From: J Pain. 2012 Jan 24. [Epub ahead of print]

A controlled experimental study was performed to examine the efficacy of the endogenous pain inhibitory systems and whether this (mal)functioning is associated with symptom increases following exercise in patients with chronic whiplash associated disorders. In addition, 2 types of exercise were compared. Twenty-two women with chronic whiplash associated disorders and 22 healthy controls performed a submaximal and a self-paced, physiologically limited exercise test on a cycle ergometer with cardiorespiratory monitoring on 2 separate occasions. Pain pressure thresholds, health status, and activity levels were assessed in response to the 2 exercise bouts.

In chronic whiplash associated disorders, pain pressure thresholds decreased following submaximal exercise, whereas they increased in healthy subjects. The same effect was established in response to the self-paced, physiologically limited exercise, with exception of the pain pressure thresholds at the calf which increased. A worsening of the chronic whiplash associated disorders symptom complex was reported post-exercise. Fewer symptoms were reported in response to the self-paced, physiologically limited exercise.

These observations suggest abnormal central pain processing during exercise in patients with chronic whiplash associated disorders. Submaximal exercise triggers post-exertional malaise, while a self-paced and physiologically limited exercise will trigger less severe symptoms, and therefore seems more appropriate for chronic whiplash associated disorders patients.

The results from this exercise study suggest impaired endogenous pain inhibition during exercise in people with chronic whiplash associated disorders. This finding highlights the fact that one should be cautious when evaluating and recommending exercise in people with chronic whiplash associated disorders, and that the use of more individual, targeted exercise therapies is recommended.

From: Mymensingh Med J. 2011 Oct;20(4):645-51.

In order to find out the fluctuation of pain by weather change, a descriptive cross-sectional study was conducted among 138 individuals having musculoskeletal disorders (MSDs) attending the out patient department (OPD) of Physical Medicine and Rehabilitation, Bangabandhu Sheikh Mujib Medical University (BSMMU) Hospital, Dhaka, during March 2004 to June 2004. Data were collected by face to face interview employing a pre-tested interview schedule containing structured questions. Among 138 respondents, male were predominant (52.2%). Mean age of the respondents was 39.42±10.79 years, while the most common age group was found as ’31 to 40 years’. By occupation, majority were housewives (40.58%), followed by businessmen (29.71%), service holder (15.22%), laborer (7.97%), and students (6.52%). The primary sites of pain were back and low back (38.4%), knee (24.6%), leg (8.7%), ankle and heel (8.0%), hand and wrist (6.5%), neck (5.8%), shoulder (5.8%), and elbow (2.2%). Highest number (47.8%) patients reported aching pain, while one fifth (20.3%) of them experienced burning pain.

About 36.2 percent respondents mentioned ‘prolonged standing’ as the main cause of pain aggravation, while almost half (48.6%) of the patients perceived that ‘application of heat’ was the key relieving factor of their pain. About two third (63%) of the respondents were sensitive to weather change; among them 56.3 percent reported that their pain increased during cold weather. Moreover, more than two third (67.4%) study-patients experienced deterioration of pain due to seasonal variation; of them 59.1 percent reported that their pain was exacerbated in winter season. Of all respondents, less than one third (30.4%) experienced aggravation of pain due to lunar change; of them majority (85.7%) experienced increased pain during dark fortnights. The study concluded that weather change might have an important role in fluctuation of pain among individuals having musculoskeletal disorders.

From: Pain. 2011 Nov 7. [Epub ahead of print]

The authors investigated the association of chronic pain with physical and mental comorbidity in the New Zealand population by measuring chronic pain status separate from comorbid conditions. Models of allostatic load provided a conceptual basis for considering multi-morbidity as accumulated comorbid load and for using both discrete conditions and cumulative measures in analyses. The nationally representative cross-sectional survey data included self-reported doctor-diagnosed chronic physical and mental health conditions, Kessler 10-item scale scores, an independent measure of chronic pain, and sociodemographic characteristics.

The population prevalence of chronic pain is 16.9%, and a quarter (26%) of the population report 2 or more comorbid physical conditions statistically associated with chronic pain. Results indicate that accumulated comorbid load is independently associated with chronic pain. Six physical conditions independently associated with chronic pain increase the risk of chronic pain in an additive manner, and residual accumulated load further increases risk for 2 or more conditions.

Anxiety and depression interacts synergistically with arthritis and neck and back disorders to increase the odds of reporting chronic pain beyond an additive model. This synergistic effect is not apparent for other conditions or for additional comorbid load. Results imply that measurement of chronic pain independent of comorbid conditions and adjustment for comorbid conditions is important for more accurate prevalence estimates and understanding relationships between conditions. Future epidemiological research might usefully incorporate independent measurement of chronic pain alongside adjustment for specific physical and mental health conditions as well as accumulated comorbid load.

From: BMC Musculoskelet Disord. 2011 Oct 12;12(1):230

Neck shoulder pain remains a major problem in work tasks with high exposure to awkward working positions, repetitive movements and movements with high precision demands. The trapezius muscle is considered particularly affected. The prevalence of chronic neck shoulder pain appears to be higher in women than in men. It causes high socioeconomic costs and significant loss of quality of life for the individual. Because of limited knowledge of the mechanisms involved in transition from acute to chronic pain, attempts to develop effective treatments have had limited success. The clinical manifestations of chronic pain conditions include both somatic (e.g., sensory disturbances, facilitated pain responses in association with movements, tense muscles with hyperalgesia for mechanical pressure/manual palpation) and psychological symptoms (e.g., sleeping problems, anxiety, and depressive symptoms).

Sensory hypersensitivity (central sensitization is sometimes used as a synonym while others use central sensitization as a term for specific mechanisms in the central nervous system (CNS)) is a common feature of several chronic neck shoulder pain conditions, particularly those with higher levels of pain intensity and disability. At the clinical examination, this can be manifested as increased sensitivity to manual palpation (i.e., pressure), but increased sensitivity to other sensory modalities, e.g., heat or cold, have also been described. Hypersensitivity to mechanical pressure or thermal pain is sometimes confined to the neck shoulder area but may also be present in remote pain-free areas, even though the clinical routine examination does not reveal clinical anatomical widespread pain and/or generalized hyperalgesia for different types of stimuli. Widespread deep tissue hyperalgesia has been found in patients with fibromyalgia, tension–type headache, whiplash associated disorders, idiopathic neck pain, epicondylalgia, low back pain, pelvic pain syndrome, and osteoarthritis.

It is generally acknowledged that the presence of widespread sensory hypersensitivity provides indication of augmented central pain processing mechanisms. Peripheral and central sensitization and alterations in descending inhibition mechanisms of nociception have been suggested as three of the underlying mechanisms of chronic musculoskeletal pain in general. It the context of muscle pain it has been suggested that neurobiological sensitization operating at somatic, cognitive and behavioral levels may increase the prevalence of e.g., sleeping problems, anxiety and depressive symptoms. Another explanation may be that such symptoms are secondary consequences of living with chronic pain.

Pain induction in an anatomical region distant from the clinical pain region is a common strategy to investigate signs of central sensitization and/or alterations in descending inhibition of neural activity and nociception at the spinal cord level. Assessments of pain sensitivity in deep tissue of non-painful regions of the body may be of importance for better understanding of the development of widespread hypersensitivity. Pressure pain thresholds using algometry have been used extensively to map mechanical sensitivity of mainly deep tissues such as muscles. Another modality (i.e., chemical) of the pain sensitivity of muscle can be investigated using the intramuscular hypertonic saline model with the opportunity to assess both aspects of sensitization and referred pain. The hypertonic saline model has been used extensively to characterize the sensory and motor effects involved in muscle pain, as the quality of the induced pain is comparable to acute clinical muscle pain and shows both localized and referred pain characteristics.

The anatomical spreading of experimentally induced muscle pain seems to alter in chronic musculoskeletal pain conditions; for example, patients with fibromyalgia experience stronger pain and larger primary and referred pain areas after hypertonic saline-evoked muscle pain compared with pain free controls. Such manifestations were present in the lower limb muscles, where these patients typically do not experience ongoing pain. Extended referred pain areas from the tibialis anterior muscle have also been found in patients with chronic whiplash associated disorders.

Both algometry and pain induction using the intramuscular saline model are psychophysical tests; i.e., an objective stimuli but a subjectively reported response by the tested subject. Noxious psychophysical tests require cooperation from the subject and attention, concentration, motivation and mood can reasonably affect the reports of the subjects tested. A bio-psycho-social model is preferred in clinical management of chronic pain since a blend of factors – neurobiological, psychological, coping styles, and contextual factors – contributes to the development and maintenance of chronic pain. Moreover, psychological factors, e.g., anxiety, depressive symptoms and fear, appear to play prominent roles in maladaptive responses to pain and in pain perpetuation. Hence, it is reasonable to assume that the psychological status can influence the reports of pain thresholds during psychophysical tests in chronic pain conditions.

Chronic whiplash associated disorders has been relatively extensively investigated concerning spreading of hyperalgesia as mentioned above. Studies of how widespread sensory hypersensitivity is in non-traumatic neck shoulder pain disorders, e.g., chronic neck shoulder pain, are, however, sparse and inconclusive and psychological aspects have not been extensively investigated in relation to pain responses to sensory tests in these patients.

The aim of this explorative study was to further investigate signs of sensory hypersensitivity, in terms of lowered pressure pain thresholds and more intense responses to painful hypertonic saline infusion, and the possible relationships to different psychological factors (sleeping problems, depression, anxiety, catastrophizing, and fear-avoidance beliefs) in women with chronic neck shoulder pain, and various extent of regional pain, compared with healthy controls.

Major results of the present study were:

The present study suggests that central sensitization mechanisms are involved in chronic nontraumatic neck shoulder pain without simultaneous clinical widespread pain since sensory hypersensitivity was found in areas distant to the region of clinical pain. A long history of chronic pain and high neck shoulder pain intensities were associated with low pressure pain thresholds both in the region of clinical pain and in distant pain free areas. Both pressure pain thresholds and chemically induced pain intercorrelated with intensity and area size of the clinical pain. Only the sensitivity to chemically induced pain was associated with the psychological status of the chronic non-traumatic neck shoulder pain but without simultaneous anatomically widespread clinical pain subjects.

From: J Sport Rehabil. 2011 Aug 8. [Epub ahead of print]

Rehabilitation professionals treat individuals suffering from chronic low back pain using a variety of treatment approaches including manual therapy and the prescription of therapeutic exercises. The use of manual therapy, specifically joint mobilization of the lumbar spine, may significantly decrease a patient’s pain and contribute to improvement in his or her functioning. Exercise may also improve pain and functioning, with some patients reporting gains up to 1 year after the last treatment session. Numerous investigations have assessed the potential benefits associated with either joint mobilization or therapeutic exercise for patients with acute or subacute low back pain or chronic low back pain.

Despite the literature to guide clinical decision making, clinicians often struggle to successfully or expeditiously treat patients with low back pain. A recent trend reported in the literature has been to use treatment-based classifications or clinical prediction rules. These reports provide evidence or clinical suggestions for treating patients with acute or subacute low back pain.

To the best of the authors’ knowledge, there is a lack of these types of reports that address evaluation and treatment for patients with chronic low back pain. When treating patients with chronic low back pain it is not uncommon for some rehabilitation professionals to use 1 treatment approach primarily or exclusively. Using a treatment program supported by the research literature should generate the most effective outcomes for patients with chronic low back pain.

From: Eur Spine J. 2011 Aug 26. [Epub ahead of print]

The eitiology of low back pain is usually multifactoral. Based on previous literature reviews, it was found that there are three main risk factors for recurrent and chronic low back pain: 1) history of low back pain with associated limitations and treatments, 2) dissatisfaction at work, and 3) poor general medical condition. Other risk factors such as socioeconomic and employment status, psychological status, and physically demanding work are also suggested.

The differences in sagittal spino-pelvic alignment between adults with chronic low back pain and the normal population are still poorly understood. In particular, it is still unknown if particular patterns of sagittal spino-pelvic alignment are more prevalent in chronic low back pain. The current study helps to better understand the relationship between sagittal alignment and low back pain.

To compare the sagittal spino-pelvic alignment of patients with chronic low back pain with a cohort of asymptomatic adults. Sagittal spino-pelvic alignment was evaluated in prospective cohorts of 198 patients with chronic low back pain and 709 normal subjects. The two cohorts were compared with respect to the sacral slope, pelvic tilt, pelvic incidence, lumbar lordosis, lumbar tilt, lordotic levels, thoracic kyphosis, thoracic tilt, kyphotic levels, and lumbosacral joint angle. Correlations between parameters were also assessed.

Sagittal spino-pelvic alignment is significantly different in chronic low back pain with respect to sacral slope, pelvic incidence, lumbar tilt, lordotic levels, thoracic kyphosis, thoracic tilt and lumbosacral joint angle, but not pelvic tilt, lumbar lordosis, and kyphotic levels. Correlations between parameters were similar for the two cohorts. As compared to normal adults, a greater proportion of patients with low back pain presented low sacral slope and lumbar lordosis associated with a small pelvic incidence, while a greater proportion of normal subjects presented normal or high sacral slope associated with normal or high pelvic incidence.

Sagittal spino-pelvic alignment was different between patients with chronic low back pain and controls. In particular, there was a greater proportion of chronic low back pain patients with low sacral slope, low lumbar lordosis and small pelvic incidence, suggesting the relationship between this specific pattern and the presence of chronic low back pain.

From: Mol Pain. 2011 Aug 25;7(1):65. [Epub ahead of print]

Chronic low back pain is a complex continuum of painful conditions that includes both axial and radicular pain: Axial low back pain is defined as spontaneous or movement-evoked pain or discomfort localized to the spine and low back region. Non-axial, radiating low back pain is pain in one or both legs. Often referred to as radicular pain or sciatica, it usually follows the course of the sciatic nerve. Current diagnostic and therapeutic approaches to chronic back pain are limited by our narrow understanding of the underlying biological mechanisms. There are many potential causes of chronic low back pain including degenerative disc disease. While natural age-related degeneration of intervertebral discs is common, chronic low back pain is associated with increased signs of disc degeneration. Like most other conditions, back pain is the product of genetic and environmental influences.

SPARC (secreted protein, acidic, rich in cysteine; aka osteonectin or BM-40) is an evolutionarily conserved collagen-binding protein present in intervertebral discs. SPARC is known to influence bone remodeling, collagen fibrillogenesis, and wound repair. Decreased expression of SPARC has been associated with aging and degeneration in human intervertebral discs. Furthermore, targeted deletion of the SPARC gene results in accelerated disc degeneration in the aging mouse and a behavioral phenotype resembling chronic low back pain in humans. The genetic evidence from mice and the clinical observation that SPARC is down-regulated in humans with disc degeneration suggests that long-term down-regulation of SPARC expression may play a critical role in chronic low back pain. What are the mechanisms that could lead to lasting down-regulation of genes such as SPARC?

One mechanism that is now well established for stable, long-term programming of gene expression is DNA methylation. The DNA is covalently modified by the addition of methylmoieties by an enzymatic DNA methyltransferase reaction that catalyzes the transfer of a methyl group from the methyl donor S-adenosyl methionine. What distinguishes DNA methylation in vertebrate genomes is the fact that not all CpGs are methylated in any given cell type, generating cell type-specific patterns of methylation, which confer upon a genome its cell type-specific identity. Active regulatory regions of the chromatin, which enable gene expression, are associated with hypomethylated DNA, whereas hypermethylated DNA is packaged in inactive chromatin resulting in gene silencing. Patterns of DNA methylation are generated during gestation and until recently were believed to be restricted to life-long programming of cell typespecific gene expression. However, recent data suggests that DNA methylation is dynamic in adult non-dividing cells and is responsive to environmental signals. It might therefore play a role in the modulation of gene function in response to a plethora of environmental signals after birth and throughout life.

The authors tested the hypothesis that DNA methylation occurring later in life or in pathological conditions might play a role in chronic low back pain. The possibility that DNA methylation might precipitate chronic pain through down-regulation of expression of critical genes such as SPARC has not been previously addressed.

The results are consistent with the hypothesis that alterations in DNA methylation associate with chronic low back pain and intervertebral disc degeneration in mice and in humans with chronic low back pain. This data provides the first line of evidence that supports the hypothesis that DNA methylation is involved in chronic pain.

This study provides the first line of evidence that DNA methylation is involved in chronic pain. Specifically, we present evidence from both mouse and human studies supporting the hypothesis that DNA methylation of the SPARC promoter is increased with age and intervertebral disc degeneration, resulting in the silencing of a gene that is protective against accelerated disc degeneration. The SPARC gene is likely to be just one example of many pain-relevant genes that are similarly regulated by DNA methylation in both peripheral tissues and in the central nervous system.

Epigenetic modifications are at the interface between environment and genetics, creating a mechanism by which life experience can lead to long-lasting changes in gene expression. If DNA methylation is implicated in chronic pain, it will provide not only new understanding of the underlying mechanisms involved in generation and maintenance of chronic pain, but also new therapeutic possibilities.

From: PLoS One. 2011;6(6):e21194. Epub 2011 Jun 16

Whiplash associated disorders are a well-documented health outcome following a motor vehicle crash. Nearly 50% report persistent symptoms up to two years post injury. Resultant costs for medical and rehabilitative care in the western-world are high. Despite such a large socio-economic problem, reasons for the high rate of transition to chronic pain remain elusive.

Factors associated with poor recovery are not conclusive and rather limited to self-report measures. These include initial higher levels of pain, recognised as the most consistent predictor of poor outcome, with measures of sensory hyperalgesia and posttraumatic stress also showing some prognostic capacity. By virtue of their self-report nature, these factors are open to bias, but no verifiable structural changes (e.g. radiological findings) have shown to be associated with the transition to chronicity. This has contributed to the scepticism surrounding the whiplash condition.

However, recent data has demonstrated structural muscle changes in patients with chronic whiplash associated disorders. Muscle fatty infiltrates on magnetic resonance imaging (MRI) were found in the neck extensor muscles of participants with chronic whiplash associated disorder. These findings were not present in those with chronic non-traumatic neck pain or in healthy controls; suggesting traumatic factors play a role in their development. It is possible the presence of widespread muscle fatty infiltrates is in some way associated with the development of chronic pain following whiplash injury. As the muscle changes have been only established in chronic whiplash associated disorders, it is necessary to now determine how soon following injury they occur and whether they uniquely manifest in those who transition.

The underlying mechanisms contributing to the development of muscle fatty infiltrates are also unknown, but knowledge of such processes may assist in developing more informed and effective early interventions. A relationship with higher pain levels seems reasonable since the muscle changes are not apparent in non-traumatic neck pain, a condition with recognized lower levels of pain than whiplash associated disorders. The widespread findings of neck muscle fatty infiltrates suggest that disuse or lack of neck range of motion may also be a contributing factor. Additionally, stress related processes have shown to negatively affect muscle tissue. Posttraumatic stress symptoms are common to whiplash associated disorders, and associated with poor recovery. A significant, albeit weak, relationship between muscle fatty infiltrates and posttraumatic stress in chronic whiplash associated disorders has been reported. The relationship between these factors at the acute stage and the development of muscle fatty infiltrates remains unknown. The authors therefore hypothesise that the development of muscle fatty infiltrates will be associated with initial pain levels but that this relationship may be mediated by reduced neck range of motion and symptoms of posttraumatic stress symptoms.

The aims of this study were to 1) investigate the temporal development of muscle fatty infiltrates following whiplash injury, 2) investigate differences in muscle fatty infiltrates between those who recover and those who report persistent symptoms at six months post injury, investigate the relationship between initial pain levels and muscle fatty infiltrates at 6 months post injury and whether this relationship is mediated by loss of neck range of motion and symptoms of posttraumatic stress disorder.

This study provides the first objective evidence for the differential development of muscle fatty infiltrates in participants with varying levels of functional recovery following whiplash injury. Previous investigations of whiplash have attempted to identify and link structural pathology with symptoms but without consistent results. However, these studies did not focus on muscular tissues. This study has uniquely 1) identified longitudinal structural muscle pathology with MRI between 4-weeks and 3-months post injury, 2) used these findings to differentiate between those with varying levels of functional recovery, and 3) shown that the relationship between muscle fatty infiltrates at 6-months post injury and initial pain intensity is mediated by post traumatic stress disorder symptoms.

All of the groups entered the study at 4-week post-injury with similar levels of muscle fatty infiltrates. However, the group with poor functional recovery at 6-months uniquely demonstrated increased muscle fatty infiltrates between 4-weeks and 3-months post-injury and these changes persisted at 6-months. The participants reporting mild pain and disability and recovery did not demonstrate such changes. This is interesting and suggests the possibility of a more severe injury in those with poor functional recovery. There are various processes that could underlie the development of such muscle degeneration and these require consideration.

Physiologic response to injured cervical structures includes profound neuroinflammatory changes in the dorsal root ganglia and spinal cord, which, similar to other chronic pain disorders, could lead to persistent pain states in whiplash associated disorders. While this study did not explore the specific role of inflammation on outcomes, the widespread muscle changes and associated higher pain could be consistent with a local and/or systemic inflammatory response from damaged somatic structures and attendant alterations in pain processing from and within the peripheral and/or central nervous systems.

It remains possible that the expression of fat cells is the result of an injury induced inflammatory response and the subsequent increase in DNA synthesis of the many different cells within the peri-muscular connective tissue e.g. mast cells, satellite cells, muscle precursor cells, fibroblasts and preadipocytes. These cells, after injury, are responsible for secreting pro-inflammatory cytokines that could stimulate their trans-differentiation into adipose tissue. While causal inference between muscle fatty infiltrates and poor recovery cannot be drawn from the results of this study, it is possible that the presence of muscle fatty infiltrates (which is not patient dependent), is the result of an initial and persistent inflammatory response to injured anatomical tissues. As such, changes in muscle structure may represent an objective MRI marker for injury. Further study investigating the influence of an early and persistent local and/or systemic inflammatory response to whiplash injury on neck muscle fatty infiltrates development and the transition to chronic pain is warranted and well underway.

Complex, physiological factors related to disuse may also stimulate and produce structural muscle changes. Postural muscles demonstrate rapid accumulations of intermuscular fat after 4-weeks of disuse. Reduced cervical range of motion following whiplash is common and associated with higher levels of pain and poor functional recovery. The authors therefore tested a potential disuse model where reduced cervical range of motion mediated the effect of initial pain intensity on the development of muscle fatty infiltrates. While initial pain intensity significantly influenced the development of muscle fatty infiltrates at 6-months, the mediational effect of reduced range of motion in this relationship was not supported. Suggesting that pain and range of motion interact separately and/or possibly in tandem through other biopsychosocial pathways].

On the contrary, the relationship between high initial pain and muscle fatty infiltrates was mediated by the presence of post traumatic stree disorder symptoms at 4-weeks post-injury. To knowledge, this is the first study on whiplash to demonstrate a relationship between symptoms of post traumatic stree disorder (a psychological finding) and objective longitudinal data for muscle degeneration (a physical pathology). Support for a psychobiologic link is available. Induced sympathetic nervous system activation that may occur in tandem with posttraumatic stress symptoms is centrally programmed and has shown to exert a number of actions at the muscle level. While these actions are beneficial in the acute stage of stress, prolonged stress can negatively impact the muscle system. Excessive sympathetic outflow can produce vasoconstriction resulting in metabolic consequences such as hypoxia and toxaemia. Under this condition, intra-myocellular oxidative stresses may be responsible for inducing muscle damage. The persistent presence of oxidative stress can dramatically affect the contractility of skeletal muscle as well as induce fibrotic degeneration, commonly seen in other painful conditions (e.g. fibromyalgia) and possibly the fatty muscle changes observed in this study.

Furthermore, this may be especially important for some cases of traumatic whiplash when considering the potential for even greater consequences on health outcomes as has been observed in other populations with post traumatic stree disorder. For example, exposure to extreme stress can activate various biological processes including the release of cortisol by the adrenal glands. Sustained hypercortisolemia can profoundly impact overall health status, including the degeneration of skeletal muscle. Additional biological consequences associated with exposure to extreme stress include autonomic reactivity, disturbed sleep, lowered immunity and altered perception of symptoms. A potential conclusion to be drawn on the basis of such information is that increased levels of muscle fatty infiltrates could be related to alterations of the neuroendocrine system in some patients following whiplash, suggesting a neuro-psycho-biological link with poor outcomes. Further research to investigate the activation of various biological processes in tandem with stress system responses following whiplash is warranted and required.

This is the first study to demonstrate an association between structural muscle changes and transition to chronicity in whiplash associated disorders. These changes were predicted by higher initial pain intensity and the effect of pain intensity on muscle fatty infiltrates was mediated by symptoms of post traumatic stree disorder. While this study utilized a relatively small sample, the low variability found within groups (Figure 2, Table 2) supports the strength of the MRI measure for detecting group differences in muscle fatty infiltrates. The results of this study can therefore be interpreted with confidence in the statistical power of our analyses.

These findings may therefore have implications for the whiplash condition where the early assessment and management of stress responses may attenuate some physical aspects of the condition. This and other questions related to the origin of muscle degeneration following traumatic whiplash injury and the overall contribution to long-term outcomes requires further evaluation.

From: BMC Musculoskelet Disord. 2011 Jun 8;12(1):129. [Epub ahead of print]

Whiplash injury occurs due to an acceleration-deceleration energy transfer to the neck resulting from motor-vehicle collisions, and the term whiplash associated disorders was introduced in order to describe the sign and symptoms associated with the injury.

The prognosis of whiplash injuries show highly variable results and may be due to differences in study populations and definitions of outcome. Usually the prognosis of whiplash is favorable and self-limited. The natural course for those that report symptoms after a whiplash trauma will in most cases be rapid improvement of pain and disability the first three months. Beyond three months there is usually little improvement. It is not clear which patients are at risk of delayed recovery following whiplash injury, but a slow or poor recovery of neck pain seems to be associated with psychological factors, compensation or legal factors and initial self reported symptom severity. The course of recovery in whiplash associated disorders is very similar to the course of neck pain in the general population.

Headache, neck pain and other subjective complaints are common in the general population, and both headache and neck pain are equally frequent in patients with and without a history of whiplash. Headache is commonly reported after a whiplash trauma, but the validity of the acute and chronic whiplash headache included in the ICHD-2 criteria are questionable and represents most likely occurrences of pre-accidental primary headaches like migraine and tension type headache, The prognosis of headache after a whiplash trauma is good and similar to non-traumatized controls.

The construct validity of the whiplash syndrome is questionable, and several studies report an association between whiplash injury and a wide variety of symptoms and pain in other areas not restricted to the head and neck region. Two studies have specifically evaluated the risk factors associated with the occurrence of wide spread bodily pain after motor vehicle collision, but these studies included insurance claimants and it is therefore not known whether there is an increased prevalence of musculoskeletal complaints among subject with self reported whiplash injury in the general population. Thus the main purpose of the present study was to study the relationship between self reported whiplash injury and chronic musculoskeletal complaints and headache in a large unselected adult population.

In this large population-based, cross-sectional study, self-reported whiplash injury was associated with increased prevalence of headache and chronic musculoskeletal complaints, which was evident for all anatomical sites. Individuals with a combination of headache and chronic musculoskeletal complaints were five times more likely to report whiplash injury than those without any complaints.

The life-time prevalence of having sustained a whiplash trauma in our study was 2.9% and is much lower than the 15.9% reported in a population-based cross-sectional study among the Saskatchewan population. Published reports from the Confederation of Norwegian Enterprise comprising all the Norwegian government insurance companies indicate that the most common cause of whiplash, a rear end collision, in year 2000 involved 54000 vehicles and half of these were hit from behind, i.e. 27000 people. Over a 10 year period one can calculate that approximately 270 000, i.e. 6% of the population, will be involved in such collision. In addition comes all other traffic and sport accidents. This means that the percentage who have sustained on an accident with whiplash mechanism within a relevant time period is probably much higher than the 2.9% who self report a whiplash accident. It is therefore very likely that whiplash traumas were grossly under-reported in the present study, and that selective reporting, e.g. among those with complaints may be present.

The present results are in accordance with previous cross-sectional studies, reporting a wide variety of health complaints among persons with self-reported whiplash injury and a Swedish cohort study showed that persons with chronic pain after a whiplash injury had an increased risk for pain from different anatomical sites. There are some that argue that these symptoms might reflect central sensitization but there is also a strong association between whiplash injury and psychiatric disorders, which might reflect a reversed causality, that is, increased risk of future self-reported whiplash injury in individuals who already have anxiety and depression. Thus, the strong relationship between whiplash injury and the combination of headache and chronic musculoskeletal complaints in the present study may, at least in part, reflect personality traits rather than biological mechanisms.

It should be emphasized that in studies dealing with subjective complaints like headache, musculoskeletal pain and psychiatric symptoms, the results may be influenced by a tendency to answer in a similar way all questions regarding complaints (reporting bias). The results from the present cross-sectional study must be evaluated with caution. It cannot be determined whether whiplash injury causes neither musculoskeletal complaints nor headache, or whether other risk factors or a shared susceptibility causes these associations. Secondly, since both headache, chronic musculoskeletal complaints and whiplash injury are based on self-report, individuals with neck pain and other pain are more likely to remember and report a previous neck trauma than those without complaints, i.e. differential information (recall bias).

Even though the use of validated questionnaires reduces the risk for misclassification, the questionnaire-based diagnoses are not optimal when compared to interview diagnoses. There is a possibility of non-differential misclassification of diagnosis that might weaken real associations, but the authors think this is a minor problem as the prevalence of headache and musculoskeletal complaints in the current population is consistent with data from other population-based studies in the Western countries.

In addition the large and unselected population and the high participating rate, reduces the risk of selection bias. Selective participation was unlikely, since neither headache, neck distortion nor chronic musculoskeletal complaints were the main objectives. The impact of non-participants has been discussed in more detail previously, but the large sample size decreased the risk of chance findings and the wide range of data made it possible to adjust for potential confounding variables.

Subjects with self reported whiplash injury had significantly more headache and musculoskeletal complaints than those without, and may in part be due to selective reporting. The causal mechanism remains unclear and cannot be addressed in the present study design.

From: Man Ther. 2011 May 30. [Epub ahead of print]

Central sensitization provides an evidence-based explanation for many cases of ‘unexplained’ chronic musculoskeletal pain. Prior to commencing rehabilitation in such cases, it is crucial to change maladaptive illness perceptions, to alter maladaptive pain cognitions and to reconceptualise pain. This can be accomplished by patient education about central sensitization and its role in chronic pain, a strategy known as pain physiology education. Pain physiology education is indicated when: 1) the clinical picture is characterized and dominated by central sensitization; and 2) maladaptive illness perceptions are present. Both are prerequisites for commencing pain physiology education. Face-to-face sessions of pain physiology education, in conjunction with written educational material, are effective for changing pain cognitions and improving health status in patients with various chronic musculoskeletal pain disorders. These include patients with chronic low back pain, chronic whiplash, fibromyalgia and chronic fatigue syndrome. After biopsychosocial assessment pain physiology education comprises of a first face-to-face session explaining basic pain physiology and contrasting acute nociception versus chronic pain (Session 1). Written information about pain physiology should be provided as homework in between session 1 and 2. The second session can be used to correct misunderstandings, and to facilitate the transition from knowledge to adaptive pain coping during daily life. Pain physiology education is a continuous process initiated during the educational sessions and continued within both the active treatment and during the longer term rehabilitation program.

Over the past decades, scientific understanding of unexplained chronic pain disorders has increased substantially. It has become clear that the majority of cases of chronic musculoskeletal pain are characterized by alterations in central nervous system processing. More specifically, the responsiveness of central neurons to input from unimodal and polymodal receptors is augmented, resulting in a pathophysiological state corresponding to central sensitization, characterized by generalized or widespread hypersensitivity. Central sensitization encompasses impaired functioning of brain-orchestrated descending anti-nociceptive (inhibitory) mechanisms, and (over) activation of descending and ascending pain facilitatory pathways. The net result is augmentation rather than inhibition of nociceptive transmission. In addition to the switch in balance between inhibitory and facilitatory pathways, central sensitization entails altered sensory processing in the brain. Indeed, a modulated pain signature arises in the brain of patients with central sensitization. The altered pain neuromatrix comprises of a) increased activity in brain areas known to be involved in acute pain sensations e.g. the insula, anterior cingulate cortex and the prefrontal cortex, but not in the primary or secondary somatosensory cortex; and b) brain activity in regions generally not involved in acute pain sensations e.g. various brain stem nuclei, dorsolateral frontal cortex and parietal associated cortex. Cognitive emotional sensitization refers to the capacity of forebrain centres in exerting powerful influences on various nuclei of the brainstem, including the nuclei identified as the origin of the descending facilitatory pathways. The activity in descending pathways is not constant but can be modulated, for example by the level of vigilance, attention and stress.

From a musculoskeletal perspective, it is important to realize that distal/peripheral mechanisms take part in the pathophysiology of central sensitization as well. Many cases of chronic musculoskeletal pain evolve from traumatic or non-traumatic local nociceptive musculoskeletal problems characterized by a period of massive peripheral input in the (sub)acute to chronic stage (e.g. chronic whiplash associated disorders or patients reporting a history of several surgical procedures). In response the central nervous system modulates the sensitivity of the somatosensory system. In addition, once central sensitization is established in cases of chronic musculoskeletal pain, it remains highly plastic: any new peripheral injury may serve as a new source of bottom-up (peripheral) nociceptive input, which in turn sustains or aggravates the process of central sensitization. Without new peripheral input, central sensitization does not resolve quickly, but rather sustains the chronic nature of the condition.

From a clinical perspective, it remains challenging for clinicians to implement science into practice. Clinical guidelines for the recognition and treatment of central sensitization in patients with chronic musculoskeletal pain have been provided, yet many issues remain. For example, how should clinicians apply the science of central sensitization and chronic pain to a case of chronic whiplash where the patient is sceptical about the biopsychosocial model, and convinced that the initial neck trauma caused severe cervical damage that remains invisible to modern imaging methods? Or a patient with moderate hip osteoarthritis saying ‘The cartilage of my hips is melting away due to erosion, which in turn is triggered by overuse of my lower limbs’ and ‘I will not participate in exercise therapy because it will worsen my hip pain and hence the erosion of my cartilage’. Likewise, a patient with fibromyalgia convinced that her pain and related symptoms are due to an undetectable or ‘new’ virus, is unlikely to adhere to conservative interventions.

It is clear that initiating a treatment like graded activity is unlikely to be successful in these patients. Prior to commencing treatment in such cases the gap between the perceptions of the patient and their health care professional about pain and its treatment should be narrowed. Therefore it is crucial to change the patient’s maladaptive illness perceptions and maladaptive pain cognitions and to reconceptualise pain before initiating the treatment. This can be accomplished by patient education about central sensitization and its role in chronic pain, a strategy frequently referred to as ‘pain (neuro)physiology education’ or ‘pain biology education’. Patients with ‘unexplained’ chronic musculoskeletal pain who are misinformed about pain, consider their pain as more threatening and demonstrate lower pain tolerance, more catastrophic thoughts and less adaptive coping strategies. Treatment adherence for active treatments is often low in these patients. Therefore, education will increase motivation for rehabilitation in those with chronic musculoskeletal pain due to central sensitization. This requires a biopsychosocial assessment and an in-depth education of altered central nervous system processing of nociceptive and non-nociceptive input. This is the focus of the present paper.

The article provides a brief overview of the clinical evidence of pain physiology education in patients with chronic musculoskeletal pain. The largest part of the paper is dedicated to practice guidelines on how to apply pain physiology education in patients with chronic musculoskeletal pain.

How to explain central sensitization to patients with ‘unexplained’ chronic musculoskeletal pain: Practice guidelines