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

annotated by Devin J. Starlanyl

 

 

References for Research Purposes

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NOTE:  New Nomenclature

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

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

 

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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.

 

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

 

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

 

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

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

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

 

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

 

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

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

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

Scharf, M.B., Baumann, M., Berkowitz, D.V. 2003.  The effects of sodium oxybarate on clinical symptoms and sleep patterns in patients with fibromyalgia.  J Rheumatol 30(5):1070-4. Sodium oxybarate reduced pain, fatigue and sleep abnormalities in FMS patients.  [This medication, Xyrem, is an orphan drug for use in conditions of cataplexy associated with narcolepsy.  Cataplexy is a sudden loss of muscle control that can occur after a trigger such as laughter or a surprise.  It is not to be taken lightly and can cause serious side effects, including pain, dizziness, sleep disorder and vomiting.  It should not be used by people with sleep apnea, and I am not at all comfortable with its use in a central nervous system disorder such as FMS.  DJS]

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

 

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

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

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

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

 

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

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

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

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

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

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.

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

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.

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

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

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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.

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

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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].

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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.

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

 

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

 

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

 

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

 

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

 

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

 

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

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

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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]

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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.

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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.

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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.

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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.

 

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

 

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

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

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

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Sist, T., 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.

 

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

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]

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

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

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

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

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

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

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

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

 

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

 

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

 

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

Smith, 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., 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.”

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.

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

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

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

Soyupek F, 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.

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

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

 

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

 

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

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

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

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

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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. 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.”

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.

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.

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

Staud R. 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, 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, 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. 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, 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, 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, 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.  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%).”