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

annotated by Devin J. Starlanyl

 

 

References for Research Purposes

On This Page
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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 18th 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.”

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 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.”

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. 

Arnstein, P. M.  1997.  The neuroplastic phenomenon: a physiologic link between chronic pain and learning.  J Neurosci Nurs 29(3):179-186.

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]

Asa, P. B., Y. Cao and R. F. Garry.  2000.  Antibodies to squalene in Gulf War syndrome. Exp Mol Pathol 68(1):55-64. 

Asaki S, Sekikawa M, Kim YT. 2006.  Sensory innervation of temporomandibular joint disk.  J Orthop Surg. 14(1):3-8.  “Free nerve endings and sensory nerve end organs are present in the disk parenchyma of the human temporomandibular joint and are associated with sensation and proprioception, just as they are in the acetabular labrum, glenoid labrum, triangular fibrocartilage complex, and meniscus.”

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.  

Ashburn, M. A. and P. S. Staats.  1999.  Management of chronic pain.  Lancet 353(9167):1865-9.

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]

 

Asmundson, G. J., P. J. Norton and G. R. Norton.  1999.  Beyond pain: the role of fear and avoidance in chronicity.  Clin Psych Rev 19(1):97-119.  

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.

Assimos, D. G., P. Langenstroer, R. F. Leinbach, N. S. Mandel, J. M. Stern and R. P. Holmes. 1999.  Guaifenesin- and ephedrine-induced stones. J Endourol 13(9):665-7.

Attal, N., L. Brasseur, F. Parker, M. Chauvin and D. Bouhassira.  1998. Effects of gabapentin on the different components of peripheral and central neuropathic pain syndromes: a pilot study. Eur Neurol 40(4):191-200. 

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.   TrPs on the contralateral side of the body exhibited a local twitch response after dry needling TrPs.  The group with active TrPs had motor unit potentials (MUPs) activated in a specific muscle on both sides of the body when the TrP on one side was needled.  This did not happen if the TrP was latent.  [If there are active TrPs on one side of the body, the corresponding muscles should be checked for latent TrPs and if those TrPs are present, they may need to be treated. DJS] 

 

Audette JF, Ryan AH. 2004.  The role of acupuncture in pain management.  Phys Med Rehabil Clin N Am. 15(4):749-772.

 

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.”

Auleciems, L. M.  1995.  Myofascial pain syndrome: a multidisciplinary approach.  Nurs Pract 20(4):18. 

Austin, James H. 1999.  Zen and the Brain.  MIT Press: Cambridge MA.

Auvenshine, R. C.  1997.  Psychoneuroimmunology and its relationship to the differential diagnosis of temporomandibular disorders.  Dent Clin North Am 41(2):279-296.

Auvinet B, Bileckot R, Alix AS et al. 2006.  Gait disorders in patients with fibromyalgia.  Joint Bone Spine. [Mar 15 Epub ahead of print]  “Gait during stable walking was severely altered in the patients.  Walking speed was significantly diminished as a result of reductions in stride length and cycle frequency.  The resulting bradykinesia was the best factor for separating the two groups.  Regularity was affected in the patients; this variable is interesting because it is independent of age and sex in healthy, active adults.  Measuring the variables that characterize relaxed walking provides useful quantitative data in patients with fibromyalgia.”  [Unfortunately, these patients were not evaluated for co-existing myofascial TrPs which are often the cause of gait disturbance. DJS]

Avery, D. H., K. Dahl, M. V. Savage, G. L. Brengelmann, L. H. Larsen, M. A. Kenny, D. N. Eder, M. V. Vitiello and P. N. Prinz.  1997.  Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression.  Biol Psychiatry 41(11): 1109-1123.

Azad SC, Huge V, Schops P et al. 2005.  [Endogenous cannabinoid system.  Effect on neuronal plasticity and pain memory] Schmerz 19(6):521-527. [German]  “The endogenous cannabinoid system is involved in the control of neuroplasticity as part of pain processing.  Cannabinoids prevent the formation of LTP (long-term potentiation) in the amygdala via activation of CBI receptors.”

Azuma, J., T. Kishi, R. H. Williams and K. Folkers. 1976.  Apparent deficiency of Vitamin B6 in typical individuals who commonly serve as normal controls. Res Commun Chem Pathol Pharmacol 14(2):343-66

Babu AS, Mathew E, Danda D et al. 2007.  Management of patients with fibromyalgia using biofeedback: a randomized control trial.  Indian J Med Sci. 61(8):455-461.  “Biofeedback as a treatment modality reduces pain in patients with FMS, along with improvements in FIQ (fibromyalgia impact questionnaire), SMWT (six-minute walk test) and the number of tender points.”

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.

Bachmann, G. A. 1999.  Vasomotor flushes in menopausal women.  Am J Obstet Gynecol 180(3):312-6.

Baconnier, S., S. B. Lang, M. Polomska et al. Calcite microcrystals in the pineal gland of the human brain: First physical and chemical studies. Bioelectromagnetics 23(7):488-495. A new form of crystallization that is separate and different from the hydroxyapatite concretions often described has been found in the pineal gland. This calcium, carbon and oxygen crystallization may have piezoelectric properties. Tests are in progress to determine function and formation of these crystals. 

Bagge, E., B. A. Bengtsson, L. Carlsson and J. Carlsson. 1998. Low growth hormone secretion in patients with fibromyalgia-a preliminary report on 10 patients and 10 controls. J Rheumatol 25(1):145-148.

Bagis S., Tamer L., Sahin G. et al. 2003.  Free radicals and antioxidants in primary fibromyalgia: an oxidative stress disorder?  Rheumatol Int. [Epub Dec 20 ahead of print].  This study indicates that free radical levels may cause FMS.

Baik, H. W. and R. M. Russell.  1999.  Vitamin B12 deficiency in the elderly.  Annu Rev Nutr 19:357-77.  

Bajaj P, Bajaj P, Madsen H et al. 2003.  Endometriosis is associated with central sensitization: a psychophysical controlled study.  J Pain 4(7):372-380.

Baker, B. A.  1986.  The muscle trigger: evidence of overload injury.  J Neuro Ortho Med Surg 7(1):35-44.  ISSN 0271-1575/86-0701.

Baker K, Barkhuizen A. 2006.  Pharmacologic treatment of fibromyalgia.  Curr Psychiatry Rep. 8(6):464-469.  “Fibromyalgia is a syndrome of widespread pain, non-restorative sleep, disturbed mood, and fatigue.  Optimal treatment involves a multidisciplinary approach with a team of health care providers using pharmacologic and nonpharmacologic treatment.  Because of the heterogeneity of the illness, management should be individualized for the patient.  Pharmacologic treatment should address issues of pain control, sleep disturbance, fatigue and any underlying coexisting mood disorder.  Nonpharmacologic treatment should include patient education, a regular exercise and stretching program, and cognitive behavioral therapy.  All of these are essential to improving functional capacity and quality of life.  This review provides general guidelines in initiating a successful pharmacologic treatment program for patients with fibromyalgia.”

Bakker, S. J., J. C. ter Maaten, C. Popp-Snijders, R. J. Heine and R. O. Gans. 1999.  Triiodo-thyronine:   a link between the insulin resistance syndrome and blood pressure?  J Hypertens 17(12 Pt 1):1725-30.

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.”

Baldweg, S. E., A. Golay, A. Natali, B. Balkau, S. Del Prato and S. W. Coppack.  2000.  Insulin resistance, lipid and fatty acid concentrations in 867 healthy Europeans.  Eur J Clin Invest 30(1):45-52.

Baldwin, C. M., I. R. Bell and M. K. O’Rourke.  1999.  Odor sensitivity and respiratory complaint profiles in a community-based sample of asthma, hay fever, and chemical odor intolerance.  Toxicol Ind Health 15(3-4):403-9.

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.

Banahan, B. F. 3rd and E. M. Kolassa.  1997. A physician survey on generic drugs and substitution of critical dose medications.  Arch Intern Med 157(18):2080-2088.

Bani, D., L. Ballati, E. Masini, M. Bigazzi and T. B. Sacchi.  1997.  Relaxin counteracts asthma-like reaction indused by inhaled antigen in sensitized guinea pigs.  Endocrinology 138(5): 1909-1915.

Bani, D. 1997. Relaxin: a pleiotropic hormone. Gen Pharmacol 28(1):13-22.

Banic B, Petersen-Felix S, Andersen OK et al. 2004.  Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia.  Pain 107(1-2):7-15.  This study gives evidence for spinal cord hyperexcitability with hyperalgesia and allodynia in fibromyalgia patients and in post-whiplash patients with chronic pain, in spite of the absence of tissue damage.

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.”

Bannwarth, B.  1999.  Risk-benefit assessment of opioids in chronic noncancer pain.  Drug Saf 21(4):283-96.

Banovac, K., K. Renfree, A. L. Makowski, L. L. Latta and R. D. Altman.  1995. Fracture healing and mast cells.  J Orthop Trauma 9(6):482-90. 

Baran, H., K. Jellinger and L. Deecke.  1999.  Kynurenine metabolism in Alzheimer’s disease. J Neural Transm 106(2):165-81.  Blockade of NMDA receptors by KYNA may be responsible for impaired memory, learning and cognition in AD patients.

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.”

 

Baraniuk JN, Petrie KN, Le U et al. 2004.  Neuropathology in Rhinosinusitis. Am J Respir Crit Care Med [Epub]

Baraniuk, J. N. , D. Clauw, A. Yuta, M. Ali, E. Gaumond, N. Upadhyayula, K. Fujita and T. Shimizu. 1998.  Nasal secretion analysis in allergic rhinitis, cystic fibrosis, and nonallergic fibromyalgia/chronic fatigue syndrome subjects. Am J Rhinol 12(6):435-40.

Barbara G, Stanghellini V, DeGiorgio R et al. 2004.  Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.  Gastroenterology 126(3):693-702.  The pain of IBS may be in part provoked by release of mast cells in the colon.

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]

 

Barkhuizen A. 2002.  Rational and targeted pharmacologic treatment of fibromyalgia.  Rheum Dis Clin North Am 28(2):261-90. "Pharmacologic agents remain an important component of FM management.  Addressing the main symptoms of pain, disturbed sleep, mood disturbances, fatigue, and associated conditions is essential to improve patient functioning and enhanced quality of life."

Barnes, J. 1996. Myofascial release for craniomandibular pain and dysfunction.  Int J Orofascial Myology 22:20-22.

Barnes, J. 1990. Myofascial Release. MFR Seminars, 10 S. Leopard Road, Suite One, Paoli, PA. 19301.

Barton, A., B. Pal, P. J. Whorwell and D. Marshall.  1999.  Increased prevalence of sicca complex and fibromyalgia in patients with irritable bowel syndrome. Am J Gastroenterol 94(7):1898-901.

Barzilai, N., L. She, B. Q. Liu, P. Vuguin, P. Cohen, J. Wang and L. Rossetti.  1999.  Surgical removal of visceral fat reverses hepatic insulin resistance.  Diabetes 48(1):94-8.  

Barzilai, N., J. Wang, D. Massilon, P. Vuguin, M. Hawkins and L. Rossetti. 1997. Leptin selectively decreases visceral adiposity and enhances insulin action. J Clin Invest 100(12):3105-3110. 

Batterman S.D., Batterman S.C. 2002. Delta-V, spinal trauma, and the myth of the minimal damage accident.  J Whiplash and Rel Dis 1(1):41-52.

Bassoe, C. F. 1995.  The skinache syndrome.  J R Soc Med 88:565-569.

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.”

Beal, M. W.  1998. Women’s use of complementary and alternative therapies in reproductive health care.  J Nurse Midwifery 43(3):224-34.

Beard, J. L., M. J. Borel and J. Derr.  1990.  Impaired thermoregulation and thyroid function in iron-deficiency anemia.  Am J Clin Nutr 52(5):813-9.

Becker, N., A. B. Thomsen, A. K. Olsen, P. Sjogren, P. Bech and J. Erikson.  1998. [No title available]. Ugeskr Laeger 160(47):6816-9. [Danish].  

Becker, N., A. Bondegaard Thomsen, A. K. Olsen, P. Sjogren, P. Bech and J. Erikson.  1997. Pain epidemiology and health related quality of life in chronic non-malignant pain patients referred to as Danish multidisciplinary pain center.  Pain 73(3):393-400.

Becker, N., P. Sjogren, P. Bech, A. K. Olsen and J. Eriksen.  2000.  Treatment outcome of chronic non-malignant pain patients managed in a Danish multidisciplinary pain center compared to general practice: a randomized controlled trial.  Pain 84(2):203-11.  

Bell IR, Lewis DA 2nd, Lewis SE et al. 2004.  EEG alpha sensitization in individualized homeopathic treatment of fibromyalgia.  Int J Neurosci. 114(9):1195-1220.  

 

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.”

Bell, I. R., C. M. Baldwin, M. Fernandez and G. E. Schwartz.  1999.  Neural sensitization model for multiple chemical sensitivity: overview of theory and empirical evidence.  Toxicol Ind Health 15(3-4):295-304.

Bell, I. R., M. J. Szarek, D. R. Dicenso, C. M. Baldwin, G. E. Schwartz and R. R. Bootzin.  1999. Patterns of waking EEG spectral power in chemically intolerant individuals during repeated chemical exposures.  Int J Neurosci 97(1):41-59.

Bell, I. R., C. M. Baldwin and G. E. Schwartz.  1998.  Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia.  Am J Med 105(3A):74S-82S. 

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. 

Bellamy N, Sothern RB, Campbell J. 2004.  Aspects of diurnal rhythmicity in pain, stiffness, and fatigue in patients with fibromyalgia.  J Rheumatol 31(2):379-89.  This study indicates that there are indications that pain, stiffness and fatigue show daily and possibly weekly patterns.  The awareness of these patterns can be useful for scheduling activities, measurement in clinical trials, and perhaps timing administration of medications for when they are most needed.

Bellastella, A., G. Pisano, S. Iorio, D. Pasquali, F. Orio, T. Venditto and A. A. Sinisi.  1998. Endocrine secretions under abnormal light-dark cycles and in the blind.  Horm Res 49(3-4):153-7. 

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. Investigati