CCI)-induced rats (neuropathic pain induction) were shown to have increased serum levels of CCL3 and CCR5. Even more interesting, an intrathecal injection of the anti-inflammatory cytokine, IL-4, and the CCL3-neutralizing antibody, reduced the CCI-induced neuropathic pain, estimated by a plantar test [7]. Other studies have also shown that the selective genetic impairment of the highlighted pro-inflammatory cytokines attenuated nerve-injury induced pain behavior, observed in neuropathic pain models [8]. Particularly, Zarpelon et al. revealed that CCI-induced rats showed reduced mechanical hyperalgesia when the IL-33 receptor gene, IL-33R (ST2), was knocked out, compared to the wild-type mice [9].
On the other hand, one study showed that blood levels of anti-inflammatory cytokines (such as IL-10 and IL-4) of Complex Regional Pain Syndrome (CRPS) patients were lower compared to the control [10]. A recent study also shows a distinction of the significant increases of pro-inflammatory cytokines based on the part of the back affected. There were more significant elevations (p<0.05, student�s t test) of pro-inflammatory cytokines in the plasma of lower back pain patients than in upper back patients, when compared to controls [11]. There has also been a study focusing on the levels of the aforementioned cytokines in patients with painful neuropathy in contrast with painless neuropathy and healthy control subjects. Patients with a painful neuropathy had about double the level of IL-2 expression (p = 0.001), TNF expression (p < 0.0001) and protein levels (p = 0.009) than the controls. The study further indicated there was about double the IL-2 and TNF level expression (p = 0.03; p = 0.001) and protein levels in painful neuropathy (p = 0.04; p = 0.04) than patients with painless neuropathy. On the contrary, levels of mRNA expression of the anti-inflammatory cytokines, IL-10 and IL-4 were considerably lower in patients with painful neuropathy than in patients with painless neuropathy (p =0.001) [12].
Several other studies, focused on the antagonist and agonist effects of some drugs targeting pro-inflammatory and anti-inflammatory cytokines, also have pointed out their significance with pain. Certain known analgesics were seen to reduce the levels of pro-inflammatory cytokines in the studies reviewed. There was a study about (CCI)-induced rats, in which case, this induced injury significantly, elevated the levels of pro-inflammatory cytokines, and decreased the serum levels of anti-inflammatory cytokines. Omeprazole, a known remedy for stomach pain, was observed to reduce the levels of pro-inflammatory cytokines (TNF-?, IL-1?, and IL-6) to normal, compared with the CCI control. It is important to note that this was while curbing the CCI-induced neuropathic pain, measured with the paw withdrawal latency [13]. Zhou et al. also highlighted the significance of certain drugs in determining the correlation between cytokines and neuropathic pain. CCI was again, used to induce neuropathic pain on rat models; and in turn, Paenoflorin, an established analgesic [14] was administered. Once Paenoflorin was introduced, significant decreases in serum levels of pro-inflammatory cytokines of CCI-induced rats (IL-1?, IL-6, TNF-?, and CXCL1) were observed, compared to the CCI-control [15]. The cytokines identified here, are the ones that showed correlation in various studies reviewed.
Even though cytokines are the key chronic pain biomarkers, according to the studies reviewed, there are still other proteins and nucleotides that have been observed to associate with chronic pain disorder. Two studies laid emphasis on regulatory microRNAs (miRNAs), which are small non-coding RNA molecules involved in post-transcriptional gene regulation. miRNAs achieve this by binding to mRNAs and degrading them or repressing their functions. Orlova et al. showed that 60% of CRPS patients in their study showed a significant down-regulation of 18 different miRNAs. The rest of the patients, however, showed variable (contradicting) miRNA levels. miRNA levels show variability, depending on the gene being regulated [5]. Tao et al. revealed that an increased inflammatory stimulation by the cytokine IL-1? in normal and osteoarthritis chondrocytes produced a significant down-regulation of the miRNA, miR-558, and a significant up-regulation of miR-21 in DRG neurons. A connection between IL-1? and miR-21 was attributed to AP-1, which is a transcription factor located in the promoter site of the mRNA, and is activated by IL-1? [4]. siRNAs have the same features as miRNAs, in the sense, that they are regulatory nucleotides. They also show variability, depending on the gene being regulated. SIRT1, a deacetylase, functions in regulating various pathways, including inflammation. It was observed that an intrathecal injection of SRT170, an SIRT1 agonist, reduced serum levels of NF-?B, a transcription factor for pro-inflammatory cytokines, in CCI-induced rat models. When SRT170-siRNA (a regulator of the regulator) was administered before SRT170, there was no agonistic effect [16].
Dr. Alex Jimenez’s Insight
A biomarker is most accurately defined as any measurement which demonstrates an interaction between a biological system and the possibility of a chemical, physical or biological hazard. However, biomarkers are often most commonly associated with medicine. In this setting, these can be utilized to determine the effects a particular treatment may have on a patient as well as for determining the risk a patient may have of developing certain health issues. An example of a diagnostic use of biomarkers includes the measurement of biomarkers in blood to evaluate the severity of a heart attack. In the same manner, blood samples can be analyzed and biomarkers can be measured in the instance of chronic pain.
Discussion
Chronic neuropathic pain affects a tremendous amount of the population. There are few effective therapies. However, outcomes are hard to determine due to the subjective nature of pain. We would like to devise a strategy that would establish objectivity of pain assessment. After review of various studies relating to pain biomarkers, we found that serum levels of pro-inflammatory cytokines and chemokines, such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, were significantly up-regulated during chronic pain experience. On the other hand, anti-inflammatory cytokines such as IL-10 and IL-4 were found to show significant down-regulation during chronic pain state. Regulatory miRNAs, siRNAs, and deacetylases that coincide with these cytokines, also showed negative correlation, corresponding to the cytokine they were regulating.
The authors would like to apply this knowledge to SCS, a therapy for chronic neuropathic pain, in an attempt to develop a biomarker profile to help predict success. This study will be a prospective study including patients scheduled for SCS. One month before SCS surgery, patients will complete a survey assessing their subjective level of pain on the visual analog scale and subjective level of function. Patients will also have venipuncture performed, and serum will be analyzed for levels of pain biomarkers. After SCS surgery, patients will be followed at 6 more time points: 2 weeks, 1 month, 3 months, 6 months, 1 year, and 2 years. At each time point, the survey will be re-administered and blood work will be repeated. By evaluating patients pre-operatively and post-operatively, we will be able to assess subjective and objective levels of pain, allowing us to analyze trends in pain biomarkers in the context of patient-reported pain measurement. The duration of this study will be 4 years. Each subject will participate in this study for a total period of 25 months, which will allow us to follow these patients for 2 years postoperatively.
Conclusion
The review of various studies relating to inflammation- and/or nerve injury-induced chronic pain disorder led us to hypothesize that the application of the spinal cord stimulation procedure should relatively reduce serum pro-inflammatory cytokines, and relatively increase serum levels of anti-inflammatory cytokines. This should, in turn, help us understand the mechanism of spinal cord stimulation, thereby optimizing the efficaciousness of the procedure, and perhaps allow us to make predictions regarding therapy success. A follow-up prospective study regarding serum biomarker profile in SCS patients is currently being undertaken.
Footnotes
Author Disclosure:The authors declare no conflicts of interest.
Disclosure of Funding:This work was supported by grants from the University of Medicine and Dentistry of New Jersey and the National Institutes of Health, Bethesda, Maryland (grant numbers: NS072206, HL117684, and DA033390).
In conclusion,�diagnostic biomarkers have the potential of leading new personalized therapeutics in the treatment of chronic pain health issues, such as low back pain, disc degeneration and neuropathic pain. Several research studies like the ones above have been established to ultimately help healthcare professionals understand better ways to reduce or eliminate the pain and discomfort associated with these chronic pain problems. Furthermore, biomarkers can be essential diagnostic tools for the evaluation and treatment of a variety of health issues. Information referenced from the National Center for Biotechnology Information (NCBI).�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Back Pain
Back pain is one of the most prevalent causes for disability and missed days at work worldwide. As a matter of fact, back pain has been attributed as the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience some type of back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
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Arthritis pain is a complex phenomenon involving intricate neurophysiological processing at all levels of the pain pathway. The treatment options available to alleviate joint pain are fairly limited, and most arthritis patients report only modest pain relief with current treatments. A better understanding of the neural mechanisms responsible for musculoskeletal pain and identifying new targets will help develop future pharmacological therapies. This article reviews some of the latest research into factors that contribute to joint pain and covers areas such as cannabinoids, proteinase-activated receptors, sodium channels, cytokines, and transient receptor potential channels. The emerging hypothesis that osteoarthritis may have a neuropathic component is also discussed.
Introduction
The world health organization ranks musculoskeletal disorders as the most frequent cause of disability in the modern world, affecting one in three adults [1]. Even more alarming is that the prevalence of these diseases is rising while our knowledge of their underlying causes is fairly rudimentary.
Fig. 1 A schematic illustrating some of the targets known to modulate joint pain. Neuromodulators can be released from nerve terminals as well as mast cells and macrophages to alter afferent mechanosensitivity. Endovanilloids, acid, and noxious heat can activate transient receptor potential vanilloid type 1 (TRPV1) ion channels leading to the release of algogenic substance P (SP), which subsequently binds to neurokinin-1 (NK1) receptors. Proteases can cleave and stimulate protease-activated receptors (PARs). Thus far, PAR2and PAR4have been shown to sensitize joint primary afferents. The endocannabinoid anandamide (AE) is produced on demand and synthesized from N-arachidonoyl phosphatidylethanolamine (NAPE) under the enzymatic action of phospholipases. A portion of AE then binds to cannabinoid-1 (CB1) receptors leading to neuronal desensitization. Unbound AE is rapidly taken up by an anandamide membrane transporter (AMT)before being broken down by a fatty acid amide hydrolase (FAAH)into ethanolamine (Et) and arachidonic acid (AA). The cytokines tumor necrosis factor-?(TNF-?), interleukin-6 (IL-6) and interleukin1-beta (IL-1?) Can bind to their respective receptors to enhance pain transmission. Finally, tetrodotoxin (TTX)-resistant sodium channels (Nav1.8) are involved in neuronal sensitization.
Patients yearn for their chronic pain to disappear; however, currently prescribed analgesics are largely ineffective and are accompanied by a wide range of unwanted side effects. As such, millions of people worldwide are suffering from the debilitating effects of joint pain, for which there is no satisfactory treatment [2].
More than 100 different forms of arthritis have osteoarthritis (OA) being the most common. OA is a progressively degenerative joint disease that causes chronic pain and loss of function. Commonly, OA is the inability of the joint to repair damage effectively in response to excessive forces being placed on it. The biological and psychosocial factors that comprise chronic OA pain are not well understood, although ongoing research unravels the complex nature of disease symptoms [2]. Current therapeutics, such as non-steroidal anti-inflammatory drugs (NSAIDs), provide some symptomatic relief, reducing the pain for short periods of time, but do not alleviate pain across the patient’s lifespan. Furthermore, high-dose NSAIDs cannot be taken repeatedly over many years, as this can lead to renal toxicity and gastrointestinal bleeding.
Traditionally, arthritis research has focused largely on the articular cartilage as a primary target for the therapeutic development of novel OA drugs for disease modification. This chondrogenic focus has shed new light on the intricate biochemical and biomechanical factors that influence chondrocyte behavior in diseased joints. However, as the articular cartilage is aneural and avascular, this tissue is unlikely to be the source of OA pain. This fact, coupled with the findings that there is no correlation between the damage of articular cartilage and pain in OA patients [3,4] or preclinical models of OA [5], has caused a shift in focus to develop drugs for effective pain control. This article will review the latest findings in joint pain research and highlight some of the emerging targets that may be the future of arthritis pain management (summarized in Fig. 1)
Cytokines
The actions of various cytokines in joint neurophysiology studies have featured quite prominently recently. Interleukin-6 (IL-6), for example, is a cytokine that typically binds to the membrane-bound IL-6 receptor (IL-6R). IL-6 can also signal by binding with a soluble IL-6R (SIL-6R) to produce an IL-6/sIL-6R complex. This IL-6/sIL-6R complex subsequent lybinds to a transmembrane glycoprotein subunit 130(gp130), thereby allowing IL-6 to signal in cells that do not constitutively express membrane-bound IL-6R [25,26]. IL-6 and SIL-6R are key players in systemic inflammation and arthritis, as upregulation of both has been found in RA patients’ serum and synovial fluid [27,29]. Recently, Vazquez et al.observed that co-administration of IL-6/sIL-6R into rat knees caused inflammation-evoked pain, as revealed by an increase in the response of spinal dorsal horn neurons to mechanical stimulation of the knee and other parts of the hindlimb [30]. Spinal neuron hyperexcitability was also seen when IL-6/sIL-6R was applied locally to the spinal cord. Spinal application of soluble gp130 (which would mop up IL-6/sIL-6R complexes, thereby reducing trans-signaling) inhibited IL-6/sIL-6R-induced central sensitization. However, acute application of soluble gp130 alone did not reduce the neuronal responses to already established joint inflammation.
The transient receptor potential (TRP) channels are non-selective cation channels that act as integrators of various physiological and pathophysiological processes. In addition to thermosensation, chemosensation, and mechanosensation, TRP channels are involved in the modulation of pain and inflammation. For example, TRP vanilloid-1 (TRPV1) ion channels have been shown to contribute to joint inflammatory pain as thermal hyperalgesia was not evocable in TRPV1 mono arthritic mice [31]. Similarly, TRP ankyrin-1 (TRPA1)ion channels are involved in arthritic mechano hypersensitivity as blockade of the receptor with selective antagonists attenuated mechanical pain in the Freunds complete adjuvant model inflammation [32,33]. Further evidence thatTRPV1 may be involved in the neurotransmission of OA pain comes from studies in which neuronal TRPV1 expression is elevated in the sodium monoiodoacetate model of OA [34]. In addition, systemic administration of the TRPV1 antagonist A-889425 reduced the evoked and spontaneous activity of spinal-wide dynamic range and nociception-specific neurons in the monoiodoacetate model [35]. These data suggest that endovanilloids could be involved in central sensitization processes associated with OA pain.
There are currently known to be at least four polymorphisms in the gene that encodes TRPV1, leading to an alteration in the structure of the ion channel and impaired function. One particular polymorphism (rs8065080) alters the sensitivity of TRPV1 to capsaicin, and individuals carrying this polymorphism are less sensitive to thermal hyperalgesia [36]. A recent study examined whether OA patients with the rs8065080 polymorphism experienced altered pain perception based on this genetic anomaly. The research team found that patients with asymptomatic knee OA were more likely to carry the rs8065080 gene than patients with painful joints [37]. This observation indicates that OA patients with normal functioning; TRPV1 channels have an increased risk of joint pain and re-affirms the potential involvement of TRPV1 in OA pain perception.
Conclusion
While the hurdle of treating arthritis pain effectively remains, great leaps are being made in our understanding of the neurophysiological processes responsible for the generation of joint pain. New targets are being discovered continually, while the mechanisms behind known pathways are being further defined and refined. Targeting one specific receptor or ion channel is unlikely to be the solution to normalizing joint pain, but rather a polypharmacy approach is indicated in which various mediators are used in combination during specific phases of the disease. Unraveling the functional circuitry at each level of the pain pathway will also improve our knowledge of how joint pain is generated. For example, identifying the peripheral mediators of joint pain will allow us to control nociception within the joint and likely avoid the central side effects of systemically administered pharmacotherapeutics.
FACETOGENIC PAIN
FACET SYNDROME & FACETOGENIC PAIN
Facet syndrome is an articular disorder related to the lumbar facet joints and their innervations and produces both local and radiating facetogenic pain.
Excessive rotation, extension, or flexion of the spine (repeated overuse) can result in degenerative changes to the joint’s cartilage. In addition, itt may involve degenerative changes to other structures, including the intervertebral disc.
CERVICAL FACET SYNDROME & FACETOGENIC PAIN
Axial neck pain (rarely radiating past the shoulders), most common unilaterally.
Pain with and/or limitation of extension and rotation
Tenderness upon palpation
Radiating facetogenic pain locally or into the shoulders or upper back, and rarely radiate in the front or down an arm or into the fingers as a herniated disc might.
LUMBAR FACET SYNDROME & FACETOGENIC PAIN
Pain or tenderness in the lower back.
Local tenderness/stiffness alongside the spine in the lower back.
Pain, stiffness, or difficulty with certain movements (such as standing up straight or getting up from a chair.
Pain upon hyperextension
Referred pain from upper lumbar facet joints can extend into the flank, hip, and upper lateral thigh.
Referred pain from lower lumbar facet joints can penetrate deep into the thigh, laterally and/or posteriorly.
L4-L5 and L5-S1 facet joints can refer to pain extending into the distal lateral leg, and in rare instances, to the foot
EVIDENCE-BASED MEDICINE
Evidence-based Interventional Pain Medicine according to Clinical Diagnoses
12. Pain Originating from the Lumbar Facet Joints
Abstract
Although the existence of a facet syndrome had long been questioned, it is now generally accepted as a clinical entity. Depending on the diagnostic criteria, the zygapophysial joints account for between 5% and 15% of cases of chronic, axial low back pain. Most commonly, facetogenic pain results from repetitive stress and/or cumulative low-level trauma, leading to inflammation and stretching of the joint capsule. The most frequent complaint is axial low back pain with referred pain perceived in the flank, hip, and thigh. No physical examination findings are pathognomonic for diagnosis. The strongest indicator for lumbar facetogenic pain is pain reduction after anesthetic blocks of the rami mediales (medial branches) of the rami dorsales that innervate the facet joints. Because false-positive and, possibly, false-negative results may occur, results must be interpreted carefully. In patients with injection-confirmed zygapophysial joint pain, procedural interventions can be undertaken in the context of a multidisciplinary, multimodal treatment regimen that includes pharmacotherapy, physical therapy, and regular exercise, and, if indicated, psychotherapy. Currently, the gold standard for treating facetogenic pain is radiofrequency treatment (1 B+). The evidence supporting intra-articular corticosteroids is limited; hence, this should be reserved for those who do not respond to radiofrequency treatment (2 B1).
Facetogenic Pain emanating from the lumbar facet joints is a common cause of low back pain in the adult population. Goldthwaite was the first to describe the syndrome in 1911, and Ghormley is generally credited with coining the term �facet syndrome� in 1933. Facetogenic pain is defined as pain that arises from any structure that is part of the facet joints, including the fibrous capsule, synovial membrane, hyaline cartilage, and bone.35
More commonly, it is the result of repetitive stress and/or cumulative low-level trauma. This leads to inflammation, which can cause the facet joint to be filled with fluid and swell, resulting in stretching of the joint capsule and subsequent pain generation.27 Inflammatory changes around the facet joint can also irritate the spinal nerve via foraminal narrowing, resulting in sciatica. In addition, Igarashi et al.28 found that inflammatory cytokines released through the ventral joint capsule in patients with zygapophysial joint degeneration may be partially responsible for the neuropathic symptoms in individuals with spinal stenosis. Predisposing factors for zygapophysial joint pain include spondylolisthesis/lysis, degenerative disc disease, and advanced age.5
I.C ADDITIONAL TESTS
The prevalence rate of pathological changes in the facet joints on radiological examination depends on the mean age of the subjects, the radiological technique used, and the definition of abnormality. Degenerative facet joints can be best visualized via computed tomography (CT) examination.49
NEUROPATHIC PAIN
Pain initiated or caused by a primary lesion or dysfunction in the somatosensory nervous system.
Neuropathic pain is usually chronic, difficult to treat, and often resistant to standard analgesic management.
Abstract
Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibers (A?, A? and C fibers) and central neurons, and affects 7-10% of the general population. Multiple causes of neuropathic pain have been described. Its incidence is likely to increase due to the aging global population, increased diabetes mellitus, and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signaling, alterations in ion channels, and variability in how pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. Furthermore, the burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes, and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain due to increased drug prescriptions and visits to health care providers and the morbidity from the pain itself and the inciting disease. Despite challenges, progress in understanding the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain.
PATHOGENESIS OF NEUROPATHIC PAIN
PERIPHERAL MECHANISMS
After a peripheral nerve lesion, neurons become more sensitive and develop abnormal excitability and elevated sensitivity to stimulation.
This is known as…Peripheral Sensitization!
CENTRAL MECHANISMS
As a consequence of ongoing spontaneous activity in the periphery, neurons develop an increased background activity, enlarged receptive fields, and increased responses to afferent impulses, including normal tactile stimuli. This is known as…Central Sensitization!
Chronic neuropathic pain is more frequent in women (8% versus 5.7% in men) and in patients >50 years of age (8.9% versus 5.6% in those <49 years of age), and most commonly affects the lower back and lower limbs, neck and upper limbs24. Lumbar and cervical painful radiculopathies are probably the most frequent cause of chronic neuropathic pain. Consistent with these data, a survey of >12,000 patients with chronic pain with both nociceptive and neuropathic pain types, referred to pain specialists in Germany, revealed that 40% of all patients experienced at least some characteristics of neuropathic pain (such as burning sensations, numbness, and tingling); patients with chronic back pain and radiculopathy were particularly affected25.
The contribution of clinical neurophysiology to the comprehension of the tension-type headache mechanisms.
Abstract
So far, clinical neurophysiological studies on tension-type headache (TTH) have been conducted with two main purposes: (1) to establish whether some neurophysiological parameters may act as markers of TTH, and (2) to investigate the physiopathology of TTH. Regarding the first point, the present results are disappointing since some abnormalities found in TTH patients may also be frequently observed in migraineurs. On the other hand, clinical neurophysiology has played an important role in the debate about the pathogenesis of TTH. Studies on the exteroceptive suppression of the temporalis muscle contraction have detected a dysfunction of the brainstem excitability and suprasegmental control. A similar conclusion has been reached using trigeminocervical reflexes, whose abnormalities in TTH have suggested a reduced inhibitory activity of brainstem interneurons, reflecting abnormal endogenous pain control mechanisms. Interestingly, the neural excitability abnormality in TTH seems to be a generalized phenomenon, not limited to the cranial districts. Defective DNIC-like mechanisms have indeed been evidenced also in somatic districts by nociceptive flexion reflex studies. Unfortunately, most neurophysiological studies on TTH are marred by serious methodological flaws, which should be avoided in future research to clarify the TTH mechanisms better.
References:
Neurophysiology of arthritis pain. McDougall JJ1 Linton P.
Pain originating from the lumbar facet joints. van Kleef M1,Vanelderen P,Cohen SP,Lataster A,Van Zundert J,Mekhail N.
Neuropathic painLuana Colloca,1Taylor Ludman,1Didier Bouhassira,2Ralf Baron,3Anthony H. Dickenson,4David Yarnitsky,5Roy Freeman,6Andrea Truini,7Nadine Attal, Nanna B. Finnerup,9Christopher Eccleston,10,11Eija Kalso,12David L. Bennett,13Robert H. Dworkin,14and Srinivasa N. Raja15
The contribution of clinical neurophysiology to the comprehension of the tension-type headache mechanisms. Rossi P1, Vollono C, Valeriani M, Sandrini G.
Doctor of Chiropractic Near Me: Mike Melgoza is an active individual who engages in a variety of strenuous physical activities on a regular basis, as a result, however, he began to experience chronic pain symptoms due to improper technique and repetitive movements. Although Mike Melgoza works out of town, he visits Dr. Alex Jimenez every time he begins to experience pain to receive chiropractic care. Mike Melgoza recommends Dr. Alex Jimenez as the non-surgical choice for chronic pain. Mike Melgoza trusts Dr. Jimenez to care for his health.
Doctor Of Chiropractic Near Me
Before you go to a chiropractor to deal with your chronic pain symptoms, it’s important to understand what exactly is causing your pain. Your physician will perform a physical exam as well as some tests to help them diagnose the source of the patient’s pain. As soon as you’re diagnosed with a pain illness, your chiropractor will create a treatment program. Your treatment plan may include spinal manipulation, manual therapies, and therapeutic exercises. Work with your chiropractor to develop a treatment plan. Once your pain is fully addressed, you should be able to slowly resume daily activities.
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
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Getting a good night�s sleep is absolutely integral to good spinal health. Sometimes, though that isn�t possible. According to the National Sleep Foundation, 92 percent of people believe that a�comfortable mattress is important for good, restful sleep. A bad mattress, or one that is old, or one that is simply wrong for your body can contribute to sleep deprivation, lower back pain, headaches, stiff neck, and anxiety and depression. With so much at stake, it�s easy to see just how important it is to select a good mattress.
Ask About How The Mattress Is Made
Learn about the construction� and what the different components mean for your comfort. Different mattresses have different coils and they are arranged differently. The padding can vary in thickness. The depth can range from 7 inches to 18 inches on the average. Understanding the various components can make it easier for you to find the one that is right for you.
Look For Comfort, As Well As, Support
A good mattress is comfortable and has good support. Support is good but if you don�t have comfort then it won�t be effective.
If it is too firm (too much support) it will cause pain on your body�s pressure points. You want your hips and shoulders to slightly sink into the mattress. However, if you prefer a mattress that is firmer to support your back, you can get one with padding on top.
Don�t Let Price Be The Determining Factor
You naturally want to get the most for your dollar, but remember that you get what you pay for. A cheap mattress can translate to a poor quality one.
Look for quality and value rather than price. If money is an issue, do some comparison shopping to find the mattress you want for the best price.
Sales are another way to save money on a purchase, but look out for advertising gimmicks. Know the meaning of the terms that are used and know what you are looking for before you go for that so-called great deal.
Educate Yourself On The Different Mattress Types
Do you want a memory foam or would latex work better for you? What exactly is an innerspring mattress? Are adjustable beds really all they are cracked up to be? Do some research and brush up on the different�types of mattresses�so that you can approach your shopping trip with confidence and as an educated consumer. It will definitely work in your favor.
In The End, It�s All About Personal Preference
There is no mattress that is a one size (or type) fits all. Different people will respond differently to mattresses. The best thing to do is try them out. Spend at least 20 minutes laying down before you make the decision to purchase or not.
Finally, if you find that your�quality of sleep�has recently gotten worse, that you are tossing and turning or wake up with pain in your back, neck, or head, it could be time to change your mattress � or pillow. If you can see your mattress sagging, that could be another indication that it is time to get a new one.
Mattresses are designed to withstand a certain degree of wear and tear, but they don�t last forever. The quality, the weight and other factors contribute to how quickly it wears out. So if you notice any of the warning signs it may be time to get a new mattress so that you can get back to peaceful, restful sleep.
Injury Medical Clinic: Back Pain Care & Treatments
Doctors define chronic pain, as any pain that lasts for 3 to 6 months or more. The pain effects an individual’s mental health and day to day life. Pain comes from a series of messages that run through the nervous system. Depression seems to follow pain. It causes severe symptoms that affect how an individual feels, thinks, and how the handle daily activities, i.e. sleeping, eating and working. Chiropractor, Dr. Alex Jimenez delves into potential biomarkers that can help in finding and treating the root causes of pain and chronic pain.
The first step in successful pain management is a comprehensive biopsychosocial assessment.
The extent of organic pathology may not be accurately reflected in the pain experience.
The initial assessment can be used to identify areas that require more in-depth evaluation.
Many validated self-report tools are available to assess the impact of chronic pain.
Assessment Of Patients With Chronic Pain
Chronic pain is a public health concern affecting 20�30% of the population of Western countries. Although there have been many scientific advances in the understanding of the neurophysiology of pain, precisely assessing and diagnosing a patient’s chronic pain problem is not straightforward or well-defined. How chronic pain is conceptualized influences how pain is evaluated and the factors considered when making a chronic pain diagnosis. There is no one-to-one relationship between the amount or type of organic pathology and pain intensity, but instead, the chronic pain experience is shaped by a myriad of biomedical, psychosocial (e.g. patients’ beliefs, expectations, and mood), and behavioral factors (e.g. context, responses by significant others). Assessing each of these three domains through a comprehensive evaluation of the person with chronic pain is essential for treatment decisions and to facilitate optimal outcomes. This evaluation should include a thorough patient history and medical evaluation and a brief screening interview where the patient’s behavior can be observed. Further assessment to address questions identified during the initial evaluation will guide decisions as to what additional assessments, if any, may be appropriate. Standardized self-reported instruments to evaluate the patient’s pain intensity, functional abilities, beliefs and expectations, and emotional distress are available, and can be administered by the physician, or a referral for in depth evaluation can be made to assist in treatment planning.
Pain is an extremely prevalent symptom. Chronic pain alone is estimated to affect 30% of the adult population of the USA, upwards of 100 million adults.1
Despite the soaring cost of treating people with chronic pain, relief for many remains elusive and complete elimination of pain is rare. Although there have been substantial advances in the knowledge of the neurophysiology of pain, along with the development of potent analgesic medications and other innovative medical and surgical interventions, on average the amount of pain reduction by available procedures is 30�40% and this occurs in fewer than one-half of treated patients.
The way we think about pain influences the way in which we go evaluate pain. Assessment begins with history and physical examination, followed, by laboratory tests and diagnostic imaging procedures in an attempt to identify and/or confirm the presence of any underlying pathology causing the symptom/s or the pain generator.
In the absence of identifiable organic pathology, the healthcare provider may assume that the report of symptoms stems from psychological factors and may request a psychological evaluation to detect the emotional factors underlying the patient’s report. There is duality where the report of symptoms are attributed to either somatic or psychogenic mechanisms.
As an example, the organic bases for some of the most common and recurring acute (e.g. headache)3 and chronic [e.g. back pain, fibromyalgia (FM)] pain problems are largely unknown,4,5 while on the other hand, asymptomatic individuals may have structural abnormalities such as herniated discs that would explain pain if it were present.6,7�There is a lacking in adequate explanations for patients with no identified organic pathology who report severe pain and pain-free individuals with significant, objective pathology.
Chronic pain affects more than just the individual patient, but also his or her significant others (partners, relatives, employers and co-workers and friends), making appropriate treatment essential. Satisfactory treatment can only come from comprehensive assessment of the biological aetiology of the pain in conjunction with the patient’s specific psychosocial and behavioral presentation, including their emotional state (e.g. anxiety, depression, and anger), perception and understanding of symptoms, and reactions to those symptoms by significant others.8,9 A key premise is that multiple factors influence the symptoms and functional limitations of individuals with chronic pain. Therefore, a comprehensive assessment is needed that addresses biomedical, psychosocial, and behavioral domains, as each contributes to chronic pain and related disability.10,11
Comprehensive Assessment Of An Individual With Chronic Pain
Turk and Meichenbaum12 suggested that three central questions should guide assessment of people who report pain:
What is the extent of the patient’s disease or injury (physical impairment)?
What is the magnitude of the illness? That is, to what extent is the patient suffering, disabled, and unable to enjoy usual activities?
Does the individual’s behavior seem appropriate to the disease or injury, or is there any evidence of symptom amplification for any of a variety of psychological or social reasons (e.g. benefits such as positive attention, mood-altering medications, financial compensation)?
To answer these questions, information should be gathered from the patient by history and physical examination, in combination with a clinical interview, and through standardized assessment instruments. Healthcare providers need to seek any cause(s) of pain through physical examination and diagnostic tests while concomitantly assessing the patient�s mood, fears, expectancies, coping efforts, resources, responses of significant others, and the impact of pain on the patients� lives.11 In short, the healthcare provider must evaluate the �whole person� and not just the pain.
The general goals of the history and medical evaluation are to:
(i) determine the necessity of additional diagnostic testing
(ii) determine if medical data can explain the patient’s symptoms, symptom severity, and functional limitations
(iii) make a medical diagnosis
(iv) evaluate the availability of appropriate treatment
(v) establish the objectives of treatment
(vi) determine the appropriate course for symptom management if a complete cure is not possible.
Significant numbers of patients that report chronic pain demonstrate no physical pathology using plain radiographs, computed axial tomography scans, or electromyography (an extensive literature is available on physical assessment, radiographic and laboratory assessment procedures to determine the physical basis of pain),17 making a precise pathological diagnosis difficult or impossible.
Despite these limitations, the patient’s history and physical examination remain the basis of medical diagnosis, can provide a safeguard against over-interpreting findings from diagnostic imaging that are largely confirmatory, and can be used to guide the direction of further evaluation efforts.
In addition, patients with chronic pain problems often consume a variety of medications.18 It is important to discuss a patient’s current medications during the interview, as many pain medications are associated with side-effects that may cause or mimic emotional distress.19 Healthcare providers should not only be familiar with medications used for chronic pain, but also with side-effects from these medications that result in fatigue, sleep difficulties, and mood changes to avoid misdiagnosis of depression.
The use of daily diaries is believed to be more accurate as they are based on real-time rather than recall. Patients may be asked to maintain regular diaries of pain intensity with ratings recorded several times each day (e.g. meals and bedtime) for several days or weeks and multiple pain ratings can be averaged across time.
One problem noted with the use of paper-and-pencil diaries is that patients may not follow the instruction to provide ratings at specified intervals. Rather, patients may complete diaries in advance (�fill forward�) or shortly before seeing a clinician (�fill backward�),24 undermining the putative validity of diaries. Electronic diaries have gained acceptance in some research studies to avoid these problems.
Research has demonstrated the importance of assessing overall health-related quality of life (HRQOL) in chronic pain patients in addition to function.31,32 There are a number of well established, psychometrically supported HRQOL measures [Medical Outcomes Study Short-Form Health Survey (SF-36)],33 general measures of physical functioning [e.g. Pain Disability Index (PDI)],34 and disease-specific measures [e.g. Western Ontario MacMaster Osteoarthritis Index (WOMAC);35 Roland-Morris Back Pain Disability Questionnaire (RDQ)]36 to assess function and quality of life.
Disease-specific measures are designed to evaluate the impact of a specific condition (e.g. pain and stiffness in people with osteoarthritis), whereas generic measures make it possible to compare physical functioning associated with a given disorder and its treatment with that of various other conditions. Specific effects of a disorder may not be detected when using a generic measure; therefore, disease-specific measures may be more likely to reveal clinically important improvement or deterioration in specific functions as a result of treatment. General measures of functioning may be useful to compare patients with a diversity of painful conditions. The combined use of disease-specific and generic measures facilitates the achievement of both objectives.
The presence of emotional distress in people with chronic pain presents a challenge when assessing symptoms such as fatigue, reduced activity level, decreased libido, appetite change, sleep disturbance, weight gain or loss, and memory and concentration deficits, as these symptoms can be the result of pain, emotional distress, or treatment medications prescribed to control pain.
Instruments have been developed specifically for pain patients to assess psychological distress, the impact of pain on patients� lives, feeling of control, coping behaviors, and attitudes about disease, pain, and healthcare providers.17
For example, the Beck Depression Inventory (BDI)39 and the Profile of Mood States (POMS)40 are psychometrically sound for assessing symptoms of depressed mood, emotional distress, and mood disturbance, and have been recommended to be used in all clinical trials of chronic pain;41 however, the scores must be interpreted with caution and the criteria for levels of emotional distress may need to be modified to prevent false positives.42
Lab Biomarkers For Pain
Biomarkers are biological characteristics that can be used to indicate health or disease. This paper reviews studies on biomarkers of low back pain (LBP) in human subjects. LBP is the leading cause of disability, caused by various spine-related disorders, including intervertebral disc degeneration, disc herniation, spinal stenosis, and facet arthritis. The focus of these studies is inflammatory mediators, because inflammation contributes to the pathogenesis of disc degeneration and associated pain mechanisms. Increasingly, studies suggest that the presence of inflammatory mediators can be measured systemically in the blood. These biomarkers may serve as novel tools for directing patient care. Currently, patient response to treatment is unpredictable with a significant rate of recurrence, and, while surgical treatments may provide anatomical correction and pain relief, they are invasive and costly. The review covers studies performed on populations with specific diagnoses and undefined origins of LBP. Since the natural history of LBP is progressive, the temporal nature of studies is categorized by duration of symptomology/disease. Related studies on changes in biomarkers with treatment are also reviewed. Ultimately, diagnostic biomarkers of LBP and spinal degeneration have the potential to shepherd an era of individualized spine medicine for personalized therapeutics in the treatment of LBP.
Biomarkers For Chronic Neuropathic Pain & Potential Application In Spinal Cord Stimulation
This review was focused on understanding which substances inside the human body increase and decrease with increasing neuropathic pain. We reviewed various studies, and saw correlations between neuropathic pain and components of the immune system (this system defends the body against diseases and infections). Our findings will especially be useful for understanding ways to reduce or eliminate the discomfort, chronic neuropathic pain brings with it. Spinal cord stimulation (SCS) procedure is one of the few fairly efficient remedial treatments for pain. A follow-up study will apply our findings from this review to SCS, in order to understand the mechanism, and further optimize efficaciousness.
Pro-inflammatory cytokines such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, have been found to play significant roles in the amplification of chronic pain states.
After review of various studies relating to pain biomarkers, we found that serum levels of pro-inflammatory cytokines and chemokines, such as IL-1?, IL-6, IL-2, IL-33, CCL3, CXCL1, CCR5, and TNF-?, were significantly up-regulated during chronic pain experience. On the other hand, anti-inflammatory cytokines such as IL-10 and IL-4 were found to show significant down-regulation during chronic pain state.
Biomarkers For Depression
A plethora of research has implicated hundreds of putative biomarkers for depression, but has not yet fully elucidated their roles in depressive illness or established what is abnormal in which patients and how biologic information can be used to enhance diagnosis, treatment and prognosis. This lack of progress is partially due to the nature and heterogeneity of depression, in conjunction with methodological heterogeneity within the research literature and the large array of biomarkers with potential, the expression of which often varies according to many factors. We review the available literature, which indicates that markers involved in inflammatory, neurotrophic and metabolic processes, as well as neurotransmitter and neuroendocrine system components, represent highly promising candidates. These may be measured through genetic and epigenetic, transcriptomic and proteomic, metabolomic and neuroimaging assessments. The use of novel approaches and systematic research programs is now required to determine whether, and which, biomarkers can be used to predict response to treatment, stratify patients to specific treatments and develop targets for new interventions. We conclude that there is much promise for reducing the burden of depression through further developing and expanding these research avenues.
References:
Assessment of patients with chronic pain�E. J. Dansiet and D. C. Turk*t�
Inflammatory biomarkers of low back pain and disc degeneration: a review.
Khan AN1, Jacobsen HE2, Khan J1, Filippi CG3, Levine M3, Lehman RA Jr2,4, Riew KD2,4, Lenke LG2,4, Chahine NO2,5.
Biomarkers for Chronic Neuropathic Pain and their Potential Application in Spinal Cord Stimulation: A Review
Chibueze D. Nwagwu,1 Christina Sarris, M.D.,3 Yuan-Xiang Tao, Ph.D., M.D.,2 and Antonios Mammis, M.D.1,2
Biomarkers for depression: recent insights, current challenges and future prospects. Strawbridge R1, Young AH1,2, Cleare AJ1,2.
Why Chiropractic Combined With Glucosamine & Chondroitin Sulfates Are A Win-Win For Degenerative Disc Disease Sufferers.
The most effective treatments are often found in the natural ones. The human body has this incredible ability to provide its own healing. Often we can aid that process through nutrition, exercise, and lifestyle changes. While there are some people who do reach for medications and invasive means of pain control, the truth is the best cure is the natural one. This is also true of degenerative disc disease. There are several natural treatments that help relieve the pain and even stop the progression of the disease. Common treatments include chiropractic, glucosamine, and chondroitin sulfates.
What Is Degenerative Disc Disease (DDD)?
In a healthy spine the discs that lie between the vertebrae and cushion them are filled with fluid. They allow the spine to move, flex, bend, and twist. Over time they may lose some of their cushion as part of the aging process.
Degenerative disc disease occurs when the discs of the spine collapse and degrade. In extreme cases, the discs can completely collapse causing the vertebrae�s facet joints to rub against each other. This leads to osteoarthritis. The condition is accompanied by pain, inflammation, and loss of mobility.
How Do Glucosamine & Chondroitin Sulfates Help Degenerative Disc Disease?
Glucosamine and chondroitin sulfates are substances that occur naturally in the body. It is an essential element in cartilage maintenance and regeneration. They help to form new cartilage from within existing cartilage. They can actually help to rebuild the discs that have begun to degrade. Often they are taken as nutritional supplements.
Studies show that long term use of glucosamine and chondroitin sulfate do indeed not just help arrest the development of spinal disc degeneration, they can also help to reverse the symptoms, especially if begun in the early stages of the disease. Treatment that incorporates these supplements result in decreased pain and improved range of motion. Patients may also notice strengthening of the back and increased flexibility. This is true even in patients who are older, in their 50�s and 60�s.
Patients may start noticing a decrease in pain as early as six months after beginning to take the supplement. After taking it consistently, the other benefits present over time. What is also important to note is that neither glucosamine nor chondroitin sulfate cause any adverse side effects. These supplements are safe and effective.
Chiropractic For Degenerative Disc Disease
Chiropractic is a complementary treatment to combine with glucosamine and chondroitin sulfate for degenerative disc disease. Chiropractic alone is very effective for many spine and neck disorders, including degenerative disc disease. It is a natural, non-invasive treatment that does not use medications but instead incorporates lifestyle changes, diet, and exercise recommendations to provide whole body wellness. While chiropractic works very well to treat pain, improve mobility, and increase flexibility, it has actually been proven to stop the progression of degenerative disc disease and even reverse its effects.
Using chiropractic for degenerative disc disease and combining it with supplements that include glucosamine and chondroitin sulfate is a very effective system for relieving the pain and other symptoms. In several studies, many patients saw improvement and decrease in symptoms faster than patients who used the supplements alone. Combining these treatments is usually the best course of action to help patients suffering from this devastating disease.
When treating any condition, it is always best to go the most natural route possible. The fewer synthetic substances and manufactured toxins that are introduced into the body, the better chance the patient has of a more thorough and faster healing or at the very least a dramatic decrease in symptoms.
Injury Medical Clinic: Herniated Disc Treatment & Recovery
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
Abstract
References:
