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Neck PainArticle 1 | Article 2 | Article 3 | Article 4 | Article 5 | Article 6Article 7 | Article 8 | Article 9 Chronic whiplash and central sensitization; an evaluation of the role of a myofascial trigger points in pain modulation Michael D Freeman1,2 , Ake Nystrom3 and Christopher Centeno4 Journal of Brachial Plexus and Peripheral Nerve Injury 2009, 4:2doi:10.1186/1749-7221-4-2 The electronic version of this article is the complete one and can be found online at: http://www.jbppni.com/content/4/1/2 Received: 1 December 2008 Abstract Objective Design Setting Subjects Intervention Outcome measures: pre and post injection cervical range of motion, pressure pain thresholds (ppt) over the infraspinatus, wrist extensor, and tibialis anterior muscles. sensitivity to light (photophobia) and subjects' perception of pain using a visual analog scale (vas) were also evaluated before and after injections. only the ppt was evaluated in the asymptomatic controls. Results Conclusion Introduction Chronic pain from injury, including injury from whiplash trauma, is associated with centrally mediated hyperalgesia, also known as central sensitization. [1] Several authors have described lowered pain thresholds in uninjured tissues, and explained the finding as the expression of an abnormal processing of nociceptive information in the brain and spinal cord. [2-7] Others have postulated that chronicposttraumatic myalgia (muscle pains) mayperpetuateandaccentuate thepain status of afflicted patients, [8,9] and Ge et al. recently reported experimental evidence of a physiologic link between myofascial trigger points and central sensitization in patients with shoulder pain of myofascial origin. [10] In contrast, Curatolo et al, in a study of chronic whiplash patients, reported that anesthetic infiltration of painful or tender points did not alter the signs of central sensitization. [11] An explanation for this discrepancy may lie in the definition of what constitutes a myofascial pain generator. While both 'tender points' and myofascial trigger points are painful to palpation, only myofascial trigger points will fasciculate or "twitch" when probed with a needle. [12] The presence of a twitch response to needle probing has been experimentally demonstrated as a necessary prerequisite for trigger point deactivation and pain relief with local anesthetic injection. [13] Based on these previously reported findings, it is reasonable to hypothesize that anesthetization of carefully identified trigger points may alter findings of central sensitization in patients with chronic neck pain. In the present study the authors set out to evaluate whether anesthetic infiltration of myofascial trigger points in patients with chronic and refractory neck pain can affect pain thresholds in uninjured parts of the body. Methods Seventeen participants were recruited from a group of twenty-threepatients who were referred for surgical evaluation for chronic and refractory neck pain. Inclusion criteria were as follows: 1. Male or female, 19–65 years of age. 2. Intrusive daily neck pain for at least 12 months. 3. Failure of conservative therapies, e.g. physical therapy, chiropractic manipulation, or acupuncture. Exclusion criteria included signs or symptoms of radiculopathy or myelopathy, or radiographic evidence of significant spine pathology. Institutional Review Board oversight and approval was provided by the Spinal Injury Foundation in Westminster, Colorado. Pre-intervention evaluations 2. Pressure pain thresholds (PPT) were determined on one side of the body using algometry as described by Koelbaek-Johansen et al. [2] Laterality was determined according to subjects' indication of the side with the most intense symptoms. Left was chosen as the default side ifa patient could not differentiate one side as more symptomatic then the other. The calibrated algometer had a range of 0.5 – 25 lbs (1.1–13.4 kg) distributed over a 1 cm circular tip. Test sites were in three different muscles: infraspinatus – 3 cm inferior to the scapular spine and 3 cm lateral to the medial scapular border; wrist extensor – 5 cm distal to the lateral epicondyle with forearm in full supination; tibialis anterior – 5 cm distal to the tibial tuberosity, and 2 cm lateral to the anterior tibial margin. Pain thresholds were determined by slowly and gradually increasing the pressure of the algometer tip against the marked test site. Identical protocols were used to assess pain thresholds in the study group and the control group, and all subjects were blinded with to the values recorded from each test. 3. Presence or absence of photophobia was determined by shining light from an ophthalmoscope into the ipsilateral eye for 3 seconds. Photophobia was considered present if the subject confirmed immediate onset or worsening of periocular pain or headaches. This evaluation was only performed on the study subjects. 4. Subjective assessment of neck painwas madeusing a visual analogue scale (VAS) graded 0–10. This evaluation was only performed on the study subjects. Intervention Post-intervention evaluation Control Group Statistical analysis Results Of the 23 patients presenting for evaluation 17 fit the inclusion criteria. The 6 patients who were excluded either had chronic pain that was not in the neck or had neck pain for less than 12 months. The 17 remaining patients consisted of14 (82%) female and 3 (18%) male subjects ranging in age from 26 to 59, with a mean age of 42.4 (SD 9.7). The duration of symptoms ranged from 1.5 to 18 years, with a mean duration of 8.7 years (SD 6.0). All except one described a traumatic episode as the precipitating factor for their neck pain, and most were injured in a traffic crash. (Table 1) Six subjects described current or past suicidal ideationbecause ofunremitting pain. Although all subjects used non-steroidal anti-inflammatory drugson a regularbasis, none reportedmore than occasional opioid use. All of the patients had been diagnosed with a chronic pain syndrome that was intended to describe their unremitting symptoms of neck pain, including myofascial pain syndrome, fibromyalgia syndrome, or simply "chronic neck pain." None of the subjects had been diagnosed with radiculopathy or myelopathy or cervical central stenosis, although there were several with nonspecific diagnoses of cervical spondylosis. Table 1. Attibuted cause of chronic neck pain As would be expected in a population of chronic neck pain patients, pre-injection CROMin the study group was generally lower thanstandard reference values. [14] Following the TP injection all subjects demonstrated an increase in CROM in all directions. (Figure 1; Table 2) Table 2. Pre and post injection cervical range of motion Table 3. Pre-injection PPT values, and pooled mean used for comparison with post-injection PPT Table 4. Pre and post injection changes in PPT, all measurements taken within 1 minute of the final injection Table 5. Pressure pain threshold for the controls A 57% reductionin neck pain was documented witha drop inVAS from a 6.1 (SD 1.5) before the trigger point injections, to 2.6 (SD 1.8) after the trigger point injections (p = < 0.001). (Figure 3). As the anesthetic wore off, however, all pre-injection symptoms returned to baseline over a matter of hours to several days. Figure 3. Pre and post injection subjective pain level. Discussion The present data demonstrate a remarkably rapid change in central sensitization symptoms following the anesthetizing of painful trigger points. Since the infraspinatus PPT site was relatively close to areas that had been infiltrated with anesthetic, the wrist extensor and tibialis anterior pressure sites may be considered more reliable indicators of alterations in centralpain modulation within the study group; however, there were little differences among the three tested sitesand threshold increases were uniform. Symptoms of light sensitivity (photophobia) resolved in all but 2 of the 11 subjects for the duration of the anesthetic. This result suggestsa central mechanism as the mediator between the myofascial trigger points andlight sensitivity; however, the phenomenon requires further investigation. The methods used in the present study were quite elementary; the outcome was simply the perception of eye or head discomfort when an opthalmoscope set on highest intensity was shined in the eye for 3 seconds. More precise methods of measuring eye discomfort thresholds vs. light intensity would have been required in order to draw any detailed quantitative conclusions. In contrast, the increase in cervical range-of-motion observed in the symptomatic cohort following the injections suggests that the initial finding of reduced motion was either a result of peripherally modulated pain inhibition (from the trigger points) or centrally mediated pain inhibition, or both. Differences in the techniques adopted to identify and inject trigger points may explain why the present resultsdiffer from those of Curatolo et al, who found no changes in central sensitization with tender point (as opposed to trigger point) injections. Despite the difference in outcome between the present study and what was described by Curatolo et al., the hypothesis introduced by these authors, that central modulation of pain is maintained by continued peripheral nociception arising from painful muscles in the neck, provides a comprehensive explanatory model for our results. While physiological and anatomical characteristics of myofascial trigger pointsare not completely understood, it is reasonable to posit that these entities initially arise as a protective response to injury. Why such focal pain generators persist and remain active after a reasonable healing period for soft tissue injury remains unclear. A nuisance effect that we attempted to control for was the potential impact of the infusion of intramuscular lidocaine on the pain thresholds of the symptomatic subjects. Prior authors have noted a decrease in experimentally induced hyperalgesia following intravenous (IV) administration of lidocaine. [15] Wu et al. also demonstrated a significant decrease in stump and phantom pain in an amputee population after 42 minutes of IV lidocaine infusion. [16] As opposed to the methods used in the present investigation, these studies involved IV infusions of lidocaine. Thus, the purpose of the control group in the present study was to evaluate the effect on pain thresholds of nonspecific IM lidocaine administration. This is not to say that the present design is ideal; a randomized controlled trial, in which the controls were identical to the cases (both groups with chronic neck pain) would have been preferable. For this reason it is reasonable to interpret the results of the present study with a modicum of caution. The most important conclusion to be drawn from our results, relate to the immediate and substantial changes in peripheral pain thresholds observed in the study group, where some participants had been symptomatic for more than two decades. It has been postulated that central sensitization is an expression of permanent structural or biochemical changes (neuroplasticity) in the central nervous system,[17] and therefore unlikely to change regardless of intervention Our findings therefore serve as an argument for central sensitization as a neuromodulatory process perpetuated by, and dependent upon peripheral sources of nociception referred to as trigger point. Rather than a neuroplastic condition, central sensitization may be a neuro elastic phenomenon. Our results also argue against psychological components as an etiological factor rather than consequence of chronic pain after whiplash injury. [18] While it has been suggested that litigation or monetary issues may augment chronic symptoms,[19] none of the subjects in the present study were involved in litigation and no reasonable interpretation of the present data allows for any attribution of the observations to financial motivation or emotional liability. The number of subjects in the present study compares with previously published reports within the same field of investigation, in which the authors have presented data based on studies of 11–29 subjects. [1,3,5,6] Nonetheless, some degree of caution is warranted in extrapolating the results of this study to the general chronic neck pain population before further randomized and placebo-controlled trials help bolster the validity of the conclusions presented here. It is important to note that the success of the injections may largely depend upon the skill and experience of the operator [11]. It is reasonable to suggest, based upon our conclusions and those of prior authors, that algometry of both symptomatic and asymptomatic body sites may have a practical clinical application in the contemporary evaluation of treatment success in chronic neck pain patients. Permanent solutions for the chronic pain conditions of the subjects in the present study are few; one suggestion is to surgically excise or ablate symptomatic trigger points that are associated with a decrease in local and generalized pain following anesthetization. [20] Such an approach, although intriguing, requires further description and study. Conclusion Lowered pain thresholds related to chronic neck pain may rapidly reversed by precise location and anesthetization of trigger points. While the full implications of this finding are yet to be determined; treatments aimed at permanent ablation of peripheral pain generators may offer a means of long term relief for this patient population. The results of the present study refute claims that some or all of the pain experienced by chronic whiplash patients arises from psychosocial issues, as the only treatment experienced by the study subjects was directed at the identified trigger points. Although encouraging, further study is needed to explore the ramifications of these findings. Competing interests The authors declare that they have no competing interests. Authors' contributions MF: Research design, data collection, data analysis, writing and editing of manuscript. AN: Research design, study execution, writing and editing of manuscript. CC: Research design, editing of manuscript. All authors read and approved the final manuscript. Acknowledgements The authors gratefully acknowledge the statistical review provided by Prof. Mike Hand.
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