References for Research Purposes

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.

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

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

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

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

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.

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

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.

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

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

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.

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.”

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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]

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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]

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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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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.

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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.”

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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

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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]

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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.

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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.]

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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, 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. 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%).”

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. 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. 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, 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."

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

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

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

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

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

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

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

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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.

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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.”

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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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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.

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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.”

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Werle E, Jakel HP, Muller A et al. 2005. Serum hyaluronic acid levels are elevated in arthritis patients, but normal and not associated with clinical data in patients with fibromyalgia syndrome. Clin Lab. 51(1-2):11-19. “The present study with a quite large cohort including patients with arthritis and FM demonstrates that serum levels of HA in FM are neither elevated nor associated with any relevant clinical data of this disease and, therefore, have no diagnostic or prognostic value in Germans.” [There are several conflicting studies. Some show elevated hyaluronic acid in FMS, and some show normal levels. Perhaps there are other combined factors, such as co-existing TrPs and glucose metabolism disorders such as insulin resistance or diabetes, that are muddying the waters. Patients must be checked for co-existing conditions and these conditions must be taken into consideration in research. FMS is heterogeneous. DJS]

Werner A, Malterud K. 2003. It is hard work behaving as a credible patient: encounters between women with chronic pain and their doctors. Soc Sci Med. 57(8):1409-1419. “In various studies during the last decade, women with medically unexplained disorders have reported negative experiences during medical encounters. Accounts of being met with skepticism and lack of comprehension, feeling rejected, ignored, and being belittled, blamed for their condition and assigned psychological explanation models are common. Attempting to fit in with normative, biomedical expectations of correctness, they tested strategies such as appropriate assertiveness, surrendering, and appearance. The informants were not only struggling for their credibility. Their stories illustrated a struggle for the maintenance of self esteem or dignity as patients and as women. [It is often overwhelming when one experiences invisible chronic pain and must attempt to convey the expanse of the symptoms to the care provider while maintaining self esteem in spite of frequent lack of support. DJS]

Werner A, Steihaug S, Malterud K. 2003. Encountering the continuing challenges for women with chronic pain: recovery through recognition. Qual Health Res. 13(4):491-509. “This work is based on experiences from a group treatment for women with chronic musculoskeletal pain. The authors explored the nature and consequences of the reported benefits from being met with recognition in the groups. Recognition had enhanced strength, confidence, and awareness expressed as increased bodily, emotional and social competence. This competence provided tools to handle their pain and illness."

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White KP, Thompson J. 2003. Fibromyalgia syndrome in an Amish community: a controlled study to determine disease and symptom prevalence. J Rheumatol. 30(8):1835-1840. “To estimate the point prevalence of fibromyalgia syndrome (FM) in Amish adults and to compare the prevalence of chronic pain, chronic widespread pain, FM, chronic fatigue, and debilitating fatigue in the Amish versus non-Amish rural and urban controls. The prior assumption was that, if litigation and/or compensation availability have major effects on FM prevalence, then FM prevalence in the Amish should approach zero. FM is relatively common among the Amish.” [This study refutes the claim of some doctors, lawyers and insurance companies that FMS is an invalid diagnosis, and that the frequency of FMS symptoms is motivated by financial rewards. In Amish society, there are no financial rewards for FMS, yet the incidence of FMS among the Amish was the same as in the non-Amish population. DJS]

White KP. 2004. Fibromyalgia: The answer is blowin’ in the wind. J Rheumatol 31(4):636-639. This eloquent editorial expresses the frustration of one expert fibromyalgia researcher as he tries to understand why “...are those who oppose the FM concept so verbal and destructive, many going out of their way to write position papers about an area in which they have done no research, and seem so oblivious and impervious to the research of others?" It is specific, accurate and clear. Legal advocates take note.

White KP, Nielson WR, Harth M, et al.2002. Does the label "fibromyalgia" alter health status, function, and health service utilization? A prospective, within-group comparison in a community cohort of adults with chronic widespread pain. Arthritis Rheum 15:47(3):260-5. "The FM label does not have a meaningful adverse affect on clinical outcome over the long term."

White KP, Harth M. 2001. Classification, epidemiology, and natural history of fibromyalgia. Curr Pain Headache Rep 5(4):320-9. "Clinic studies have found MF to be common in countries worldwide; these include studies in specialty and general clinics. The FM to be between 0.5% and 5%. Although some authors claim that an epidemic of FM has been fueled by an over-generous Western compensation system, there are no data that demonstrate an increasing incidence or prevalence of FM; moreover, existing data refute any association between FM prevalence and compensation. Claims that the FM label itself causes illness behavior and increased dependence on the medical system also are not supported by existing research."

White, K.,P., Speechley, M., Harth, M., Ostbye, T. 2000. Co-existence of chronic fatigue syndrome with fibromyalgia syndrome in the general population. Indicators of more disability than the "pain alone group" argues against FMS and CFS patients being chronic complainers who abuse the health care system as suggested by Haddler. A refined subgroup classification of FMS and CFS may be appropriate in further analyses and therapeutic studies.

White, K. P., S. Carette, M. Harth and R. W. Teasell. 2000. Trauma and fibromyalgia: is there an association and what does it mean? Semin Arthritis Rheum 29(4):200-16.

White, K. P. and M. Harth. 1999. The occurrence and impact of generalized pain. Baillieres Best Pract Res Clin Rheumatol 13(3):379-89.

White, K. P., M. Speechley, M. Harth and T. Ostbye. 1999. The London Fibromyalgia Epidemiology Study: comparing the demographic and clinical characteristics in 100 random community cases of fibromyalgia versus controls. J Rheumatol 26(7):1577-85.

White, K. P., M. Speechley, M. Harth and T. Ostbye. 1999. Comparing self-reported function and work disability in 100 community cases of fibromyalgia syndrome versus controls in London, Ontario: the London Fibromyalgia Epidemiology Study. Arthritis Rheum 42(1):76-83

White, K. P., M. Speechley, M. Harth and T. Ostbye. 1999. The London Fibromyalgia Epidemiology Study: direct health care costs of fibromyalgia syndrome in London, Canada. J Rheumatol 26(4):885-9.

White MF. 2003. Insulin signaling in health and disease. Science 302(5651):1710-1711. “The close association between obesity and insulin resistance, and their progression to type II diabetes, is a serious health problem. Whether better management of chronic inflammation can improve insulin action . . . and restore central nervous system appetite control is an important area of investigation.”

White RL, Cohen SP. 2007. Return-to-duty rates among coalition forces treated in a forward-deployed pain treatment center: a prospective observational study. Anesthesiology 107(6):1003-1008. To avoid recurrent or chronic pain, non-battle-related injuries must be treated promptly in war zones. Methods used included trigger point injections and nerve blocks. This produced a high return to duty rate.

Whorwood CB, Donovan SJ, Flanagan D et al. 2002. Increased glucocorticoid receptor expression in human skeletal muscle cells may contribute to the pathogenesis of the metabolic syndrome. Diabetes 51(4):1066-1075. [This study links skeletal muscle tissue and regulation of intracellular cortisol to metabolic syndrome, including insulin resistance and abdominal obesity. DJS]

Wiersinga WM, Thyroid Hormone Replacement Therapy. Horm Res Jan;56 Suppl S1:74-81, 2001. A combination of T(4) and T(3) replacement, not T(4) alone, is necessary to ensure that all tissues are properly supplied with thyroid hormone in thyroidectomized rats. Many physicians have seen some hypothyroid patients who have hypothyroid symptoms in spite of therapy. A slow-release preparation of both T(4) and T(3) may be more effective than T(4) alone.

Wieseler-Frank J, Maier SF, Watkins LR. 2005. Immune-to-brain communication dynamically modulates pain: physiological and pathological consequences. Brain Behav Immun. 19(2):104-111. “This review is an examination of how activation of immune-like glial cells within the spinal cord can amplify pain by modulating the excitability of spinal neurons. This recently recognized role of spinal cord glia and glially derived proinflammatory cytokines as powerful modulators of pain is exciting as it may provide novel approaches for controlling human chronic pain states that are poorly controlled by currently available therapies.”

Wieseler-Frank J, Maier SF, Watkins LR. 2004. Glial activation and pathological pain. 45(2-3):389-395. In chronic pain states, “…neuronal function is indeed altered, [but] there is significant evidence showing that exaggerated pain is regulated by the activation of astrocytes and microglia [types of glial cells]. In exaggerated pain, astrocytes and microglia are activated by neuronal signals including substance P, glutamate, and fractalkine.” The glial cells then release other substances, including proinflammatory cytokines that further act on other glia and neurons. This “…review describes glia as newly recognized mediators of exaggerated pain, and as new therapeutic targets.” The glial-neuron interactions are likely to play a significant role in phenomenon besides pain.

Wigers SH, Finset A. 2007. Multidimensional rehabilitation of fibromyalgia syndrome versus singular treatment regimens. J Musculoskel Pain 15 (Supp 13):60 item 107. [Myopain 2007 Poster] “MDR (multidimensional rehabilitation) within a biopsychosocial model induces rapid and broad therapeutic effects with long-lasting impact in FMS. MDR is indicated to be superior to singular treatment regimens.”

Wigers SH, Finset A. 2007. [Rehabilitation of chronic myofascial pain disorders.] Tidsskr Nor Laegeforen 127(5):604-608. [Norwegian] “Our findings confirm the existing evidence-based guidelines by showing that multidimensional rehabilitation is an effective intervention for patients with widespread chronic pain.” This study included patients with fibromyalgia and patients with myofascial pain. Some patients who went through the program no longer met the criteria for FM. With this kind of rehabilitation, more patients returned to work or had fewer sick days, but also more received disability pensions. This kind of multidimensional rehab seems to help patients find the best quality of life and return to the highest function possible, recognizing that for some patients, this still means disability.

Wijnhoven H, Vet H, Smit H, et al. Hormonal and reproductive factors are associated with chronic low back pain and chronic upper extremity pain in women - the MORGEN study. 2006. Spine 31(13):1496-1502. “In adult women, hormonal and reproductive factors are associated with chronic musculoskeletal pain in general. Factors related to increased estrogen levels may specifically increase the risk of chronic LBP (low back pain).

Wik G, Fischer H, Finer B et al. 2006. Retrospenial cortical deactivation during painful stimulation of fibromyalgic patients. Int J Neurosci. 116(1):1-8.

Wik, G., Fischer, H., Bragee, B. et al. 2003. Retrospinal cortical activation in the fibromyalgia syndrome. Neuroreport 14(4):619-21. This study confirms that patients with FMS have lower cerebral blood flow in areas associated with cognitive pain processing than healthy controls.

Wik, G., H. Fischer, B. Bragee, B. Finer and M. Fredrikson. 1999. Functional anatomy of hypnotic analgesia: a PET study of patients with fibromyalgia. Eur J Pain 3(1):7-12.

Wikner, J., U. Hirsch, L. Wetterberg and S. Rojdmark. 1998. Fibromyalgia-a syndrome associated with decreased nocturnal melatonin secretion. Clin Endocrinol(Oxf) 49(2):179-83.

Wikstrom EA, Tillman MD, Chmielewski TL et al. 2006. Measurement and evaluation of dynamic joint stability of the knee and ankle after injury. Sports Med. 36(5):393-410. “Evidence suggests that surgery and aggressive rehabilitation will not necessarily restore the deficits in dynamic joint stability caused by injury to the anterior cruciate ligament or lateral ankle ligaments.” “A quick return to play could start a vicious cycle of chronic injuries or permanent disability.”

Wilder-Smith CH, Robert-Yap J. 2007. Abnormal endogenous pain modulation and somatic and visceral hypersensitivity in female patients with irritable bowel syndrome. World J Gastroenterol. 13(27):3699-3704. “A majority of IBS patients had abnormal endogenous pain modulation and somatic hypersensitivity as evidence of central sensitization.”

Wilke, W. S. 1995. Treatment of "resistant" fibromyalgia. Rheum Dis Clin North Am 21(1): 247-260.

Willert RP, Delaney C, Kelly K et al. 2007. Exploring the neurophysiological basis of chest wall allodynia induced by experimental oesophageal acidification – evidence of central sensitization. Neurogastroenterol Motil. 19(4):270-278. “NMDA receptor antagonism reversed both visceral and somatic pain hypersensitivity but did not affect CEP (chest wall evoked potentials) latencies. These data provide objective neurophysiological evidence that CS contributes to the development of somatic allodynia following visceral sensitization.”

Willert RP, Woolf CJ, Hobson AR et al. 2004. The development and maintenance of human visceral pain hypersensitivity is dependent on the N-methyl-d-aspartate receptor. Gastroenterology 126(3):683-692.

Williams DA, Gracely RH. 2007. Biology and therapy of fibromyalgia. Functional magnetic resonance imaging findings in fibromyalgia. Arthritis Res Ther. 8(6):224. “This article provides an overview of the nociceptive system as it functions normally, reviews functional brain imaging methods, and integrates the existing literature utilizing fMRI to study central pain mechanisms in fibromyalgia.”

Williams DA, Gendreau M, Hufford MR et al. 2004. Pain assessment in patients with fibromyalgia syndrome: a consideration of methods for clinical trials. Clin J Pain 20(5):348-356. “Pain assessment methods relying on recall might contribute to an apparent improvement in clinical trials in the absence of an intervention; such an effect has been considered a ‘placebo response’. Future clinical trials might consider using a real-time approach to pain assessment, which in this study appeared to mitigate against seeing improvement in the absence of an intervention and demonstrated higher levels of patient adherence.” [Some FMS studies that have relied on patient memories may be suspect. DJS]

Williams DA, Gendreau M, Hufford MR et al. 2004. Pain assessment in patients with fibromyalgia syndrome: a consideration of methods for clinical trials. Clin J Pain 20(5):348-356. This study took a close look at the means of assessment of FMS pain. The results indicate that studies depending on patient recall of pain may be misleading, and “...contribute to an apparent improvement in clinical trials in the absence of intervention; such effect has been considered a ‘placebo response.’ The effect may instead be due to inaccurate patient recall. This may be a “wild” factor in a large number of clinical studies.

Williams RE, Hartmann KE, Sandler RS et al. 2005. Recognition and treatment of irritable bowel syndrome among women with chronic pelvic pain. Am J Obstet Gynecol. 192(3):761-767. “IBS is not consistently diagnosed and treated even in a pelvic pain clinic. “...treatment of IBS may reduce the overall abdominal pain of these patients.”

Wilson, J. 1999. Acknowledging the expertise of patients and their organizations. BMJ 319(7212):771-4.

Wilson, R. B., O. S. Gluck, J. R. Tesser, J. C. Rice, A. Meyer and A. J. Bridges. 1999.Antipolymer antibody reactivity in a subset of patients with fibromyalgia correlates with severity. J Rheumatol 26(2):402-7.

Wilson VE, Peper E. 2004. The effects of upright and slumped postures on the recall of positive and negative thoughts. Appl Psychophysiol Biofeedback 29(3):189-195. “...positive thoughts are more easily recalled in the upright posture.” The head-forward, shoulder slumped posture is not only a perpetuating factor for TrPs, but can affect your emotional state as well.

Wine WA. 2007. Chronic pain and cannabinoids. J Musculoskel Pain 15 (Supp 13):61 item 108. [Myopain 2007 Poster] “Fifty-nine patients are studied in a case series extending over a year and the data is presented in table form.” “Different combinations of cannabinoids worked effectively with different types of fibromyalgia.” “Improvement in pain scores, improvement in mood, and improvement in sleep architecture were all noted in our population; as well as an ability to titrate down other medications and decrease ADI effects.” [This agrees with the large file folder of research I have accumulated concerning chronic pain and symptom relief from cannabinoids. DJS]

Winfield JB. 2007. Pain and arthritis. N C Med J. 68(6):444-446. “Overcome your negative bias against fibromyalgia and review recent discoveries that have led to classification of fibromyalgia as a biologically-based neurosensory disorder. Use the simple and convenient ways that are available to measure pain and its concomitants (fatigue, poor sleep, depression, anxiety, and impaired physical functioning) both at initial evaluation and in follow-up visits as a guide to therapy. Do not fear use of opioids; just be careful with this class of drug.”

Winfield, J. B. 1998. Pain in fibromyalgia. Rheum Dis Clin North Am 25(1):55-79.

Wingenfeld K, Wagner D, Schmidt I et al. 2007. The low-dose dexamethasone suppression test in fibromyalgia. J Psychosom Res. 62(1):85-91. “Our results suggest increased sensitivity to glucocorticoid feedback, manifested at the adrenal level, in FMS.”

Winkelman JW. 2003. Treatment of nocturnal eating syndrome and sleep-related eating disorder with topiramate. Sleep Med. 4(3):243-246. “Sleep-related eating disorder (SRED) and nocturnal eating syndrome (NES) combine features of sleep disorders and eating disorders.” “Topiramate may be of benefit for patients with NES or SRED in reducing nocturnal eating, improving nocturnal sleep, and producing weight loss.”

Wise SK, Wise JC, Delgaudio JM. 2006. Gastroesophageal reflux and laryngopharyngeal reflux in patients with sleep-disordered breathing. Otolaryngol Head Neck Surg 135(2): 253-257. [These conditions can activate myofascial TrPs. DJS.]

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Wittrup, I. H. , A. Wiik and B. Danneskiold-Samsoe. 1999. Antibody profile in patients with fibromyalgia compared to healthy controls. J Musculoskel Pain 7(1-2):273-277.

Wogoman, H., M. Steinberg and A. J. Jenkins. 1998. Acute intoxication with guaifenesin, diphenhydramine, and chlorphenhydramine. Am J Forensic Med Path 20(2):199-202.

Wolf K, Raedler T, Henke K et al. 2005. The face of pain – a pilot study to validate the measurement of facial pain expression with an improved electromyogram method. Pain Res Manag. 10(1):15-19. Tightening of the muscles, especially the orbicularis oculi and specific mouth muscles, can be significantly activated with pain. [This tightening itself may initiate, activate or perpetuate TrPs in the area, causing more pain. DJS]

Wolfe F, Michaud K. 2004. Severe rheumatoid arthritis (RA), worse outcomes, comorbid illness, and sociodemographic disadvantage characterize RA patients with fibromyalgia. J Rheumatol 31(4):695-700. A percentage of patients with severe RA may have co-existing FMS.

Wolfe, F. and J. Anderson. 1999. Silicone filled breast implants and the risk of fibromyalgia and rheumatoid arthritis. J Rheumatol 26(9):2025-8.

Wolfe, F. and D. J. Hawley. 1999. Evidence of this older symptom appraisal and fibromyalgia: increased rates of reported comorbidity and comorbidity severity Clin Exp Rheumatol 17(3):297-303.

Wolfe, F. 1999. "Silicone related symptoms" are common in patients with fibromyalgia: no evidence for a new disease. J Rheumatol 26(5):1172-5.

Wolfe, F. 1998. What use are fibromyalgia control points? J Rheumatol 25(3):546-550.

Wolfe, F. 1997. The fibromyalgia problem. J Rheumatol 24(7):1247-9.

Wolfe, F., I. J. Russell, G. Vipraio, K. Ross and J. Anderson. 1997. Serotonin levels, pain threshold, and fibromyalgia symptoms in the general population. J Rheumatol 24(3):555-559.

Wolfe, F., Anderson J., D. Harkness, R. M. Bennett, X. J. Caro, D. L. Goldenberg, I. J. Russell and M. B. Yunus. 1997. Health status and disease severity of fibromyalgia: results of a six-center longitudinal study. Arthritis Rheum 40(9):1571-1579.

Wolfe, F., J. Anderson, D. Harkness, R. M. Bennett, X. J. Caro, D. L. Goldenberg, I. J. Russell and M. B. Yunus. 1997. A prospective, longitudinal, multicenter study of service utilization and costs in fibromyalgia. Arthritis Rheum 40(9):1560-1570.

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Wolfe, F., Smythe H. A. , Yunus M. B. , Bennett R, M. Bombadier C., Goldenberg D. L. Tugwell P., Campbell S. M. Ables M., Clark P. et al. "The American College of Rheumatology 1990 Criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee." Arth Rheum 33(2):160-172.

Wolfe U, Comee JA, Sherman BS. 2007. Feeling darkness: a visually induced somatosensory illusion. Percept Psychophys. 69(6):879-886. “This reveals that the integration of vision with touch and proprioception is not restricted to higher-level spatial vision, but is instead a more fundamental aspect of sensory processing than has been previously shown.” [This study may have some relevance to patients with FM and CMP. DJS]

Wood PB, Schweinhardt P, Jaeger E et al. 2007. Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 25(12):3576-3582.

Wood PB, Kablinger AS, Caldito GS. 2005. Open trial of pindolol in the treatment of fibromyalgia. Ann Pharmacother 39(11):1812-1816. In this small group (n=20), pindolol, which works by affecting beta-androgenic receptors to down-regulate the hyperactive sympathetic nervous system, improved the general FMS parameters.

Wood PB. 2004. Fibromyalgia syndrome: a central role for the hippocampus — a theoretical construct. Jour of Musculoskel Pain 12(1):19-26. “Fibromyalgia is characterized by abnormalities that appear to be related to hippocampal dysfunction, including hyperactivity of both corticotropin-releasing hormone neurons and the sympathetic nervous system, impaired declarative memory, and enhanced NMDA receptor-mediated nociception. It is therefore postulated that stress-induced, NMDA receptor-mediated dysfunction within the hippocampus plays a central role in the etiopathogenesis and clinical phenomena of fibromyalgia.”

Wood PB. 2004. Stress and dopamine: implications for the pathophysiology of chronic widespread pain. Med Hypotheses 62(3):420-424. “…prolonged stress produces both reduction of dopamine output…and persistent hyperalgesia in the context of chronic stress…”

Woodward, M. 1999. Insomnia in the elderly. Aust Fam Physician 28(7):653-8.

Woolf CJ. 2007. Central sensitization: uncovering the relation between pain and plasticity. Anesthesiology 106(4):864-867. “Electrophysiological analysis of the injury-induced increase in excitability of the flexion reflex shows that it in part arises from changes in the activity of the spinal cord. The long-term consequences of noxious stimuli result, therefore, from central as well as from peripheral changes.”

Worthman, C. M. and M. K. Melby. In press. Toward a comparative developmental ecology of human sleep. In Adolescent Sleep Patterns: Biological, Social, and Psychological Influences, M. A. Carskadon, ed. New York: Cambridge University Press.

Wreje U, Brorsson B. 1995. A multicenter randomized controlled trial of injections of sterile water and saline for chronic myofascial pain syndromes. Pain 61(3):441-444. “Injections of sterile water are substantially more painful but demonstrate no better clinical outcome than similar injections of saline as a method to treat patients with chronic myofascial pain syndrome.”

Wright EF. 2000. Referred craniofacial pain patterns in patients with temporomandibular disorder. J Am Dent Assoc. 131(9):1307-1315. “Patients with TMD often report referred craniofacial pain arising from palpation of the head and neck region. The author found that the pattern between referred pain source and

site was consistent and predictable.”

Wu, CT, JC Yu, CC Yeh, ST Liu, CY Li, ST Ho and CS Wong. 1999. Preincisional dextromethorphan treatment decreases postoperative pain and opioid requirement after laparoscopic cholecystectomy. Anesth Analg 88(6):1331-4.

Wu G, Ren X. 2009. Speed effect of selected Tai Chi Chuan movement on leg muscle activity in young and old practitioners. Clin Biomech. [Apr 6 Epub ahead of print]. “The activation duration and function of leg muscles, especially the knee extensor muscle, are significantly affected by the speed on the selected Tai Chi Chuan movement. Practicing Tai Chi Chuan at different speed may alter the role of muscular function in movement control.”

Wu G, Ringkamp M, Hartke TV et al. 2001. Early onset of spontaneous activity in uninjured c-fiber nociceptors after injury to neighboring nerve fibers. J Neurosci 21(8):RC140. [This study links uninjured C-fibers to central sensitization. DJS]

Wu SK, Hong CZ, You JY et al. 2005. Therapeutic effect on the change of gait performance in chronic calf myofascial pain syndrome: a time series case study. J Musculoskeletal Pain 13(3). This case study documents the changes brought about by therapy for biomechanical abnormality in gait due to myofascial TrPs in the calf muscle, including perpetuating factor abatement. [ This study demonstrates an aspect of myofascial TrPs that often goes unrecognized. Gait can be profoundly disturbed by myofascial TrPs, and this can lead to chronic pain and imbalances throughout the body. If the TrPs are recognized promptly and dealt with thoroughly, the impact on the patient’s life can be greatly lessened. DJS]

Wu T, Giovannucci E, Pischon T et al. 2004. Fructose, glycemic load, and quantity and quality of carbohydrate intake in relation to plasma C-peptide concentrations in US women. Am J Clin Nutr. 80(4):1043-1049. Some foods, such as high-fructose corn syrup, may be linked to the development of insulin resistance. DJS]

Xiao Y, Upadhyaya B, Haynes WL et al. 2007. G protein coupled receptor dysfunction in a subgroup of fibromyalgia syndrome patients. J Musculoskel Pain 15 (Supp 13):62 item 110. [Myopain 2007 Poster] This study found a genetically based functional defect in the G stimulator or peripheral blood mononuclear cells in patients with FM. This indicates more phenotype and genotype Gs protein research is warranted in FM patients, with implications as to the causal mechanisms and potential treatments of FM.

Xu L, Gao PY. 2006. “Palpation by imaging”: magnetic resonance elastography. Chin Med Sci J. 21(4):281-286. This is a report on an exciting imagery technique that may be able to document changes in elasticity of tissue, and thus the difference between healthy tissue and tissue affected by pathologies.

Xu L, Lin Y, Xi ZN et al. 2007. Magnetic resonance elastography of the human brain: a preliminary study. Acta Radiol. 48(1):112-115. This new technology propagates shear waves in brain tissue to differentiate brain tissue types, and may be able to directly assess elasticity of brain tissue. It may become a significant imaging technique.

Xu YL, Reinscheid RK, Huitron-Resendiz S et al. 2004. Neuropeptide S: a neuropeptide promoting arousal and anxiolytic-like effects. Neuron 43(4):487-497. “NPS could be a new modulator of arousal and anxiety. The LC region encompasses distinct nuclei expressing different arousal-promoting neurotransmitters.” Neuropeptide S could be a previously unexpected modulator of wakefulness and anxiety.

Yaksh, T. L., X. Y. Hua, I. Kalcheva, N. Nozaki-Taguchi and M. Marsala. 1999. The spinal biology in humans and animals of pain states generated by persistent small afferent input. Proc Natl Acad Sci 96(14):7680-6.

Yamada T, Funahashi M, Murayama T. 2005. [Clinical evaluation of 30 patients with interstitial cystitis complicated by fibromyalgia] Nippon Hinyokika Gakkai Zasshi 96(5):554-559. [Japanese] “Approximately 11% of patients with IC have a complication of FM. They feel isolated due to the lack of understanding of the disease and endure generalized intolerable pain.”

Yamada, H., T. Okumura, W. Motomura, Y. Kobayashi and Y Kohgo. 2000. Inhibition of food intake by central injection of anti-orexin antibody in fasted rats. Biochem Biophys Res Commun267(2):527-531.

Yang H, Meng X, Zhu Y. 2000. [The position of submaxillary transcutaneous electrical stimulation for obstructive sleep apnea syndrome] Zhonghua Er Bi Yan Hou Ke Za Zhi 35(1):55-58. [Chinese] “Submaxillary electrical stimulation with fixed provocative locus is effective for the treatment of OSAS.”

Yang H, Meng XG, Zhu YZ et al. 2000. [Clinical study of effects of submaxillary transcutaneous electrical stimulation of genioglossus on obstructive sleep apnea syndrome] Lin Chuang Er Bi Yan Hou Ke Za Zhi 14(6):250-252. [Chinese] “Submaxillary electrical stimulation is effective to the treatment of OSAS and its curative effect perhaps has a close relationship with obstructive level of with upper airway. Stimulating upper airway dilating muscle which formed mainly by genioglossus could push the tongue ahead and effectively open pharyngeal cavity.” [Sleep apnea can be affected by tightened muscles. DJS]

Yang EV, Glaser R. Stress-induced immunomodulation and the implications for health. Int Innumopharmacol Feb;2(2-3):315-24,2002.

Yang, J. 1994. Intrathecal administration of oxytocin induces analgesia in low back pain involving the endogenous opiate peptide system. Spine 19(8):867-871.

Yang M, Li ZS, Xu XR et al. 2006. Characterization of cortical potentials evoked by oesophageal balloon distention and acid perfusion in patients with functional heartburn. Neurogastroenterol Motil. 18(4):292-299. “These findings provide the evidence that central sensitization contributes to the development and maintenance of oesophageal hypersensitivity.” [This would indicate that FMS patients may be especially sensitive to developing reflux. Care may be needed to avoid TrPs in the high abdominal oblique muscles that could contribute to and be perpetuated by GERD. DJS]

Yap A.U., Tan K.B., Chua E.K et al. 2002. Depression and somatization in patients with temporomandibular disorders. J Prosthet Dent 88(5):479-84. “Within the limits of this study, patients diagnosed with myofascial pain and other joint conditions (group E) has significantly higher levels of depression (P=.03) and somatization (P=.03) than patients diagnosed with only disk displacements (group B).” [It would be interesting to find out how the levels of “depression and somatization” changed if the clinicians doing this study took into account that myofascial pain is not a “joint condition”, myofascial TrPs can occur body-wide and could be a factor in this study, and that patients should also be screened for coexisting fibromyalgia. DJS]

Yap EC. 2007. Myofascial pain – an overview. Ann Acad Med Singapore. 36(1):43-46. “With rehabilitation, many patients do not have to continue to suffer unnecessary pain that affects their daily activities and quality of life. Early diagnosis and management may also help reduce psychosocial complications and financial burden of chronic pain syndrome.”

Yaron, I., D. Buskila, I Shirazi, I. Neumann, O. Elkayam, D. Parran and M. Yaron. 1997. Elevated levels of hyaluronic acid in the sera of women with fibromyalgia. J Rheumatol 24(11):2221-4.

Yavuz, S, I Fresko, V Hamuryudan, S Yurdakul and H Yazici. 1998. Fibromyalgia in Behcet’s syndrome. J Rheumatol 25(11):2219-20.

Yeh GY, Mietus JE, Peng CK et al. 2007.

Enhancement of sleep stability with Tai Chi exercise in chronic heart failure: preliminary findings using an ECG-based spectrogram method. Sleep Med. [Aug 2 Epub ahead of print] “Tai Chi exercise may enhance sleep stability in patients with chronic heart failure. This sleep effect may have a beneficial impact on blood pressure, arrhythmogenesis and quality of life.” [T’ai chi could be very beneficial to patients with FM as well as those with CHF, as it impacts both sleep quality and blood pressure, as well as improving balance and other effects shown in other studies. DJS]

Yeh SH, Chuang H, Lin LW et al. 2006. Regular tai chi chuan exercise enhances functional mobility and CD4CD25 regulatory T cells. Br J Sports Med. 40(3):239-243. “The duration and vigor of physical exercise are widely considered to be critical elements that may positively or negatively affect physical health and immune response.” “A 12-week program of regular TCC exercise enhances functional mobility, personal health expectations, and regulatory T cell function.”

Yehuda R. 2004. Risk and resilience in posttraumatic stress disorder. J Clin Psychiatry 65 Suppl 1:29-36. Patients with increased heart rate and relatively low cortisol levels at the time of trauma may be at greater risk of developing PSTD. [Spending more time to evaluate patients at the time of trauma, including soft tissue injury and potential central insult, may provide significant measures to help prevent the development of costly and life-altering chronic disease states. DJS.]

Yehuda R, McFarlane AC, Shalev AY. 1998. Predicting the development of posttraumatic stress disorder from the acute response to a traumatic event. Biol Psychiatry 44(12):1305-1313. “Posttraumatic stress disorder (PTSD) is a psychiatric condition that is directly precipitated by an event that threatens a person’s life or physical integrity and that invokes a response of fear, helplessness, or horror. Only a proportion of those exposed to fear-producing events develop or sustain PTSD. These studies have demonstrated increased heart rate and lower cortisol levels at the time of the traumatic event in those who have PTSD at a follow-up time compared to those who do not. Certain features associated with PTSD, such as intrusive symptoms and exaggerated startle responses, are only manifest weeks after the trauma. The findings suggest that the development of PTSD may be facilitated by an atypical biological response in the immediate aftermath of a traumatic event, which in turn leads to a maladaptive psychological state.” [Examination for these factors during follow-up care, and additional support to those at risk, may prevent or minimize this chronic illness. This would also be a good time to check for developing soft tissue injury and central sensitization, and would be preventative medicine that could provide significant results for the patients and the health care system. DJS]

Yehuda, R., A. C. McFarlane and A. Y. Shalev. 1998. Predicting the development of post-traumatic stress disorder from the acute response to a traumatic event. Biol Psychiatry 44(12):1305-13.

Yokoe T, Minoguchi K, Matsuo H et al. 2003. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation 107(8):1129-1134. Effective CPAP therapy can affect levels of irritation-producing biochemicals.”

Yonkers, K. A., U. Halbreich, E. Freeman, C. Brown, J. Endicott, E. Frank, B. Parry, T. Pearlstein, S. Severino, A. Stout, A. Stone and W. Harrison. 1997. Yoshinoya, S. Y. Mizoguchi, Y. Hashimoto, A. Yamada, S. Uchida, A. Taniguchi, E. Nishioka and T. Miyamoto. 1991. [Serum concentration of hyaluronic acid in healthy populations and patients with rheumatoid arthritis–relationship to clinical disease activity of RA]. Ryumachi 31(4):381-90 [Japanese].

Yoshihara T, Shigeta K, Hasegawa H et al. 2005. Neuroendocrine responses to psychological stress in patients with myofascial pain. J Orofac Pain 19(3):202-208. “These results suggest that both the sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenocortical systems are more highly activated in response to psychological stress in patients with myofascial pain than in healthy individuals.”

Younger J, Mackey S. 2009. Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study. Pain Med. [Apr 22 Epub ahead of print]. “We conclude that low-dose naltrexone may be an effective, highly tolerable, and inexpensive treatment for fibromyalgia.”

Youngstedt, S. D., D. F. Kripke, M. R. Klauber, R. S. Sepulveda and W. J. Mason. 1998.Periodic leg movements during sleep and sleep disturbances in elders. J Gerontol A Biol Sci Med Sci 53(5):M391-4.

Ytterberg SR, Mahowald ML, Woods SR. 1998. Codeine and oxycodone use in patients with chronic rheumatic disease pain. Arthritis Rheum. 41(9):1603-1612. “Prolonged treatment of rheumatic disease pain with codeine or oxycodone was effective in reducing pain severity and was associated with only mild toxicity. Doses were stable for prolonged periods of time, with escalations of the opioid dose almost always related to worsening of the painful condition or a complication thereof, rather than the development of tolerance to opioids. Doubts or concerns about opioid efficacy, toxicity, tolerance, and abuse or addiction should no longer be used to justify withholding opioids from patients with well-defined rheumatic disease pain.”

Yuen KC, Bennett RM, Hryciw CA et al. 2007. Is further evaluation for growth hormone (GH) deficiency necessary in fibromyalgia patients with low serum insulin-like growth factor (IGF)-I levels? Growth Horm IGF Res. [Feb 5 Epub ahead of print].

Yunus MB. 2007. Role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain. Best Pract Res Clin Rheumatol. 21(3):481-497. “Patients with widespread pain or fibromyalgia syndrome have many symptoms besides musculoskeletal pain: e.g., fatigue, sleep difficulties, a swollen feeling in tissues, paresthesia, cognitive dysfunction, dizziness, and symptoms of overlapping conditions such as irritable bowel syndrome, headaches and restless legs syndrome.” “Evaluation of a patient presenting with widespread pain includes history and physical examination to diagnose both fibromyalgia and associated or concomitant conditions.” “Patients with rheumatoid arthritis and systemic lupus erythematosus should be evaluated for fibromyalgia, since 20-30% of them have associated fibromyalgia, requiring a different treatment approach.”

Yunus MB. 2007. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Semin Arthritis Rheum. [Mar 10 Epub ahead of print] “Each patient, irrespective of diagnosis, should be treated as an individual considering both the biological and psychosocial contributions to his or her symptoms and suffering.”

Yunus MB. 2004. Suffering, science and sabotage. J Musculoskel Pain 12(2):3-18. This courageous editorial takes the medical profession to task for its frequent judgmental attitude and mistreatment of patients with FMS and other central sensitivity syndromes. It is specific, clear, detailed and referenced.

Yunus MB. 2002. A comprehensive medical evaluation of patients with fibromyalgia syndrome. Rheum Dis Clin North Am 28(2):201-17. "Fibromyalgia syndrome (FMS) is a common and distressful condition. It is imperative that all physicians do their best to help these suffering patients with understanding and respect, since the primary responsibility of a physician is to ameliorate suffering of a patient, irrespective of the type of the disease or the illness. (The authors use the terms "disease" and "illness" synonymously, since any distinction between these two terms are really pointless because the word "disease" means lack of ease or presence of suffering.) It is clear that a physician cannot optimize management of a patients with FMS without a thorough medical and psychologic evaluation."

Yunus, M. B., F. Inanici, J. C. Aldag and R. F. Mangold. 2000. Fibromyalgia in men: comparison of clinical features with women. J Rheumatol 27(2):485-90

Yunus, M. B. , M. A. Kahn, K. K. Rawlings, J. R. Green, J. M. Olson and S. Shah. 1999. Genetic linkage analysis of multicase families with fibromyalgia syndrome. J Rheumatol 26(2):408-12.

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Zachrisson O, Colque-Navarro P, Gottfries CG et al. 2004. Immune modulation with a staphylococcal preparation in Fibromyalgia/Chronic Fatigue Syndrome: Relation between antibody levels and clinical improvement. Eur J Clin Microbiol Infect Dis 23(2):98-105. This study did not differentiate between fibromyalgia and chronic fatigue and did not account for any co-existing conditions. Since CFIDS is an illness of exclusion, this is not logical and the conclusions must be suspect.

Zammit, G. J., J. Weiner, N. Damato, G. P. Sillup and C. A. McMillan. 1999. Quality of life in people with insomnia. Sleep 22 Suppl 2:S379-85.

Zanchet EM, Longo I, Cury Y. 2004. Involvement of spinal neurokinins, excitatory amino acids, proinflammatory cytokines, nitric oxide and prostanoids in pain facilitation induced by Phoneutria nigriventer spider venom. Brain Res. 102(1):101-111. Central sensitization can be caused by this spider venom.

Zautra AJ, Fasman R, Parish BP et al. 2006. Daily fatigue in women with osteoarthritis, rheumatoid arthritis, and fibromyalgia. Pain. [Oct 19 Epub ahead of print] “Results indicated that FMS patients had higher overall levels of and greater daily variability in fatigue compared with the other pain groups.”

Zenz, M., M. Strumpf and M. Tryba. 1992. Long-term oral opioid therapy in patients with chronic nonmalignant pain. J Pain Symptom Manage 7(2):69-77.

Zhou J, Law HKW, Yan Cheung C et al. 2006. Differential expression of chemokines and their receptors in adult and neonatal macrophages infected with human or avian influenza viruses. J Infect Dis 194(1):61-70. One of the reasons that the human variant of avian flu is so devastating to adults is that it precipitates a cytokine storm. [What this will mean to fibromyalgia patients who are already in a cytokine storm generated by FMS remains to be seen. Pentoxifylline has been indicated as helpful to mediate pro-inflammatory cytokines. (See Gutierrez-Reyes G et al 2006) DJS]

Zhuo M. 2007. A synaptic model for pain: long-term potentiation in the anterior cingulated cortex. Mol Cells. 23(3):259-271. “Long-term potentiation (LTP), mostly intensely studies in the hippocampus and amygdale, is proposed to be a cellular model for learning and memory.” “ACC (anterior cingulate cortex) LTP may serve as a cellular model for studying central sensitization that related to chronic pain, as well as pain-related cognitive emotional disorders.”

Zieglgansberger W. 2004. Mechanisms of the transition from acute to chronic pain. J Musculoskeletal Pain 12(3/4):13. “Objectives: Chronic pain states may arise from synaptic and cellular plasticity in a variety of distinct systems. Novel compounds and new regimes for drug treatment to prevent activity-dependent long-term changes are emerging.” “Conclusions: ‘Memory traces’ of pain are not necessarily permanent but can gradually diminish spontaneously or can be reversed by adequate therapeutic intervention. In the absence of reinforcement, the behavioral responses resulting from aversive memories will gradually diminish to be finally extinct. In a recent study we showed that in mice that were deficient in cannabinoid receptor 1 the extinction of aversive memory was impaired. (Marsicano et al., Nature 418, 2002).”

Zih FS, Costa DD, Fitzcharles MA. 2004. Is there benefit in referring patients with fibromyalgia to a specialist clinic? J Rheumatol 31(12):2468-2471. These authors state that care of fibromyalgia patients in a specialist clinic is of value for discovery of co-existing treatable conditions, and is of questionable use in FMS. [Co-existing conditions (such as myofascial trigger points) must be identified and brought under control as much as possible. That is part of the treatment of fibromyalgia. A great deal depends on the ability of the primary physician, and of the pain clinic, to do this. DJS]

Zijlstra TR, Braakman-Jansen LM, Taal E et al. 2007. Cost-effectiveness of spa treatment for fibromyalgia: general health improvement is not for free. Rheumatology [Jul 17 Epub ahead of print]. “The temporary improvement in quality of life due to an adjuvant treatment course of spa therapy for patients with FM is associated with limited incremental costs per patient.”

Zimmermann, M. 1991. Pathophysiology mechanisms of fibromyalgia. Clin J Pain 7 (Suppl1):S8-S15.

Zink, T. and J. Chaffin. 1998. Herbal "health" products: what family physicians need to know. Am Fam Physician 58(5):1133-40.

Zisapel, N. 1999. The use of melatonin for the treatment of insomnia. Biol Signals Recept8(1-1):84-9.

Ziem, G. and J. McTamney. 1997. Profile of patients with chemical injury and sensitivity. Environ Health Perspect 105 Suppl 2:417-436.

Zeisel, S. H. 1986. Dietary influences on neurotransmission. Adv Pediatr 33:23-47.

Zink, T. and J. Chaffin. 1998. Herbal ‘health’ products: what family physicians need to know. Am Fam Physician 58(5):1133-40.

Zink W, Graf BM. 2004. Local anesthetic myotoxicity. Reg Anesth Pain Med. 29(4):333-340. “All local anesthetic agents that have been examined are myotoxic, whereby procaine produces the least and bupivacaine the most severe muscle injury.” [Bupivicaine (Marcaine) should not be used for trigger point injections. Procaine is much less myotoxic. DJS]

Zohn, D. A. 1997. Relationship of joint dysfunction and soft-tissue problems. In: Phys Med Rehab Clin North Am 8(1):69-86.

Zohn, D. and D. Clauw. 1999. Skin rolling as a diagnostic test for fibromyalgia. J Musculoskel P 7(3):127-136.

Zuo Y, Perkins NM, Tracey DJ et al. 2003. Inflammation and hyperalgesia induced by nerve injury in the rat: a key role of mast cells. Pain 105(3):467-79. “Treatment with histamine receptor antagonists suppressed the development of hyperalgesia following nerve injury and alleviated hyperalgesia once it was established.”

Zwerling C, Sprince NL, Davis CS et al. 1998. Occupational injuries among older workers with disabilities: a prospective cohort study of the Health and Retirement Survey, 1992 to 1994. Am J Public Health 88(11):1691-1695. “Poor sight and poor hearing, as well as work disabilities in general, are associated with occupational injuries among older workers.” [Disabled workers are at risk for on-the-job injury. Preventive measures could be instituted that would allow for their inclusion in the workforce without the increased safety concerns. Greater awareness and job adaptation is required on the part of the employers and insurance companies. DJS]

Zwerling C, Whitten PS, Davis CS et al. 1997. Occupational injuries among workers with disabilities: the National Health Interview Survey, 1985-1994. JAMA 278(24):2163-2166. “Workers with disabilities, especially sensory impairments, appear to have an elevated risk for occupational injury. Further research in the design and evaluation of improved workplace accommodations for workers with these disabilities is needed.” [This study identifies preventive measures that could save enormous impact on quality of life, health care costs and avoid increased loss to the work force. DJS]

Zwerling C, Whitten PS, Davis CS et al. 1998. Occupational injuries among older workers with visual, auditory, and other impairments. A validation study. J Occup Environ Med. 40(8):720-723. “As the workforce ages, more attention must be paid to the accommodation of disabilities in the workplace, especially sensory impairments — poor vision and hearing.” [Preventive measures, if instituted early and universally, may result in a tremendous long-term savings in both suffering and in financial costs. This public health impact will be increasing as the work force grows older. DJS]

[No authors listed]. 1997. Practice guidelines for chronic pain management. A report by the American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology 86(4):995-1004

[No authors listed]. 1999. Multiple chemical sensitivity: a 1999 consensus. Arch Environ Health 54(3):147-9.

[No authors listed] 1999. Insomnia: assessment and management in primary care.National Heart, Lung, and Blood Institute Working Group on Insomnia. Am Fam Physician 59(11):3029-38.

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