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.”

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]

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

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.

 

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.”

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.” 

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]

 

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.

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, 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.”

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, 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.

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.

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.

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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.

Schwarz, 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 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 3^rd. 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.

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.

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.

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]

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."

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

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, 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. "Our results indicate that cetylated derivatives of fatty acids can effectively reduce pain and symptoms associated with neck MPS, when combined with physical therapy."

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.

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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

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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.”

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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.

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.

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.

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.

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."

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.

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.

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.

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.

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.

 

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.

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.

Slotkoff, A. T., D. A. Radulovic and D. J. Clauw. 1997. The relationship between fibromyalgia and the multiple chemical sensitivity syndrome. Scand J Rheumatol 26(5):364-367.

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. L. 1986. Patient education: tuning in to the needs of the elderly. Medical Times114(10):27-31.

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 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 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, 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]  

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.

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 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 3^rd, 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, 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. 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, 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, 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."

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."

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.

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. 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. 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. 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. 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, 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."

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, 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]

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."

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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.”

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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.

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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.”

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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."

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.

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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.

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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."

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]

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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.”

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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]

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.

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.”

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."