January 2011 References Devin J. Starlanyl for http://www.sover.net/~devstar
Note: This is somewhat longer than usual, as some of these articles are from the Journal of Musculoskeletal Pain’s International Myopain Society’s presentation issue.
Aliyev R, Vieth T, Geiger G. 2010. Traditional Chinese medicine in diagnosis and treatment of fibromyalgia syndrome. Georgian Med News. (188):38-45. “Fibromyalgia Syndrome (FS) is known for the difficulties arising from classification. The accompanying pain in skeletal muscles, myofascial peri-articular structures and a number of polymorphic symptoms cannot be separated into complexes of symptoms. The application of principles of Traditional Chinese Medicine (TCM) helps in analyzing the symptoms of FS to detect a leading syndrome and thereby establish an individual therapy. Medical histories and objective examinations of 25 patients with FS and 22 patients with vertebrogenic pain syndromes were analyzed according to TCM. A questionnaire was used to determine the leading constitutional type according to the 5-elements-theory. Analyses of the results showed that 83% of patients with FS were of constitutional type of the element earth. The following syndromes were found to be important in FS: 1) liver-Qi-stagnation, 2) Yin and blood deficiency of the liver, 3) Yang-weakness of the spleen and kidney, 4) Yin-weakness of the kidney. Applying TCM for FS allows for separating a group of symptoms and thus individual therapy. The determination of the constitutional type according to the 5-elements-theory may be used for a better understanding of the disharmony pattern.”
Aparicio VA, Ortega FB, Heredia JM et al. 2011. Handgrip strength test as a complementary tool in the assessment of fibromyalgia severity in women. Arch Phys Med Rehabil. 92(1):83-88. “Handgrip strength is reduced in women with FM as well as those with severe FM from their peers with moderate FM. Identification of women who fail to meet the suggested standards can be a helpful and informative tool for clinician.” [As trigger points are known to cause grip strength failure and also to co-exist with FM, it is most likely that the failure of handgrip strength had nothing or little to do with FM, and was probably caused by coexisting TrPs. DJS]
Bazzichi L, Ciregia F, Giusti L et al. 2009. Detection of potential markers of primary fibromyalgia syndrome in human saliva. Proteomics Clin Appl. 3(11):1296-1304. “In the last few years, many attempts have been carried out for the research of specific biological biomarkers in fibromyalgia (FM) since, so far, no laboratory tests have been appropriately validated for the diagnosis and the prognostic stratification of the disease. In our study for the first time, we carried out a proteomic analysis of the whole saliva of FM patients in order to evaluate salivary biomarkers. Twenty-two FM patients with all fulfilling the American College of Rheumathology diagnostic criteria for FM and 26 sex-and age-matched healthy subjects were enrolled in the study. The most relevant observation which emerged from the data analysis was the exclusive and significant over-expression of transaldolase and phosphoglycerate mutase I. These findings were validated by Western blot analysis and the total optical density confirmed the significant up-regulation of transaldolase and phosphoglycerate mutase I in FM samples with respect to healthy subjects. It was noteworthy that seven further salivary proteins resulted differentially expressed. These preliminary results demonstrated the utility of salivary proteomic analysis in the identification of salivary biomarkers in FM patients and in clarifying some of the pathogenetic aspects of the disease.”
Boehm A, Eisenberg E, Lampel S. 2010. The Contribution of Social Capital and Coping Strategies to Functioning and Quality of Life of Patients with Fibromyalgia. Clin J Pain. [Dec 20 Epub ahead of print]. “Bonding social capital, problem-solving coping strategies, and the duration of FM contribute positively to functioning and QoL (quality of life) of FM patients; whereas, emotional-focused coping strategies do the opposite. Further research to test the effects of strengthened social capital and enhanced problem-solving rather than emotion-focused coping strategies on functioning and QoL of FM patients is warranted.”
Brage S, Ihlebaek C, Natvig B et al. 2010. [Musculoskeletal disorders as causes of sick leave and disability benefits] Tidsskr Nor Laegeforen. 130(23):2369-2370. [Norwegian] “Of the musculoskeletal disorders, low back conditions are the most frequent causes of sick leave and disability benefits, and account for 11 and 9% respectively. Neck and shoulder disorders are also common causes of sick leave, while osteoarthritis and fibromyalgia are common causes of disability benefits and each account for 5% of all new cases. The labor and welfare administration should continue to focus on musculoskeletal disorders to prevent long-term sick leave and permanent absence from work.”
Cady RJ, Hirst JJ, Durham PL. 2010. Dietary grape seed polyphenols repress neuron and glia activation in trigeminal ganglion and trigeminal nucleus caudalis. Mol Pain. 6:91. “Results from our study provide evidence that grape seed extract may be beneficial as a natural therapeutic option for temporomandibular joint disorders by suppressing development of peripheral and central sensitization.”
Correa A, Miro E, Martinez MP et al. 2010. Temporal preparation and inhibitory deficit in fibromyalgia syndrome. Brain Cogn. [Dec 10 Epub ahead of print]. “Cognitive deficits in fibromyalgia may be specifically related to controlled processes, such as those measured by working memory or executive function tasks. This hypothesis was tested here by measuring controlled temporal preparation (temporal orienting) during a response inhibition (go no-go) task. Temporal orienting effects (faster reaction times for targets appearing at temporally attended vs. unattended moments) and response inhibition were impaired in fibromyalgia compared to the control group. It is concluded that frontal networks underlying attentional control (temporal orienting and response inhibition) can be a dysfunctional neurocognitive mechanism in fibromyalgia.”
Culpepper L. 2010. Pharmacologic therapy for fibromyalgia. J Clin Psychiatry. 71(12):e34. “While nonpharmacologic strategies can help patients understand and accept the diagnosis of fibromyalgia, pharmacologic therapy can provide important additional symptom relief and improvement in functioning. Pharmacologic therapy must be individualized based on a comprehensive evaluation of the patient and continued assessment of symptoms and response to treatment. Patient symptoms and impairments related to each of the dimensions of the ‘fibromyalgia triad’ (pain, sleep dysfunction, and mood disorders) as well as any other comorbidities, past experiences with treatment, and patient preferences should guide therapy selection.”
Fernandez-de-las-Penas C. 2010. New evidence for trigger point involvement in tension-type headaches. J Musculoskel Pain. 18(4):354-360. “Tension-type headache (TTH) is the most common form of headache and its chronic form (chronic tension-type headache (CTTH)) is one of the most neglected and difficult headaches to treat. TTH is an overarching syndrome of ‘featureless’ headaches characterized by nothing but pain in the head. The term ‘tension-type’ has been chosen by the International Headache Society (ICHD-II) to offer a new heading underlining the uncertain pathogenesis, but indicating that some form of muscle tension may play a role. Hyperalgesic and allodynic responses support the role of both peripheral and central mechanisms in the development of the clinical picture of CTTH. In fact, it is suggested that central sensitization, a reduction in inhibitory pain mechanisms, and peripheral sensitization of muscle nociceptors are mechanisms involved in perceived pain in CTTH. Subjects who develop TTH have showed normal tenderness scores and pressure pain threshold levels before the beginning of the symptoms, which suggests that the mechanical hypersensitivity is rather a consequence than a risk factor for the development of TTH.” “Previous studies have found that TTH patients described their head pain as pressing, tightening, or soreness. Dull and tight heaviness are also pain quality features of TTH attacks. These pain features resemble the descriptions of clinically referred pain elicited by TrPs as described by Simons et al.” “Recent clinical studies have clearly demonstrated the relevance of active TrPs in CTTH. In fact, recent studies have described the referred pain elicited from two extra-ocular muscles, i.e., superior oblique and lateral rectus in patients with CTTH.”
Fernandez-Lao C, Cantarero-Villanueva I, Fernanndez-de-Las-Penas C et al. 2010. Widespread Mechanical Pain Hypersensitivity as a Sign of Central Sensitization after Breast Cancer Surgery: Comparison between Mastectomy and Lumpectomy. Pain Med. [Dec 10 Epub ahead of print]. “The current study found widespread pressure pain hyperalgesia in women who received breast cancer surgery suggesting central spreading sensitization. The degree of central sensitization was similar between lumpectomy and mastectomy surgery.”
Finan PH, Zautra AJ, Davis MC et al. 2010. COMT moderates the relation of daily maladaptive coping and pain in fibromyalgia. Pain. [Dec 2 Epub ahead of print]. “Forty-five women with fibromyalgia (FM) engaged in a 30-day electronic diary assessment, recording daily ratings of pain and 2 forms of maladaptive coping: pain catastrophizing and pain attention. Participants were genotyped for the val(158)met single nucleotide polymorphism (rs4680) in the catechol-O-methyltransferase (COMT) gene. COMT genotype moderated the daily relations of both maladaptive coping processes and pain. FM women with the homozygous met/met genotype evidenced more pain on days when pain catastrophizing was elevated relative to heterozygous and homozygous val(158) carriers. FM women with the homozygous met/met genotype evidenced more pain on days when pain attention was elevated relative to those with the homozygous val/val genotype. Evidence is presented to suggest that these are independent effects. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process, which has been previously characterized in a sample of postoperative shoulder pain patients. Further, the findings advance our understanding of the role of COMT in FM, suggesting that genetic variation in the val(158)met polymorphism may affect FM pain through pathways of pain-related cognition. This study examined 2 forms of maladaptive coping: pain catastrophizing and pain attention. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process and suggest that genetic variation in the val(158)met polymorphism may affect fibromyalgia pain through pathways of pain-related cognition.”
Gerwin R. 2010. Myofascial pain syndrome: here we are; where must we go? J Musculoskel Pain. 18(4):329-347. “MPS was first defined clinically by Janet Travell, MD, and later by David Simons, MD. Pain neurophysiology has only recently provided the basis for understanding the sensorimotor manifestations of MPS. This article reviews the current state of knowledge concerning MPS. MPS is a form of myalgia characterized by local regions of muscle hardness and tenderness that cause referred pain. The signature feature is the trigger point, a tender, taut band of muscle that can be painful spontaneously or when stimulated. The active trigger point has identifiable pathophysiologic changes. Levels of substance P, calcitonin gene related peptide, bradykinin, and assorted cytokines, are elevated, indicating a chemical inflammation. Trigger point milieu pH is low, about pH 5, consistent with hypoxia and ischemia. Persistent, low-amplitude, high-frequency electrical discharges that look like endplate potentials characteristic. The taut band can be visualized using high definition ultrasonograpy and magnetic resonance sonography. Central scanning. The role of MPS in headache and pelvic pain has been extensively studied in the last few years. Although great progress has been made, studies are still needed to substantiate the energy crisis hypothesis of trigger point formation, to understand the nature of sustained muscle contraction that forms the taut band and of referred pain in humans, and to develop a more rationale and effective treatment.”
“Nociceptive activity from TrPs activates spinal cord dorsal horn neurons and sensitizes the central nervous system, causing central sensitization, hyperalgesia, and referred pain. Muscle weakness without atrophy occurs due to TrP-induced motor inhibition. Restricted range of motion occurs because of the shortening of the contracted taut band, and perhaps because of pain. The range of motion in hypermobile individuals must be interpreted cautiously, because it can appear to be normal, but can still be restricted. Impaired reciprocal inhibition results in co-contraction of agonists and antagonists, thus interfering with fine motor control and coordination. Autonomic disturbances can accompany TrP activation leading to changes in skin temperature and color, piloerection (goosebumps), and lacrimation (tearing). The clinically evident progression from a non-tender taut band to a tender taut band suggests that the first change in muscle is the development of the contracted, taut group of muscle fibers that can become painful when sufficiently stressed.”
“Myofascial pain syndrome presents as acute and chronic muscle pain. It may be regional or widespread. It may be accompanied by a sensory component of parasthesias or dysesthesias. MPS may persist long after the initiating cause of pain has resolved. Thus, myofascial pain can be complex.” “Muscles harboring a TrP are often weak. Weakness in affected muscles occurs without atrophy, and is not neuropathic or myopathic. It is rapidly reversible immediately on inactivation of the TrP, suggesting that it is caused by the inhibition of muscle action a TrP in one muscle can inhibit effort or contractile force in another muscle.” “The TrP causes a disordered recruitment of muscles that work together to produce an action.” “Reciprocal inhibition, whereby contraction of one muscle is inhibited by the contraction of its antagonist muscle, is reduced or absent when the activated muscle contains a TrP. The lack of reciprocal inhibition causes co-contraction that reduces the quality of movement and leads to clumsiness and an incoordination of fine movement.” “The range of motion around a joint moved by muscles with TrPs is often limited. The end range may be painful, but limitation of the range may be painless unless the patient is pushed to move beyond comfort. Limitation of range of motion is not a reliable indicator of the presence of a TrP in persons who are hypermobile.
Changes in spatial distribution also occur with muscle contraction, the changes correlating with the duration of contraction. This suggests that a more long-lasting nociceptive irritant like a TrP would also cause a functional spatial reorganization of muscle activity. The TrP is a tender focus in muscle, the region of tenderness always located on the taut band. The region of greatest hardness is usually also the region of greatest tenderness. A tender TrP always means that there is hyperalgesia or allodynia.”
“Miniature endplate potentials are thought to be the result of spontaneous release of acetylcholine from motor nerve potentials. It is now clear that motor endplates are more widely distributed throughout the muscle than just the endplate zone. A greater endplate activity and consequently greater focal muscle sarcomere compression can be thought of as being associated with greater local muscle injury and local release of nociceptive substances.” “It is likely that TrPs are first formed as latent TrPs and then become tender as muscle is activated. Latent TrPs exist without spontaneous pain. Furthermore, TrP tenderness does not occur except in regions of muscle hardness, but regions of muscle hardness occur without local or referred pain. Hence, muscle hardness or the taut band that occurs in the absence of pain may be the first abnormality, and the active TrP is a more activated TrP.” “Current thinking in keeping with the expanded integrated hypothesis of the TrP is that localized ischemia is associated with the acute development and maintenance of the TrP. Localized ischemia results from capillary compression within the taut band. In turn, the release of vasodilating substances such as calcitonin gene-related peptide (CGRP) and substance P leads to localized non-inflammatory edema that further compresses capillaries. The initial change in the muscle associated with the TrP seems to be a motor abnormality, the development of the taut band.”
“Sympathetic modulation of the SEA is the most important concept because of the important role the sympathetic nervous system plays in maintaining the abnormal electrical activity at the TrP. A post-synaptic muscle dysfunction that increases intracellular calcium concentration through a leaky ryanidine receptor calcium channel on the sarcoplasmic reticulum membrane or through adrenergic-mediated second-messenger systems involving protein kinase C and cyclic adenosine monophosphate (cAMP), initiating actin-myosin interaction, may also result in muscle fibril contraction. Calcium channel activity is important in the generation of TrP endplate noise.” “The association of endplate noise and the trigger zone has led to the suggestion that the trigger zone is where the endplate zone is located and that is in mid-belly of the muscle. However, the muscle mid-belly is not always obvious and depends on the specific anatomy of the muscle.” “The myofascial trigger zone or region is hypoxic, a region of severe oxygen desaturation at the core surrounded by a region of increased oxygenation, consistent with capillary compression and ischemia. The core is ischemic and the surrounding zone hyperemic. Temperature studies of the trigger zone showed an increase in temperature in the TrP region, consistent with a hyperemic outer area but inconsistent with a hypoxic trigger zone core.” “TrP tenderness is associated with central sensitization and hypersensitivity, as is the case with other tissues. Central sensitization is the mechanism through which referred pain occurs. One of the consequences of central sensitization is the activation of otherwise ineffective (sometimes called ‘sleeping’) synaptic connections from one afferent nerve fiber to many recipient nociceptive neurons. A single dorsal horn neuron will thus respond to a larger pool of afferent fiber connections, thereby greatly expanding its receptive field.” “The most common referred pain patterns are within the same or adjacent spinal segments as that of the primary sensory nerve. Thus, TrPs in muscles innervated predominantly by the C5 nerve root refer pain largely to the C5 dermatome and myotome, overlapping into the C4 and C6 innervated areas. Because muscle innervation is relatively constant, segmental referred pain patterns tend to be relatively constant from one person to another. The activation of latent TrPs in one muscle results in increased motor activity in a distant muscle latent TrP in the same segmental level.” “The segmental spread of referred pain can also be bilateral.” “In summary, central sensitization and widespread pain referral is clinically important because individuals who have had seemingly local injury producing persistent pain can develop extraordinarily widespread pain with hyperalgesia or allodynia that appears to involve most of the body.” “The proposal discussed herein is that muscle overuse, or bio-mechanical stress, is the cause of the TrP. Supramaximal muscle contraction or overloaded eccentric contraction can damage muscle and lead to pain, including delayed onset muscle soreness. Repetitive strain is a variant of muscle overload and is thought to have the same effect. The maintenance of fixed positions for long periods of time and sustained contraction of muscle as a result of emotional stress (anxiety, fear, and depression) are also thought to produce muscle overuse. There has long been a concern about the overlap of FMS and MPS, a concern now resolved with the understanding that FMS is a central pain disorder and MPS has a major central hypersensitization component. Therefore, it is not surprising that there are TrPs at many if not all of the sites selected for tender point assessment in FMS and that TrPs present as a comorbid finding in FMS can contribute to pain in FMS. Thus, the concurrence of the two conditions in individual patients with clinical pain syndromes is to be expected. Nearly one-quarter of patients with chronic cervical myofascial pain met the criteria for FMS. An earlier study found that 75 percent of subjects with FMS had clinically significant MPS. TrPs may be a peripheral pain generator initiating or sustaining FMS, or may occur secondarily to the development of central sensitization in FMS. No study has looked at the effect of treating TrPs on comorbid FMS.” “the hyperirritable nodule does not have to be a palpable nodule at all. However, the taut band is a constant finding in active and latent TrPs, and is the only consistent objective finding on physical examination.” “Dommerholt and Gerwin (unpublished data) found that identification of a taut band, tenderness of the taut band, and reproduction of the patient's pain were sufficient to guide effective treatment and presented this concept at the International Myopain Congress in Italy in 1998.” [This is the International Myopain President’s Address from the Myopain Congress 2010, and it is dedicated to David G. Simons MD. I believe Dr. Simons is very proud of it. It is strongly suggested that interested readers obtain the whole article from Journal of Musculoskeletal Pain. In my opinion, this is the best summary of myofascial medicine available. DJS]
Giamberardino MA, Affaitati G, Costantini R. 2010. Visceral referred pain. J Musculoskel Pain. 18(4):403-410. “Visceral referred pain occurs in somatic areas neuromerically connected with the affected organs where secondary hyperalgesia takes place mostly in deep body wall tissues, extending to superficial layers in repeated/prolonged visceral processes. When two internal organs sharing part of their central sensory projection are affected, visceral pain and referred hyperalgesia from each organ are significantly enhanced (‘viscero-visceral hyperalgesia’). In this case, treatment of one visceral condition significantly improves symptoms from the other. Referred phenomena are mainly sustained by central sensitization processes, involving viscero-somatic or viscero-visceral-somatic convergent neurons, as shown by electrophysiological studies in animal models. A contribution by viscero-somatic reflexes is also present, which would account for the trophic changes of deep body wall tissues that often accompany the hyperalgesia. The expression of visceral referred pain is reduced with the aging process, which renders diagnosis more difficult in the elderly, increasing the risks in life-threatening conditions. Some of the contributing mechanisms may include age-related impaired A-Delta fiber function and a reduction in the content and turnover of neurotransmitter systems involved in nociception. Visceral referred pain and accompanying phenomena are being increasingly understood as regards their pathophysiology. This opens new avenues for treatment strategies that are more mechanism-based and not purely symptomatic.”[As it is important to understand the concepts of viscero-somatic and somato-visceral referred pain, it is also important to understand how visceral pain can lead to central sensitization. As this article demonstrates, even advanced age can lead to referred visceral pain. DJS]
Glass JM. 2010. Cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain. 18(4):367-372. “Fibromyalgia syndrome (FMS) is characterized by chronic, widespread, musculoskeletal pain, but symptoms other than pain are common. Dyscognition is a term used to refer to subjective feelings and objective performance measures of cognitive dysfunction. In this paper, the evidence for dyscognition in FMS is reviewed. Dyscognition is a prevalent symptom among patients with FMS that can be very disruptive. Studies using self-report measures support patient reports of dyscognition, demonstrating perceived problems across a number of cognitive domains. Tests using performance-based measures of cognitive function also support patient reports of dyscognition. Furthermore, these tests have thus far revealed a pattern of impairment in working memory and attention/executive control as well as memory impairment. Dyscognition is a real and troubling symptom for many patients with fibromyalgia. However, the body of research on dyscognition in FMS is still quite small. More research is needed to understand the factors that contribute to dyscognition and treatment approaches that help with dyscognition and to understand the cognitive symptoms that are affected, including neuroimaging studies.” “Although pain is the defining symptom, it is well known that other symptoms often accompany FMS, including fatigue, somatic complaints, mood disorders, and cognitive dysfunction. Researchers have used the term ‘dyscognition’ to refer to both self- reported cognitive problems and objective dysfunction seen on performance-based measures of cognition. Patients refer to the subjective experience of cognitive dysfunction as ‘fibrofog,’ and several studies point to the salience of this particular symptom. Memory and concentration problems are reported by many patients, following pain, stiffness, fatigue, and nonrestorative sleep as the most prevalent symptoms. When dyscognition problems are present, patients report that they are very disruptive.” “Glass et al. found that FMS patients reported lower memory capacity, more negative change in memory, and more anxiety about memory performance than healthy age- and education-matched controls. Of interest was the fact that patients also reported more use of strategies to support memory while at the same time reporting lower self-efficacy over memory performance. Specifically, tests that focus on working memory and on executive control of attention, as well as tests of long-term verbal episodic and semantic memory, appear to be most likely to reveal dysfunction. Working memory is the ability to briefly store a small amount of information in mind while performing other mental operations. The evidence to date suggests that the aspect of working memory that is most affected in FMS is the ability to maintain attention or to manage the items in working memory, rather than with the simple storage of items for a brief period. Consistent with this view, FMS patients perform poorly on tests that involve attentional control and the ability to ignore distraction suggest that FMS patients have a particular difficulty dealing with distraction or managing attention. This ability to manage distraction is part of a domain of cognitive abilities called executive function. In addition to working memory and attention control tests, several studies point to problems with memory function in FMS patients.” “Dick et al. found that when pain was included as a covariate in their analyses, differences between FMS patients and controls became nonsignificant. These results suggest that the most important contributor to cognitive dysfunction in FMS is pain, but this is still very much a preliminary conclusion.” [This article is a masterful presentation of what we know now about FM cognitive dysfunction. DJS]
Hayes SM, Myhal GC, Thornton JF et al. 2010. Fibromyalgia and the therapeutic relationship: where uncertainty meets attitude. Pain Res Manag. 15(6):385-391. “GPs reported insufficient knowledge and skill in diagnosing fibromyalgia, with not all believing it to be a diagnosable condition. Twenty-three per cent of GPs and 12% of specialists characterized fibromyalgia patients as malingerers. They further reported a lack of knowledge and skill in treating fibromyalgia including the pain, sleep disorders and mood disorders related to the condition Specialists shared these challenges, although to a lesser degree. Attitudinal issues centered around frustration and negative profiling of fibromyalgia patients. Findings revealed the presence of GP attitudinal and confidence challenges in caring for fibromyalgia patients. As care of fibromyalgia patients moves to general practices, these fundamental competencies must be addressed to assure that all patients receive the quality of care necessary to manage their disease and to empower physicians to be more professionally effective. As stated by one patient, ‘why are we being penalized for having this disability?’” [As the information on central sensitization mounts, it is sad to see so much evidence that so few care providers in the trenches are reading it and understanding what they read. Patients do get penalized for the ignorance of their care providers, and thus the care providers are doing them harm, failing to providing care because they do not understand fibromyalgia (and other central sensitization states), or myofascial trigger points, two of the three most common causes of musculoskeletal pain. DJS]
Hoffmann RG, Kotchen JM, Kotchen TA et al. 2010. Temporomandibular Disorders and Associated Clinical Comorbidities. Clin J Pain. [Dec 20 Epub ahead of print]. “The TMJD (temporomandibular joint and muscle disorders) -affected individuals were on average 41 years of age and predominantly female (90%). Nearly 60% of both men and women reported recent pain of moderate-to-severe intensity with a quarter of them indicating interference or termination of work-related activities. In the case-control comparison, a higher frequency of headaches, allergies, depression, fatigue, degenerative arthritis, fibromyalgia, autoimmune disorders, sleep apnea, and gastrointestinal complaints were prevalent among those affected with TMJD. Many of the associated comorbid conditions were over 6 times more likely to occur after TMJD was diagnosed. Among a wide array of treatments used (46 listed), the most effective relief for most affected individuals (91%) was the use of thermal therapies-hot/cold packs to the jaw area or hot baths. Nearly 40% of individuals affected with TMJD patients reported one or more surgical procedures and nearly all were treated with one or many different medications. Results of these treatments were generally equivocal. Although potentially limited to the most severe TMJD affected individuals, the survey results provide a comprehensive dataset describing the clinical manifestations of TMJD. The data provide evidence that TMJD represent a spectrum of disorders with varying pathophysiologies, clinical manifestations, and associated comorbid conditions. The findings underscore the complex nature of TMJD, the need for more extensive interdisciplinary basic and clinical research, and the development of outcome-based strategies to more effectively diagnose, prevent, and treat these chronic, debilitating conditions.” [It is unfortunate that these patients were not assessed for co-existing myofascial trigger points, which can cause TMJD, are treatable, and are often components of other co-morbidities as well. DJS]
Hussain SA, Al-Khalifa II, Jasim NA et al. 2010. Adjuvant use of melatonin for treatment of fibromyalgia. J Pineal Res. [Dec 16 Epub ahead of print]. “Using melatonin (3mg or 5mg/day) in combination with 20 mg/day fluoxetine resulted in significant reduction in both total and different components of FIQ score compared to the pretreatment values. In conclusion, administration of melatonin, alone or in a combination with fluoxetine, was effective in the treatment of patients with FMS.”
Kawase T, Maki A, Takata Y et al. 2010. Effects of neck muscle vibration on subjective visual vertical: comparative analysis with effects on nystagmus. Eur Arch Otorhinolaryngol. [Dec 23 Epub ahead of print]. “In patients with unilateral vestibular dysfunction, vibratory stimulation to the neck muscles not only induces shift of the subjective visual vertical (SVV), but also enhances the generation of nystagmus. In the present study, the effects of neck vibration on the SVV were compared with those on nystagmus in patients with unilateral vestibular schwannoma (14 patients; 6 males and 8 females, mean age 54.2Â years). The results indicated that the presence of nystagmus and magnitude of the SVV were generally correlated, neck vibration significantly increased the abnormal shift of the SVV and the presence of nystagmus, and the effects of vibration to the ipsilateral dorsal neck were significantly larger than those to the contralateral dorsal neck on the SVV, whereas no significant difference was observed in slow phase velocity of nystagmus. The present study suggests that both SVV and nystagmus induced by vibration have many similar clinical features and may be important in assessing the unilateral vestibular dysfunction.” [Vestibular dysfunction is a common but often undiagnosed co-existing disorder of FM and CMP. DJS]
Mayoral del Moral O. 2010. Dry needling treatments for myofascial trigger points. J Musculoskel Pain. 18(4):411-416. “There exist different dry needling techniques that can be used in the treatment of trigger points. These techniques seem to be effective in treating this condition. There seems to be an increasing number of indications of these techniques within the context of myofascial pain syndrome. Dry needling techniques are rapidly expanding among healthcare providers. More research is needed to know the mechanisms of dry needling in order to improve its efficiency and the patients’ tolerance of the techniques.” There are multiple dry needling techniques, and all require training and experience.
Mense S. 2010. How do muscle lesions such as latent and active trigger points influence central nociceptive neurons? J Musculoskel Pain. 18(4):348-353. “Spontaneous pain is mainly due to ongoing activity in nociceptive neurons in the spinal cord. Allodynia and hyperalgesia can be explained by a sensitization of central nociceptive neurons (central sensitization). One mechanism of central sensitization is the release of substance P together with glutamate from presynaptic terminals of nociceptive fibers from muscle. Other steps of sensitization are the opening of N-methyl-d-aspartate channels on postsynaptic neurons and the de novo synthesis of ion channels. The current concept of pain referral assumes that the efficacy of synaptic connections of central dorsal horn neurons can change under the influence of a nociceptive input. Thus, ineffective synaptic connections can become effective. Pain referral appears to reflect the formation of new effective central nervous connections.” “Myofascial TrPs are not merely a peripheral phenomenon, the input from TrPs leads to hyperexcitability of central neurons that manifests itself in allodynia, hyperalgesia, and pain referral. These central changes are mainly based on an increase in the synaptic efficacy of central connections induced by nociceptive input.” “Allodynia (pain evoked by stimuli that are not normally painful) and hyperalgesia (stronger than usual pain evoked by a painful stimulus) can be explained by a sensitization of central nociceptive neurons (central sensitization).” “One mechanism of central sensitization is the release of the neuromodulator SP together with glutamate from presynaptic terminals of nociceptive fibers from muscle.” [This article explains how TrPs can cause central sensitization states such as FM, and that glial cell activation is a critical part of this process. DJS]
Mizumura K, Murase S, Taguchi T. 2010. Animal models of myofascial trigger points. J Musculoskel Pain. 18(4):361-366. “The sensitization of muscle nociceptors to mechanical stimulation by NGF up-regulated in the muscle after LC is considered to be a mechanism for mechanical hyperalgesia after exercise. Determining whether there is any difference in expression of NGF or sensitivity of muscle nociceptors in the TrP and in other areas will be an important key for clarifying the mechanism of TrPs.” This article also explains mechanisms involved in delayed onset muscle soreness.
Pavlou M, Quinn C, Murray K et al. 2010. The effect of repeated visual motion stimuli on visual dependence and postural control in normal subjects. Gait Posture. [Dec 6 Epub ahead of print]. “Patients with vestibular dysfunction, migraine and/or anxiety may experience visual vertigo (VV), whereby symptoms are provoked by disorienting visual environments (e.g., supermarkets). Patients with VV over rely on vision for balance (i.e., visually dependent). Visual vertigo significantly improves when vestibular rehabilitation incorporates exposure to optokinetic stimulation (OKS). However, whether OKS exposure induces a reduction in visual dependency is unknown. This study investigated this issue by measuring visual dependency before and after repeated OKS exposure. Twenty-six healthy subjects (10 males; mean age 29.8 years, range 20-42 years) were randomly allocated into an OKS group who underwent graded OKS exposure for five consecutive days, or a no intervention control group. Assessment included the 'Rod and Frame' and 'Rod and Disc' tests where subjects set the subjective visual vertical in darkness, facing a tilted luminous frame or luminous rotating disc, respectively. Postural sway measures were obtained with eyes open, closed and facing the rotating disc. Results showed significant reductions in subjective vertical tilt with the frame and rotating disc for the OKS group only. Total sway path and mean deviation induced by the rotating stimulus decreased significantly only for the OKS group (p<0.01), as did the Kinetic Quotient (disc rotation/eyes open sway path ratio; p=0.04). The Romberg Quotient (eyes closed/eyes open ratio) showed no change. Findings suggest visual dependency, both at a perceptual and a postural level, can be reduced with short-term graded OKS exposure in healthy subjects. This has important implications for treatment of patients with VV and balance disorders.”
Ricci NA, Aratani MC, Dona F et al. 2010. [A systematic review about the effects of the vestibular rehabilitation in middle-age and older adults.] Rev Bras Fisioter.14(5):361-371. [Portuguese] “The studies included in this review provide evidence for the positive effects of VR (vestibular rehabilitation) in elderly and middle-aged adults with vestibular disturbances.”[Vestibular dysfunction is a frequent co-existing condition in patients with FM and CMP. DJS]
Robinson ME, Craggs JG, Price DD et al. 2010. Gray Matter Volumes of Pain-Related Brain Areas are Decreased in Fibromyalgia Syndrome. J Pain. [Dec 9 Epub ahead of print].
“Fibromyalgia (FM) is a chronic, widespread musculoskeletal pain disorder that is very prevalent in the general population (approximately 5%). Accumulating evidence suggests that FM is associated with central pain processing abnormalities, i.e., central sensitization. Several previous studies of chronic pain patients, including FM, have shown gray matter atrophy of brain areas associated with sensory and affective pain processing. These findings, however, have not been confirmed in all FM studies. In this study, we investigated gray matter volumes of brain areas associated with pain-related areas of FM patients identified by functional brain imaging
Using a more stringent analysis than other VBM (voxel-based morphometric) studies, we provide evidence for decreased gray matter volumes in a number of pain-related brain areas in FM. Although the mechanisms for these gray matter changes are presently unclear, they may contribute to some of the core features of this chronic disorder including affective disturbances and chronic widespread pain. Increasing evidence supports the association of chronic pain with accelerated gray matter atrophy in pain disorders like low back pain, IBS, and FM syndrome. However, cause-effect relationships between chronic pain and decreased gray matter volumes have not been established yet and will require future prospective studies.”
Roosink M, Renzenbrink GJ, Buitenweg JR et al. 2010. Somatosensory Symptoms and Signs and Conditioned Pain Modulation in Chronic Post-Stroke Shoulder Pain. J Pain. [Dec 16 Epub ahead of print]. “Persistent shoulder pain is a common complication after stroke. Its etiology and underlying mechanisms are not well understood and treatment is generally unsatisfactory. The objective of this study was to assess the role of central sensitization and disinhibition in chronic stroke patients with chronic PSSP (n = 19), pain-free stroke patients (n = 29), and healthy controls (n = 23). Sensory abnormalities were more frequently observed and more severe in patients with PSSP, including positive signs such as allodynia at the affected side and generalized hyperalgesia at the unaffected side. CPM was similar in stroke patients and healthy controls. This study showed that chronic PSSP was associated with several positive and negative somatosensory signs, implicating a role for central sensitization and possibly for disinhibition. Since the causal relationship remains unclear, and may be related to either neuroplasticity induced by ongoing nociception as well as to the neuropathic brain lesion, prospective studies are warranted. The assessment of somatosensory symptoms and signs and endogenous pain modulation demonstrated a role for central sensitization and possibly for disinhibition in chronic PSSP. Prevention and treatment of PSSP could benefit from a more detailed analysis of both peripheral and central pain mechanisms.” [It would be interesting to check these patients for those TrPs that cause shoulder pain. It is very likely that there are treatable myofascial components to post-stroke pain. DJS]
Schleip R, Zorn A, Klinger W. 2010. Biomechanical properties of fascial tissues and their role as pain generators. J Musculoskel Pain. 18(4):393-395. “In addition to a tensional load bearing function of tendons and ligaments, muscles transmit a significant portion of their force via their epimysia to laterally positioned tissues, such as to synergistic or antagonistic muscles. Fascial tissues are commonly used as elastic springs (catapult action) during oscillatory movements, such as walking, hopping, or running, in which the supporting skeletal muscles contract rather isometrically. They are prone to viscoelastic deformations such as creep, hysteresis, and relaxation. Such temporary deformations alter fascial stiffness and may take several hours for recovery. There is a gradual transition zone between reversible viscoelastic deformation and complete tissue tearing. Micro tearing of collagenous fibers and their interconnections has been documented in this zone. Fascia is densely innervated by myelinated nerve endings, which are assumed to serve a proprioceptive function. These are Pacini (and paciniform) corpuscles, Golgi tendon organs, and Ruffini endings. In addition they are innervated by free endings, containing substance P, suggestive of a nociceptive function. New findings suggest that nociceptive activity of epimysial fasciae play a major role in delayed onset muscle soreness subsequent to repetitive concentric exercise. “Fascial tissues serve important load bearing functions. The innervation of fascia indicates a sensory role as an organ for propriocepton, and also a potential nociceptive function. Micro tearing and/or inflammation of fascia can be a direct source of musculoskeletal pain. Fascia may be an indirect source of back pain.” “Following the proposed comprehensive terminology of the 1st Fascia Research Congress, this brief review considers all collagenous connective tissues as ‘fascial tissues’ whose morphology is dominantly shaped by tensional loading and which can be seen to be part of an interconnected tensional network throughout the whole body.” “Fascial tissues serve important load bearing functions. Severe tensional loading can induce temporary viscoelastic deformation and even micro tearing. The innervation of fascia indicates a potential nociceptive function. Micro tearing and/or inflammation of fascia can be a direct source of musculoskeletal pain. In addition, fascia may be an indirect source of, e.g., back pain, due to a sensitization of fascial nerve endings associated with inflammatory processes in other tissues within the same segment.”
Siler AC, Gardner H, Yanit K et al. 2010. Systematic Review of the Comparative Effectiveness of Antiepileptic Drugs for Fibromyalgia. J Pain. [Dec 9 Epub ahead of print]. “Fibromyalgia is a difficult-to-treat chronic pain syndrome that affects 2% of the US population. Pregabalin is an antiepileptic recently FDA approved for fibromyalgia treatment. Other antiepileptics have been suggested for treatment. This systematic review examines the relative benefits and harms of antiepileptic drugs in the treatment of fibromyalgia. A literature search was conducted and 8 studies matched criteria (7 studies of pregabalin, 1 of gabapentin). Both drugs reduced mean pain scores more than placebo at a modest rate (pregabalin, 38% to 50%; gabapentin, 51%). In a 6-month trial of pregabalin responders, 32% continued to have response at 6 months, with a mean time to loss of response of 34 days. Compared to placebo, the drugs had similarly high rates of adverse events and withdrawals. Without a head-to-head trial it is not possible to conclude if 1 antiepileptic is more effective or harmful than the other, although limited evidence suggests potential differences. Future studies must directly compare the drugs, include a more broadly defined population, examine long-term benefits and harms, and include cointerventions. We conclude that pregabalin and gabapentin are modestly effective for the treatment of fibromyalgia but that their long-term safety and efficacy remain unknown. This systematic review evaluates the benefits and harms of using the antiepileptic drugs gabapentin and pregabalin for the treatment of fibromyalgia. Conclusions from this paper can help clinicians to more effectively treat the pain associated with fibromyalgia.”
Spaeth M. 2010. Fibromyalgia syndrome treatment from a multidimensional perspective. J Musculoskel Pain. 18(4):373-379. “Fibromyalgia syndrome (FMS) is a pain syndrome which is not due to tissue damage or inflammation, and is thus fundamentally different from rheumatic disorders and many other pain conditions. Presenting as a ‘prototype’ of a ‘central pain’ disease, FMS widespread pain is often associated with a wide range of other symptoms such as sleep disturbance, fatigue, cognitive disturbance, stiffness, and depressive symptoms. The underlying mechanisms involved in the development of central sensitization both explain the clinical variety of symptoms (heterogeneity) and provide targets for pharmacologic and nonpharmacologic treatment strategies.” “Nonpharmacologic therapies include education, exercise, cognitive behavioral therapy, and other multidimensional therapeutic approaches. These should enable the patient to develop his or her own disease management strategies, in which drugs can be incorporated. Pharmacologic treatment targets several mechanisms involved in the development of central sensitization.” “The role of nonrestorative, unrefreshing sleep has been underestimated for many years. Recently, clinical trials have been published, emphasizing the important role of improved sleep quality. There was significant benefit on many disease domains by giving sodium oxybate. The complex symptomatology of FMS will continue to require a multidisciplinary approach including education and exercise, in addition to drug therapy to achieve the most efficient management of FMS, thus indicating a strong need for further and more extended studies targeting the benefits from using combinations of pharmacologic and nonpharmacologic treatments. Comorbid mood and anxiety disorders have often led to the misconception that FMS is a pure psychiatric illness. Now there is increasing evidence that FMS subgroups exist, presenting with a broad variety of different comorbidities and a varying extent of these comorbidities.” “There is increasing evidence that nonrestorative sleep and its influence on peripheral functions promote hyperalgesia, fatigue and bodily hypersensitivity. The fragmentation of slow-wave sleep increases sensitivity to pain as well as to nonpainful stimuli such as loud sounds and bright light. Fragmented sleep is a result of periodic arousal disturbances and has been demonstrated in FMS patients using polysomnography; the high index of such arousal disturbances in FMS patients is an indicator of sleep instability and is associated with unrefreshing, less efficient sleep, and is correlated to the severity of clinical symptoms in FMS patients. Neurotransmitter functions and dysfunctions in FMS patients also contribute to hypersensitivity and disordered sleep. Sodium oxybate increases slow-wave sleep decreases alpha intrusions into nonrapid eye movement slow-wave sleep and reduces pain and fatigue associated with FMS. The most recent study with sodium oxybate in FMS could demonstrate significant improvement in a composite score including pain, rated on a visual analog scale, the fibromyalgia impact questionnaire score, and patient global assessment.” [It is extremely sad, seeing the evidence supporting the ability of sodium oxybate to provide restorative, refreshing sleep, that the FDA has denied its use for FM patients. The denial was due to admitted fear that it would be abused by patients who might sell it for use as a date-rape drug rather than use it. That is quite a commentary on our focus on the “War on Drugs,” which, in this instance, has become a “War on Chronic Pain Patients.” They say they need more studies. Perhaps they should read this article. DJS]
Strimpakos N. 2011. The assessment of the cervical spine. Part 1: Range of motion and proprioception. J Bodyw Mov Ther. 15(1):114-124. “Neck pain and headache of cervical origin are complaints affecting an increasing number of the general population. Mechanical factors such as sustained neck postures or movements and long-term abnormal physiologic loads on the neck are believed to affect the cervical structures and compromise neck function. A comprehensive assessment of neck function requires evaluation of its physical parameters such as range of motion, proprioception, strength and endurance/fatigue. The complicated structure of the cervical spine however, makes it difficult for any clinician to obtain reliable and valid results. The aim of the first part of this systematic critical review is to identify the factors influencing the assessment of range of motion and proprioception of the cervical spine.”
Tiidus PM. 2010. Skeletal muscle damage and repair: classic paradigms and recent developments. J Musculoskel Pain. 18(4):396-402. This article explains the processes involved in muscle damage and repair, including muscle swelling, delayed onset muscle soreness, secondary injury related to the inflammatory response, and effects of sex hormones (and the loss of same on the aging), NSAIDS, and the arachidonic cascade on muscle repair. For example, NSAIDS may reduce the rate of post-injury repair, and estrogens and testosterone may enhance muscle recovery in multiple ways. The latter can be of significance to those of older years.
Torres-Oviedo G, Bastian AJ. 2010. Seeing is believing: effects of visual contextual cues on learning and transfer of locomotor adaptation. J Neurosci. 30(50):17015-17022. “Devices such as robots or treadmills are often used to drive motor learning because they can create novel physical environments. However, the learning (i.e., adaptation) acquired on these devices only partially generalizes to natural movements. What determines the specificity of motor learning, and can this be reliably made more general? Here we investigated the effect of visual cues on the specificity of split-belt walking adaptation. We evaluated the adaptation of temporal and spatial features of gait (i.e., timing and location of foot landing), their transfer to walking over ground, and washout of adaptation when subjects returned to the treadmill. Removing vision during both training (i.e., on the treadmill) and testing (i.e., over ground) strongly improved the transfer of treadmill adaptation to natural walking. Removing vision only during training increased the transfer of temporal adaptation, whereas removing vision only during testing increased the transfer of spatial adaptation. This dissociation reveals differences in adaptive mechanisms for temporal and spatial features of walking. Finally training without vision increased the amount that was learned and was linked to the variability in the behavior during adaptation. In conclusion, contextual cues can be manipulated to modulate the magnitude, transfer, and washout of device-induced learning in humans. “
Wang CF, Pancaro C, Gerner P et al. 2011. Prolonged Suppression of Postincisional Pain by a Slow-release Formulation of Lidocaine. Anesthesiology. 114(1):135-149. “Postoperative pain can occur despite nerve blocks during the surgical period. Here we tested Xybrex (Orthocon, Inc. Irvington, NY), a slow-release formulation of lidocaine that blocks rat sciatic nerve for 1-2 days, for its ability to suppress postincisional pain. Implants of slow-release lidocaine formulations are most effective against postincisional pain when placed at the ipsilateral nerve innervating the area of incision. Contralateral nerve implants are somewhat less effective, probably acting by releasing lidocaine into the systemic circulation. There appears to be a differential role of central sensitization between postincisional allodynia and hyperalgesia.” [Although this study was done in rats, it may have important ramifications in preventing one cause of central sensitization in humans. DJS]
Watson NF, Buchwald D, Goldberg J et al. 2010. Is Chiari-I Malformation Associated with Fibromyalgia? Neurosurgery. [Nov 30 Epub ahead of print]. “Most patients with FM do not have CIM pathology. Future studies should focus on dynamic neuroimaging of craniocervical neuroanatomy in patients with FM.” [We know that TrPs, and even turning the head can narrow the canal. Surgery should never be done lightly. DJS]
Wick JY, Zanni GR. 2010. Tiptoeing around gait disorders: multiple presentations, many causes. Consult Pharm. 25(11):724-737. “Walking appears to be a simple innate ability, but it is an extraordinarily complex process involving three major afferent systems (visual, proprioception, and vestibular). Humans' unique gait is established around age seven. Velocity and step-length change with age, but the overall package we call gai remains stable. Age is the single most important factor in changing gait, with some normal changes expected. Gait disorders, beyond what are normal age-related changes, are common among elders. At 60 years of age, 15% of elders have gait problems, increasing to 82% for those 85 years of age and older. Abnormal gait movement can be broadly defined as hyperkinetic (too much movement) and hypokinetic (too little movement). Gait disorders are classified into lowest level (affecting one afferent system), middle level (more afferent system involvement), and highest level (characterized by planning deficits) disorders. Gait disturbances may be a manifestation of underlying conditions or may be drug-induced. To treat gait disorders appropriately, clinicians must review the patient's disease progression, medication status, and environmental conditions. Physical therapy, medication changes, and, rarely, surgery can help improve gait.” [Patient education is also a vital component of physical retraining and therapy, and possible TrPs must also be taken into consideration when confronting gait irregularities. DJS]
Wood PB. 2010. Neuroimaging in fibromyalgia syndrome. J Musculoskel Pain. 18(4):387-392. “Fibromyalgia is associated with a variety of brain abnormalities demonstrable by neuroimaging that correlate with patients' symptoms. Future neuroimaging studies that take into account distinguishing characteristics among different populations of FMS patients may help to improve approaches to treatment and provide insight as to the pathophysiology of symptoms in addition to chronic widespread pain.”
Zhang L, Berta T, Xu ZZ et al. 2010. TNF-alpha contributes to spinal cord synaptic plasticity and inflammatory pain: Distinct role of TNF receptor subtypes 1 and 2. Pain. [Dec 13 Epub ahead of print]. “Tumor necrosis factor-alpha (TNF-alpha) is a key proinflammatory cytokine…. Our findings support a central role of TNF-alpha in regulating synaptic plasticity (central sensitization) and inflammatory pain via both TNFR1 and TNFR2. Our data also uncover a unique role of TNFR2 in mediating early-phase inflammatory pain. TNF-alpha is shown to play a critical role in regulating spinal cord synaptic plasticity and central sensitization, and TNFR1 and TNFR2 play a distinct role in regulating different phases of inflammatory pain.”