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).

Aarflot, T. and D. Bruusgaard. 1996. Association between chronic widespread musculoskeletal complaints and thyroid autoimmunity. Results from a community survey. Scand J Prim Health Care 14(2):111-115.

Abajo, F.J., Rodriguex L.A.G., Montero, D. 1999. Association between selective serotonin reuptake inhibitors in gastrointestinal bleeding: population based control study. The concomitant use of NSAIDs or aspirin with SSRIs poses a significantly increased risk of GI bleeding. The possible etiological mechanism is the lower level of platelet serotonin in patients on SSRIs.

Abbasi, F., T. McLaughlin, C. Lamendola and G. M. Reaven. 2000. Insulin regulation of plasma free fatty acid concentrations is abnormal in healthy subjects with muscle insulin resistance. Metabolism 49(2):151-4.

Abbott RB, Hui KK, Hays RD et al. 2007. A randomized controlled trial of Tai Chi for tension headaches. Evid Based Complement Alternat Med. 4(1):107-113. “A 15 week intervention of Tai Chi practice was effective in reducing headache impact and also effective in improving perceptions of some aspects of physical and mental health.”

Abdel-Moty E, Khalil T, Rosomoff H. 1999. The effects of the Aqua-PT on myofascial pain. Paper presented at the 18^th Annual Scientific Meeting of the American Pain Society, Oct 21-24, Greater Fort Lauderdale/Broward County Convention Center. This paper, studying 123 patients with myofascial pain as a primary diagnosis, indicates that 15 minute therapy sessions on an aqua massage unit may provide some relief from myofascial pain.

Abeles AM, Pillinger MH, Solitar BM et al. 2007. Narrative review: the pathophysiology of fibromyalgia. Ann Intern Med. 146(10):726-734.

Abitbol, J., P. Abitbol and B. Abitbol. 1999. Sex hormones and the female voice. J Voice 13(3):424-46.

Acasuso-Diaz, M. and E. Collantes-Estevez. 1998. Joint hypermobility in patients with fibromyalgia syndrome. Arthritis Care Res 11(1):39-42.

Achermann, J. C. and J. L. Jameson. 1999. Fertility and infertility: genetic contributions from the hypothalamic-pituitary-gonadal axis. Mol Endocrinology. 13(6):812-8.

Acheson DW, Luccioli S. 2004. Microbial-gut interactions in health and disease. Mucosal immune responses. Best Pract Res Clin Gastroenterol 18(2):387-404. This is a good review, including functions of the GI mucosal barrier and permeable membrane, or Leaky Gut Syndrome.

Adak B, Tekeoglu I, Ediz L et al. 2005. Fibromyalgia frequency in hepatitis B carriers. J Clin Rheumatol. 11(3):157-159. “The present study suggests that chronic hepatitis B carriage appears to increase the risk of FM and many of the typically associated symptoms.”

Adam TC, Epel ES. 2007. Stress, eating and the reward system. Physiol Behav. 91(4):449-458. Chronic stress may be worsening the obesity epidemic due to the loss of glucocorticoid regulation by insulin and leptin.

Adams PJ, Snutch TP. 2007. Calcium channelopathies: voltage-gated calcium channels. Subcell Biochem. 45:215-251. Genetically caused minute changes in calcium ion channels can have a wide spectrum affect on “...mammalian developmental, physiological and behavioral functions.” Agents that act on selective calcium channel activity may be important medications for the future.

Adams, W. R., K. J. Spolnik and J. E. Bouquot. 1999. Maxillofacial osteonecrosis in a patient with multiple “idiopathic” facial points. J Oral Pathol Med 28(9):423-32. Called NICO (neuralgia-inducing cavitational osteonecrosis). The underlying problem is vascular insufficiency.

Adcock KG, Kyle PB, Deaton JS et al. 2007. Pharmacokinetics of intranasal and intratracheal pentoxifylline in rabbits. Pharmacotherapy. 27(2):200-206. “The pharmacokinetic profiles after intranasal and intratracheal administration of pentoxifylline appear similar to those after intravenous administration.” [Since intrathecal glial cell modulation works well in rats to diminish or relieve central sensitization, this use of intranasal pentoxifylline may have potential for FMS. DJS]

Adiguzel O, Kaptanoglu E, Turgut B et al. 2004. The possible effect of clinical recovery on regional cerebral blood flow deficits in fibromyalgia: a prospective study with semi-quantitative SPECT. South Med J. 97(7):651-655. “...these findings could indicate that deficits in cerebral blood flow in fibromyalgia improve parallel to clinical recovery.”

Adler GK, Geenen R. 2005. Hypothalamic-pituitary-adrenal and autonomic nervous system functioning in fibromyalgia. Rheum Dis Clin North Am 31(1):187-202. “In general, there seems to be a reduction in some neuroendocrine and autonomic nervous system (ANS) responses to applied stresses in individuals who have fibromyalgia.”

Adler GK, Manfredsdottir VF, Creskoff KW. 2002. Neuroendocrine abnormalities in fibromyalgia. Curr Pain Headache Rep 6(4): 289-98. "A combination of multiple, mild impaired responses may lead to more profound physiologic and clinical consequences as compared with a defect in only one system, and could contribute to the symptoms of fibromyalgia."

Adler, G. K., B. T. Kinsley, S. Hurwitz, C. J. Mossey and D. L. Goldenberg. 1999. Reduced hypothalamic pituitary and sympathoadrenal responses to hypoglycemia in women with fibromyalgia syndrome. Am J Med 106(5):534-43.

Adler MW, Rogers TJ. 2005. Are chemokines the third major system in the brain? J Leukoc Biol. [Oct 4 Epub ahead of print] The authors propose that the endogenous chemokine system in the brain interacts with the neurotransmitter and neuropeptide systems to govern brain function. [There are abundant chemokine receptors in the glial cells, and activated intrathecal glia have been implicated in the inception and maintenance of chronic pain states. Imbalance of specific neuopeptides, and neurotransmitters and cytokines have been implicated in fibromyalgia, and biochemicals belonging to these systems are released during myofascial trigger point twitch. DJS]

Adriaensen H, Vissers K, Noorduin H et al. 2003. Opioid tolerance and dependence: an inevitable consequence of chronic treatment? Acta Anaesthesiol Belg. 54(1):37-47. “Although opioids provide effective analgesia, largely unsubstantiated concern about opioid-induced tolerance, physical dependence and addiction have limited their appropriate use. As a consequence, many patients receive inadequate treatment for both malignant and non-malignant pain. However, it has been shown that analgesic tolerance develops less frequently during chronic opioid administration in a clinical context than in animal experiments.”

Affaitati G, Fabrizio A, Savini A et al. 2009. A randomized, controlled study comparing a lidocaine patch, a placebo patch, and anesthetic injection for treatment of trigger points in patients with myofascial pain syndrome: evaluation of pain and somatic pain thresholds. Clin Ther. 31(4):705-720. The lidocaine patch seems effective and acceptable to patients with myofascial pain. [This may be useful in sports therapy, or very early detection of single TrPs. The patch in the study was applied to THE trigger point. For those of us with chronic myofascial pain, having dozens or even hundreds of TrPs, lidocaine patch therapy may not be helpful. DJS]

Aftimos, S. 1989. Myofascial pain in children. N Z Med J 102(874):440-441.

Agargun, M. Y. , I. Tekeoglu, A. Gunes, B. Adak, H. Kara and M. Ercan. 1999. Sleep quality and pain threshold in patients with fibromyalgia. Compr Psychiatry 40(3):226-8.

Ahmadpour, S. and U. M. Kabadi. 1997. Pancreatic alpha-cell function in idiopathic reactive hypoglycemia. Metabolism 46(6):639-643.

Aikins, Murphy P. 1998. Alternative therapies for nausea and vomiting of pregnancy. Obstet Gynecol 91(1):149-155.

Airaksinen, O. and P. J. Pontinen. 1992. Effects of electrical stimulation of myofascial trigger points with tension headache. Acupunct Electrother Res 17(4):285-290.

Akassoglou K., Strickland S. 2002. Fibrin inhibits nerve regeneration by arresting schwann cell differentiation. Glia (Suppl 1):S42 [Abstract]. “These results provide the first indication that fibrin, a blood-derived protein, which becomes a component of the extracellular matrix of the nervous system in pathological states, can affect repair by negatively regulating myalination. Dysregulation of fibrin clearance and/or deposition could play a role in traumatic injuries of the nervous system, as well as in demyelinating diseases such as multiple sclerosis.”

Akkasilpa S, Goldman D, Magder LS et al. 2005. Number of fibromyalgia tender points is associated with health status in patients with systemic lupus erythematosus. J Rheumatol. 32(1):48-50. “A strong association between the number of FM TPs and health status was found in patients with SLE. The number of TPs, and not just the presence/absence of FM, is associated with health status in SLE.”

Al-Alawi A, Mulgrew A, Tench E et al. 2006. Prevalence, risk factors and impact on daytime sleepiness and hypertension of periodic leg movements with arousals in patients with obstructive sleep apnea. J Clin Sleep Med. 2(3):281-287. “Risk factors for PLMS include preexisting medical conditions -- particularly depression, fibromyalgia, and diabetes mellitus -- increasing age, predisposing medications, obesity and OSA.”

Al-Shenqiti AM, Oldham JA. 2005. Test-retest reliability of myofascial trigger point detection in patients with rotator cuff tendonitis. Clin Rehabil. 19(5):482-487. “The presence or absence of the taut band, spot tenderness, jump sign and pain recognition was highly reliable between sessions. Referred pain and local twitch response reliability varied depending on the muscle being studied.” [Again, both training and experience are vital to reliably diagnose and treat TrPs. DJS]

Alanoglu E, Ulas UH, Ozdag F. et al. 2004. Auditory event-related brain potentials in fibromyalgia syndrome. Rheumatol Int. [Epub Feb 21 ahead of print]. “...FM affects quality of life and dysfunction in cognitive abilities can be determined by brain event-related potentials.”

Alarcon, G. S., and L. A. Bradley. 1998. Advances in the treatment of fibromyalgia: current status and future directions. Am J Med Sci 315 (6):397-404.

Albright, G. L. and A. A. Fischer. 1990. Effects of warming imagery aimed at trigger-point sites on tissue compliance, skin temperature, and pain sensitivity in biofeedback-trained patients with chronic pain: a preliminary study. Percept Mot Skills 71(3 Pt 2):1163-70.

Album D, Westin S. 2007. Do diseases have a prestige hierarchy? A survey among physicians and medical students. Soc Sci Med. [Sep 10 Epub ahead of print] Medical specialties and illnesses are considered to have a ranking among doctors and medical students. “Myocardial infarction, leukemia and brain tumor were among the highest ranked, and fibromyalgia and anxiety neurosis were among the lowest.” “Low prestige scores are given to diseases and specialties associated with chronic conditions located in the lower parts of the body or having no specific bodily location, with less visible treatment procedures, and with elderly patients.” [It seems we have a lot of educating to do, and it is no wonder FM patients are considered to have a self-esteem problem. See: “Bennett RM. 2007. Do patients’ perceptions of negative physician attitudes influence fibromyalgia symptoms and status?” This would seem to indicate that some doctors could be major perpetuating factors. DJS.]

Aldridge, R., E. B. Cady, D. A. Jones and G. Obletter. 1986. Muscle pain after exercise is linked with an inorganic phosphate increase as shown by 31P NMR. Biosci Rep 6(7):663-7.

Alexander, R. W. , L. A. Bradley, G. S. Alarcon, M. Triana-Alexander, L. A. Aaron, K. R. Alberts, M. Y. Martin and K. E. Stewart. 1998. Sexual and physical abuse in women with fibromyalgia: association with outpatients health care utilization and pain medication usage. Arthritis Care Res 11(2):102-15.

Alford, F. P., F. L. Hew, M. C. Christopher and C. Rantzau. 1999. Insulin sensitivity in growth hormone (GH)-deficient adults and effect of GH replacement therapy. J Endocrinol Invest 22(5 Suppl):28-32.

Alix ME, Bates DK. 1999. A proposed etiology of cervicogenic headache: the neurophysiologic basis and anatomic relationship between the dura mater and the rectus posterior capitis minor muscle. J Manipulative Physiol Ther. 22(8):534-539. This study found bridges formed of connective tissue at the atlanto-occipital junction between the rectus capitis posterior and the dorsal spinal dura. Tightness of these connections may be associated with headache. “The dura-muscular, dura-ligamentous connections in the upper cervical spine and occipital areas may provide anatomic and physiologic answers to the cause of the cervicogenic headache.”

Allcock N, McGarry J, Elkan R. 2002. Management of pain in older people within the nursing home: a preliminary study. Health Soc Care Comm. 10(6):464-471. “It has been estimated that approximately two-thirds of people aged 65 years and over experience chronic pain, and that the prevalence of chronic pain in nursing home residents is between 45% and 80%. Overall, 37% of nursing home residents were identified as experiencing chronic non-malignant pain.”

Allegrante, J. P. 1996. The role of adjunctive therapy in the management of chronic nonmalignant pain. Am J Med 101(1A):33S-39S.

Allen, G., B. S. Galer and L. Schwartz. 1999. Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain 80(3):539-44

Almeida, TF, Roizenblatt, S, Benedito, Silva AA, et al. 2003. The effect of combined therapy (ultrasound and interferential current) on pain and sleep in fibromyalgia. Pain 104(3):665-672. Combined therapy with pulsed ultrasound and interferential current can be an effective therapy for pain and sleep dysfunction in fibromyalgia patients.

Alonso-Ruiz, A., A. De la Hoz-Martinez and A. C. Zea-Mendoza. 1985. Fibromyalgia syndrome as a late complication of toxic-oil syndrome. J Rheumatol 12(6):1207-1208.

Altindag O, Gur A, Calgan N et al. 2007. Paraoxonase and arylesterase activities in fibromyalgia. Redox Rep. 12(3):134-138. “Patients with fibromyalgia might be prone to development of atherosclerosis with reduced paraoxonase and arylesterase activities.”

Altindag O, Celik H. 2006. Total antioxidant capacity and the severity of the pain in patients with fibromyalgia. Redox Rep. 11(3):131-135. “Increased oxidative stress may play a role in the etiopathogenesis of the disease.” Antioxidant supplements may be a useful part of therapy.

Alvarez DJ, Rockwell PG. 2002. Trigger points: diagnosis and management. Am Fam Physician 65(4):653-660. “Trigger points are discrete, focal, hyperirritable spots located in a taut band of skeletal muscle. They produce pain locally and in a referred pattern and often accompany chronic musculoskeletal disorders. Acute trauma or repetitive microtrauma may lead to the development of stress on muscle fibers and the formation of trigger points. Patients may have regional, persistent pain resulting in a decreased range of motion in the affected muscles. These include muscles used to maintain body posture, such as those in the neck, shoulders, and pelvic girdle. Trigger points may also manifest as tension headache, tinnitus, temporomandibular joint pain, decreased range of motion in the legs, and low back pain. Palpation of a hypersensitive bundle or nodule of muscle fiber of harder than normal consistency is the physical finding typically associated with a trigger point. Palpation of the trigger point will elicit pain directly over the affected area and/or cause radiation of pain toward a zone of reference and a local twitch response. Various modalities, such as the Spray and Stretch technique, ultrasonography, manipulative therapy and injection, are used to inactivate trigger points. Trigger-point injection has been shown to be one of the most effective treatment modalities to inactivate trigger points and provide prompt relief of symptoms.”

Alvarez, L. B. , J Teran, J. L. Alonso, J. Alegre, I. Arroyo and J. L. Viejo. 1992. Lack of association between fibromyalgia and sleep apnea syndrome. Ann Rheum Dis 51(1):108-11.

Aly T.A., Tahaka Y., Aizawa T. et al. 2002. Medial superior cluneal nerve entrapment neuropathy in teenagers: a report of two cases. Tohoku J Exp Med 197(4):229-31. Nerve entrapment causing pain radiating down the low back may be caused by myofascial trigger points, but these are often misdiagnosed. These two patients completely recovered after trigger point therapy, even though they had been misdiagnosed and in pain for a long time.

Amador NJ, Shivers K, Weiner J et al. Program 51.16/M8. Estrus cycle effects on behavioral and physiological responses to formalin-induced inflammatory pain. Georgia World Congress Center Atlanta, GA. Society for Neuroscience, Presentation.: Oct 14, 2006. Both physiological and behavioral changes to inflammatory pain can vary significantly with the estrus cycle in rats. Hormones may physically affect perceptions of pain.

Ambalavanar R, Moutanni A, Dessem D. 2006. Inflammation of craniofacial muscle induces widespread mechanical allodynia. Neurosci Lett. [Feb 27 Epub ahead of print]

Ambrogio, N., J. Cuttiford, S. Lineker and L. Li. 1998. A comparison of three types of neck support in fibromyalgia patients. Arthritis Care Res 11(5):405-10.

Ames BN, Elson-Schwab I, Silver EA. 2002. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. Am J Clin Nutr. 75(4):616-658. This article concerns increasing developments in the science of genomics. They have already found over 50 genetic diseases that can be helped by high doses of the vitamin component of coenzymes, restoring metabolic paths. [From what we have learned in the study of genomics and epigenomics, each human being has significantly different nutrient requirements, and this may be profoundly affected by differences in intestinal permeability. The use of healthy food and supplements as medicine may become more accepted as research unfolds. DJS]

Amital D, Fostik L, Polliack ML et al. 2006. Posttraumatic stress disorder, tenderness, and fibromyalgia syndrome: are they different entities? J Psychosom Res. 61(5):663-669. This study concerned comorbidity of FMS in male patients with PTSD that occurred after an intensive, initial combat-related traumatic event. [In these patients, and not necessarily all male patients as the study concluded, the occurrence, degree and impact of PTSD is often significantly related to co-existing FMS. FMS may be amplifying more than pain. DJS]

Ammer, K. and P. Melnizky. 1999. [Medicinal baths for treatment of generalized fibromyalgia.] Forsch Komplementarmed 6(2):80-5. [German] .

Anand KJ. 2000. Pain, plasticity, and premature birth: a prescription for permanent suffering? Nat Med 6(9):971-973. Premature infants and other children requiring medical procedures require adequate pain control. Failure to provide it not only causes needless acute suffering but can change the central nervous system and cause predisposition to chronic pain.

Anand P, Aziz Q, Willert R et al. 2007. Peripheral and central mechanisms of visceral sensitization in man. Neurogastroenterol Motil. 19(1 Suppl):29-46.

Ancoli-Israel, S. and T. Roth. 1999. Characteristics of insomnia in the United States: results of the 1991 National Sleep Foundation Survey. I. Sleep 22 Suppl 2:S347-53.

Anderberg, UM, 2001.[Stress-related syndromes-contemporary illnesses.] Lakartidningen Dec;98(51-52):5860-3.[Swedish] The diagnoses of burnout, chronic fatigue syndrome and fibromyalgia syndrome may represent reactions to an overwhelming situation. The new diagnoses may indicate preliminary stages of more serious diseases such as angina pectoris or myocardial infarction. Other causes of death may be related to stress. "These circumstances reflect not only considerable suffering on the part of individuals, but also a substantial economic burden for society".

Anderberg, U. M., Z. Liu, L Berglund and F. Nyberg. 1999. Elevated plasma levels of neuro-peptide Y in female fibromyalgia patients. Eur J Pain 3(1):19-30.

Anderberg, U. M. , I. Marteinsdottir, J. Hallman and T. Backstrom. 1998. Variablility in cyclicity affects pain and other symptoms in female fibromyalgia syndrome patients. J Musculoskel Pain 6(4):5-22.

Anderson H, Arendt-Nielsen L, Svensson P et al. 2007. Spatial and temporal muscle hyperalgesia induced by nerve growth factor in humans. J Musculoskel Pain 15 (Supp 13):13 item 16. [Myopain 2007 Poster] “NGF intramuscular injection causes a time-dependent enlargement of the hyperalgesic area that is most prominent 24 hours after injection. The expansion of hyperalgesia locally and in distinct area innervated by the same nerve indicates that both peripheral and central mechanisms are involved in the NGF-induced sensitization. These findings may add to the current knowledge of the development of chronic pain conditions.”

Anderson, K. and J. M. Silver. 1998. Modulation of Anger and Aggression. Semin Clin Neuropsychiatry 3(3):232-242.

Anderson RU, Wise D, Sawyer T et al. 2005. Integration of myofascial trigger point release and paradoxical relaxation training treatment of chronic pelvic pain in men. J Urol. 174(1):155-160. Myofascial release of trigger points combined with paradoxical relaxation training can provide pain relief superior to traditional therapy.

Andersson HI. 2004. The course of non-malignant chronic pain: a 12-year follow-up of a cohort from the general population. Eur J Pain 8(1):47-53. “Mortality was significantly higher in the group initially reporting widespread pain compared with the other groups. The chronicity of widespread chronic pain supports early and intense intervention among individuals with located pain. The association between chronic widespread pain and increased mortality needs further investigation but may deepen the view of chronic pain as a public health problem.”

Andersen, S. and G. Leikersfeldt. 1996. Management of chronic non-malignant pain. Br J Clin Pract 50(6):324-330.

Anderson, R. A. 1992. Chromium, glucose tolerance, and diabetes. Biol Trace Elem Res 32:19-24.

Anderson, R. C. and J. H. Anderson. 1999. Sensory irritation and multiple chemical sensitivity. Toxicol Ind Health 15(3-4):339-45.

Anderson, R. C. and J. H. Anderson. 1998. Acute toxic effects of fragrance products. Arch Environ Health 53(2):138-46.

Andersson, M., J. R. Bagby, L. Dyrehag and C. Gottfries. 1998. Effects of staphylococcus toxoid vaccine on pain and fatigue in patients with fibromyalgia/chronic fatigue syndrome. Eur J Pain 2(2):133-142.

Andersson, M., J. R. Bagby, L. E. Dyrehag and C. G. Gottfries. 1999. Effects of staphylococcus toxoid vaccine on pain and fatigue in patients with fibromyalgia/chronic fatigue syndrome. Eur J Pain 2(2):133-142.

Andreu JL, Sanz J. 2005. [Fibromyalgia and its diagnosis.] Rev Clin Esp. 205(7):333-336. [Spanish] “Although the fibromyalgia classification criteria of the American College of Rheumatology are not diagnostic criteria, they have been extensively used to diagnose FMS in patients with chronic diffuse arthromyalgias. Fibromyalgia diagnosis reduces the patient’s anxiety, avoiding complementary expensive and unnecessary tests and it allows the patient to share his/her fears, illnesses and expectations with other human beings who suffer the same problem.”

Andrews R.C., Herlihy O., Livingstone D.E. 2002. Abnormal cortisol metabolism and tissue sensitivity to cortisol in patients with glucose intolerance. J Clin Endocrinol Metab 87(12):5587-93. “...in patients with glucose intolerance, cortisol secretion, although normal, is inappropriately high given enhanced central and peripheral sensitivity to glucocorticoids....altered cortisol action occurs not only in obesity and hypertension but also in glucose intolerance, and could therefore contribute to the link between these multiple cardiovascular risk factors.”

Andrews, R. C. and B. R. Walker. 1999. Glucocorticoids and insulin resistance: old hormones, new targets. Clin Sci (Colch) 96(5):513-523.

Angarola, R. T. 1990. National and international regulation of opioid drugs: purpose, structures, benefits and risks. J Pain Symptom Manage 5(1 Suppl):S6-S11.

Angsuwarangsee T, Morrison M. 2002. Extrinsic laryngeal muscular tension in patients with voice disorders. J Voice 16(3):333-343. “A strong relationship was found between thyrohyoid muscle tension and both gastroesophageal reflux (GER) and muscle misuse dysphonia (MMD).” [These patients were not checked for TrPs. TrPs may cause muscle tension. This may be an important connection between reflux as a perpetuating factor of myofascial TrPs. DJS]

Antoin H, Beasley RD. 2004. Opioids for chronic noncancer pain. Tailoring therapy to fit the patient and the pain. Postgrad Med. 116(3)37-40, 43-44. “…opioids can be a viable option today for successful therapy for chronic non-cancer pain.”

Anuradha, C. V. and S. D. Balakrishnan. 1999. Taurine attenuates hypertension and improves insulin sensitivity in the fructose-fed rat, and animal model of insulin resistance. Can J Physiol Pharmacol 77(10:749-54.

Apkarian AV, Sosa Y, Krauss BR et al. 2004. Chronic pain patients are impaired on an emotional decision-making task. Pain 108(1-2):129-136. “Performance on an emotional decision-making task may be impaired in chronic pain since human brain imaging studies show that brain regions critical for this ability are also involved in chronic pain. Our evidence indicates that chronic pain is associated with a specific cognitive deficit, which may impact everyday behavior especially in risky, emotionally laden situations.”

Apkarian AV, Sosa Y, Sonty S et al. 2004. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neurosci. 24(46):10410-10415. “Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.”

Appelboom, T. and A. Schoutens. 1990. High bone turnover in fibromyalgia. Calcif Tissue Int 46(5):314-317.

Arciero, P. J., M. D. Vukovich, J. O. Holloszy, S. B. Racette and W. M. Kohrt. 1999. Comparison of short-term diet and exercise on insulin action in individuals with abnormal glucose tolerance. J Appl Physiol 86(6):1930-5.

Arden Pope III, C., R. L. Verrier, E. G. Lovett, A. C. Larson, M. E. Raizenne, R. E. Kanner, J. Schwartz, G. M. Villegas, D. R. Gold and D. W. Dockery. 1999. Heart rate variability associated with particulate air pollution. Am Heart J 138(5):890-899.

Ardic F, Gokharman D, Atsu S et al. 2006. The comprehensive evaluation of temporomandibular disorders seen in rheumatoid arthritis. Aust Dent J. 51(1):23-28. “...the myofascial pain of the temporomandibular system is an important cause of pain in rheumatoid arthritis...”

Arendt-Nielsen L. 2007. Measuring muscle pain. J Musculoskel Pain 15 (Supp 13):9 item 11. [Myopain 2007 Poster] “Referred muscle pain [and the possible related hyperalgesia] is manifested in somatic structures [skin, muscles, joints, tendons]. These manifestations are of significant clinical importance for the diagnosis of pain pathologies.” “Recently we have found that patients suffering from chronic musculoskeletal pains have significantly larger referred pain areas to experimentally induced muscle pain intramuscular injection of hypertonic saline, and at the same time they show manifestations of muscle sensitization. Furthermore they show facilitated responses to a variety of other stimuli.”

Arendt-Nielsen L, Mense S, Graven-Nielsen T. 2003. [Assessment of muscle pain and hyperalgesia. Experimental and clinical findings] [German] Schmerz 17(6):445-449. “ An important part of the manifestation of pain in chronic musculoskeletal disorders may be due to peripheral and central sensitization processes, which are also involved in the transition from acute to chronic pain. Knowledge of these processes has expanded enormously in recent years; it should be utilized when new intervention strategies are designed.”

Arendt-Nielsen, L, Graven-Neilsen, T. 2003. Central sensitization in fibromyalgia and other musculoskeletal disorders. Curr Pain Headache Rep. 7(5):355-361. Tenderness and referred chronic musculoskeletal pain may be due to peripheral and central sensitization. This sensitization may be part of what changes acute pain into chronic pain.

Arendt-Nielsen, L., T. Graven-Nielson. 2002. Deep tissue Hyperalgesia. J Musculoskel Pain 10(1/2):97-119. "increased muscle sensitivity is present in musculoskeletal pain conditions and may play a role for chronification of pain, and interventions should take this aspect into consideration".

Arendt-Nielsen, L., T. Graven-Nielsen and P. Svensson. 1999. Assessment of muscle pain in humans–clinical and experimental aspects. J Musculoskel Pain 7(1-2):25-41.

Argoff, C. E. 2002. A review of the use of topical analgesics for myofascial pain. Curr Pain Headache Rep 6(5):375-8.

Arguelles LM, Afari N, Buchwald DS et al. 2006. A twin study of posttraumatic stress disorder symptoms and chronic widespread pain. Pain [May 13 Epub ahead of print] “Our findings suggest that PTSD (posttraumatic stress disorder) symptoms, as measured by IES (Impact Events Scale), are strongly linked to CWP (chronic widespread pain), but this association is not explained by a common familial or genetic vulnerability to both conditions. Future research is needed.

Ariji Y, Sakuma S, Izumi M et al. 2004. Ultrasonographic features of the masseter muscle in female patients with temporomandibular disorder associated with myofascial pain. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 98(3):337-341. Masseter muscle pain in TMD might be associated with muscle edema.

Ariji Y, Sakuma S, Izumi M et al. 2004. Ultrasonographic features of the masseter muscle in female patients with temporomandibular disorder associated with myofascial pain. Oral Surg. 98(3):337-341. [I found it very interesting that the myofascial pain in patients in this study was associated with muscle edema. DJS]

Arnold LM, Crofford LJ, Martin SA et al. 2007. The effect of anxiety and depression on improvements in pain in a randomized, controlled trial of pregabalin for treatment of fibromyalgia. Pain Med. 8(8):633-638. “The pain treatment effect of pregabalin did not depend on baseline anxiety or depressive symptoms, suggesting pregabalin improves pain in patients with or without these symptoms. Much of the pain reduction appears to be independent of improvements in anxiety or mood symptoms.”

Arnold LM, Pritchett YL, D’Souza DN et al. 2007. Duloxetine for the treatment of fibromyalgia in women: pooled results from two randomized, placebo-controlled clinical trials. J Womens Health 16(8):1145-1156. “…duloxetine is a safe and efficacious treatment for both the pain and functional impairment associated with fibromyalgia in female patients, while significantly improving quality of life.”

Arnold L, Duan W, Young, Jr. J et al. 2007. Efficacy of pregabalin monotherapy for relief of pain associated with fibromyalgia syndrome: time course and durability of pain results of a 14-week, double-blind, placebo-controlled trial. J Musculoskel Pain 15 (Supp 13):41 item 71. [Myopain 2007 Poster] “Pregabalin was associated with relief of FMS pain.”

Arnold L, Russell IJ, Duan R et al. 2007. Pregabalin monotherapy for relief of symptoms of fibromyalgia syndrome: two double-blind, randomized, controlled trials. J Musculoskel Pain 15 (Supp 13):41 item 72. [Myopain 2007 Poster] “Pregabalin 300, 450, and 600mg/d [BID] therapy was associated with significant and clinically relevant reduction of pain associated with FMS.”

Arnold LM, Goldenberg DL, Stanford SB et al. 2007. Gabapentin in the treatment of fibromyalgia: a randomized, double-blind, placebo-controlled, multicenter trial. Arthritis Rheum. 56(4):1336-1344. “Gabapentin (1,200-2,400 mg/day) is safe and efficacious for the treatment of pain and other symptoms associated with fibromyalgia.” [It would be interesting to see a comparison of the effectiveness and side-effect profile of Gabapentin and Lyrica. DJS]

Arnson Y, Amital D, Fostick L et al. 2007. Physical activity protects male patients with post-traumatic stress disorder from developing severe fibromyalgia. Clin Exp Rheumatol. 25(4):529-533. “Physical exercise in male patients with combat-related PTSD provides protection from the future development of fibromyalgia and is related in this group of patients to a better perception of their quality of life.”

Arnstein, P., M. Caudill, C. L. Mandle, A. Norris and R. Beasley. 1999. Self efficacy as a mediator of the relationship between pain intensity, disability and depression in chronic pain patients. Pain 80(3):483-91.

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Arlt, W., F. Callies, J. C. van Vlijmen, I. Koehler, M. Reincke, M. Bidlingmaier, D. Huebler, M. Oettel, M. Ernst, H. M. Schulte and B. Allolio. 1999. Dehydroepiandrosterone replacement in women with adrenal insufficiency. N Engl J Med 341(14):1013-20.

Arshad A, Ool KK. 2007. Awareness and perceptions of fibromyalgia syndrome: a survey of Southeast Asian rheumatologists. J Clin Rheumatol. 13(2):59-62.

Arshad A, Kong KO. 2007. Awareness and perceptions of fibromyalgia syndrome: a survey of Malaysian and Singaporean rheumatologists. Singapore Med J. 48(1):25-30. “This study confirmed that there was a variation of perceptions and knowledge of FMS among rheumatologists from Malaysia and Singapore.” [It is unfortunate that neither the rheumatologists surveyed nor the authors themselves understand that fibromyalgia is not a diagnosis of exclusion, and that FMS is often present as a condition interacting with other diagnoses. DJS]

Arvoid DS, Odean MJ, Dornfeld MP et al. 2009. Correlation of symptoms with vitamin D deficiency and symptom response to cholecalciferol treatment: a randomized controlled trial. Endocr Pract. 15(3):203-212. “Compared with participants in the placebo group, patients in the treatment group showed mild short-term improvement in the overall fibromyalgia impact score, but did not show significant improvement in most musculoskeletal symptoms or in activities of daily living.” [This study might have been much more helpful had it taken into account co-existing myofascial trigger points. DJS]

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Asbring P, Narvanen AL. 2003. Ideal versus reality: physicians perspectives on patients with chronic fatigue syndrome (CFS) and fibromyalgia. Soc Sci Med 57(4):711-720. “The results suggest that there is a discrepancy between the ideal role of the physician and reality in the everyday work in interaction with these patients.” “The results also illuminate the physician’s interpretations of patients in moralising terms. Conditions given the status of illness were regarded, for example, as less serious by the physicians than those with disease status. Skepticism was expressed regarding especially CFS, but also fibromyalgia. Moreover, it is shown how the patients are characterized by the physicians as ambitious, active, illness focused, demanding and medicalising. The patients in question do not always gain full access to the sick-role, in part as a consequence of the conditions not being defined as diseases.” [It is a sad reflection on the state of medical practice that many practitioners do not understand that syndromes can be every bit as serious and life-altering as diseases. Just because we do not understand the total mechanisms behind the illness does not mean the patients with these illnesses do not deserve the care given to patients who have illnesses that we do understand. DJS]

Asbring, PJ, Chronic Illness-A Disruption in Life: Identity-Transformation Among Women with Chronic Fatigue Syndrome and Fibromyalgia. Adv Nurs 34(3):312-319, 2001. FMS can profoundly affect personal identity, particularly in relation to work and social life. Some of the change was positive. The first step toward successful therapy is often the acceptance of diagnosis.

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Ashby, E.C. 1994. Chronic obscure groin pain is commonly caused by enthesopathy: 'tennis elbow' of the groin. Br J. Surg 81(11):1632-4. Groin pain may be caused by myofascial trigger points in the groin ligaments.

Ashina S, Bendtsen L, Ashina M. 2005. Pathophysiology of tension-type headache. Curr Pain Headache Rep. 9(6):415-422. “Increased excitability of the central nervous system generated by repetitive and sustained pericranial myofascial input may be responsible for the transformation of episodic tension-type headache into the chronic form. Studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of tension-type headache and that the antinociceptive effect of nitric oxide synthase inhibitors may become a novel principle in the future treatment of chronic headache.” [Nitric oxide is a focus of chronic pain research, and would give another pathway to treat it. DJS]

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Assefi, N.P., Coy, T.V., Uslan, D. et al. Financial, occupational, and personal consequences of disability patients with chronic fatigue syndrome and fibromyalgia compared to other fatiguing conditions. J Rheumatol 30(4):804-8. Patient evaluation at a chronic fatigue clinic indicated that the patients with the most extensive loss of support by friends, family, and loss of job, possessions, and recreational abilities were those with FMS alone or with CFS, and yet there were “...no reliable difference between groups in use of disability benefits.” The authors recommend “Employers and personal relations of patients with chronic fatigue should make a greater effort to accommodate the illness-related limitations of these conditions, especially for those with FMS and CFS.

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Audette JF, Blinder RA. 2003. Acupuncture in the management of myofascial pain and headache. Curr Pain Headache Rep. 7(5):395-401. Many practitioners and patients have reported benefits from the treatment of myofascial pain and headache by acupuncture.

Audette JF, Wang F, Smith H 2004. Bilateral activation of motor unit potentials with unilateral needle stimulation of active myofascial trigger points. Am J Phys Med Rehabil. 83(5):368-374. “...perception of pain and muscle dysfunction in active MTrPs may be related to abnormal central nervous system processing of sensory input at the level of the spinal cord.”

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Bach GL, Clement DB. 2007. Efficacy of Farabloc as an analgesic in primary fibromyalgia. [Jan 11 Epub ahead or print] Clin Rheumatol. This single-blind study suggests that Farabloc, an electromagnetic shielding fabric, if used as material for night clothes for fibromyalgia patients, has analgesic properties.

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Bal S, Celiker R. 2009. Health-related quality of life in patients with myofascial pain syndrome: a controlled clinical study. J Musculoskel Pain. 17(2):173-177. “There was a correlation between NHP (Nottingham Health Profile) pain score and number of trigger points. However, no correlation was found between the NHP scores and other clinical parameters, such as age, duration of pain, and visual analog scale scores.” “The results of this study suggest that MPS affects many aspects of HRQOL (health-related quality of life). Besides the clinical and laboratory evaluation, the emotional and physiological parameters should also be considered to define the health status of the patients and plan the appropriate treatment.”

Balasubramaniam R, Laudenbach JM, Stoopler ET. 2007. Fibromyalgia: an update for oral health care providers. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 104(5):589-602. “Oral health care providers may be the first to recognize signs and symptoms of this complex disorder and are often consulted to participate in the management of FM patients.” “This review will also highlight issues that are important to the oral health care provider, including orofacial manifestations and dental considerations for patients with FM.” [Many dentists and oral hygienists have no idea how much their work can impact the life of their FM patients. They don’t understand central sensitization and can cause significant needless pain that can last for weeks or longer. Many dentists are also unaware of MTPs, and thus unaware of the impact MTPs can have on equilibration. If the bite is off due to MTPs, or there is dental pain or sensitivity to pressure or cold, etc., due to MTPs, errors in “correcting” the bite can ruin the patient’s mouth, cause needless dental work, and amount to malpractice. Information has been available for a long time, and there is no excuse for dentists (nor other care providers) “not wanting to know.” DJS]

Balasubramanian V, Adalarasu K. 2007. EMG-based analysis of change in muscle activity during simulated driving. J Bodywork Move Ther. 11, 151-158. “Extensive usage of computers could cause fatigue and even lead to musculo-skeletal injuries.”

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Baliki MN, Geha PY, Apkarian AV. 2007. Spontaneous pain and brain activity in neuropathic pain: functional MRI and pharmacologic functional MRI studies. Curr Pain Headache Rep 11(3):171-177. Functional MRI may be a valid method for studying clinical pain. “...the latest results using this approach imply that distinct clinical chronic pain conditions seem to involve specific brain circuitry, which is also distinct from the brain activity commonly observed in acute pain.”

Baliki MN, Chialvo DR, Geha PY. 2006. Chronic pain and the emotional brain: Specific brain activity associated with spontaneous fluctuations of intensity of chronic back pain. Chronic pain seems to activate different areas of the brain than are activated during acute pain. Chronic pain is associated with the insula, an area of the brain that also is associated with negative emotions, response conflict, emotional memories and self-image. Chronic back pain may influence a person’s sense of being and may trigger emotional distress of itself.

Balint G. 2002. Buprenorphine treatment of patients with non-malignant musculoskeletal diseases. Clin Rheumatol 21 Duppl 1:S17-S18. “When simple analgesics are not sufficient, the use of opioid-type analgesics is justified. Buprenorphine transdermal therapeutic system (TDS) is a novel formulation of a well-tolerated and highly effective drug for satisfactory pain control that can also be used in patients with chronic non-malignant pain (CNMP) due to musculoskeletal diseases.”

Balousek S, Plane MB, Fleming M. 2007. Prevalence of interpersonal abuse in primary care patients prescribed opioids for chronic pain. J Gen Intern Med. [Jul 20 Epub ahead of print]. This study, contrary to many others, reported abuse of opioids in chronic pain patients. A large percentage of these patients, however, had suffered lifetime physical abuse and suicide attempts. The study concludes that understanding of patients' needs may be better met by screening patients taking opioids for chronic pain for a history of interpersonal abuse, and addressing those needs specifically.

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Banisadr G, Rostene W, Kitabgi P et al. 2005. Chemokines and brain functions. Curr Drug Targets Inflamm Allergy 4(3):387-399. “Chemokines are small secreted proteins that chemoattract and activate immune and non-immune cells both in vivo and in vitro. Besides their well-established role in the immune system, several recent reports have suggested that chemokines and their receptors may also play a role in the central nervous system. These proteins regulate the leukocyte infiltration in the brain during inflammatory and infectious diseases. Chemokines and their receptors are constitutively expressed by glial and neuronal cells in the CNS, where they are involved in intercellular communication. The implication of chemokines in cellular communication could allow: i) to identify a new pathway for neuron-neuron and/or glia-glia and/or neuron-glia communications that are relevant to both normal brain function and neuroinflammatory and neurodegenerative diseases; ii) to develop new therapeutic approaches for still untreatable diseases further.”

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Baraniuk JN, Casado B, Maibach H. 2005. A chronic fatigue syndrome-related proteome in human cerebrospinal fluid. BMC Neurol Dec 1:5(1):22. “This pilot study detected an identical set of central nervous system, innate immune and amyloidogenic proteins in cerebrospinal fluids from two independent cohorts of subjects with overlapping CFS (chronic fatigue syndrome), PGI (Persian Gulf War Illness) and fibromyalgia.” The conditions are different, but they may share the proteome and pathological mechanism. This study also gives an objective neuropathophysiology shared by each of these conditions. [Dr. Baraniuk stated that his research “ …provides initial evidence that chronic fatigue syndrome and its family of illnesses (i.e., FMS and GWI) may be legitimate, neurological diseases and that at least part of the pathology involves the central nervous system.” Georgetown University Medical Center public press release 12/1/05. ]

Baraniuk JN, Whalen G, Cunningham J et al. 2004. Cerebrospinal fluid levels of opioid peptides in fibromyalgia and chronic low back pain. BMC Musculoskel Disord 5(1):48. “Central nervous system opioid dysfunction may contribute to pain in fibromyalgia.”

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Bardin L, Tarayre JP, Malfetes N et al. 2003. Profound, non-opioid analgesia produced by the high-efficacy 5-HT(1A) agonist F 13640 in the formalin model of tonic nociceptive pain. Pharmacology 67(4):182-194. “These results help to establish large-magnitude 5-HT(1A) receptor activation as a new molecular mechanism of profound, central analgesia and suggest that F 13640 may be particularly effective against pain arising from severe tonic nociceptive stimulation.” [Although these studies are in early phases in rats, they provide hope that a new type of medication for chronic pain will become available that may be helpful for FMS. DJS]

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Bazzichi L, Rossi A, Massimetti G et al. 2007. Cytokine patterns in fibromyalgia and their correlation with clinical manifestations. Clin Exp Rheumatol. 25(2):225-230. “The higher levels of cytokines found in FM patients suggest the presence of an inflammatory response system (IRS) and highlight a parallel between the clinical symptoms and biochemical data. They support the hypothesis that cytokines may play a role in the clinical features of fibromyalgia. In addition, the similar cytokine patterns found in FM patients with different psychiatric profiles suggests that IRS impairment may play a specific role in the disease.”

Bazzichi L, Rossi A, Giuliano T et al. 2007. Association between thyroid autoimmunity and fibromyalgic disease severity. Clin Rheumatol. [May 9 Epub ahead of print]. “...autoimmune thyroiditis is present in an elevated percentage of FM patients…”

Bazzichi L, Giannaccini G, Betti L et al. 2006. Alteration of serotonin transporter density and activity in fibromyalgia. Arthritis Res Ther. 8(4):R99. “A change in SERT (specific serotonin transporter, and serotonin uptake) seems to occur in fibromyalgia patients, and it seems to be related to the severity of fibromyalgic symptoms.”

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Bell IR, Lewis II DA, Brooks AJ et al. 2004. Improved clinical status in fibromyalgia patients treated with individualized homeopathic remedies versus placebo. Rheumatology (Oxford) 43(5):577-582. This double-blind, randomized, parallel-group, placebo-controlled study indicates that “...individualized homeopathy is significantly better than placebo in lessening tender point pain and improving the quality of life and global health of persons with fibromyalgia.”

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Bell, I. R., C. M. Baldwin, L. G. Russek, G. E. Schwartz and E. E. Hardin. 1998. Early life stress, negative paternal relationships, and chemical intolerance in middle-aged women: support for a neural sensitization model. J Womens Health 7(9):1135-47.

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Bendiksen A, McGehee E, Handberg G. 2007. [The use of methadone in the treatment of chronic non-malignant pain in an out-patient setting] Ugeskr Laeger 169(17):1568-1572. [Danish] “Opioid treated chronic pain patients with insufficient pain relief may benefit from conversion to methadone, as 59% in our analysis achieved better pain relief, while the rotation was generally opioid-saving at the same time. The method used was safe and acceptable to the patients. The analyses did not result in any fundamental changes to the procedure.” Methodone may be a viable option for insufficiently relieved pain in chronic non-malignant pain patients.

Bendtsen L. 2000. Central sensitization in tension-type headache—possible pathophysiological mechanisms. Cephalalgia 20(5):486-508. “The stimulus-response function for palpation pressure vs. pain was found to be qualitatively altered in chronic tension-type headache patients compared with controls. The stimulus-response function was found to be qualitatively altered also in patients with fibromyalgia. It was concluded that the qualitatively altered nociception was probably due to central sensitization at the level of the spinal dorsal horn/trigeminal nucleus. Future basic and clinical research should aim at identifying the source of peripheral nociception in order to prevent the development of central sensitization and at ways of reducing established sensitization. This may lead to a much needed improvement in the treatment of chronic tension-type headache and other chronic myofascial pain conditions.”

Bendtsen, L., J. Norregaard, B. Jensen and J. Olesen.1997. Evidence of qualitatively altered nociception in patients with fibromyalgia. J Rheumatol 40(1):98-102.

Benecke R., Dressler D, Kunesch E et al. 2003. [No Title Given] Schmertz 17(6):450-458. Pain relief for myofascial pain has been reported with botox injections, but “in fibromyalgia, there seems to be no analgesic effect.”

Bengtsson, A., J. Ernerudh, M. Vrethem and T. Skogh. 1990. Absence of autoantibodies in primary fibromyalgia. J Rheumatol 17(12:1682-3.

Bengtsson, A. and K. G. Henriksson. 1989. The muscle in fibromyalgia–a review of Swedish studies. J Rheumatol Suppl Nov;(19)144-149.

Bengtsson, A. and M. Bengtsson. 1988. Regional sympathetic blockade in primary fibromyalgia. Pain 33(2):161-7.

Bengtsson A., Henriksson KG, Larsson J. 1986. Reduced high-energy phosphate levels in the painful muscles of patients with primary fibromyalgia. Arthritis Rheum. 29:817-21.

Benjamin M, Toumi H, Ralphs JR et al. 2006. Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load. J Anat. 208(4):471-490. “Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone. Consequently, they are commonly subject to overuse injuries (enthesopathies) that are well documented in a number of sports.” [These areas are often sites of attachment TrPs and these TrPs are frequently overlooked by orthopedic and surgical consultants. DJS]

Benjamin, S., Morris, S., McBeth, J., MacFarland, G.J., Silman, A.J.. 2000. The association between chronic widespread pain and mental disorder: A Population Study. Epidemiological group has tended towards viewing FMS as a somatization disorder. It was therefore important in this study that they only found three cases of somatoform disorders and came to the conclusion that somatoform disorders were uncommon in people with chronic widespread pain.

Bennett GJ. 2000. Update on the neurophysiology of pain transmission and modulation: focus on the NMDA-receptor. J Pain Symptom Manage 19(1 Suppl):S2-S6. “NMDA-receptor activation not only increases the cell’s response to pain stimuli, it also decreases neuronal sensitivity to opioid receptor agonists. In addition to preventing central sensitization, co-administration of NMDA-receptor antagonists with an opioid may prevent tolerance to opioid analgesia.”

Bennett, G. J. 2000. Update on the neurophysiology of pain transmission and modulation: focus on the NMDA-receptor. J Pain Symptom Manage 19(1 Suppl):S2-6.

Bennett R. 2007. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheum 21(3):427-445. This outstanding summary of MTPs is a comprehensive, clearly written overview of myofascial medicine. It explains why it is necessary for doctors to be trained in diagnosis of MTPs, and that they frequently occur in the presence of other conditions but, although they are exceedingly common, are often undiagnosed or misdiagnosed. [Severe CMP with central sensitization and multiple conditions are not explored, but the treatments suggested are often adequate for mild cases. It is significant that an article on MTPs written by such a respected scientist and clinician has appeared in a rheumatology journal. It is hoped that it is as well-read as it is well-written. DJS]

Bennett RM. 2007. Do patients’ perceptions of negative physician attitudes influence fibromyalgia symptoms and status? J Musculoskel Pain 15 (Supp 13):42 item 74. [Myopain 2007 Poster] “Current physicians were perceived to take the diagnosis of FMS more seriously, which in turn was related to improved FMS symptomatology. Perception that current or past physicians didn’t take FMS seriously was associated with increased anxiety. Patients may improve both physically and psychologically under the care of a physician who takes their illness seriously, whereas a negative past attitude continues to adversely influence their psychological health.” [Doctors can be serious perpetuating factors. Use care in choosing your health care team. DJS]

Bennett R. 2007. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 21(3):427-445. “Myofascial pain refers to a specific form of soft tissue rheumatism that results from irritable foci (trigger points) within skeletal muscles and their ligamentous junctions. It must be distinguished from bursitis, tendonitis, hypermobility syndromes, fibromyalgia and fasciitis. On the other hand it often exists as part of a clinical complex that includes these other soft tissue conditions, i.e., it is not a diagnosis of exclusion.”

Bennett RM. 2004. Diagnostic criteria and differential diagnosis of the fibromyalgia syndrome. J Musculoskeletal Pain 12(3/4):59-64. This article explains some of the difficulties arising from the use of 1990 ACR FMS Criteria for research as diagnostic criteria, the need for clarification of terms and training in differential diagnosis and treatment.

Bennett RM. 2004. Three years later: presidential address to MYOPAIN ’04. J Musculoskeletal Pain 12(3/4):1-12. [This is an excellent overview on some of the current developments in FMS and myofascial pain, including a summary of the reasons central sensitization is a key to FMS, and a clear look at the increase in morbidity and mortality for those with chronic pain. DJS]

Bennett R. 2005. The fibromyalgia impact questionnaire (FIQ): a review of its development, current version, operating characteristics and uses. Clin Exp Rheumatol. 23(5 Suppl 39):S154-162. The latest version of the Fibromyalgia Impact Questionnaire can be found at www.myalgia.com/FIQ/FIQ

Bennett RM, Schein J, Kosinski MR et al. 2005. Impact of fibromyalgia pain on health-related quality of life before and after treatment with tramadol/acetaminophen. Arthritis Rheum. 53(4):519-527. “Moderate-to-severe fibromyalgia pain significantly impairs HRQOL [health-related quality of life], and effective pain relief in these patients significantly increases HRQOL.”

Bennett R. 2004. Fibromyalgia: present to future. Curr pain Headache Rep. 8(5):379-384. A review of the understanding of FMS, including emerging clues and predictions on future developments.

Bennett RM. 2002. Adult growth hormone deficiency in patients with fibromyalgia. Curr Rheumatol Rep 4(4):306-12. "There is evidence that GH deficiency as defined in terms of a low insulin-like growth factor-1 (IGF-1) level occurs in approximately 30% of patients with fibromyalgia and is probably the cause of some morbidity. It seems most likely that impaired GH secretion in fibromyalgia is related to a physiologic dysregulation of the hypothalamic-pituitary-adrenal axis (HPA) with a resulting increase in hypothalamic somatostatin tone. The severe GH deficiency that occurs in a subset of patients with fibromyalgia is of clinical relevance because it is a treatable disorder with demonstrated benefits to patients."

Bennett RM. 2002. The rational management of fibromyalgia patients. Rheum Dis Clin North Am 2002. 28(2):181-99. "The exponential increase in pain research over the last 10 years has established fibromyalgia (FM) as a common chronic pain syndrome with similar neurophysiologic aberrations to other chronic pain states. As such, the pathogenesis is considered to involve an interaction of augmented sensory processing (central sensitization) and peripheral pain generators. The notion, the FM symptomatology results from an amplification of incoming sensory impulses, has revolutionized the contemporary understanding of this enigmatic problem and provided a more rational approach to treatment."

Bennett, R. M. 1999. Fibromyalgia Review. J Musculoskeletal Pain 7(4):85.

Bennett, R. M. 1999. Emerging concepts in the neural biology of chronic pain: evidence of abnormal sensory processing in fibromyalgia.. Mayo Clin Proc 74(4):385-98.

Bennett, R. M. 1998. Disordered growth hormone secretion and fibromyalgia: a review of recent findings and a hypothesized etiology. Z Rheumatol 57 Suppl 2:72-6.

Bennett, R. M., S. C. Clark and J. Walczyk. 1998. A randomized, double-blind, placebo-controlled study of growth hormone in the treatment of fibromyalgia. A J Med 104(3):227-231.

Bennett, R. M. , D. M. Cook, S. R. Clark, C. S. Burckhardt and S. M. Campbell. 1997. Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia. J Rheumatol 24(7):1384-1389.

Bennett, R. M. 1995. Fibromyalgia: The commonest cause of widespread pain. Frontiers 21(6):269-275.

Bennett, R. M. And S. Jacobsen. 1994. Muscle function and origin of pain in fibromyalgia. Ballieres Clin Rheumatol 8(4):721-746.

Bennett, R. M., S. R. Clark, S. M. Campbell and C. S. Burckhardt. 1992. Low levels of somatomedin C in patients with the fibromyalgia syndrome: a possible link between sleep and muscle pain. Arthritis Rheum 35(10):1113-6.

Bennett, R. M., S. R. Clark, S. M. Campbell, S. B. Ingram, C. S. Burckhardt, D. L. Nelson and J. M. Porter. 1991. Symptoms of Raynaud’s syndrome in patients with fibromyalgia. Arthritis Rheum 34(3):264-9.

Bennett, R.M., R. A. Gatter, S. M. Campbell, R. P. Andrews, S. R. Clark and J. A. Scarola. 1988. A comparison of cyclobenzaprine and placebo in the management of fibrositis. Arthritis Rheum 31(12):1535-1542.

Berga, S. L. 1998. Hypothalamus pituitary gonadal axis: stress-induced gonadal compromise. J Musculoskel Pain 6(3):61-70.

Berger A, Dukes E, Martin S et al. 2007. Characteristics and healthcare costs of patients with fibromyalgia syndrome. Int J Clin Pract. [Jul 26 Epub ahead of print]. “Patients with FMS have comparatively high levels of comorbidities and high levels of healthcare utilization and cost.” [Researchers are realizing that FM patients often have multiple conditions. What they do not yet understand is that many of these conditions are interactive. DJS]

Berggren-Clive, K. 1998. Out of the darkness and into the light: women’s experiences with depression after childbirth. Can J Commun Ment Health 17(1):103-20.

Bergholm U, Johansson BH. 2003. [No title given] Lakartidningen 100(47):3842-3847. [Swedish] “The late onset of symptoms can now be explained by the functional stenosis of the spinal cord and brainstem due to scar formation around the dens axis after injury. Modern neurophysiology can now explain the background of the generalized and complex picture of chronic pain and muscular and cognitive dysfunction. This new knowledge has prepared the way for more specific therapy in patients suffering from craniocervical instability symptoms and pain from disks and facet joints in the cervical spine after whiplash trauma.”

Berman, B. M., J. P. Swyers and J. Ezzo. 2000. The evidence for acupuncture as a treatment for rheumatologic conditions. Rheum Dis Clin North Am 26(1):103-15, ix-x.

Berman, B. M. and J. P. Swyers. 1999. Complementary medicine treatments for fibromyalgia syndrome. Baillieres Best Pract Res Clin Rheumatol 13(3):487-92.

Berman, B. M, B. B. Singh, S. M. Hartnoll, B. K. Singh and D. Reilly. 1998. Primary care physicians and complementary-alternative medicine: training, attitudes, and practice patterns. J Am Board Fam Pract 11(4):272-81.

Berman, B. M. and J. P. Swyers. 1997. Establishing as research agenda for investigating alternative medical interventions for chronic pain. Prim Care 24(4):743-758.

Berman SM, Naliboff BD, Suyenobu B et al. 2008. Reduced brainstem inhibition during anticipated pelvic visceral pain correlates with enhanced brain response to the visceral stimulus in women with irritable bowel syndrome. J Neurosci. 28(2):349-359.

Bernardes AT, dos Santos RM. 1997. Immune network at the edge of chaos. J Theor Biol. 186(2):173-187. Chaos system, used in mathematics, corresponds in many ways to the state of ill health, especially chronic illness.

Bernardis, L. L. and P. J. Davis. 1996. Aging and the hypothalamus: research perspectives. Physiol Behav 59(3):523-36.

Bernatsky S, Dobkin P, DeCivita M et al. 2005. Co-morbidity and physician use in fibromyalgia. Swiss Med Wkly 135(5-6):76-81. “Reported co-morbidity was classified into 4 categories: medical, psychiatric, ‘functional’ and unknown. The category for ‘functional’ conditions included disorders that have been classified by previous authors as medically unexplained symptoms such as the irritable bowel and chronic fatigue syndromes. Co-morbidity with other disorders, both functional and medical, was high in this sample. Medical and psychiatric co-morbidity were stronger determinants of high physician use than ‘functional’ co-morbidity.” [It is illogical to classify conditions together merely because medical science, or the authors, cannot explain them. DJS]

Bernstein J, Alonso DR, DiCaprio M et al. 2003. Curricular reform in musculoskeletal medicine: needs, opportunities and solutions. Clin Orthop Relat Res. (415):302-308. “Musculoskeletal medicine is not taught adequately in American medical schools and the predictable consequences are seen. Students cannot show cognitive mastery of the subject and lack confidence in this topic.” “…although inadequate education is neither new nor necessarily unique among disciplines, the coming year or two, the beginning of the Bone and Joint decade, was seen to be a particularly auspicious time for attempting curricular reform.”

Berthold U, Johansson BH. 2003. [No title given] Lakartidingen 100(47):3842-3847. [Swedish] Late symptom onset may be due to scar formation around the dens axis after whiplash injury. Functional magnetic resonance imaging (fMRI) may be a valuable source of documentation in whiplash injuries. This may be causing central pain, and muscular and cognitive dysfunctions. [Narrowing of the spinal cord and brainstem area may also be due to constricting muscles due to TrP contracture. DJS

Bezerra Rocha CA, Sanchez TG, Tesseroli de Siqueira JT. 2007. Myofascial trigger point: a possible way of modulating tinnitus. Audiol Neurootol. 13(3):153-160. “Temporary modulation of tinnitus was frequently observed (55.9%) during digital pressure, mainly in the masseter.” “An association between tinnitus and the presence of myofascial trigger points was observed, as well as a laterality association between the ear with the worst tinnitus and the side of the body with more myofascial trigger points. Thus, this relationship could be explained not only by somatosensory-auditory system interactions but also by the influence of the sympathetic system.”

Biasi, G., A. Fioravani, A. Franci and R. Marcolongo. 1994. [The role computerized telethermography in the diagnosis of fibromyalgia syndrome.] Minerva Med 85(9):451-4. [Italian]

Bieber C, Muller KG, Blumenstiel K et al. 2008. A shared decision-making communication training program for physicians treating fibromyalgia patients: effects of a randomized controlled trial. J Psychosom Res. 64(1):13-20. “SDM (shared decision making) with FMS patients might be a possible means to achieve a positive quality of physician-patient interaction. A specific SDM communication training program teaches physicians to perform SDM and reduces frustration in patients.”

Bieber C, Muller KG, Blumenstiel K et al. 2006. Long-term effects of a shared decision-making intervention on physician-patient interaction and outcome in fibromyalgia: A qualitative and quantitative 1-year follow-up of a randomized controlled trial. Patient Educ Couns. [Jul 25 Epub ahead of print] Shared decision making can be a critical step in producing both doctor and patient satisfaction in fibromyalgia care.

Billiard M, Bentley A. 2004. Is insomnia best categorized as a symptom or a disease? Sleep Med. 5 Suppl 1:S35-40. It is important to discover if co-existing conditions are causing the insomnia, or simply co-existing. If co-existing, it is important to discover the cause of the insomnia and get that under control.

Binhi VN. 2005. Stochastic dynamics of magnetosomes and a mechanism of biological orientation in the geomagnetic field. Bioelectromagnetics [Nov 10 Epub ahead of print]. Magnetosomes embedded in the cytoskeleton (skeletal structure of the cells) may be what allows migratory animals to orient themselves. They are sensitive to the Earth’s magnetic field. [The possibility of magnetosomes in cytoskeletons of those people electromagnetically sensitive or electromagnetically sensible exists. DJS]

Birch, S. 2003. Trigger point–acupuncture point correlations revisited. J Altern Complement Med 9(1):91-103. Earlier research (Melzack et al 1977) claimed 71% correspondence of trigger points to traditional acupuncture points. This study finds that result is “conceptually not possible,” and that there is no more than a 40% correlation and more likely 18% to 19% correlation between the two. The author did find that another class of acupuncture points, “a she” points, had a very high correlation to trigger points.

Birch, S. and R. N. Jamison. 1998. Controlled trial of Japanese acupuncture for chronic myofascial neck pain: assessment of specific and nonspecific effects of treatment. Clin J Pain 14(3):248-55.

Birdsall, T. C. 1998. 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Altern Med Rev 3(4):271-80.

Birkmayer W. and P. Riederer. 1989. Understanding the Neurotransmitters: Key to the Workings of the Brain. Translated from German by Karl Blau. NY: Springerer-Verlag.

Birketvedt, G. S. , J. Florholmen, J. Sundsfjord, B. Osterud, D. Dinges, W. Bilker and A. Stunkard. 1999. Behavioral and neuroendocrine characteristics of the night-eating syndrome. JAMA 282(7):657-63.

Bishnoi, A., H. E. Carlson, B. L. Gruber, L. D. Kaufman, J. L. Bock and K. Lidonnici. 1994. Effects of commonly prescribed nonsteroidal anti-inflammatory drugs on thyroid hormone measurements. Am J Med 96(3):235-8.

Bjorntorp P. 2001. Do Stress reactions cause abdominal obesity and comorbidities? Obes Rev 2(2):73-86. Long-term activation of the Hypothalamus-Pituitary Adrenal (HPA) Axis and sympathetic nervous system [commonly part of FMS DJS] may be the prelude to many serious illnesses. This includes Metabolic Syndrome. It is important to prevent and/or treat abnormal stress activation. "...it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abnormal abdominal obesity with its associated comorbidities."

Bjorntorp, P., G. Holm and R. Rosamund. 1999. Hypothalamus arousal, insulin resistance and Type 2 diabetes mellitus. Diabet Med 16(5):373-83.

Black, D. W., B. N. Doebbeling, M. D. Voelker, W. R. Clarke, R. F. Woolson, D. H. Barrett and D. A. Schwartz. 1999. Quality of life and health-services utilization in a population-based sample of military personnel reporting multiple chemical sensitivities. J Occup Environ Med 41(10):928-33.

Black, K. M., P. McClure and M. Polansky. 1996. The influence of different sitting positions on cervical and lumbar posture. Spine 21(1):65-70.

Blackman, J. D., V. L. Towle, G. F. Lewis, J. P. Spire and K. S. Polonsky. 1990. Hypoglycemic thresholds for cognitive dysfunction in humans. Diabetes 39(7):828-835.

Blacksher E. 2002. On being poor and feeling poor: low socioeconomic status and the moral self. Theor Med Bioeth. 23(6):455-470. “Persons of low socioeconomic status generally experience worse health and shorter lives than their better off counterparts. They also suffer a greater incidence of adverse psychosocial characteristics, such as low self-esteem, self-efficacy, and self-mastery and increased cynicism and hostility. Chronic socioeconomic deprivation can create environments that undermine the development of self and capacities constitutive to moral agency — i.e., the capacity for self-determination and crafting a life of one’s own. This moral harm is particularly salient in modern Western societies, especially in the United States, where success and failure is attributed to the individual, with little notice of the larger social and political realities that inform an individual’s circumstances and choices.”

Blanco I, Arbesu D, Al Kassam D et al. 2006. Alphal-antitrypsin polymorphism in fibromyalgia syndrome patients from the Asturias province in northern Spain: a significantly higher prevalence of the PI*Z deficiency allele in patients than in the general population. J Musculoskel Pain 14(3):5-12. A gene has been found that is twice as high in FMS patients as in this general population. The gene is associated with AT, an anti-inflammatory substance, and may indicate that “...at least a subset of FMS subjects could suffer from an inflammatory process, mediated by cytokines, proteases, and inflammation mediators normally inhibited by AT.” [This study indicates that if there is a triggering event that causes inflammation in the extra cellular matrix and the patient lacks these anti-inflammatory modulators due to genetics, the central sensitization process of FMS could begin. DJS]

Blashki G, McMichael T, Karoly DJ. 2007. Climate change and primary health care. 36(12):986-989. “Climate change has substantial potential health effects. These include heat stress related to heat waves; injuries related to extreme weather events such as storms, fires and floods; infectious disease outbreaks due to changing patterns of mosquito borne and water borne diseases; poor nutrition from reduced food availability and affordability; the psychosocial impact of drought; and the displacement of communities. Primary health care has an important role in preparing for and responding to these climate change related threats to human health.” [Patients with weather-reactive health conditions should be environmental activists. We are the canaries in the mines. Sensitivity to pollution in all its forms has made us the first to be aware, but we will not be the last to be affected. DJS]

Bliddal H, Danneskiold-Samsoe B. 2007. Chronic widespread pain in the spectrum of rheumatological diseases. Best Pract Res Clin Rheumatol. 21(3):391-402. “Evidence points to central sensitization as an important neurophysiological aberration in the development of FMS. Importantly, these neurological changes may result from inadequately treated chronic focal pain problems such as osteoarthritis or myofascial pain.” “Fibromyalgia patients need recognition of their pain syndrome if they are to comply with treatment. Lack of empathy and understanding by healthcare professionals often leads to patient frustration and inappropriate illness behavior, often associated with some exaggeration of symptoms in an effort to gain some legitimacy for their problem.”

Blunz, K. L., M. H. Rajwani and R. C. Guerriero. 1997. The effectiveness of chiropractic management of fibromyalgia patients: a pilot study. J Manipulative Physiol Ther 20(6):389-399.

Blyth FM, March LM, Brnabic AJ et al. 2004. Chronic pain and frequent use of health care. Pain 111(1-2):51-58. “There was a strong association between pain-related disability and greater use of services.”

Bohme K. 2002. Buprenorphine in a transdermal therapeutic system — a new option. Clin Rheumatol 21 Suppl 1:S13-S16. “Typical opioid-related adverse events were reported with a low incidence and mild intensity. Clinical benefit, coupled with a high level of patient compliance and improved quality of life, substantiate the usefulness of buprenorphine TDS in a practical setting.”

Bolgla LA, Malone TR. 2004. Plantar fasciitis and the Windlass Mechanism: A biochemical link to clinical practice. J Alth Train 39(1):77-82. “This model provides a means for describing plantar fasciitis conditions such that clinicians can formulate a potential causal relationship between conditions and their treatments. [This article is relevant to and can be useful in the treatment of myofascial TrPs, and would have benefitted by their inclusion. DJS]

Bonadonna R. Meditation’s impact on chronic illness. Holistic Nurs Pract 17(6):309-319. This article points out that more research needs to be done on the effect of living mindfully on chronic illness and urges the practice of meditation as part of treatment regimens.

Bongers, K. M., J. P. ter Bruggen and C. L. Franke. 1991. [The exploding head syndrome]. Ned Tijdschr Geneeskd 135(14):617-618. [Dutch]

Bonifazi M, Lisa Suman A, Cambiaggi C et al. 2006. Changes in salivary cortisol and corticosteroid receptor-alpha mRNA expression following a 3-week multidisciplinary treatment program in patients with fibromyalgia. Psychoneuroendocrinology 31(9):1076-1086. “One of the active mechanisms underlying the effects of our treatment is an improvement of HPA axis function, consisting in increased resiliency and sensitivity of the stress system probably related to stimulation of GR-alpha synthesis by the components of the treatment.”

Boninger M.L., Cooper R.A., Fitzgerald S.G. et al. 2003. Investigating neck pain in wheelchair users. Am J Phys Med Rehabil 82(3):197-202. Palpation for trigger points (TrPs) reproduced pain in 54% of the wheelchair user patients who had experienced recent neck pain. Myofascial TrPs may be a significant contributor to neck pain in wheelchair users. [Not only neck pain. Janet Travell mentioned how much the wheelchair was “vexing” the TrPs in her legs, and indicated that the use of the chair, although she was generally able to get up and about for specific needs, could be a perpetuating factor for many TrPs. DJS]

Bonneau, R. H., P. Mormede, G. P. Vogler, G. E. McClearn and B. C. Jones. 1998. A genetic basis for neuroendocrine-immune interactions. Brain Behav Immun 12(2):83-9.

Booth, F. W., S. E. Gordon, C. J. Carlson and M. T. Hamilton. 2000. Waging war on modern chronic diseases: primary prevention though exercise biology. J Appl Physiol 88(2):774-787.

Borenstein, D. 1995. Prevalence and treatment outcome of primary and secondary fibromyalgia in patients with spinal pain. Spine. 20(7):796-800.

Borg-Stein J. 2006. Treatment of fibromyalgia, myofascial pain, and related disorders. Phys Med Rehabil Clin N Am. 17(2):491-510. This is an overview of treatment considerations for these patients.

Borg-Stein J, Wilkins A. 2006. Soft tissue determinants of low back pain. Curr Pain Headache Rep. 10(5):339-344. Low back pain patients are often incorrectly labeled. It is important to recognize and treat the soft tissue cause of the low back pain. These conditions may be found alone or in combination: ligamentous, non ligamentous, discogenic and facet. All contributing causes must be evaluated and treated.

Borg-Stein J. 2002. Cervical myofascial pain and headache. Curr Pain Headache Rep 6(4):324-30. Myofascial pain from trigger points is a treatable component or cause of many headaches.

Borg-Stein J. 2002. Management of peripheral pain generators in fibromyalgia. Rheum Dis Clin North Am 28(2):305-17. "Fibromyalgia is a widespread chronic pain disorder that is characterized in part by central sensitization and increased pain response to peripheral nociceptive and non-nociceptive stimuli. Part of the comprehensive pain management of patients with fibromyalgia should include a thoughtful evaluation and search for peripheral pain generators that either are associated with fibromyalgia or are coincidentally present. The identification and treatment of these pain generators lessens the total pain burden, facilitates rehabilitation and decreases the stimuli for ongoing central sensitization."

Borg-Stein, J. and J. Stein. 1996. Trigger points and tender points. Rheum Disease Clin North Am 22(2):305-22.

Borman, P. and Celiker, R. 1999. A comparative analysis of quality of life in rheumatoid arthritis and fibromyalgia. J Musculoskeletal Pain 7(4).

Borman, P., R. Celiker and Z. Hascelik. 1999. Muscle performance in fibromyalgia syndrome. Rhematol Int 19(1-2):27-30.

Botwin KP, Patel BC. 2007. Electromyographically guided trigger point injections in the cervicothoracic musculature of obese patients: a new and unreported technique. Pain Physician 10(6):753-756. “This technique helps confirm proper needle placement within the cervicothoracic musculature in an obese patient in whom the musculature is not readily palpated. This, thus, reduces the potential for a pneumothorax by an improperly placed injection.”

Bou-Holaigah, I., H. Calkins, J. A. Flynn, C. Tunin, H. C. Chang, J. S. Kan and P. C. Rowe. 1997. Provocation of hypotension and pain during upright tilt table testing in adults with fibromyalgia. Clin Exp Rheumatol 15(3):239-246.

Bou-Holaigah, I., P. C. Rowe, J. Kan and H. Calkins. 1995. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA 274(12):961-967.

Bourdette DN, McCauley LA, Barkhuizen A, Johnston W, Wynn M, Joos SK, Storzbach D, Shuell T, Sticker D. 2001. Symptom factor analysis, clinical findings, and functional status in a population-based case control study of Gulf War unexplained illness. J Occup Environ Med Dec;43(12):1026-40. More than half of the veterans with unexplained musculoskeletal pain met the criteria for fibromyalgia. Many with unexplained fatigue met the criteria for chronic fatigue syndrome.

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Boyum, A., P. Wiik, E. Gustavsson, O. P. Veiby, J. Reseland, A. H. Haugen and P. K. Opstad. 1996. The effect of strenuous exercise, calorie deficiency and sleep deprivation on white blood cells, plasma immunoglobulins and cytokines. Scand J Immunol 43(2):228-235.

Bradley LA, McKendree-Smith NL. Central nervous system mechanisms of pain in fibromyalgia and other musculoskeletal disorders: behavioral and psychologic treatment approaches. Curr Opin Rheumatol Jan;14(1):45-51,2002. The neuromatrix is a construct that helps in understanding the interaction between physiologic mechanisms and psychosocial factors in the development and maintenance of chronic pain. The efficacy of cognitive-behavioral interventions for patients with fibromyalgia has not been established. Cognitive-behavior therapy will benefit some patients but not others.

Bradley, LA, A. Sotolongo, KR Alberts, G. S. Alarcon, J. M. Mountz, H-G Liu, et al. 1999. Abnormal regional cerebral blood flow in the caudate nucleus among fibromyalgia patients and non-patients os associated with insidious symptom onset. J Musculoskel Pain 7(1-2):285-292.

Bradley, L. A. and K. R. Alberts. 1998. Psychological and behavioral approaches to pain management for patients with rheumatic disease. Rheum Dis Clin North Am 25(1):215-32, viii.

Brady, C., D. Taylor and M. O'Brien. 1993. Whiplash and temporomandibular joint dysfunction. J Ir Dent Assoc 39(3):69-72.

Brainard GC, Hanifin JP. 2005. Photons, clocks and consciousness. J Biol Rhythms 20(4):314-325. “Light profoundly impacts human consciousness through the stimulation of the visual system and powerfully regulates the human circadian system, which, in turn, has a broad regulatory impact on virtually all tissues in the body.” This includes the neuroendocrine system. The use of specific wavelength light at specific times of the day may be very helpful in resetting biological clocks.

Branco, J., A. Atalaia and T. Paiva. 1994. Sleep cycles and alpha-delta sleep in fibromyalgia syndrome. J Rheumatol 21(6):1113-1117.

Branco, J. C. , V. Tavares, I. Abreu and R. L. Humbel. 1994. [Viral infection and fibromyalgia.] J Rheumatol 7(6):337-341. [Portugese]

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Brattberg, G. 1999. Connective tissue massage in the treatment of fibromyalgia. Eur J Pain 3(3):235-244.

Brault JR, Siegmund GP, Wheeler JB. 2000. Cervical muscle response during whiplash: evidence of a lengthening muscle contraction. Clin Biomech 15(6):426-435. “The cervical muscles contract rapidly in response to impact and the potential exists for muscle injury due to lengthening contractions. The clinician should recognize the role of cervical retraction in the mechanism of whiplash injury and avoid aggressive motion in that plane during diagnosis and treatment.”

Brault, J. R., G. P. Siegmund and J. B. Wheeler. 2000. Cervical muscle response during whiplash: evidence of a lengthening muscle contraction. Clin Biomech (Bristol, Avon) 15(6):426-435.

Braus DF. 2004. [Neurobiology of learning – the basis of an alteration process.] 31 (Suppl 2):215-223. [German] “...there is now increasing evidence that the plasticity of the human brain, i.e. its remarkable ability to adapt to and change with experience, is, under normal conditions, a lifelong phenomenon.” “The capability to modify the biochemistry of synapses as well as the growth and change in terms of rewiring of synapses, dendritic branching and glial cell proliferation via the dialogue of synapses and genes, results in specific changes in neuronal connectivity and function.” “...neurotransmitter systems modulate neuronal plasticity on the neuronal level; on the behavioral level they influence affect, emotion, positive motivation and the correct evaluation of environmental stimuli. Experience, action as well as learning and memory are influenced by these systems.” [Superb paper with great significance in FMS. DJS]

Breau, L. M., P. J. McGrath and L. H. Ju. 1999. Review of juvenile primary fibromyalgia and chronic fatigue syndrome. J Dev Behav Pediatr 20(4):278-88.

Brecher LS, Cymet TC. A practical approach to fibromyalgia. 2001. J Am Osteopath Assoc (4 Suppl Pt 2):S12-7. "The term fibromyalgia refers to a collection of symptoms with no clear physiologic cause, but the symptoms together constitute a clearly recognizable and distinct pathologic entity. Diagnostic criteria serve as guidelines for diagnosis, not as absolute requirements. Treatment of fibromyalgia, which is an ongoing process, remains individualized. It is goal-oriented, directed at helping patients get restorative sleep, alleviating the somatic pains, keeping patients productive, and regulating schedules. Because fibromyalgia is chronic and may affect all areas of an individual's functioning, the physician needs to also evaluate the social support systems of patients with fibromyalgia."

Brenne, E., K. van der Hagen, E. Maehlum and S. Husebo. 1997. [Treatment of chronic pain with amitriptyline. A double-blind dosage study with determination of serum levels]. Tidsskr Nor Laegeforen 117(24):3491-3494 [Norwegian].

Brietzke, S. E., Mair, E. A. 2001. Injection snoreplasty: how to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg 124(5):503-10. Injection of a sclerotherapy agent, Sotradecol, into the soft palate, reduces or eliminates palatal flutter snoring. It is a simple, safe and effective office treatment for primary snoring.

Briley M. 2003. New hope in the treatment of painful symptoms in depression. Curr Opin Investig Drugs 4(1):42-45. “Recent, principally open, trials with members of the new select serotonin and norepinephrine reuptake inhibitor class of antidepressants such as venlafaxine, milnacipran and duloxetine...suggest that these compounds may be effective in relieving pain both associated with, and independent of, depression.”

Brisby H. 2006. Pathology and possible mechanisms of nervous system response to disc degeneration. J Bone Joint Surg Am. 88 Suppl 2:68-71. “Disc deterioration and/or degeneration may influence the nervous system by stimulation of nociceptors in the anulus fibrosus, causing nociceptive pain that is often referred to as discogenic pain. The stimulation of the nociceptors may be of mechanical or inflammatory origin. Deterioration of a disc with loss of normal structure and weight-bearing properties may lead to abnormal motions that cause mechanical stimulation.” “A large number of inflammatory and signaling substances, such as tumor necrosis factor and interleukins (interleukin-1beta, interleukin-6, and interleukin-8) may also play a role in the development of back pain. Independent of stimulus of the nociceptors, the pain impulses are conducted through myelinated A delta fibers and unmyelinated C fibers to the dorsal root ganglion and continue by way of the spinothalamic tract to the thalamus and the somatosensory cortex.” “Disc deterioration also influences other spinal structures, such as facet joints, ligaments, and muscles, which can also become pain generators. Thus, disc degeneration may be responsible for the development of chronic low-back pain without being the actual pain focus.” “The altered magnitude of perceived pain is often referred to as neural plasticity and is considered to play a critical role in the evolution of chronic pain.”

Brisby H. 2006. Pathology and possible mechanisms of nervous system response to disc degeneration. J Bone Joint Surg Am. 88 Suppl 2:68-71. “Deterioration of a disc with loss of normal structure and weight-bearing properties may lead to abnormal motions that cause mechanical stimulation. This theory is supported by the fact that patients commonly experience an increase in pain with weight-bearing and certain movements.” “A large number of inflammatory and signaling substances, such as tumor necrosis factor and interleukins (interleukin-1beta, interleukin-6, and interleukin-8), may also play a role in the development of back pain.” “Disc deterioration also influences other spinal structures, such as facet joints, ligaments, and muscles, which can also become pain generators. Thus, disc degeneration may be responsible for the development of chronic low-back pain without being the actual pain focus. Both nociceptive and neuropathic pain can be modulated at higher centers, both at the spinal and the supraspinal levels (central sensitization). The altered magnitude of perceived pain is often referred to as neural plasticity and is considered to play a critical role in the evolution of chronic pain.”

Brockow T, Wagner A, Franke A et al. 2007. A randomized controlled trial on the effectiveness of mild water-filtered near infrared whole-body hyperthermia as an adjunct to a standard multimodal rehabilitation in the treatment of fibromyalgia. Clin J Pain. 23(1):67-75. “The study indicates that NI-WBH (whole body hyperthermia) is a worthwhile adjunct to MR (multimodal rehabilitation) in the treatment of FM.” [It would be useful to compare the efficacy of this type of hyperthermia with a warm water bath of the same temperature. DJS]

Broderick JE, Junghaenel DU, Turk DC. 2004. Stability of patient adaptation classifications on the multidimensional pain inventory. Pain 109(1-2):94-102. “The implications of this study is that for a sizable number of chronic pain patients, MPI classifications may not be stable, trait-like characterizations.” [This agrees with my observation in the 2nd edition Survival Manual. Chronic pain can often cause patients to answer in a way that may indicate antisocial or other psychological characteristics in a healthy person. For example, you often leave a party early because you are in pain, not because you want to avoid contact.]

Broide, R. S. and F. M. Leslie. 1999. The alpha 7 nicotinic acetylcholine receptor in neuronal plasticity. Mol Neurobiol 20(1):1-16.

Brown, C. S., N. Parker, F. Ling and J. Wan. 2000. Effects of magnets on chronic pelvic pain. Obstet Gynecol 95(4 Suppl 1):S29.

Brown, C. R. 1996. Pain management NICO. The Implant Report 8(9):916.

Brown MM, Jason LA. 2007. Functioning in individuals with chronic fatigue syndrome: increased impairment with co-occurring multiple chemical sensitivity and fibromyalgia. Dyn Med. 6(1):6. “…having more than one illness exacerbates one’s disability beyond CFS alone.”

Brown SL, Duggiraia HJ, Pennello G. 2002. An Association of Silicone-gel Breast Implant Rupture and Fibromyalgia. Curr Rheumatol Rep 4(4):293-8. "Silicone-gel breast implant rupture is common. Silicone-gel from ruptured implants may escape the scar capsule that forms around breast implants and become 'extracapsular silicone'. Our previously published study found that women with extracapsular silicone-gel were at higher risk of reporting that they were diagnosed with fibromyalgia."

Bruce, E. 1995 Myofascial pain syndrome: early recognition and comprehensive management. AAOHN J 43(9):469-474.

Bruehl S, Chung OY. 2004. Interactions between the cardiovascular and pain regulatory systems: an updated review of mechanisms and possible alterations in chronic pain. Neurosci Biobehav Rev. 28(4):395-414. Theoretical possibilities and clinical implications are discussed in this article.

Bruehl S, Chung OY, Ward P et al. 2004. Endogenous opioids and chronic pain intensity: interactions with level of disability. Clin J Pain 20(5):283-292. Among more disabled chronic pain patients, endogenous opioid system dysfunction may contribute to hyperalgesia. Among less disabled patients, chronic pain itself may initiate central sensitization. [Even chronic pain from TrPs. DJS]

Brunner E.J., Hemingway H., Walker B.R. et al. 2002. Adrenocortical, autonomic, and inflammatory causes of the metabolic syndrome: nested case-control study. Circulation 106(21):2659-65. “Neuroendocrine stress axes are activated in MS [Metabolic Syndrome]. There is relative cardiac sympathetic predominance. The neuroendocrine changes may be reversible. This case-control study provides the first evidence that chronic stress may be a cause of MS.”

Bruno, R. L. 1998. Abnormal movements in sleep as a post-polio sequelae. Am J Phys Med Rehabil 77(4):339-43.

Bruno, R. L., S. J. Creange and N. M. Frick. 1998. Parallels between post-polio fatigue and chronic fatigue syndrome: a common pathophysiology? Am J Med 105(3A):66S-73S.

Brunson KL, Kramar E, Lin B et al. 2005. Mechanisms of late-onset cognitive decline after early-life stress. Jour of Neuro. 25(41):9328-9338. “A short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans.” [This may explain at least part of why some of a subset of FMS patients have greater cognitive impairment when they reach middle age. This may be very significant, and an initiating factor that can be prevented. DJS]

Bryant, R. A. and A. G. Harvey. 1999. Postconcussive symptoms and posttraumatic stress disorder after mild traumatic brain injury. J Nerv Ment Dis 187(5):302-5.

Buchgreitz L, Lyngberg AC, Bendtsen L et al. 2007. Increased pain sensitivity is not a risk factor but a consequence of frequent headache: a population-based follow-up study. Pain. [Nov 29 Epub ahead of print]. “…increased pain sensitivity is a consequence of frequent tension-type headache, not a risk factor, and support that central sensitization plays an important role or the chronification of tension-type headache.”

Buchgreitz L, Lyngberg A, Bendtsen L et al. 2007. Increased prevalence of tension-type headache over a 12-year period is related to increased pain sensitivity. A population study. Cephalalgia. 27(2):145-152. Tension-type headache in women may be one cause of central sensitization.

Buchner RL, Snyder AZ, Shannon BJ et al. 2005. Molecular, structural, and functional characterization of Alzheimer’s Disease; Evidence for a relationship between default activity, amyloid, and memory. J Neurosci 25(34):7709-7717. Chronically activated areas of the brain produce more amyloid beta. That is the substance implicated in Alzheimer’s. [What this means for patients with FMS who have rapid-fire synapses, if anything, remains to be seen, but it is an area of research to watch. DJS]

Buckelew, S. P., R. Conway, J. Parker, W. E. Deuser, J. Read, T. E. Witty, J. E. Hewett, M. Minor, J. C. Johnson, L. Van Male, M. J. McIntosh, M. Nigh and D. R. Kay. 1998. Biofeedback/relaxation training and exercise interventions for fibromyalgia: a prospective trial. Arthritis Care Res 11(3);196-209.

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Bugajski, J. 1996. Role of prostaglandins in the stimulation of the hypothalamic-pituitary-adrenal axis by adrenergic and neurohormone systems. J Physiol Pharmacol 47(4):559-575.

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Burchard, J. F., D. H. Nguyen, L. Richard, S. N. Young, M. P. Heyes and E. Block. 1998. Effects of electromagnetic fields on the levels of biogenic amine metabolites, quinolinic acid, and beta-endorphin in the cerebrospinal fluid of dairy cows. Neurochem Res 23(12):1527-31.

Burckhardt CS. 2004. Fibromyalgia: novel therapeutic aspects. J Musculoskeletal Pain 12(3/4):65-72. “Overall, there is moderate to strong evidence of the effectiveness of some nonpharmacologic approaches to fibromyalgia treatment. Novel treatments from a wide group of practitioners and health perspectives are beginning to emerge as legitimate strategies. An individualized approach that incorporates patient’s abilities, preferences, physical and psychological characteristics is critical to the success of treatment.”

Burckhardt CS, Clark SR, Bennett RM. 2005. Long-term follow-up of fibromyalgia patients who completed a structured treatment program versus patients in routine treatment. J Musculoskeletal Pain 13(1). “Patients treated in a comprehensive program had consistently lower FMS impact, depression, pain, and fatigue scores over time. Patients who did not enter or complete the program were as likely to take sleep medication, exercise or use self-management techniques over time but did not perceive themselves to be doing as well as those who completed the program.”

Burckhardt CS. 2005. Educating patients: self-management approaches. Disabil Rehabil. 27(12):703-709. “Programs that combine education with cognitive-behavioral techniques and exercise are most effective in enhancing self-efficacy and decreasing symptoms of FMS.”

Burckhardt, C. S. , S. R. Clark and R. M. Bennett. 1993. Fibromyalgia and quality of life: a comparative analysis. .J Rheumatol 20(3):475-9.

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Burgunder, J. M. 1998. Pathophysiology of akinetic movement disorders: a paradigm for studies in fibromyalgia? Z Rheumatol Suppl 57(2):27-30.

Burns, J. W., B. J. Johnson, J. Devine, N. Mahoney and R. Pawl. 1998. Anger management style and the prediction of treatment outcome among male and female chronic pain patients. Behav Res Ther 36(11):1051-62.

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Burwinkle T, Robinson JP, Turk DC. 2005.

Fear of movement: factor structure of the Tampa Scale of Kinesiophobia in patients with fibromyalgia syndrome. J Pain 6(6):384-391. The Tampa Scale of Kinesiophobia may not be applicable to fibromyalgia patients, and its assessment measurement properties are “problematic.” [It may be even less applicable for myofascial pain patients. DJS.]

Bushnell, M. C., C. Villemure, I Strigo et al. 2001. Imaging pain in the brain: The role of the cerebral cortex in pain perception and modulation. J Musculoskel Pain 10(1/2):59-72. Fibromyalgia may involve dysfunctional pain processing in the forebrain. "…activity in this network can be modulated by cognitive state, as well as by pharmaceutical treatments", resulting in pain control.

Buskila D, Sarzi-Puttini P, Ablin JN. 2007. The genetics of fibromyalgia syndrome. Pharmacogenomics 8(1):67-74. “The mode of inheritance in FMS is unknown, but it is most probably polygenic. Recognition of these gene polymorphisms may help to better subgroup FMS patients and to guide a more rational pharmacological approach.”

Buskila D, Press J, Abu-Shakra M. 2003. Fibromyalgia in systemic lupus erythamatosus: prevalence and clinical implications. Clin Rev Allergy Immunol Aug:25(1):25-8. “Fibromyalgia (FM) is common in SLE patients, and is the source of many of the symptoms and much of the disability in these patients.”

Buskila D., Neumann L., 2000. Musculoskeletal Injury as a Trigger for Fibromyalgia/Post-traumatic Fibromyalgia. Curr Rheumatol Rep 2(2):104-108. Soft tissue trauma to the neck can result in an increased incidence of FM compared with other injuries.

Buskila, D, Neumann L, Odes LR, et al. 2001. The prevalence of musculoskeletal pain and fibromyalgia in patients hospitalized on internal medicine wards. Semin Arthritis Rheum 30(6):411-7. Pain syndromes and related symptoms are prevalent among hospitalized patients on the medicine wards. Care providers need to be aware of these syndromes, regardless of the reason for the patient's hospitalization.

Buskila, D. 1999. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol 11(2):119-26.

Buskila, D., L. R. Odes, L. Neumann and H. S. Odes. 1999. Fibromyalgia in inflammatory bowel disease. J Rheumatol 26(5):1167-71.

Buskila, D., L. Neumann, D. Sibirski and P. Shvartzman. 1997. Awareness of diagnostic and clinical features in fibromyalgia among family physicians. Fam Pract 14(3):238-241.

Buskila, D. and L. Neumann. 1997. Fibromyalgia syndrome (FM) and nonarticular tenderness in relatives of patients with FM. J Rheumatol 24(5):941-944.

Buskila, D., L Neumann, G. Vaisberg, D. Alkalay and F. Wolfe. 1997. Increased rates of fibromyalgia following cervical spine injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum 40(3):446-452.

Buskila, D., A. Shnaider, I. Neumann, D. Zilberman, N. Hilzenrat and E. Sikuler. 1997. Fibromyalgia in hepatitis C virus infection. Another infectious disease relationship. Arch Intern Med 157(21):2497-500.

Buskila, D., L. Neumann, I. Hazanov and R. Carmi. 1996. Familial aggregation in the fibromyalgia syndrome. Semin Arthritis Rheum 26(3):605-611.

Buskila, D., L. Neumann, E. Hershman, A. Gedalia, J. Press and S. Sukenik. 1995. Fibromyalgia syndrome in children–an outcome study. J Rheumatol 22(3):525-528.

Buskila, D., J. Press, A. Gedalia, M. Klein, L. Newman, R. Boehm and S. Sukenik. 1993. Assessment of nonarticular tenderness and prevalence of fibromyalgia in children. J Rheumatol 20(2):368-70.

Buskila, D., D. D. Gladman, K.V. Straaton P. Langevitz, S.Urowicz and H. A. Smythe. 1990. Fibromyalgia in human immunodeficiency syndrome virus infection. J Rheumatol 17(9):1202-12-6.

Butkevich I.P., Vershinina E.A. 2003. Maternal stress differently alters nociceptive behaviors in the formalin test in adult female and male rats. Brain Res 961(1):159-65. Prenatal stress alters pain receptor behaviors in offspring.

Butt AM, Hamilton N, Hubbard P et al. 2005. Synantocytes: the fifth element. J Anat. 207(6):695-706. There is a possible form of glial cells apart from the astrocytes, oligodendrocytes and microglia. It expressed the NG2 chondroitin sulphate proteoglycan (CSPG). The majority of the NG-2-expressing glial cells in the adult CNS is a specific cell the authors name syantocytes, and they are an integral part of the tripartite synapse, integrating commmunication between the neuron and glial cell. “Neuronal activity, glutamate and adenosine triphosphate (ATP) act on synatocyte receptors and evoke raised intracellular calcium. This may affect ion channels and receptor profiles, and their activation may result in glial scar formation. [This may be an important factor in FMS and CMP interconnection. DJS]

Cabral GA, Marciano-Cabral F. 2005. Cannabinoid receptors in microglia of the central nervous system: immune functional relevance. J Leukoc Biol. [Oct 4 Epub ahead of print] “The recognition that microglia express cannabinoid receptors and that their activation results in modulation of select cellular activities suggests that they may be amenable to therapeutic manipulation for ablating untoward inflammatory responses in the central nervous system.”

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Cairns BE. 2007. The role of peripheral glutamate and glutamate receptors in muscle pain. J Musculoskel Pain 15 (Supp 13):8 item 10. [Myopain 2007 Poster] “These findings suggest that elevations of interstitial glutamate concentration alter musculoskeletal pain sensitivity in a sex-related manner through activation of peripheral NMDA receptors.”

Cairns V, Godwin J. 2005. Post-Lyme borreliosis syndrome: a meta-analysis of reported symptoms. Int J Epidemiol. [Epub ahead of print July 22] “This meta-analysis provides strong evidence that some patients with LB have fatigue, musculoskeletal pain, and neurocognitive difficulties that may last for years despite antibiotic treatment.”

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Calandre EP, Morillas-Arques P, Rodriguez-Lopez CM et al. 2007. Pregabalin augmentation of quetiapine therapy in the treatment of fibromyalgia: an open-label, prospective trial. Pharmacopsychiatry 40(2):68-71. “...the use of pregabalin can be a useful augmentation strategy in fibromyalgia patients partially responding to quetiapine.”

Calandre EP, Hidalgo J, Garcia-Leiva JM et al. 2006. Trigger point evaluation in migraine patients: an indication of peripheral sensitization linked to migraine predisposition? Eur J Neurol. 13(3):244-249. “Trigger points were found in 92 (93.9%) migraineurs and in nine (29%) controls.” “These data indicate that nociceptive peripheral sensitization is a usual finding in migraine, and that central sensitization can develop in patients with frequent attacks and long-lasting disease. Trigger points’ detection in migraine patients could be useful when applying therapies like acupuncture, needling or botulinum toxin injections directed to reduce peripheral sensitization.” [This may be another indication wherein the central sensitization found in FMS acts synergically with the peripheral pain stimuli from trigger points. DJS]

Calandre EP, Hidalgo J, Garcia-Leiva JM et al. 2006. Trigger point evaluation in migraine patients: an indication of peripheral sensitization linked to migraine predisposition? Eur J Neurol. 13(3):244-249. “These data indicate that nociceptive peripheral sensitization is a usual finding in migraine, and that central sensitization can develop in patients with frequent attacks and long-lasting disease. Trigger points’ detection in migraine patients could be useful.” [This may indicate another connection with central sensitization of FMS and TrPs. DJS]

Caldarella MP, Giamberardino MA, Sacco F et al. 2006. Sensitivity disturbances in patients with irritable bowel syndrome and fibromyalgia. Am J Gastroenterol. 101(12):2782-2789. “Our observations seem to indicate that, although sharing a common hypersensitivity background, multiple mechanisms may modulate perceptual somatic and visceral responses in patients with IBS and FM.”

Calder, AA. 1994. Prostaglandins and biological control of cervical function. Aust N Z Obstet Gynaecol 34(3):347-51.

Calis M, Gokee C, Ates F et al. 2004. Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome. J Endocrinol Invest 27(1):42-46. This study indicated that the HPA axis is underactivated in primary FMS patients. [The disparity of this conclusion with other researchers’ findings could be that there are several phases of HPA activation, and once the system has been stressed for a period of time, the imbalance causes a decreased response. We don’t know. DJS]

Calvo MS, Whiting SJ. 2003. Prevalence of vitamin D insufficiency in Canada and the United States: importance to health status and efficacy of current food fortification and dietary supplement use. Nutr Rev. 61(3):107-113. “Several recent studies have identified a surprisingly high prevalence of vitamin insufficiency in otherwise healthy adults living in Canada and the United States. Dietary Vitamin D is not reaching the population in greatest need, nor is it very protective against insufficiency.”

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Cambron JA, Dexheimer J, Coe P. 2006. Changes in blood pressure after various forms of therapeutic massage: a preliminary study. J Altern Complement Med. 12(1):65-70. “Increases in BP were noted for potentially painful massage techniques, including trigger point therapy.” [There are a lot of different TrP massage therapy techniques and they were not differentiated here. TrP therapists must be careful to keep the pain level low to prevent the possibility of central sensitization. This paper shows that there may be other possible effects of painful therapies. DJS]

Camparis CM, Formigoni G, Teixeira MJ et al. 2006. Sleep bruxism and temporomandibular disorder: clinical and polysomnographic evaluation. Arch Oral Biol. [Apr 1 Epub ahead of print]. “The polysomnographic characteristics of patients with sleep bruxism, with and without orofacial pain, are similar. More studies are necessary to clarify the reasons why some sleep bruxism patients develop chronic (facial) myofascial pain, and others do not.”

Camparis CM, Formigoni G, Teixeira MJ et al. 2005. Clinical evaluation of tinnitus in patients with sleep bruxism: prevalence and characteristics. J Oral Rehabil. 32(11):808-814. “Tinnitus frequency was higher in patients with sleep bruxism and chronic facial pain. Myofascial pain, numbers of areas painful to palpation in the masticatory and cervical muscles, higher levels of depression and tooth absence without prosthetic replacement were more frequent in the group with tinnitus.”

Cannon DE, Dillingham TR, Miao H et al. 2007. Musculoskeletal disorders in referrals for suspected cervical radiculopathy. Arch Phys Med Rehabil. 88(10):1256-1259. “Musculoskeletal disorders are common in patients with suspected cervical radiculopathy.” “The presence of musculoskeletal disorders should not preclude electrodiagnostic testing when otherwise indicated.”

Cantini, F., F. Bellandi, L. Niccoli and O. Di Munno. 1994. Fluoxetin combined with cyclo-benzaprine in the treatment of fibromyalgia. Minerva Med 85(3):97-100 [Italian].

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Caraco Y, Sheller J, Wood AJ. 1996. Pharmacogenetic determination of the effects of codeine and prediction of drug interactions. J Pharmacol Exp Ther. 278(3):1165-1174. Codeine, hydrocodone, and oxycodone are dependent on metabolism by CYP2D6. Patients who lack the enzyme CYP2D6 or have inhibited CYP2D6 are not candidates for these medications. Patients on these medications should not be put on medications that inhibit this enzyme. [Lack of phenotyping test subjects and avoidance of inhibitors may have resulted in incorrect conclusions in some opioid trials for chronic pain. Metabolic testing may be a valuable tool to help decide which patients will find opioids more effective in controlling pain. DJS]

Caraco Y, Sheller J, Wood AJ. 1999. Impact of ethnic origin and quinidine coadministration on codeine’s disposition and pharmacodynamic effects. J Pharmacol Exp Ther. 290(1):413-422. Chinese patients varied greatly from Caucasian patients in CYP2D6 activity. “..Chinese patients produce less morphine from codeine, exhibit reduced sensitivity to that morphine, and therefore might experience reduced analgesic effect in response to codeine. Quinidine-induced inhibition of codeine metabolism is ethnically dependent as well. The reduction is significantly greater in Caucasians. [Clinicians need to be aware that different ethnic populations may react differently to medications. DJS]

Carames J, Carvalhao F, Real Dias MC. 2009. [Myofascial trigger point disease – a multidisciplinary disorder] Acta Reumatol Port. 34(1):38-43. [Portuguese] “The articles and texts reviewed underline the need for an early diagnosis of this disease in order to treat its aetiology and avoid the chronicity of symptoms.”

Cardenal, A., I. Masuda, W. Ono, A. L. Haas, L. M. Ryan, D. Trotter and D. J. McCarty. 1998. Serum nucleotide pyrophosphohydrolase activity; elevated levels in osteoarthritis, calcium pyrophosphate cyrstal {NOTE EDITOR, “CRYSTAL” IS MISSPELLED IN ARTICLE} deposition disease, scleroderma, and fibromyalgia. J Rheumatol 25(11):2175-80.

Carette, S., M. J. Bell, W. J. Reynolds, B. Haraoui, G. A. McCain, V. P. Bykerk, S. M. Edworthy, M. Baron, B. E. Koehler, A.G. Fam et al. 1994. Comparison of amitriptyline, cyclobenzaprine, and placebo in the treatment of fibromyalgia. A randomized, double-blind clinical trial. Arthritis Rheum 37(1):32-40.

Carli G., Suman A.L., Biasi G. et al. 2002. Reactivity to superficial and deep stimuli in patients with chronic musculoskeletal pain. Pain 100(3):259-69. Even when patients who have pain in many regions of the body do not have 11 of 18 tender points required for the technical diagnosis of fibromyalgia, the nociceptive system is already dysfunctional. The dysfunction becomes more severe as the tender points increase, and becomes greatest in patients who have fibromyalgia. [This study indicates that patients who do not yet have the 11 of 18 tender points may benefit from aggressive pain control to prevent further central sensitization. DJS]

Carlson CR, Okeson JP, Falace DA et al. 1993. Reduction of pain and EMG activity in the masseter region by trapezius trigger point injection. Pain 55(3):397-400. “Sources of deep pain can produce heterotopic sensory and motor changes in distant anatomical regions.”

Carmona L. 2002. More evidence on the dysautonomic nature of fibromyalgia: The association with short stature. Arthritis Rheum 46(1):1415-1416. This is especially interesting in that the author found a significant correlation with FMS and short women.

Caro XJ, Winter EF, Dumas AJ. 2008. A subset of fibromyalgia patients have findings suggestive of chronic inflammatory demyelinating polyneuropathy and appear to respond to IVIg. Rheumatology 47(2):208-211. “A significant subset of FMS subjects have clinical and EDX (electrodiagnostic) findings suggestive of CIDP. IVIg (intravenous immunoglobin) treatment shows promise in treating this subset.”

Caro, X. J. , F. Wolfe, W. H. Johnston and A. L. Smith. 1986. A controlled and blinded study of immune L. reactive deposition at the dermal-epidermal junction of patients with primary fibrositis syndrome. J. Rheumatol 13(6):1086-1092.

Carrillo-de-la-Pena MT, Vallet M, Perez MI et al. 2006. Intensity dependence of auditory-evoked cortical potentials in fibromyalgia patients: a test of the generalized hypervigilance hypothesis. J Pain 7(7):480-487. “Defects in an inhibitory system protecting against overstimulation may be a crucial factor in the pathophysiology of FM.” FMS patients may have hypersensitivity to stimuli, especially loud noise. [This study suggests mechanisms which may explain part of the auditory segment of allodynia often associated with FMS. DJS]

Carter, J. E. 1999. A systematic history for the patient with chronic pelvic pain. JSLS 3(4); 245-52.

Carter, J. E. 1998. Surgical treatment for chronic pelvic pain. J Soc Laparoendosc Surg 2(2):129-39.

Cartwright, R., A. Luten, M. Young, P. Mercer and M. Bears. 1998. Role of REM sleep and dream affect in overnight mood regulation: a study of normal volunteers. Psychiatry Res 81(1):1-8.

Cartwright, R. D. and E. Wood. 1991. Adjustment disorders of sleep: the sleep effects of a major stressful event and its resolution. Psychiatry Res 39(3):199-209.

Cassidy, C. M. 1998. Chinese medicine users in the United States. Part I: Utilization, satisfaction, medical plurality. J Altern Complement Med 4(1):17-27.

Cavriani G, Domingos HV, Oliveira-Filho RM et al. 2007. Lymphatic thoracic duct ligation modulates the serum levels of IL-1beta and IL-10 after intestinal ischemia/reperfusion in rats with the involvement of tumor necrosis factor alpha and nitric oxide. Shock. 27(2):209-213. [This study may be relevant to glial cell research and central sensitization. DJS]

Cayea D, Perera S, Weiner DK. 2006. Chronic low back pain in older adults: what physicians know, what they think they know, and what they should be taught. J Am Geriatr Soc. 54(11):1772-1777. “PCPs did not feel ‘very confident’ in their ability to diagnose any of the contributors of CLBP listed (most items <40%). PCPs felt most confident in detecting scoliosis and least confident detecting myofascial pain of the piriformis muscle.” “The results point to a need for more PCP education about CLBP in older adults. It also suggests that accurate needs assessment should not rely on physician confidence ratings alone.”

Cedraschi C, Desmeules J, Rapiti E et al. 2004. Fibromyalgia: a randomised, controlled trial of a treatment programme based on self management. Ann Rheum Dis 63(3):290-296. Appropriate 6 week pool-based exercise and education resulted in sustained (at least 6 months) improved quality of life for FMS patients. These patients were not screened for co-existing chronic myofascial pain.

Cenevic C, Maloney G, Mehta N. 2006. Myofascial pain may mimic trigeminal neuralgia. Cephalalgia 26:899-901.

Ceru-Bjork C, Andersson I, Rossner S. 2001. Night eating and nocturnal eating – two different or similar syndromes among obese patients? Int J Obes Relat Metab Disord. 25(3):365-372. “The main objective of this study was to identify subjects with (1) night eating syndrome (defined as morning anorexia, evening hyperphagia and insomnia) and (2) nocturnal eating syndrome (defined as eating at night after having gone to bed.)...Fourteen percent of the patients at our obesity unit met the criteria for night eating and/or nocturnal eating syndrome.”

Cervero, F. and J. M. Laird. 1996. Mechanisms of touch-evoked pain (allodynia): a new model. Pain 1996 68(1):13-23.

Cervero, F. 1995. Visceral pain: mechanisms of peripheral and central sensitization. Ann Med 27(2):235-9.

Ceylan Y, Hizmetli S, Silig Y. 2004. The effects of infrared laser and medical treatments on pain and serotonin degradation products in patients with myofascial pain syndrome. A controlled trial. Rheumatol Int. 24(5):260-263. IR laser may be highly effective for pain reduction in MPS patients.

Ceylan Y., Hizmetli S., Silig Y. 2003. The effects of infrared laser and medical treatments on pain and serotonin degradation products in patients with myofascial pain syndrome. A controlled trial. Rheumatol Int. [Epub Nov 20 ahead of print]. This study indicates that infrared laser treatment is effective for myofascial pain.

Chaitow L. 2007. Chronic pelvic pain: Pelvic floor problems, sacroiliac dysfunction and the trigger point connection. J Bodywork Move Ther 11(4):327-339. This review is packed with information. Chronic pelvic pain is poorly understood and may have far-reaching connections including breathing dysfunction and sacroiliac and urethral instability. This review includes excellent illustrations, clear explanations of the connections of specific links between symptoms and often unsuspected causes, and methods of examination and treatment. The importance of pelvic muscle tone is often greatly underestimated, and often much can be done to relieve symptoms often thought of as untreatable.

Chan K, Qin L, Lau M et al. 2004. A randomized, prospective study of the effects of Tai Chi Chun exercise on bone mineral density in postmenopausal women. Arch Phys Med Rehabil. 85(5):717-722. The practice of t’ai chi chuan may retard some bone loss.

Chan R, Lee M, Lee S. 2007. Needle electrical intramuscular stimulation for MPS: the VAS change of pain perception. J Musculoskel Pain 15 (Supp 13):14 item 18. [Myopain 2007 Poster] “NEIMS yield a good immediate pain relief [VAS drop about 2 scales] to the MPS patients. The effect can last for around one week. There is no treatment-tolerance after multiple NEIMS treatments.”

Chandler TJ, Kibler WB. 1993. A biomechanical approach to the prevention, treatment and rehabilitation of plantar fasciitis. Sports Med 15(5):344-352. [Understanding biomechanics of the foot may help treat and reduce recurrence of plantar fasciitis. This article would have benefitted greatly by inclusion of data concerning myofascial TrPs. DJS]

Chandra, S. and R. K. Chandra. 1986. Nutrition, immune response, and outcome. Prog Food Nutr Sci 10(1-2):1-65.

Chang CC, Chang ST. 2009. Excessive yawning induced by stimulation of myofascial trigger point-case report. Eur J Neurol. 16(6):e118-119.

Chang L, Berman S, Mayer EA, 2003. Brain responses to visceral and somatic stimuli in patients with irritable bowel syndrome with and without fibromyalgia. Am J. Gastroenterol 98(6):1354-1361. Irritable bowel syndrome and fibromyalgia may have similar central pathophysiologic mechanisms.

Chao J. 2005. Retrospective analysis of kadian (morphine sulfate sustained-release capsules) in patients with chronic, nonmalignant pain. Pain Med. 6(3):262-265. “Kadian® use did not result in escalation of dose strength or frequency, and was safe and efficacious regardless of patient age.”

Chao JD, Memmel HC, Redding JF. 2002. Reduction mammaplasty is a functional operation, improving quality of life in symptomatic women: a prospective, single-center breast reduction outcome study. Plast Reconstr Surg. 110(7):1644-1652. “Reduction for symptomatic breast hypertrophy can effect a statistically significant improvement in these objective measures of pain, disability, muscle weakness and poor posture.”

Chao Y.F., Chen S.Y., Lan C. et al. 2002. The cardiorespiratory response and energy expenditure of “Tai-Chi-Qui-Gong. Am J Chin Med 30(4):451-461. T’ai chi is a low intensity valid alternative exercise program for cardiopulmonary rehabilitation.

Chaplan, S. R., F. W. Bach, S. L. Shafer and T. L. Yaksh. 1995. Prolonged alleviation of tactile allodynia by intravenous lidocaine in neuropathic rats. Anesthesiology 83(4):775-785.

Chapman, C. R. and J. Gavrin. 1999. Suffering: the contributions of persistent pain. Lancet 353(9171):2233-7.

Chappell AS, Littlejohn G, Kajdasz DK et al. 2009. A 1-year safety and efficacy study of duloxetine in patients with fibromyalgia. Clin J Pain. 25(5):365-375.

Chau KW, Mao DW. 2006. The characteristics of foot movements in Tai Chi Chuan. Res Sports Med. 14(1):19-28. “The movements classified are shown to simulate balance, flexibility and proprioception, and functional training. The findings partially explain the relationship between practicing TCC (t’ai chi chuan) and its health benefits.”

Chawla PS, Kochar MS. 1999. Effect of pain and nonsteroidal analgesics on blood pressure. WMJ 98(5):22-25, 29. “NSAIDs antagonize the antihypertensive effect of diuretics, beta-blockers and ACE inhibitors more than that of calcium-channel blockers. The elderly and those with salt-sensitive hypertension experience greater rise in blood pressure with NSAIDs. Physicians should avoid NSAIDs and instead use alternative analgesics such as acetaminophen and physical therapy for control of pain. Since both pain and hypertension are common, it is important that their relationship be well understood by the primary care physicians.”

Check JH, Katsoff B, Citerone T et al. 2005. A novel highly effective treatment of interstitial cystitis causing chronic pelvic pain of bladder origin: case reports. Clin Exp Obstet Gynecol 32(4):247-249. Dextroamphetamine sulfate seems to be helpful for this condition.

Check JH, Katsoff D, Kaplan H et al. 2007. A disorder of sympathomimetic amines leading to increased vascular permeability may be the etiologic factor in various treatment refractory health problems in women. Med Hypotheses. [Aug 30 Epub ahead of print] “There is an evidence that increased capillary permeability in the standing position is related to a deficit in the sympathetic nervous system.” “One of the most common manifestations is the inability to lose weight despite proper dieting. A randomized study comparing the efficacy of a diuretic, a converting enzyme inhibitor, spironolactone and a sympathomimetic amine on weight loss in diet refractory women found that only the latter in the form of dextroamphetamine sulfate demonstrated significant weight reduction over a six month time span.” “The diagnosis of a deficit in sympathomimetic amines is established by demonstrating an abnormal clearance of a water load in the erect position and exclusion of other conditions that are associated with an abnormal free water clearance, e.g., hypothyroidism, renal or liver disease or congestive heart failure.” “There are several conditions that have proven refractory to conventional theory that respond quickly and effectively to sympathomimetic amines. There have been many anecdotal reports of relieving intractable pain syndromes quickly and efficiently with sympathomimetic amine theory, despite failure with a multitude of other therapies. These include interstitial cystitis and pelvic pain that was attributed to endometriosis, gastrointestinal pain including esophagitis and gastroparesis, headaches, joint pain, fibromyalgia, and carpal tunnel syndrome. It is not clear if the improvement in pain is related to a decrease in fluid retention or a direct effect of the sympathomimetic amines on the sympathetic nervous system.” “These studies strongly suggest that physicians be aware of this condition involving a deficit in the sympathetic nervous system when faced with various enigmatic complaints especially if standard therapy has not proven effective.” [This review has made connections that may explain why an FM subset of patients and those with other conditions respond to some stimulants and other medications in this class. DJS]

Check JH, Shanis BS, Shapse D et al. 1995. A randomized comparison of the effect of two diuretics, a converting enzyme inhibitor, and a sympathomimetic amine on weight loss in diet-refractory patients. “...the results suggest that some women who are recalcitrant to dietary weight loss may have a mild type of water retention that is refractory to diuretics but responsive to amphetamines.”

Check, J. H. , H. g. Adelson and C. H. Wu. 1982. Improvement of cervical factor with guaifenesin. Fertil Steril 37(5):707-708.

Chen CL, Robert JJ, Orr WC. 2008. Sleep symptoms and gastroesophageal reflux. J Clin Gastroenterol. 42(1):13-17. “Nighttime heartburn together with sleep complaints is associated with excessive gastroesophageal reflux.”

Chen CL, Broom DC, Liu Y et al. 2006. Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain. Neuron. 49(3):365-377. “In mammals, the perception of pain is initiated by the transduction of noxious stimuli through specialized ion channels and receptors expressed by nociceptive sensory neurons.” “Thus, Runx1, a Runt domain transcription factor, coordinates the phenotype of a large cohort of nociceptors, a finding with implications for pain therapy.”

Chen CS, Ingber DE. 1999. Tensegrity and mechanoregulation: from skeleton to cytoskeleton. Osteoarthritis Cartilage. 7(1):81-94. This article explains how factors affecting one portion of the body can affect the whole, down to the molecular level.

Chen I, Kurz J, Pasanen M et al. 2005. Racial differences in opioid use for chronic nonmalignant pain. J Gen Intern Med. 20(7):593-598. “Equal treatment by race occurs in nonopioid-related therapies, but white patients are more likely than black patients to be treated with opioids.”

Chen JJ, Wang JY, Chang YM et al. 2007. Regional cerebral blood flow between primary and concomitant fibromyalgia patients: a possible way to differentiate concomitant fibromyalgia from the primary disease. Scand J Rheumatol. 36(3):226-232. “Reduced rCBF at cortical regions, in addition to previously reported areas at the thalamus and the subcortical nucleus, in FM patients was demonstrated in this study. The perfusion deficit areas were similar between primary and concomitant FM when the underlying disease activity was quiescent. The feasibility of using this neuroimaging rheumatoid arthritis (RA)-associated depression and neuropsychiatric lupus, should be considered.”

Chen, J. T. S. M. Chen, T. S. Kuan, K. C. Chung and C. Z. Hong. 1998. Phentolamine effect on the spontaneous electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle. Arch Phys Med Rehabil 79(7):790-4.

Chen KH, Hong CZ, Kuo FC et al. 2007. Electrophysiological effects of therapeutic laser on trigger spots of rabbit skeletal muscles. J Musculoskel Pain 15 (Supp 13):24 item 38. [Myopain 2007 Poster]

Chen KW, Hassett AL, Hou F et al. 2006. A pilot study of external qigong therapy for patients with fibromyalgia. J Altern Complement Med. 12(9):851-856. “Treatment with EQT resulting in complete recovery for some FMS patients suggests that TCM may be very effective for treating pain and the multiplicity of symptoms associated with FMS. Larger controlled trials of this promising intervention are urgently needed.”

Chen Q, Basford J, An KN. 2008. Ability of magnetic resonance elastography to assess taut bands. Clin Biomech [Jan 16 Epub ahead of print]. “This study suggests that magnetic resonance elastography may have a potential for objectively characterizing myofascial taut bands that have been up to now detectable only by the clinician’s fingers.”

Chen Q, Bensamoun S, Basford JR et al. 2007. Identification and quantification of myofascial taut bands with magnetic resonance elastography. Arch Phys Med Rehabil. 88(12):1658-1661. “Our findings suggest that MRE can quantitate asymmetries in muscle tone that could previously only be identified subjectively by examination.” This includes myofascial trigger points

Chen, S. M., J. T. Chen, T. S. Kuan and C. Z. Hong. 1998. Myofascial trigger points in intercostal muscles secondary to herpes zoster infection of the intercostal nerve. Arch Phys Med Rehabil 79(3):336-338.

Cheng XF, Tan J, Tan KL. 2005. [Clinical analysis of six cases with juvenile primary fibromyalgia syndrome.] Zhonghua Er Ke Za Zhi 43(11):863-865. [Chinese] “Juvenile primary FMS may not be a rare disease and the clinicians should pay more attention to it for avoiding misdiagnosis.”

Cheras, P. A., A. N. Whitaker, E. A. Blackwell, T. J. Sinton, M. D. Chapman and K. A. Peacock. 1997. Hypercoagulability and hypofibrinolysis in primary osteoarthritis. Clin Orthop (334):57-67.

Cheshire, W. P., S. W. Abashian and J. D. Mann. 1994. Botulinum toxin in the treatment of myofascial pain syndrome. Pain 59(1):65-9.

Chevlen, E. 2000. Morphine with dextromethorphan; conversion from other opioid analgesics. J Pain Symptom Manage 19(1 Suppl):S42-9. MS:DM appears safe and effective in treating moderate to severe chronic pain.

Chim D, Brodsky M, Hui KK. 2007. Teaching medical students trigger point techniques. Fam Med. (1):8. “Myofascial pain is underemphasized in medical education and underrecognized in clinical practice.”

Chiu, H. F., T. Leung, L. C. Lam, Y. K. Wing, D. W. Chung, S. W. Li, I. Chi, W. T. Law and K. W. Boey. 1999. Sleep problems in Chinese elderly in Hong Kong. Sleep 22(6):717-26.

Chiu KC, Chu A, Go VLW et al. 2004. Hypovitaminosis D is associated with insulin resistance and B cell dysfunction. Amer Jour Clinical Nut. 79(5):820-825. This may be very pertinent as I have observed insulin resistance to be a common perpetuating factor for both FMS and CMP, and vitamin D insufficiency is implicated as one cause of musculoskeletal pain.

Cho JW, Chu K, Jeon BS. 2001. Case of essential palatal tremor: atypical features and remarkable benefit from botulinum toxin injection. Mov Disord. 16(4):779-782. An injection of Botox into the tensor veli palatini muscles cured essential palatal tremor. [The patient had some control over the tremor before treatment. Could there have been myofascial TrPs? DJS.]

Cho, Z. H., S. C. Chung, J. P. Jones, J. B. Park, H. J. Park, H. J. Lee, E. K. Wong and B. I. Min. 1998. New findings of the correlation between acupoints and corresponding brain cortices using function MRI. Proc Natl Acad Sci U S A 95(5):2670-2673.

Choileain NN, Redmond HP. 2006. Cell response to surgery. Arch Surg. 141(11):1132-1140. “Surgical trauma produces profound immunological dysfunction. Therapeutic strategies directed at restoring immune homeostasis should aim to redress the physiological proinflammatory-anti-inflammatory cell imbalance associated with major surgery.”

Chou KC. 2004. Insights from modeling three-dimensional structures of the human potassium and sodium channels. J Proteome Res. 3(4):856-861. Research in ion channel dysfunction may be revealing new strategies for treatment of chronic pain.

Chou LW, Hsieh YL, Kao MJ et al. 2009. Remote influences of acupuncture on the pain intensity and the amplitude changes of endplate noise in the myofascial trigger point of the upper trapezius muscle. Arch Phys Med Rehabil. 90(6):905-912. Trapezius TrP symptoms were reduced after acupuncture at remote sites. This study was interesting in that both subjective (pain) and objective (electrical endplate noise) qualities were decreased after the acupuncture.

Chow DH, Leung KT, Holmes AD. 2007. Changes in spinal curvature and proprioception of schoolboys carrying different weights of backpack. Ergonomics. [Sep 19 Epub ahead of print]. “Carriage of a loaded backpack causes immediate changes in spinal curvature and appears to have a direct effect on the repositioning consistency.” Patents and teachers must be made aware of the dangers posed to the youth of our country by carrying heavy backpacks.

Chow RT, Barnsley L, Heller GZ et al. 2004. A pilot study of low-power laser therapy in the management of chronic neck pain. Musculoskel Pain 12(2):71-81.

Chow R, Barnsley L, Heller GZ et al. 2003. Efficacy of 300 mW, 830 nm laser in the treatment of chronic neck pain: a survey in a general practice setting. J Musculoskel Pain 11(3):13-21. “Low level laser therapy using this wavelength and power of infrared laser may provide a non-drug, non-invasive option for the management of neck pain.”

Chu J. 2000. Twitch-obtaining intramuscular stimulation (TOIMS): long term observations in the management of chronic partial cervical radiculopathy. Electromyogr Clin Neurophysiol 40(8):503-510. “Observations suggest TOIMS to have potential value in the long-term management of partial cervical radiculopathy related myofascial pain.”

Chu J, Takehara I, Li TC et al. 2004. Electrical twitch obtaining intramuscular stimulation (ETOIMS) myofascial pain syndrome in a football player. Br J Sports Med. 38(5):E25. ETOIMS may be helpful in reducing pain and increasing and maintaining range of motion in MPS.

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Ciccone DS, Elliott DK, Chandler HK et al. 2005. Sexual and physical abuse in women with fibromyalgia syndrome: a test of the trauma hypothesis. Clin J Pain 21(5):378-386. "With the exception of rape, no self-reported sexual or physical abuse event was associated with FMS in this community sample. [Emphasis mine. DJS] In accord with the trauma hypothesis, however, posttraumatic stress disorder was more prevalent in the FMS group. Chronic stress in the form of posttraumatic stress disorder but not major depressive disorder may mediate the relationship between rape and FMS.”

Ciccone DS, Just N, Bandilla EB et al. 2000. Psychological correlates of opioid use in patients with chronic nonmalignant pain. A preliminary test of the downhill spiral hypothesis. J Pain Symptom Manage 20(3):180-192. “There was no evidence that higher levels of opioid use were associated with higher levels of disability or depression.”

Cimbiz A, Beydemir F, Manisaligil U. 2006. Evaluation of trigger points in young subjects. J Musculoskel Pain 14(4):27-35. It is necessary to diagnose and treat myofascial TrPs promptly in young patients, as they can become chronic and worsen with time.

Cimbiz A, Bayazit V, Hallaceli H et al. 2005. The effect of combined therapy (spa and physical therapy) on pain in various chronic diseases. Complement Ther Med. 13(4):244-250. “The patients with ankle arthrosis, fibromyalgia and cervical disc herniation reported the highest VAS (Visual Analog Scale) score before treatment program. After the therapy program, VAS scores were seen to decrease compared to before treatment.” “To decrease pain and high blood pressure without hemodynamic risk, a combined spa and physical therapy program may help to decrease pain and improve hemodynamic response in patients with irreversible pathologies.”

Cimen A, Celik M, Erdine S. 2004. Myofascial pain syndrome in the differential diagnosis of chronic abdominal pain. Agri. 16(3):45-47. MPS may be misdiagnosed as visceral disease if the clinician is not trained in its diagnosis.

Cinar, Y., G. Demir, M. Pac and A. B. Cinar. 1999. Effect of hematocrit on blood pressure via hyperviscosity. Am J Hypertens 12(7):739-43.

Cioni B, Meglio M. 2007. Motor cortex stimulation for chronic non-malignant pain: current state and future prospects. Acta Neurochir Suppl. 97(Pt 2):45-49. “MCS may act by rebalancing the control of non-nociceptive sensory inputs over nociceptive afferents at cortical, thalamic, brainstem and spinal level. In addition, it may interfere with the emotional component of nociceptive perception.” MCS may be a promising new therapy for chronic pain.

Cisler TA. 1994. Whiplash as a total-body injury. J Am Osteopath Assoc 94(2):145-148. “Physicians must recognize whiplash injury as a manifestation of total-body trauma and treat accordingly, with particular emphasis on alleviating abnormal tension of the fascia. Precise description of the accident, followed by healing methods tailored to well-defined bodily injury, aids in effective management.”

Citak-Karakaya I, Akbayrak T, Demirturk F et al. 2006. Short- and long-term results of connective tissue manipulation and combined ultrasound therapy in patients with fibromyalgia. Manipulative Psysiol Ther. 29(7):524-528. “Methods used in this study seemed to be helpful in improving pain intensity, complaints of nonrestorative sleep, and impact on functional activities in patients with FM.”

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E. J. Scheines and D. P. Carinalli. 2000. The effect of melatonin in patients with fibromyalgia: a pilot study. Clin Rheumatol 19(1):9-13.

Clark, F., S. P. Azen, R. Zemke, J. Jackson, M. Carlson, D. Mandel, J. Hay, K. Josephson, B. Cherry, C. Hessel, J. Palmer and L. Lipson. 1997. Occupational therapy for independent-living older adults. A randomized controlled trial. JAMA 278(16):1321-6. Significant benefits for the OT preventive treatment group were found across various health, function, and quality-of-life domains. Preventive health programs based on OT may mitigate against the health risks of older adulthood.

Clark, F. J., R. C. Burgess, J. W. Chapin and W. T. Lipscomb. 1985. Role of intramuscular receptors in the awareness of limb position. J Neurophysiol 54(6):1529-40.

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Clark, P., R. Burgos-Vargas, C. Medina-Palma, P. Lavielle and F. F. Marina. 1998. Prevalence of fibromyalgia in children: a clinical study of Mexican children. J Rheumatol 25(10):2009-14.

Clauw DJ. 2007. Clinical studies and their implications for the management of fibromyalgia syndrome. J Musculoskel Pain 15 (Supp 13):6 item 7. [Myopain 2007 Poster] Possibly the most common association in FM studies is the amplification of sensory stimuli, including pressure, pain, heat, electricity and noise. Regional pain conditions that often occur with FM and are associated with central sensitization, such as IBS, have similar amplification, with “...augmented central processing of pain as a finding common to all of these conditions.” [Many of the conditions mentioned, such as tension headache, TMD and low back pain have myofascial components. DJS] There is one or more dysfunctions in the descending pain pathway in FM. Indications are that there may be genetic defects involved in the metabolism of pro-nociceptive or anti-nociceptive biochemicals. “Drugs that decrease the release of pro-nociceptive substances (e.g. pregabalin) may be acting via this mechanism to ‘decrease the volume’ setting in FMS.” “...studies suggest that the biological basis for the effectiveness of cognitive behavioral approaches can be objectively measured using functional imaging.” Research suggests that decreasing restorative sleep and exercise may help initiate or worsen FM, and focusing on restoring these areas may help restore function and reduce pain.

Clauw DJ, Crofford LJ. 2003. Chronic widespread pain and fibromyalgia: what we know, and what we need to know. Best Pract Res Clin Rheumatol. 17(4):685-701. “These conditions respond best to a combination of symptom-based pharmacological therapies, and non-pharmacological therapies such as exercise and cognitive behavioral therapy. In contrast to drugs that work for peripheral pain due to damage or inflammation, neuroactive compounds [especially those that raise central levels of noradrenaline (norepinephrine) or serotonin] are most effective for treating central pain.”

Clauw, D. 2002. Fibromyalgia associated syndromes. J Musculoskel Pain 10(1/2)201-214. " …chronic multisystem illnesses such as fibromyalgia are extremely common. Hallmarks of these syndromes include non-nociceptive pain, fatigue, memory difficulties, and dysfunction of visceral organs".

Clauw, D. J. and G. P. Chousos. 1997. Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation 4(3):134-53.

Clauw, D. J. , M. Schmidt, D. Radulovic, A. Singer, P. Katz, and J. Bresettte..1997. The relationship between fibromyalgia and interstitial cystitis. J Psychiatr Res 31(1):125-31.

Cleveland, C. H. Jr., R. H. Fisher, E. P. Brestel, J. D. Esinhart and W. J. Metzger. 1992. Chronic rhinitis: an underrecognized association with fibromyalgia. Allergy Proc 13(5):263-267.

Coderre, T. J. and J. Katz. 1997. Peripheral and central hyperexcitability: differential signs and symptoms in persistent pain. Behav Brain Sci 20(3):404-19.

Cogan J, Camus M, Saucier JF et al. 2006. A new application of sound resonance technology therapy for the treatment of fibromyalgia: a retrospective analysis. Complement Ther Clin Pract. 12(3):206-212. “Conclusions: This retrospective analysis suggests considerable and rapid relief of the symptoms of fibromyalgia following the use of the three-phase SRTT treatment protocol, which appears to be maintained over several years. Although these results are not conclusive, they are remarkable as no other therapy reported in the scientific literature seems as efficacious for fibromyalgia. A follow-up study using an RCT design is warranted.”

Cohen, H., L. Neumann, Y. Haiman et al. 2002. Prevalence of post-traumatic stress disorder in fibromyalgia patients: Overlapping syndromes or post-traumatic fibromyalgia syndrome? Semin Arthritis Rheum 23(1):38-50. In this study, 57% of the FMS patients tested had significant levels of PTSD symptoms.

Cohen, H., L. Neumann, M. Shore, M. Amir, Y. Cassuto and D. Buskila. 2000. Autonomic dysfunction in patients with fibromyalgia: application of power spectral analysis of heart rate variability. Semin Arthritis Rheum 2000 Feb;29(4):217-27

Cohen, S., E. Frank, W. J. Doyle, D. P. Skoner, B. S. Rabin and J. M. Gwaltney, Jr. 1998. Types of stressors that increase susceptibility to the common cold in healthy adults. Health Psychol 17(3):214-23.

Cohen, S., W. J. Doyle, D. P. Skoner, B. S. Rabin and J. M. Gwaltney, Jr. 1997. Social ties and susceptibility to the common cold. JAMA 277(24):1940-4.

Cole JA, Rothman KJ, Cabral HJ et al. 2006. Migraine, fibromyalgia and depression among people with IBS: a prevalence study. BMC Gastroenterol. 6:26. “People in the IBS cohort had a 40% to 80% higher prevalence odds of migraine, fibromyalgia and depression.”

Cook DB, Nagelkirk PR, Poluri A et al. 2006. The influence of aerobic fitness and fibromyalgia on cardiorespiratory and perceptual responses to exercise in patients with chronic fatigue syndrome. Arthritis Rheum. 54(10):3351-3362. “These results suggest that aerobic fitness and a concurrent diagnosis of FM are likely explanations for currently conflicting data and challenge ideas implicating metabolic disease in the pathogenesis of CFS.”

Cook DB, Lange G, Ciccone DS et al. 2004. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol 31(2):364-78. This study provides “...further evidence for a physiological explanation for FM pain.”

Covelli, V., A. B. Maffione, C. Nacci, E. Tato and E. Jirillo. 1998. Stress, neuropsychiatric disorders and immunological effects exerted by benzodiazepines. Immunopharmacol Immunotoxicol 20(2):199-209.

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Colborn, T. 1994. The wildlife/human connection: modernizing risk decisions. Environ Health Perspect 102 Suppl 12:55-9.

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Colburn KK, Rambharose JA, Malto MC et al. 2006. Abnormally low antibody markers of elastin synthesis in patients with fibromyalgia syndrome. J Musculoskel Pain. 14(3):13-19. This study showed altered elastin metabolism in FMS patients. This alteration, if significant, could affect elastic tissue in areas such as the lungs and other organs, skin, and blood vessels. [These patients were not screened for co-existing myofascial TrPs. DJS]

Colcombe SJ, Kramer AF, Erickson KI et al. 2004. Cardiovascular fitness, cortical plasticity and aging. Proc Natl Acad Sci U S A 101(9):3316-3321. Brain function in sedentary seniors can be improved with moderate regular walking exercise.

Collop N. 2007. The effect of obstructive sleep apnea on chronic medical disorders. Cleve Clin J Med. 74(1):72-78. “Evidence is mounting that obstructive sleep apnea causes or contributes to many chronic medical diseases, and that treatment with continuous positive airway pressure (CPAP) often improves concomitant diseases.” [This can be beneficial for some chronic pain patients, as OSA is often a perpetuating factor or interactive diagnosis. DJS]

Conigliaro, D. A. 1996. Opioids for chronic non-malignant pain. J Fla Med Assoc 83(10):708-711.

Conte, PM, Walco, GA, Kimura, Y. 2003. Temperament and stress response in children with juvenile primary fibromyalgia syndrome. Arthritis Rheum 48(10):2923-30. This article may help care providers recognize children who are at risk for development of a chronic pain condition and may be a valuable tool in helping to prevent that from happening.

Cook, I. A., A. F. Leuchter, M. Morgan et al. 2002. Early changes in prefrontal activity characterize clinical responders to antidepressants. Neuropsychopharmacology 27(1):120-31. Quantatative EEG (QEEG) of the prefrontal region of the brain may be a valuable tool that might indicate which patients are responding to a specific antidepressant within 48 hours to 1 week after beginning therapy.

Coplan, J. D., H. Tamir, D. Calaprice, M. DeJesus, M. de la Nuez, D. Pine, L. A. Papp, D. F. Klein and J. M. Gorman. 1999. Plasma anti-serotonin and serotonin anti-idiotypic antibodies are elevated in panic disorder. Neuropsychopharmacology 20(4):386-91.

Corvo G, Tartaro G, Giudice A et al. 2003. Distribution of craniomandibular disorders, occlusal factors and oral parafunctions in a paediatric population. Eur J Paediatr Dent. 4(2):84-88. Early diagnosis and correction of muscle dysfunctions are critical to avoid later TMJD. [Myofascial TrPs are a very common and generally unrecognized cause of many of these dysfunctions DJS.]

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Couppe C, Torelli P, Fugisang-Frederiksen A et al. 2007. Myofascial trigger points are very prevalent in patients with chronic tension-type headache: a double-blinded controlled study. Clin J Pain. 23(1):23-27. “These findings suggest that active TrPs are much more frequent in CTTH (chronic tension type headaches) than in controls and the number and pain intensity of TrPs may be used to distinguish between the two groups.”

Cox GR, Barish RA. 1991. Delayed presentation of unstable cervical spine injury with minimal symptoms. J Emerg Med 9(3):123-127. “Physicians must aggressively search for injuries whenever a history of neck pain is present or a strong mechanism of injury exists, even if the patient has been ambulatory for days or weeks following the injury."

Cox JJ, Reimann F, Nicholas AK. 2006. An SCN9A channelopathy causes congenital inability to experience pain. Nature 444:894-898. A genetic mutation can cause the inability to feel pain through a sodium channelopathy. Studying this may offer insights into chronic pain. [Myofascial pain may also be a channelopathy. DJS]

Crago BR, Gray MR, Nelson LA et al. 2003. Psychological, neuropsychological, and electrocortical effects of mixed mold exposure. Arch Environ Health 58(8):452-463. Mold exposure can lead to “...organic-based dysregulation of emotions and cognitive functioning as a result of toxic or metabolic encephalopathy...” Abnormalities in the frontal and prefrontal lobes of the brain were “...significantly and consistently related to deficits in cognitive functioning and mold-exposure measures.” “Patients reported a loss of their sense of self, of their usual ways of doing things, and even of their personality. They were painfully aware of their deficits and were constantly frustrated by their loss of cognitive efficiency and frequent mistakes.”

Craig, AD. 2003. Interoception: the sense of the physiological condition of the body. Curr Opin Neurobiol 13:500-505. Both fibromyalgia and chronic myofascial trigger points may be associated with autonomic symptoms. There may be mechanoreceptive and proprioceptive dysfunction. This article discusses the interoceptive system, which includes vasomotor activity, hunger, thirst and internal sensations. “These findings explain the distinct nature of pain, temperature, itch, sensual touch and other bodily feelings from cutaneous mechanoreception (somatosensory touch) and they identify the long-missing peripheral and central afferent complement to the efferent autonomic nervous system. I agree with the author that this study may have profound clinical significance.

Craig KD, Lilley CM, Gilbert CA. 1996. Social barriers to optimal pain management in infants and children. Clin J Pain 12(3):232-242. Care providers need to be aware that infants and children need adequate pain control.

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Crofford LJ, Rowbotham MC, Mease PJ et al. 2005. Pregabalin for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 52(4):1264-1273. “Conclusion: Pregabalin at 450 mg/day was efficacious for the treatment of FMS, reducing symptoms of pain, disturbed sleep, and fatigue compared with placebo. Pregabalin was well tolerated and improved global measures and health-related quality of life.”

Crofford LJ. 2004. Pharmaceutical treatment options for fibromyalgia. Curr Rheumatol Rep. 6(4):274-280. There are multiple mechanisms causing a wide variety of fibromyalgia symptoms. “Understanding specific etiologic factors and pathogenic mechanisms in individual patients will allow clinicians to determine treatments that are most effective for a given patient.” [Look for the perpetuating factors. DJS]

Crawford, LJ. 1998. Neuroendocrine findings and patients with fibromyalgia. J Musculoskel Pain 6(3):69.

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Crotti FM, Carai A, Carai M et al. 2005. TOS pathophysiology and clinical features. Acta Neurochir Suppl. 92:7-12. “In all patients neurological, vascular and myofascial pain symptoms were observed before the operation. Neurological and vascular pain disappeared after surgery, while the myofascial pain remained. In TOS, therefore, there is a pain loop that cannot be resolved by surgical therapy alone. The connection between myofascial pain syndrome and TOS might explain the many controversial opinions regarding frequency, results and surgical possibilities of this lesion.” [Thoracic Outlet Syndrome is a description, not a diagnosis. Clinicians must learn to look for the reasons for constriction. It is often caused by muscles contractured due to myofascial TrPs. The sooner the TrPs are treated the less the chance for fibrosis or calcification. DJS]

Crotti FM, Carai A, Carai M et al. 2005. Entrapment of crural branches of the common peroneal nerve. Acta Neurochir 92:69-70. “Failed back surgery syndrome (FBSS) occurs in 30% of operated patients and represents a heavy problem both regarding disability and costs in first world countries. Among FBSS we found the possibility of a double crush syndrome: a disco-radicular conflict and a peripheral nerve entrapment. The latter, disguised by root compression symptoms, becomes evident only after spinal surgery. We found peroneal nerve crural branches entrapped where they crossed the fascia to reach the subcutaneous layer. Most of the patients were found to have myofascial pain syndrome (MPS).” [Again, myofascial TrPs are often the cause of nerve entrapment. Clinicians (and insurance companies) need to be aware of this. Doctors need to be trained in diagnosis and treatment of TrPs to help minimize the pain and costs of chronic care. DJS]

Crow T, Kasper D. 2006. A myofascial trigger point on the skull: treatment improves peak flow values in acute asthma patients. AAOJ 16(1):23-25. Nine chronic asthma patients, varying from mild to severe cases, were given manual therapy of an MTP on the left parietal eminence. The air flow rate of 5 patients was restored to from 96-108%, and the other 4 restored to between 66 and 88% expected flow amount based on body size. [This is an early study, lacking much specific data, but it does imply that it is worth checking asthma patients for MTPs in the skull and treating any that are found. DJS]

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Csaba G, Kovacs P, Tothfalusi L et al. 2005. Prolonged effect of stress (water and food deprivation) at weaning or in adult age on the triiodothyronine and histamine content of immune cells. Horm Metab Res. 37(11):711-715. “Not only fetal or neonatal stress has long-lasting consequences, but also stress events in later periods of life in cells (organs) that are continuously differentiating.” A significant change in rat T3 metabolism due to neonatal stress was evident. The histamine content of granulocytes was also changed significantly. [Similar changes have been noted in adult FMS patients. DJS.]

Csako G, McGriff NJ, Rotman-Pikielny P, Sarlis NJ, Pucino F. 2001. Exaggerated levothyroxine malabsorption due to calcium carbonate supplementation in gastrointestinal disorders. Ann Pharmacother Dec:35(12):1578-83. Calcium carbonate can decrease absorption of levothyroxine especially if the patient has a preexisting malabsorption disorder.

Cubukcu S, Alimoglu MK, Samanci N et al. 2007. Isokinetic and isometric muscle strength of the knee flexors and extensors in patients with the fibromyalgia syndrome and chronic myofascial pain syndrome. J Musculoskel Pain 15(3):49-55. “Muscular performance in both of FMS and MPS patients groups was low compared to HNCs (healthy normal controls]. The FMS patients showed lower isokinetic flexion and isometric extension strength than the MPS patients at some particular speeds.” [The MTP patient’s muscle weakness may be due to latent MTPs in the area. DJS]

Cueco RT, Salvat I, Montull S et al. 2007. Evaluation of the skin rolling procedure as a diagnostic test for fibromyalgia syndrome. J Musculoskel Pain 15 (Supp 13):44 item 77. [Myopain 2007 Poster] “Toughness and stiffness felt in the application of the SRP (skin rolling procedure) is not a valuable diagnostic tool in FMS and cannot be used as a diagnostic test.” [This “test” can be exceedingly painful to patients with CMP and central sensitization. They may have tissue adhesed from skin to the bone, and releasing stuck fascia by this method may increase central sensitization. DJS]

Cummings M. 2003. Myofascial pain from pectoralis major following trans-axillary surgery. Acupuncture Med 21(3):105-107. Myofascial referred pain and nerve entrapment symptoms can occur at a post-surgical drain site.

Cummings, M. 2003. Referred knee pain treated with electroacupuncture to iliopsoas. Acupunct Med 21(1-2):32-35. This is a showcase of what can happen when care providers don’t understand myofascial medicine. The patient developed knee pain after standing for a prolonged time. Tests indicated arthritis and left hip dysplasia, but no knee abnormalities. After multiple surgical techniques, including femoral osteotomy, lateral shaft graft and total hip replacement, the knee pain was still present on follow-up. After two treatments with electroacupuncture to the iliopsoas muscle, the knee pain was gone. How might the practice of medicine, and the costs of same, be changed if the care providers were trained in the diagnosis and treatment of myofascial trigger points?

Curatolo M, Arendt-Nielsen L, Petersen-Felix S. 2004. Evidence, mechanisms, and clinical implications of central hypersensitivity in chronic pain after whiplash injury. Clin J Pain 20(6):469-476. “Central hypersensitivity may explain exaggerated pain in the presence of minimal nociceptive input arising from minimally damaged tissue. This could account for pain and disability in the absence of objective signs of damage in patients with whiplash. Central hypersensitivity may provide a neurobiological framework for the integration of peripheral and supraspinal mechanisms in the pathophysiology of chronic pain after whiplash.”

Da Costa D, Abrahamowicz M, Lowensteyn I et al. 2005. A randomized clinical trial of an individualized home-based exercise program for women with fibromyalgia. Rheumatology (Oxford) [Epub ahead of print July 19] “Home-based exercise, a relatively low-cost treatment modality, has the potential to improve important health outcomes in FM.”

Da Costa, D., P. L. Dobkin, M. A. Fitzcharles, P. R. Fortin, A. Beaulieu, M. Zummer, J. L. Senecal, J. R. Goulet, E. Rich, D. Choquette and A. E. Clark. 2000. Determinants of health status in fibromyalgia: a comparative study with systemic lupus erythematosus. J Rheumatol 27(2):365-72.

Daali Y, Cherkaoui S, Doffey-Lazeyras F et al. 2008. Development and validation of a chemical hydrolysis method for dextromethorphan and dextrophan determination in urine samples: application to the assessment of CYP2D6 activity in fibromyalgia patients. J Chromatogr B Analyt Technol Biomed Life Sci. 861(1):56-63

D’Adamo PJ, Kelly GS. 2001. Metabolic and immunologic consequences of ABH secretor and Lewis subtype status. Altern Med Rev. 6(4):390-405. “Determining ABH secretor phenotype and/or Lewis (Le) blood group status can be useful to the metabolically-oriented clinician. Lewis typing is one genetic marker which might help identify subpopulations of individuals genetically prone to insulin resistance, autoimmunity and heart disease.” ABH secretor status and Lewis blood groups may provide some clues that insulin resistance or other metabolic abnormalities may be present.

Dainoff MJ, Cohen BG, Dainoff MH. 2005. The effect of an ergonomic intervention on musculoskeletal, psychosocial, and visual strain of VDT data entry work: the United States part of the international study. Int J Occuip Saf Ergon. 11(1):49-63. “...extensive, intensive and relatively expensive ergonomic intervention and training...” can prevent further injury, improve health, and avoid further costs to the company. “The cost of this intervention was estimated as $2,200 per employee, while the cost of a single worker’s compensation case could be as high as $75,000.” [The problem now is to get the employers and 3^rd party insurance payers to realize that preventative ergonomic medicine is cost effective. DJS]

Dall’Alba PT, Sterling MM, Treleaven JM et al. 2001. Cervical range of motion discriminates between asymptomatic persons and those with whiplash. Spine 26(19):2090-2094. “Range of motion was reduced in all primary movements in patients with persistent whiplash-associated disorder.” [Decreased range of motion is often caused by myofascial trigger points. DJS]

Dalmau-Carola J. 2005. Myofascial pain syndrome affecting the piriformis and the obturator internus muscle. Pain Pract. 5(4):361-363. “The obturator internus muscle is an external rotator of the hip. Obturator internus injury may occur and be hidden by the piriformis syndrome. Clinical symptoms may offer some clues to the clinician. The selective injection technique described here facilitates precise diagnosis.”

Dalpiaz AS, Lordon SP, Lipman AG. 2004. Topical lidocaine patch therapy for myofascial pain. J Pain Palliat Care Pharmacother 18(3):15-34.

Dalpiaz AS, Dodds TA. 2002. Myofascial pain response to topical lidocaine patch therapy: case report. J Pain Palliat Care Pharmacother. In the case described, pain was decreased and function improved with the use of lidocaine patch.

D'Ambrogi E, Giacomozzi C, Macellari V et al. 2005. Abnormal foot function in diabetic patients: the altered onset of Windlass mechanism. Diabetic Med 22(12):1713-1719. “Increased thickness of Achilles tendon and plantar fascia, more evident in the presence of neuropathy...might play a significant role in the overall alteration of the biomechanics of the foot-ankle complex.” [Diabetic neuropathy might be a significant perpetuating factor to myofascial TrPs. DJS]

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Danneskiold-Samsøe B, Bartels EM, Genefke I. 2007. Treatment of torture victims – a longitudinal clinical study. Torture. 17(1):11-7. “A high percentage of the torture victims in our study suffered from fibromyalgia prior to treatment. A multidisciplinary treatment involving individualized physiotherapy and psychotherapy had a significant effect on musculoskeletal pain in torture victims. Following nine months of treatment, only one torture victim in our study could be classified as suffering from fibromyalgia when applying the fibrositis index.”

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Dargaud J, Lamotte C, Dainotti JP et al. 2001. [Venous drainage and innervation of the maxillary sinus] Morphologie 85(270):11-13. [French] Although not mentioning myofascial TrPs specifically, this study indicates how maxillary sinus congestion could be caused by blood vessel entrapment by pterygoid TrPs.

Da Silva GD, Lorenzi-Filho G, Lage LV. 2007. Effects of yoga and the addition of tui na in patients with fibromyalgia. J Altern Complement Med. 13(10):1107-1114. Some yoga techniques may be helpful for some FM patients. Patients who experienced a type of soft tissue masssage, tui na, reported less pain than patients who took part in yoga, but the patients with yoga improved more over the long term. [This study did not screen patients for co-existing MTPs, but may indicate that while massage may ease the pain, stretching and breathing properly may be a better alternative than passive treatment if one has to choose between the two. DJS]

Daub CW. 2007. A case report of a patient with upper extremity symptoms: differentiating radicular and referred pain. Chiropr Osteopat. 15(1):10. “During the first episode the patient was diagnosed with a cervical radiculopathy.” “Approximately eighteen months later the patient again experienced a severe acute flare-up of the upper extremity symptoms. Although the subjective complaint was similar, it was determined that the pain generator of this episode was an active trigger point of the infraspinatus muscle. A diagnosis of myofascial referred pain was made and a protocol of manual trigger point therapy and functional postural rehabilitative exercises improved the condition.” “Conservative manual therapy and rehabilitative exercises may be an effective treatment for certain cases of cervical radiculopathy and myofascial referred pain.” [We will never know how much surgery and other invasive procedures are unnecessary until we start assessing soft tissue pain generators such as myofascial trigger points. DJS]

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Decharms RC, Maeda F, Glover GH et al. 2005. Control over brain activation and pain learned by using real-time functional MRI. Proc Natl Acad Sci. U S A 102(51):18626-18631. “These findings show that individuals can gain voluntary control over activation in a specific brain region given appropriate training, that voluntary control over activation in rACC (the rostral anterior cingulate cortex) leads to control over pain perception, and that these effects were powerful enough to impact severe, chronic clinical pain.”

Decker MW, Meyer MD, Sullivan JP. 2001. The therapeutic potential of nicotinic acetylcholine receptor agonists for pain control. Expert Opin Investig Drugs 10(10):1819-1830. “Preclinical findings suggest that nAChR agonists have the potential to be highly efficacious treatments in a variety of pain states.”

Dedert EA, Studts JL, Weissbecker I et al. 2004. Religiosity may help preserve the cortisol rhythm in women with stress-related illness. Int J Psychiatry Med. 34(1):61-77. “...religiosity may have a protective effect on the physiological effects of stress among women with fibromyalgia.”

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Degotardi PJ, Klass ES, Rosenberg BS et al. 2005. Development and evaluation of a cognitive-behavioral intervention for juvenile fibromyalgia. J Pediatr Psychol. [August 24 Epub ahead of print] “Children with fibromyalgia can be taught CBT strategies that help them effectively manage this chronic and disabling musculoskeletal pain disorder.”

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Delaney J.P., Leong K. S., Watkins A. et al. 2002. The short-term effects of myofascial trigger point massage therapy on cardiac autonomic tone in healthy subjects. J Adv Nurs 27(4):364-71. TrP massage to the head, neck and shoulder increased cardiac parasympathetic activity and improved relaxation even in healthy individuals.

de Las Penas CF, Cuadrado ML, Gerwin RD et al. 2005. Referred pain from the trochlear region in tension-type headache: a myofascial trigger point from the superior oblique muscle. Headache 45(6):731-737. This blinded, controlled study indicates that myofascial trigger points in the superior oblique muscle may cause or contribute to typical tension headache pain. [This study confirms the presence of myofascial trigger points in at least one of the extrinsic eye muscles, as per the 2^nd edition of “Fibromyalgia and Chronic Myofascial Pain: A Survival Manual. TrPs in the extrinsic eye muscles may be diagnosed and treated by use of eye exercises in that book.]

DeLeo JA, Tanga FY, Tawfik VL. 2004. Neuroimmune activation and neuroinflammation in chronic pain and opioid tolerance/hyperalgesia. Neuroscientist 10(1):40-52. Modulation of central nervous system glial cells and
proinflammatory cytokines may not only contribute to central sensitization but also decrease the effectiveness of opioids. The role of neuroinflammation and interstitial swelling can be integral parts of central sensitization. “…there is now increasing evidence suggesting that the CNS mounts an organized innate immune response during systemic infection and neuronal injury.” Also interesting is the observation of cellular adhesion molecules in the lumbar spinal cord following peripheral inflammatory stimuli. This may indicate a similar process occurring in the central nervous system similar to the myofascial cellular adhesion in response to mechanical or biochemical trauma.

DeLeo JA, Tanga FY, Tawfik VL. 2004. Neuroimmune activation and neuroinflammation in chronic pain and opioid tolerance/hyperalgesia. Neuroscientist 10(1):40-52. Modulation of central nervous system glial cells and pro-inflammatory cytokines may not only contribute to central sensitization but also decrease the effectiveness of opioids. The role of neuroinflammation and interstitial swelling can be integral parts of central sensitization. "…there is now increasing evidence suggesting that the CNS mounts an organized innate immune response during systemic infection and neuronal injury." Also interesting is the observation of cellular adhesion molecules in the lumbar spinal cord following peripheral inflammatory stimuli. This may indicate a similar process occurring in the central nervous system similar to the myofascial cellular adhesion in response to mechanical or biochemical trauma.

Dellon AL, Shookster LA, Maloney CT Jr et al. 2003. Diagnosis of compressive neuropathies in patients with fibromyalgia. J Hand Surg [Am] 28(6):894-7. This article suggests that the Tinel sign may be a valid tool for identification of arm peripheral nerve compression in fibromyalgia. It neglects to screen patients for myofascial trigger points, which may be the cause of such nerve entrapment.

Delorme T, Boureau F, Eymard B et al. 2004. Clinical study of chronic pain in hereditary myopathies. Eur J Pain 8(1):55-61. This study of 68 consecutive and unselected adult patients at a multidiciplinary consultation for hereditary myopathies found that 46 of them had chronic pain, mostly musculoskeletal. 50% had symptoms of myofascial pain and 26% had symptoms of fibromyalgia. [It would be interesting to study how many of the relatives with hereditary myopathies also had these co-existing conditions. Clinicians must become aware that these illness are frequent companions to other chronic illnesses, and that prompt diagnosis, recognition, and treatment of the individual TrPs and central sensitization may considerably improve the patient=s quality of life. DJS]

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DeMaria Jr. S, Hassett AL, Sigal LH. 2007. N-methyl-D-aspartate receptor-mediated chronic pain: new approaches to fibromyalgia syndrome etiology and therapy. J Musculoskel Pain 15(2):33-39. NMDA receptors are good targets for FMS pharmaceutical chronic pain remediation. NMDA receptor modulation shows more promise than blockade. Dextromethorphan, ifenprodil, memantine and other low-affinity NMDA antagonists show promise.

De Meirleir K., Bisbal C., Campine I., De Becker P., Salehzada T., Demettre, D., Lebleu B. 2000. A 37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome. Am J Med 108(2):99-105. There may be a way to distinguish chronic fatigue syndrome patients from patients with fibromyalgia or depression with a biochemical marker.

DeMeo MT, Mutlu EA, Keshavarzian A et al. 2002. Intestinal permeation and gastrointestinal disease. J Clin Castroenterol. 34(4):385-396. “The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier.” “Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation.” [More information is coming out concerning the relationship between permeable bowel and chronic illness. What can be done to heal the bowel is to remove irritants, replace lost enzymes, reinnoculate healthy organisms with probiotics, and repair the mucosa. Detailed information can be found in the Textbook of Functional Medicine, (see Galland, L. and www.functionalmedicine.org). DJS.]

Demeter P, Vardi VK, Magyar P. 2004. [Study on connection between gastroesophageal reflux disease and obstructive sleep apnea] Orv Hetil. 145(37):1897-1901. [Hungarian] “The study reveals that in patients with severe obstructive sleep apnea, erosive reflux disease is more frequent and a positive correlation can be found between severity of reflux disease and sleep apnea as well.”

Demeter P, Pap A. 2004. The relationship between gastroesophageal reflux disease and obstructive sleep apnea. Gastroenterol 39(9):815-820. Reflux is more likely to occur during sleep. Also, “...the transdiaphragmatic pressure increases in parallel with the growing intrathoracic pressure generated during obstructive apnea episodes.”

Demeter P, Vardi VK, Magyar P. 2004. [Study of connection between gastroesophageal reflux disease and obstructive sleep apnea] Orv Hetil. 145(37):1897-1901. [Hungarian] “The study reveals that in patients with severe obstructive sleep apnea, erosive reflux disease is more frequent and a positive correlation can be found between severity of reflux disease and sleep apnea as well.”

Demitrack, M. A. and L. J. Crofford. 1998. Evidence for and pathophysiologic implications of hypothalamic-pituitary-adrenal axis dysregulation in fibromyalgia and chronic fatigue syndrome. Ann NY Acad Sci 840:(684-697.

De Noronha M, Refshauge KM, Herbert RD et al. 2006. Do voluntary strength, proprioception, range of motion, or postural sway predict occurrence of lateral ankle sprain? Br J Sports Med. 40(10):824-828. “...people with reduced ankle dorsiflexion range may be at increased risk of ankle sprain.” [The reduced ROM is often due to TrPs. DJS]

Deodhar, A. A. , R. A. Fisher, C. V. Blacker and A. D. Woolf. 1994. Fluid retention syndrome and fibromyalgia. Br J Rheumatol 33(6):576-582.

DePedro JA, Perez-Caballer AJ, Dominguez J et al. 2005. Pulsed electromagnetic fields induce peripheral nerve regeneration and endplate enzymatic changes. Bioelectromagnetics 26(1):20-27. This study on the ability of electromagnetic field ability to induce changes in the endplate enzymes may be significant, as that is where the central TrPs occur.

DePedro JA, Perez-Caballer AJ, Dominguez J et al. 2005. Pulsed electromagnetic fields induce peripheral nerve regeneration and endplate enzymatic changes. Bioelectromagnetics 26(1):20-27. This study demonstrated effects of pulsed electromagnetic fields on motor endplates. Since motor endplates are the areas of dysfunction implicated in the formation and perpetuation of myofascial TrPs, this study may suggest some mechanisms involved in the benefits of some types of specific electronic therapies.

DeQuervain, D.J., Roozendaal, B., Nitsch, R.M., McGaugh, J.L., Hock, C. 2000. Acute cortisone administration impairs retrieval of long term declarative memory in humans. Most patients with FMS and other chronic pain syndromes report more stress in their lives. The major endocrine manifestation of stress is increased secretion of cortisol. Could this, in part, be an explanation for so-called "fibro fog" - the impaired memory problems described by many FMS patients? In this study, cortisol had a selective effect of interfering with delayed recall, but not immediate recall or recognition memory. This study is also relevant to the cognitive defects often described by lupus patients who are often treated with intermittently high doses of corticosteroids.

Deroo BJ, Korach KS. 2006. Estrogen receptors and human disease. J Clin Invest. 116(3):561-570. “Estrogens influence many physiological processes in mammals, including but not limited to reproduction, cardiovascular health, bone integrity, cognition, and behavior. Given this widespread role for estrogen in human physiology, it is not surprising that estrogen is also implicated in the development or progression of numerous diseases, which include but are not limited to various types of cancer (breast, ovarian, colorectal, prostate, endometrial), osteoporosis, neurodegenerative diseases, cardiovascular disease, insulin resistance, lupus erythematosus, endometriosis, and obesity. In many of these diseases, estrogen mediates its effects through the estrogen receptor (ER), which serves as the basis for many therapeutic interventions.” Now that we are aware of the 2nd estrogen receptor and its differences, new medications may be specifically tailored to estrogen receptor beta. More tools are being developed for preventative medicine.

Devor M. 2006. Sodium channels and mechanisms of neuropathic pain. J Pain 7 Suppl 1:S3-S12. “Neuropathic pain is a complex outcome of multiple pathophysiological changes that develop in the peripheral nervous system (PNS) and the central nervous system (CNS) following nerve injury or disease. All or most of the CNS changes are thought to be due to abnormal signaling from the PNS, notably electrical hyperexcitability of peripheral sensory neurons. Because hyperexcitability is associated with abnormal sodium channel regulation, this process is a prime target for therapeutic intervention.”

Demco L. 2004. Pain mapping of adhesions. J Am Assoc Gynecol Laparosc. 11(2):181-183. [This is an interesting study. I would like such a study in which the tissue (and surrounding tissue) was also examined for evidence of TrPs. DJS]

DeMeo DL, Zanobetti A, Litonjua AA et al. 2004. Ambient air pollution and oxygen saturation. Am J Respir Crit Care Med. 170(4):383-387. Air pollution can cause reduced oxygen saturation in the body. This study discusses possible mechanisms. [Anything that reduces oxygen availability is a perpetuating factor for both FMS and CMP. DJS]

De Renzi, E., F. Lucchelli, S. Muggia and H. Spinnler. 1995. Persistent retrograde amnesia following a minor trauma. Cortex 31(3):531-542 .

de Ridder, D., M. Depla, P. Severens and M. Malsch. 1997. Beliefs on coping with illness: a consumer’s perspective. Soc Sci Med 44(5):553-9.

Dertwinkel, R., A. Wiebalck, M. Zenz and M. Strumpf. 1996. [Oral opioids for long-term treatment of chronic non-cancer pain]. Anaesthesist 45(6):495-505 [German].

de Sa Pinto AL, de Barros Holanda PM, Radu AS et al. 2006. Musculoskeletal findings in obese children. J Paediatr Child Health 42(6):341-4. “The present data suggest that obesity has a negative impact on osteoarticular health by promoting biomechanical changes in the lumbar spine and lower extremities.” [This research would suggest that other factors that cause biomechanical changes in the lumbar spine and lower extremities, such as muscle contracture due to TrPs, could also contribute to OA. DJS]

Despres JP, Golay A, Sjostrom L et al. 2005. Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia. N Engl J Med. 353(20):2121-2134. [This medication may be a promising one for patients with Metabolic Syndrome. DJS]

Dhein, S., R. Gerwin, U. Ziskoven, M. Schott, A. F. Rump, Y. Zhao, A. Salameh and W. Klaus. 1993. Propranolol unmasks class III like electrophysiological properties of norepinephrine. Naunyn Schmiedebergs Arch Pharmacol 348(6):643-649.

Diaz, J. H. and H. J. Gould 3^rd. 1999. Management of post-thoracotomy pseudoangina and myofascial pain with botulinum toxin. Anesthesiology 91(3):877-9. Diaz: Louisiana State University Medical Center, Multidisciplinary Pain Mastery Center, New Orleans 70112.

Dechene, L. 1993. Chronic fatigue syndrome: influence of histamine, hormones and electrolytes. Med Hypotheses 40(1):55-60.

Denko CW, Malemud CJ. 2004. Serum growth hormone and insulin but not insulin-like growth factor-1 levels are elevated in patients with fibromyalgia syndrome. [Jul 24 Epub ahead of print] “Basal serum GH and fasting serum insulin levels appear to be valuable surrogate markers in clinically active, normoglycemic fibromyalgia patients.” [These may be associated with perpetuating factors of insulin resistance and lack of restorative sleep. DJS]

Dick BD, Rashiq S. 2007. Disruption of attention and working memory traces in individuals with chronic pain. Anesth Analg 104(5):1223-1229. This research indicates that the maintenance of memory trace is affected by chronic pain. Spatial memory was particularly affected. "...pain may disrupt the maintenance of the memory trace that is required to hold information for processing and to later retain it for storage in longer-term memory stores.”

Dickenson AH, Carpenter K, Suzuki R. 1999. Pain relief. IDrugs 2(11):1130-1132. “…excitability blockers acting on sodium and calcium channels, progress in drugs acting at glutamate receptors, cannabinoid receptors, capsaicin analogs, novel opioids acting at receptors other than the mu receptor for morphine, substance P antagonists and cyclooxygenase (COX)-2 inhibitors as being of particular interest.” [Cannabinoids seem to be of increasing interest for the control of chronic pain. DJS]

Dickenson, A. H. 1997. NMDA receptor antagonists: interactions with opioids. Acta Anaesthesiol Scan 41(1 Pt 2):112-115.

Dickman R, Feroze H, Fass R. 2006. Gastroesophageal reflux disease and irritable bowel syndrome: a common overlap syndrome. Curr Gastroenterol Rep 8(4):261-265. GERD patients with IBS are less likely to respond to anti-reflux medications than patients without IBS and also perceive their symptoms to be more severe. [The latter could be due to the central sensitization aspects of IBS. DJS]

Dickstein, J. B., H. Moldofsky, F. A. Lue and J. B. Hay. 1999. Intracerebroventricular injection of TNF-alpha promotes sleep and is recovered in cervical lymph. Am J Physiol 276(4 Pt 2):

Dietz GP, Valbuena PC, Dietz B et al. 2006. Application of a blood-brain-barrier-penetrating form of GDNF in a mouse model for Parkinson’s disease. Brain Res. 1082(1):61-66. [Although this is a rat study, it is an important step in finding a biochemical that can cross the blood-brain barrier and perhaps influence the development of central sensitization. DJS]

Dijk DJ. 2008. Slow-wave sleep, diabetes, and the sympathetic nervous system. Proc Natl Acad Sci U S A. 105(4):1107-1108. Slow wave (delta) sleep has a profound impact on brain regulatory functions, including glucose regulation and the development of insulin resistance. [It is becoming more recognized that preventative medicine must include assurance of restorative sleep. DJS]

DiLorenzo L, Traballesi M, Morelli D et al. 2004. Hemiparetic shoulder pain syndrome treated with deep dry needling during early rehabilitation: a prospective, open-label, randomized investigation. J Musculoskel Pain 12(2):25-34. Deep dry needling was associated with significant reduction of pain during sleep and physiotherapy.

Dimitrova S, Stoilova I, Cholakov I. 2004. Influence of local geomagnetic storms on arterial blood pressure. Bioelectromagnetics 25(6):408-414. “Arterial bp was found to increase with the increase of the GMA level, and systolic and diastolic bp were found to increase significantly from the day before till the second day after the geomagnetic storm. These effects were present irrespective of sex and medication.” [FMS hypersensitivity to stimuli may cause greater sensitivity to geomagnetic effects. DJS.]

Dinerman, H. D. L. Goldenberg and D. T. Felson. 1986. A prospective evaluation of 118 patients with the fibromyalgia syndrome: prevalence of Raynaud’s phenomenon, sicca symptoms, ANA, low complement, and Ig deposition at the dermal-epidermal junction. J Rheumatol 13(2):368-73.

Dinges, D. F., M. T. Orne, W. G. Whitehouse and E. C. Orne. 1987. Temporal placement of a nap for alertness: contributions of circadian phase and prior wakefulness. Sleep 10(4):313-29.

Dirlewanger, M., P. H. Schneiter, N. Paquot, E. Jequier, V. Ray and L. Tappy. 2000. Effects of glucocorticoids on hepatic sensitivity to insulin and glucagon in man. Clin Nutr 19(1):29-34.

Di Stefano, G. and B. P. Radanov. 1995. Course of attention and memory after common whiplash: 82-year prospective study with age, education and gender pair-matched patients. Acta Neurol Scand 91(5):346-352.

Djouhri L, Koutsikou S, Fang X et al. 2006. Spontaneous pain, both neuropathic and inflammatory, is related to frequency of spontaneous firing in intact C-fiber nociceptors. “Spontaneous pain is a poorly understood aspect of human neuropathic pain.” “Some types of spontaneous pain after nerve injury may result from cumulative neuroinflammation.”

Dobkin PL, Sita A, Sewitch MJ. 2006. Predictors of adherence to treatment in women with fibromyalgia. Clin J Pain. 22(3):286-294. “Adherence is influenced by both clinical (patient-physician discordance and pain) and psychological (distress) factors in women with FM. Improvements in these domains may improve adherence in FM.”

Dobkin PL, Abrahamowicz M, Fitzcharles MA et al. 2005. Maintenance of exercise in women with fibromyalgia. Arthritis Rheum. 53(5):724-731. “The maintenance of an exercise program in women with FM appears to be contingent on being able to deal with stress, pain, barriers to exercise, and disability.”

Doggweiler-Wiygul R, 2004. Urological myofascial pain syndromes. Curr Pain Headache Rep 8(6):445-451. It can be difficult to distinguish pain from visceral organs and pain due to myofascial trigger points that refer to the same areas. Visceral pain can also be a perpetuating factor of TrPs, although the TrPs themselves can perpetuate the pain and other symptoms long after the visceral problem is under control.

Doggweiler-Wiygul R., Wiygul J.P. Interstitial cystitis, pelvic pain, and the relationship to myofascial pain and dysfunction: a report on four patients. World J Urol 20(5):310-4. “Referred pain and motor activity to the pelvic floor muscles (sphincters), as well as to the pelvic organs, can be the sole cause of IC, IPP, and irritative voiding dysfunction...”

Dohrenbusch, R., H. Sodhi , J. Lamprecht and E. Genth. 1997. Fibromyalgia as a disorder of perceptual organization? An analysis of acoustic stimulus processing in patients with widespread pain. Z Rheumatol 56(6):334-341.

Dommerholt JD, Bron C, Frannsen J. 2006. Myofascial trigger points: An evidence-informed review. J Man Manip Ther 14(4):203-221. This excellent review includes history, examination procedures, and a good overview of the evidence-based material on MTPs. Although it is written for manual therapists, it is worthy reading for all care providers, including physicians.

Dommerholt, Jan, 2000. Fibromyalgia: time to consider a new taxonomy? Persons with fibromyalgia have altered nociception, hyperalgesia, allodynia, and hypervigilance. The term "fibromyalgia" does not describe the etiology of the syndrome adequately.

Donahue, R. P. , R. J. Prineas, R. DeCarlo Donahue, P. Zimmet, J. A. Bean, M. De Courten, G. Collier, R. B. Goldberg, J. S. Skyler and N. Schneiderman. 1999. Is fasting leptin associated with insulin resistance among nondiabetic individuals? The Miami Community Health Study. Diabetes Care 22(7):1092-6.

Donaldson CCS, Nelson DV, Schulz R. 1998. Disinhibition in the gamma motoneuron circuitry: a neglected mechanism for understanding myofascial pain syndromes? Applied Psycho Biofeedback 23(1):43-57.

Donaldson, C. C. , D. V., Nelson and R. Schulz. 1998. Disinhibition in the gamma motoneuron circuitry: a neglected mechanism for understanding myofascial pain syndromes? Appl Psychophysiol Biofeedback 23(1):43-57.

Donaldson, C.C.S., G. E. Sella and H. H. Mueller. 1998. Fibromyalgia: a retrospective study of 252 consecutive referrals. Can J Clin Med 5(6):1-10.

Donaldson IM. 2000. The functions of the proprioceptors of the eye muscles. Philos Trans R Soc Lond B Sci. 355(1404):1685-1754. “...there are excellent grounds for believing that the receptors in the extraocular muscles are indeed proprioceptors...”

Donnelly JM, Palubinskas L. 2007. Prevalence and inter-rater reliability of trigger points. J Musculoskel Pain 15 (Supp 13):16 item 21. [Myopain 2007 Poster] This research not only confirmed that practitioners skilled in palpation had excellent inter-rater reliability for MTPs, but also found that many healthy college students had taut bands and MTPs. [It would be interesting to follow these students and find out if these latent MTPs caused restricted range of motion, if there were one or more perpetuating factors, and if they activated at a later time. DJS]

Donnelly, J. M. 2002. Physical therapy approach to fibromyalgia with myofascial trigger points: a case report. J Musculoskel Pain 10(1/2)177-190. This report indicates that a well educated and function-oriented patient coupled with a care provider who is well-trained in the recognition of fibromyalgia and myofascial trigger points can work as a team to significantly improve the patient’s quality of life, improving function and decreasing pain level.

Doron Y, Peleg R, Peleg A et al. 2004. The clinical and economic burden of fibromyalgia compared with diabetes mellitus and hypertension among Bedouin women in the Negev. Fam Pract. 21(4):415-419. “Conclusions: FM patients consume health care resources to a similar extent to patients with other chronic diseases such as diabetes mellitus and hypertension, but the latter usually receive much more attention from the health care system. Greater awareness of this disorder can improve management and facilitate planning of health care resources, thus improving quality of care.”

Dorsher PT. 2009. Myofascial referred-pain data provide physiologic evidence of acupuncture meridians. J Pain. [Apr 29 Epub ahead of print]. “This article demonstrates that myofascial referred-pain data provide independent physiologic evidence of acupuncture meridians. The acupuncture tradition provides pain practitioners with millennia of accumulated clinical experience treating pain (and visceral) disorders and offers the potential for novel pain treatment approaches and understanding of pain neurophysiology.”

Dorsher PT. 2007. Subcutaneous trigger point causing radiating post-surgical pain. J Musculoskel Pain 15 (Supp 13):16 item 22. [Myopain 2007 Poster] A visible subcutaneous trigger point overlying the latissimus dorsi muscle was difficult to anesthetize. It produced referred arm and back pain, but range of motion was normal. The pain improved with a mild opioid, Flexeril, physical therapy including massage and exercises. [Subcutaneous trigger points are not well known or documented. Much research is needed on trigger points in nonmyofascial tissues. DJS]

Dreon, D. M., H. A. Fernstrom, P. T. Williams and R. M. Krauss. 1999. A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins. Am J Clin Nutr 69(3):411-8.

Drewes, A. M. , K. D. Kielson, S. J. Taagholt, K. Bjerregard, L. Svendsen and J. Gade. 1995. Sleep intensity in fibromyalgia: focus on the micro-structure of the sleep process. Br J Rheumatol 34(7):629-635.

Dreyer L, Mellemkjaer L, Kendall S et al. 2007. Increased cancer risk in patients referred to hospital with suspected fibromyalgia. J Rheumatol. 34(1):201-206. This study found no association between these two conditions. [Any chronic unrelieved pain, or any other chronic or sufficiently acute central nervous system stimulation, might provoke central sensitization and FMS. DJS]

Duan B, Wu LJ, Yu YQ et al. 2007. Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity. J Neurosci. 27(41):11139-11148. “Specific blockade of Ca2+-permeable ASIC1a channels thus may have antinociceptive effect by reducing or preventing the development of central sensitization induced by inflammation.” [This is another indication of calcium ion channel dysfunction affecting the chronic pain state, and may lead to new avenues of prevention and treatment of same. DJS]

Dubner, R. 1991. Basic mechanisms of pain associated with deep tissues. Can J Physiol Pharmacol 69(5):607-609.

Duclos M, Gatta B, Corcuff JB et al. 2001. Fat distribution in obese women is associated with subtle alterations of the hypothalamic-pituitary-adrenal axis activity and sensitivity to glucocorticoids. Clin Endocrinol 55(4):447-454. [This study shows another connection between HPA axis dysfunction and abdominal obesity. Insulin resistance, abdominal obesity and other pieces of the metabolic syndrome are perpetuating factors of both FMS and myofascial TrPs. DJS]

Dubner, R. and K. M. Hargreaves. 1989. The neurobiology of pain and its modulation. Clin J Pain 5(Suppl 2):S1-S4.

Dubousset J. 2003. [Spinal instrumentation, source of progress, but also revealing pitfalls.] Bull Acad Natl Med 187(3):523-533. [French] Most surgeons do not check their patients presurgically for the presence of biomechanical or soft tissue dysfunctions. Even bone evaluations are rarely done except supine views. Computer simulation may help to remedy this lack, and may reduce needless surgery and minimize failed surgeries.

Dulloo, A. G., C. Duret, D. Rohrer, L. Girardier, N. Mensi, M. Fathi, P. Chantre and J. Vandermander. 1999. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr 70(6):1040-5.

Dummer JS, Dinges DF. 2005. Neurocognitive consequences of sleep deprivation. Semin Neurol. 25(1):117-129. “Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation also results in neurocognitive performance decrements similar to those seen in sleep restriction studies.”

Duncan B, White A, Rahman A. 2007. Acupuncture in the treatment of fibromyalgia in tertiary care – a case series. Acupunct Med. 25(4):137-147. “Acupuncture appears to offer symptomatic improvement to some patients with fibromyalgia in a tertiary clinic who have failed to respond to other treatments. In view of its safety, further acupuncture research is justified in this population.”

Dunnett AJ, Roy D, Stewart A et al. 2007. The diagnosis of fibromyalgia in women may be influenced by menstrual cycle phase. J Bodywork Move Ther. 11, 99-105. “…sensitivity to pressure and pain varies over the course of the menstrual cycle, requiring clinical adjustments in palpation-based diagnostic models and treatment modalities.”

Dunteman, E., M. S. Turner and R. Swarm. 1996. Pseudo--spinal headache. Reg Anesth 21(4):358-360.

DuPont, J. S. Jr. DDS. 1999. Trigger Point Identification and Treatment with Microcurrent. J Craniomandib Pract 17(4):293-296.

Duric V, McCarson KE. 2006. Persistent pain produces stress-like alterations in hippocampal neurogenesis and gene expression. J Pain 7(8):544-555. “Persistent pain induces stress-like damaging modulatory effects in the hippocampus, which is one of the limbic regions involved in the pathophysiology of depression. Targeting these mechanisms (which are potential contributors to the emotional impact of pain) may provide novel therapeutic approaches for relieving depression-like aspects of chronic pain.”

Dutra EH, Maruo H, Vianna-Lara MS. 2006. Electromyographic activity evaluation and comparison of the orbicularis oris (lower fascicle) and mentalis muscles in predominantly nose- or mouth-breathing subjects. Am J Orthod Dentofacial Orthop. 129(6):722.e1-9. [Although TrPs were not specifically mentioned, this study indicated that mouth breathing influences EMG activity of specific muscles, and that could increase the chance of TrP formation. DJS]

Dwight, M. M., L. M. Arnold, H. O’Brien, R. Metzger, E. Morris-Park and P. E. Peck Jr. 1998. An open clinical trial of venlafaxine treatment of fibromyalgia. Psychosomatics 39(1):14-17.

Dykman, K. D., C. Tone, C. Ford and R. A. Dykman. 1998. The effects of nutritional supplements on the symptoms of fibromyalgia and chronic fatigue syndrome. Integr Physiol Behav Sci 33(1):61-71.

Ebener, M. K. 1999. Older adults living with chronic pain: an opportunity for improvement. J Nurs Care Qual 13(4):1-7.

Edwards J. 2005. The importance of postural habits in perpetuating myofascial trigger point pain. Acupunct In Med. 23(2):77-82. This article is a collection of examples indicating how bracing arms or knees, leg crossing and side-leaning, arm crossing, sitting with legs tucked sideways, habitual undesirable sleeping positions, and “...any habitual posture that gives rise to [prolonged contraction of muscle fibres may cause motor endplate dysfunction and the development of an MTrP...” [ The author believes that habitual dysfunctional postures may occur without other perpetuating factors and may be often untreated and correctable perpetuating factors. We both believe that this knowledge would be very empowering to TrP patients and should be part of the educational process. DJS]

Edwards J, Knowles N. 2003. Superficial dry needling and active stretching in the treatment of myofascial pain — a randomized controlled trial. Acupunct Med 21(3):80-86. “SDN followed by active stretching is more effective than stretching alone in deactivating TrPs (reducing their sensitivity to pressure), and more effective than no treatment in reducing subjective pain. Stretching without prior deactivation may increase TrP sensitivity.”

Edwards RR, Bingham CO 3^rd, Bathon J et al. 2006. Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases. Arthritis Rheum. 55(2):325-332. “There appear to be multiple mechanisms by which catastrophizing exerts its harmful effects, from maladaptive influences on the social environment to direct amplification of the central nervous system’s processing of pain.” “Catastrophizing is a critically important variable in understanding the experience of pain in rheumatologic disorders as well as other chronic pain conditions. Pain-related catastrophizing may be an important target for both psychosocial and pharmacologic treatment of pain.”

Eichling PS, Sahni J. 2005. Menopause related sleep disorders. J Clin Sleep Med. 1(3):291-300. “The ‘domino theory’ of sleep disruption leading to insomnia followed by depression has the most scientific support. Estrogen itself may also have an antidepressant as well as a direct sleep effect. Treatment of insomnia in responsive individuals may be a major remaining indication for hormone therapy.” “Due to the general under-recognition of SDB, health care providers should not assume sleep complaints are due to vasomotor related insomnia/depression without considering SDB.” “Sleep complaints are almost universal in FM. There are associated polysomnogram (PSG) findings.” “Treatment of sleep itself seems to improve, if not resolve FM. Menopausal sleep disruption can exacerbate other pre-existing sleep disorders including RLS and circadian disorders.”

Einarson, A. and G. Koren. 1999. Dextromethorphan. Extrapolation of findings from reproductive studies in animals to humans. Can Fam Physician 45:2309-10.

Eisen SA, Kang HK, Murphy FM et al. 2005. Gulf War veterans’ health: medical evaluation of a U.S. cohort. Ann Intern Med. 142(11):881-890. “Gulf War deployment is associated with an increased risk for fibromyalgia, the chronic fatigue syndrome, skin conditions, dyspepsia, and a clinically insignificant decrease in the SF-36 physical component score.”

Eisinger J, Ayavou T, Zakarian H et al. 2007. Fibromyalgia [FMS], Nitric Oxide [NO] and Insulin: Probable links between metabolic changes, inflammation and apoptosis: Taxonomy and description. J Musculoskel Pain 15 (Supp 13):45 item 78. Insulin modulates inflammation [TNF, cytokines], vasodilatation [NO], vasoconstriction [ET], energy metabolism, ROS and aptosis. Its role in FM is probably underestimated.

Eisinger J. 2007. Dysautonomia, fibromyalgia and reflex dystrophy. Arthritis Res Ther. 9(4):105. “Fibromyalgia could be a generalized sympathetic dystrophy since both conditions are activated by trauma and partly linked to sympathetic mechanisms. Yet they differ on several points: hormonal and neurochemical abnormalities are observed in fibromyalgia whereas activation by peripheral trauma and hyperosteolysis are observed in reflex sympathetic dystrophy.”

Eisinger J. 2006. Fibromyalgia: terra incognita. J Musculoskel Pain 14(4):5-9. This perceptive editorial provides charts that may be valuable tools for indicating subsets of FMS, as well as possible treatment options.

Eisinger, J. 2003. [Clinical evaluation of fibromyalgia] Rev Med Interne 24(4):237-42. [French]. The use of blood pressure tensiometetry is a new, easier and alternative way to screen for fibromyalgia.

Eisinger J, Milliat M, Garnier R, Starlanyl D. 2000. [Commentaries sur un questionnaire "fibromyalgie" detaille.] Myalgies 1(3):1-3 insert. [French].

Eisinger J, Starlanyl D, Blotman F, Bueno L et al. 2000. [Protocole d’informations anonyme sure les fibromyalgiques.] Med du Sud-Est 1:9-13. [French].

Eisinger, J. B. 1999. Hypothyroidism treatment: one hormone or two? Myalgies 2(Suppl 2):1-3. [French]

Eisinger, J. 1998. Place du syndrome polymyalgies-hypothryroïdie instable dans le cadre des manifestations musculaires des hypothyroïdiens traités. Lyon Méditerranée Médical - Médecine du Sud-est 34(5,6):4-6.

Eisinger, J. B. 1998. Alcohol, thiamin and fibromyalgia. J Am Col Nutri 17(3):300-303.

Eisinger, J., A. Plantamura and T. Ayavou. 1994. Glycolosis abnormalities in fibromyalgia.. J Am Col Nutri 13(2) 144-148.

Eisinger, J., A. Plantamura, P. A. Marie and T. Ayavou. 1994. Selenium and magnesium status and fibromyalgia. Magnes Res 7(3-4):285-8.

Eken C, Durmaz D, Erol B. 2009. Successful treatment of a persistent renal colic with trigger point injection. Am J Emerg. Med. 27(2):252.e3-4. “We present a case of renal colic successfully treated by trigger point injection that was refractory to 150 microg fentanyl and 5 mg morphine.”

Elert J, Kendall SA, Larsson B et al. 2001. Chronic pain and difficulty in relaxing postural muscles in patients with fibromyalgia and chronic whiplash associated disorders. J Rheumatol 28(6):1361-1368. Some “… groups of patients with chronic pain have increased muscle tension and decreased output during dynamic activity compared to pain-free controls. However, the results indicated there is heterogeneity within groups of patients with the same chronic pain disorder and that not all patients with chronic pain have increased muscle tension.”

Elie, R., E. Ruther, I. Farr, G. Emilien and E. Salinas. 1999. Sleep latency is shortened during 4 weeks of treatment with zaleplon, a novel nonbenzodiazepine hypnotic. Zaleplon Clinical Study Group. J Clin Psychiatry 60(8):536-44.

El Maghraoui A, Tellal S, Achemial L et al. 2006. Bone turnover and hormonal perturbations in patients with fibromyalgia. Clin Exp Rheumatol. 24(4):428-431. “Our study showed that patients with FM had low bone resorption and normal bone formation compared to a control group. This was not related to several hormonal perturbations observed in these patients and may reflect functional impairment as suggested in previous studies.”

Eltiti S, Wallace D, Zougkou K et al. 2006. Development and evaluation of the electromagnetic hypersensitivity questionnaire. Bioelectromagnetics. [Sep 29 Epub ahead of print] The electromagnetic sensitivity questionnaire was developed with eight subscales: neurovegetative, skin, auditory, headache, cardiorespiratory, cold related, locomotor and allergy. This scale provides “...an index of the type and intensity of the symptoms commonly experienced by people believing themselves to be EHS and a screening tool that researchers can use to pre-select the most sensitive individuals...”

Elvin A, Siosteen AK, Nilsson A et al. 2006. Decreased muscle blood flow in fibromyalgia patients during standardized muscle exercise: a contrast media enhanced color doppler study. Eur J Pain 10(2):137-144. “…muscle ischemia can contribute to pain in FM, possibly by maintaining the central nervous changes such as central sensitization/disinhibition. US with contrast can be a new valuable approach to assess muscle perfusion in pain patients during standardized exercise.”

Enestrom, S., A. Bengtsson, and T. Frodin. 1997. Dermal IgG deposits and increase of mast cells in patients with fibromyalgia–relevant findings or epiphenomena? Scand J Rheumatol 26(4):308-313.

Enge, C. C. Jr. 2002. Caring for medically unexplained physical symptoms after toxic environmental exposures: effects of contested causation. Environ Health Perspect 110(Suppl 4):641-7. Contested causation may have serious deletory effects on the patient, and on the patient-care provider relationship.

Engel CC Jr. 2002. Caring for medically unexplained physical symptoms after toxic environmental exposures: effects of contested causation. Environ Health Perspect 110 Suppl 4:641-647. The adversarial experience when outside parties refuse to believe that patients have become ill after toxic exposure may be toxic in itself. Medically unexplained physical symptoms, [or care providers who do not understand the cause or mechanisms of the symptoms DJS] “…may erode patient-provider trust, test the provider’s issues of compensation, reparation and blame. These issues may distract patients and providers from therapeutic goals.”

Eraso RM, Bradford NJ, Fontenot CN et al. 2007. Fibromyalgia syndrome in young children: onset at age 10 years and younger. Clin Exp Rheumatol. 25(4):639-644. “FMS in young children of 10 years old and younger is frequently under-recognized. As compared with the older group, stiffness, subjective joint swelling, abdominal pain, initial presentation on wheelchair and a higher mean count of tender points at diagnosis were significantly more common in the younger age group. However, the type of medications used and outcome were similar in both groups.” [We have to stop believing that FM is an illness that presents predominantly in middle aged women. Men, children of both genders and the elderly can have FM too, and these groups are often undiagnosed or misdiagnosed. DJS]

Erikstrup C, Pedersen LM, Heickendorff L, et al. 2001. Production of hyaluronan and chondroitin sulphate proteoglyucans from human arterial smooth muscle- the effect of glucose, insulin, IGF-I or growth hormone. Eur J Endocrinol 145(2):193-8.Chondroitin sulphate proteoglycan CSPG. Insulin and hGH can influence the accumulation of hyaluronan and CSPG.

Epstein, S. A. , G. Kay, D. Clauw, R. Heaton, D. Kelin, L. Krupp, J. Kuck, V. Leslie, D. Masur, M. Wagner, R. Waid and S. Zisook. 1999. Psychiatric disorders in patients with fibromyalgia. A multicenter investigation. Psychosomatics 40(1):57-63.

Ernberg M, Lundeberg T, Kopp S. 2000. Pain and allodynia/hyperalgesia induced by intramuscular injection of serotonin in patients with fibromyalgia and healthy individuals. Pain 85(1-2):31-39. “5-HT injected into the masseter muscle of healthy female subjects elicits pain and allodynia/hyperalgesia, while no such responses occur in patients with fibromyalgia.”

Ernst, E. 1998. Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review. Br J Sports Med 32(3):212-4.

Escalante, A. and M. Fischbach. 1998. Musculoskeletal manifestations, pain, and quality of life in Persian Gulf War veterans referred for rheumatologic evaluation. J Rheumatol 25(11):2228-35. .

Escalante Pulido, J. M. and M. Alpizar Salazar. 1999. Changes in insulin sensitivity, secretion and glucose effectiveness during menstrual cycle. Arch Med Res 30(1):19-22.

Esenyel M, Caglar N, Aldemir T. 2000. Treatment of myofascial pain. Am J Phys Med Rehabil. 79(1):48-52. “When combined with neck stretching exercises, ultrasound treatment and trigger point injections were found to be equally effective.”

Esenyel M, Walsh K, Walden JG et al. 2003. Kinetics of high-heeled gait. J Am Podiatr Med Assoc. 93(1):27-32. “Reduced effectiveness of the ankle plantar flexors during late stance results in a compensatory enhanced hip flexor “pull-off” that assists in limb advancement during the stance-to-swing transition. Larger muscle moments and increased work occur at the hip and knee, which may predispose long-term wearers of high-heeled shoes to musculoskeletal pain.” [Janet Travell indicated high heeled shoes, and any non-flexible soled shoe, can be perpetuating factors of many TrPs. DJS]

Esposito K, Pontillo A, Giugliano F. et al. 2003. Association of low interleukin-10 levels with the metabolic syndrome in obese women. J Clin Endocrinol Metab 88(3):1055-1058. Circulating levels of the anti-inflammatory cytokine IL-10 are elevated in obese and non-obese women compared with obese women who had metabolic syndrome. [This may be significant in chronic pain states, especially if metabolic syndrome is a perpetuating factor. DJS]

Estivill, E. and V. de la Fuente. 1999. [No title available]. Rev Neurol 28(10):962-3. Ropinirol, treatment of initial phase of Parkinson’s disease. Restless legs syndrome.

Esty, ML. 2006. Reflections on FMS treatment, research and neurotherapy: Cautionary tales. (see Kravitz HM, Esty ML, Karz RS et al. 2006.) J Neurother 10(2/3):63-68.

Ettlin T. 2004. Trigger point injection treatment with the 5-HT3 receptor antagonist tropisetron in patients with late whiplash-associated disorder. First results of a multiple case study. Scand J Rheumatol Suppl (119):49-50. “The study demonstrated more than 50% pain relief for more than two weeks in 52% of the 73 treatment sessions. The duration of effectiveness of the injections showed great intraindividual and interindividual variation.”

Evans, R. W., R. I. Evans and M. J. Sharp. 1994. The physician survey on the post-concussion and whiplash syndromes. Headache 34(5):268-274.

Evengard, B., C. G. Nilsson, G. Lindh, L. Lindquist, P. Eneroth, S. Fredrikson, L. Terenius and K. G. Henriksson. 1998. Chronic fatigue syndrome differs from fibromyalgia. No evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic fatigue syndrome. Pain 78(2):153-5.

Evans, R. W. 1992. Some observations on whiplash injuries. Neurol Clin 10(4):975-997.

Everett CF, Morice AH. 2004. Gastroesophageal reflux and chronic cough. Minerva Gastroenterol Dietol. 50(3):205-213. “Gastroesophageal reflux (GOR) disease is one of the 3 commonest causes of chronic cough. It can be difficult to diagnose as the traditionally recognized symptoms of GOR, such as heartburn an acid regurgitation, are often absent.” [GERD is an important perpetuating factor of myofascial TrPs. Without the typical presenting symptoms, it may be missed. DJS]

Everson, M. P., S. D. Kotler and W. D. Blackburn, Jr. 1999. Stress and immune dysfunction in Gulf War veterans. Ann N Y Acad Sci 876:413-8.

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