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Fibromyalgia (FMS) and
Chronic Myofascial Pain (CMP)
For Doctors and 
Other Health Care Providers

annotated by Devin J. Starlanyl

 

 

References for Research Purposes

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NOTE:  New Nomenclature

All material written by me after October 1, 2007, will have the following changes in nomenclature.  I regret any confusion caused by this change, but deem it necessary due to the changes in our current understanding of the conditions involved.

 
The abbreviation for myofascial trigger point, "TrP," is replaced by "MTP." 
 
The term Myofascial Pain Syndrome (MPS) will no longer be used, as current research shows it is not a syndrome but a true myopathy, and thus a true disease.  
 
There are acute MTPs and chronic myofascial pain (CMP) due to MTPs.  Where applicable, CMP will be separated into CMP Stage 1 (without central sensitization) and CMP Stage 2 (with central sensitization).
 
Fibromyalgia (FM) will replace the former term fibromyalgia syndrome (FMS).

 

Saa'd S, Many A, Jacob G et al. 2012. High prevalence of fibromyalgia symptoms among healthy full-term pregnant women. Rheumatol Int. [Dec 22 Epub ahead of print]. "A VAS recording pain intensity during delivery was documented. Out of 100 women recruited, 27 (27 %) fulfilled Modified FMS criteria. Only one of these women fulfilled ACR 1990 criteria, women who fulfilled the ACR criteria differed significantly from women who did not fulfill these criteria on a broad range of parameters including widespread pain and fatigue, social functioning, emotional well-being, role limitation and physical functioning. A significant correlation was found between length of stage 2 and results of the FIQ as well as with components of the SF-36. The intensity of pain during birth however was not correlated with the presence of FMS criteria. FMS symptoms were highly prevalent among healthy pregnant women at term. The presence of such symptoms may impact on the course of delivery and the need for anesthesia. Evaluating for features of centrally mediated pain may be of clinical relevance for physicians involved in the treatment of pregnant women." [These women were not examined for co-existing TrPs, which often occur during pregnancy. DJS]

Sabayan B, Bagheri M, Borhani Haghighi A. 2007.  Possible joint origin of restless leg syndrome (RLS) and migraine.  Med Hypotheses. [Jan 25 Epub ahead of print]

Sabido-David C, Faravelli L, Salvati P. 2004.  The therapeutic potential of Na(+) and Ca(2+) channel blockers for pain management.  Expert Opin Investig Drugs 13(10):1249-1261.  This paper suggests promising targets for pain control.

Sachs, C. and E. Svanborg. 1991. The exploding head syndrome: polysomnographic recordings and therapeutic suggestions. Sleep 14(3):263-266.

Sadownik LA. 2014. Etiology, diagnosis, and clinical management of vulvodynia. Int J Womens Health. 6:437-449. "Chronic vulvar pain or discomfort for which no obvious etiology can be found, i.e., vulvodynia, can affect up to 16% of women. It may affect girls and women across all age groups and ethnicities. Vulvodynia is a significant burden to society, the health care system, the affected woman, and her intimate partner. The etiology is multifactorial and may involve local injury or inflammation, and peripheral and or central sensitization of the nervous system. An approach to the diagnosis and management of a woman presenting with chronic vulvar pain should address the biological, psychological, and social/interpersonal factors that contribute to her illness. The gynecologist has a key role in excluding other causes for vulvar pain, screening for psychosexual and pelvic floor dysfunction, and collaborating with other health care providers to manage a woman's pain. An important component of treatment is patient education regarding the pathogenesis of the pain and the negative impact of experiencing pain on a woman's overall quality of life. An individualized, holistic, and often multidisciplinary approach is needed to effectively manage the woman's pain and pain-related distress."

Sadrediny S, Molaeephard M, Mir-Ahmadi M. 2009.  Sexual disorder improvement: a target or a way in treatment of fibromyalgia.  A case report and brief review.  Mod Rheumatol. [Oct 3 Epub ahead of print]  “Previous studies had shown the relation between fibromyalgia (FM) and sexual impairment as a symptom of established disease, which causes often serious problems in partners’ relationship.  We described a middle-aged man with FM who was refractory to conventional treatments after an 8-year history of generalized chronic pain.  He underwent multiple treatment modalities, such as tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and nonpharmacological therapies, with no dramatic success.  Psychiatric assessment revealed a homosexual tendency.  He and his wife were informed about the problem.  A change in sexual behavior caused a significant resolution of symptoms over a 6-month period, and he no longer receives medication for FM.  This is the first case report to demonstrate the efficacy of sexual disorder improvement in the treatment of refractory FM.”  [It is a medical fact that homosexuality is biochemical and not an aberration, and that repression of one’s natural tendencies can cause extended grief and psychological stress which can of themselves cause chronic pain.  I have seen patients who had been diagnosed with fibromyalgia who were relieved of their pain when they switched their careers (for example, one man had wanted to be a forest ranger but his parents wanted him to be an accountant.  Going into nature-related work relieved his pain.)  Being true to one’s own true nature is an important part of healthy living. DJS]

Safarpour D, Jabbari B. 2010. Botulinum Toxin A (Botox) for Treatment of Proximal Myofascial Pain in Complex Regional Pain Syndrome: Two Cases. Pain Med. [Aug 23 Epub ahead of print]. In this practice the authors have observed that it is common to have patients with myofascial TrPs on one side develop TrPs on the opposite side in the same location. "We describe two such patients in detail with their treatment. Patient 1. A 48-year-old woman experienced severe allodynia, swelling and autonomic changes in the right hand after surgery for carpal tunnel syndrome. Over the succeeding months, she developed painful trigger points in the right trapezius and upper back muscles which was treated with administration of botulinum toxin A (BoNT-A) into the trigger points (20 unit/point). Patient 2. A 41-year-old woman following a traumatic forearm injury suffered from CRPS1(chronic regional pain syndrome) affecting the left hand and forearm. Proximal MFPS (myofascial pain syndrome) gradually developed on the same side over 12 months and was treated with administration of BoNT-A into the trapezius, splenius capitis, and rhomboid muscle trigger points. Results. In both patients treatment with BoNT-A improved the proximal pain of MFPS and the distal symptoms of CRPS1. Conclusion. proximal MFPS develops ipsilateral to the distal painful limb in patients with CRPS1. Administration of BoNT-A into the affected proximal muscles may alleviate both MFPS and the distal allodynia, discoloration and, tissue swelling of CRPS."

Sagaram S., Walji M., Bernstam E. 2002.  Evaluating the prevalence, content and readability of complementary and alternative medicine (CAM) web pages on the Internet.  Proc AMIA Symp 672-6.  It is difficult for consumers of CAM to find reliable information on the Internet, as many websites are focused on selling products and make claims without medical references.

Sagberg, F. 1999. Road accidents caused by drivers falling asleep. Accid Anal Prev 31(6):639-49.

Saggini R, Giamberardino MA, Gatteschi L et al. 1996.  Myofascial pain syndrome of the peroneus longus: biomechanical approach.  Clin J Pain. 12(1):30-37.  “Both anatomical and biomechanical alterations of the dynamics of movement play a role in the painful symptoms of MPS of the peroneus longus, but the biomechanical factor is by far the more prominent.”

Saggini R, Bellomo RG, Affaitati G et al. 2006.  Sensory and biomechanical characterization of two painful syndromes in the heel.  J Pain [Sep 30 Epub ahead of print].  Entrapment syndrome of the nerve to abductor digiti quinti and myofascial syndrome of the abductor hallucis may have similar symptoms but distinct patterns and treatments.

Sahelian, R. and S. Borken. 1998. Dehydroepiandrosterone and cardiac arrhythmia. Ann Intern Med 129(7):588.

Sahin U, Tecer A, Irencin S et al. 2007.  Myofascial pain syndrome and trauma in torture survivors.  J Musculoskel Pain 15 (Supp 13):37 item 63.  [Myopain 2007 Poster]  “MPS is a quite common cause of acute and chronic pain in torture survivors.  Overstretch, direct trauma and psychological stress are the main factors.  Relations between torture and MPS should be recognized by health professionals.”

Saito, K., J. S. Crowley, S. P. Markey and M. P. Heyes. 1993. A mechanism for increased quinolinic acid formation following acute systemic immune stimulation. J Biol Chem 268(21): 15496-15503.

Sakamoto Y, Akita K. 2004.  Spatial relationships between masticatory muscles and their innervating nerves in man with special reference to the medial pterygoid muscle and its accessory muscle bundle. Surg Radiol Anat.  26(2):122-127.

Salaffi F, De Angelis R, Carotti M et al. 2014. Fibromyalgia in patients with axial spondyloarthritis: epidemiological profile and effect on measures of disease activity. Rheumatol Int. [Feb 8 Epub ahead of print.] "FM is common in axial-SpA and more prevalent in female patients. Our findings suggest that ASDAS (Ankylosing Spondylitis Disease Activity Score) is better than BASDAI (Bath Ankylosing Spondylitis Activity Disease Activity Index) in distinguishing patients with disease activity from those with functional impairment. The use of ASDAS may be very useful in clinical practice as it allows treating patients with the most appropriate therapy."

Salek AK, Khan MM, Ahmed SM et al. 2005.  Effect of aerobic exercise on patients with primary fibromyalgia.  Mymensingh Med J. 14(2):141-144.  “From this study it was observed that aerobic exercise showed no significant benefit to fibromyalgia patients.”  [Since this contradicts other studies, it may be the type and duration of the exercise as well as the presence of co-existing myofascial TrPs that contributed to this result. DJS]

Salemi S, Aeschlimann A, Wollina U et al. 2007.  Up-regulation of delta-opioid receptors and kappa-opioid receptors in the skin of fibromyalgia patients.  Arthritis Rheum. 56(7):2464-2466.

Sales Pinto LM, de Carvalho JJ, Cunha CO et al. 2013. Influence of Myofascial Pain on the Pressure Pain Threshold of Masticatory Muscles in Women with Migraine. Clin J Pain. [Jan 16 Epub ahead of print]. "We found that all groups had significantly lower PPT values compared with asymptomatic women, with lower values seen in group II (women with migraine and myofascial pain). Women with a migraine and myofascial pain showed significantly lower PPT values compared with women with a migraine only, and also when compared with women with myofascial pain only …Migraine, especially when accompanied by myofascial pain, reduces the PPT of masticatory muscles, suggesting the importance of masticatory muscle palpation during examination of patients with migraine."

Salgueiro M, Aira Z, Buesa I et al. 2011. Is psychological distress intrinsic to fibromyalgia syndrome? Cross-sectional analysis in two clinical presentations. Rheumatol Int. [Nov 8 Epub ahead of print]. "The present data suggest that associated psychological distress and maladaptive emotional responses that are commonly attributed to the general FMS population may be largely a distinguishing feature of one subset of patients."

Salinsky M, Storzbach D, Munoz S. 2010. Cognitive effects of pregabalin in healthy volunteers: A double-blind, placebo-controlled trial. Neurology. 74(9):755-61. Background: “Antiepileptic drugs (AEDs) can be associated with neurotoxic side effects including cognitive dysfunction, a problem of considerable importance given the usual long-term course of treatment. Pregabalin is a relatively new AED widely used for the treatment of seizures and some types of chronic pain including fibromyalgia. We measured the cognitive effects of 12 weeks of pregabalin in healthy volunteers.”  “At conventional doses and titration, pregabalin induced mild negative cognitive effects and neurotoxicity complaints in healthy volunteers. These effects are one factor to be considered in the selection and monitoring of chronic AED therapy. …This study provides Class I evidence that pregabalin 300 mg BID negatively impacts cognition on some tasks in healthy volunteers.” [This is important research. There seems to be a tendency for those in the field of complex chronic pain conditions, and for patients with these conditions,  to search for “magic wand” cures. We haven’t found one for FM yet. This medication causes neurotoxicity in healthy individuals. We already know that neurotoxins are produced by the body each time a TrP twitches, and that TrPs are common if not ubiquitous in FM patients. Some FM patients may produce quinolinic acid (instead of the healthy amount of needed serotonin) by means of the kynurenine pathway. One thing we don’t need is more neurotoxicity.  DJS]

Saljo, A, Huang, YL, Hansson, HA. 2003.  Impulse noise transiently increased the permeability of nerve and glial cell membranes, an effect accentuated by a recent brain injury. Neurotrauma 20(8):787-794.  Even one intense pulse noise can cause diffuse brain injury, although without visible hemorrhage or gross structural damage.  Intense noise damages both the nerve cells and the glial cells.  “The abnormal membrane permeability and the associated cytoskeletal changes may initiate events, which eventually result in progressive diffuse brain injury.

Sallinen M, Kukkurainen ML, Peltokallio L. 2011. Finally heard, believed and accepted - Peer support in the narratives of women with fibromyalgia. Patient Educ Couns. [Mar 16 Epub ahead of print]. "Long-term fibromyalgia patients saw peer support as an impetus to an ongoing process of reconstruction of identity, illness acceptance and coping with fibromyalgia....In addition to up-dating their knowledge about fibromyalgia and its treatment, long term patients may need arenas where they can share and compare their experiences to those of other patients with a long history of fibromyalgia.

Sallinen M, Kukkurainen ML, Peltokalio L et al. 2009.  Women’s narratives on experiences of work ability and functioning in fibromyalgia.  Musculoskeletal Care. [Oct 21 Epub ahead of print]  “Four types of experience concerning work ability were identified in the narratives: confusion, coping with fluctuating symptoms, being ‘in between’ and being over the edge of exhaustion.  Severe pain and fatigue symptoms, combined with a demanding life situation and ageing, seemed to lead to substantial decrease in work ability and functioning over the long term.  In the narratives, vocational rehabilitation or adjustments to work tasks were rarely seen or were started too late to be effective.  Exploring the life stories of women with fibromyalgia can reveal the perceived causes and consequences of fibromyalgia related to work ability or disability, which can be utilized in developing client-centered rehabilitation approaches and effective interventions to support work ability and avoid premature retirement in fibromyalgia patients.”

Salminen, J. J., J. Pentti and P. Terho. 1992. Low back pain and disability in 14-year-old school children. Acta Paediatr 81(12):1035-9.

Salmon P, Hall GM. 2003.  Patient empowerment and control: a psychological discourse in service of medicine.  Soc Sci Med 57(10):1969-1980.

Salnik M, Li J, McFann K et al. 2007.  Frequency specific microcurrent for facet syndrome pain.  J Musculoskel Pain 15 (Supp 13):37 item 64.  [Myopain 2007 Poster]  “In this study, FSM significantly reduced FS pain and warrants testing in a randomized placebo-controlled trial.”  [This is yet another study that indicates that FSM is capable of successfully treating multiple conditions. DJS]

Salomons TV, Moayedi M, Erpelding N et al. 2014. A brief cognitive-behavioral intervention for pain reduces secondary hyperalgesia. Pain. [Feb 22 Epub ahead of print.] "Repeated exposure to pain can result in sensitization of the central nervous system enhancing subsequent pain and potentially leading to chronicity. The ability to reverse this sensitization in a top-down manner would be of tremendous clinical benefit but the degree that this can be accomplished volitionally remains unknown(intervention could modify pain perception and reduce central sensitization (as reflected by secondary hyperalgesia). In each of eight sessions, two groups of healthy human subjects received a series of painful thermal stimuli that resulted in secondary hyperalgesia. One group ("Regulate") was given brief pain-focused cognitive training at each session while the other group ("Control") received a non-pain focused intervention. The intervention selectively reduced pain unpleasantness but not pain intensity in the Regulate group. Furthermore, secondary hyperalgesia was significantly reduced in the Regulate group compared with the Control group. Reduction in secondary hyperalgesia was associated with reduced pain catastrophizing, suggesting that changes in central sensitization are related to changes in pain-related cognitions. Thus, we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughts."

Salter MW. 2004. Cellular neuroplasticity mechanisms mediating pain persistence. J Orofac Pain 18(4):318-324.  Central sensitization mechanisms are becoming more understood. The role of microglia in central sensitization may give insight to new diagnostic and treatment strategies.

Salter MW, DeKoninck Y. 1999.  An ambiguous fast synapse: a new twist in the tale of two transmitters.  Nat Neurosci. 2(3):199-200.  When microglia are stimulated they can release a protein called brain-derived neutrotrophic factor (BDNF).  BDNF can change pain neurons in the spinal cord so that they are excited rather than inhibited by GABA.  If this pathway can be stopped, the neuropathic pain process may be prevented as well.  This could prevent many cases of chronic pain.

 

Salter MW. 2005.  Cellular signaling pathways of spinal pain neuroplasticity as targets for analgesic development.  Curr Top Med Chem. 5(6):557-567.  “Central to the mechanisms for pain hypersensitivity is the NMDA receptor, the activity of which is facilitated by convergent intracellular biochemical cascades in dorsal horn neurons.  Cellular changes are not restricted to neurons in the dorsal horn, however, and there is growing evidence for involvement of glia, and of glia-neuronal signaling, in initiating the sustaining enhancement of nociceptive transmission.  This expanded understanding of cellular and molecular signaling mechanisms in the dorsal horn, that includes both neurons and glia, provides a basis of creating new types of strategies for management, and also for diagnosis, of chronic pain.”

Salter, M.W. 2002.  The neurobiology of central sensitization.  J Musculoskel Pain 10(1/2):23-33.  Glutamic excitatory synaptic activity in the dorsal horn contributes to central sensitization.  It is produced by calcium entry through the NMDA glutamic receptor which initiates an intracellular cascade, significantly contributing to pain hypersensitivity.

Salvador J, Iriarte J, Silva C et al. 2004.  [The obstructive sleep apnoea syndrome in obesity: a conspirator in the shadow]  Rev Med Univ Navarra 48(2):55-62. [Spanish]  In cases of OSA, positive pressure therapy can improve cardiovascular risk and cognitive deficits.

Saman Y, Bamiou DE, Gleeson M et al. 2012. Interactions between stress and vestibular compensation - A review. Front Neurol. 3:116. "Elevated levels of stress and anxiety often accompany vestibular dysfunction, while conversely complaints of dizziness and loss of balance are common in patients with panic and other anxiety disorders. The interactions between stress and vestibular function have been investigated both in animal models and in clinical studies. Evidence from animal studies indicates that vestibular symptoms are effective in activating the stress axis, and that the acute stress response is important in promoting compensatory synaptic and neuronal plasticity in the vestibular system and cerebellum. The role of stress in human vestibular disorders is complex, and definitive evidence is lacking. This article reviews the evidence from animal and clinical studies with a focus on the effects of stress on the central vestibular pathways and their role in the pathogenesis and management of human vestibular disorders."

Samborski W, Lezanska-Szpera M, Rybakowski JK. 2004.  Effects of antidepressant mirtazapine on fibromyalgia symptoms.  Rocz. Akad Med Bialymst. 49:265-269.  The majority of FMS patients (who also had depression) in this study had reduced symptoms with mirtazapine therapy.  More studies are needed.

Samborski W, Lezanska-Szpera M, Rybakowksi JK. 2004.  [No Title Given]  Pharmacopsychiatry 37(4):168-170.  This Polish study indicates that mirtazapine may be helpful in FMS

Samborski, W., T. Stratz, T. Schochat, P. Mennet and W. Muller. 1996. Biochemical changes in fibromyalgia. Z Rheumatol 55(3):168-173. [German]

Samimagham H, Haghighi A, Tayebi M et al. 2014. Prevalence of fibromyalgia in hemodialysis patients. Iran J Kidney Dis. 8(3):236-239. "…there was a higher prevalence of fibromyalgia in hemodialysis patients than previously reported. Sleep disturbances and depression levels correlated with fibromyalgia." Free Article

Sampson SM, Rome JD, Rummans TA. 2006.  Slow-frequency rTMS reduces fibromyalgia pain.  Pain Med. 7(2):115-118.  “Evidence suggests that fibromyalgia (FM) is a centrally mediated pain disorder.”  “Repetitive transcranial magnetic stimulation (rTMS) is a new antidepressant treatment, which may also be useful in treating chronic pain.”  “These preliminary findings suggest a possible role for rTMS in treating FM.”

Samraj GP, Kuritzky L, Curry RW. 2005.  Chronic pelvic pain in women: evaluation and management in primary care.  Compr Ther. 31(1):28-39.  [The authors are to be congratulated in their recognition of myofascial trigger points as one of the most common sources of chronic pelvic pain.  Clinicians need to be aware that terms such as levator ani syndrome, pelvic floor tension myalgia, pudendal neuralgia and cramps are descriptions, not diagnoses, and they may frequently be caused by TrPs.  You must find the source of the pain, or other such as vaginismus, and that often requires knowledge of diagnosis and treatment of TrPs. DJS]

Samuel AN, Peter AA, Ramanathan K. 20007.  The association of active trigger points with lumbar disc lesions.  J Musculoskel Pain 15(2):11-18.  “...there is a possibility of a myofascial pain syndrome component when there is lumbar disc disease, and it also corresponds to the same myotome level of the lesion.”

Sanchez AI, Valenza MC, Martinez MP et al. 2013. Gender differences in pain experience and physical activity of fibromyalgia syndrome patients. J Musculoskel Pain. 21(2):147-155. Abnormal pain processing in FM patients is similar in males as in females, with lower pain thresholds and higher pain levels. "In women with FMS, only sleep quality was significantly correlated with physical activity."

Sanchez RJ, Uribe C, Li H et al. 2011. Longitudinal evaluation of health care utilization and costs during the first three years after a new diagnosis of fibromyalgia. Curr Med Res Opin. [Jan 18 Epub ahead of print]. "An FM diagnosis was associated with increased utilization and pain-related medication cost up to the first 6 months post-diagnosis followed by stabilization over 3 years post-diagnosis. Less use of recommended therapies relative to other therapies suggests that further dissemination of treatment guidelines is needed. An increase in non-pain medications over the observation period accounted for the majority of pharmacy costs. These pharmacy costs may be related to an increasing prevalence of comorbid conditions."

Sanchez TG, Bezerra CA.  2003.  Trigger points: Occurrence in tinnitus patients and ability to modulate tinnitus.  Otolaryngol Head Neck Surg. 129(2):241.  “Tinnitus could be modulated with stimulation of TrPs in the splenius capitis, deep masseter, and sternocleidomastoid muscles.”

Sanchez del Río-Gonzalez M. 2012. [Chronic migraine: pathophysiology]. Rev Neurol. 54 Suppl 2:S13-19 [Article in Spanish]. "Chronic migraine is considered a complication of episodic migraine. Several risk factors, which may be modifiable or non-modifiable, make varying contributions to the progression towards chronification. Every year 2.5% of patients with episodic migraine go on to suffer chronic migraine. Experimental studies point to a dysfunction in the descending pain modulatory system that would facilitate nociceptive afferents, in the absence of damage to tissues, and so chronic migraine would share a pathogenesis that is similar to that of fibromyalgia, irritable bowel syndrome or chronic tension-type headache (conditions that frequently coexist). This paper reviews the risk factors and the scientific evidence of the possible pathogenic mechanisms involved in the progression towards chronification."

Sanchez-Valiente, S. 1998. [Treatment of neuropathic pain with gabapentin++]. Rev Neurol26(152):618-20 [Spanish].

Sandberg M, Lindberg LG, Gerdle B. 2004.  Peripheral effects of needle stimulation (acupuncture) on skin and muscle blood flow in fibromyalgia.  Eur J Pain 8(2):163-171.  "...in FMS patients subcutaneous needle insertion was followed by a significant increase in both skin and muscle blood flow, in contrast to healthy subjects where no significant blood flow increase was found following the subcutaneouos needling.... muscle blood flow may be related to a greater sensitivity to pain and other somatosensory input in FMS."

Sandeberg, M., T. Lundeberg and B. Gerdle. 1999. Manual acupuncture in fibromyalgia: a long-term pilot study. J Musculoskel Pain 6(4):39-58.

Sandlund J, Djupsjobacka M, Ryhed B et al. 2006.  Predictive and discriminative value of shoulder proprioception tests for patients with whiplash-associated disorders.  J Rehabil Med. 38(1):44-49.   “The results show that, at the group level, patients with whiplash-associated disorders have impaired shoulder proprioception.”

Sandyk, R. 1997. Treatment of electromagnetic fields improves dual-task performance (talking while walking) in multiple sclerosis. Int J Neurosci 92(1-2):95-102.

Sandyk, R. 1997a. Immediate recovery of cognitive functions and resolutions of fatigue by treatment with weak electromagnetic fields in a patient with multiple sclerosis. Int J Neurosci 90(1-2):59-74.

--- 1997b. Progressive cognitive improvement in multiple sclerosis from treatment with electromagnetic fields. Int J Neurosci 89(1-2):39-51.

Sandyk, R. 1996. Effect of weak electromagnetic fields on the amplitude of the pattern reversal VEP response in Parkinson’s disease. Int J Neurosci 84(1-4):165-175.

Sang, C. N. 2000. NMDA-receptor antagonists in neuropathic pain: experimental methods to clinical trials. J Pain Symptom Manage 19(1 Suppl)S:21-5.

Sanita PV, de Alencar FGP. 2009.  Myofascial pain syndrome as a contributing factor in patients with chronic headaches.  J Musculoskel Pain. 17(1):15-25.  “Subjects with chronic headaches had a higher prevalence of TrPs, and headache complaints could be reproduced during stimulation of active TrPs that were localized more frequently in temporalis and occiptofrontalis muscles.  The presence of TrPs may be a contributing factor in the initiation and/or perpetuation of chronic headaches.”

San Pedro, E. C., J. M. Mountz, J. D. Mountz, H. G. Liu, C. R. Katholi and G. Deutsch. 1998.Familial painful restless legs syndrome correlates with pain dependent variation of blood flow to the caudate, thalamus, and anterior cingulate gyrus. J Rheumatol 25(11):2270-5.

Sann, H. and F. K. Pierau. 1998. Efferent functions of C-fiber nociceptors. Z Rheumatol. 57 Suppl 2:8-13.

Santelmann H, Laerum E, Ronnevig J et al. 2001.  Effectiveness of nystatin in polysymptomatic patients.  Fam Pract 18(3):258-265.  This study found that patients with multiple symptoms such as fatigue, cognitive dysfunctions, lack of coordination, dizziness, headache, burning or tearing of the eyes, IBS, musculoskeletal aches, respiratory tract symptoms, vaginal and/or urinary burning or itching and many others found symptom relief after treatment with an anti-fungal medication.  Relief was even more significant if the therapy was coupled with a sugar and yeast-free diet.

Sañudo B, Galiano D. 2009. Using cardiovascular parameters and symptom severity to prescribe physical activity in women with fibromyalgia. Clin Exp Rheumatol. 27(5 Suppl 56):S62-66. “Subjects were submitted twice to a maximum treadmill incremental test until participants achieved volitional exhaustion (VO2max). Expired respiratory gases, ventilator parameters and heart rate (HR) were measured continuously through exercise, and rate perceived exertion (RPE) was assessed once a minute during the test….Peak VO2 values for the moderately affected group (Group 1) were significantly different from those of severely affected group (Group 2) (26.2+/-2.1 ml x kg(-1) x min(-1) (Group 1) and 22.1+/-2.5 ml x kg(-1) x min(-1) (Group 2)). Additionally taking into account VO2 at ventilatory threshold (VO2VT), significant differences between groups were found in both tests. Some notable differences in all parameters evaluated were also found…..This study has demonstrated that the aerobic capacity of patients with FMS was different according to how severely affected they were by the condition; therefore, physical activity of the same intensity should not be prescribed for both groups.” 

Sapolsky, R.M. 1999.  Glucorticoids, stress, and their adverse neurological effects: relevance to aging.  Exp Gerontol 34(6):721-32.  Adrenal hormones are critical for survival of acute stressors, but excesses of these stress hormones can harm the central nervous system, especially the hippocampus, causing damage “... including disruption of synaptic plasticity, atrophy of dentritic processes, compromising the ability of neurons to survive a variety of coincident insults and, at an extreme, overt neuron death.”  [This can have implications when the HPA axis is in constant overdrive. DJS]

Sarchielli P, Mancini ML, Floridi A et al. 2007.  Increased levels of neurotrophins are not specific for chronic migraine: evidence from primary fibromyalgia syndrome.  J Pain [Jul 3 Epub ahead of print].

Sari H, Akarirmak U, Uludag M. 2012. Active myofascial trigger points might be more frequent in patients with cervical radiculopathy. Eur J Phys Rehabil Med. 48(2):237-244. Of 128 female and 116 male patients, some with active trigger points and some without, the patients with active trigger points were more likely to have co-existing cervical radiculopathy.  The authors conclude that cervical root compression would be the initiator or maintainer of an active TrP, and that treating cervical radiculopathy may help co-existing TrPs. They did find that many of the "healthy controls" had latent TrPs in the muscles checked. [It could be that since latent TrPs can cause muscle contraction, weakness and dysfunction without pain, latent TrPs may be the beginning of the process that eventually leads to cervical compression and active TrPs—although we don't know for sure in which order this occurs. DJS]

Sarkar S, Woolf CJ, Hobson AR et al. 2006.  Perceptual wind-up in the human esophagus is enhanced by central sensitization.  Gut. [Feb 21 Epub ahead of print]  [FMS patients have central sensitization, and many have GERD.  It may be relevant to check for symptom-free “silent” GERD and sleep apnea in FMS patients. DJS]

Sarnoch, H., Adler F., Scholz O. B. 1997. Relevance of muscular sensitivity, muscular activity, and cognitive variables for pain reduction associated with EMG biofeedback in fibromyalgia. Percept Motor Skills 84 (3 pt1): 1043-1050.

Sarrafzadeh J, Ahmadi A, Yassin M. 2011. The effects of pressure release, phonophoresis of hydrocortisone, and ultrasound on upper trapezius latent myofascial trigger point. Arch Phys Med Rehabil. [Oct 7 Epub ahead of print]. "Our results indicate that all 3 treatments used in this study were effective for treating MTP. According to this study, PhH (phonophoresis of hydrocortisone) is suggested as a new method effective for the treatment of MTP." [This is of some concern, as cortisone has never been recommended for myofascial trigger points, and can have formidable side-effects. Sicne TrPs are rarely found singly, and body-wide TrPs are not uncommon, the use of such a therapy must be decided carefully on a patient to patient basis. DJS]

Sarrel, P. M. 2000. Effects of hormone replacement therapy on sexual psychophysiology and behavior in postmenopause. J Womens Health Gend Based Med 9(Suppl 1):S25-32.

Sarrel, P. M. 1999. Psychosexual effects of menopause: role of androgens. Am J Obstet Gynecol 180(3 Pt 2):319-24.

Sarrel, P., B. Dobay and B. Wiita. 1998. Estrogen and estrogen-androgen replacement in post-menopausal women dissatisfied with estrogen-only therapy. Sexual behavior and neuroendocrine responses. J Reprod Med 43(10):847-56.

Sarro Alvarex S. 2002  [Psychiatric view of fibromyalgia.] Actas Esp Psiquiatr 30(6):392-6. [Spanish]  “Rheumatic fibromyalgia, also known as fibrositis or myofascial pain, is a common syndrome... . This article intends to offer an up-to-date and complete information about this entity, focused on psychiatric aspects, to better identify and manage such a puzzling disease.”  [These authors do not even know that fibromyalgia and myofascial pain are separate conditions, and thus is based on a faulty premise. DJS]

Sarzi-Puttini P, Atzeni F, Cazzola M. 2010. Neuroendocrine therapy of fibromyalgia syndrome: an update. Ann NY Acad Sci. 1193(1):91-97. “Studies predicting treatment response indicate that it is useful if not essential to tailor the choice of treatment components to the needs of individual patients.”

Sasama J, Sherris DA, Shin SH et al. 2005.  New paradigm for the roles of fungi and eosinophils in chronic rhinosinusitis.  Curr Opin Otolaryngol Head Neck Surg. 13(1):2-8.  “New results suggest a broader role for fungi in the pathophysiology of chronic rhinosinusitis, linking the eosinophilic inflammation to the presence of certain molds in the nasal and paranasal cavities.  Although fungi are commonly found in nearly everyone, only chronic rhinosinusitis patients respond to them with an eosinophilic inflammation.  These findings support a shift in the etiologic understanding of chronic rhinosinusitis away from a bacteriologic infectious pathogenesis to a fungal-driven inflammatory pathophysiology.”

Savage, M. K. and D. J. Reed. 1994. Oxidation of pyridine nucleotides and depletion of ATP and ADP during calcium- and inorganic phosphate-induced mitochondrial permeabilitytransition. Biochem Biophys Res Communications 200(3):1615-1620.

Savage, S. R. 1999. Opioid use in the management of chronic pain. Med Clin North Am 83(3):761-86.

Savage, S. R. 1996. Long-term opioid therapy: assessment of consequences and risks. J Pain Symptom Manage 11(5):274-286.

Sawynok J. 2014. Topical and peripheral ketamine as an analgesic. Anesth Analg. 119(1):170-178. "Ketamine, in subanesthetic doses, produces systemic analgesia in chronic pain settings, an action largely attributed to block of N-methyl-D-aspartate receptors in the spinal cord and inhibition of central sensitization processes. N-methyl-D-aspartate receptors also are located peripherally on sensory afferent nerve endings, and this provided the initial impetus for exploring peripheral applications of ketamine. Ketamine also produces several other pharmacological actions (block of ion channels and receptors, modulation of transporters, anti-inflammatory effects), and while these may require higher concentrations, after topical (e.g., as gels, creams) and peripheral application (e.g., localized injections), local tissue concentrations are higher than those after systemic administration and can engage lower affinity mechanisms. Peripheral administration of ketamine by localized injection produced some alterations in sensory thresholds in experimental trials in volunteers and in complex regional pain syndrome subjects in experimental settings, but many variables were unaltered. There are several case reports of analgesia after topical application of ketamine given alone in neuropathic pain, but controlled trials have not confirmed such effects. A combination of topical ketamine with several other agents produced pain relief in case, and case series, reports with response rates of 40% to 75% in retrospective analyses. In controlled trials of neuropathic pain with topical ketamine combinations, there were improvements in some outcomes, but optimal dosing and drug combinations were not clear. Given orally (as a gargle, throat swab, localized peritonsillar injections), ketamine produced significant oral/throat analgesia in controlled trials in postoperative settings. Topical analgesics are likely more effective in particular conditions (patient factors, disease factors), and future trials of topical ketamine should include a consideration of factors that could predispose to favorable outcomes."

Sayar K, Aksu G, Ak I et al. 2003.  Venlafaxine treatment of fibromyalgia.  Ann Pharmacother 37(11):1561-5.  “Blockade of both norepinephrine and serotonin reuptake might be more effective than blockade of either neurotransmitter alone in the treatment of fibromyalgia.”

Sberly JZ, Vernon H, Lee D et al. 2013. Immediate effects of spinal manipulative therapy on regional antinociceptive effects in myofascial tissues in healthy young adults. J Manipulative Physiol Ther. [July 3 Epub ahead of print]. This study used patients with TRPs in the infraspinatus and gluteus medius muscles. Spinal manipulation therapy (SMT) to the C5-C6 spine significantly improved pressure pain thresholds short-term (15 minutes) in the test infraspinatus muscle in healthy young adults. No significant increases were found in control infraspinatus and gluteus medius muscles of patients who received sham SMT.

Scarbrough E, Crofford LJ. 2007.  Why is the management of fibromyalgia syndrome so difficult for rheumatologists?  Nat Clin Pract Rheumatol. [Jul 24 Epub ahead of print].  This paper makes a good case for much needed education for primary care providers in the diagnoses and treatment of fibromyalgia and myofascial pain due to trigger points.  These conditions are multifactorial and require time and specificity for each patient.  [Each patient is different, and cookbook medicine is unlikely to be useful in dealing with these conditions, thus the patients are often seen as “difficult,” whereas it is the illness(es) that are difficult to manage unless adequate training, patience and perseverance is part of practice. DJS]

Scarpina F, Van der Stigchel S, Nijboer TC et al. 2013. Prism adaptation changes the subjective proprioceptive localization of the hands. J Neuropsychol. [Nov 13 Epub ahead of print]. "Prism adaptation involves a proprioceptive, a visual and a motor component. As the existing paradigms are not able to distinguish between these three components, the contribution of the proprioceptive component remains unclear. In the current study, a proprioceptive judgment task, in the absence of motor responses, was used to investigate how prism adaptation would specifically influences the felt position of the hands in healthy participants. The task was administered before and after adaptation to left and right displacing prisms using either the left or the right hand during the adaptation procedure. The results appeared to suggest that the prisms induced a drift in the felt position of the hands, although the after-effect depended on the combination of the pointing hand and the visual deviation induced by prisms. The results are interpreted as in line with the hypothesis of an asymmetrical neural architecture of somatosensory processing. Moreover, the passive proprioception of the hand position revealed different effects of proprioceptive re-alignment compared to active pointing straight ahead: different mechanisms about how visuo-proprioceptive discrepancy is resolved were hypothesized." Abnormal visual prisms affect proprioceptive sense.

Schaefer C, Chandran A, Hufstader M et al. 2011. The Comparative Burden of Mild, Moderate and Severe Fibromyalgia: Results from a Cross-Sectional Survey in the United States. Health Qual Life Outcomes. 9(1):71. "FM imposes a substantial humanistic burden on patients in the United States, and leads to substantial productivity loss, despite treatment. This burden is higher among subjects with worse FM severity."

 

Schaefer KM. 2005.  The lived experience of fibromyalgia in African American women.  Holist Nurs Pract. 19(1):17-25.  “Data analysis revealed the following themes: (a) managing the symptoms, (b) becoming a self-advocate, (c) medications camouflage the pain, (d) coming to grips with the illness means making changes, (e) being accused of ‘taking a free ride’ angers them, (f) support comes from self and spiritual connections, and (g) a certain amount of secrecy makes it easier to live with the illness.  Recommendations focus on using a holistic approach to help African American women achieve or maintain their integrity.” 

 

Schaefer KM. 2004.  Breastfeeding in chronic illness: the voices of women with fibromyalgia. MCN Am J Matern Child Nurs. 29(4):248-253.  Breast-feeding infants while simultaneously dealing with the fatigue, pain and muscle stiffness of FMS and the lack of safe medication can be frustrating. Education for prospective mothers and their health care providers is important.

Schaefer, K. M. 1997. Health patterns of women with fibromyalgia. J Adv Nurs 26(3):565-571.

Schaible HG, Schmelz M, Tegeder I. 2006.  Pathophysiology and treatment of pain in joint disease.  Adv Drug Deliv Rev. 58(2):323-342.   “Deep somatic pain originating in joints and tendons is a major therapeutic challenge.  Spontaneous pain and mechanical hypersensitivity can develop as a consequence of sensitization of primary afferents directly involved in the inflammatory process, but also following sensitization of neuronal processing in the spinal cord (central sensitization) or higher centres.”  “New targets for analgesic therapy include sensory proteins at the nociceptive nerve endings such as the activating TRPV and ASIC channels, but also inhibitory opioid and cannabinoid receptors.  Therapeutic targets are also found among the axonal channels that set membrane potential and modulate discharge frequency such as voltage sensitive sodium channels and various potassium channels.”

Schanberg, L. E., F. J. Keefe, J. C. Lefebvre, D. W. Kredich and K. M. Gil. 1998. Social context of pain in children with Juvenile Primary Fibromyalgia Syndrome: parental pain history and family environment. Clin J Pain 14(2):107-115.

Scharf MB, Cohen AP. 1998.  Diagnostic and treatment implications of nasal obstruction in snoring and obstructive sleep apnea.  Ann Allergy Asthma Immunol 81(4):279-287.  “In predisposed individuals, OSA, sleep fragmentation, and the sequelae of disturbed sleep often result from nasal obstruction.....nasal obstruction frequently leads to nocturnal mouth breathing, snoring, and ultimately to OSA.”  Congestion can cause sleep fragmentation (found in a subset of FMS patients).

Scharf, M.B., Baumann, M., Berkowitz, D.V. 2003.  The effects of sodium oxybarate on clinical symptoms and sleep patterns in patients with fibromyalgia.  J Rheumatol 30(5):1070-4. Sodium oxybarate reduced pain, fatigue and sleep abnormalities in FMS patients. 

Scheen, A. J. 1999. [Does chronic sleep deprivation predispose to metabolic syndrome?] Rev Med Liege 54(11):898-900 [French].

Scheidt CE, Mueller-Becsangele J, Hiller K et al. 2013. Self-reported symptoms of pain and depression in primary fibromyalgia syndrome and rheumatoid arthritis. Nord J Psychiatry. [Apr 16 Epub ahead of print]. "FMS patients in tertiary referral centers suffer from higher levels of pain intensity than RA patients. Depression predicts levels of pain in FMS but not in RA and is therefore an important target of intervention."

Schein, O. D., M. C. Hochberg, B. Munoz, J. M. Tielsch, K. Bandeen-Roche, T. Provost, G. J.Anhalt and S. West. 1999. Dry eye and dry mouth in the elderly: a population-based assessment. Arch Intern Med 159(12):1359-63.

Scheuler, W., D. Stinshoff and S. Kubicki. 1983. The alpha sleep pattern: different from other sleep patterns and effects of hypnotics. Neuropsychobiology 10(2-3):183-9.

Schey R, Dickman R, Parthasarathy S et al. 2007. Sleep deprivation is hyperalgesic in patients with gastroesophageal reflux disease. Gastroenterology 133(6):1787-1795. “Sleep deprivation is hyperalgesic in patients with GERD and provides a potential mechanism for increase in GERD symptom severity in sleep-deprived patients.”

Schjerning Olsen AM, Fosbel EL, Lindhardsen J. 2012. Long-term cardiovascular risk of NSAID use according to time passed after first-time myocardial infarction: A nationwide cohort study. Circulation. [Sept 10 Epub ahead of print]. "The use of NSAIDS is associated with persistently increased coronary risk regardless of time elapsed after first-time MI. We advise long-term caution in using NSAIDS for patients after MI."

Schleicher H, Alonso C, Shirtcliff EA et al. 2005.  In the face of pain: the relationship between psychological well being and disability in women with fibromyalgia.  Psychother Psychosom. 74(4):231-239.  “Self-acceptance, environmental mastery, purpose in life, and positive relations with others emerged as four important constructs in the association between PWB [psychological well-being] and disability.”

Schleip R. 2003. Fascial plasticity—a new neurobiological explanation: Part I. J Bdywrk Move Ther 7(1):11-19. This article explains some of the mechanisms that may be involved during myofascial release of tight tissues. The fascia and the nervous system are interconnected, and the response of the tissue to bodywork may be more due to its effects on the nervous system self-regulatory mechanisms than on biophysics. Fascia holds a great number of mechanoreceptors sensitive to pressure, and manual therapy can cause these to soften tissues and relax the tension of the sympathetic nervous system. This article stresses the importance of the myotendinous junctions and the tendons themselves. Golgi receptors, arranged in series with fascial fibers, respond to slow stretch by communicating through the spinal cord with the alpha motor neurons, getting the to lower their firing rate. This can soften the related muscle fibers. 90% of the Golgi receptors found in dense connective tissue lives in myotendinous junctions, other attachments, joint capsules, and peripheral joint ligaments. This article covers information on the interstitial (Types III and IV) receptor fibers, the most numerous. Most of them have autonomic functions. Interstitial, diffuse swelling is often seen in fibromyalgia and insulin resistance. "While many of the nerve fibers in a typical motor nerve have a vasomotor function, which regulates blood flow, the largest group of these fibers are sensory nerves." Some kinds of interstitial receptors are both high pressure sensitive and pain receptors. When pain and its resultant biochemical changes surround these receptors, they will fire in a strong and chronic manner, leading to pain without mechanical irritation. [This may explain some of the autonomic effects associated with myofascia trigger points. DJS]

Schleip R. 2003. Fascial plasticity—a new neurobiological explanation: Part II. J Bdywrk Move Ther :7(2)104-116. This article explains how mechanical stimulation of fascial receptors can change the viscosity of the ground substance. The widespread network of interfascial autonomic nerves and sensory nerve endings and capillaries. There are also smooth muscle cells imbedded within fascia that likely are involved in setting up tension states in the fascia. "With fibromyalgia the main understanding has been that the pain receptors are in the muscle tissue. Yet now we know that there are many sensory receptors, including pain receptors in fascia, which points our attention to fibromyalgia, as well as many other kinds of soft-tissue pain syndromes to a much higher value of therapeutic interventions in the fascia itself….Any intervention on the fascia is also an intervention on the autonomic system. "

Schleip R, Jäger H, Klingler W et al. 2012. What is 'fascia'? A review of different nomenclatures. J Bodyw Mov Ther. 16(4):496-502.

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."

Schlesinger N. 2004.  Clues to pathogenesis of fibromyalgia in patients with sickle cell disease.  J Rheumatol 31(3):598-600.  There is a high frequency of FMS in sickle-cell patients.  FMS flare may be misinterpreted as sickle-cell crisis.

Schley M, Legler A, Skopp G et al. 2006.  Delta-9-THC based monotherapy in fibromyalgia patients on experimentally induced pain, axon reflex flare, and pain relief.  Curr Med Res Opin. 22(7):1269-1276.  “A sub-population of FM patients reported significant benefit from the delta-9-THC monotherapy.  The unaffected electrically induced axon reflex flare, but decreased pain perception, suggests a central mode of action of the cannabinoid.”

Schmechel DE, Edwards C. 2012. Fibromyalgia, mood disorders, and intense creative energy: A1AT polymorphisms are not always silent. Neurotoxicology. [Mar 10 Epub ahead of print]. "Persons with single copies of common alpha-1-antitrypsin polymorphisms such as S and Z are often considered 'silent carriers'. Published evidence however supports a complex behavioral phenotype or trait - intense creative energy ("ICE") -associated with A1AT polymorphisms. We now confirm that phenotype and present an association of fibromyalgia syndrome (FMS) and A1AT in a consecutive series of neurological patients....Our findings support the ICE behavioral phenotype for A1AT polymorphism carriers and the reported association with anxiety and bipolar spectrum disorders. We now extend that phenotype to apparent vulnerability to inflammatory muscle disease in a spectrum from JRA to fibromyalgia (FMS) and specific behavioral subsets of ADD, PTSD, and specific late onset neurological syndromes (FTD-PD and PPA). High and low risk FMS subsets can be defined using A1AT, MTHFR and APOE genotyping. Clinical diagnoses associated with A1AT polymorphisms included fibromyalgia, JRA/JIA, bipolar disorder, PTSD, primary progressive aphasia and FTDPD, but not most Alzheimer Disease subtypes. These results support an extended phenotype for A1AT mutation carriers beyond liver and lung vulnerability to selective advantages: ICE phenotype and disadvantages: fibromyalgia, affective disorders, and selected late onset neurological syndromes."

Schmelz M. 2006.  [Interactions between itch and pain.]  Hautarzt [Apr 5 Epub ahead of print]  [German]  “Chronic inflammatory diseases can locally sensitize nerve endings and thereby contribute to itch.  ….there is increasing evidence that also central processing of itch can be sensitized in pruritus patients.  Interestingly, this pattern of peripheral and central sensitization in pruritus has striking similarities to the one observed in chronic pain patients.  The presumed similarities in underlying sensitizing mechanisms between itch and pain has major therapeutic consequences as successful therapies for chronic pain might be used also in chronic itch.”

Schmelz, M., R. Schmidt, A. Bickel, H. E. Torebjork and H. O. Handwerker. 1998. Innervation territories of a single sympathetic C-fibers in human skin. J Neurophysiol 79(4):1653-60.

Schmelz, M., R. Schmidt, A. Bickel, H. O. Handwerker and H. E. Torebjork. 1997. Specific C-receptors for itch and human skin. J Neurosci 17(20:8003-8008.

Schmid M, Schieppati M. 2004.  Neck muscle fatigue and spatial orientation during stepping in place in humans.  J Appl Physiol. [Epub ahead of print]  “Neck proprioceptive input, as elicited by muscle vibration, can produce destabilizing effects on stance and locomotion.  Neck muscle fatigue produces destabilizing effects on stance, too.  Neck muscle fatigue can also perturb the orientation in space during a walking task.  The neck represents a complex source of inputs capable of modifying our orientation in space during a locomotor task.”

Schmid, P. 1999. [No title available}. Schwiz Med Wochenschr 129(38):1368-80. [German] .

Schmidt, C. W. 1999. Poisoning young minds. Environ Health Perspect 107(6):A302-A307.

Schmidt-Wilcke T, Luerding R, Weigand T et al. 2007.  Striatal grey matter increase in patients suffering from fibromyalgia – a voxel-based morphometry study.  Pain [Jun 21 Epub ahead of print].  “Our data suggest that fibromyalgia is associated with structural changes in the CNS of patients suffering from this chronic pain disorder.  They might reflect either a consequence of chronic nociceptive input or they might be causative to the pathogenesis of fibromyalgia.”

Schneider C, Palomba D, Flor H. 2004.  Pavlovian conditioning of muscular responses in chronic pain patients: central and peripheral correlates.  Pain 112(3):239-247.  “These data confirm the hypothesis of enhanced muscular responding in chronic pain patients and suggest a dissociation of muscular and central processes during aversive conditioning in the patients that might contribute to the chronicity problem.”

Schneider, M. J. 1996. Chiropractic management of myofascial and muscular disorders. Advances in Chiropractic 3:55-85.

Schneider, M.. J. 1995. Tender Points/fibromyalgia vs. trigger points/myofascial pain syndrome: a need for clarity in terminology and differential diagnosis. J Manip. Physiol Ther 18(6):398-406.

Schneider, M. J. 1992. Soft tissue effects of sacroiliac and lumbosacral join manipulation. Chiropractic Technique 136-142.

Schneider, M. J. 1991. The traction methods of Cox and Leander: the neglected role of the multifidus muscle in low back pain. Chiro Tech 3(3):109-115.

Schneider W, Dvorak J. 1996.  [Functional treatment of diseases and injuries of the cervical spine]  Orthopade. 25(6):519-523. [German]  “The clinical findings and pain symptoms determine the functional treatment of the cervical spine disorders.  Acute pain syndromes are to be approached by passive procedures, such as massage, electrotherapy, trigger point treatment.  Could the pain reaction be reduced, the mobilizing techniques, including manipulation are indicated, followed by training therapy/reconditioning of shoulder girdle muscles.  The patients are also to be instructed to perform home exercise program aiming the stabilization of cervical spine.”

Schneider-Helmert D. 2003.  [Do we need polysomnography in insomnia?]  Schweiz Rundsch Med Prax. 92(48):2061-2066. [German]  “In the field of differential diagnosis, overlapping of insomnia with other disturbances within and outside the range of sleep medicine is frequent.  Special problems arise in chronic non-organic pain.  It is clear from all these aspects that PSG [polysomnography–sleep study] is indispensable in insomnia.”  [This is an important study. Lack of restorative sleep plays an important role in many cases of fibromyalgia, and not enough is done to track down the causes of non-restorative sleep.  Too often it is just dismissed as part of FMS, when there often may be components that are treatable. DJS]

 

Schneider-Helmert D, Whitehouse I, Kumar A et al. 2001.  Insomnia and alpha sleep in chronic non-organic pain as compared to primary insomnia. Neuropsychobiology 43(1):54-58.  This study indicates that insomnia in chronic pain patients may not be due to the pain itself.  It should not be dismissed as a given part of the chronic pain picture.  “It is suggested that insomnia in chronic pain patients should be taken seriously and treated by its specific methods.”

Schnurr, R. F. and M. R. MacDonald. 1995. Memory complaints in chronic pain. Clin J Pain11(2):103-11. These finding suggest that memory complaints may be related not only to depression but also to the presence of chronic pain.

Schochat T, Raspe H. 2003.  Elements of fibromyalgia in an open population.  Rheumatology 42(7):829-835.  “Subjects could be identified who met the tender point criterion of the ACR without a history of widespread pain.”  [These patients were not screened for co-existing myofascial TrPs.]

 

Schochat T, Beckmann C. 2003.  [Sociodemographic characteristics, risk factors and reproductive history in subjects with fibromyalgia — results of a population-based case-control study] [German]  Z Rheumatol. 62(1):46-59.  The factors of low social level, low alcohol intake, rare pregnancy and late start of first menstruation were more common among FMS patients than other chronic pain patients or people without chronic pain. 

Schochat T, Beckmann C 2003.  [Sociodemographic characteristics, risk factors and reproductive history in subjects with fibromyalgia – results of a population-based case-control study.]  Z Rheumatol 62(1):46-59.  [German]  “The associations with a low social level, low alcohol intake, late menarche and rare pregnancies are specific for subjects with fibromyalgia. These factors distinguish subjects with fibromyalgia from subjects with other chronic pain conditions as well as from subjects with no chronic pain.  The same hormonal factors responsible for a delayed menarche and a reduced fertility may be relevant in the development of fibromyalgia.”

Schoenberger NE, Shif SC, Esty ML et al. 2001.  Flexyx neurotherapy system in the treatment of traumatic brain injury: an initial evaluation.  J Head Trauma Rehabil 16(3):260-274.  This type of brain wave modulation neurotherapy appears to be a promising therapy for traumatic brain injury.

Schonen J. 2004.  Tension-type headache and fibromyalgia: what’s common, what’s different?  Neurol Sci 25 (Suppl 3):S157-159.

 

Schoofs N, Bambini D, Ronning P et al. 2004.  Death of a lifestyle: the effects of social support and healthcare support on the quality of life of persons with fibromyalgia and/or chronic fatigue syndrome.  Orthop Nurs. 23(6):364-374.  “Social support, unlike healthcare support, is related to quality of life (QOL).  Subjects suffering from CFS and/or FMS do not experience high levels of social support.”

Schraer, CD, SO Ebbesson, AI Adler, JS Cohen, EJ Boyko and ED Nobmann. 1998.  Glucose tolerance and insulin-resistance syndrome among St. Lawrence Island Eskimos.  Int J Circumpolar Health 57 Suppl 1:348-54.

Schreuder, BJ. 1999.  [Cognitive ego-disturbances in the elderly who have become victims of organized violence].  Z Gerontol Geriatr 32(4):266-272 [German].

Schrier M, Amital D, Arnson Y et al. 2011. Association of fibromyalgia characteristics in patients with non-metastatic breast cancer and the protective role of resilience. Rheumatol Int. [Sep 8 Epub ahead of print]. "Women with breast cancer tend to develop chronic widespread pain syndromes more often than do healthy women."

Schroeder B, Sanfilippo JS, Hertweck SP. 2000.  Musculoskeletal pelvic pain in a pediatric and adolescent gynecology practice.  J Pediatr Adolesc Gynecol. 13(2):90. “MS (musculoskeletal) etiologies of pelvic pain are common in the adolescent age group and respond well to physical therapy.  Physical therapy might be employed as an early intervention prior to surgery in adolescent girls with unexplained pelvic pain.”  Research indicates that these patients are NOT good candidates for surgery as often the pain is myofascial in origin, and surgery is seldom needed if the cause of the pain can be found.

Schroder, H, E Navarro, A Tramullas, J Mora and D Galiano. 2000.  Nutrition antioxidant status and oxidative stress in professional basketball players: effects of a three compound antioxidative supplement.  Int J Sports Med 21(2):146-50.

Schubert MS. 2004.  Allergic fungal sinusitis. Otolaryngol Cli North Am. 37(2):301-326.  

Schuh-Hofer S, Wodarski R, Pfau DB et al. 2013. One night of total sleep deprivation promotes a state of generalized hyperalgesia: a surrogate pain model to study the relationship of insomnia and pain. Pain. 154(9):1613-1621. "Our findings show that a single night of TSD is able to induce generalized hyperalgesia and to increase State Anxiety scores. In the future, TSD may serve as a translational pain model to elucidate the pathomechanisms underlying the hyperalgesic effect of sleep disturbances."

Schuler M, Njoo N, Hestermann M et al. 2004. Acute and chronic pain in geriatrics: clinical characteristics of pain and the influence of cognition.  Pain Med. 5(3):253-262.

Schultz, R. L. and Feitis R. 1996. The Endless Web: Fascial Anatomy and Physical Reality. North Atlantic Books, Berkeley, CA.

Shultz SP, Driban JB, Swanik CB. 2007. The evaluation of electrodermal properties in the identification of myofascial trigger points. Arch Phys Med Rehabil 88(6):780-784. The area of a TrP, either active or latent, has significant increased skin electrical resistance that decreases as with the distance from the TrP.

Schumacher, M., Avellana-Adalid V., Baron-Van Evercooren A. et al. 2002.  Steroid synthesis and metabolism by glia: tropic and protective effects.  Glia (Suppl 1):S4 [Abstract].

Schwabe, C. and E. E. Bullesbach. 1990. Relaxin. Comp Biochem Physiol [B] 96(1):15-21.

Schwaller F, Fitzgerald M. 2014. The consequences of pain in early life: injury-induced plasticity in developing pain pathways. Eur J Neurosci. 39(3):344-352. "Pain in infancy influences pain reactivity in later life, but how and why this occurs is poorly understood. Here we review the evidence for developmental plasticity of nociceptive pathways in animal models and discuss the peripheral and central mechanisms that underlie this plasticity. Adults who have experienced neonatal injury display increased pain and injury-induced hyperalgesia in the affected region but mild injury can also induce widespread baseline hyposensitivity across the rest of the body surface, suggesting the involvement of several underlying mechanisms, depending upon the type of early life experience. Peripheral nerve sprouting and dorsal horn central sensitization, disinhibition and neuroimmune priming are discussed in relation to the increased pain and hyperalgesia, while altered descending pain control systems driven, in part, by changes in the stress/HPA axis are discussed in relation to the widespread hypoalgesia. Finally, it is proposed that the endocannabinoid system deserves further attention in the search for mechanisms underlying injury-induced changes in pain processing in infants and children."

Schwarcz, R., C. Speciale and E. D. French. 1987. Hippocampal kynurenines as etiological factors in seizure disorders. Pol J Pharmacol Pharm 39(5):485-494.

Schwartz M.J., Offenbacher M., Neumeister A. et al. 2002. Evidence for an altered tryptophan metabolism in fibromyalgia. Neurobiol Dis 11(3):434-442.  This study shows an altered tryptophan metabolism in a subgroup of fibromyalgia patients.

Schwartz MJ, Offenbaecher M, Neumeister A et al.  2003.  Experimental evaluation of an altered tryptophan metabolism in fibromyalgia.  Adv Exp Med Biol. 527:265-275.  “These data demonstrate an altered TRP metabolism in a subgroup of FM patients, where the TD seems to activate 5-HT metabolism and IL-6 production.”

Schwartz, M. J., M. Spath, H. Muller-Bardorff, D. E. Pongratz, B. Bondy and M. Ackenheil. 1999.   Relationship of substance P, 5-hydroxyindole acetic acid and tryptophan in serum of fibromyalgia patients. Neurosci Lett 259(3):196-8.

Schwartz N, Temkin P, Jurado S et al. 2014. Chronic pain: Decreased motivation during chronic pain requires long-term depression in the nucleus accumbens. Science 345(6296):535-542. This study was undertaken to find if reduces motivation in chronic pain states in mice are due to dysfunction sin neural circuits. These researchers found that a dysfunction in neural circuitry was required in chronic pain states before depression of specific excitatory synaptic transmissions reduced motivation to initiate or complete goal-directed tasks. This neural defect dampens the pleasure response areas. The researchers believe that this isn't the only reason for reduced motivation in chronic pain states, but it does validate the feelings of chronic pain patients.

Schwartz RG, Gall NG, Grant AE. 1984.  Abdominal pain in quadriparesis: myofascial syndrome as unsuspected cause.  Arch Phys Med Rehabil. 65(1):44-46.  “This is a case report of a 47-year-old man with C6 quadriparesis who presented with tenderness in the right lower quandrant of his abdomen which was diagnosed as iliocostalis myofascial syndrome.  Diagnosis of nephrolithiasis and appendicitis were considered, but the complete blood count, abdominal x-ray, intravenous pyelogram, and sonogram were all normal.  His symptoms became progressively more severe over the ensuing 2-week period.  Examination at that time revealed extreme tenderness to light touch in the right lower quandrant, right flank, and right posterior subcostal area.  A trigger point in the right iliocostalis muscle referred pain to the right lower quandrant.  In the absence of evidence of internal derangement a diagnosis of iliocostalis myofascial syndrome was made.  A 3-day course of ‘spray and stretch’ to the iliocostalis cleared the symptoms.  This case illustrates that myofascial syndrome should be considered in the differential diagnosis of soft tissue pain in the patient with spinal cord injury and sensory sparing.”

Schweinhardt P, Lee M, Tracey I. 2006.  Imaging pain in patients: is it meaningful?  Curr Opin Neurol. 19(4):392-400.  “Results to date strongly support the notion that neuroimaging will aid our understanding of basic mechanisms contributing to the generation of chronic pain states.”

Sciotti V.M. , Mittak V.L. , DiMArco L.M. et al. 2002. Clinical precision of myofascial trigger point location in the trapezius muscle.  Pain 93(3)259-226.

Scott NA, Guo B, Barton PM et al. 2009.  Trigger point injections for chronic non-malignant musculoskeletal pain: a systematic review.  Pain Med. 10(1):54-69.  “TPI (trigger point injection) is a safe procedure when used by clinicians with appropriate expertise and training.  It relieved symptoms when used as a sole treatment for patients with chronic head, neck, shoulder, and back pain or whiplash syndrome, regardless of the injectant used, and may be a useful adjunct to intra-articular injection in the treatment of osteoarthritis pain.  Although the addition of TPI to stretching exercises augments treatment outcomes, this was also true of other therapies such as ultrasound and laser.”  “The only advantage of injecting anesthetic into trigger points may be to reduce the pain of the needling process, which may not be an insignificant benefit.”

Seaman, D. R. and C. Cleveland 3rd. 1999. Spinal pain syndromes: nociceptive, neuropathic, and psychologic mechanisms. J Manipulative Physiol Ther 22(7):458-72.

Sears, Barry. 1999. The Anti-Aging Zone HarperCollins Inc New York.

Seas, K. L. and H. W. Clark. 1993. Opioid use in the treatment of chronic pain: assessment of addiction. J Pain Symptom Manage 8(5):257-264.

Seed SM, Dunican KC, Lynch AM et al. 2012. An update in options for the treatment of pain: a review of new opioid formulations. Hosp Pract (Minneap). 40(1):166-175. "This article reviews new opioid options for the treatment of pain management and requirements of the Risk Evaluation and Mitigation Strategies program."

Seegal, R. F., J. R. Wolpaw and R. Dowman. 1989. Chronic exposure of primates to 60-Hz electric and magnetic fields: II. Neurochemical effects. Bioelectromagnetics 10(3):289-301.

Seematter G, Binnert C, Martin JL et al. 2004.  Relationship between stress, inflammation and metabolism.  Curr Opinion Clin Nutr Metab Care 7(2):169-173.  The HPA axis stress response mobilizes neuroendocrine response systems that can institute a metabolic cascade with far-reaching consequences.  “They also exert anti-insulin actions and may in the long-term induce a state of insulin resistance.  In addition, stress stimulates inflammatory mediators in mononuclear cells.  Given the possible role of low-grade inflammation in chronic metabolic disorders, this suggests that stress may be a factor in the development of insulin resistance and the metabolic syndrome.”   Stress and causes of same, including pain, must be controlled.

Seematter G, Binnert C, Martin JL et al. 2004.  Relationship between stress, inflammation and metabolism.  Curr Opin Clin Nutr Metab Care 7(2):169-173.  “Recent work performed in the field has indicated that stress may be a significant factor in the pathogenesis of metabolic disorders.  Nutritional intervention or pharmacological agents targeted at modulating stress should be investigated.”

Seers, K. 1996. "The patients’ experiences of their chronic non-malignant pain." J Adv Nurs 24(6):1160-1168.

Sees, K. L. and H. W. Clark. 1993. Opioid use in the treatment of chronic pain: assessment of addiction. J Pain Sympt Manage 8(5):257-64.

Segal NA, Glass NA, Felson DT et al. 2010. The effect of quadriceps strength and proprioception on risk for knee osteoarthritis. Med Sci Sports Exerc. [Mar 25 Epub ahead of print]. “…quadriceps strength protected against incident symptomatic but not radiographic knee OA (osteoarthritis) regardless of JPS (joint position strength)...”

Segerstrom SC, Miller GE. 2004.  Psychological stress and the human immune system: a meta-analytic study of 30 years of inquiry.  Psychol Bull 130(4):601-630.  “Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity.  Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity.  Chronic stressors were associated with suppression of both cellular and humoral measures.  Effects of event sequences varied according to the kind of event (trauma vs. loss).  In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.”

Segura-Jimenez V, Carbonell-Baeza A, Aparicio VA et al. 2012. A Warm Water Pool-Based Exercise Program Decreases Immediate Pain in Female Fibromyalgia Patients: Uncontrolled Clinical Trial. Int J Sports Med. [Dec 20 Epub ahead of print]. Fibromyalgia is characterized by chronic and extended musculoskeletal pain. The combination of exercise therapy with the warm water may be an appropriate treatment. However, studies focusing on the analysis of immediate pain during and after an exercise session are rare. This study aimed to determine the immediate changes of a warm water pool-based exercise program (12 weeks) on pain (before vs. after session) in female fibromyalgia patients. 33 Spanish women with fibromyalgia were selected to participate in a 12 week (2 sessions/week) low-moderate intensity warm water pool-based program. We assessed pain by means of a Visual Analogue Scale before and after each single session….a warm water pool-based exercise program for 12 weeks (2 times/week) led to a positive immediate decrease in level of pain in female patients with fibromyalgia. Improvements were higher in older women and in those with more intense pain.

Segura-Jimenez V, Romero-Zurita, Carbonell-Baeza A et al. 2013. Effectiveness of Tai-Chi for Decreasing Acute Pain in Fibromyalgia Patients. Int J Sports Med. [Nov 7 Epub ahead of print]. "Tai-Chi has shown benefits in physical and psychological outcomes in diverse populations. We aimed to determine the changes elicited by a Tai-Chi program (12 and 24 weeks) in acute pain (before vs. after session) in fibromyalgia patients. We also assessed the cumulative changes in pain brought about by a Tai-Chi program….In conclusion, a low-moderate intensity Tai-Chi program for 12 weeks (3 times/week) decreased levels of acute pain in fibromyalgia patients. A longer period is necessary (e. g. 24 weeks) for observing cumulative changes in pain."

Seibold, J. R., P. J. Clements, D. E. Furst, M. D. Mayes, D. A. McCloskey, L. W. Moreland, B. White, F. M. Wigley, S. Rocco, M. Erikson, J. F. Hannigan, M. E. Sanders and E. P. Amento.1998. Safety and pharmacokinetics of recombinant human relaxin in systemic sclerosis. J Rheumatol 25(2):302-307.

Seidel MF, Weinreich GF, Stratz T et al. 2007.  5-HT3 receptor antagonists regulate autonomic cardiac dysfunction in primary fibromyalgia syndrome.  Rheumatol Int. [Jul 19 Epub ahead of print].  “Tropisetron reduced not only pain perception but also had a favorable effect on cardiac dysfunction during treatment.”  [This medication seems to be effective for both FM and myofascial pain, as well as cardiac dysfunction. DJS]

 

Sendur OF, Gurer G, Bozbas GT. 2006.  The frequency of hypermobility and its relationship with clinical findings of fibromyalgia patients.  Clin Rheumatol. [Apr 25 Epub ahead of print]  “...more severe clinical findings were observed in FM patients with hypermobility when compared with ones without.”

Senior BA, Khan M, Schwimmer C et al. 2001.  Gastroesophageal reflux and obstructive sleep apnea.  Laryngoscope 111(112):2144-6.  “These results suggest a potential relationship between OSA and GER...”  Treatment of one may significantly impact the other in some patients.

Seo HG, Bang MS, Chung SG et al. 2012. Effect of electrical stimulation on botulinum toxin A therapy in patients with chronic myofascial pain syndrome: A 16-week randomized double-blinded study. Arch Phys Med Rehabil. [Oct 31 Epub ahead of print]. Short-term electrical stimulation may affect reduction in pain after BTX-A injection at TrPs in patients with chronic MPS on the neck and shoulder regions. Based on the results, it seems that sensory electrical stimulation was superior to motor electrical stimulation as an adjuvant therapy of BTX-A injection in the patients with chronic MPS. Further studies are warranted to investigate the method facilitating the effect of BTX-A on MPS.

Seok J, Warren HS, Cuenca AG et al. 2013. Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Natl Acad Sci USA. [Feb 11 Epub ahead of print]. This study shows that the commonly used mouse as an experimental model does not translate well to human applications in the context of inflammatory disease. How a mouse responds in an experiment does not indicate how a human will respond. [One very small step for mouse-kind. DJS]

Sephton SE, Salmon P, Weissbecker I et al. 2007.  Mindfulness meditation alleviates depressive symptoms in women with fibromyalgia: results of a randomized clinical trial.  Arthritis Rheum. 57(1):77-85.  “This meditation-based intervention alleviated depressive symptoms among patients with fibromyalgia.”

Sepici V, Tosun A, Kokturk O. 2007.  Obstructive sleep apnea syndrome as an uncommon cause of fibromyalgia: a case report.  Rheumatol Int. [Jun 23 Epub ahead of print].

Sergey A, Dzugan R, Arnold Smith R. 2002.  Hypercholesterolemia treatment: a new hypothesis or just an accident?  Med Hypoth 59(6):751-756.  This team’s “...findings support the hypothesis that hypercholesterolemia is a compensatory mechanism for life-cycle related down-regulation of steroid hormones and that broadband steroid hormone restoration is associated with a substantial drop in serum TC in many patients.”  This may be very important in treating FMS patients who often have many hormonal axes imbalanced.  It is vital that the hormone levels be tests and the normal amounts restored using natural hormones.

Sergi, M., M. Rizzi, A. Braghiroli, P. S. Puttini, M. Greco, M. Cazzola and A. Andreoli. 1999.  Periodic breathing during sleep in patients affected by fibromyalgia syndrome.  Eur Respir J 14(1):203-8.

Serra E, Spaeth M, Carbonell J et al. 2010. Development of the Fibromyalgia Burden Assessment: measuring the multifaceted burden of fibromyalgia. Clin Exp Rheumatol. 28(6 Suppl 63):S87-93. "The FMBA is a self-reported questionnaire allowing the assessment and a better understanding of the impacts of fibromyalgia and the burden associated with these on patients' daily lives. It is available in UK English, French, German and Spanish. Its scoring and validation remain to be undertaken."

Serra J, Collado A, Sola R et al. 2013. Hyperexcitable C nociceptors in fibromyalgia. Ann Neurol. [Nov 16 Epub ahead of print]. "Microneurography was used to record from C nociceptors of 30 female patients meeting criteria for fibromyalgia and compared with recordings from 17 female patients with small fiber neuropathy and 9 female controls…. The mechano-sensitive nociceptors in the fibromyalgia patients behaved normally, but the silent nociceptors in 76.6% of fibromyalgia patients exhibited abnormalities. Spontaneous activity was detected in 31% of silent nociceptors in fibromyalgia, 34% in small fiber neuropathy, and 2.2% in controls. Sensitization to mechanical stimulation was found in 24.2% of silent nociceptors in fibromyalgia, 22.7% in small fiber neuropathy, and 3.7% in controls. Abnormally high slowing of conduction velocity when first stimulated at 0.25 Hz was more common in fibromyalgia. Interpretation: We show for the first time that the majority of fibromyalgia patients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small fiber neuropathy, but high activity-dependent slowing of conduction velocity is more common in fibromyalgia patients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia."

Settipane, R. A. 1999.  Complications of allergic rhinitis.  Allergy Asthma Proc 20(4):209-13.

Sewitch MJ, Dobkin PL, Bernatsky S. et al. 2004. Medication non-adherence in women with fibromyalgia.  Rheumatology (Oxford) 43(5):648-654.  ”Overall non-adherence was predicted by higher patient-physician discordance...The therapeutic relationship, in addition to clinical and psychosocial characteristics, influenced non-adherence to medication.”

Shadmehr A, Jafarian Z, Tavakol K et al. 2013. Effect of pelvic compression on the stability of pelvis and relief of sacroiliac joint pain in women: A case series. J Musculoskel Pain. 21(1):31-36. "Pelvic compression significantly reduced the EMG (electromyographic) activity from six muscles....pelvic compression can improve both the motor control and stability of the pelvis, while reducing joint pain in women suffering from sacroiliac symptoms."

Shaffer SM, Brismee JM, Sizer PS et al. 2014. Temporomandibular disorders. Part 2: conservative management. J Man Manip Ther. 22(1):13-23. "Appropriate management of temporomandibular disorders (TMD) requires an understanding of the underlying dysfunction associated with the temporomandibular joint (TMJ) and surrounding structures. A comprehensive examination process, as described in part 1 of this series, can reveal underlying clinical findings that assist in the delivery of comprehensive physical therapy services for patients with TMD. Part 2 of this series focuses on management strategies for TMD. Physical therapy is the preferred conservative management approach for TMD. Physical therapists are professionally well-positioned to step into the void and provide clinical services for patients with TMD. Clinicians should utilize examination findings to design rehabilitation programs that focus on addressing patient-specific impairments. Potentially appropriate plan of care components include joint and soft tissue mobilization, trigger point dry needling, friction massage, therapeutic exercise, patient education, modalities, and outside referral. Management options should address both symptom reduction and oral function. Satisfactory results can often be achieved when management focuses on patient-specific clinical variables."

Shah MA, Feinberg S, Krishnan E. 2006.  Sleep-disordered breathing among women with fibromyalgia syndrome.  J Clin Rheumatol. 12(6):277-281.  “A large proportion of women with fibromyalgia in a general rheumatology practice had sleep-disordered breathing, which can be detected using sleep polysomnograms.”

Shah JP, Parikh S, Danoff J et al. 2007.  Re: the myofascial trigger point region: correlation between the degree of irritability and the prevalence of endplate noise.  Am J Phys Med Rehabil. 86(12 :1033-1034.

Shah JP, Danoff JV, Desai MJ et al. 2008.  Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points.  Arch Phys Med Rehabil. 89(1):16-23.  “We have shown the feasibility of continuous, in vivo recovery of small molecules from soft tissue without harmful effects.  Subjects with active MTPs in the trapezius muscle have a biochemical milieu of selected inflammatory mediators, neuropeptides, cytokines, and catecholamines different from subjects with latent or absent MTPs in their trapezius.  These concentrations also differ quantitatively from a remote, uninvolved site in the gastrocnemius muscle.  The milieu of the gastrocnemius in subjects with active MTPs in the trapezius differs from subjects without active MTPs.”

Shah J. 2007.  Uncovering the biochemical milieu of myofascial trigger points using in-vivo microdialysis.  J Musculoskel Pain 15 (Supp 13):2 item 2.  [Myopain 2007 Poster]  The use of in-vivo sampling by microdialysis acupuncture needle “...provides us the unprecedented ability to safely explore and measure the local biochemical milieu of TrPs before, during and after a local twitch response.”  “...the local biochemical milieu does appear to change after a LTR.”  “...the vicinity of the active TrP exhibits a unique biochemical milieu of substances associated with pain and inflammation .... analyte abnormalities may not be limited to local areas of active TrPs.”

Shah JP, Phillips TM, Danoff JV et al. 2005.  An in-vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle.  J Appl Physiol. 99(5):1977-1984.  This article describes a ground-breaking technique for measuring minute amounts of biochemicals in the body.  In this case, the biochemicals released in the interstitial fluid surrounding myofascial TrPs during TrP twitch were analyzed.  They found a sensitized and sensitizing soup of over 30 biochemicals released.  In the active TrP patient group, bradykinins, calcitonin gene-related peptide, IL-$, serotonin, tumor necrosis factor-", and norepinephrine were significantly higher and the pH dropped significantly than in the control group or the group with latent TrPs.  Substance P and CGRP dropped significantly after the TrP twitch release.  This study may indicate some of the cause of TrP pain, and also highlight promising targets for TrP pain relief.  [It also indicates some ways active TrPs can aggravate the central sensitization of fibromyalgia. DJS]

Shaheen NJ, Madanick RD, Alattar M et al. 2007.  Gastroesophageal Reflux Disease as an etiology of sleep disturbance in subjects with insomnia and minimal reflux symptoms: a pilot study of prevalence and response to therapy.  Dig Dis Sci. [Nov 6 Epub ahead of print].  “Despite the lack of GERD symptoms, a significant minority of subjects with sleep disturbance have abnormal acid exposures.  These preliminary data suggest that aggressive treatment of GERD in such patients may result in improvement in sleep efficiency.”  [Care providers should first attempt to normalize the gut flora with the use of healthy diet, probiotics, prebiotics, supplements and non-invasive care such as frequency specific stimulation. DJS]

 

Shan G, Daniels D, Gu R.  2004.  Artificial neural networks and center-of-pressure modeling: a practical method for sensorimotor-degradation assessment.  J Aging Phys Act. 12(1):75-89.  “Tai Chi slowed down the effects of sensorimotor aging.”

Shanahan, F. 1999.  Brain-gut axis and mucosal immunity: a perspective on mucosalpsychoneuroimmunology.  Semin Gastrointest Dis 10(1):8-13.

Shankar H, Cummings C. 2012. Ultrasound Imaging of Embedded Shrapnel Facilitates Diagnosis and Management of Myofascial Pain Syndrome. Pain Pract [Oct 24 Epub ahead of print]. "Trigger points can result from a variety of inciting events including muscle overuse, trauma, mechanical overload, and psychological stress....A veteran was referred to the pain clinic for management of his severe headache following a gunshot wound to the neck with shrapnel embedded in the neck muscles a few years prior to presentation. He had no other comorbid conditions. Physical examination revealed a taut band in the neck. An ultrasound imaging of the neck over the taut band revealed the deformed shrapnel located within the levator scapulae muscle along with an associated trigger point in the same muscle. Ultrasound guided trigger point injection, followed by physical therapy resolved his symptoms."

Shankar H, Reddy S. 2012. Two- and Three-Dimensional Ultrasound Imaging to Facilitate Detection and Targeting of Taut Bands in Myofascial Pain Syndrome. Pain Med. [Jun 8 Epub ahead of print]. This is a case report using ultrasound elastography. Conservative TrP therapy had been insufficient to resolve pain and reduced range of motion of the shoulder. "Three-dimensional ultrasound images provided evidence of aberrancy in the architecture of the muscle fascicles around the taut bands compared to the adjacent normal muscle tissue during serial sectioning of the accrued image. On two-dimensional ultrasound imaging over the palpated taut band, areas of hyperechogenicity were visualized in the trapezius and supraspinatus muscles. Subsequently, the patient received ultrasound-guided real-time lidocaine injections to the trigger points with successful resolution of symptoms....This is a successful demonstration of utility of ultrasound imaging of taut bands in the management of myofascial pain syndrome. Utility of this imaging modality in myofascial pain syndrome requires further clinical validation." [This method is a research method and not presently accessible for clinical applications. DJS]

Shankland II W. E. 1995. Craniofacial pain syndromes that mimic temporomandibular joint disorders. Ann Acad Med Singapore 24(1):83-112.

Shankland, II W. E., J. A. Negulesco and B. O’Brian. 1996. The pre-anterior belly of the temporalis muscle; a preliminary study of a newly described muscle. Cranio 14(2):106-112.

Shankland, II W. E. 1995. Craniofacial pain syndromes that mimic temporomandibular joint disorders. Ann Acad Med Singapore 24(1):83-112.

Shanks, N., R. J. Windle, P. Perks, S. Wood, C. D. Ingram and S. L. Lightman. 1999. The hypothalamic-pituitary-adrenal axis response to endotoxin is attenuated during lactation. J Neuroendocrinol 11(11):857-65.

Shannon, C. N. and A. P. Baranowski. 1997. Use of opioids in non-cancer pain. Br J Hosp Med58(9):459-463.

Shanoudy H, Soliman A, Moe S, Hadian D et al. 2001. manifestations of Asick euthyroid@ syndrome in patients with compensated chronic heart failure. J Card Fail 7(2):146-52. "Patients with compensated CHF display the derangements in thyroid hormone metabolism of impaired peripheral conversion of T(4) and t(3) and increased production of rT(3) in the presence of normal dynamic function of the hypothalamic-pituitary-thyroid axis, which are consistent with early manifestations of a sick euthyroid state."

Shapir E, Cohen H, Calzolari A et al. 2008.  Electronic structure of single DNA molecules resolved by transverse scanning tunnelling spectroscopy.  Nat Mat (7):68-74.  The DNA molecule is laterally electrically conductive across the helix.  [This may be a method whereby some electroceutical devices, such as frequency specific microcurrent and electroacupuncture, change the body chemistry even below the cellular level, effecting healing through the DNA.  DJS]

Shapiro, R. S. 1994. Legal bases for the control of analgesic drugs. J Pain Symptom Manage9(3):153-159.

Sharan D, Ajeesh PS, Rameshkumar R et al. 2012. Risk factors, clinical features, and outcome of treatment of work related musculoskeletal disorders in on-site clinics among IT companies in India. Work. Suppl 1:5702-5704. This study focused on the IT (information technology) profession and workplace risk in India. It found poor office ergonomics; lack of keyboard and/or mouse tray and foot rest; and improper monitor height to be the most common risk factors. The most common musculoskeletal disorders were myofascial pain syndrome (49.2%), thoracic outlet syndrome (25%), and fibromyalgia (8.5%). The body regions affected mostly were neck (64.9%), shoulder 42.1%), lower back (56.5%), and thigh (34.2%). The patients were treated with the RECOUP protocol designed by Dr. Sharan, and the patients were satisfied with their progress.

Sharan D, Jacob BN, Ajeesh PS et al. 2011. The effect of cetylated fatty esters and physical therapy on myofascial pain syndrome of the neck. J Bodyw Mov Ther. 15(3):363-374. Myofascial pain patients were treated with either a combination of cetylated fatty ester complex (CFEC) and 1.5% menthol or a control cream of 1.5% menthol. The patients treated with the compound containing the CFEC experienced significantly improved symptoms compared with those who used the menthol cream. [Patients on guaifenesin should be aware that the cream available in the USA, Celadrin, has significant peppermint oil and would be contraindicated due to the salicylates in it. DJS]

Sharan D, Manjula M, Urmi D et al. 2014. Effect of yoga on the Myofascial Pain Syndrome of neck. Int J Yoga. 7(1):54-59. "Myofascial Pain Syndrome (MPS) refers to pain attributed to muscle and its surrounding fascia, which is associated with "myofascial trigger points" (MTrPs). MTrPs in the trapezius has been proposed as the main cause of temporal and cervicogenic headache and neck pain. Literature shows that the prevalence of various musculoskeletal disorders (MSD) among physiotherapists is high. Yoga has traditionally been used to treat MSDs in various populations. But there is scarcity of literature which explains the effects of yoga on reducing MPS of the neck in terms of various physical parameters and subjective responses. Therefore, a pilot study was done among eight physiotherapists with minimum six months of experience. A structured yoga protocol was designed and implemented for five days in a week for four weeks. The outcome variables were Disability of Arm, Shoulder and Hands (DASH) score, Neck Disability Index (NDI), Visual Analogue Scale (VAS), Pressure Pain Threshold (PPT) for Trigger Points, Cervical Range of Motion (CROM) - active & passive, grip and pinch strengths. The variables were compared before and after the intervention. Finally, the result revealed that all the variables ….improved significantly after intervention."

Sharan D, Mohandoss M, Ranganathan R et al. 2014. Musculoskeletal disorders of the upper extremities due to excessive usage of hand held devices. Ann Occ Env Med. 26:22. This retrospective study from India was held on 70 subjects with upper extremity MSD from handheld devices. "All of the subjects reported pain in the thumb and forearm with associated burning, numbness and tingling around the thenar aspect of the hand, and stiffness of wrist and hand. 43 subjects had symptoms on the right side; 9 on the left and 18n had bilateral symptoms.…All the subjects were diagnosed to have tendinosis of the extensor pollicis longus and myofascial pain syndrome affecting the 1st interossei, thenar group of muscles and extensor digitorum communis….All subjects recovered completely following the rehabilitation."

Sharan D, Rajkumar JS, Mohandoss M. 2014. Myofascial low back pain treatment. Curr Pain Headache Rep.18(9):449. "Myofascial pain is a common musculoskeletal problem, with the low back being one of the commonest affected regions. Several treatments have been used for myofascial low back pain through physical therapies, pharmacologic agents, injections, and other such therapies. This review will provide an update based on recently published literature in the field of myofascial low back pain along with a brief description of a sequenced, multidisciplinary treatment protocol called Skilled Hands-on Approach for the Release of myofascia, Articular, Neural and Soft tissue mobilization (SHARANS) protocol. A comprehensive multidisciplinary approach is recommended for the successful management of individuals with myofascial low back pain."

Sharkey SW, Lesser JR, Zenovich AG et al. 2005.  Acute and reversible cardiomyopathy provoked in stress in women from the United States.  Circulation. 111(4):472-479.  Profound psychological stress can trigger reversible cardiac events including chest pain and cardiac dysfunction.

Sharpe, M. H. and T. S. Miles. 1993. Position sense at the elbow after fatiguing contractions. Exp Brain Res 94(1):179-82.

Sharpley, A., A. Clements, K. Hawton and M. Sharpe. 1997. Do patients with "pure" chronic fatigue syndrome (neurasthenia) have abnormal sleep? Psychosom Med 59(6):592-6.

Shaver, J. L. , M. Lentz, C. A. Landis, M. M. Heitkemper, D. S. Buchwald and N. F. Woods. 1997. Sleep, psychological distress, and stress arousal in women with fibromyalgia. Res Nurs Health 20(3):247-257.

Shaw S, Lee A. 2010. Student nurses' misconceptions of adults with chronic nonmalignant pain.  Pain Manag Nurs. 11(1):2-14. Earlier research has identified chronic pain as a leading cause of disability..... The knowledge and attitudes of nurses have been found to affect patient experience and treatment..... The student nurses who participated in this study demonstrated that they held misconceptions about adults with chronic nonmalignant pain to a considerable degree. Students enrolled in semester six held the misconceptions to a slightly lesser degree than those enrolled in semesters one and four. The process of undergraduate education needs to equip nursing students with accurate knowledge about chronic nonmalignant pain and encourage them to develop the appropriate attitudes for working with patients experiencing it.

Shaywitz, S. E., B. A. Shaywitz, K. R. Pugh, R. K. Fulbright, Skudlarski P, W. E. Mencl, R. T. Constable, F. Naftolin, S. F. Palter, K. E. Marchione, L. Katz, D. P. Shankweiler, J. M. Fletcher, C. Lacadie, M. Keltz, J. C. Gore. 1999. Effect of estrogen on brain activation patterns in postmenopausal women during working memory tasks. JAMA 281(13):1197-202

Shear, D. A., J. Dong, K. L. Haik-Creguer, T. J. Bazzett, R. L. Albin and G. L. Dunbar. 1998.Chronic administration of quinolinic acid in the rat striatum causes spatial learning deficits in a radial arm water maze task. Exp Neurol 150(2):305-311.

Sheehan, J., J. McKay, M. Ryan, N. Walsh and D. O’Keefe. 1996. "What cost chronic pain?" Ir Med J 89(6):218-219.

Sheon, R. P. 1997. Repetitive strain injury. 2. Diagnostic and treatment tips on six common problems. The Goff Group. Postgrad Med 102(4):72-78.

Sherman KJ, Cherkin DC, Deyo RA et al. 2006.  The diagnosis and treatment of chronic back pain by acupuncturists, chiropractors, and massage therapists.  Clin J Pain. 22(3):227-234.  “Information on the care patients routinely received from CAM (complementary and alternative) providers will help physicians better understand these increasingly popular forms of care.”

Sherwin, B. B. 1998. Estrogen and cognitive functioning in women. Proc Soc Exp Biol Med217(1):17-22.

Sherwin, B. B. 1997. Estrogens effects on cognition in menopausal women. Neurology 48(5 Suppl 7):A21-6.

Sheth T, Pitchumoni CS, Das KM. 2014. Musculoskeletal manifestations in inflammatory bowel disease: A revisit in search of immunopathophysiological mechanisms. J Clin Gastroenterol. [Jan 31 Epub ahead of print.] "Inflammatory bowel diseases are chronic inflammatory disorders of multiple organ systems, primarily involving the gut, with chronic relapsing and remitting course. Musculoskeletal involvement is the most common extraintestinal manifestation. Distinct cell-mediated and humoral immunopathophysiological mechanisms have been identified underlying gut and joint inflammation in patients with inflammatory bowel disease and arthritis. Genetic polymorphisms in genes coding for NOD2 and IL12/IL23 complex lead to impaired antigenic handling in the gut and local immune dysregulation. The gut-synovial axis hypothesis implicates both environmental and host factors acting as triggers to initiate inflammation in genetically predisposed individuals, leading to priming of Th1 and Th17 lymphocytes in the gut and subsequent homing to the synovial tissue. Similar to gut, antibody-dependent cell-mediated cytotoxicity and complement-mediated cell lysis may also contribute to the joint damage. Involvement of peripheral joints occurs in 2 distinct manners, one being oligoarticular asymmetric arthritis associated with active disease and the other being polyarticular symmetric involvement of small joints. The axial involvement may include asymptomatic sacroiliitis, inflammatory back pain, and ankylosing spondylitis, running an independent clinical course. Noninflammatory involvement of the musculoskeletal system may present as osteopenia, osteonecrosis, fibromyalgia, or myopathies, leading to significant impact on quality of life."

Shi, D., O. Nikodijevic, K. A. Jacobson and J. W. Daly. 1994. Effects of chronic caffeine on adenosine, dopamine and acetylcholine systems in mice. Arch Int Pharmacodyn Ther 328(3):261-287.

Shilo, L., Y. Dagan, Y. Smorjik, U. Weinberg, S. Dolev, B. Komptel, H. Balaum and L. Shenkman. 1999. Patients in the intensive care unit suffer from severe lack of sleep associated with loss of normal melatonin secretion pattern. Am J Med Sci 317(5):278-81.

Shin HJ, Shin JC, Kim WS et al. 2014. Application of ultrasound-guided trigger point injection for myofascial trigger points in the subscapularis and pectoralis muscles to post-mastectomy patients: a pilot study. Yonsei Med J. 55(3):792-799. "In post-mastectomy patients with shoulder pain, US-guided trigger point injections of the subscapularis and/or pectoralis muscles are effective for both diagnosis and treatment when the cause of shoulder pain is suspected to originate from active MTrPs in these muscles, particularly, the subscapularis."

Shinozaki T, Sakamoto E, Shilba S et al. 2006.  Cervical plexus block helps in diagnosis of orofacial pain originating from cervical structures.  Tohoku J Exp Med. 210(1):41-47.

Shmushkevich Y, Kalichman L. 2013. Myofascial pain in lateral epicondylalgia: A review. J Bodyw Mov Ther. 17(4):434-439. "There is an ongoing debate about the myofascial component, characterized by the presence of myofascial trigger points (MTrPs) in lateral epicondylalgia (LE)…." The objectives of this study were: "To review current evidence of the association between myofascial pain and LE, including efficacy of treatment, focusing on myofascial pain….PubMed, Google Scholar and PEDro databases were searched without search limitations from inception until October 2012 for terms relating to LE and MTrPs….Two observational studies showed a high prevalence of MTrPs in LE patients compared to healthy controls. Three randomized controlled trials demonstrated significant improvement in pain and functional outcomes after application of soft tissue techniques, focusing on the myofascial component. Myofascial pain and MTrPs may be part of the LE etiology. Treatment focusing on the myofascial component seems to be effective in reducing pain and improving function in patients with LE. Additional trials are essential to attain a solid conclusion." [Since some studies still use the term "myofascial pain" to mean TMJD, and so very many researchers are not even aware of myofascial trigger points or lack the training and experience needed to palpate them, previous research is only as good as the training. There should be no "ongoing debate" about the myofascial component of LE. There are only those experienced and well-trained in the techniques of palpating TrPs and those who are not. Disagreements between those who are trained and those who are not, does not constitute a true debate. To have a controversy, there must be science on both sides. Researchers who do not understand the ubiquity of TrPs are churning out incomplete and often flawed research. Quantity does not equal quality. The "debate" will continue until they all become enlightened. Until then, bad research will beget more bad research. This study is not bad, but reflects the need for education. DJS]

Shoaib, M., L. S. Swanner, S. Yasar and S. R. Goldberg. 1999. Chronic caffeine exposure potentiates nicotine self-administration in rats. Psychopharmacology (Berl) 142(4):327-33.

Shochat, T., I Haimov and P. Lavie. 1998. Melatonin–the key to the gate of sleep. Ann Med30(1):109-14.

Shoskes DA, Berger R, Elmi A et al. 2007.  Muscle tenderness in men with chronic prostatitis/chronic pelvic pain syndrome: the chronic prostatitis cohort study.  J Urol. [Dec 12 Epub ahead of print].  "Myofascial pain is a possible etiology for category III chronic prostatitis/chronic pelvic pain syndrome, either secondary to infection/inflammation or as the primary cause."  "Abdominal/pelvic tenderness is present in half of the patients with chronic pelvic pain syndrome…."

Sidell, N. L. Adult adjustment to chronic illness: a review of the literature. Health Soc Work 22(1):5-11.

Sido B, Dumoulin FL, Homann J et al. 2013. [Surgical interventions in patients with mast cell activation disease: Aspects relevant for surgery using the example of a cholecystectomy.] Chirurg. [Dec 15 Epub ahead of print.] [Article in German] "Systemic mast cell activation disease (MCAD) is characterized by an increased and unregulated release of mast cell mediators which can evoke a multifaceted clinical picture often resembling irritable bowel syndrome or fibromyalgia. Because of the considerable prevalence (~ 17 %) of MCAD surgeons are frequently unwittingly confronted with MCAD patients in whom unexpected intraoperative and postoperative complications may occur. Therefore, knowledge of the particular requirements is of relevance for surgical treatment of MCAD patients….Due to the high prevalence of MCAD in the general population it can be assumed that the frequency in the surgical patient population is similar. If a patient has MCAD, specific characteristics should be taken into account in the surgical procedure to avoid increased operative and complication risks resulting from MCAD."

Siedentopf F. 2009. [Chronic pelvic pain in women from a gynecologic viewpoint]  Urologe A. 48(10):1193-1194, 1196-1198. [German]   It is rather amazing that the most common cause of chronic pelvic pain, the myofascial trigger point, is not included in this article.

Siedentopf F, Sillem M. 2014. [Chronic pelvic pain in women.] Schmerz. 28(3):300-304. [Article in German.] "Chronic pelvic pain in women represents a difficult diagnostic and therapeutic problem in the gynecological practice which is always a challenge when dealing with affected women….Important diagnostic steps are recording the patient history, a gynecological examination and laparoscopy. Multidisciplinary therapeutic approaches are considered to be very promising. Basic psychosomatic care and psychotherapy should be integrated into the therapeutic concept at an early stage."

Siegan, J. B., A. T. Hama and J. Sagen. 1997. Suppression of neuropathic pain by a naturally derived peptide with NMDA antagonist activity. Brain Res 755(2):331-334.

Siegel, D. M. , D. Janeway and J. Baum. 1998. Fibromyalgia syndrome in children and adolescents: clinical features at presentation and status at follow-up. Pediatrics 101(3 Pt 1):377-382.

Siegmeth, W. 1999. [No title available]. Wien Med Wochenschr 149(19-20):558-60 [German].

Siegmund G.P., Brault J.R., Chimich D.D. 2002.  Do cervical muscles play a role in whiplash injury?  J Whiplash and Rel Dis 1(1):23-40.  “...initially-relaxed cervical muscles have the potential to alter the head and neck kinematics and Kinematics resulting from whiplash events.”

Sigal, L. H. , D. J. Chang and V. Sloan.1998. 18 tender points and the "18 wheeler" sign: clues to the diagnosis of fibromyalgia. JAMA 279(6):434.

Sigmundsson H. 2005.  Disorders of motor development (clumsy child syndrome).  J Neural Transm Suppl. (69):51-68.  “Research has shown that about 6-10% of children have motor competences well below the norm.  It is unusual for motor problems to simply disappear over time.  In the absence of intervention the syndrome is likely to manifest itself.”  “...clumsiness must be seen as a neurological insufficiency.”

 

Sigmundsson H. 2003.  Perceptual deficits in clumsy children: inter- and intra-modal matching approach — a window into clumsy behavior.  Neural Plast. 10(1-2):27-38.  There are many informational deficits that can contribute to clumsy behavior.  Sensory integration dysfunction must be considered as well as proprioception and visual-perceptual and visual motor deficits.

Sikdar S, Ortiz R, Gebreab T et al. 2010. Understanding the vascular environment of myofascial trigger points using ultrasonic imaging and computational modeling. Conf Proc IEEE Eng Med Biol Soc. 1:5302-5305. "Recently, our research group has developed new ultrasound imaging methods to visualize and characterize MTrPs and their surrounding soft tissue. The goal of this paper was to quantitatively analyze Doppler velocity waveforms in blood vessels in the neighborhood of MTrPs to characterize their vascular environment.... 16 patients with acute neck pain were recruited for the study and the blood vessels in the upper trapezius muscle in the neighborhood of palpable MTrPs were imaged using Doppler ultrasound. Preliminary findings show that symptomatic MTrPs have significantly higher peak systolic velocities and negative diastolic velocities compared to latent MTrPs and normal muscle sites. Using compartment modeling, we show that a constricted vascular bed and an enlarged vascular volume could explain the observed flow waveforms with retrograde diastolic flow."

Sikdar S, Shah JP, Gebreab T et al. 2009. Novel Applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehab. 90(11):1829-1838. Nine subjects meeting Travel land Simons criteria for trigger points were assessed with physical evaluation, pressure algometry, and 3 types of ultrasound including grayscale 2D US, vibration sonoelastography and Doppler. The imaging techniques were capable of distinguishing myofascial trigger points from surrounding tissue. Tau bands were not investigated; only the contraction nodules. The studies support Simons' Integrated Hypothesis of Trigger Point Formation, indicating areas of hypoxic energy crisis and/or tissue damage at the contraction nodules. Although the operator was blinded as to the location of the nodules, the imaging made it obvious, as they were easily differentiated from the surrounding tissue. The authors warn that "…this study is exploratory and descriptive, and the findings are from a small number of subjects." They are also exceedingly expensive research studies and dependent on one operator, and in no way can be construed as clinically available. With the use of all of these types of techniques, it is possible to image myofascial trigger points. It may be some time in the future before any clinical use can be made of this, but the authors are working on standardizing the technique. [After this study from the National Institutes of Health—and others, there is absolutely no way that anyone can logically deny the existence of myofascial trigger points. The evidence was always there right under (trained, experienced) fingers. DJS]

Sil S, Lynch-Jordan A, Ting TV et al. 2012. The influence of family environment on long-term psychosocial functioning of adolescents with juvenile fibromyalgia. Arthritis Care Res (Hoboken). [Dec 19 Epub ahead of print]. "Results indicated that family environment during early adolescence significantly predicted greater depressive symptoms in early adulthood for both the JFM group and healthy controls. In particular, a controlling family environment (use of rules to control the family and allowing little independence) during early adolescence was the driving factor in predicting poorer long-term emotional functioning for patients with JFM. Family environment did not significantly predict longer-term physical impairment for either group."

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."

Silva KM, Tucano SJ, Kumpel C et al. 2012. Effect of hydrotherapy on quality of life, functional capacity and sleep quality in patients with fibromyalgia. Rev Bras Reumatol. 52(6):851-857. [English, Portuguese]. "Hydrotherapy improves sleep quality, physical function, professional status, psychological disorders and physical symptoms in patients with fibromyalgia."

Silva MP, Barrett JM, Williams JD. 2004.  A retrospective review of outcomes of fibromyalgia patients following physical therapy treatments.  J Musculoskel Pain 12(2):83-92.  Upledger’s cranio-sacral release therapy may be effective to decrease pain levels and medication and increase quality of life for FMS patients.

 

Silver DS, Wallace DJ. 2002. The management of fibromyalgia-associated syndromes.  Rheum Dis Clin North Am 28(2):405-17. "Most of the six million Americans with fibromyalgia have at least one associated syndrome which mandates specialized attention in addition to traditional therapeutic approaches.  The successful treatment of fibromyalgia-associated syndromes improves the symptoms, quality of life, and prognosis of fibromyalgia."

Silver, I. A., J. Deas and M. Erecinska. 1997. Ion homeostasis in brain cells: differences in intracellular ion responses to energy limitation between cultured neurons and glial cells. Neuroscience 78(2):589-601.

Simeonova M, Gimsa J. 2006.  The influence of the molecular structure of lipid membranes on the electric field distribution and energy absorption.  Bioelectromagnetics [Aug 17 Epub ahead of print]

Simms, R. W. 1998. Fibromyalgia is not a muscle disorder. Am J Med Sci 315(6):346-350.

Simms, R. W. , C. A. Zerbini, N. Ferrante, J. Anthony, D. T. Felson and D. E. Craven. 1992. Fibromyalgia syndrome in patients infected with human immunodeficiency virus. the Boston City Hospital Clinical AIDS Team. Am J Med 92(4):368-374.

Simon, J., E. Klaiber, B. Wiita (yes 2 "i"s), A. Bowen and H. M. Yang. 1999. Differential effects of estrogen-androgen and estrogen-only therapy on vasomotor symptoms, gonadotropin secretion, and endogenous androgen bio availability in post menopausal women. Menopause 6(2):138-46.

Simonnet G. 2005.  [Complexity and physiological logic of analgesic effects of opioids]  Rev Med Suisse. 1(25):1682-1685. [French]  “NMDA receptor antagonists and specific diets able to negatively modulate NR2B subunit containing NMDA receptors prevented abnormal pain hypersensitivity, partially reversed chronic pain and restored the opioid effectiveness on opioid-resistant pain models.”

 

Simons DG. 1991.  Symptomatology and clinical pathophysiology of myofascial pain.  Schmerz. 5(Supp 1):S29-37.  “Myofascial pain syndromes, fibromyalgia, and articular dysfunctions may all be contributing to our patients’ ubiquitous musculoskeletal pain problems that generally are poorly understood and poorly managed.”  [So many years later, and this is still the case.  One must wonder what it will take for the medical world to be equal to the paradigm change that it will take to bring myofascial pain into mainstream medicine, reducing so much needless pain, misery and cost. DJS]

 

Simons DG, Hong CZ, Simons LS. 2002.  Endplate potentials are common to midfiber myofascial trigger points. Am J Phys Med Rehabil. 81(3):212-222.  “Endplate noise was significantly more prevalent in myofascial trigger points than in sites that were outside of a trigger point but still within the endplate zone.  Endplate noise seems to be characteristic of, but is not restricted to, the region of a myofascial trigger point.”

 

Simons DG. 2004.  New aspects of myofascial trigger points: etiological and clinical.  J Musculoskeletal Pain 12(3/4):15-21.  This article clearly explains the evidence backing the integrated hypothesis for TrP formation, including information on biopsies and on the release of sensitizing substances documented by the work of Shah (see Shah JP, Phillips TM, Danoff JV et al. 2005. et al.).  It explains that it is a ...“serious mistake to consider the TrP in isolation.”  Patients often have clusters or chains of TrPs, and clinicians need to be on the alert that when one TrP is present in a patient with chronic symptoms (not always pain–TrPs can cause muscle dysfunctions including weakness as well as other symptoms before they cause pain), it is important to take into account the possible presence of other TrPs adding to the symptom load and maintaining chronicity.

 

Simons DG. 1981.  Myofascial trigger points: a need for understanding.  Arch Phys Med and Rehab. 62:97-99.  We need to clear up the terminology associated with myofascial TrPs.  There are neurophysiological mechanisms that can explain the TrP.

 

Simons DG, Mense S. 1998.  Understanding and measurement of muscle tone as related to clinical muscle pain.  Pain 75(1):1-17.  “Thixotropy of muscle is a ubiquitous and functionally important phenomenon that is not commonly recognized.  A clinical pain condition associated with increased muscle tension is tension-type headache, which is largely muscular in origin; it is often caused by myofascial trigger points.”  Diagnoses of muscle tension and muscle spasm must be differentiated.

Simons DG. 1995.  Myofascial pain syndrome: One term but two concepts; a new understanding.  J Musculoskeletal Pain 3(1):7-14.  This paper is of vital importance.  It explains how some researchers have been using the term “myofascial pain syndrome (MPS)” as synonymous with temporomandibular dysfunction (TMJD), without explaining the definition.  [This practice is common in papers written by dentists.  This dangerous practice can lead to misleading or erroneous conclusions.  Others build on these conclusions, not realizing that authors are using the term MPS to mean TMJD, and may assume that they refer to myofascial pain due to trigger points that may occur in all four quadrants of the body.  Authors must be careful to define their terms. DJS] 

Simons DG, Mense S.  Diagnosis and therapy of myofascial trigger points.  Schmertz 17(6):419-424.  This verifies by muscle biopsy the segmental shortening of sarcomere groupings in individual muscle fibers, suggesting the mechanism behind myofascial trigger point taut band formation. It presents an integrated hypothesis for the pathophysiology of myofascial trigger points, beginning with the release of excess acetylcholine from dysfunctional motor endplates. [German]

Simons D. G. 2001.  Do endplate noise and spikes arise from normal motor endplates?  Am J. Phys Med Rehabil 80(2):134-40.  Endplate noise may be a commonly misunderstood phenomenon and needs to be more carefully assessed in regards to association with myofascial trigger points.

Simons, DG. 1999. Diagnostic criteria of myofascial pain caused by trigger points. J Musculoskel Pain 7(1-2):111-120.

Simons, D. G. 1993. Examining for myofascial trigger points. Arch Phys Med Rehabil 74:676.

Simons, D. G. and W. C. Stolov. 1976. Microscopic features and transient contraction of palpable bands in canine muscles. Am J Phys Med 55:65-88.

Simpson, J. J. and W. E. Davies. 1999. Recent advances in the pharmacological treatment of tinnitus. Trends Pharmacol Sci 20(1):12-8.

Simpson KH. 2002.  Individual choice of opioids and formulations: strategies to achieve the optimum for the patient.  Clin Rheumatol 21 Suppl 1:S5-S8.  “Recent years have seen a gradual shift towards the use of opioid therapy in chronic non-malignant pain (CNMP) following recognition that at least a subpopulation of such patients appears to benefit from long-term opioid treatment.  Misconceptions about opioids and the associated risk of dependence stemmed from older research that was fundamentally flawed.  Opioid treatment must therefore be individualized for each patient, based on a clear understanding of drug absorption, metabolism, toxic and binding characteristics, using opioid switching strategies where appropriate.  Practical guidelines for opioid therapy in MNMP include regular and systematic checks of treatment results to adjust therapy or each individual patient and to ensure optimum benefit.”

Simunovic, Z., T. Trobonjaca and Z. Trobonjaca. 1998. Treatment of medial and lateral epicondylitis–tennis and golfer’s elbow–with low level laser therapy: a multicenter double-blind, placebo-controlled clinical study on 324 patients. J Clin Laser Med Surg 16(3):145-51.

Simunovic, Z. 1996. Low level laser therapy with trigger points technique: a clinical study on 243 patients. J Clin Laser Med Surg 14(4):163-167.

Sinaii N, Cleary S.D, Ballweg M.L. et al. 2002.  High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among women with endometriosis: a survey analysis.  Hum Reprod 17(10):2715-24.

Singh, B. B., B. M. Berman, V. A. Hadhazy and P. Creamer. 1998. A pilot study of cognitive behavioral therapy in fibromyalgia. Altern Ther Health Med 4(2):67-70.

Singh, G., D. R. Ramey, D. Morfeld, H. Shi, H. T. Hatoum and J. F. Fries. 1996. Gastrointestinal tract complications of nonsteroidal anti-inflammatory drug treatment in rheumatoid arthritis. A prospective observational cohort study. Arch Intern Med 156(14):1530-1536.

Singh RB, Kartik C, Otsuka K et al. 2002.  Brain-heart connection and the risk of heart attack. Biomed Pharmacother. 56 Suppl 2:257s-265s.  This article connects recent research linking conditions such as diabetes, ambient pollution, insulin resistance and mental stress with heart attack risk, gives some perpetuating factors of chest pain, and lists some possible protective mechanisms.

Sinz, E. H., P. M. Kochanek, M. P. Heyes, S. R. Wisniewski, M. J. Bell, R. S. Clark, S. T. DeKosky, A. R. Blight and D. W. Marion. 1998. Quinolinic acid is increased in CSF and associated with mortality after traumatic brain injury in humans. J Cereb Blood Flow Metab18(6):610-615.

Sirvent P, Mercier J, Vassort G et al. 2005.  Simvastatin triggers mitochondria-induced Ca2+ signaling altercation in skeletal muscle.  Biochem Biophys Res Commun 329:1067-1075.  This article is vitally important for physicians who have patients with myofascial TrPs.  Simvastatin, and, by biochemical inference, statin medications, triggers flood of intra-cellular calcium.  Increased release of Ca2+ is an essential part of the formation of myofascial TrPs, according to Simons’ integrated hypothesis.  The addition of statins could cause a flare of TrP symptoms that would not abate until statins are discontinued.  [This would mesh with personal observations and communications from myofascial pain specialists who have observed that many of their patients do not improve until they are off statins.  DJS]

Sist T, Wong C. 2000.  Difficult problems and their solutions in patients with cancer pain of the head and neck areas.  Curr Rev Pain. 4(3):206-214.  Often, pain in cancer patients is attributed to tumor regrowth when it is due to something else.  These authors urge careful consideration of alternatives and the possibility of mixed pain generators, including myofascial trigger points.

Sist, T., Miner, M.., Lema, M.,. 1999. Characteristics of postradical neck pain syndrome: a report of 25 cases. These results indicate that postoperative neuropathic pain and postoperative TrP pain can be present concurrently, that TrPs can be a common cause of postoperative pain, and that each type of pain requires its own specific treatment for relief.

Sitges C, Garcia-Herrera M, Pericas M et al. 2007.  Abnormal brain processing of affective and sensory pain descriptors in chronic pain patients.  J Affect Disord. [Apr 13 Epub ahead of print]

Siu AM, Chan CC, Poon PK. 2006.  Evaluation of the chronic disease self-management program in a Chinese population.  Patient Educ Couns. [Jul 25 Epub ahead of print]  “The CDSMP participants demonstrated significantly higher self-efficacy in managing their illness, used more cognitive methods to manage pain and symptoms, and felt more energetic than the subjects in the comparison group.”

Sivertsen B, Lallukka T, Salo P et al. 2013. Insomnia as a risk factor for ill health: results from the large population-based prospective HUNT Study in Norway. J Sleep Res. [Oct 30 Epub ahead of print.] "We conclude that insomnia predicts cumulative incidence of several physical and mental conditions. These results may have important clinical implications, and whether or not treatment of insomnia would have a preventive value for both physical and mental conditions should be studied further."

Sivri, A., A. Cindas, F. Dincer and B. Sivri. 1996. Bowel dysfunction and irritable bowel syndrome in fibromyalgia patients. Clin Rheumatol 15(3):283-286.

Sjogren P, Christrup LL, Petersen MA et al. 2005.  Neuropsychological assessment of chronic non-malignant pain patients treated in a multidisciplinary pain centre.  Eur J Pain 9(4):453-0462.  “MMSE [Mini Mental State Examination] seems to be too insensitive for detecting the milder forms of cognitive impairment found in chronic non-malignant patients.” 

Sjolund, K. F., M. Segerdahl and A. Sollevi. 1999. Adenosine reduces secondary hyperalgesiain two human models of cutaneous inflammatory pain. Anesth Analg 88(3):605-10.

Skargren, E. I. , B. E. Oberg, P. G. Carlsson and M. Gade. 1997. Cost and effectiveness analysis of chiropractic and physiotherapy treatment for low back and neck pain. Six-month follow-up. Spine 22(18):2167-2177.

Skootsky, S. A., B. Jaeger and R. K. Oye. 1989. Prevalence of myofascial pain in general internal medicine practice. West J Med 151(2):157-160.

Skorupska E, Rychlik M, Pawelec W et al. 2014. Trigger point-related sympathetic nerve activity in chronic sciatic leg pain: a case study. Acupunct Med. [Jun 26 Epub ahead of print.] "We report the case of a 22-year-old Caucasian European man who presented with a 3-year history of chronic sciatic-type leg pain. In the third year of symptoms, coexistent myofascial pain syndrome was diagnosed. Acupuncture needle stimulation of active trigger points under infrared thermovisual camera showed a sudden short-term vasodilatation (an autonomic phenomenon) in the area of referred pain. The vasodilatation spread from 0.2 to 171.9 cm2 and then gradually decreased.… It is not yet known whether the vasodilatation observed was evoked exclusively by dry needling of active trigger points. The complex condition of the patient suggests that other variables might have influenced the infrared thermovision camera results. We suggest that it is important to check if vasodilatation in the area of referred pain occurs in all patients with active trigger points."

Skrabek RQ, Galimova L, Ethansand Daryl K. 2007.  Nabilone for the treatment of pain in fibromyalgia.  [Oct 30 Epub ahead of print].  “To our knowledge, this is the first randomized, controlled trial to assess the benefit of nabilone, a synthetic cannabinoid, on pain reduction and quality of life improvement in patients with fibromyalgia.  As nabilone improved symptoms and was well-tolerated, it may be a useful adjunct for pain management in fibromyalgia.”  [Cannabinoids are increasingly being researched for chronic pain, with positive results. DJS]

Slater ME, De Lima J, Campbell K et al.  Opioids for the management of severe chronic nonmalignant pain in children: a retrospective 1 year practice survey in a children’s hospital.  Pain Med. [Epub ahead of print]  Function was improved in these children when they received adequate pain control.  Pediatric patients with severe nonmalignant chronic pain should not be denied opioids if they are needed as part of a pain management strategy.

Sloan P. 2008. Review of oral oxymorphone in the management of pain. Ther Clin Manag 4(4):777-787. Oxymorphone is available in both sustained-release and immediate release forms. This opioid does not have an NSAID or acetaminophen included, and has been successful for relief of chronic pain.

Slocumb, J. C. 1984. Neurological factors in chronic pelvic pain: trigger points and the abdominal pelvic pain syndrome. Am J Obstet Gynecol 149(5):536-43.

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Smania N, Corato E, Fiaschi A et al. 2005.  Repetitive magnetic stimulation - a novel therapeutic approach for myofascial pain syndrome.  J Neurol. [Epub ahead of print]  “Our results strongly suggest that at medium and longer term intervals peripheral rMS may be more effective than TENS for the treatment of myofascial pain.”

Smania N., Corato E., Fiaschi A. et al. 2003.  Therapeutic effects of peripheral repetitive magnetic stimulation on myofascial pain syndrome.  Clin Neurophysiol.  This study indicated that peripheral repetitive magnetic stimulation may have therapeutic effects on myofascial head and neck TrP pain and ROM.  The improvement noted lasted at least one month.

Smart, P. A., G. W. Waylonis and K. V. Hackinshaw. 1997. Immunologic profile of patients with fibromyalgia. Am J Phys Med Rehabil 76(3):231-4.

Smith D, Wilkie R, Uthman O et al. 2014. Chronic pain and mortality: a systematic review. PLoS One. 9(6):e99048. "This review showed a mildly increased risk of death in people with chronic pain, particularly from cancer. However, the small number of studies and methodological differences prevented clear conclusions from being drawn. Consistently applied definitions of chronic pain and further investigation of the role of health, lifestyle, social and psychological factors in future studies will improve understanding of the relationship between chronic pain and mortality." Free Article

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Smith EK, Magarey M, Argue S et al. 2009.  Muscular load to the therapist’s shoulder during three alternative techniques for trigger point therapy.  J Bodyw Mov Ther. 13(2):171-181.  “While there is evidence that the TTT (treatment-tool technique) decreases the muscular load to the shoulder of the contact arm, there is no indication of where this load is redistributed.”

Smith H, Elliott J. 2001.  Alpha2 receptors and agonists in pain management.  Curr Opin Anaesthesiol. 14(5):513-518.  “It has been noted that these agents can enhance analgesia provided by traditional analgesics, such as opiates, and may result in opiate-sparing effects.  This has important implications for the management of acute postoperative pain and chronic pain states…”

Smith, H.S., Audette J., Royal M.A. 2002.  Botuminum toxin in pain management of soft tissue syndrome.  Clin J Pain.  These authors suggest that because botulinum toxin has been used successfully for pain associated with myofascial trigger points, and it admits that central sensitization may be part of many chronic pain syndromes, it suggests that botulinum toxin therapy may be “particularly useful” in many soft tissue syndromes such as fibromyalgia when other approaches have failed.  [This paper ignores the specific mechanism of the myofascial trigger point (MTrP), as we believe it to be, with a release of excess acetylcholine at the motor endplate causing the release of excess calcium and the formation of MTrPs.  Botulinum toxin specifically interrupts acetylcholine in this process.  Logic indicates that one cannot extrapolate that the use of botulinum locally would be of any benefit in the control of a chronic central pain state, unless the peripheral pain generators perpetuating that state are MTrPs.  In that case, the MTrPs must first be shown to respond to local injection using the proper technique incorporating positioning of involved muscles, palpation for TrPs, injection of all related MTrPs, and full ROM stretch.  If this releases the muscle, but the release does not hold for a significant time in spite of the identification and control of all perpetuating factors, it would then be the time for consideration of more aggressive methods.]

Smith J.A., Lumley M.A., Longo D.J. 2002.  Contrasting emotional approach coping with passive coping for chronic myofascial pain.  Ann Behav Med 24(4):326-35. Emotional-approach coping (emotional processing and emotional expression) was related to less pain in myofascial pain patients, especially women, and less depression in men.  The use of passive pain coping strategies are associated with worse pain and adjustment.  Some emotion-focused types of pain coping may be adaptive.

Smith JD, Terpening CM, Schmidt SO et al. 2001. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins.  Ann Pharmacother 35(6):702-706.  A subset of FMS patients may improve significantly with the elimination of excitotoxins such as monosodium glutamate and aspartame from their diet.

Smith MT, Moore BJ. 2012. Pregabalin for the treatment of fibromyalgia. Expert Opin Pharmacother. 13(10):1527-1533. "This review addresses pregabalin pharmacokinetics, efficacy and adverse event (AE) profiles from randomized controlled trials and open-label extension studies in patients with FM. These effects are compared with those of the serotonin norepinephrine reuptake inhibitors, duloxetine and milnacipran that also have FDA approval for the treatment of fibromyalgia….At the approved dosages, oral pregabalin has at most a moderate therapeutic benefit above placebo with tolerable side-effects, in no more than 50% of patients with FM. Durability of clinically meaningful...pain relief in pregabalin-responders has been demonstrated for at least 6-months, but longer-term studies are required as most patients have symptoms for decades. Exclusion of patients with common co-morbidities from the pregabalin RCTs in FM raises questions on the generalizability of the RCT findings to the typical patient seen in clinical practice and so additional investigation is required."

Smith MT, Perlis ML, Haythornthwaite JA. 2004.  Suicidal ideation in outpatients with chronic musculoskeletal pain: an exploratory study of the role of sleep onset insomnia and pain intensity.  Clin J Pain. 20(2):111-118.  “Chronic pain patients who self-reported severe and frequent initial insomnia with concomitant daytime dysfunction and high pain intensity were more likely to report passive suicidal ideation, independent from the effects of depression severity.”  More attention needs to be focused on controlling factors leading to suicidal ideation in chronic pain patients.

Smith MT, Edwards RR, Robinson RC et al. 2004.  Suicidal ideation, plans, and attempts in chronic pain patients: factors associated with increased risk.  Pain 111(1-2):201-208.  “Demographics, pain severity, and depression severity were not associated with suicidal ideation in multivariate analyses.”

Smith MT, Edwards RR, Robinson RC et al. 2004.  Suicidal ideation, plans, and attempts in chronic pain patients: factors associated with increased risk.  Pain 111(1-2):201-208.  “These findings highlight the need for routine evaluation monitoring of suicidal behavior in chronic pain, especially for patients with histories of suicide, those taking potentially lethal medications, and patients with abdominal pain.”

Smith PF. 2012. Dyscalculia and vestibular function. Med Hypotheses. [Jul 21 Epub ahead of print]. "A few studies in humans suggest that changes in stimulation of the balance organs of the inner ear (the 'vestibular system') can disrupt numerical cognition, resulting in 'dyscalculia', the inability to manipulate numbers. Many studies have also demonstrated that patients with vestibular dysfunction exhibit deficits in spatial memory....It is suggested that there may be a connection between spatial memory deficits resulting from vestibular dysfunction and the occurrence of dyscalculia, given the evidence that numerosity is coupled to the processing of spatial information (e.g., the 'spatial numerical association of response codes ('SNARC') effect')."

Smith PF, Darlington CL. 2013. Personality changes in patients with vestibular dysfunction. Front Hum Neurosci. 7:678. "The vestibular system is a sensory system that has evolved to detect linear and angular acceleration of the head in all planes so that the brain is not predominantly reliant on visual information to determine self-motion. Since the vestibular system first evolved in invertebrate species in order to detect gravitational vertical, it is likely that the central nervous system has developed a special dependence upon vestibular input. In addition to the deficits in eye movement and postural reflexes that occur following vestibular dysfunction, there is convincing evidence that vestibular loss also causes cognitive and emotional disorders, some of which may be due to the reflexive deficits and some of which are related to the role that ascending vestibular pathways to the limbic system and neocortex play in the sense of spatial orientation. Beyond this, however, patients with vestibular disorders have been reported to experience other personality changes that suggest that vestibular sensation is implicated in the sense of self. These are depersonalization and derealization symptoms such as feeling "spaced out", "body feeling strange" and "not feeling in control of self". We propose in this review that these symptoms suggest that the vestibular system may make a unique contribution to the concept of self through information regarding self-motion and self-location that it transmits, albeit indirectly, to areas of the brain such as the temporo-parietal junction (TPJ)." [I have observed that many patients with fibromyalgia and chronic myofascial pain also have co-existing (and often undiagnosed) vestibular dysfunction. This co-existing condition may be a cause of significant symptoms. DJS]

Smith PF, Zheng Y. 2013. From ear to uncertainty: vestibular contributions to cognitive function. Front Integr Neurosci. 7:84. "In addition to the deficits in the vestibulo-ocular and vestibulo-spinal reflexes that occur following vestibular dysfunction, there is substantial evidence that vestibular loss also causes cognitive disorders, some of which may be due to the reflexive deficits and some of which are related to the role that ascending vestibular pathways to the limbic system and neocortex play in spatial orientation. In this review we summarize the evidence that vestibular loss causes cognitive disorders, especially spatial memory deficits, in animals and humans and critically evaluate the evidence that these deficits are not due to hearing loss, problems with motor control, oscillopsia or anxiety and depression. We review the evidence that vestibular lesions affect head direction and place cells as well as the emerging evidence that artificial activation of the vestibular system, using galvanic vestibular stimulation (GVS), can modulate cognitive function."

Smith SC, Wagner MS. 2014. Clinical endocannabinoid deficiency (CECD) revisited: Can this concept explain the therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuro Endocrinol Lett. 35(3):198-201. "Subsequent research has confirmed that underlying endocannabinoid deficiencies indeed play a role in migraine, fibromyalgia, irritable bowel syndrome and a growing list of other medical conditions. Clinical experience is bearing this out. Further research and especially, clinical trials will further demonstrate the usefulness of medical cannabis. As legal barriers fall and scientific bias fades this will become more apparent."

Smith, W. A. 1998. Fibromyalgia Syndrome. Nurs Clin North Am 33(4):653-669.

Smith WR, White PD, Buchwald D. 2006.  A case control study of premorbid and currently reported physical activity levels in chronic fatigue syndrome.  BMC Psychiatry 6:53.  “Patients with chronic, unexplained, disabling fatigue reported being more active before becoming ill than healthy controls.  This finding could be explained by greater premorbid activity levels that could predispose to illness, or by an overestimation of previous activity.”

Smith-Coggins, R., M. R. Rosekind, K. R. Buccino, D. F. Dinges and R. P. Moser. 1997. Rotating shift work schedules: can we enhance physician adaptation to night shifts? Acad Emerg Med 4(10):951-61.

Smythe HA. 2004.  Fibromyalgia among friends. J Rheumatol 31(4):627-630.  This editorial describes anti-fibromyalgia bias that is blatant in material from some medical authors, in spite of scientific evidence that it is real.  Legal advocates should take note of this. 

Smythe, H. 1998.  Examination for tenderness: learning to use 4 kg force.  J Rheumatol 25(1):149-151.

Snyder-Mackler L, Barry AJ, Perkins AI et al. 1989.  Effects of helium-neon laser irradiation on skin resistance and pain in patients with trigger points in the neck or back.  Phys Ther. 69(5):336-341.  “The purpose of this double-blind study was to ascertain the effects of helium-neon (He-Ne) laser irradiation on skin resistance and pain in patients with trigger points in the neck or low back.”  “Results indicated a statistically significant increase in skin resistance and a decrease in pain following laser treatment.”

Snyder-Mackler, L., A. Delitto, S. W. Stralka and S. L. Bailey. 1994. Use of electrical stimulation to enhance recovery of quadriceps femoris muscle force production in patients following anterior cruciate ligament reconstruction. Phys Ther 74(10):901-907.

Soderberg, S., B. Lundman and A. Norberg. 1999. Struggling for dignity: the meaning of women’s experiences of living with fibromyalgia. Qual Health Res 9(5):575-87.

Soderberg, S., B. Lundman and A. Norberg. 1997. Living with fibromyalgia: sense of coherence, perception of well-being, and stress in daily life. Res Nurs Health 20(6):495-503.

Sohn W. 2001.  [The path to pain management on WHO. Step III.  Towards a better understanding of the treatment of severe chronic pain] Fortschr Med Orig. 119 Suppl 2:81-89. [German]  “Many patients with severe chronic pain continue to receive inadequate treatment.  The reason is often a lack of proper communication between patient and physician.”

Soin A, Cheng J, Brown L et al. 2008.  Functional outcomes in patients with chronic nonmalignant pain on long-term opioid therapy.  Pain Pract. 8(5):379-384.  “We conclude that judicious use of opioids therapy may lead to improvement in perceived quality of life and certain aspects of functional capacity and daily activities in a highly selected group of patients with CNMP (chronic nonmalignant pain) who have not responded to other therapeutic modalities for over 6 months.”

Sok SR, Erien JA, Kim KB. 2003.  Effects of acupuncture therapy on insomnia.  J Adv Nurs 44(4):375-384.  Acupuncture may have a significant effect on insomnia.

Solberg Nes L, Carlson CR, Crofford LJ et al. 2010. Self-regulatory deficits in fibromyalgia and temporomandibular disorders. Pain. [Jun 17 Epub ahead of print]. "Chronic pain conditions such as fibromyalgia (FM) and temporomandibular disorders (TMDs) are accompanied by complex interactions of cognitive, emotional, and physiological disturbances. Such conditions are complicated and draining to live with, and successful adaptation may depend on ability to self-regulate. Self-regulation involves capacity to exercise control and guide or alter reactions and behavior, abilities essential for human adjustment. Research indicates that self-regulatory strength is a limited source that can be depleted or fatigued, however, and the current study aimed to show that patients with FM and TMD are vulnerable to self-regulatory fatigue as a consequence of their condition…. Patients displayed significantly less capacity to persist on the subsequent task compared with controls. In fact, patients exposed to low self-regulatory effort displayed similar low persistence to patients and controls exposed to high self-regulatory effort, indicating that patients with chronic pain conditions may be suffering from chronic self-regulatory fatigue….Impact of chronic pain conditions on self-regulatory effort was mediated by pain, but not by any other factors. The current study suggests that patients with chronic pain conditions likely suffer from chronic self-regulatory fatigue, and underlines the importance of taking self-regulatory capacity into account when aiming to understand and treat these complex conditions. "

Solerte, S. B., M. Rondanelli, R. Giacchero, M. Stabile, E. Lovati, L. Cravello, B. Pontiggia, G. Vignati and E. Ferrari, MF. 1999. Serum glucagon concentration and hyperinsulinaemia influence renal haemodynamics and urinary protein loss in normotensive patients with central obesity. Int J Obes Relat Metab Disord 23(9):997-1003.

Solomon, C. G., J. S. Carroll, K. Okamura, S. W. Graves and E. W. Seely. 1999. Higher cholesterol and insulin levels in pregnancy are associated with increased risk for pregnancy-induced hypertension. Am J Hypertens 12(3):276-82.

Solomon, D. H. and M. H. Liang. 1997. Fibromyalgia: scourge of humankind or bane of a rheumatologist's existence? Arthritis and Rheumatism 40:1553-1555.

Solomon L, Schnitzler CM, Browett JP. 1982.  Osteoarthritis of the hip: the patient behind the disease.  Ann Rheum Dis. 41(2):118-125.  “...appearances of hip OA are determined by 3 interacting factors: mechanical stress, cartilage degeneration, and bone response.”  [Mechanical stress could be supplied by the presence of myofascial TrPs, especially in the attachment regions.  DJS]  

Sommer C. 2013. [Neuropathic pain: Pathophysiology, assessment, and therapy.] Schmerz. [Nov 13 Epub ahead of print]. [Article in German] "Neuropathic pain is caused by lesions in the somatosensory system. Characteristic but not exclusive features are spontaneous burning pain, electrifying and shooting pain, hyperalgesia, and allodynia. The basic concept of the pathophysiology of neuropathic pain is the combination of peripheral and central sensitization. Knowledge on the molecular mechanisms has grown exponentially in recent years. The problem lies in identifying the individual mechanisms and in determining a comprehensive concept. Progress has also been made in assessment, e.g., methods for detecting dysfunction of nociceptors have significantly improved. In addition, there are many more therapeutic options available than 15 years ago. The drugs available include antidepressants, anticonvulsants, opioids, and topical medications."

Soppi, M. and E. Beneforti. 1999. Muscular pain in some rheumatic diseases. J Musculoskel Pain 7(1-2):225-229

Sorensen, J., A. Bengtsson, J. Ahlner, K. G. Henriksson, L. Ekselius, and M. Bengtsson. 1997. Fibromyalgia--are there different mechanisms in the processing of pain? A double blind crossover comparison of analgesic drugs. J Rheumatol 24(8):1615-1621.

Sorensen, J., A. Bengtsson, E. Backman, K. G. Henriksson and M. Bengtsson. 1995. Pain analysis in patients with fibromyalgia. Effects of intravenous morphine, lidocaine, and ketamine.Scand J Rheumatol 24(6):360-365.

Sorg, B. A. and T. Hochstatter. 1999. Behavioral sensitization after repeated formaldehyde exposure in rats. Toxicol Ind Health 15(3-4):346-55.

Sorond FA, Hurwitz S, Salat De et al. 2013. Neurovascular coupling, cerebral white matter integrity, and response to cocoa in older people. Neurology Aug 7 [Epub ahead of print] Neurovascular coupling is associated with cognitive function. Both can be improved in individuals with impaired cognitive function between the ages of about 67 to 78 if they consume cocoa every day.

Sorrell MR. 2010. Myofascial examination leads to diagnosis and successful treatment of migraine headache. J Musculoskel Pain. 18(1). “The myofascial examination of the head and neck reproduced the headache pain of most patients having migraine. The PTS (physical therapist supervised stretching of involved muscles along their lengths) is effective in treating these headaches. The myofascial examination should be used to determine treatment for migraineurs.” 

Sorrell MR, Flanagan W. 2003.  Treatment of chronic resistant myofascial pain using a multidisciplinary protocol [The Myofascial Pain Program].  J Musculoskel Pain 11(1):5-9.  Multidisciplinary treatment including myofascial technique physical therapy, surface electromyography and biofeedback training, medication and trigger point injections can significantly produce pain relief, mood elevation and increase ability to function, even in patients who have symptoms resistant to other therapies.

Sorrell MR, Flanagan W, McCall JL. 2003.  Symptom duration affects the outcome of multidisciplinary treatment of myofascial pain.  The method of assessment influences the understanding of the results.  J Musculoskel Pain 11(1):11-16.  The earlier the patient enters a multidisciplinary treatment program that understands myofascial pain, the better the results.

Sorrell MR, Flanagan W, McCall JL. 2003.  The effect of depression and anxiety on the success of multidisciplinary treatment of chronic resistant myofascial pain.  J Musculoskel Pain 11(1):17-20. Co-existing depression significantly reduced positive outcome of this treatment

Sousa AS, Macedo R, Santos R et al. 2013. Influence of wearing an unstable shoe construction on compensatory control of posture. Hum Mov Sci. 32(6):1353-1364. "These findings demonstrate that WUS (wearing unstable shoes) led to a reorganization of the postural control system associated to improved performance of some components of postural control responses."

Sousa RF, Gazzola JM, Gananca MM et al. 2011. Correlation between the body balance and functional capacity from elderly with chronic vestibular disorders. Braz J Otorhinolaryngol. 77(6):791-798. [Article in English, Portuguese] "Vestibular disorders are common among the elderly, mainly resulting in dizziness and imbalance - symptoms which can impact daily routine activities.....There is a positive correlation between body balance and functional capacity in elderly patients with peripheral vestibular disorders, that is: the better the balance, the better the individual's functional capacity. In addition, a worse functional capacity increases the individual's risk of falling." [Vestibular dysfunction is also common in FM patients, and must be considered. DJS]

Southwick, S. M., C. A. Morgan 3rd, D. S. Charney and J. R. High. 1999. Yohimbine use in a natural setting: effects on posttraumatic stress disorder. Biol Psychiatry 46(3):442-4.

Sowers, J. R. and B. Draznin. 1998. Insulin, cation metabolism and insulin resistance. J Basic Clin Physiol Pharmacol 9(2-4):223-33.

Soyupek F, Guney M, Kaplan O et al. 2013. Is fibromyalgia syndrome common in the patients with primary dysmenorrhea? J Musculoskel Pain 21(2):156-160. Fibromyalgia was more frequent in primary dysmenorrhea patients, especially symptomatic ones. [These patients were not checked for co-existing chronic myofascial pain. Since trigger points can cause dysmenorrhea and drive FM central sensitization, these patients may have had primary myofascial pain due to trigger points that caused the dysmenorrhea and subsequently, the FM. DJS]

Soyupek F, Soyupek S, Akkus S et al. 2007.  The coexistence of the fibromyalgia syndrome and the overactive bladder syndrome.  J Musculoskel Pain 15(3):31-37.  “Our findings suggest that there is an association between OBS and FMS, especially in female patients.”  The authors remind readers that both FM and OBS are chronic.

Soyupek F, Yildiz S, Akkus S et al. 2010. The frequency of fibromyalgia syndrome in patients with polycystic ovary syndrome. J Musculoskel Pain 18(2):120-126. This interesting article reports that 32% of FM patients in the study had polycystic ovary syndrome (PCOS). Only 7.7% of the healthy controls had PCOS. Insulin resistance is a common co-existing condition in FM patients, and PCOS is common in insulin resistance. It would be most interesting to learn what percentage of these patients also had insulin resistance. It is suspected that FM and insulin resistance are interactive diagnoses. DJS]

Spaeth M, Alegre C, Perrot S et al. 2013. Long-term tolerability and maintenance of therapeutic response to sodium oxybate in an open-label extension study in patients with fibromyalgia. Arthritis Res Ther. 15(6):R185. "The long-term safety and therapeutic response of sodium oxybate (SXB) in fibromyalgia syndrome (FM) patients were assessed for a combined period of up to 1 year in a prospective, multicenter, open-label, extension study in patients completing 1 of 2 phase 3 randomized, double-blind, controlled, 14-week trials that examined the efficacy and safety of SXB 4.5 g, SXB 6 g, and placebo for treatment of FM….Maintenance of SXB therapeutic response was demonstrated with continued improvement from controlled-study baseline in pain VAS, Fibromyalgia Impact Questionnaire (FIQ) total scores, and other measures. Responder analyses showed that 68.8% of patients achieved ≥ 30% reduction in pain VAS and 69.7% achieved ≥ 30% reduction in FIQ total score at study endpoint….The long-term safety profile of SXB in FM patients was similar to that in the previously reported controlled clinical trials. Improvement in pain and other FM clinical domains was maintained during long-term use."

Spaeth M. 2011. [Fibromyalgia]. Z Rheumatol. 70(7):573-587. [German]. "Although chronic musculoskeletal pain represents the main symptom of fibromyalgia, those affected usually experience many and various accompanying symptoms of differing frequency and extent. While symptoms such as non-restful sleep, daytime fatigue, impaired memory and concentration, morning stiffness, as well as digestive and urination disorders help to establish the diagnosis, they represent a particular disease burden on patients, those around them and on the social system. Pathogenetic research is focused increasingly on a central dysregulation in pain perception and pain processing, leading to the concept of 'central sensitization' as a final common pathway for fibromyalgia and similar syndromes. This supports the recommendations for prompt multimodal therapy based on pharmaco-, functional and behavioral therapy."

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]

Spaeth M. 2009.  Epidemiology, costs, and the economic burden of fibromyalgia.  Arthritis Res Ther. 11(3):117.  “Despite the differences between healthcare and sociopolitical systems in various countries, more recent results from epidemiological research now clearly demonstrate the socioeconomic burden of fibromyalgia and its comorbidities.  The costs of the disease, calculated in single studies and countries, allow estimates for populations in other countries.  The alarming results highlight the urgent need both for more research (including pathophysiology and epidemiology) and for the acceptance of emerging treatment challenges.”  [The central sensitization of fibromyalgia occurs worldwide, and is a significant burden on the patient and the health care system.  Most cases of FM are preventable.  It’s long past time for the medical community to devote resources to research and vigorous treatment, rather than wasting resources in denying the existence of FM. DJS]

Spaeth M, Bennett RM, Benson BA et al. 2012. Sodium oxybate therapy provides multidimensional improvement in fibromyalgia: results of an international phase 3 trial. Ann Rheum Dis. [Jan 31 Epub ahead of print]. "Along with pain and fatigue, non-restorative sleep is a core symptom of fibromyalgia." This study of 573 FM patients meeting the 1990 ACR criteria... .."were randomly assigned to placebo, SXB (sodium oxybate) 4.5 g/night or SXB 6 g/night." Assessment included pain, ..."function, sleep quality, effect of sleep on function, fatigue, tenderness, health-related quality of life and subject's impression of change in overall wellbeing....Significant improvements in pain, sleep and other symptoms associated with fibromyalgia were seen in SXB treated subjects compared with placebo....These results, combined with findings from previous phase 2 and 3 studies, provide supportive evidence that SXB therapy affords important benefits across multiple symptoms in subjects with fibromyalgia.

Spaeth M, Rizzi M, Sarzi-Puttini P. 2011. Fibromyalgia and sleep. Best Pract Res Clin Rheumatol. 25(2):227-239. "Chronic pain in fibromyalgia patients, together with its associated symptoms and co-morbidities, is now considered a result of dysregulated mechanisms in the central nervous system (CNS). As fibromyalgia patients often report sleep problems, the physiological processes that normally regulate sleep may be disturbed and overlap with other CNS dysfunctions. Although the mechanisms potentially linking chronic widespread pain, sleep alterations and mood disorders have not yet been proven, polysomnography findings in patients with fibromyalgia and non-restorative sleep and their relationships with clinical symptoms support the hypothesis of a conceptual common mechanism called 'central sensitization'. Food and Drug Administration (FDA)-approved drugs for the treatment of fibromyalgia may benefit sleep, but their label does not include the treatment of fibromyalgia-associated sleep disorders. Non-pharmacological therapies (including a thorough sleep assessment) can be considered in the first-line treatment of non-restorative sleep, although they have not yet been fully investigated in patients with fibromyalgia. Both pharmacological and non-pharmacological treatments should be used cautiously in patients with fibromyalgia, bearing in mind the patients' underlying disorders and the potential interactions of the therapies."

Spaggiari, M. C., F. Granella, L. Parrino, C. Marchesi, I. Melli and M. G. Terzano. 1994. Nocturnal eating syndrome in adults. Sleep 17(4):339-44.

Spath M, Stratz T, Farber L et al. 2004.  Treatment of fibromyalgia with tropisetron — dose and efficacy correlations.  Scand J Rheumatol Suppl (119):63-66.  Tropisetron therapy may need to be tailored to subgroups of FMS patients.

 

Spath M, Stratz T, Neeck G et al. 2004.  Efficacy and tolerability of intravenous tropisetron in the treatment of fibromyalgia.  Scand J Rheumatol. 33(4):267-270.  Intravenous tropisetron, a 5-HT3 receptor blocker, provided significant pain relief for the FMS patients in this prospective trial.

 

Spath M, Neeck G. 2002.  [The expert assessment of fibromyalgia.]  Z Rheumatol 61(6):661-6. [German]   Pain amplification syndromes are well documented and have been researched for a decade.  The validity of the reality of fibromyalgia has no place in an expert assessment.  “The sociomedical implications (of fibromyalgia) are obvious and considerable...”  Assessments must be specific to the individual, focusing on evaluation of specific impairments and disabilities and how these handicaps affect function.

Sperber, A. D., S. Carmel, Y. Atzmon, I. Weisberg, Y. Shalit, L. Neumann, A. Fich and D. Buskila. 1999. The sense of coherence index and the irritable bowel syndrome. A cross-sectional comparison among irritable bowel syndrome patients with and without coexisting fibromyalgia, irritable bowel syndrome non-patients, and controls. Scand J Gastroenterol 34(3):259-63.

Sperber, A. D., Y. Atzmon, L. Neumann, I. Weisberg, Y. Shalit, M. Abu-Shakrah, A. Fich and D. Buskila. 1999. Fibromyalgia in the irritable bowel syndrome: studies of prevalence and clinical implications. Am J Gastroenterol 94(12):3541-6.

Sperber AD, Dekel R. 2010. Irritable Bowel Syndrome and Co-morbid Gastrointestinal and Extra-gastrointestinal Functional Syndromes. J Neurogastroenterol Motil. 16(2):113-119. "Many IBS patients have at least one co-morbid somatic complaint and many meet diagnostic criteria for other functional disorders. Patients with IBS and another functional disorder, in comparison with patients with IBS only, have more severe IBS symptoms, a higher rate of psychopathology, greater impairment of quality of life, and more illness-related work absenteeism. Estimates of the prevalence of IBS in patients with fibromyalgia range from 30-35% to as high as 70%. Studies of IBS among patients with chronic fatigue syndrome have reported a prevalence ranging from 35-92%.....It has been suggested that the presence of multiple co-morbid disorders may be a marker for psychological influences on etiology. This raises the question of whether the functional syndromes represent the same pathophysiological process, i.e., are the same entity that has been separated into different clinical entities because of medical sub-specialization, or are indeed separate disorders. While the answer to this question awaits further research, it would appear that most functional patients who meet formal diagnostic criteria for more than one functional disorder manifest one disorder clinically more that the others and seek consultation differentially for that set of symptoms.

Spevak C. 1997.  Asystole during trigger point injections in a patient with panic disorder.  Reg Anesth. 22(6):583.  [This article is a vital reminder that TrP injections can be painful and complex, and that it takes more than a glance at a TrP diagram to be able to perform them adequately.  Patients must be carefully assessed and pain and anxiety must be brought under control, and the protocol followed, with the pain and anxiety level kept below danger level.  One must always monitor for symptoms of shock or other severe reaction and be ready to handle whatever may come.  The best preventative is a well-educated and prepared patient and care provider.  DJS]

Spiro, H. 1992. What is empathy and can it be taught? Ann Intern Med 116(10):843-6.

Spitzer AR, Boyle JT, Tuchman DN et al. 1984.  Awake apnea associated with gastroesophageal reflux: a specific clinical syndrome.  J Pediatr 104(2):200-205.

Spitzer AR, Broadman M. 2010. Treatment of the narcoleptiform sleep disorder in chronic fatigue syndrome and fibromyalgia with sodium oxybate. Pain Pract. 10(1):54-59. "Sixty percent of patients treated with oxybate experienced significant relief of pain, while 75% experienced significant relief of fatigue. We postulate that the response to oxybate in CFS and FM suggests a disturbance of sleep similar to narcolepsy. These findings support this novel approach to intervention and further research."

Spitznagle TM, McCurdy Robinson C. 2014. Myofascial Pelvic Pain. Obstet Gynecol Clin North Am. 41(3):409-432. "Individuals with pelvic pain commonly present with complaints of pain located anywhere below the umbilicus radiating to the top of their thighs or genital region. The somatovisceral convergence that occurs within the pelvic region exemplifies why examination of not only the organs but also the muscles, connective tissues (fascia), and neurologic input to the region should be performed for women with pelvic pain. The susceptibility of the pelvic floor musculature to the development of myofascial pain has been attributed to unique functional demands of this muscle. Conservative interventions should be considered to address the impairments found on physical examination."

Sprott H, Salemi S, Gay RE et al. 2004.  Increased DNA fragmentation and ultrastructural changes in fibromyalgic muscle fibres.  Ann Rheum Dis. 63(3):245-251.  This study found a significantly high rate of DNA fragmentation in FMS patient samples (55.4%) compared with healthy controls (4.1%).  Myofibers and actin filaments were disorganized, and the number of mitochondria were significantly lower in FMS patients.

Sprott, H., L. A. Bradley, S. J. Oh, W. Wintersberger, G. S. Alarcon, H. G. Mussell, A. Tseng, R. E. Gay and S. Gay. 1998. Immunohistochemical and molecular studies of serotonin, substance P., galanin, pituitary adenylyl cyclase-activating polypeptide, and secretoneurin in fibromyalgia to muscle tissue. Arthritis Rheum 41(9):1689-94.

Sprott, H., A. Muller and H. Hartmut. 1997. Collagen crosslinks in fibromyalgia. Arthritis Rheum 40(8):1450-1454.

Srbely JZ, Dickey JP, Bent LR et al. 2009.  Capsaicin-induced central sensitization evokes segmental increases in trigger point sensitivity in humans.  J Pain. [Dec 14 Epub ahead of print]  “This study investigated whether inducing central sensitization evokes segmental increases in trigger point pressure sensitivity.”  “These results demonstrate that increases in central sensitization evoke increases in trigger point pressure sensitivity in segmentally related muscles.”  “Myofascial pain is the most common form of musculoskeletal pain.  Myofascial trigger points play an important role in the clinical manifestation of myofascial pain syndrome.  Elucidating the role of central sensitization in the pathophysiology of trigger points is fundamental to developing optimal strategies in the management of myofascial pain syndrome.”

Srbely JZ, Dickey JP. 2007.  Randomized controlled study of the anti-nociceptive effect of ultrasound on trigger point sensitivity: novel applications in myofascial therapy?  Clin Rehabil. 21(5):411-417.   “Ultrasound may be a useful clinical tool for the treatment and management of trigger points and myofascial pain syndromes.”

Srbely JZ, Dickey JP, Lee D et al. 2010. Dry needle stimulation of myofascial trigger points evokes segmental anti-nociceptive effects. J Rehabil Med. 42(5):463-468. "One intervention of dry needle stimulation to a single trigger point (sensitive locus) evokes short-term segmental anti-nociceptive effects. These results suggest that trigger point (sensitive locus) stimulation may evoke anti-nociceptive effects by modulating segmental mechanisms, which may be an important consideration in the management of myofascial pain."

Srbely JZ, Vernon H, Lee D et al. 2013. Immediate effects of spinal manipulative therapy on regional antinociceptive effect in myofascial tissues in healthy young adults. J Manipulative Physiol Ther. 36(6):333-341. This study had as its participants healthy students from Guelph University with identifiable (assumedly latent) trigger points in the infraspinatus and gluteus medius myofascia. They tested the effects on pain sensitivity in these muscles after one single high-velocity, low amplitude rotary spinal thrust spinal manipulative therapy on the C5-C6. The treatment resulted in short-term increases in pain sensitivity in the muscles tested. This did not occur in students in a control group who received sham treatment. [The effects on pain sensitivity in the buttocks and shoulder after a chiropractic technique performed on the spinal area of the neck (in healthy students who probably had latent trigger points) are interesting. I'd like to see a study with comparison of Activator and manual techniques compared, using patients with active trigger points in the same muscles, including patients who have central sensitization. DJS]

Srdic, F., Sarhus, M., Topuz, O. 2002.  Comparisons of two different techniques of electrotherapy on myofascial pain.  J Back Musculoskel Rehab 16:11-16.  Electrotherapy can be useful to treat myofascial pain.

Srikuea R, Symons TB, Long DE et al. 2012. Fibromyalgia is associated with altered skeletal muscle characteristics which may contribute to post-exertional fatigue in post-menopausal women. Arthritis Rheum. [Nov 1 Epub ahead of print]. "Peripheral mechanisms i.e. altered muscle fiber size distribution and decreased capillary density may contribute to post-exertional fatigue in subjects with FM. Understanding these defects in fibromyalgic muscle may provide valuable insight for treatment." [The authors of this study from Thailand may have been looking at co-existing myofascial trigger points. DJS]

Srinivasan AK, Kaye JD, Moldwin R. 2007.  Myofascial dysfunction associated with chronic pelvic floor pain: management strategies.  Curr Pain Headache Rep. 11(5):359-364.

Staedt, J., H. Hunerjager, E. Ruther and G. Stoppe. 1998. Pergolide: treatment of choice in restless legs syndrome (RLS) and nocturnal myoclonus syndrome (NMS). Long term follow up on pergolide. Short communication. J Neural Transm 105(2-3):265-8.

Staedt, J., G. Stoppe, A. Kogler, H. Riemann, G. Hajak, D. L. Munz, D. emrich and E. Ruther. 1995. Nocturnal myoclonus syndrome (periodic movements in sleep) related to central dopamine D2-receptor alteration. Eur Arch Psychiatry Clin Neurosci 245(1):8-10.

Stahl SM, Briley M. 2009.  Why psychiatrists should not ignore pain in their patients – focus on fibromyalgia?  Hum Psychopharmacol. 24 Suppl 1:S1-2.

St. Amand, R. Paul and Claudia C. Marek. 1999. What Your Doctor May Not Tell You About Fibromyalgia. Warner Books: New York.

Stair S., K. Carlson, S. Shuster et al. 2002. Mystixin peptides reduce hyaluran deposition and edema formation. Eur J Pharmacol 450(3):291.

Stamer UM, Bayerer B, Stuber F. 2005.  Genetics and variability in opioid response.  Eur J Pain. 9(2):101-104.  “In pain therapy, the genetic background influencing the efficacy of opioid therapy is of special interest.  CYP2D6 genetic variability is supposed to be a major factor of adverse drug reaction, possibly influencing hospital stay and total costs.  Further candidate genes involved in pain perception, pain processing and pain management like opioid receptors, transporters and other targets of pharmacotherapy are under investigation.  Aspects of genetic differences influencing efficacy, side effects and adverse outcome of pharmacotherapy will be of importance for future pain management.”

 

Stander S, Schmelz M. 2006.  Chronic itch and pain – similarities and differences.  Eur J Pain [May 4 Epub ahead of print]  “Classical inflammatory mediators such as bradykinin have been shown to sensitize nociceptors for both itch and pain.  Also regulation of gene expression induced by trophic factors, such as NGF, plays a major role in persistently increased neuronal sensitivity for itch and pain.  Finally, itch and pain exhibit corresponding patterns of central sensitization.”

Stander S, Steinhoff M, Schmetz M et al. 2003.  Neurophysiology of pruitis: cutaneous elicitation of itch.  Arch Dermatol 139(11):1463-1470.  This article is important because it indirectly explains how itch can be a manifestation of both fibromyalgia and/or myofascial pain.  It covers receptor systems, itch generation by both peripheral and central nervous systems, as well as mechanical, chemical (including biochemical) triggers. This paper may be of help in documenting itch associations with the above-mentioned conditions.

Stark, F. M. and H. M. Sobetzko. 1999. Approaches to coping with chronic fatigue syndrome. Zentralbl Hyg Umweltmed 202(2-4):179-90.

Starlanyl DJ. 2006. Comment on Canadian consensus document on fibromyalgia syndrome.  J Musculoskel Pain. 14(4):75-81.  In the original document, there seemed to be confusion between symptoms due to FMS and those that were due to co-existing myofascial TrPs.  This offers clarifications.

Starlanyl DJ, Jeffrey JL, Roentsch G, Taylor-Olson C.  The effect of transdermal T3 (3,3’,5-triiodothyronine) on geloid masses found in patients with both fibromyalgia and myofascial pain: double-blinded, N of 1 clinical study.  [Submitted for review Aug 15, 2001.]

Starlanyl, D.  T’ai Chi Chuan and Musculoskeletal Pain.  T’ai Chi Magazine.  [Accepted for publication July 2001.]

Starlanyl DJ and Jeffrey JL. 2001.  The presence of geloid masses in a patient with both fibromyalgia and chronic myofascial pain. Phys Ther Case Rep 4(1):22-31.

Starlanyl D. J. and M. E. Copeland. 2001. Fibromyalgia and Chronic Myofascial Pain: A Survival Manual. Edition 2. Oakland: New Harbinger Publications.

Starlanyl DJ. 1999. The Fibromyalgia Advocate. Oakland: New Harbinger Publications.

Starlanyl D J 1997. Chronic Myofascial Pain Syndrome: A Guide to the Trigger Points. Oakland: New Harbinger. 2 hour video.

Starlanyl DJ. 1997.  Fibromyalgia and Myofascial Pain Syndrome: A Special Challenge.  Clin Bull Myofas Ther 2 (2/3): 75-89.

Starlanyl DJ. 1995.  "Comment on Granges and Littlejohn's. "Prevalence of myofascial pain syndrome in fibromyalgia and regional pain syndrome: A comparative study."  J Musculoskel Pain 3 (1):129-132.

Starlanyl DJ 1994.  "Comment on article by Hong, Chen, Pon and Yu, "Intermediate effects of various physical medicine modalities on pain threshold of an active myofascial trigger point."  J Musculoskel Pain 2 (2):141-142.

Staud R. 2013. The important role of CNS facilitation and inhibition for chronic pain. Int J Clin Rheumtol. 8(6):639-646. "Multiple studies have demonstrated that the pain experience among individuals is highly variable. Even under circumstances where the tissue injuries are similar, individual pain experiences may vary drastically. However, this individual difference in pain sensitivity is not only related to sensitivity of peripheral pain receptors, but also to variability in CNS pain processing. Peripheral impulses derived from tissue receptors undergo modification in dorsal horn neurons that can either result in inhibition or facilitation of pain. Such influences are particularly apparent in inflammation where not only peripheral, but also central, pain modulatory mechanisms can significantly increase nociceptive pain. Emotional state, level of anxiety, attention and distraction, memories, stress, fatigue and many other factors can either increase or reduce the pain experience. Increasing evidence suggests that 'bottom-up' and 'top-down' modulatory circuits within the spinal cord and brain play an important role in pain processing, which can profoundly affect the experience of pain."

Staud R. 2012. Peripheral and Central Mechanisms of Fatigue in Inflammatory and Noninflammatory Rheumatic Diseases. Curr Rheumatol Rep. [Jul 17 Epub ahead of print]. "Whereas many studies have focused on disease activity as a correlate to these patients' fatigue, it has become apparent that other factors, including negative affect and pain, are some of the most powerful predictors for fatigue. Conversely, sleep problems, including insomnia, seem to be less important for fatigue. There are several effective treatment strategies available for fatigued patients with rheumatologic disorders, including pharmacological and nonpharmacological therapies."

Staud R. 2011. Evidence for Shared Pain Mechanisms in Osteoarthritis, Low Back Pain, and Fibromyalgia. Curr Rheumatol Rep. [Aug 11 Epub ahead of print]. "Osteoarthritis (OA), low back pain (LBP), and fibromyalgia (FM) are common chronic pain disorders that occur frequently in the general population. They are a significant cause of dysfunction and disability. Why some of these chronic pain disorders remain localized to few body areas (OA and LBP), whereas others become widespread (FM), is unclear at this time. Genetic, environmental, and psychosocial factors likely play an important role...... Ineffective endogenous pain control and central sensitization are important features of OA, LBP, and FM patients."

Staud R. 2011. Sodium oxybate for the treatment of fibromyalgia. Expert Opin Pharmacother. [Jun 16 Epub ahead of print]. "Introduction: Gamma-hydroxybutyrate (GHB) is a short-chain fatty acid that is synthesized within the CNS, mostly from its parent compound gamma amino butyric acid (GABA). GHB acts as a neuromodulator/neurotransmitter to affect neuronal activity of other neurotransmitters and so, stimulate the release of growth hormone. Its sodium salt (sodium oxybate: SXB) was approved by the Food and Drug Administration (FDA) for the treatment of narcolepsy. SXB has shown to improve disrupted sleep and increase NR3 (slow-wave restorative) sleep in patients with narcolepsy. It is rapidly absorbed and has a plasma half-life of 30 - 60 min, necessitating twice-nightly dosing. Most of the observed effects of SXB result from binding to GABA-B receptors. Areas covered: Several randomized, controlled trials demonstrated significantly improved fibromyalgia (FM) symptoms with SXB. As seen in narcolepsy trials, SXB improved sleep of FM patients, increased slow-wave sleep duration as well as delta power, and reduced frequent night-time awakenings. Furthermore, FM pain and fatigue was consistently reduced with nightly SXB over time. Commonly reported adverse events included headache, nausea, dizziness and somnolence. Despite its proven efficacy, SXB did not receive FDA approval for the management of FM in 2010, mostly because of concerns about abuse. Expert opinion: Insomnia, fatigue and pain are important clinical FM symptoms that showed moderate improvements with SXB in several large, well-designed clinical trials. Because of the limited efficacy of currently available FM drugs additional treatment options are needed. In particular, drugs like SXB - which belong to a different drug class than other Food and Drug Administration (FDA)-approved FM medications such as pregabalin, duloxetine and milnacipran - would provide a much-needed addition to presently available treatment options. However, the FDA has set the bar high for future SXB re-submissions, with requirements of superior efficacy and improved risk mitigation strategies. At this time, no future FDA submission of SXB for the fibromyalgia indication is planned."

Staud R. 2011. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol. 25(2):155-164. "Clinical symptoms of chronic widespread pain (CWP) conditions like fibromyalgia (FM), include pain, stiffness, subjective weakness, and muscle fatigue. Muscle pain in CWP is usually described as fluctuating and often associated with local or generalized tenderness (hyperalgesia and/or allodynia). This tenderness related to muscle pain depends on increased peripheral and/or central nervous system responsiveness to peripheral stimuli, which can be either noxious (hyperalgesia) or non-noxious (allodynia). For example, patients with muscle hyperalgesia will rate painful muscle stimuli higher than normal controls, whereas patients with allodynia may perceive light touch as painful, something that a 'normal' individual will never describe as painful. The pathogenesis of such peripheral and/or central nervous system changes in CWP is unclear, but peripheral soft tissue changes have been implicated. Indirect evidence from interventions that attenuate tonic peripheral nociceptive impulses in patients with CWP syndromes like FM suggest that overall FM pain is dependent on peripheral input. More importantly, allodynia and hyperalgesia can be improved or abolished by removal of peripheral impulse input. Another potential mechanism for CWP pain is central disinhibition. However, this pain mechanism also depends on tonic impulse input, even if only inadequately inhibited. Thus, a promising approach to understanding CWP is to determine whether abnormal activity of receptors in deep tissues is fundamental to the development and maintenance of this chronic pain disorder.....Most CWP patients present with focal tissue abnormalities including myofascial trigger points, ligamentous trigger points or osteoarthritis of the joints and spine. While not predictive for the development of CWP, these changes nevertheless represent important pain generators that may initiate or perpetuate chronic pain. Local chemical mediators, including lactic acid, adenosine triphosphate (ATP) and cytokines, seem to play an important role in sensitizing deep tissue nociceptors of CWP patients. Thus, the combination of peripheral impulse input and increased central pain sensitivity may be responsible for widespread chronic pain disorders including FM."

Staud R. 2010. Is It All Central Sensitization? Role of Peripheral Tissue Nociception in Chronic Musculoskeletal Pain. Curr Rheumatol Rep. [Sep 30 Epub ahead of print]. "Fibromyalgia syndrome (FM) is a highly prevalent musculoskeletal disorder that is often accompanied by somatic hyperalgesia (enhanced pain from noxious stimuli). Neural mechanisms of somatic hyperalgesia have been analyzed via quantitative sensory testing of FM patients. Results of these studies suggest that FM pain is associated with widespread primary and secondary cutaneous hyperalgesia, which are dynamically maintained by tonic impulse input from deep tissues and likely by brain-to-spinal cord facilitation. Enhanced somatic pains are accompanied by mechanical hyperalgesia and allodynia in FM patients as compared with healthy controls. FM pain is likely to be at least partially maintained by peripheral impulse input from deep tissues. This conclusion is supported by results of several studies showing that injection of local anesthetics into painful muscles normalizes somatic hyperalgesia in FM patients." [This work agrees with the research showing the FM patients have TrPs, and that TrP-pain generation is a common factor sustaining central sensitization. DJS]

Staud R. 2010. Pharmacological treatment of fibromyalgia syndrome: new developments.  Drugs. 70(1):1-14.  “Duloxetine and milnacipran, two highly selective serotonin-norepinephrine (noradrenaline) reuptake inhibitors, and the alpha(2)delta agonist pregabalin have been approved by the US FDA for the treatment of fibromyalgia symptoms.  In general, about half of all treated patients seem to experience a 30% reduction of symptoms, suggesting that many patients with fibromyalgia will require additional therapies.  Thus, other forms of treatment, including exercise, cognitive behavioral therapies and self-management strategies, may be necessary to achieve satisfactory treatment outcomes.  Despite promising results of pilot trials, RCTs (randomized controlled trials) with dopamine receptor agonists and sodium channel antagonists have so far been disappointing for patients with fibromyalgia.  However, new pharmacological approaches for the treatment of fibromyalgia pain and insomnia using sodium oxybate appear to be promising.”

Staud R. 2009.  Abnormal pain modulation in patients with spatially distributed chronic pain: fibromyalgia.  Rheum Dis Clin North Am. 35(2):263-274.  “Many chronic pain syndromes are associated with hypersensitivity to painful stimuli and with reduced endogenous pain inhibition.  These findings suggest that modulation of pain-related information may be linked to the onset or maintenance of chronic pain.  The combination of heightened pain sensitivity and reduced pain inhibition seems to predispose individuals to greater risk for increased acute clinical pain.  It is unknown whether such pain processing abnormalities may also place individuals at increased risk for chronic pain.”

Staud R. 2008. Heart rate variability as a biomarker of fibromyalgia syndrome.  Fut Rheumatol. 3(5):475-483. “HRV (heart rate variability) has been shown to correlate with FM pain and is sensitive to change; in particular, pain related to physical and mental stressors.  Thus, ANS (autonomic nervous system) dysfunction as assessed by HRV analysis may serve as a useful biomarker, and may become part of future FM diagnostic criteria and serve as a surrogate end point in clinical trials.”

Staud R. 2007.  Mechanisms of acupuncture analgesia: effective therapy for musculoskeletal pain?  Curr Rheumatol Rep. 9(6):473-481.    Acupuncture relief may take some time “...to develop and resolve."  “…some forms of AP are more effective for providing analgesia than others.”  Particularly, electro-AP seems best to activate powerful opioids and non-opioid analgesic mechanisms.”

Staud R. 2007.  The role of peripheral input for chronic pain syndromes like fibromyalgia.  J Musculoskel Pain 15 (Supp 13):7 item 8.  [Myopain 2007 Poster]  Indications are that the diffuse, bodywide pain of FM is maintained by peripheral pain stimuli.  “Most FMS patients present with focal tissue abnormalities including myofascial trigger points [TrPs], ligamentous trigger points, or osteoarthritis of the joints and spine.  While not predictive for the development of FMS, these changes nevertheless represent important pain generators that may initiate or perpetuate chronic pain.  Thus spatially limited forms of musculoskeletal pain, including MPS, may develop in some patients into widespread chronic pain syndromes like FMS.”

Staud R. 2006.  Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome.  Arthritis Res Ther. 8(3):208  “Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition.  However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both.  It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain.   “Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state.”

Staud R. 2004.  Fibromyalgia pain: do we know the source? Curr Opin Rheumatol 16(2):157-63.  This review brings together studies that show that the mechanism behind FMS may be biochemicals released due to acute or repetitive injury (traumatic or biochemical) “...may be responsible for long-term activation of spinal cord glia and dorsal horn neurons, thus resulting in central sensitization.”  This conceptual understanding may aid us in discovering more effective therapies and treatment strategies in the future.  It is also an important step in defining the mechanism of FMS, and this may lead to a change in classification from syndrome to disease.

Staud R.  2004.  Predictors of clinical pain intensity in patients with fibromyalgia syndrome.  Curr Rheumatol Rep. 6(4):281-286.  “The magnitude of wind-up after-sensations appeared to be one of the best predictors for clinical pain intensity of fibromyalgia syndrome patients (27%).”

Staud R. 2002.  Evidence of involvement of central neural mechanisms in generating fibromyalgia pain.  Curr Rheumatol Rep 4(4):299-305. "Fibromyalgia syndrome (FMS) is characterized by widespread pain, fatigue, sleep abnormalities, and distress.  Abnormal temporal summation of second pain (wind-up) and central sensitization have been described recently in patients with FMS.  Wind-up and central sensitization, which rely on activation of nocicepto-specific neurons and wide dynamic range neurons in the dorsal horn of the spinal cord.  Other abnormal central pain mechanisms recently detected in patients with FMS include diffuse noxious inhibitory controls.  These pain inhibitory mechanisms rely on spinal cord and supraspinal systems involving pain facilitatory and pain inhibitory pathways.  Brain-imaging techniques that can detect neuronal activation after nociceptive stimuli have provided additional evidence for abnormal central pain mechanism in FMS.  Brain images have corroborated the augmented reported pain experience of patients with fibromyalgia during experimental pain stimuli.  In addition, thalamic activity, which contributes significantly to pain processing, was decreased in fibromyalgia.  However, central pain mechanisms of fibromyalgia may not depend exclusively on neuronal activation.  Neuroglial activation has been found to play an important role in the induction and maintenance of chronic pain."

Staud R, Cannon RC, Mauderli AP et al. 2003.  Temporal summation of pain from mechanical stimulation of muscle tissue in normal controls and subjects with fibromyalgia syndrome.  Pain 102(1-2):87-95.  “Temporal summation for FMS subjects occurred at substantially lower forces and at a lower frequency of stimulation.  Furthermore, painful after-sensations were greater in amplitude and more prolonged for FMS subjects.”  “Abnormal input from muscle nociceptors appears to underlie production of central sensitization in FMS that generalizes to input from cutaneous nociceptors,”

Staud R, Koo E, Robinson ME et al. 2007.  Spatial summation of mechanically evoked muscle pain and painful aftersensations in normal subjects and fibromyalgia patients.  Pain. [Apr 23 Epub ahead of print].  “…decreasing pain in some muscle areas by local anesthetics or other means may improve overall clinical pain of FM patients.”  [This is another indication that control of peripheral pain stimuli such as caused by myofascial trigger points and arthritis can be a significant part of chronic pain treatment in FM. DJS]

Staud R, Nagel S, Robinson ME et al. 2009.  Enhanced central pain processing of fibromyalgia patients is maintained by muscle afferent input: a randomized, double-blind, placebo-controlled study.  Pain. [Jun 18 Epub ahead of print].  “Lidocaine injections increased local pain thresholds and decreased remote secondary heat hyperalgesia in FM patients, emphasizing the important role of peripheral impulse input in maintaining central sensitization in this chronic pain syndrome; similar to other persistent pain conditions such as irritable bowel syndrome and complex regional pain syndrome.” [This is yet another study showing that peripheral pain sensations such as those caused by myofascial TrPs are sufficient to maintain the central sensitization state of FM and may be important to maintaining other chronic conditions. DJS]

Staud R, Price DD, Robinson ME et al. 2004.  Body pain area and pain-related negative affect predict clinical pain intensity in patients with fibromyalgia.  J Pain 5(6):338-343.  “The number of painful body areas obtained by body pain diagrams is a better predictor of clinical pain intensity than TPS in FM patients.”  [It would be helpful if these patients were checked for co-existing myofascial TrPs.  It could be that the presence of co-existing myofascial TrPs is the better predictor of clinical pain intensity. DJS]

Staud R, Price DD, Robinson ME et al. 2004.  Body pain area and pain-related negative affect predict clinical pain intensity in patients with fibromyalgia. J Pain 5(6):338-343.  The combination of charts showing painful body areas, tender point counts, and pain-related negative emotions gave a much more accurate representation of pain intensity in FMS patients than did simple counting of tender points.

Staud R, Price DD, Robinson ME et al.  2004.  Maintenance of windup of second pain requires less frequent stimulation in fibromyalgia patients compared to normal controls.  Pain 110(3):689-696.  “Unlike NC (normal control) subjects, FM subjects showed enhanced second pain during WU-M (wind-up maintenance) stimuli at very low stimulus frequencies, indicating central sensitization.  Increased WU sensitivity, enhanced WU-M, and increased WU-related aftersensations help account for persistent pain conditions in FM subjects.”  [Patients with FMS may respond to lower stimuli to maintain a state of central sensitization.  Myofascial trigger points that would not cause central sensitization in healthy individuals may be sufficient to maintain central sensitization in patients with FMS. DJS]

Staud R, Robinson ME, Goldman CT et al. 2011. Attenuation of experimental pain by vibro-tactile stimulation in patients with chronic local or widespread musculoskeletal pain. Eur J Pain. [Feb 19 Epub ahead of print]. "One form of endogenous pain inhibition, diffuse noxious inhibitory controls (DNIC), has been found to be abnormal in some chronic pain patients and evidence exists for deficient spatial summation of pain, specifically in FM. Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders, like neck and back pain. Whereas DNIC reduces pain through activation of nociceptive afferents, vibro-tactile pain inhibition involves innocuous A-beta fiber.....To assess endogenous analgesic mechanisms of study subjects, vibro-tactile conditioning stimuli were simultaneously applied with test stimuli either homotopically or heterotopically. Additionally, the effect of distraction on experimental pain was assessed. Homotopic vibro-tactile stimulation resulted in 40% heat pain reductions in all subject groups.....Conclusions: Vibro-tactile stimulation effectively recruited analgesic mechanisms not only in NC (normal pain-free controls) but also in patients with chronic musculoskeletal pain, including FM. Distraction did not seem to contribute to this analgesic effect."

Staud R, Robinson ME, Price DD. 2007.  Temporal summation of second pain and its maintenance are useful for characterizing widespread central sensitization of fibromyalgia patients.  J Pain. [Aug 1 Epub ahead of print].  “Perspective:  The pain of FM seems to be accompanied by generalized central sensitization, involving the length of the spinal neuroaxis.  Thus, widespread central sensitization appears to be a hallmark of FM and may be useful for the clinical case definition of this prevalent pain syndrome.  In addition, measures of widespread central sensitization, like TSSP-M (temporal summation of second pain and maintenance), could also be used to assess treatment responses of FM patients.”

Staud R, Robinson ME, Weyl EE et al. 2010. Pain variability in fibromyalgia is related to activity and rest: role of peripheral tissue impulse input. J Pain. [May 6 Epub ahead of print]. “FM is a pain-amplification syndrome that depends at least in part on peripheral tissue impulse input. Whereas muscle activity increased overall pain, short rest periods produced analgesic effects.” [This indicates that in cases of FM, short rest periods may enable us to accomplish some activities. This agrees with Travell and Simons’ recommendations for myofascial trigger points, which often cause the peripheral pain stimuli maintaining FM central sensitization. We must remember to rest every 20 minutes, or whatever our time limit is for each task. DJS] 

Staud R, Smitherman ML. 2002.  Peripheral and central sensitization in fibromyalgia: pathogenetic role. Curr Pain Headache Rep 6(4):259-66. "Patients with fibromyalgia show psychophysical evidence of mechanical, thermal and electrical hyperalgesia. Peripheral and central abnormalities of nociception have been described in fibromyalgia. Important nociceptor systems in the skin and muscles seem to undergo profound changes..."  "These include sensitization of vanilloid receptor, acid-sensing ion channel receptors, and purino-receptors. Tissue mediators of inflammation and nerve growth channel receptors can excite these receptors and cause extensive change in pain sensitivity, but patients with fibromyalgia lack consistent evidence for inflammatory soft tissue abnormalities."

Staud R, Vierck CJ, Robinson ME et al. 2006.  Overall fibromyalgia pain is predicted by ratings of local pain and pain-related negative affect – possible role of peripheral tissues.  Rheumatology (Oxford) [Apr 18 Epub ahead of print]  “We hypothesized that the overall clinical pain is largely determined by the pain intensity of local body areas.  Thus, we assessed the role of local body pains as predictors of overall clinical pain in FM patients.”  “Peripheral factors (maximal/average local pain and number of painful body areas) predicted most of the variance of overall clinical FM pain, suggesting that the input of pain by the peripheral tissues is clinically relevant.  About 19% of the pain variance was predicted by PRNA.  Thus, peripheral pain and negative affect appear to be particularly relevant for overall FM pain and may represent important targets for future therapies.”

Staud R, Vierck CJ, Robinson ME et al. 2005.  Effects of the N-Methyl-D-Aspartate receptor antagonist Dextromethorphan on temporal summation of pain are similar in fibromyalgia patients and normal control subjects.  Jour Pain 6(5):323-332.

Staud R, Weyl EE, Bartley E et al. 2013. Analgesic and anti-hyperalgesic effects of muscle injections with lidocaine or saline in patients with fibromyalgia syndrome. Eur J Pain. [Nov 5 Epub ahead of print.] This double-blind controlled study of 62 women with fibromyalgia utilized injection into trapezius and gluteal trigger points with either saline or lidocaine. The results indicate that injection of peripheral trigger point pain generators can reliably and significantly reduce clinical fibromyalgia pain. This research strongly suggests that, at least in women, it is the input from peripheral pain generators such as trigger points that maintain the mechanical and heat hyperalgesia of fibromyalgia. "…effects of muscle injections on hyperalgesia were greater for lidocaine than saline; the effects on clinical pain were similar for both injectates."

Staud R, Weyl EE, Price DD et al. 2012. Mechanical and Heat Hyperalgesia Highly Predict Clinical Pain Intensity in Patients with Chronic Musculoskeletal Pain Syndromes. J Pain. [Jun 26 Epub ahead of print]. "Multiple abnormalities in pain processing have been reported in patients with chronic musculoskeletal pain syndromes. These changes include mechanical and thermal hyperalgesia, decreased thresholds to mechanical and thermal stimuli (allodynia), and central sensitization, all of which are fundamental to the generation of clinical pain.....we hypothesized that quantitative sensory tests may provide useful predictors of clinical pain intensity of such patients..... Using either heat or pressure pain ratings as well as tender point counts and negative affect as predictors, up to 49.4% of the patients' variance of clinical pain intensity could be estimated....Simple tests of mechanical and heat hyperalgesia can predict large proportions of the variance in clinical pain intensity of chronic musculoskeletal pain patients and thus are feasible to be included in clinical practice and clinical trials."

Staud R, Weyl EE, Riley JL 3rd et al. 2014. Slow temporal summation of pain for assessment of central pain sensitivity and clinical pain of fibromyalgia patients. PLoS One. 9(2):e89086. "In healthy individuals slow temporal summation of pain or wind-up (WU) can be evoked by repetitive heat-pulses at frequencies of ≥ .33 Hz. Previous WU studies have used various stimulus frequencies and intensities to characterize central sensitization of human subjects including fibromyalgia (FM) patients. However, many trials demonstrated considerable WU-variability including zero WU or even wind-down (WD) at stimulus intensities sufficient for activating C-nociceptors. Additionally, few WU-protocols have controlled for contributions of individual pain sensitivity to WU-magnitude, which is critical for WU-comparisons. ….Slope of WU-RF, which is representative of central pain sensitivity, was significantly steeper in FM patients than NC (normal controls) ....Compared to single WU series, WU-RFs integrate individuals' pain sensitivity as well as WU and WD. Slope of WU-RFs was significantly different between FM patients and NC. Therefore WU-RF may be useful for assessing central sensitization of chronic pain patients in research and clinical practice." Free PMC Article

Stearns, V., C. Isaacs, J. Rowland, J. Crawford, M. J. Ellis, R. Kramer, W. Lawrence, J. J. Hanfelt and D. F. Hayes. 2000. A pilot trial assessing the efficacy of paroxetine hydrochloride(Paxil) in controlling hot flashes in breast cancer survivors. Ann Oncol 11(1):17-22.

Stecco A, Gesi M, Stecco C et al. 2013. Fascial components of the myofascial pain syndrome. Curr Pain Headache Rep. 17(8):352. "Myofascial pain syndrome (MPS) is described as the muscle, sensory, motor, and autonomic nervous system symptoms caused by stimulation of myofascial trigger points (MTP). The participation of fascia in this syndrome has often been neglected. Several manual and physical approaches have been proposed to improve myofascial function after traumatic injuries, but the processes that induce pathological modifications of myofascial tissue after trauma remain unclear. Alterations in collagen fiber composition, in fibroblasts or in extracellular matrix composition have been postulated. We summarize here recent developments in the biology of fascia, and in particular, its associated hyaluronan (HA)-rich matrix that address the issue of MPS."

Stecco A, Meneghinie A, Stern R et al. 2014. Ultrasonography in myofascial neck pain: randomized clinical trial for diagnosis and follow-up. Surg Radiol Anat. 36(3):243-253. "This study compared active and passive cervical range of motion, along with a neck disability questionnaire. "The fascial thickness of the sternal ending of the sternocleidomastoid and medial scalene muscles was also analyzed by ultrasonography. …. There were significant differences between healthy subjects and patients with CNP in the thickness of the upper side of the sternocleidomastoid fascia and the lower and upper sides of the right scalene fascia both at the end of treatment as during follow-up." There was a significant difference in pain, as well as the amount of loose connective tissue after treatment. "The variation of thickness of the fascia correlated with the increase in quantity of the loose connective tissue but not of dense connective tissue."

Stecco A, Stecco C, Macchi V et al. 2011. RMI study and clinical correlations of ankle retinacula damage and outcomes of ankle sprain. Surg Radiol Anat. [Feb 9 Epub ahead of print]. Alterations shown by MRI in ankle retinacula from trauma or chronic ankle instability corresponds to proprioceptive damage noted by photography and clinical exam. This indicates that the ankle reticulinum are not passive stabilizers but also involved in proprioceptive function. Deep massage of the ankle retinacula alleviated these symptoms. The authors state that adaptive fibrosis may develop as a consequence of unremitting non-physiological tension in a fascial segment. The deep friction massage changes the nature of the ground substance, restoring glide. They believe this to be due to changes in the myofascia rather than to bones or ligaments. [Correspondence with the authors revealed that they also have found trigger points in retinacula. DJS]

Stecco C, Gagey O, Belloni A et al. 2007. Anatomy of the deep fascia of the upper limb. Second part: study of innervation. Morphologie 91(292):38-43. This study indicates that the flexor retinaculum has more proprioceptive functions, whereas the tendons were primarily mechanical in function. "…the fascia is a membrane that extends throughout the whole body and numerous muscular expansions maintain it in a basal tension. During a muscular contraction these expansions could also transmit the effect of the stretch to a specific area of the fascia, stimulating the proprioceptors in that area."

Stecco C, Macchi V, Porzionato A et al. 2010. The ankle retinacula: morphological evidence of the proprioceptive role of the fascial system. Cells Tissues Organs 192(3):200-210. "The retinacula are not static structures for joint stabilization, like the ligaments, but a specialization of the fascia for local spatial proprioception of the movements of the foot and ankle. Their anatomical variations and accessory bundles may be viewed as morphological evidence of the integrative role of the fascial system in peripheral control of articular motility."

Stecco C, Stern R, Prozionato A et al. 2011. Hyaluronan within fascia in the etiology of myofascial pain. Surg Radiol Anat 33(10):891-896. This study focused on hyaluronic acid in the fascial layers. "The HA within the deep fascia facilitates the free sliding of two adjacent fibrous fascial layers, thus promoting the normal function associated with the deep fascia. If the HA assumes a more packed confirmation, or more generally, if the loose connective tissue inside the fascia alters its density, the behavior of the entire deep fascia and the underlying muscle would be compromised, This, we predict, may be the basis of the common phenomenon known as "myofascial pain." This study describes the fascial reservoir as a "…reservoir of water and ions for surrounding tissues. It may also function as a reservoir to accumulate and remove various degradation products and toxic substances…A fundamental element of the loose connective tissue (ground substance) is the HA, and its concentration determines, together with the temperature and other physical parameters, the density of the matrix. " The study proposes the mechanism of increasing viscosity of ground substance, and proposes a new type of cell they call the "fasciacyte." [This study confirms increased hyaluronic acid in myofascial pain areas (what we found in the geloid mass over areas of resistant TrPs), and gives new anatomical fascial insights and a new direction in what may be a promising way to relieve and even reverse myofascial pain. DJS]

Stejskal V, Ockert K, Bjørklund G. 2013. Metal-induced inflammation triggers fibromyalgia in metal-allergic patients. Neuro Endocrinol Lett. 34(6):559-565. "Fifteen female FM patients were included in the study. Metal allergy was measured by a lymphocyte transformation test, MELISA®….All FM patients tested positive to at least one of the metals tested. The most frequent reactions were to nickel, followed by inorganic mercury, cadmium and lead. Some healthy controls responded to inorganic mercury in vitro but most of the tests were negative. Objective examination 5 years later showed that half of the patients no longer fulfilled the FM diagnosis, 20% had improved and the remaining 30% still had FM. All patients reported subjective health improvement."

Sterling M, Jull G, Vicenzino B et al. 2003.  Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery.  Pain 104(3):509-517.  “These findings suggest that those with persistent moderate/severe symptoms at six months display, soon after injury, generalized hypersensitivity suggestive of changes in central pain processing mechanisms.  This phenomenon did not occur in those who recover or those with persistent mild symptoms.”
 

Sterling M, Jull G, Vicenzino B et al. 2003.  Development of motor system dysfunction following whiplash injury.  Pain 103(1-2):65-73.  “This study identifies, for the first time, deficits in the motor system, as early as one month post whiplash injury, that persisted not only in those reporting moderate/severe symptoms at three months but also in subjects who recovered and those with persistent mild symptoms.”

 

Sterling M, Jull G, Wright A. 2001.  The effect of musculoskeletal pain on motor activity and control.  J Pain 2(3):135-145.  “Aberrant movement patterns and postures are obvious to clinicians managing patients with musculoskeletal pain.  Some changes in motor function that occur in the presence of pain are less apparent.  Clinical and basic science investigations have provided evidence of the effects of nociception on aspects of motor function.  Recent research has seen the emergence of a new model in which patterns of muscle activation and recruitment are altered in the presence of pain (neuromuscular activation model).  These changes seem to particularly affect the ability of muscles to perform synergistic functions related to maintaining joint stability and control.  These changes are believed to persist into the period of chronicity.  It is apparent that people experiencing musculoskeletal pain exhibit complex motor responses that may show some variation with the time course of the disorder.”

 

Sterling M, Kenardy J, Jull G et al. 2003.  The development of psychological changes following whiplash injury.  Pain 106(3):481-489.  “This study identifies, for the first time, deficits in the motor system, as early as 1 month post whiplash injury, that persisted not only in those reporting moderate/severe symptoms at 3 months but also in subjects who recovered and those with persistent mild symptoms.”

Sterling M., Jull G, Wright A. 2001.  The effect of musculoskeletal pain on motor activity and control.  J Pain 2(3):135-145.  This article relates how muscle activation and recruitment patterns are influenced by pain, affecting the ability of muscles to perform synergistically. This can affect joint stability and control of muscle function. This is important, as it isn’t only the specific pain that must be treated, but associated muscle weakness and dysfunction must also be recognized and addressed for function to be restored.

Sterling M., Treleven J., Edwards S. et al. 2002.  Pressure pain thresholds in chronic Whiplash Associated Disorder: further evidence of altered central pain processing. Central sensitization may occur after whiplash.  J Musculoskel Pain 10(3):69-81.

Sterling M, Jull G, Wright A. 2001. The effect of musculoskeletal pain on motor activity and control. [No journal listed] 2(3):135-145. Patterns of muscle activation and recruitment are altered in the presence of pain.  "These changes seem to particularly affect the ability of muscles to perform synergistic functions related to maintaining joint stability and control.  It is apparent that people experiencing musculoskeletal pain exhibit complex motor responses that may show some variation with the time course of the disorder."

Stella, N., P. Schweitzer and D. Piomelli. 1997. A second endogenous cannabinoid that modulates long-term potentiation. Nature 388(6644):773-778.

Stelmack, R. M. 1990. Biological bases of extraversion: psychophysiological evidence. J Pers58(1):293-311.

Stephan AH, Madison DV, Mateos JM et al. 2013. A dramatic increase of C1q protein in the CNS during normal aging. J Neurosci. 33(33):13460-13474. "The decline of cognitive function has emerged as one of the greatest health threats of old age. Age-related cognitive decline is caused by an impacted neuronal circuitry, yet the molecular mechanisms responsible are unknown. C1q, the initiating protein of the classical complement cascade and powerful effector of the peripheral immune response, mediates synapse elimination in the developing CNS. Here we show that C1q protein levels dramatically increase in the normal aging mouse and human brain, by as much as 300-fold. This increase was predominantly localized in close proximity to synapses and occurred earliest and most dramatically in certain regions of the brain, including some but not all regions known to be selectively vulnerable in neurodegenerative diseases, i.e., the hippocampus, substantia nigra, and piriform cortex. C1q-deficient mice exhibited enhanced synaptic plasticity in the adult and reorganization of the circuitry in the aging hippocampal dentate gyrus. Moreover, aged C1q-deficient mice exhibited significantly less cognitive and memory decline in certain hippocampus-dependent behavior tests compared with their wild-type littermates. Unlike in the developing CNS, the complement cascade effector C3 was only present at very low levels in the adult and aging brain. In addition, the aging-dependent effect of C1q on the hippocampal circuitry was independent of C3 and unaccompanied by detectable synapse loss, providing evidence for a novel, complement- and synapse elimination-independent role for C1q in CNS aging." [The microglial cells that help prune developing brain cells early in life may be part of the problem of aging. Dysfunctional glial cells could be responsible for some of the symptoms of fibromyalgia that seem to be an advanced aging process. If so, the ability of this C1q deficient mouse may hold some clues to a work-around of fibromyalgia cognitive deficits in the future. DJS]

Stevensen, C. 1995. The role of shiatsu in palliative care. Complement Ther Nurs Midwifery1(2):51-58.

Stewart, D. P., J. Kaylor and E. Koutanis. 1996. Cognitive deficits in presumed minor head injured patients. Acad Emerg Med 3 (1):21-26.

Stewart, J. M., M. H. Gewitz, A. Weldon and J. Munoz. 1999. Patterns of orthostatic intolerance: the orthostatic tachycardia syndrome and adolescent chronic fatigue. J Pediatr 135(2 Pt 1):218-25.

Stewart WF, Ricci JA, Chee E et al. 2003.  Lost productive time and cost due to common pain conditions in the US workforce. JAMA 290(18):2443-2454.  Pain is not only a common disability keeping people from the workforce, but AMost of the pain-related lost productive time occurs while employees are at work and is in the form of reduced performance.@

Stiasny-Kolster K, Magerl W, Oertel WH et al. 2004.  Static mechanical hyperalgesia without dynamic tactile allodynia in patients with restless legs syndrome.  Brain [Epub Feb 25 ahead of print]

Stoll, B. A. 1999. Western nutrition and the insulin resistance syndrome: a link to breast cancer. Eur J Clin Nutr 53(2):83-7.

Stormorken H, Brosstad F. 2005.  [Frequent urination—an important diagnostic marker in fibromyalgia]  Tidsskr Nor Laegeforen 125(1):17-19. [Norwegian]  “An abnormally high frequency of urination is a characteristic feature in fibromyalgia and a useful diagnostic variable.  The pattern is that of urge, sometimes with incontinence.”  [This study would have been more useful had the patients been screened for co-existing myofascial TrPs that can cause the same symptoms and yet can respond immediately to appropriate treatment. DJS.]

Stratz T, Fiebich B, Haus U et al. 2004.  Influence of tropisetron on the serum substance P levels in fibromyalgia patients.  Scand J Rheumatol Suppl (119):41-43.  “It is possible that the responders to tropisetron represent a subgroup of FM patients for whom substance P and 5-HT3 receptors play key roles in the development of the pain symptoms.”

Stratz T, Muller W. 2004.  Treatment of chronic low back pain with tropisetron.  Scand J Rheumatol Suppl (119):76-78.  Some patents with myofascial pain syndromes and painful tendinopathies were helped by tropisetron injections.

Straub RH, Buttgereit F, Cutulo M. 2011. Alterations of the hypothalamic-pituitary-adrenal axis in systemic immune disease—a role for misguided energy regulation. Clin Exp Rheumatol. 29(5 Suppl 68):S23-31. This review covers the anti-inflammatory role of a balanced HPA axis, its relationship to some other hormones and some other informational substances, and how an unbalanced HPA axis can drive glucocorticoid resistance and lead to chronic inflammatory diseases such as metabolic syndrome.

Straub, T. A. 1999. Endoscopic carpal tunnel release: a prospective analysis of factors associated with unsatisfactory results. Arthroscopy 15(3):269-74.

Streit RS. 2014. NTOS symptoms and mobility: A case study on neurogenic thoracic outlet syndrome involving massage therapy. J Bodyw Mov Ther. 18:42-48. "Neurogenic thoracic outlet syndrome (NTOS) is a neuromuscular condition affecting brachial plexus functionality. NTOS is characterized by paresthesia, pain muscle fatigue, and restricted mobility in the upper extremity. This study quantified massage therapy's possible contribution to treatment of NTOS. A 24-year-old female with NTOS received eight treatments over 35 days. Treatment included myofascial release, trigger point therapy, cross fiber friction, muscle stripping, and gentle passive stretching. Abduction and lateral rotation at the glenohumeral (GH joint) assessments measured range of motion (ROM). A resisted muscle test evaluated upper extremity strength. The client rated symptoms daily via a visual analog scale (VAS). Findings showed improvement in ROM at the GH joint. VAS ratings revealed a reduction in muscle weakness, pain, numbness, and 'paresthesia'. Results suggest massage may be useful as part of a broad approach to managing NTOS symptoms and improving mobility."

Stricker, R. B., B. Goldberg and W. L. Epstein. 1997. Topical immune modulation (TIM): a novel approach to the immunotherapy of systemic disease. Immunol Lett 59(3):145-50.

Striffler, J. S., J. S. Law, M. M. Polansky, S. J. Bhathena, and R. A. Anderson. 1995. Chromium improves insulin response to glucose in rats. Metabolism 44(10):1314-1320.

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."

Strobel, E. S., M. Krapf, M. Suckfull, W. Bruckle, W. Fleckenstein and W. Muller. 1997. Tissue oxygen measurement and 31 P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia. Rheumatol Int 16(5):

Stryła W, Pogorzała AM, Stępień J. 2013. Proprioception exercises in medical rehabilitation. Pol Orthop Traumatol. 78:5-27. "Proprioception, or kinesthesia, is the sense of orientation responsible for perception of body and relative position of its parts. Kinesthesia is received by receptors located in muscles and tendons. In this study a set of proprioception developing exercises was presented. Proprioception should be restored in case of musculoskeletal and neurological disorders. Proprioception training can also be used as a prophylaxis before starting various sporting activities. Proprioception developing exercises have significant meaning for the elderly, who are at risk of balance disorders. These exercises help developing motor memory and at the same time protect from falls." [All care providers must understand that myofascial TrPs can have associated proprioceptive and/or autonomic dysfunction. DJS]

Stuifbergen AK, Phillips L, Carter P et al. 2010. Subjective and objective sleep difficulties in women with fibromyalgia syndrome. J Am Acad Nurse Pract. 22(10):548-556. "Sleep problems are a major concern among women with FMS. Those with concurrent depressive symptoms, high pain, and limited functioning may be candidates for in-depth sleep assessment and behavioral programs to improve sleep." [When pain is a major cause of sleep impairment, the causes of pain must be addressed. Co-existing sleep dysfunctions, such as obstructive sleep apnea, must also be addressed. Myofascial trigger points may be major components of these. Often, the psychological support is needed to address the failure of medicine to promptly and adequately address the causes of pain and dysfunction and support the patients with these conditions. DJS]

Stuifbergen AK, Phillips L, Voelmeck W et al. 2006.  Illness perceptions and related outcomes among women with fibromyalgia syndrome.  Womens Health Issues 16(6):353-360.  “Emotional representations explained 41% of the variance in mental health scores and 17% in reported health behaviors.  Overall, this sample of women with FMS had fairly negative perceptions of their illness.  As suggested by Leventhal’s model, cognitive and emotional representations predicted different outcomes.”

Sturgeon JA, Yeung EW, Zautra AJ. 2014. Respiratory Sinus Arrhythmia: a Marker of Resilience to Pain Induction. Int J Behav Med. [Jan 14 Epub ahead of print.] There may be significant individual differences in physiological regulatory responses to the experience of pain and stress. Respiratory sinus arrhythmia is a physiological indicator that may have implications for efficient physiological responses to pain and stress….Fifty-nine women (33 with fibromyalgia and 26 healthy controls) were exposed to repeated thermal pain stimuli and were asked to rate their feelings of fatigue after each block of thermal pain exposures….Self-reported fatigue affect increased during pain induction, but greater respiratory sinus arrhythmia predicted less-pronounced increases in fatigue affect across induction trials. Respiratory sinus arrhythmia appears to be a promising indicator of physiological resilience to pain, predicting an attenuated effect of repeated pain exposure on self-reported fatigue. Implications of efficient regulation of pain, fatigue, and long-term physical health are discussed.

Sturnieks DL, Tiedemann A, Chapman K et al. 2004.  Physiological risk factors for falls in older people with lower limb arthritis.  J Rheumatol. 31(11):2272-2279.  “A physiological falls-risk profile based on mean test scores for the arthritis group highlights deficits in muscular strength, knee proprioception, and standing balance, indicating the need for targeted falls prevention intervention in this population.”

Sturzenegger, M. G. Di Stefano, B. P. Radanow and A. Schnidrig. 1994. Presenting symptoms and signed after whiplash injury: the influence of accident mechanisms. Neurology 44(4):688-693.

Suarez-Almazor, M. E., L. Gonzalez-Lopez, J. I. Gamez-Nava, E. Belseck, C. J. Kendall and P. Davis. 1998 Utilization and predictive value of laboratory tests in patients referred to rheumatologists by primary care physicians. J Rheumatol 25(10:1980-5.

Subramaniam, V., M. W. Stewart and J. F. Smith. 1999. The development and impact of a chronic pain support group: a qualitative and quantitative study. J Pain Symptom Manage 17(5):376-83.

Sucher BM. 1995.  Palpatory diagnosis and manipulative management of carpal tunnel syndrome: Part 2. ‘Double crush’ and thoracic outlet syndrome.  J Am Osteopath Assoc. 95(8):471-479.  “The physician treating carpal tunnel syndrome needs to be aware of the possible concomitant occurrence of thoracic outlet syndrome, the so-called double crush syndrome.  Palpation is used to differentiate carpal tunnel syndrome from thoracic outlet syndrome.  Such palpatory examination assists the physician in planning the initial treatment, including osteopathic manipulation and self-stretching maneuvers, targeted specifically at the most clinically significant pathologic region.  Supplemental physical medicine modalities such as ultrasound may enhance the treatment response. Some illustrative cases are reported.”  [Carpal tunnel syndrome often co-exists with TOS.   Myofascial trigger points can cause symptoms of both, so the examining clinician needs to look for patterns, and for TrPs.  DJS]

Sucher, B. M. 1993. Myofascial release of carpal tunnel syndrome. J Am Osteopath Assoc 93(1):92-94.

Sugawa T, Fujiwara Y, Okuyama M et al. 2007.  [Prevalence, diagnosis and treatment of extraesophageal manifestation of GERD] Nippon Rinsho. 65(5):946-950. [Japanese]   “Gastroesophageal reflux disease (GERD) is associated with a variety of extraesophageal symptoms including asthma, chronic cough, laryngeal disorders, and various ENT symptoms.  Recent studies suggest that GERD underlies or contributes to chronic sinusitis, chronic otitis media, dental erosion and obstructive sleep apnea syndrome (OSAS).”

Sugimoto Y, Iba Y, Nakamura Y et al. 2004. Pruritus-associated response mediated by cutaneous histamine H3 receptors.  Clin Exp Allergy 34(3):456-459.  Histamine 1 receptor antagonists have been a primary treatment for itching.  Histamine 3 receptor antagonists may also be useful.

Suleiman S, Johnston DE. 2001.  The abdominal wall: an overlooked source of pain.  Am Fam Physician 64(3):431-438.  “When abdominal pain is chronic and unremitting, with minimal or no relationship to eating or bowel function but often a relationship to posture (i.e., lying, sitting, standing), the abdominal wall should be suspected as the source of pain.  Frequently, a localized, tender trigger point can be identified, although the pain may radiate over a diffuse area of the abdomen.  If tenderness is unchanged or increased when abdominal muscles are tensed (positive Carnett’s sign), the abdominal wall is the likely origin of pain.  Most commonly, abdominal wall pain is related to cutaneous nerve root irritation or myofascial irritation.  The pain can also result from structural conditions, such as localized endometriosis or rectus sheath hematoma, or from incisional or other abdominal wall hernias.  If hernia or structural disease is excluded, injection of a local anesthetic with or without a corticosteroid into the pain trigger point can be diagnostic and therapeutic.”

Sullivan MD, Cahana A, Derbyshire S et al. 2013. What does it mean to call chronic pain a brain disease? J Pain. 14(4):317-322. "When considering the significance of neuroimaging results, it is important to remember that "disease" is a concept that arises out of clinical medicine, not laboratory science. Following Canguilhem, we believe that disease is best defined as a structural or functional change that causes disvalue to the whole organism. It is important to be cautious in our assertions about chronic pain as a brain disease because these may have negative effects on 1) the therapeutic dialogue between clinicians and patients; 2) the social dialogue about reimbursement for pain treatments and disability due to pain; and 3) the chronic pain research agenda.... We should not see pain caused by the brain alone. Pain is not felt by the brain, but by the person….conceiving of chronic pain as a brain disease can have negative consequences for research and clinical care of patients with chronic pain."

Sullivan SK, Petroski RE, Verge G et al. 2004.  Characterization of the interaction of indiplon, a novel pyrazolopyrimidine sedative-hypnotic, with the GABA receptor.  J Pharmacol Exp Ther 311(2):537-546.  Indiplon had a higher binding to GABA A receptors than zolpidem or zaleplon, according to this study.  Indiplon may be a promising new tool for the treatment of sleep disorders.

Suma S, Veerendra Kumar B. 2012. Temporomandibular disorders and functional somatic syndromes: Deliberations for the dentist. Indian J Dent Res. 23(4):529-536. "Temporomandibular disorder (TMD) is an umbrella term for a collection of disorders affecting the temporomandibular joint (TMJ) and associated tissues…. Management is dictated by the cause. The most 'famed' causes include trauma, inflammation, aging, parafunctional habits, infections, neoplasms, and stress; and these are always considered in the differential diagnosis of TMJ pain. There are some less 'famed' causes of TMD, which are characterized by increased pain sensitivity due to psychosocial factors; these include myofascial pain syndrome and functional somatic syndromes (FSS) such as fibromyalgia and chronic fatigue syndrome. They present with chronic pain, fatigue, disability, and impairment in ability to perform daily activities."

Sumen A, Sarsan A, Alkan H et al. 2014. Efficacy of low level laser therapy and ?ntramuscular electrical stimulation on myofascial pain syndrome. J Back Musculoskelet Rehabil. [Jul 24 Epub ahead of print.] "Myofascial pain syndrome (MPS) which is an important cause of musculoskeletal pain has shown a dramatic increase in recent years….An improvement was found in all parameters for all groups, except for the pain threshold within the control group at the end of the treatment and one month after the treatment. It was found that pain score was significantly lower in Group 1 and 2 at one month after the treatment compared to Group 3. Similarly, it was found that pain threshold score was significantly higher in Group 2 at one month after the treatment compared to Group 3….In this study we observed that both LLLT and IMS treatments added on to stretching are effective in improving pain parameters in patients with MPS."

Summers J, Johnson S, Pridmore S et al. 2004. Changes to cold detection and pain thresholds following low and high frequency transcranial magnetic stimulation of the motor cortex.  Neurosci Lett. 368(2):197-200.  RTMS may reduce sensory threshold changes that may benefit people in chronic pain.

Sundblom, D. M., S. Haikonen, J. Niemi-Pynttari and I. Tigerstedt. 1994. Effect of spiritual healing on chronic idiopathic pain: a medical and psychological study. Clin J Pain 10(4):296-302.

Sundstrom I., D. Ashbrook and T. Backstrom. 1997. Reduced benzodiazepine sensitivity in patents with premenstrual syndrome: a pilot study. Psychoneuroendocrinology 22(1):25-38.

Sullivan, J. A. 1999. Pediatric flatfoot: evaluation and management. J Am Acad Orthop Surg 7(1):44-53.

Suskind AM, Berry SH, Suttorp MJ et al. 2012. Health-related quality of life in patients with interstitial cystitis/bladder pain syndrome and frequently associated comorbidities. Qual Life Res. [Oct 7 Epub ahead of print]. "To estimate the association of chronic non-urologic conditions [i.e., fibromyalgia (FM), chronic fatigue syndrome (CFS), and irritable bowel syndrome (IBS)] with health-related quality of life (HRQOL) in patients with interstitial cystitis/bladder pain syndrome (IC/BPS).....In patients with IC/BPS, the presence of FM, CFS, and IBS has a significant association with HRQOL, equivalent in impact to the bladder symptoms themselves. These results emphasize the importance of a multidisciplinary approach to treating patients with IC/BPS and other conditions."

Sutbeyaz ST, Sezer N, Koseoglu F et al. 2009.  Low-frequency pulsed electromagnetic field therapy in fibromyalgia: a randomized, double-blind, sham-controlled clinical study.  Clin J Pain. 25(8):722-728.  “Low-frequency PEMF (pulsed electromagnetic field) therapy might improve function, pain, fatigue, and global status in FM patients.”

Suzuki R, A. H. Dickenson. 2002. The pharmacology of Central Sensitization. J Musculoskel Pain 10(1/2):35-43. As research discovers how the pain processing system works, we have a much better chance of coming up with pharmacological methods to treat it.

Suzuki R, Dickenson AH. 2002.  Neuropharmacologic targets and agents in fibromyalgia. Curr Pain Headache Rep 6(4):267-73. Fibromyalgia pain is commonly poorly managed. Patients often have fatigue, sleep disturbances and anxiety. Some medications that target the central nervous system may help a number of these symptoms.

Svebak S, Hagen K, Zwart JA. 2006.  One-year prevalence of chronic musculoskeletal pain in a large adult Norwegian county population: relations with age and gender – the HUNT study.  J Musculoskel Pain 14(1):21-28.  “Nearly half of the adult population reported chronic MSCs during the last year.  The high degree of interference with daily activities and work capacity should be motivation for better preventive strategies in the future.”

Sverdrup B 2004.  Use less cosmetics – suffer less from fibromyalgia?  J Womens Health 13(2):187-194.  Reduced use of cosmetics resulted in a reduction in FMS symptoms.

Svendsen KB, Andersen S, Arnason S et al. 2005.  Breakthrough pain in malignant and non-malignant diseases: a review of prevalence, characteristics and mechanisms.  Eur J Pain. 9(2):195-206.  “Breakthrough pain or transient worsening of pain in patients with an ongoing steady pain is a well known feature in cancer pain patients, but it is also seen in non-malignant pain conditions with involvement of nerves, muscles, bones or viscera.  We suggest that peripheral and/or central sensitization (hyperexcitability) may play a major role in many causes of BTP.”

Swenson CJ. 2002.  Ethical issues in pain management.  Semin Oncol Nurs 18(2):135-142.  “The oncology patient continues to have inadequate pain control.  With the acknowledgment that we have the technical skills and the physiological knowledge to reduce pain, yet it is not being done, health care professionals have begun to explore the ethics behind pain.”

Swerdlow B, Dieter JN. 1992.  An evaluation of the sensitivity and specificity of medical thermography for the documentation of myofascial trigger points.  Pain. 48(2):205-213.

Swezey RL and J Adams. 1999.  Fibromyalgia: a risk factor for osteoporosis. J Rheumatol 26(12):2642-4.

Swick TJ. 2011. Sodium oxybate: a potential new pharmacological option for the treatment of fibromyalgia syndrome. Ther Adv Musculoskelet Dis. 3(4):167-178. "Fibromyalgia syndrome (FMS) is a common disorder, characterized by diffuse pain and tenderness, stiffness, fatigue, affective disorders and significant sleep pathology. A new set of diagnostic criteria have been developed which should make it easier for a busy clinician to diagnose the condition. US Food and Drug Administration (FDA) approved medications for the treatment of FMS have, for the most part, been geared to modulate the pain pathways to give the patient some degree of relief. A different kind of pharmacological agent, sodium oxybate (SXB), is described that is currently approved for the treatment of excessive daytime sleepiness and cataplexy in patients with narcolepsy. SXB, an endogenous metabolite of the inhibitory neurotransmitter gamma-hydroxybutyrate, is thought to act independently as a neurotransmitter with a presumed ability to modulate numerous other central nervous system neurotransmitters. In addition SXB has been shown to robustly increase slow wave sleep and decrease sleep fragmentation. Several large clinical trials have demonstrated SXB's ability to statistically improve pain, fatigue and a wide array of quality of life measurements of patients with fibromyalgia. SXB is not FDA approved to treat fibromyalgia."

Switlick T, Kernozek TW, Meardon S. 2014. Differences in Joint Position Sense and Vibratory Threshold in Runners With and Without a History of Over-Use Injury. J Sport Rehabil. [Jun 23 Epub ahead of print.] "A relationship between altered postural control and injury has been reported in sports. Sensorimotor function serves a fundamental role in postural control and is not often studied in runners. Persons who sustain running injury may have altered sensorimotor function contributing to risk of injury or re-injury….Differences in ankle eversion proprioception between runners with a history of ankle and foot injuries and non-injured runners were observed. Runners with a history of injury also displayed an increased vibratory threshold in the arch region compared to non-injured runners. Poor ankle joint position sense and increased plantar sensitivity suggest altered sensorimotor function following injury. These factors may influence underlying postural control and contribute to altered loading responses commonly observed in injured runners." [These symptoms strongly suggest associated trigger points, both active and latent, and patients should be assessed for TrPs before they continue running. DJS]

Sztajnbok FR, Serra CR, Rodrigues MC et al. 2001.  [Rheumatic diseases in adolescence.]  J Pediatr 77 Suppl 2:S234-244.  This review lists many conditions, including fibromyalgia and growing pains, but does not specifically mention myofascial trigger points.  It does state: “It is important that health professionals diagnose these diseases as early as possible so that prompt action can be taken and prognosis can be improved.”  [Portuguese]

Szygula-Jurkiewicz B, Hudzik B, Nowak J et al. 2004.  [Sleep apnea syndrome in patients with chronic heart failure]  Wiad Lek. 57(3-4):161-165. [Polish]  “Sleep apnea syndrome (SAS) in patients with chronic heart failure (CHF) increases the risk of death.  Obstructive apneas (OSAHS) may lead to central apneas by frequent arousals, decreased left ventricular function and prolongation of circulation."

Taccola, A., D. Miotti and M. Zambelli. 1998. [Occupational exposure to vibration: Raynaud’s phenomenon and the vascular response to methacholine iontophoresis]. G Ital Med Lav Ergon 20(4):243-8 [Italian].

Taddio A, Katz J. 2005.  The effects of early pain experience in neonates on pain responses in infancy and childhood.  Paediatr Drugs 7(4):245-257.  “Pre-term infants that are hospitalized as neonates and subjected to painful procedures appear to have a dampened response to painful procedures later in infancy.  Full-term neonates exposed to extreme stress during delivery, or to a surgical procedure, react to later noxious procedures with heightened behavioral responsiveness.  Studies in which analgesic agents (local anesthetics or opioids) have been administered prior to noxious procedures demonstrate less procedural pain and a reduction in the magnitude of long-term changes in pain behaviors.”  [Adequate pain control from infancy may prevent sensitizing the central nervous system and lessen the chance of developing FMS.  DJS]

Taggart HM, Arslanian CL, Bae S et al. 2003.  Effects of T’ai Chi exercise on fibromyalgia symptoms and health-related quality of life.  Orthop Nurs 22(5):353-60.  “T’ai Chi is potentially beneficial to patients with FM.”  [The high drop-out rate in the study may be due to lack of modification of the training, or to co-existing myofascial trigger points.  See reference article under “Starlanyl DJ, published in T’ai Chi Magazine.”

Tagoe CE, Zezon A, Khattri S et al. 2013. Rheumatic manifestations of euthyroid, anti-thyroid antibody-positive patients. Rheumatol Int. [Jan 5 Epub ahead of print]. The aim of this study is to define the rheumatic manifestations of euthyroid patients with chronic lymphocytic thyroiditis (CLT) but without a well-defined connective tissue disease…..[This study found that] Rheumatic manifestations frequently occur in patients with CLT in the absence of overt thyroid dysfunction and mimic the presentation of the well-defined connective tissue diseases."

Taguchi T. 2005.  [The indication and clinical value of neural blocks for low back pain.]  Clin Calcium 15(3):337-342. [Japanese]  Trigger point blocks are included in this article.

Tague SE, Smith PG. 2010. Vitamin D receptor and enzyme expression in dorsal root ganglia of adult female rats: Modulation by ovarian hormones. J Chem Neuroanat. [Oct 20 Epub ahead of print]. "Vitamin D insufficiency impacts sensory processes including pain and proprioception, but little is known regarding vitamin D signaling in adult sensory neurons. These findings (in rats) imply that vitamin D signaling may play a specialized role in a neural cell population that is primarily nociceptive."

Tai CF, Baraniuk JN. 2003.  A tale of two neurons in the upper airways: pain versus itch.  Curr Allergy Asthma Rep. 3(3):215-220.  Connections between itch and pain and unmyelinated type C neurons.

Tai CF, Baraniuk JN. 2002.  Upper airway neurogenic mechanisms.  Curr Opin Allergy Clin Immunol. 2(1):11-19.  This article links dysfunctional Type C nociceptive nerves, involved in some types of chronic pain and itch, as contributors of “...allergic rhinitis, infectious rhinitis, nasal hyperresponsiveness, and possibly sinusitis.”

Taimela, S., M. Kankaanpaa and S. Luoto. 1999. The effect of lumbar fatigue on the ability to sense a change in lumbar position. A controlled study. Spine 24(13):1322-7.

Takagi, A. 1999. [Effect of caffeine on tension development of skeletal muscle of mdx mouse]. Rinsho Shinkeigaku 39(2-3):311-5. [Japanese]

Talebian S, Otadi K, Ansari NN et al. 2012. Postural control in women with myofascial neck pain. J Musculoskel Pain. 20(1):25-30.Patients with myofascial TrPs in the neck area had difficulty standing on foam flooring, both with one-foot standing and bipedal standing. Foam flooring affected both the control group and the patient group, but the patients had a faster sway velocity and significantly greater displacement distance. The study revealed that patients with cervical TrPs have standing deficits in standing balance with the eyes open or closed. Postural impairments could be from proprioceptor dysfunction associated with neck TrPs. The use of foam flooring as a standing surface significantly worsened postural control, both during one-legged and bipedal stances. The foam disrupts the sensory information from cutaneous mechanoreceptors on the soles of the feet, contributing to postural instability that increased with TrP-related neck pain. Patients did recruit the ankle tissues in an attempt to compensate for the postural imbalance, stressing those muscles. [This has direct application for those patients who exercise on foam matted surfaces, for t'ai chi chuan, yoga and other forms in which postural balance is of importance. DJS.]

Tamim H, Castel ES, Jamnik V et al. 2009. Tai Chi workplace program for improving musculoskeletal fitness among female computer users.  Work. 34(3):331-338.  “Results showed that the TC (Tai Chi) program was effective in improving musculoskeletal fitness and psychological well-being.”  “Significant improvements in physiological and psychological measures were observed, even at the large class sizes tested here, suggesting that TC has considerable potential as an economic, effective and convenient workplace intervention.”

Tamimi MA, McCeney MH, Krutsch J. 2009.  A case series of pulsed radiofrequency treatment of myofascial trigger points and scar neuromas.  Pain Med. 10(6):1140-1143.  “…PRF (pulsed radiofrequency) could be a minimally invasive, less neurodestructive treatment modality for these painful conditions and that further systematic evaluation of this treatment approach is warranted.”

Tamisier R, Pepin JL, Wuyam B et al. 2004.  Expiratory changes in pressure: flow ratio during sleep in patients with sleep-disordered breathing.  Sleep 27(2):240-248. 

Tampin B, Briffa NK, Slater H. 2012. Self-reported sensory descriptors are associated with quantitative sensory testing parameters in patients with cervical radiculopathy, but not in patients with fibromyalgia. Eur J Pain. [Oct 26 Epub ahead of print]. "The painDETECT questionnaire (PD-Q) has been used as a tool to characterize sensory abnormalities in patients with persistent pain. This study investigated whether the self-reported sensory descriptors of patients with painful cervical radiculopathy (CxRAD) and patients with fibromyalgia (FM), as characterized by responses to verbal sensory descriptors from PD-Q (sensitivity to light touch, cold, heat, slight pressure, feeling of numbness in the main area of pain), were associated with the corresponding sensory parameters as demonstrated by quantitative sensory testing (QST)....Clinicians and researchers should be cautious about relying on PD-Q (as a stand-alone screening tool to determine sensory abnormalities in patients with FM."

Tampin B, Slater H, Hall T. 2012. Quantitative sensory testing somatosensory profiles in patients with cervical radiculopathy are distinct from those in patients with nonspecific neck-arm pain. Pain. [Sep 11 Epub ahead of print]. The aim of this study was to establish the somatosensory profiles of patients with cervical radiculopathy and patients with nonspecific neck-arm pain associated with heightened nerve mechanosensitivity (NSNAP). Sensory profiles were compared to healthy control (HC) subjects and a positive control group comprising patients with fibromyalgia (FM)....Despite commonalities in pain characteristics between the two neck-arm pain groups, distinct sensory profiles were demonstrated for each group. [It would be extremely helpful to discover what percentage of these patients had co-existing myofascial trigger points referring to the upper limb and/or neck. DJS]

Tanaka M, Ishii A, Watanabe Y. 2014. Regulatory mechanism of performance in chronic cognitive fatigue. Med Hypotheses. 82(5):567-571. "Chronic cognitive fatigue is characterized by a sensation of long-lasting fatigue that impairs cognitive functions. Facilitation and inhibition systems in the central nervous system play primary roles in determining the output to the peripheral system, that is, performance. Sensory input from the peripheral system to the central nervous system activates the inhibition system to limit performance, whereas motivational input activates the facilitation system to enhance performance. The dysfunction of the facilitation system and central sensitization and classical conditioning of the inhibition system play important roles in the pathophysiology of chronic cognitive fatigue. Because the dorsolateral prefrontal cortex receives input from both the facilitation and inhibition systems to determine performance, metabolic, functional, and structural impairments of the dorsolateral prefrontal cortex induced by repetitive and prolonged overwork, stress, and stress responses contribute to the impaired functioning and cognitive performance that occur in people with chronic cognitive fatigue. This hypothesis of the regulatory mechanism of performance provides a new perspective on the neural mechanisms underlying chronic cognitive fatigue."

Tander B, Atmaca A, Aliyazicioglu Y et al. 2007.  Serum ghrelin levels but not GH, IGF-1 and IGFBP-3 levels are altered in patients with fibromyalgia syndrome.  Joint Bone Spine. [Jun 29 Epub ahead of print]  “Our results suggest that low levels of ghrelin in FMS are not related to the changes in hypothalama-pituitary-IGF-1 axis but may be related to some symptoms of FMS.  Our results need to be clarified by further studies.” [This may explain some of the abdominal fat pad, some of the glycolysis abnormalities, and some overeating issues in some patients with FM. DJS]

Tang B, Ji Y, Traub RJ. 2007.  Estrogen alters spinal NMDA receptor activity via a PKA signaling pathway in a visceral pain model in the rat.  Pain [Dec 7 Epub ahead of print].  “Pain symptoms in several chronic pain disorders in women, including irritable bowel syndrome, fluctuate with the menstrual cycle..”  The estrogen beta receptor may be in part responsible.

Tang S, Calkins H, Petri M. 2004.  Neurally mediated hypotension in systemic lupus erythematosus patients with fibromyalgia. Rheumatology (Oxford) 43(5):609-614.  In SLE patients, “...NMH has no impact on quality of life above that determined by FM, and has no significant association with FM status.  Identification of NMH may be important in selected patients with SLE who have chronic fatigue, but NMH cannot explain the increased prevalence of FM in SLE.”

Tanrikut A, Nadire O, Huseyin AK et al. 2001.  High voltage galvanic stimulation in myofascial pain syndrome.  J Muscoloskel Pain 11(2):11-15.  HGVS can be a useful treatment for myofascial pain.

Tanriverdi O. 2014. Is a new perspective for definition and diagnostic criteria of fibromyalgia in early stage cancer patients necessary? Med Hypotheses. [Jan 27 Epub ahead of print.] "Fibromyalgia is a most common pain syndrome characterized by the presence of chronic widespread pain and tenderness with manual palpation. However there is not enough data about frequency of fibromyalgia syndrome in patients with cancer. How often FM is being used in oncological practice and how are we managing this case by medical oncologists. Widespread pain index and symptom severity scale are not clear enough in patients with cancer when ACR-2010 diagnostic criteria for FM are considered. In conclusion, there is it may more prevalence of fibromyalgia in patients with cancer. For the diagnosis of fibromyalgia, (there may need to) be new diagnostic criteria for early-stage cancer patients."

Targino RA, Imamura M, Kaziyama HH et al. 2002.  Pain treatment with acupuncture for patients with fibromyalgia.  Curr Pain Headache Rep. 6(5):379-383.  This review is a comparison of acupuncture and other therapies in the relief of FMS.  Traditional acupuncture resulted in FMS improvement.

Tasali E, Leproult R, Ehrmann DA et al. 2008. Slow-wave sleep and the risk of type 2 diabetes in humans.  Proc Natl Acad Sci U S A 105(3):1044-1049.  “These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis.  Furthermore, our data suggest that reduced sleep quality with low levels of SWS (slow-wave sleep), as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes.”

Tassain V, Attal N, Fletcher D et al. 2003.  Long term effects of oral sustained release morphine on neuropsychological performance in patients with chronic non-cancer pain.  Pain 104(1-2):389-400. “...twelve months treatment with oral morphine does not disrupt cognitive functioning in patients with chronic non-cancer pain and instead results in moderate improvement of some aspects of cognitive functioning as a consequence of the pain relief and concomitant improvement of well-being and mood.”

Tauben DJ, Loeser JD. 2013. Pain education at the University of Washington School of Medicine. J Pain. 14(5):431-437. "There is a compelling need for implementation of new approaches to pain medicine education in both medical and other health science schools in response to the increasing evidence of inadequate and insufficient pain medicine education in both the U.S. and elsewhere. The UWSOM has recently increased pain curriculum time spent and the future practice relevance of its pain education by implementing a 4-year integrated curriculum tailored to match both the learning level and clinical experience, including most of the ISAP's recommended content, while emphasizing the educational needs of future primary care physicians, those who are and will continue to manage the vast majority of patients seeking medical advice and treatment of both acute and chronic pain."

Taubes G. 2003.  Neuroscience.  Insulin insults may spur Alzheimer's disease.  Science 301(5629):40-41.  Patients with type II diabetes and insulin resistance may have an increased incidence of Alzheimer’s disease.  Any diet that increases insulin levels may also predispose toward the development of Alzheimer’s.

Tawfik VL, Nutile-McMenemy N, Lacroix-Fralish ML, DeLeo JA.  Efficacy of propentofylline, a glial modulating agent, on existing mechanical allodynia following peripheral nerve injury.  Brain Behav Immun 2006 [Aug 30 Epub ahead of print].

Taylor AG, Anderson JG, Riedel SL et al. 2013. A randomized, controlled, double-blind pilot study of the effects of cranial electrical stimulation on activity in brain pain processing regions in individuals with fibromyalgia. Explore (NY). 9(1):32-40. "The observed decrease in activation in the pain processing regions may indicate a decrease in neural activity in these regions that may be related to decreased pain. This is the first randomized, controlled trial of CES in patients diagnosed with fibromyalgia to report functional magnetic resonance imaging data."

Taylor-Piliae RE, Froelicher ES. 2004.  Effectiveness of T'ai Chi exercise in improving aerobic capacity: meta-analysis.  J Cardiovasc Nurs 19(1):48-57.  T'ai chi may be considered aerobic exercise.  "The greatest benefit was seen from the classical Yang style T'ai Chi when performed for one year by sedentary adults with an initial low level of physical activity habits."

Teachey WS. 2004.  Otolaryngic myofascial pain syndromes.  Curr Pain Headache Rep. 8(6):457-462.  Many unexplained ear, nose, throat, head and neck dysfunctions that cannot be explained otherwise fit the diagnosis of myofascial dysfunction, and TrP therapy is effective for these symptoms.

Tecco S, Marzo G, Crincoli V et al. 2012. The prognosis of myofascial pain syndrome (MPS) during a fixed orthodontic treatment. Cranio. 30(1):52-71. "Among treatments in the literature for myofascial pain syndrome (MPS), the most reliable therapies in dentistry are spray and stretch, and, although less frequently used, anesthetic injection. Adult MPS subjects are often treated using fixed orthodontic therapy for resolution of malocclusion....The purpose of this study was to analyze the prognosis of MPS during orthodontic treatment of subjects with malocclusion, initially diagnosed as having MPS. The analysis covered the medical records of 91 young adult Caucasians scheduled for orthodontic treatment for various malocclusions. Thirty-seven of the patients were initially diagnosed as also having MPS (T0). Thirty patients began the orthodontic treatment and were recalled for a re-evaluation of MPS after dental alignment and dental class correction was achieved (T1). A wait-and-see strategy was applied in seven subjects who were included as the control subjects. They received no treatment for MPS. At T1, a statistically significant decrease was observed in the study group in the presence of any clicking or creaking noises from the jaw joint, a significant jaw joint and jaw muscle pain reduction, and a quality of life improvement. Among patients who were depressed at the beginning of treatment, the majority felt better at the follow-up evaluation. On muscular palpation, a statistically significant decrease was found on the visual analogic scale value of the middle fibers of the temporalis muscle, temporalis tendon, clavicular and sternal division of the sternocleidomastoid muscle, masseter muscles, and posterior cervical muscles. The temporalis and the masseter muscles showed a significant decrease in the number of subjects with trigger points (TrPs) in all areas in the study group, after treatment. The digastric and sternocleidomastoid muscles also showed a significant reduction in the number of subjects with TrPs. Subjects with MPS and malocclusion were treated using a fixed orthodontic treatment. They showed improvement, although no resolution, in the signs and symptoms of MPS, compared with the untreated control group."

Tegeder I, Costigan M, Griffin RS et al. 2006.  GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence.  Nat Med. 12(11):1269-1277.  This study indicates a genetic rate-limiting essential cofactor that influences neuropathic and inflammatory pain, as well as the formation of several biochemicals such as serotonin.  “BH4 is therefore an intrinsic regulator of pain sensitivity and chronicity, and the GTP cyclohydrolase haplotype is a marker for these traits.”  Researchers are searching for potential GTP inhibitor medications.

 

Teitelbaum JE, Johnson C, St Cyr J. 2006.  The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study.  J Altern Complement Med. 12(9):857-862.  “D-ribose significantly reduced clinical symptoms in patients suffering from fibromyalgia and chronic fatigue syndrome.”

Teixeira MJ, Yeng LT, Garcia OG et al. 2011. Failed back surgery pain syndrome: therapeutic approach descriptive study in 56 patients. Rev Assoc Med Bras. 57(3):286-291. [English, Portuguese] "The authors show the clinical evaluation and follow-up results in 56 patients diagnosed with a failed back surgery pain syndrome. ... In patients with a post-laminectomy syndrome, postoperative pain was more severe than preoperative pain from a herniated disk. A myofascial component was found in most patients."

Tekin L, Akarsu S, Durmuṣ O et al. 2012. The effect of dry needling in the treatment of myofascial pain syndrome: a randomized double-blinded placebo-controlled trial. Clin Rheumatol. [Nov 9 Epub ahead of print]. "The present study shows that the dry needling treatment is effective in relieving the pain and in improving the quality of life of patients with MPS."

Tekkok S.B., Ye Z.C., Brown A.M. et al. 2002.  Glutamate and aspartate are released from mouse optic nerve during oxygen/glucose deprivation.  Glia (Suppl 1):S66 [Abstract].

Tennant F. 2009.  Brain atrophy with chronic pain – A call for enhanced treatment.  Pract Pain Manage. 9(2):12-14,44.  Chronic pain can cause areas of the brain to shrink by as much as 11%, similar to that lost by 1-2 decades of aging.  “The decrease in the prefrontal cortex and the thalamus…was related to the duration of time spent in pain.  Every year of pain appeared to decrease grey matter by 1.3 cubic centimeters….Brain atrophy, along with altered brain physiology and neurochemistry, now joins the risk profile of undertreated chronic pain.”  [This study was done on chronic back pain patients.  It indicates that undertreated pain is an interactive condition of itself, although a preventable one. DJS]

Tennant F, Hermann L. 2001.  (231) use of transmucosal fentanyl in non-malignant, chronic pain.  Pain Med. 2(3):252-253.  “Reported reasons for widespread patient acceptance included TF’s fast action, fewer bed-bound days, increased energy, decreased use of other opioids, less depression, and fewer emergency room visits.  This pilot study indicates that TF is effective and desired as a preferential opioid for breakthrough pain by a high percentage of chronic, non-malignant pain patients.”

Tepper S J. 2004.  New thoughts on sinus headache.  Allergy Asthma Proc 25(2):95-96. “Sinus headaches are usually severely disabling migraines, misdiagnosed and mistreated, with 61% of patients receiving antibiotic prescriptions for noninfectious causes, thus failing the patients and, in addition, contributing to a serious public health problem.”

Terkelsen AJ, Gierthmuhlen J, Finnerup NB et al. 2014. Bilateral Hypersensitivity to Capsaicin, Thermal, and Mechanical Stimuli in Unilateral Complex Regional Pain Syndrome. Anesthesiology. [Mar 11 Epub ahead of print.] "Complex regional pain syndrome is multifactorial. Exaggerated inflammatory responses to limb injury may be involved. The authors hypothesized that capsaicin-induced pain and neurogenic inflammation (skin perfusion and flare area) are increased in patients with complex regional pain syndrome compared with that in controls…. The main finding is bilaterally increased capsaicin-induced pain in patients compared with controls. The flare response to capsaicin was normal, suggesting that the increased pain response was not due to increased neurogenic inflammation. The bilateral hypersensitivity to painful chemical, thermal, and mechanical stimuli not confined to the innervation area of a peripheral nerve or root cannot be explained by a regional change and may partly be due to central sensitization."

Terman, M. and J. S. Terman. 1999. Bright light therapy: side effects and benefits across the symptom spectrum. J Clin Psychiatry 60(11):799-808.

Ternov, K., M. Nilsson, L. Lofberg, L. Algotsson and J. Akeson. 1998. Acupuncture for pain relief during childbirth. Acupunct Electrother Res 23(1):19-26.

Tershner SA, Mitchell JM, Fields HL. 2000.  Brainstem pain modulating circuitry is sexually dimorphic with respect to mu and kappa opioid receptor function.  Pain 85(1-2):153-159.  “There are sex differences in the pain modulating potency of the opioid analgesics...”

Theadom A, Cropley M, Humphrey KL. 2007.   Exploring the role of sleep and coping in quality of life in fibromyalgia.  J Psychosom Res. 62(2):145-151.  “Sleep quality was significantly predictive of pain, fatigue, and social functioning in patients with FMS....Interventions designed to improve sleep quality may help to improve health-related quality of life for patients with FMS.”

Theoharides TC. 2007.  Treatment approaches for painful bladder syndrome/interstitial cystitis.  Drugs. 67(2):215-235.  “Lack of early diagnosis and treatment [of painful bladder] can affect outcomes and leads to the development of hyperalgesia/allodynia.”

Thiagarajah AS, Eades LE, Thomas PR et al. 2014. GILZ: Glitzing up our understanding of the glucocorticoid receptor in psychopathology. Brain Res. [Jun 12 Epub ahead of print.] "Dysfunction of the hypothalamic-pituitary-adrenal axis, particularly the glucocorticoid receptor, is a commonly implicated link between stress and psychopathology. GR abnormalities are frequently reported in depression, and these anomalies must be resolved before depressive symptoms remit. This biological finding is rendered clinically relevant by the knowledge that only select antidepressants alter GR function. The relationship between GR dysfunction and other diseases associated with psychiatric stress, such as post-traumatic stress disorder (PTSD) and fibromyalgia, is also documented. However, as laboratory constraints limit the utility of GR testing, other measures of GR activity, such as levels of GR-induced genes, may have greater clinical value. In this review, glucocorticoid-induced leucine zipper (GILZ), a product of GR-initiated gene transcription, will be discussed in the context of GR dysfunction in psychopathology."

Thieme K, Gracely RH. 2009.  Are psychological treatments effective for fibromyalgia pain?  Curr Rheumatol Rep. 11(6):443-450.  This is a review based on literature search, and so based on studies that do not take into consideration the co-existing conditions including TrPs, which now have been found to occur in all FM patients.  This may have something to do with the FM heterogenicity mentioned in this review.  It basically compared the effects of different types of psychological treatments.  Remembering the above caveats, relaxation as a single therapy was shown to be not helpful, hypnotherapy and writing intervention were mildly effective, but operant-behavioral therapy and cognitive behavioral therapy were considered effective for FM pain.  [Although psychological mechanisms can be helpful adjuncts, if FM pain is being maintained by myofascial TrPs, and they are due to defects in calcium channels, psychological methods cannot be considered treatment of FM pain, but they can help people with FM cope with the pain, the other symptoms, and the lack of support and understanding by others, often including the medical care team.  Adequate pain control and identification and control of TrP perpetuating factors might do a great deal more to help “FM” pain. DJS]

Thieme K, Turk DC. 2005.  Heterogeneity of psychophysiological stress responses in fibromyalgia syndrome patients.  Arthritis Res Ther. 8(1):R9  “The identification of low baseline muscle tension in FMS is discrepant with other chronic pain syndromes and suggests that unique psychophysiological features may be associated with FMS.  The different psychophysiological response patterns within the patient sample support the heterogeneity of FMS.”

Thimineur M, De Ridder D. 2007.  C2 area neurostimulation: a surgical treatment for fibromyalgia.  Pain Med. 8(8):639-646.  “C2 area scalp stimulation may diminish pain and related symptoms in patients with FM.”

Thomas CH. 2010. Spinal cord mechanisms of chronic pain and clinical implications. Curr Pain Headache Rep. 14(3):213-220. “In chronic pain states, painful stimuli trigger afferent fibers in the dorsal horn to release neuropeptides and neurotransmitters. These events induce multiple inflammatory and neuropathic processes in the spinal cord dorsal horn, and trigger modification and plasticity of local neural circuits. As a result, ongoing noxious signals to the brain are amplified and prolonged, a phenomenon known as central sensitization.”

Thomas HV, Stimpson NJ, Weightman AL et al. 2006.  Systematic review of multi-symptom conditions in Gulf War veterans.  Psychol Med. 36(6):735-747.  “Studies were included if they compared the prevalence of chronic fatigue syndrome, multiple chemical sensitivity, CDC-defined chronic multi-symptom illness, fibromyalgia, or symptoms of either fatigue or numbness and tingling…”  “The results support the hypothesis that deployment to the Gulf War is associated with greater reporting of multi-symptom conditions.”

Thomas K, Shankar H. 2013. Targeting myofascial taut bands by ultrasound. Curr Pain Headache Rep. 17(7):349. "Myofascial pain syndrome (MPS) is a frequent diagnosis in chronic pain and is characterized by tender, taut bands known as trigger points. The trigger points are painful areas in skeletal muscle that are associated with a palpable nodule within a taut band of muscle fibers. Despite the prevalence of myofascial pain syndrome, diagnosis is based on clinical criteria alone. A growing body of evidence that suggests that taut bands are readily visualized under ultrasound-guided exam, especially when results are correlated with elastography, multidimensional imaging, and physical exam findings such as local twitch response."

Thomas M., Sing H., Belenky G., Holcomb H., Mayberg H., Dannals R., Wagner H., Thorne D., Popp K., Rowland L., Welsh A., Balwinski S., Redmond D. 2000. Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J Sleep Res 9(4):335-352. Sleep deprivation can cause dysfunction in the brain, primarily in the thalamus.  Short-term sleep deprivation produces global decreases in brain activity and dsyfunction in higher-order cognitive processes.

Thomas RJ. 1995.  Excitatory amino acids in health and disease.  J Am Geriatr Soc. 43(11):1279-1289.  “Pharmacological manipulation of the excitatory amino acid receptors is likely to be of benefit in important and common diseases of the nervous system.”  Only a few neurotransmitter modulators now available have acceptable therapeutic indices.  New medications in this field may have applications in chronic pain therapy.

 

Thomas RJ, Terzano MG, Parrino L et al. 2004.  Obstructive sleep-disordered breathing with a dominant cyclic alternating pattern — a recognizable polysomnographic variant with practical clinical implications.  Sleep 27(2):229-234.  “This variant of sleep apnea may reflect a dominant component of respiratory instability and periodic breathing coupled with upper-airway obstruction.  Besides positive airway pressure, measures to treat periodic breathing may be required.

Thomas, S. A. and R. D. Palmiter. 1997. Disruption of the dopamine beta-hydroxylase gene in mice suggests roles for norepinephrine in motor function, learning, and memory. Behav Neurosci 111(3):579-589.

Thomas, S. A. and R. D. Palmiter 1997b. Impaired maternal behavior in mice lacking norepinephrine and epinephrine. Cell 91(5):583-592.

Thomas, S.P., 2000. A phenomenologic study of chronic pain. West J Nurs Res 22(6):683-99.  This paper called chronic nonmalignant pain "a force or monster that cannot be tamed", in which "time seemed to stop; the future was unfathomable".

Thomas, T. J. 1988. Fibrositis in men. West Virginia Med J 84:235-6.

Thomason HC 3rd, Bos GD, Renner JB. 2001.  Calcifying tendinitis of the gluteus maximus.  Am J Orthop. 30(10):757-758.

Thompson JM. 2012. Exercise in muscle pain disorders. PM R. 4(11):889-893. "Muscle pain disorders range from local or regional (myofascial pain) to widespread (fibromyalgia). Many people with muscle pain have decreased fitness. Exercise intolerance is a common feature as well, and yet exercise plays an important role in the treatment of muscle pain disorders. Results of studies have shown repeatedly, via multiple modes and methods of delivery, that exercise is at least as effective as the best pharmacologic treatments. An understanding by clinicians and their patients of the unique benefits of a carefully crafted exercise program is one step in the successful management of these often frustrating muscle pain disorders." Mayo School of Graduate Medical Education

Thompson JM, Luedtke CA, Oh TH. 2010. Direct medical costs in patients with fibromyalgia: Cost of illness and impact of a brief multidisciplinary treatment program. Am J Phys Med Rehabil. [Oct 21 Epub ahead of print]. "Patients with clinically diagnosed fibromyalgia incur direct medical costs about twice that of their matched controls. This increased cost is related to the severity of their symptoms as measured by the Fibromyalgia Impact Questionnaire and was not impacted by participation in a brief cognitive behaviorally based fibromyalgia treatment program."

Thornton EW, Sykes KS, Tang WK. 2004.  Health benefits of T'ai Chi exercise: improved balance and blood pressure in middle-aged women.  Health Promot Int 19(1):33-38.  “Elderly T'ai chi practitioners attained the same level of balance control performance as did young, healthy subjects when standing under reduced or conflicting somatosensory, visual, and vestibular conditions."

Thorson, K. 1999. Is fibromyalgia a distinct clinical entity? The patient’s evidence. Baillieres Best Pract Res Clin Rheumatol 13(3):463-7.

Thoss, F., B. Bartsch, D. Tellschaft and M. Thoss. 1999. Periodic inversion of the vertical component of the Earth’s magnetic field influences fluctuation of visual sensitivity in humans. Bioelectromagnetics 20(7):459-461.

Tiedemann AC, Sherrington C, Lord SR. 2007.  Physical and psychological factors associated with stair negotiation performance in older people.  J Gerontol A Biol Sci Med Sci. 62(11):1259-1265.  “An inability to negotiate stairs is a marker of disability and functional decline and can be a critical factor in loss of independence in older people.”  “In community-dwelling older people, impaired stair negotiation is associated not only with reduced strength but also with impaired sensation, strength, and balance; reduced vitality; presence of pain; and increased fear of falling.” [T’ai chi chuan may be useful to prevent or improve this problem.  Improvement of proprioception and muscle function, including range of motion, through the treatment of co-existing MTPS should also be considered.  Latent MTPs may be common but unsuspected in elderly patients with restricted range of motion. DJS]

Tietjen GE, Brandes JL, Peterlin BL et al. 2009.  Allodynia in migraine: association with comorbid pain conditions.  Headache. 49(9):1333-1344.  “Symptoms of CA (cutaneous allodynia) in migraine were associated with current anxiety, depression, and several chronic pain conditions.  A graded relationship was observed between number of allodynic symptoms and the number of pain conditions, even after adjusting for confounding factors.  This study also presents the novel association of CA symptoms with younger age of migraine onset, and with cigarette smoking, in addition to confirming several previously reported findings.”

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.

Tiihonen, M., M. Partinen and S. Narvanen. 1993. The severity of obstructive sleep apnea is associated with insulin resistance. J Sleep Res 2(1):56-61.

Tikiz C, Muezzinoglu T, Pirildar T et al. 2005.  Sexual dysfunction in female subjects with fibromyalgia.  J Urol. 174(2):620-623.  “Female patients with FM have distinct sexual dysfunction compared with healthy controls and coexistent MD has no additional negative effect on sexual function.  Thus, female subjects with FM should be evaluated in terms of sexual function to provide better quality of life.”

Timmerman GM, Calfa NA, Stuifbergen AK. 2013. Correlates of body mass index in women with fibromyalgia. Orthop Nurs. 32(2):113-119. "The findings support a growing body of evidence that excess weight is negatively related to quality of life and pain in women with FMS."

Ting TV, Hashkes PJ, Schikler K et al. 2012. Pediatr Rheumatol Online J. 10(1):16. The role of benign joint hypermobility in the pain experience in Juvenile Fibromyalgia: an observational study. "Juvenile Fibromyalgia (JFM) is characterized by chronic widespread musculoskeletal pain and approximately 40% of children and adolescents with JFM also suffer from benign joint hypermobility (HM)....The presence of HM among adolescent patients with JFM appears to be associated with enhanced physiologic pain sensitivity, but not self-report of clinical pain. Further examination of the mechanisms for increased pain sensitivity associated with HM, especially in adolescents with widespread pain conditions such as JFM is warranted."

Tishler, M., Smorodin, T., Vanzina-Amit, M., et al. 2003. Fibromyalgia in diabetes mellitus.  Rheumatol Int [***epub ahead of print].  “Fibromyalgia is a common finding in patients with types 1 and 2 diabetes, and its prevalence could be related to control of the disease.  As with other diabetes complications, FM might be prevented by improved control of blood glucose levels.”

Tishler, M., Y. Barak, D. Paran and M. Yaron. 1997. Sleep disturbances, fibromyalgia and primary Sjogren's syndrome. Clin Exp Rheumatol 15(1):71-74.

Tizabi, Y., R. L. Copeland Jr., R. Brus and R. M. Kostrzewa. 1999. Nicotine blocks quinpirole-induced behavior in rats: psychiatric implications. Psychopharmacology (Berl) 145(4):433-441.

Tobbackx Y, Meeus M, Wauters L. 2012. Does acupuncture activate endogenous analgesia in chronic whiplash-associated disorders? A randomized crossover trial. Eur J Pain. [Sep 11 Epub ahead of print]. "It was shown that one session of acupuncture treatment results in acute improvements in pressure pain sensitivity in the neck and calf of patients with chronic WAD. Acupuncture had no effect on conditioned pain modulation or temporal summation of pressure pain. Both acupuncture and relaxation appear to be well-tolerated treatments for people with chronic WAD. These findings suggest that acupuncture treatment activates endogenous analgesia in patients with chronic WAD."

Toda K. 2007.  The prevalence of fibromyalgia in Japanese workers.  Scand J Rheumatol. 36(2):140-144.  “FM is a common musculoskeletal disorder among Japanese adult workers, especially among female workers.”

Toda K, Harada T, Ishizaki F et al. 2006.  Parkinson disease patient with fibromyalgia: a case report.  Parkinsonism Relat Disord. [Jul 5 Epub ahead of print].  This report indicates that pain in Parkinson’s disease patients may be from other sources, including FMS.  [The pain could also be due to myofascial TrPs. DJS]

Todisco T, Todisco C, Bruni L et al. 2004.  Chin stimulation: a trigger point for provoking acute hiccups.  Respiration. 71(1):104.

Tolk J, Kohnen R, Muller W. 2004.  Intravenous treatment of fibromyalgia with the 5-HT3 receptor antagonist tropisetron in a rheumatological practice.  Scand J Rheumatol Suppl. (119):72-75.  “IV tropisetron treatment represents a promising option for the treatment of FM even though the study design incorporated many imponderables.”

Toms J. 2012. [Updated view of fibromyalgia]. Cas Lek Cesk. 151(9):415-419 [Czech]. "Fibromyalgia is a chronic syndrome characterized by dysfunction of pain processing and regulation....The absence of objective diagnostic tests often results in delayed diagnosis and patient fluctuation among a number of specialists with uncertainty and fear of a serious disease. The treatment is based on the individually adjusted and multidisciplinary approach to the patient, combining pharmacological and non-pharmacological therapy."

Ton E, Bakker MF, Verstappen SM on behalf of the Utrecht Rheumatoid Arthritis Cohort Study. 2011. Look Beyond the Disease Activity Score of 28 Joints (DAS28): Tender Points Influence the DAS28 in Patients with Rheumatoid Arthritis. J Rheumatol. [Oct 15 Epub ahead of print]. "DAS28 is influenced by tender points, even in the non-fibromyalgia range, falsely suggesting higher disease activity and decreasing the sensitivity of the DAS28 criterion of low disease activity or remission. When applying DAS28-guided "tight control" or "treat-to-target" treatment strategies in RA, evaluation of not only the DAS28, but also its individual components along with a full joint and physical evaluation including assessment of TP is required to reliably estimate the individual's disease activity, which guides therapeutic decisions."

Torma LM, Houck GM, Wagnild GM et al. 2012. Growing Old with Fibromyalgia: Factors That Predict Physical Function. Nurs Res. 62(1):16-24. "Resilience, a novel variable in fibromyalgia research, was a unique predictor of physical function. Further research is needed to learn more about the relationships between resilience, fibromyalgia impact, and the aging process."

Torpy, D. J. and G. P. Chrousos. 1996. The three-way interactions between the hypothalamic-pituitary-adrenal and gonadal axes and the immune system. Baillieres Clin Rheumatol 10(2):181-98.

Torres Lacomba M, Mayoral del Moral O, Coperias Zazo JL et al. 2010. Incidence of myofascial pain syndrome in breast cancer surgery: a prospective study. Clin J Pain. 26(4):320-325. “Pain after breast cancer therapy is a recognized complication found to have an adverse impact on patient's quality of life, increasing psychosocial distress.....The objective of this study was to assess the incidence of myofascial pain syndrome prospectively 12 months after breast cancer surgery....Each participant was assessed preoperatively, postoperatively between day 3 and day 5, and at 1, 3, 6, and 12 months after surgery. A physical therapist, expert in the diagnosis of myofascial pain syndrome, performed follow-up assessments. Pain descriptions by the patients and pain pattern drawings in body forms guided the physical examination. The patients were not given any information concerning myofascial pain or other muscle pain syndromes....One year follow-up was completed by 116 women. Of these, 52 women developed myofascial pain syndrome.... CONCLUSION: Myofascial pain syndrome is a common source of pain in women undergoing breast cancer surgery that includes axillary lymph node dissection at least during the first year after surgery. Myofascial pain syndrome is one potential cause of chronic pain in breast cancer survivors who have undergone this kind of surgery.”

Torres M, Mayoral del Moral O, Yuste MJ et al. 2007.  Prevalence of myofascial pain syndrome in breast cancer.  J Musculoskel Pain 15 (Supp 13):29 item 47.  [Myopain 2007 Poster]  “The prevalence of regional MPS in breast cancer suggests that it may be an important cause of pain following cancer treatment such as surgery, radiotherapy, chemotherapy or hormonal therapy.”

Torres R, Vasques J, Duarte JA et al. 2010. Knee proprioception after exercise-induced muscle damage. Int J Sports Med. [Mar 18 Epub ahead of print] “…eccentric exercise leading to muscle damage alters joint proprioception, suggesting that there might be impairment in the intrafusal fibres of spindle muscles and in the tendon organs."

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. "

Torresani C, Bellafiore S, De Panfilis G. 2009.  Chronic urticaria is usually associated with fibromyalgia syndrome.  Acta Derm Venereol. 89(4):389-392.  “A total of 126 patients with chronic urticaria were investigated for fibromyalgia syndrome.  The corresponding proportion for 50 control dermatological patients was 16%, which is higher than previously published data for the Italian general population (2.2%).  It is possible that dysfunction cutaneous nerve fibers of patients with fibromyalgia syndrome may release neuropeptides, which, in turn, may induce dermal microvessel dilatation and plasma extravasation.  Furthermore, some neuropeptides may favor mast cell degranulation, which stimulates nerve endings, thus providing positive feedback.  Chronic urticaria may thus be viewed in many patients, as a consequence of fibromyalgia syndrome; in fact, skin neuropathy (fibromyalgia syndrome) may trigger neurogenic skin inflammation (chronic urticaria).”

Toto BJ. 1993.  Chiropractic correction of congenital muscular torticollis.  J Manipulative Physiol Ther. 16(8):556-559.  “Treatments included chiropractic manipulation, trigger point therapy, specific stretches, pillow positioning and exercises.  Excellent results were obtained.  Conclusion: Suggests that chiropractic intervention is a viable treatment option for congenital muscular torticollis.  Further studies should be performed to compare the effectiveness of other treatment options.”

Touch EA, White AR, Richards S et al. 2007.  Variability of criteria used to diagnose myofascial trigger point pain syndrome-evidence from a review of the literature.  Clin J Pain. 23(3):278-286.  [While it is true that far too many authors of papers confuse myofascial pain as TMJ, it is unfortunate that these authors did not differentiate between the two, in spite of the clear distinction in the articles: Simons DG. 1995.  Myofascial pain syndrome: One term but two concepts; a new understanding. J Musculoskeletal Pain 3(1):7-14 and Simons DG. 2004.  New aspects of myofascial trigger points: etiological and clinical. J Musculoskeletal Pain 12(3/4):15-21.  The authors have noted an important truth.  Far too many articles purporting to be on myofascial pain do not specify the criteria that have been used.  Also, I believe that far too many articles on any kind of pain, including fibromyalgia, do not take into consideration co-existing myofascial trigger points may be influencing their research and lead to faulty or biased conclusions. DJS]

Tough EA, White AR, Richards SH et al. 2010. Myofascial trigger point needling for whiplash associated pain - A feasibility study. Man Ther. [Jun 24 Epub ahead of print]. Forty-one patients with recent whiplash injury were tested in this study to see if phase III study specific needling therapy of myofascial TrPs was warranted. It is, and is being planned.

Townsley P, Ravenscroft A, Bedforth N. 2011. Ultrasound-guided spinal accessory nerve blockade in the diagnosis and management of trapezius muscle-related myofascial pain. Anaesthesia. [Mar 18 Epub ahead of print]. "We report the first description of ultrasound-guided spinal accessory nerve blockade using single-shot and subsequently continuous infusion (via a perineural catheter) local anesthetic techniques, for the diagnosis and treatment of myofascial pain affecting the trapezius muscle.... We have demonstrated that the spinal accessory nerve is identifiable in the posterior triangle of the neck and can be blocked successfully using ultrasound guidance. This technique can aid the diagnosis and treatment of myofascial pain originating from the trapezius muscle."

Tozzi P. 2014. Does fascia hold memories? J Bodyw Move Ther. 18(2):259-265. "Many bodyworkers, at some point in their practice, have experienced phenomena that may be interpreted as representing a release of memory traces when working on dysfunctional tissues. This feeling may have been accompanied by some type of sensory experience, for the therapist and/or the patient. In some cases, early traumatic experiences may be recalled. When this happens, the potency of the memory may be erased or eased, along with restoration of tissue function. Hence the questions: can memories be held in the fascia? And are these memories accessible during manual fascial work?" "…it is suggested that a possibility may exist that manual therapy might affect various forms of memory, producing profound tissue changes from subatomic to global effects." [This fascinating editorial mentions some of the possible mechanisms of cellular memory. DJS]

Trampas A, Kitsios A, Sykaras E et al. 2010. Clinical massage and modified Proprioceptive Neuromuscular Facilitation stretching in males with latent myofascial trigger points. Phys Ther Sport. 11(3):91-98.

Tran MT, Arendt-Nielsen L, Kupers R et al. 2012. Multiple chemical sensitivity: On the scent of central sensitization. Int J Hyg Environ Health. [Apr 7 Epub ahead of print]. "Increased capsaicin-induced secondary punctate hyperalgesia was demonstrated in MCS patients without comorbid, overlapping disorders, suggesting facilitated central sensitization in MCS."

Travell J. 1981.  Identification of myofascial trigger point syndromes: a case of atypical facial neuralgia.  Arch Phys Med Rehabil. 62(3):100-106.  “A case report describes in detail the treatment of a patient who, for 13 years, had suffered from a medically enigmatic, intense right facial pain with severe dysfunction and who is now pain-free, with a full schedule of unrestricted activities 23 years later.”  [One cannot help but grieve for the patient’s 13 years lost to needless intense pain. DJS]

 

Travell JG. 1977. A trigger point for hiccup.  J Am Osteopath Assoc. 77(4):308-312.  This TrP is found in the uvula, and can be treated by stimulation with the end of a cold spoon.  [Spray with appropriate anesthetic or application of oral anesthetic can often work as well.  DJS]

 

Tremblay A, Pelletier C, Doucet E et al.  2004.  Thermogenesis and weight loss in obese individuals: a primary association with organochlorine pollution.  Int. Jour Obesity 28(7):936-939.  Many toxic chemicals can be stored in fat.  Weight loss may release toxic chemicals that slow and otherwise affect the body’s metabolism, contributing to feelings of malaise and difficulty losing weight. 

Triadafilopoulos, G. , R. W. Simms and D. L. Goldenberg. 1991. Bowel dysfunction in fibromyalgia syndrome. Dig Dis Sci 36(1):59-64.

Triano, J. J., M. McGregor and D. R. Skogsbergh. 1997. Use of chiropractic manipulation in lumbar rehabilitation. J Rehabil Res Dev 34(4):394-404.

Trimble, M. H. and R. M. Enoka. 1991. Mechanisms underlying the training effects associated with neuromuscular electrical stimulation. Phys Ther 71(4):273-280.

Trinanes Y, Gonzalez-Villar A, Gomez-Perretta C et al. 2014. Suicidality in chronic pain: Predictors of suicidal ideation in fibromyalgia. Pain Pract. [Apr 1 Epub ahead of print.] "Fibromyalgia (FM) has been associated with a higher prevalence of suicidal behavior. Nevertheless, much remains unknown about suicide risk factors for this chronic pain disorder. In the present study, the relationship of suicidal ideation in FM with a number of sociodemographic, clinical, and psychological variables was analyzed…. The prevalence of suicidal ideation among FM patients was 32.5%. Significant differences between patients with vs. without suicidal ideas emerged mainly for the various indices of depression. Patients with suicidal ideation also reported higher levels of anxiety, more day dysfunction due to sleepiness and more limitations due to emotional and physical problems. Logistic regression analysis revealed that cognitive depression symptoms such as BDI Self-Blame cluster are the more closely related to suicide ideation…. The presence of suicidal ideation in FM patients is closely related to comorbid depression, anxiety and to a higher impact of the disease in daily life."

Trujillo KA, Akil H. 1994.  Inhibition of opiate tolerance by non-competitive N-methyl-D-aspartate receptor antagonists.  Brain Res. 633(1-2):178-188.  “...NMDA receptors may have a fundamental role in the development of opiate tolerance....non-competitive NMDA receptor antagonists may be effective adjuncts to opiates in the treatment of chronic pain.”

Trujillo, K. A. and H. Akil. 1994. Inhibition of opiate tolerance by non-competitiveN-methyl-D-aspartate receptor antagonists. Brain Res 633(1-2):178-88.

Tsai CT, Hsieh LF, Kuan TS et al. 2009.  Injection in the cervical facet joint for shoulder pain with myofascial trigger points in the upper trapezius muscle.  Orthopedics. 32(8).  “This study demonstrates that intra-articular or peri-articular injection into the cervical facet joint region can effectively inactivate the upper trapezius myofascial trigger point secondary to the facet lesion.”  [Trigger points have perpetuating factors.  If the TrPs return in spite of appropriate treatment, the perpetuating factor must be identified and brought under control.  In this case, the perpetuating factor was a facet joint problem. DJS]

Tsai CT, Hsieh LF, Kuan TS et al. 2009.  Remote effects of dry needling on the irritability of the myofascial trigger point in the upper trapezius muscle.  Am J Phys Med Rehabil. [Apr 28 Epub ahead of print].  “This study demonstrated the remote effectiveness of dry needling.  Dry needling of a distal myofascial trigger point can provide a remote effect to reduce the irritability of a proximal myofascial trigger point.”

Tsang WW, Wong VS, Fu SN et al. 2004.  T'ai Chi improves standing balance control under reduced or conflicting sensory conditions.  Arch Phys Med Rehabil 85(1):129-137.  "…T'ai Chi exercise can be a good choice of exercise for middle-aged adults, with potential benefits for ageing as well as the aged."

Tsao JC, Meldrum M, Kim SC et al. 2007.  Treatment preferences for CAM in children with chronic pain.  Evid Based Complement Alternat Med. 4(3):367-374.  “This study examined treatment preferences in chronic pediatric pain patients offered a choice of CAM therapies for their pain.  Participants were 129 children (94 girls) (mean age = 14.5 years +/- 2.4; range = 8-18 years) presenting at a multidisciplinary, tertiary clinic specializing in pediatric chronic pain.”  “Patients with a diagnosis of fibromyalgia (80%) were the most likely to try CAM versus those with other pain diagnoses.”  “When given a choice of CAM therapies, this sample of children with chronic pain, irrespective of pain diagnosis, preferred non-invasive approaches that enhanced relaxation and increased somatic control.  Longer duration of pain and greater impairment in functioning, particularly during family activities increased the likelihood that such patients agreed to engage in CAM treatments, especially those that were categorized as mind-based modalities.”  [Children get FM.  They also get MTPs.  Many suffer needlessly because of the mistaken belief that they do not.  Pediatricians need to become aware that many children are suffering needlessly and perhaps unknowingly, because they have no frame of reference.  They have always hurt.  Seek and ye shall find. DJS]

Tschopp, K. P. and C. Gysin. 1996. Local injection therapy in 107 patients with myofascial pain syndrome of the head and neck.  ORL J Otorhinolaryngol Relat Spec 58(6):306-310.

Tsen, L. C. and W. R. Camann. 1997. Trigger point injections for myofascial pain during epidural analgesia for labor. Reg Anesth 22(5):466-468.

Tsigos C, Chrousos G. 2002. Hypothalamic-pituitary- adrenal axis, neuroendocrine factors and stress.  J Psychosom Res 53(4):865.  When the stress response system is disrupted, many other hormones and informational substances can be affected, including sex hormones, growth hormone and thyroid hormone.

Tsuchie H, Miyakoshi N, Kasukawa Y et al. 2013. High prevalence of abdominal aortic aneurysm in patients with chronic low back pain. Tohoku J Exp Med. 230(2):83-86. "The prevalence of LBP (low back pain) is high in AAA (abdominal aortic aneurysm) patients, and doctors who treat chronic LBP should be aware of AAA as a potential cause of LBP." [This study is included here to alert readers that abdominal aortic aneurysm is common in low back pain patients and must be assessed and can mimic symptoms of spinal or myofascial pain. DJS]

Tu CH, Niddam DM, Chao HT et al. 2010. Brain morphological changes associated with cyclic menstrual pain. Pain.150(3):462-468. "Primary dysmenorrhea (PDM) is the most prevalent gynecological disorder for women in the reproductive age. PDM patients suffer from lower abdominal pain that starts with the onset of the menstrual flow. Prolonged nociceptive input to the central nervous system can induce functional and structural alterations throughout the nervous system. In PDM, a chronic viscero-nociceptive drive of cyclic nature, indications of central sensitization and altered brain metabolism suggest a substantial central reorganization.... Our results demonstrate that abnormal GM volume changes are present in PDM patients even in the absence of pain. These changes may underpin a combination of impaired pain inhibition, increased pain facilitation and increased affect. Our findings highlight that longer lasting central changes may occur not only in sustained chronic pain conditions but also in cyclic occurring pain conditions." [The most common cause of menstrual pain is myofascial TrPs. It is to be hoped that greater awareness will be focused on the pain generators, as well as on the pain amplifier. DJS]

Tu CH, Niddam DM, Yeh TC et al. 2013. Menstrual pain is associated with rapid structural alterations in the brain. Pain. [May 18 Epub ahead of print]. "Dysmenorrhea is the most prevalent gynecological disorder for women in the childbearing age. Dysmenorrhea is associated with central sensitization and functional and structural changes in the brain. Our recent brain morphometry study disclosed that dysmenorrhea is associated with trait-related abnormal gray matter (GM) changes even in the absence of menstrual pain, indicating that the adolescent brain is vulnerable to menstrual pain. Here we report rapid state-related brain morphological changes, i.e. between pain and pain-free states, in dysmenorrhea. We used T1-weighted anatomical magnetic resonance imaging to investigate regional GM volume changes between menstruation and peri-ovulatory phases, in 32 dysmenorrhea subjects and 32 age- and menstrual cycle-matched asymptomatic controls. An optimized voxel-based morphometry analysis was conducted to disclose the possible state-related regional GM volume changes across different menstrual phases. A correlation analysis was also conducted between GM differences and the current menstrual pain experience in the dysmenorrhea group. Compared to the peri-ovulatory phase, the dysmenorrhea subjects revealed greater hypertrophic GM changes than controls during the menstruation phase in regions involved in pain modulation, generation of the affective experience and regulation of endocrine function while atrophic GM changes were found in regions associated with pain transmission. Volume changes in regions involved in regulation of endocrine function and pain transmission correlated with the menstrual pain experience scores. Our results demonstrated that short-lasting cyclic menstrual pain is associated not only with trait-related but also rapid state-related structural alterations in the brain. Considering the high prevalence rate of menstrual pain, these findings mandate a great demand to revisit dysmenorrhea regarding its impact on the brain and other clinical pain conditions."

Tuchman M, Barrett JA, Donevan S et al. 2010. Central sensitization and Ca(V)alpha(2)delta ligands in chronic pain syndromes: pathologic processes and pharmacologic effect. J Pain. [May 14 Epub ahead of print]. “This focus article discusses how the central nervous system plasticity phenomenon, central sensitization, is established in the induction and maintenance of chronic pain, allodynia, and hyperalgesia. In addition, it explores the neurophysiologic actions of the calcium-channel ligands gabapentin and pregabalin in limiting pathological manifestations of central sensitization.”  

Tugnet N, Williams R. 2012. "My bones hurt." An unusual cause of fibromyalgia syndrome. J Musculoskel Pain 20(3):208-221. This excellent case report documents fibromyalgia caused by multiple bony hemangiomatosis. [This is a good reminder that when the central nervous system is sensitized, it has been sensitized by something. One must look for the cause. DJS]

Tuncer, T., B. Butun, M. Arman, A. Akyokus and A. Doseyen. 1997. Primary fibromyalgia and allergy. Clin Rheumatol 16(1):9-12.

Tullberg M, Ernberg M. 2006.  Long-term effect on tinnitus by treatment of temporomandibular disorders: a two-year follow-up by questionnaire.  Acta Odontol Scand. 64(2):89-96.  “The results of this study showed that TMD symptoms and signs are frequent in patients with tinnitus and that TMD treatment has a good effect on tinnitus in a long-term perspective, especially in patients with fluctuating tinnitus.”

 

Tuo KS, Cheng YY, Kao CL. 2006.  Vestibular rehabilitation in a patient with whiplash-associated disorders.  J Chin Med Assoc. 69(12):591-595.   Prompt comprehensive rehabilitation, including TrP injection, coordination and vestibular rehab, may successfully treat some cases of whiplash syndrome

 

Turk DC, Robinson JP, Burwinkle R. 2004.  Prevalence of fear of pain and activity in patients with fibromyalgia syndrome.  J Pain 5(9):483-490.  “Fear of movement is a significant concern for chronic pain sufferers because these behaviors maintain pain and increase disability.”  [While this is true of itself, care must be taken in interpreting this behavior.  It is not abnormal to avoid movements that cause pain, and to consider this as pathological shows disregard for the pain level of the patient and lack of understanding and justice. DJS]

 

Turk DC. 1997.  Evaluating the role of physical, operant, cognitive, and affective factors in the pain behaviors of chronic pain patients.  Behavior Modification 21(3):259-280.  “63 chronic pain patients diagnosed with the disorder fibromyalgia underwent medical, physical, and psychological evaluations.  The physical, cognitive, and affective factors, but not operant factors, were significantly related to observed pain behaviors.  Pain behaviors should be conceptualized as behavioral manifestation of pain based on a complex interaction of various psychological and physical factors.”

Turk, D. C., A. Okifuji, J. D. Sinclair and T. W. Starz. 1998. Interdisciplinary treatment for fibromyalgia syndrome: clinical and statistical significance. Arthritis Care Res 11(3):186-95.

Turk, D. C., A. Okifuji, T. W. Starz and J. D. Sinclair. 1996. Effects of type of symptom onset on psychological distress and disability in fibromyalgia syndrome patients. Pain 68(2-3):423-430.

Turkyilmaz AK, Kurt EE, Capkin E et al. 2012. Assessment of neuropathic pain in patients with fibromyalgia syndrome: A pilot study. J Musculoskel Pain. 20(3):170-176. [This study indicated that many patients with fibromyalgia have neuropathic pain syndromes that are associated with pain severity. Since many if not all fibromyalgia patients also have myofascial trigger points, and trigger points can cause nerve entrapment and these symptoms, it is to be hoped that future studies will include co-existing trigger points as a possible cause of these symptoms. DJS]

Turner, R. A., M. Altemus, T. Enos, B. Cooper and T. McGuiness. 1999. Preliminary research on plasma oxytocin in normal cycling women: investigating emotion and interpersonal distress. Psychiatry 62(2):97-113.

Turo D, Otto P, Gebreab T et al. 2013. Shear wave elastography for characterizing muscle tissue in myofascial pain syndrome. J Acoust Soc Am. 133(5):3358. "Myofascial pain syndrome (MPS) affects 85% of chronic pain sufferers in a specialty pain center. Neck and low-back are commonly affected by MPS. Myofascial trigger points (MTrPs) are characteristic findings of MPS and are palpable tender nodules in the muscles of symptomatic subjects. Mechanical characterization of MTrPs and surrounding tissue can offer important insight about the pathophysiology of the MPS, which is currently poorly understood. In this study, we propose an inexpensive technique, based on ultrasound shear wave elastography, to objectively measure mechanical properties of MTrPs and surrounding tissue in the upper trapezius. In an ongoing clinical study, we recruited 34 subjects: 12 healthy controls, 10 with not spontaneously painful MTrPs (latent) and 12 with symptomatic chronic neck pain (>3 months) and active (spontaneously painful) MTrPs. Shear wave elastography was performed on the upper trapezius of all subjects using the Ultrasonix RP system and an external vibrator. Voigt's model was used to estimate shear modulus G and viscosity µ of the interrogated tissue. Preliminary analysis demonstrates that symptomatic muscle tissue in subjects with neck pain is stiffer …compared to muscle in control subjects… and that active MTrPs are more viscous …than surrounding tissue…. Latent MTrPs …and surrounding tissue … are more viscous than normal tissue …."

Turo D, Otto P, Shah JP et al. 2013. Ultrasonic characterization of the upper trapezius muscle in patients with chronic neck pain. Ultrason Imaging. 35(2):173-187. "Localization, diagnosis, and clinical outcome measures of painful MTrPs (myofascial trigger points) can be improved by objectively characterizing and quantitatively measuring their properties. The goal of this study was to evaluate whether ultrasound imaging and elastography can differentiate symptomatic (active) MTrPs from normal muscle.....results suggest that active MTrPs have more homogeneous texture and heterogeneous stiffness when compared with normal, unaffected muscle. Our methods enabled us to improve the imaging contrast between suspected MTrPs and surrounding muscle. Our results indicate that in subjects with chronic neck pain and active MTrPs, the abnormalities are not confined to discrete isolated nodules but instead affect the milieu of the muscle surrounding palpable MTrPs. With further refinement, ultrasound imaging can be a promising objective method for characterizing soft tissue abnormalities associated with active MTrPs and elucidating the role of MTrPs in the pathophysiology of MPS."

Turo D, Otto P, Shah JP et al. 2012. Ultrasonic tissue characterization of the upper trapezius muscle in patients with myofascial pain syndrome. Conf Proc IEEE Eng Med Biol Soc. 2012:4386-4389. Myofascial trigger points (MTrPs) are palpable, tender nodules in skeletal muscle that produce symptomatic referred pain when palpated…. Objective characterization and quantitative measurement of the properties of MTrPs can improve their localization and diagnosis, as well as lead to clinical outcome measures. MTrPs associated with soft tissue neck pain are often found in the upper trapezius muscle. We have previously demonstrated that MTrPs can be visualized using ultrasound imaging. The goal of this study was to evaluate whether texture-based image analysis can differentiate structural heterogeneity of symptomatic MTrPs and normal muscle.

Turton, E. P., P. J. Kent and R. C Kester. 1998. The aetiology of Raynaud’s phenomenon. Cardiovasc Surg 6(5):431-40.

Tutoglu A, Boyaci A, Koca I et al. 2014. Quality of life, depression, and sexual dysfunction in spouses of female patients with fibromyalgia. Rheumatol Int. [Jan 9 Epub ahead of print.] "Being a spouse of a patient with fibromyalgia might significantly interfere with quality of life and lead to a high rate of sexual dysfunction. Spouses of patients with fibromyalgia might also be investigated for sexual dysfunction and quality of life. Treatment programs for this group should be considered."

Tuttle N. 2005.  Do changes within a manual therapy treatment session predict between-session changes for patients with cervical spine pain?  Aust J Physiother. 51(1):43-48.  “The results support the use of within-session changes in ROM [range-of-motion], centralization, and possible pain intensity as predictors of between-session changes for musculoskeletal disorders of the cervical spine.”

Tuunainen E, Poe D, Jantti P et al. 2011. Presbyequilibrium in the oldest olds, a combination of vestibular, oculomotor and postural deficits. Aging Clin Exp Res. [Mar 29 Epub ahead of print]. "Progressive loss of balance in the aged, or "presbyequilibrium," is a complex and incompletely understood process involving vestibular, oculomotor, visual acuity, proprioception, motor, organ system and metabolic weaknesses and disorders. These factors provide some potential basis for streamlining the diagnostic evaluation and aiding in planning for effective therapy. In the oldest olds, these problems are magnified, raising the need for additional expertise in their care that could be met by training specialized health care staff." [This study makes a good point. It would be interesting to include myofascial TrPs, a common cause of balance dysfunction, as part of this process. DJS]

Uceyler N, Valenza R, Stock M et al. 2006.   Reduced levels of anti-inflammatory cytokines in patients with chronic widespread pain.  Arthritis & Rheumatism. 54(8):2656-2664.  “Chronic widespread pain is associated with a lack of anti-inflammatory and analgesic Th2 cytokine activity, which may contribute to its pathogenesis.”

Uceyler N, Zeller D, Kahn AK et al. 2013. Small fibre pathology in patients with fibromyalgia syndrome. Brain. [Epub Mar 9]This case control study of 25 patients investigated shape and function of small nerve fibers through punch biopsies of the upper thigh and lower leg, plus patient neurological assessment. FM patients had increased neuropathic findings in questionnaires. Compared with healthy controls and patients with depression, FM patients had impaired small fiber function with increased cold and warm sensation thresholds and increased reaction to touch/pain stimuli. There were a smaller number of unmyelinated nerve fiber bundles in the skin of FM patients compared to the others, although mylinated nerve fibers were equal in all groups. This study indicates that pain in FM has a neuropathic nature.[These patients were not screened for co-existing myofascial trigger points and related microcirculation abnormalities and nerve entrapment. DJS]

Ueda HM, Kato M, Saifuddin M et al. 2002.  Differences in the fatigue of masticatory and neck muscles between male and female.  J Oral Rehabil. 29(6):575-582.  “The purpose of this study was to investigate the nature of fatigue and recovery of masticatory and neck muscles and the differences between sexes in normal subjects during experimentally induced loading.  Significant differences in the recovery ratios between both sexes were more prominent in the masseter muscle than in the SCM.  These results suggest that the differences in muscle endurance between sexes may have some association with higher susceptibility of craniomandibular disorders in females than in males.”

Uemoto L, Antonio C Garcia M, Vinicius D et al. 2013. Laser therapy and needling in myofascial trigger point deactivation. J Oral Sci. 55(2):175-181. Twenty-one women patients with bilateral masseter TrPs were divided into groups to receive either laser therapy, needling with local anesthetic or no treatment (control). The laser and needling groups experienced a significant decrease of pain by visual analogue scale. A significant decrease in pressure pain threshold was experienced by the local anesthetic needling group only. This study indicates that four sessions of needling with 2% lidocaine without vasoconstrictor, with intervals between 48 and 72 hours between treatments, or laser therapy at a dose of 4 J/cm2, effectively deactivated the TrPs.

Uemoto L, Nascimento de Azevedo R, Almeida Alfaya T et al. 2013. Myofascial trigger point therapy: laser therapy and dry needling. Curr Pain Headache Rep. 17(9):357. "The aim of the present review is to discuss two forms of treatment for myofascial pain: laser therapy and dry needling. Although studies have reported the deactivation of myofascial trigger points with these two methods, clinical trials demonstrating their efficacy are scarce. The literature reports greater efficacy with the use of laser over dry needling. It has been suggested that improvements in microcirculation through the administration of laser therapy may favor the supply of oxygen to the cells under conditions of hypoxia and help remove the waste products of cell metabolism, thereby breaking the vicious cycle of pain, muscle spasm and further pain. While laser therapy is the method of choice for patients with a fear of needles and healthcare professionals inexperienced with the dry needling technique, further controlled studies are still needed to prove the greater efficacy of this method."

Ulas UH, Unlu E, Hamamcioglu K et al. 2005. Dysautonomia in fibromyalgia syndrome: sympathetic skin responses and RR Interval analysis.  Rheumatol Int. [Epub ahead of print June 30]  “Sympathetic as well as parasympathetic nervous system dysfunction occurs in FM patients and this abnormality could be determined by SSR [sympathetic skin response] and RRIV [R-R interval variation] analysis.”

Ullrich A, Hauer J, Farin E. 2014. Communication preferences in patients with fibromyalgia syndrome: descriptive results and patient characteristics as predictors. Patient Prefer Adherence. 8:135-145. "Communication with patients with fibromyalgia syndrome (FMS) is often considered difficult. The primary objective of this explorative study was to describe the communication preferences of FMS patients in comparison with other chronic diseases, and the secondary objective was to identify patient-related predictors of those communication preferences….Health care providers who communicate with FMS patients should employ an open and patient-centered communication style, and affective communication components should be adapted to accommodate each patient."

Ulualp S, Brodsky L.  Nasal pain disrupting sleep as a presenting symptom of extraesophageal acid reflux in children.  Int J Pediatr Otorhrinolaryngol 69(11):1555-1557.  Acid reflux caused nasal pain and disrupted sleep in a 4 year old boy.  Treated with acid suppression.  Not tested for TrPs.

Uludag M, Kaparov A, Sari H et al. 2011. Osteopoikilosis associated with fibromyalgia and active myofascial trigger point in upper trapezius muscles. J Back Musculoskel Rehabil. 24(4):257-261. "The sclerosing bone dysplasia known as osteopoikilosis can be associated with fibromyalgia and trigger points." [This is another case of interactive diagnoses. DJS]

Umeda M, Corbin LW, Maluf KS. 2013. Pain mediates the association between physical activity and the impact of fibromyalgia on daily function. Clin Rheumatol. [Sep 13 Epub ahead of print]. "This study quantified the association between recreational physical activity and daily function in women with fibromyalgia, and determined if this association is mediated by symptoms of pain, depression, or body mass….These results indicate that the intensity of musculoskeletal pain, rather than depressive symptoms or body mass, mediates the association between physical activity and daily function among women with fibromyalgia." This study shows that pain itself is the driving factor determining the amount of activity and function in FM women, and it is not the "sedentary nature" or depression that drives the pain.

Umstadt HE. 2002.  [Botulinum toxin in oromaxillofacial surgery]  Mund Kiefer Gesichtschir. 6(4):249-260. [German]  “Abnormal activity of the masticatory or mimic muscular system, whether acquired or congenital, leads to aesthetic and/or functional impairments for the patient. Subsequently, pathological changes of the tissue structure caused by persistent dysfunction can entail chronic pain and progressive aesthetic reduction can induce psychopathological conditions in a patient.  Use of botulinum toxin A can achieve short-term correction of muscular activities with very few side effects if applied in an accurate and controlled manner.”  [Trigger points should be treated with standard management techniques before botulinum toxin is considered. DJS]

Unno N, Fink MP 1998.  Intestinal epithelial hypermobility.  Mechanisms and relevance to disease.  Gastroenterol Clin North Am 27(2):289-307.  Mechanisms and relevance of leaky gut syndrome.

Urata M, Fukuno H, Nomura M et al. 2006.  Gastric motility and autonomic activity during obstructive sleep apnea.  Aliment Pharmacol Ther. 24 Suppl 4:132-140.  “The present study suggested that, in addition to decreased pressure on the pleural cavity, factors affecting the development of RE might include abnormal gastric motility, low oxygen, and increased sympathetic nervous activity during sleep apnea.”

Urban, M. O. and G. F. Gebhart. 1999. Central mechanisms in pain. Med Clin North Am 83(3):585-96.

Uremovic M, Cvijetic S, Pasic MD et al. 2007. Impairment of proprioception after whiplash injury.  Coll Antropol. 31(3):823-827.  “…subject with recent cervical spine injury have incorrect perception of their head position.  Therefore, their rehabilitation should include the correction of proprioception and head coordination.”  [Assessment for associated MTPs in the head and neck, which may adversely affect priprioception, as well as restrict range of motion and cause other symptoms, should be done promptly, and treatment continued until the MTPs are resolved to avoid chronicity if possible. DJS]

Urresti F, Perez LG, Cueco RT. 2007.  Effectiveness of deep dry needling of trigger points in lateral pterigoid muscle.  J Musculoskel Pain 15 (Supp 13):40 item 69.  [Myopain 2007 Poster]  “LPTM (lateral pterygoid muscle) MTP appears to be a common cause of temporomandibular pain.”

Urschitz, MS, Guenther, A, Eggebrecht, E et al.  Snoring, intermittent hypoxia and academic performance in primary school children.  Am J Resp Crit Care Med 168:464-468.  Habitual snoring is significantly associated with poor academic performance.

Ursin, R., I. Endresen, H. Vaeroy and A. M. Hjelmen. 1999. Relations among muscle pain, sleep variables, and depression. J Musculoskel Pain 6(4):59-72.

Ustun N, Arslan F, Mansuroglu A et al. 2013. Efficacy of EMLA cream phonophoresis comparison with ultrasound therapy on myofascial pain syndrome of the trapezius: a single-blind, randomized clinical study. Rheumatol Int. [Oct 23 Epub ahead of print]. This study from Turkey took 50 myofascial pain syndrome patients (42 female and 8 male), and separated them into groups where they received either phonophoresis (PH) with EMLA local anesthetic (2.5% lidocaine, 2.5% prilocaine) cream, or ultrasound (US). The groups received treatment 10 minutes a day for 15 sessions on all active trapezius trigger points. The study found: "EMLA cream phonophoresis is more effective than conventional ultrasound therapy in terms of pain and associated neck disability…"

Usui C, Hatta K, Doi N et al. 2010. Brain perfusion in fibromyalgia patients and its differences between responders and poor responders to gabapentin. Arthritis Res Ther. 12(2):R64. “The present study revealed brain regions with significant hyperperfusion associated with the default-mode network, in addition to abnormalities in the sensory dimension of pain processing and affective-attentional areas in fibromyalgia patients. Furthermore, hyperperfusion in these areas was strongly predictive of poor response to gabapentin.”

Usui C, Doi N, Nishioka M et al. 2006.  Electroconvulsive therapy improves severe pain associated with fibromyalgia.  Pain. 121(3):276-280.  “Several reports have recently suggested the novel concept that fibromyalgia is due to the central nervous system becoming hyper-responsive to a peripheral stimulus....Our study clearly demonstrated that pain was significantly less severe after ECT, as indicated by the VAS scale for pain and the evaluation of TPs. A further notable observation was that thalamic blood flow was also improved.”

Usui C, Doi N, Nishioka M et al. 2006.  Electroconvulsive therapy improves severe pain associated with fibromyalgia.  Pain [Feb 20 Epub ahead of print].

Uvnas-Moberg, K. 1997. Physiological and endocrine effects of social contact. Ann N Y Acad Sci 807:146-163.

Vadivelu N, Mitra S, Narayan D. 2010. Recent advances in postoperative pain management. Yale J Biol Med. 83(1):11-25. “Good pain control after surgery is important to prevent negative outcomes such as tachycardia, hypertension, myocardial ischemia, decrease in alveolar ventilation, and poor wound healing. Exacerbations of acute pain can lead to neural sensitization and release of mediators both peripherally and centrally. Clinical wind up occurs from the processes of N-Methyl D-Aspartate (NMDA) activation, wind up central sensitization, long-term potentiation of pain (LTP), and transcription-dependent sensitization. Advances in the knowledge of molecular mechanisms have led to the development of multimodal analgesia and new pharmaceutical products to treat postoperative pain. The new pharmacological products to treat postoperative pain include extended-release epidural morphine and analgesic adjuvants such as capsaicin, ketamine, gabapentin, pregabalin dexmetomidine, and tapentadol. Newer postoperative patient-controlled analgesia (PCA) in modes such as intranasal, regional, transdermal, and pulmonary presents another interesting avenue of development.”  [This paper stresses the importance of acute pain control to help prevent central sensitization. When patients already are in a central sensitization state such as FM, such pain control is critical. DJS]

Vadivelu N, Hines RL. 2008.  Management of chronic pain in the elderly: focus on transdermal buprenorphine.  Clin Interv Aging. 3(3):421-430.  “The transdermal buprenorphine matrix allows for slow release of buprenorphine and damage does not produce dose dumping.  In addition, the long-acting analgesic property and relative safety profile makes it a suitable choice for the treatment of chronic pain in the elderly.  Its safe use in the presence of renal failure makes it an attractive choice for older individuals.  Recent scientific studies have shown no evidence of a ceiling dose of analgesia in man but only a ceiling effect for respiratory depression, increasing its safety profile.  It appears that transdermal buprenorphine can be used in clinical practice safely and efficaciously for treating chronic pain in the elderly.”

Vadivelu N, Mitra S, Schermer E et al. 2014. Preventive analgesia for postoperative pain control: a broader concept. Local Reg Anesth. 7:17-22. "Preventive analgesia reduces postoperative pain and consumption of analgesics, and this appears to be the most effective means of decreasing postoperative pain. Preventive analgesia, which includes multimodal preoperative and postoperative analgesic therapies, results in decreased postoperative pain and less postoperative consumption of analgesics."

Vaeroy, H., T. Sakurada, O. Forre, E. Kass and L. Terenius. 1989. Modulation of pain in fibromyalgia (fibrositis syndrome): cerebral spinal fluid (CFS) investigation of pain related neuropeptides with special reference to calcitonin gene related peptide (CGRP). J Rheumatol Suppl 19:94-97.

Vaeroy, H., A. Abrahamsen, O. Forre and E. Kass. 1989. Treatment of fibromyalgia (fibrositis syndrome): a parallel double-blind trial with carisoprodol, paracetamol and caffeine (Somadrilcomp) versus placebo. Clin Rheumatol 8(2):245-250.

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Valdés M, Collado A, Bargalló N et al. 2010. Increased glutamate-glutamine compounds (Glx) in the brain of patients with fibromyalgia: A MR spectroscopy study. Arthritis Rheum. [Feb 26 Epub ahead of print]  Fibromyalgia (FM) has been defined as a systemic disorder clinically characterized by pain, cognitive deficit and the presence of associated psychopathology, all of which are suggestive of a primary brain dysfunction. In order to identify the nature of this cerebral dysfunction, brain metabolites of FM patients have been studied through MR spectroscopy techniques. METHODS: Brain metabolites in amygdala, thalami and prefrontal cortex were studied through MR spectroscopy techniques in a sample of 28 women with FM, and in a control group of healthy women (n=24) of the same age. RESULTS:: Compared to healthy controls FM patients showed higher levels of glutamate compounds (Glx) (11,9+/-1,6 vs. 13,4+/-1,7 arbitrary institutional units respectively, t= 2.517, df 35, p=0.03) and a higher glutamine-glutamate/creatine ratio (Glx/Cr) (2,1+/- 0,4 in controls vs. 2,4 +/- 1,4 in FM patients, t=2.373, df 35, p=0.04) in the right amygdala. In FM patients with more pain, fatigue and depressive symptoms inositol (Ins) levels were significantly higher in the right amygdala and right thalamus. CONCLUSIONS: The distinctive metabolic features found in the right amygdala of FM patients suggest the possible existence of a neural dysfunction in emotional processing, this being a prolongation of the dysfunction in pain processing previously proposed by some authors.

Valencia-Flores M, Cardiel MH, Santiago V et al. 2004. Prevalence and factors associated with fibromyalgia in Mexican patients with systemic lupus erythematosus.  Lupus 13(1):4-10.  “Fibromyalgia is not common in Mexican patients with SLE and has a different pattern of symptoms in RP (regional pain) and NP (no pain) patients.  These data add evidence that ethnicity can play an important role in FM manifestations.” 

Valenza MC, Rodenstein DO, Fernandez-de-las-Penas C. 2011. Consideration of sleep dysfunction in rehabilitation. J Bodyw Mov Ther. 15(3):262-267. Patients with whiplash commonly have neck pain that is contributory to sleep disturbance. There is a direct relationship between pain intensity and worsening sleep quality. It is essential to treat both the causes of the pain and the sleep dysfunction components as part of management of these patients.

Valenza MC, Valenza G, Gonzalez-Jimenez E et al. 2011. Alteration in sleep quality in patients with mechanical insidious neck pain and whiplash-associated neck pain. Am J Phys Med Rehabil. [Dec 14 Epub ahead of print]. "Sleep disturbances are a common finding in individuals with neck pain and are associated with the intensity of ongoing pain in WAD (whiplash)." Inadequate sleep quality and quantity can contribute to multi-system effects. "It seems essential to address the ongoing cycle of pain and sleep disturbances as an integral part of the treatment of patients with neck pain."

Valim, V., Oliveira, L., Suda, A., et al. 2003.  Aerobic fitness effects in fibromyalgia.  J Rheumatol 30(5):1060-1069.  “...aerobic exercise is beneficial to patients with FM, but the cardiorespiratory gain is not related to improvement of FM symptoms.”

Valkeinen H, Hakkinen A, Alen M et al. 2007.  Physical fitness in postmenopausal women with fibromyalgia.  Int J Sports Med. [Oct 24 Epub ahead of print].  “A lower maximal load in the aerobic test suggests the patients’ unsatisfactory ability to stand physical loading and resist overall fatigue.  Moreover, fatigue rather than pain was the main factor to decrease the quality of life in women with fibromyalgia.  Additional efforts should be addressed to strength training, when planning health promotion and rehabilitation programs in fibromyalgia.”  [These results may be suspect as there is no allowance for co-existing MTPs that could be affecting the results.  Also, strength training, if there are MTPs, will only make them worse.  You can’t strengthen a muscle that is physiologically inhibited by MTPs.  DJS]

Vallbona, C., C. F. Hazelwood and G. Jurida. 1997. Response of pain to static magnetic fields in post-polio patients: a double-blind pilot study. Arch Phys Med Rehabil 78(11):1200-1203.

Vallejo M, Martinez-Martínez LA, Grijalva-Quijada S et al. 2013. Prevalence of fibromyalgia in vasovagal syncope. J Clin Rheumatol. 19(3):111-114. "Fibromyalgia was relatively frequent in these women with vasovagal syncope and could be associated with dysautonomic symptoms. Therefore, it seems important to search for dysautonomic comorbidities in patients with vasovagal syncope and/or fibromyalgia, to provide a patient-centered holistic approach, instead of the often currently used therapeutic partition."

Valouchova P, Lewit K. 2009.  Surface electromyography of abdominal and back muscles in patients with active scars.  J Bodywork Move Ther. 13(3):262-267.  Abdominal scars may significantly impair back mobility and add to clinical symptoms.   These scars and the tissue around them can often be treated successfully with manual methods, and this study gives objective data of surface electromyography to show this.  The “…muscles surrounded by active scar tissue are likely to harbour trigger points.”

Valrie CR, Bromberg MH, Palermo T et al. 2013. A systematic review of sleep in pediatric pain populations. J Dev Behav Pediatr. 34(2):120-128. "Findings from this review highlight the need to assess and treat sleep problems in children presenting with persistent pain. Health care providers should consider conducting routine sleep screenings, including a comprehensive description of sleep patterns and behaviors obtained through clinical interview, sleep diaries, and/or the use of standardized measures of sleep. Future research focusing on investigating the mechanisms associating sleep and pediatric persistent pain and on functional outcomes of poor sleep in pediatric pain populations is needed."

Van Cauter E, Holmback U, Knutson K et al. 2007.  Impact of sleep and sleep loss on neuroendocrine and metabolic function.  Horm Res. 67 Suppl 1:2-9.  “Laboratory studies in healthy young volunteers have shown that experimental sleep restriction is associated with a dysregulation of the neuroendocrine control of appetite consistent with increased hunger and with alterations in parameters of glucose tolerance suggestive of an increased risk of diabetes.  Epidemiologic findings in both children and adults are consistent with the laboratory data.”  Deep sleep has a significant effect on hormones.

Van Cauter E, Latta F, Nedeltcheva A et al.  2004.  Reciprocal interactions between the GH axis and sleep.  Growth Horm IGF Res. 14 Suppl A:S10-7.  “Preliminary data show decreased total sleep time and increased sleep fragmentation in GH-deficient patients as compared with normal controls.”

Van Cauter, E., L. Plat and G. Copinschi. 1998. Interrelations between sleep and the somatotropic axis. Sleep 21(6):553-66.

Van Daele DJ, McCulloch TM, Palmer PM et al. 2005.  Timing of glottic closure during swallowing: a combined electromyographic and endoscopic analysis.  Ann Otol Rhinol Laryngol. 114(6):478-487.  [This article indicates why TrPs in some of the area muscles could have some patients choking on their own saliva, “swallowing the wrong way".    In such cases, it may be wise to check the thyroarytenoid and other area muscles for TrPs.]

van de Glind G, de Vries M, Rodenburg R et al. 2007.  Resting muscle pain as the first clinical symptom in children carrying the MTTK A8344G mutation.  Eur J Paediatr Neurol. [Feb 9 Epub ahead of print]  “Fatigue in combination with recurrent resting muscle pain occurs frequently in the initial phase of various hereditary muscle disorders and in several autoimmune, endocrine and metabolic syndromes.  In the absence of obvious biochemical/metabolic abnormalities and in the lack of neurological symptoms, the complaints are frequently labeled as fibromyalgia or chronic fatigue syndrome.”  [We certainly need more research into genetic mitochondrial defects.  DJS]

van Denderen, J. C. , J. W. Boersma, P. Zeinstra, A. P. Hollander and B. R. van Neerbos. 1992. Physiolgical effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity? Scand J Rheumatol 21(1):35-7.

van der Esch M, Holla JF, van der Leeden M et al. 2014. Decrease of muscle strength is associated with increase of activity limitations in early knee osteoarthritis: 3-year results from the Cohort Hip and Cohort Knee study. Arch Phys Med Rehabil. [Jun 27 Epub ahead of print.] "In patients with early knee OA, decreased muscle strength is associated with an increase in activity limitations. Our results are a step towards understanding the role of muscle weakness in the development of activity limitations in knee OA. Further, well-designed experimental studies are indicated to establish the causal role of muscle weakness in activity limitations." [Myofascial trigger points co-exist with OA, and often cause the muscle weakness and proprioceptive dysfunctions described. It would be of value to have these patients assessed for TRPs, as the symptoms might be relieved with treatment of TrPs. DJS]

Vanderweeen L, Oostendorp RA, Vaes P et al. 1996.  Pressure algometry in manual therapy.  Man Ther. 1(5):258-265.

Van de Ven TJ, John Hsia HL. 2012. Causes and prevention of chronic postsurgical pain. Curr Opin Crit Care [Jun 22 Epub ahead of print]. "Surgical incision invariably causes some measure of nerve damage and inflammatory response that, in most cases, heals quickly without long-term negative consequence. However, a subset of these patients go on to develop lasting neuropathic pain that is difficult to treat and, in many cases, prevents the return to normal activities of life. It remains unknown why two patients with identical surgical interventions may go on to develop completely divergent pain phenotypes or no pain at all. Aggressive, early analgesic therapy has been shown to reduce the incidence of chronic postsurgical pain (CPSP), but no specific regional anesthetic technique or systemic pharmacologic therapy has been shown to prevent CPSP....Inflammation and glial cell activation have recently been shown to be just as important in the transition from normal acute pain to pathologic chronic pain as nerve injury itself and that central sensitization may not be solely due to repetitive nociceptive firing at the time of nerve injury. This has opened a number of new therapeutic possibilities for prevention of CPSP....Here, we discuss the causes of CPSP and current useful preventive strategies in the perioperative period. We also discuss future potential disease-modifying treatments of CPSP." [Since glial cells in the spinal cord have been implicated in the development of central sensitization states such as fibromyalgia, this is of interest. Histamine levels, microcirculation, and other factors affecting TrP development may be part of the answer to this puzzle. DJS]

Van Gheluwe B, Dananberg HJ, Hagman F et al. 2006.  Effects of hallux limitus on plantar foot pressure and foot kinematics during walking.  J Am Podiatr Med Assoc 96(5):428-436.  [Stiffness or contracture of the hallicis muscles, such as that due to myofascial TrPs, although largely ignored in the literature, could be a major source of gait irregularities and foot dysfunction. DJS]

Van Handel D, Fass R. 2005.  The pathophysiology of non-cardiac chest pain.  J Gastroenterol Hepatol. 20 Suppl 3:S6-S13.  Gastroesophageal reflux disease (GERD) is the most common cause of non-cardiac pain.  [But what is causing the GERD?  It would have been helpful if these patients had been checked for abdominal TrPs. DJS]

Van Houdenhove B, Luyten P. 2006.  Stress, depression and fibromyalgia.  Acta Neurol Belg. 106(4):149-156.

Van Houdenhove B, Neerinckx, E, Onghena P et al. 2002. Daily hassles reported by chronic fatigue syndrome and fibromyalgia patients in tertiary care: a controlled quantitative and qualitative study.  Psychother Psychosom 71(4):207-13. Patients with Chronic Fatigue Syndrome and FM show "a higher frequency of hassles, higher emotional impact and higher fatigue, pain depression and anxiety levels than patients with RA or MS."  The cause of the hassles are "dissatisfaction with oneself, insecurity and a lack of social recognition."  "An optimal therapeutic approach of CFS and FMS should take account of this heavy psychosocial burden, which might refer to core themes of these patients' experiences."

Van Koulil S, Kraaimaat FW, van Lankveld W et al. 2009. A patient’s perspective on multidisciplinary treatment gain for fibromyalgia: an indicator for pre-post treatment effects? Arthritis Rheum. 61(12):1626-1632.  “Results suggest that the patient’s perception of treatment gain and pre-post changes in outcomes during treatment assess different aspects of the patient’s perception of treatment gain as an independent and clinically relevant outcome, in addition to standardized trial data of pre-post assessments of health outcomes.”

van Laarhoven A, Kraaimaat F, Wilder-Smith O. 2007.  Generalized and symptom-specific sensitization of chronic itch and pain.  J Eur Acad Dermatol Venereol. 21(9):1187-1192.  “The present study provides preliminary support that both generalized and symptom-specific sensitization processes play a role in the regulation and processing of somatosensory stimulation of patients with chronic itch and pain.”

Van Middendorp H, Lumley MA, Moerbeek M et al. 2009.  Effects of anger and anger regulation styles on pain in daily life of women with fibromyalgia: a diary study.  Eur J Pain. [Apr 16 Epub ahead of print].  “Our study suggests that anger and a general tendency to inhibit anger predicts heightened pain in the everyday life of female patients with fibromyalgia.  Psychological intervention could focus on healthy anger expression to try to mitigate the symptoms of fibromyalgia.”

van Oosterwijck J, Meeus M, Paul L et al. 2013. Pain physiology education improves health status and endogenous pain Inhibition in fibromyalgia: A double-blind randomized controlled trial. Clin J Pain. [Jan 30 Epub ahead of print]. "These results suggest that FM patients are able to understand and remember the complex material about pain physiology. Pain physiology education seems to be a useful component in the treatment of FM patients as it improves health status and endogenous pain inhibition in the long term."

Van Oosterwijck J, Nijs J, Meeus M et al. 2012. Evidence for central sensitization in chronic whiplash: A systematic literature review. Eur J Pain. [Sep 25 Epub ahead of print]. "It has been suggested that sensitization of the central nervous system plays an important role in the development and maintenance of chronic (pain) complaints experienced by whiplash patients. According to the PRISMA guidelines, a systematic review was performed to screen and evaluate the existing clinical evidence for the presence of central sensitization in chronic whiplash....These studies evaluated the sensitivity to different types of stimuli (mechanical, thermal, electrical). Findings suggest that although different central mechanisms seem to be involved in sustaining the pain complaints in whiplash patients, hypersensitivity of the central nervous system plays a significant role.....international guidelines for the definition, clinical recognition, assessment and treatment of central sensitization are warranted."

van Uden-Kraan CF, Drossaert CH, Taal E et al. 2010. Patient-initiated online support groups: motives for initiation, extent of success and success factors. J Telemed Telecare. 16(1):30-34. “We studied the success and success factors of online support groups (OSGs) for patients, and the motives and goals of people who start such groups. We interviewed 23 webmasters of OSGs for patients with breast cancer, fibromyalgia and arthritis. The majority were women (n = 20) and most were patients (n = 21). Analysis of the interviews revealed that webmasters had altruistic and intrinsic motives for initiating an online support group. They defined success as the fulfillment of the goals they had in mind when they initiated their groups. To be able to make a group successful, decisions about its organization and management need to be coherent with these goals. Most webmasters stressed that promoting the group, keeping it alive and moderating the messages were vital success factors during the evolution stage. Management of the OSGs took up much of the webmasters' time and energy. On average webmasters were occupied with the group for 10-15 hours a week. Our study provides an overview of the pros and cons of differing decisions that have to be made when initiating an OSG.”

van Uden-Kraan CF, Drossaert CH, Taal E et al. 2008.  Empowering processes and outcomes of participation in online support groups for patients with breast cancer, arthritis, or fibromyalgia.  Qual Health Res. 18(3):405-417.  “Empowering outcomes mentioned were being better informed; feeling confident in the relationship with their physician, their treatment, and their social environment; improved acceptance of the disease; increased optimism and control; enhanced self-esteem and social well-being; and collective action.”  “...participation in online support groups can make a valuable contribution to the emergence of empowered patients.” [It is vitally important that the support groups be positive and empowering.   Negative groups that are exclusive or stressful can have an equally undermining effect on patient quality of life. DJS]

Van Wilgen CP, Dijkstra PU, Van Der Laan BF et al. 2004.  Morbidity of the neck and head and neck cancer therapy.  Head Neck 26(9):785-791.  The authors found that 46% of the post-surgery cancer patients had myofascial pain.  [This indicates that at least some of the pain, loss of range of motion and muscle weakness the patients with co-existing myofascial pain sustained could be either eliminated or minimized by adequate treatment of the myofascial component. DJS]

van Wilgen CP, Keizer D. 2012. The sensitization model to explain how chronic pain exists without tissue damage. Pain Manag Nurs. 13(1):60-65. "The interaction of nurses with chronic pain patients is often difficult. One of the reasons is that chronic pain is difficult to explain, because no obvious anatomic defect or tissue damage is present. There is now enough evidence available indicating that chronic pain syndromes such as low back pain, whiplash, and fibromyalgia share the same pathogenesis, namely, sensitization of pain modulating systems in the central nervous system. Sensitization is a neuropathic pain mechanism in which neurophysiologic changes may be as important as behavioral, psychological, and environmental mechanisms. The sensitization model provides nurses with an opportunity to explain pain as a physical cause related to changes in the nervous system. This explanation may improve the patient's motivation to discuss the importance of psychosocial factors that contribute to the maintenance of chronic pain. In this article, sensitization is described as a model that can be used for the explanation of the existence of chronic pain. The sensitization model is described using a metaphor. The sensitization model is a useful tool for nurses in their communication and education toward patients."

Vanhala, M. 1999.  Childhood weight and metabolic syndrome in adults.  Ann Med 31(4):236-9.

Varani, K, F Portaluppi, S Merighi, F Ongini, L Belardinelli and PA Borea. 1999.  Caffeine alters A2A adenosine receptors and their function in human platelets.  Circulation 99(19):2499-502.

Vargas A, Vargas A, Hernandez-Paz R et al. 2006.  Sphygmomanometry-evoked allodynia – a simple bedside test indicative of fibromyalgia: a multicenter developmental study.  J Clin Rheumatol. 12(6):272-274.  “Sphygmomanometry is a simple bedside test that may be useful in the recognition of patients with FM….Based on our results, we suggest searching for FM features in any person who has sphygmomanometry-evoked allodynia.”  [This article unfortunately fails to recognize that this method, possibly an easy, inexpensive way to diagnose FMS, was discovered and developed by JB Eisenger. DJS]

Vargas A, Vargas A, Hernandez-Paz R et al. 2006.  Sphygmomanometry-evoked allodynia – a simple bedside test indicative of fibromyalgia: a multicenter developmental study.  J Clin Rheumatol. 12(6):272-274.  “Sphygmomanometry is a simple bedside test that may be useful in the recognition of patients with FM.  Blood pressure testing is a universal procedure in all clinical environments.  Based on our results, we suggest searching for FM features in any person who has sphygmomanometry-evoked allodynia.”  [This supports the work of JB Eisinger and his discovery that FMS may be diagnosed by blood pressure test evoked pain. DJS]

Vargas-Alarcon G, Alvarez-Leon E, Fragoso JM et al. 2012. A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia. BMC Musculoskel Disord. 13(1):23. "A consistent line of investigation suggests that autonomic nervous system dysfunction may explain the multi-system features of fibromyalgia (FM); and that FM is a sympathetically maintained neuropathic pain syndrome....The aim of this study was to search for an association between fibromyalgia and several SCN9A sodium channels gene polymorphisms....We studied 73 Mexican women suffering from FM and 48 age-matched women who considered themselves healthy....In this ethnic group; a disabling form of FM is associated to a particular SCN9A sodium channel gene variant. These preliminary results raise the possibility that some patients with severe FM may have a dorsal root ganglia sodium channelopathy."

Vargas-Alarcon G, Fragoso JM, Cruz-Robies D et al. 2009.  Association of adrenergic receptor gene polymorphisms with different fibromyalgia syndrome domains.  Arthritis Rheum. 60(7):2169-2173.  “AR (adrenergic receptor) gene polymorphisms are related to the risk of developing FM and are also linked to different domains of the FM syndrome.”

Vaz C, Couto M, Duarte C et al. 2009.  [An unusual case of generalized pain: paramyloidosis simulating fibromyalgia]  Acta Reumatol Port. 34(2B):431-435.  [Portuguese] [Fibromyalgia central sensitization is maintained by something, whether it be myofascial TrP pain or another underlying co-existing condition.   Diagnosis does not stop with a FM label but must include searching for the cause of the central sensitization.  DJS]

Vecchiet L, Vecchiet J, Giamberardino MA. 1999.  Referred muscle pain: clinical and pathophysiologic aspects.  Curr Rev Pain 3(6):489-498.  Referred pain is common in medicine, and the average practitioner in general practice encounters it frequently.  [One wonders why the concept of referred pain from myofascial TrPs is met with such resistance. DJS]

Vecchiet, L, J Vecchiet, R Bellomo, and MA Giamberardino. 1999.  Muscle pain from physical exercise. J Musculoskel Pain 7(1-2):43-63.

Vecsei, L., G. Dibo and C. Kiss. 1998. Neurotoxins and neurodegenerative disorders. Neurotoxicology 19(4-5):511-4.

Velazquez KT, Mohammad H, Sweitzer SM. 2007.  Protein kinase C in pain: involvement of multiple isoforms.  Pharmacol Res. 55(6):578-589.  “Protein kinase C isozymes are under investigation as potential therapeutics for the treatment of chronic pain conditions.”  “…protein kinase C may function as a master regulator of the peripheral and central sensitization that underlies many chronic pain conditions.”

Veldhuijzen DS, Sondaal SF, Oosterman JM. 2012. Intact cognitive inhibition in patients with fibromyalgia but evidence of declined processing speed. J Pain. 13(5):507-515. "Patients with fibromyalgia frequently report cognitive complaints. In this study we examined performance on 2 cognitive inhibition tests, the Stroop Color-Word Test (SCWT) and the Multi-Source Interference Test (MSIT), in 35 female patients with fibromyalgia and 35 age-matched healthy female controls....For patients, pain ...correlated significantly to several indices of cognition. Psychosocial variables were not related to cognitive test performance. Fibromyalgia patients performed worse on both tests but to a similar extent for the neutral condition and the interference condition, indicating that there is no specific problem in cognitive inhibition. Evidence of decreased mental processing and/or psychomotor speed was found in patients with fibromyalgia. PERSPECTIVE: Fibromyalgia patients performed worse on interference tests, but no specific problem in cognitive inhibition was found. Decreased reaction time performance may instead point to an underlying problem of psychomotor or mental processing speed in fibromyalgia. Future studies should examine potential deficits in psychomotor function in fibromyalgia patients in more detail."

Velly AM, Look JO, Schiffman E et al. 2010. The effect of fibromyalgia and widespread pain on the clinically significant temporomandibular muscle and joint pain disorders – a prospective 18-month cohort study. J Pain. [May 11 Epub ahead of print]. “Fibromyalgia and widespread pain should receive important consideration when evaluating and developing a treatment plan for patients with TMJD (temporomandibular muscle and joint disorders).” [Consistent with current research, any chronic pain generator may promote central sensitization. What is needed is to look for the causes of the chronic pain, such as trigger points (often cause or contributor to TMJD), and treat them as promptly and effectively as possible and bring perpetuating factors under control. DJS]

Vendrig, A. A., P. F. van Akkerveeken and K. R. McWhorter. 2000. Results of a multi-modal treatment program for patients with chronic symptoms after a whiplash injury of the neck. Spine 25(2):238-44.

Venancio Rde A, Alencar FG Jr, Zamperini C. 2009.  Botulinum toxin, lidocaine, and dry-needling injections in patients with myofascial pain and headaches.  Cranio. 27(1):46-53.  “Statistically, all the groups showed favorable results for the evaluated requisites…, except for the use of rescue medication and local post injection sensitivity….”  “Considering its reduced cost, lidocaine could be adopted as a substance of choice, and botulinum toxin should be reserved for refractory cases, in which the expected effects could not be achieved, and the use of a more expensive therapy would be mandatory.”

Vera-Portocarrero LP, Zhang ET, Ossipov MH et al. 2006.  Descending facilitation from the rostral ventromedial medulla maintains nerve injury-induced central sensitization.  Neuroscience [Apr 27 Epub ahead of print]  “The results demonstrate the novel concept that once initiated, maintenance of nerve injury-induced central sensitization in the spinal dorsal horn requires descending pain facilitation mechanisms arising from the rostral ventromedial medulla.”  [Researchers are zeroing in on the mechanisms behind central sensitization.  This may give us more of a chance to control it.   DJS]

Vergne-Salle P, Dufauret-Lombard C, Bonnet C et al. 2010. A randomized, double-blind, placebo-controlled trial of dolasetron, a 5-hydroxytryptamine 3 receptor antagonist, in patients with fibromyalgia. Eur J Pain. [Oct 29 Epub ahead of print]. "Reduction in pain intensity... was significantly greater in dolasetron-treated patients...compared with placebo controls..... The most common adverse events were constipation, nausea, dizziness and headache, with no significant differences between the two groups. Intermittent IV dolasetron was safe and efficacious for the reduction of pain intensity associated with FM at 3months."

Verne GN, Robinson ME, Vase L et al. 2003.  Reversal of visceral and cutaneous hyperalgesia by local rectal anesthesia in irritable bowel syndrome (IBS) patients.  Pain 105(1-2):223-30. This article deals with altered visceral perception in IBS.  The researchers found that using topical anesthetic (lidocaine) rectally effectively decreased visceral and cutaneous hyperalgesia in these patients.  They concluded that this was a central blockade, but perhaps topical application of lidocaine on area myofascial trigger points could have been involved.  More medical researchers need to become aware of the reality and scope of myofascial trigger points.

Vgontzas A.N., Papanicolaou D.A., Bixler, E.O., Hopper K., Lotsikas A., Lin H.M., Kales A., Chrousos G.P. 2000. Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia. J. Clin Endocrinol Metab. 85(3):1151-8. Sleep apnea is associated with daytime sleepiness and fatigue, abdominal obesity, and insulin resistance.

Vgontzas, A. N. and A. Kales. 1999. Sleep and its disorders. Annu Rev Med 50:387-400.

Vgontzas, A. N. , G. Mastorakos, E. O. Bixter, A. Kales, P. W. Gold and G. P. Chrousos. 1999. Sleep deprivation effects on the activity of the hypothalamus-pituitary-adrenal and growth axes: potential clinical implications. Clin Endocrinol (Oxf) 51(2):205-215.

Viane I, Crombez G, Eccleston C et al. 2003.  Acceptance of pain is an independent predictor of mental well-being in patients with chronic pain: empirical evidence and reappraisal.  “Acceptance of chronic pain is best conceived of as the shift away from pain to non-pain aspects of life, and the shift away from a search for a cure with an acknowledgment that pain may not change.”

Vicennati, V., Pasquali R. 2000. Abnormalities of the hypothalamic-pituitary-adrenal axis in nondepressed women with abdominal obesity and relations with insulin resistance: evidence for a central and a peripheral alteration. J. Clin Endocrinol Metab 85(11):4093-8. HPA-axis dysfunction is associated with abdominal obesity and insulin resistance. [HPA-axis dysfunction is also associated with FMS. DJS].

Vierck CJ Jr. 2006.  Mechanisms underlying development of spatially distributed chronic pain (fibromyalgia).  Pain [Jul 12 Epub ahead of print]   “It appears that central mechanisms of FM pain are dependent on abnormal peripheral input(s) for development and maintenance of this condition.”

Vierck CJ Wong F, King CD et al. 2013. Characteristics of Sensitization Associated With Chronic Pain Conditions. Clin J Pain. [Apr 25 Epub ahead of print]. "The widespread sensitization for irritable bowel syndrome and TMD participants does not rely on mechanisms of spatial and temporal summation often invoked to explain widespread hyperalgesia associated with chronic pain. Increased sensitivity during descending series of stimulation of an arm or leg but not the face indicates a propensity for sensitization of nociceptive input to the spinal cord. Abnormally prolonged sensitization for FM participants reveals a unique influence of widespread chronic pain referred to deep somatic tissues."

Vilar B, Busserolles J, Ling B et al. 2013. Alleviating Pain Hypersensitivity through Activation of Type 4 Metabotropic Glutamate Receptor. J Neurosci. 33(48):18951-18965. "Hyperactivity of the glutamatergic system is involved in the development of central sensitization in the pain neuraxis, associated with allodynia and hyperalgesia observed in patients with chronic pain. Herein we study the ability of type 4 metabotropic glutamate receptors (mGlu4) to regulate spinal glutamate signaling and alleviate chronic pain. We show that mGlu4 are located both on unmyelinated C-fibers and spinal neurons terminals in the inner lamina II of the spinal cord where they inhibit glutamatergic transmission through coupling to Cav2.2 channels. Genetic deletion of mGlu4 in mice alters sensitivity to strong noxious mechanical compression and accelerates the onset of the nociceptive behavior in the inflammatory phase of the formalin test. However, responses to punctate mechanical stimulation and nocifensive responses to thermal noxious stimuli are not modified. Accordingly, pharmacological activation of mGlu4 inhibits mechanical hypersensitivity in animal models of inflammatory or neuropathic pain while leaving acute mechanical perception unchanged in naive animals. Together, these results reveal that mGlu4 is a promising new target for the treatment of chronic pain."

Villa, M., P. Mustarelli and M. Caprotti. 1991. Biological effects of magnetic fields. Life Sci 49(2):85-92.

Villalon P, Arzola JF, Valdivia J et al. 2013. The occlusal appliance effect on myofascial pain. Cranio. 31(2):84-91. "There are limited studies about the effects of occlusal appliance (OA) after three months of use. This study aimed to compare myofascial pain (MP) according to RDC/TMD, craniocervical relationships (CR) and masseter and temporalis bilateral electromyographic (EMG) activity, before and after three months of occlusal appliance use. Nineteen patients participated in this study. Cephalometric and RDC/TMD diagnostics were performed previously (baseline) and at the end of the study period (three months). EMG recordings at clinical mandibular rest position (MRP), during swallowing of saliva (SW) and during maximum voluntary clenching (MVC) were performed as follows: after one hour of use of an OA; after three months of using the OA for a minimum of 16 hours each day; and immediately after removal from the mouth. MP was relieved in all patients at the end of the study period. CR did not change significantly between baseline and after removal of the OA at the end of the study period. EMG activity during MRP, SW, and MVC decreased in both muscles after one hour using the OA and maintained the same level for the three-month period. When comparing baseline versus final EMG activity without OA, a significant decrease was only observed in the masseter muscle. The results observed in the present study are relevant to clinicians because they imply that the therapeutic effect of OA does not significantly affect the homeostasis of the craniocervical system."

Vincent A, Clauw D, Oh TH et al. 2014. Decreased physical activity attributable to higher body mass index influences fibromyalgia symptoms. PM R. [Feb 14 Epub ahead of print.] "The relationship between BMI and fibromyalgia impact was almost fully accounted for by physical factors and not psychological factors….Despite patient report that pain hinders physical activity, clinicians who encounter patients with fibromyalgia, particularly patients with increased BMI, should be cognizant to invest time and resources to counsel patients on physical factors (i.e., physical activity) that could improve the patient's symptom experience."

Vincent A, Whipple MO, Luedtke CA et al. 2011. Pain and other symptom severity in women with fibromyalgia and a previous hysterectomy. J Pain Res. 4:325-329. "Pain and other fibromyalgia symptom severity were worse in women who had had a hysterectomy with or without an oophorectomy." [It would be interesting if the Mayo Clinic did a companion study, taking into account the reason for the surgery. Many FM patients have significant pelvic pain and other symptoms due to a variety of co-existing conditions. DJS]

Viola-Saltzman M, Watson NF, Bogart A et al. 2010. High prevalence of restless legs syndrome among patients with fibromyalgia: a controlled cross-sectional study. J Clin Sleep Med. 6(5):423-427. "There is a higher prevalence and odds of RLS in those with FM compared to controls. Clinicians should routinely query FM patients regarding RLS symptoms because treatment of RLS can potentially improve sleep and quality of life in these patients." [One must wonder how many of these patients also have TrPs, as TrPs have been shown to be a factor in RLS, and these patients were not checked for co-existing TrPs. DJS]

Vitton O, Gendreau M, Gendreau J et al. 2004.  A double-blind placebo-controlled trial of milnacipran in the treatment of fibromyalgia.  Hum Psychopharmacol. 19(S1):S27.  Mililcipran may have the potential to reduce several FMS symptoms, including pain.  [Minilcipran, affecting norepinephrine and serotonin as an SNRI, has a 3:1 effect ratio of norepinephrine to serotonin. Effexor has a 1:3 ratio. DJS]

Vitali, C., A. Tavoni, B. Rossi, E. Bibolotti, C. Giannini, L. Puzzuoli, R. Cacialli and G. Pasero. 1989. Evidence of neuromuscular hyperexcitability features in patients with primary fibromyalgia. Clin Exp Rheumatol 7(4):385-390.

Vizi, E. S. and B. Lendvai. 1999. Modulatory role of presynaptic nicotinic receptors in synaptic and non-synaptic chemical communication in the central nervous system. Brain Res Brain Res Rev 30(3):219-35.

Volkers L, Mechioukhi Y, Coste B. 2014. Piezo channels: from structure to function. Pflugers Arch. [Jul 20 Epub ahead of print.] "Mechanotransduction is the conversion of mechanical stimuli into biological signals. It is involved in the modulation of diverse cellular functions such as migration, proliferation, differentiation, and apoptosis as well as in the detection of sensory stimuli such as air vibration and mechanical contact. Therefore, mechanotransduction is crucial for organ development and homeostasis and plays a direct role in hearing, touch, proprioception, and pain. Multiple molecular players involved in mechanotransduction have been identified in the past, among them ion channels directly activated by cell membrane deformation. Most of these channels have well-established roles in lower organisms but are not conserved in mammals or fail to encode mechanically activated channels in mammals due to non-conservation of mechanotransduction property. A family of mechanically activated channels that counts only two members in human, piezo1 and 2, has emerged recently. Given the lack of valid mechanically activated channel candidates in mammals in the past decades, particular attention is given to piezo channels and their potential roles in various biological functions. This review summarizes our current knowledge on these ion channels."

Volkmann, H., J. Norregaard, S. Jacobsen, B. Danneskiold-Samsoe, G. Knoke and D. Nehrdich. 1997. Double-blind, placebo-controlled cross-over study of intravenous A-adenosyl-L-methionine in patients with fibromyalgia. Scand J Rheumatol 26(3):206-11.

Vollestad NK, Mengshoel AM. 2005.  Relationships between neuromuscular functioning, disability and pain in fibromyalgia.  Disabil Rehabil. 27(12):667-673. 

Volonte C, Amadio S, Cavaliere F et al. 2003.  Extracellular ATP and neurodegeneration.  Curr Drug Targets CNS Neurol Disord. 2(6):403-412.   “...extracellular ATP plays a very complex role not only in the repair, remodeling and survival occurring in the nervous system, but even in cell death and this can occur either after normal developmental conditions, after injury, or acute and chronic diseases.  [Extracellular ATP and neurodegeneration may be involved in biochemical traumatic brain injury, a factor I believe is often unrecognized in FMS and other chronic pain patients.]

Volonte C, Amadio S, Cavaliere F et al. 2003.  Extracellular ATP and neurodegeneration.  Curr Drug Targets CNS Neurol Disord. 2(6):403-412.  “Extracellular ATP plays a very complex role not only in the repair, remodeling and survival occurring in the nervous system, but even in cell death and this can occur either after normal developmental conditions, after injury, or acute and chronic diseases.”  [This mechanism may be involved in the development of some chronic pain states. DJS]

Volz MS, Medeiros LF, Tarrago MD et al. 2013. The Relationship between Cortical Excitability and Pain Catastrophizing in Myofascial Pain. J Pain. [Jun 27 Epub ahead of print]. "Pain catastrophizing regularly occurs in chronic pain patients. ….this study explored the relationship between a neurophysiological marker of cortical excitability, as assessed by transcranial magnetic stimulation, and catastrophizing, as assessed by the Brazilian Portuguese Pain Catastrophizing Scale, in patients with chronic myofascial pain syndrome. …Our results did not suggest that these findings were influenced by other factors, such as age or medication use. Furthermore, short intracortical inhibition showed a significant association with pressure pain threshold….This study highlights the relationship between cortical excitability and catastrophizing. Cortical measures may illuminate how catastrophizing responses may be related to neurophysiological mechanisms associated with chronic pain."

Vondrackova D, Leyendecker P, Meissner W et al. 2008.  Analgesic efficacy and safety of oxycodone in combination with naloxone as prolonged release tablets in patients with moderate to severe chronic pain.  J Pain. 9(12):1144-1154. “Not only does oxycodone PR/naloxone PR demonstrate analgesic efficacy comparable with oxycodone PR, but it also improves opioids-induced bowel dysfunction, and may therefore improve the acceptability of long-term opioids treatment for chronic pain.”

von Kanel R, Muller-Hartmannsgruber V, Kokinogenis G et al. 2014. Vitamin D and Central Hypersensitivity in Patients with Chronic Pain. Pain Med. [Apr 14 Epub ahead of print.] "The findings suggest a role of low vitamin D levels for heightened central sensitivity, particularly augmented pain processing upon mechanical stimulation in chronic pain patients. Vitamin D seems comparably less important for self-reports of spontaneous chronic pain."

von Klitzing, L. 1991. A new encephalomagnetic effect in human brain generated by static magnetic fields. Brain Res 540(1-2):295-6.

Von Stulpnagel C, Reilich P, Straube A et al. 2009.  Myofascial trigger points in children with tension-type headache: a new diagnostic and therapeutic option.  J Child Neurol. 24(4):406-409.  “These preliminary findings suggest a role for active trigger points in children with tension-type headache.  Trigger point-specific physiotherapy seems to be an effective therapy in these children.”

Von Stulpnagel C, Blaschek A, Lee SH et al. 2006.  [Primary headache in children]  MMW Fortschr Med. 148(46):39-41. [German]  “...treatment of headaches is integrative and multimodal, and includes pharmacotherapy, psychological interventional measures, modification of the daily routine (e.g., drinking, sleeping) and trigger point-based physiotherapy.”

Vranesh, J. G., G. Madrid, J. Bautista, P. Ching and R.A. Hicks. 1999. Time perspective and sleep problems. Percept Mot Skills 88(1):23-4.

Vulfsons S, Ratmansky M, Kalichman L. 2012. Trigger point needling: techniques and outcome. Curr Pain Headache Rep. 16(5):407-412. "In this review we provide the updates on last years' advancements in basic science, imaging methods, efficacy, and safety of dry needling of myofascial trigger points (MTrPs). The latest studies confirmed that dry needling is an effective and safe method for the treatment of MTrPs when provided by adequately trained physicians or physical therapists. Recent basic studies have confirmed that at the site of an active MTrP there are elevated levels of inflammatory mediators, known to be associated with persistent pain states and myofascial tenderness and that this local milieu changes with the occurrence of local twitch response. Two new modalities, sonoelastography and magnetic resonance elastography, were recently introduced allowing noninvasive imaging of MTrPs. MTrP dry needling, at least partially, involves supraspinal pain control via midbrain periaqueductal gray matter activation. A recent study demonstrated that distal muscle needling reduces proximal pain by means of the diffuse noxious inhibitory control. Therefore, in a patient too sensitive to be needled in the area of the primary pain source, the treatment can be initiated with distal needling."


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