Larson, B., Bjork, J., Henriksson, K.J., Gerdle, B., Lindman, R. 2000. The prevalence of cytochrome oxidase negative and super-positive fibers and ragged red fibers in the trapezius muscle of female cleaners with and without myalgia and/or female healthy controls. Peripheral pain input from injuries, inflammation, or chronic work-related myalgia are probable sources of persistent nociceptive impulses could lead to a central sensitization.  Furthermore, once central sensitization develops, peripheral pain generators, such as myofascial trigger points, may lead to perpetuation and aggravation of central sensitization.

Laske C, Stransky E, Eschweiler GW et al. 2006.  Increased BDNF serum concentration in fibromyalgia with or without depression or antidepressants.  J Psychiatr Res.  [Apr 3 Epub ahead of print]   “Fibromyalgia (FM) is still often viewed as a psychosomatic disorder.  However, the increased pain sensitivity to stimuli in FM patients is not an ‘imagined’ histrionic phenomena.  Pain, which is consistently felt in the musculature, is related to specific abnormalities in the CNS pain matrix.  Brain-derived neurotrophic factor (BDNF) is an endogenous protein involved in neuronal survival and synaptic plasticity of the central and peripheral nervous system (CNS and PNS).  Several lines of evidence converged to indicate that BDNF also participates in structural and functional plasticity of nociceptive pathways in the CNS and within the dorsal root ganglia and spinal cord.  In the latter, release of BDNF appears to modulate or even mediate nociceptive sensory inputs and pain hypersensitivity.  We were interested if BDNF serum concentration may be altered in FM.”  “The results from our study indicate that BDNF may be involved in the pathophysiology of pain in FM.  Nevertheless, how BDNF increases susceptibility to pain is still not known.”

Ljoranson, D., Ryan, K.M., Gilson, A.M., Dahl, J.L. 2000. Trends in medical use and abuse of opioid analgesics. Between 1990-1996 the use of all agents, with the exception of meperidine, increased from between 19% and 59%.  Drug abuse due to opioids and narcotics increased by only 6.6%.  As a proportion of all drug abuse, narcotic abuse decreased by 2% in the same period.  Specifically, abuse of meperidine decreased by 39%, oxycodeine by 29%, fentanyl by 59%, and hydromorphine by 15%.  There was a 3% increase in drug abuse related to morphine.

Lowe, J.C., Honeyman-Lowe, G. 1999. Ultrasound treatment of trigger points: differences in technique for myofascial pain syndrome and fibromyalgia patients.  This is a report of clinical experience described in terms of an experimental approach without presentation of hard data. The details of treatment depend strongly on what the patient feels.  The caveat that FMS patients are prone to be hyperreactive to ultrasound therapy and need to be treated less vigorously is consistent with their strong reaction to other treatments and life experiences.  It takes much more skill and gentleness to successfully treat MTrPs of FMS patients than uncomplicated MTrPs.

Magaldi M, Moltoni L, Biasi G, Marcolongo R. 2000. Role of intracellular calcium ions in the physiopathology of fibromyalgia syndrome. Boll Soc Ital Biol Sper (1-2:)1-4. "In fibromyalgia patients the intracellular calcium concentration is significantly reduced in comparison to that of healthy controls: the reduced intracellular calcium concentration seems to be a peculiar characteristic of fibromyalgia patients and may be potentially responsible for muscular hypertonus."

Maquet D, Croisier JL, Renard C, Crielaard JM. 2002. Muscle performance in patients with fibromyalgia. Joint Bone Spine 69(3):293-9. "This study of the three pathways supplying energy to muscle confirms that muscle function is globally impaired in FMS patients.  The results suggest that the impairment predominated on aerobic processes."

Martinez-Lavin, M. 2002. The autonomic nervous system, and fibromyalgia. J Musculoskel Pain 10(1/2):221-228.  Fibromyalgia is a multisystem illness. Many researchers have found indications that fibromyalgia is a form of autonomic nervous system dysfunction. 

Martinez-Lavin, M. 2002. Management of dysautonomia in fibromyalgia. Rheum Dis Clin North Am 28(2):379-87. "The realization of dysautonomia in FM has opened the possibility for new and different therapeutic interventions.  Much more research is needed to better define the role of ANS in the pathogenesis of FM.  If this research supports current hypotheses, therapeutic trials with disciplines and substances intended to correct autonomic dysfunction will be indicated."

Meyer HP. 2002.  Myofascial pain syndrome and its suggested role in the pathogenesis and treatment of fibromyalgia syndrome. Curr Pain Headache Rep 6(4):274-83. Failure on the part of care providers to recognize myofascial pain from trigger points often leads to costly and unnecessary tests and  procedures. This failure to diagnose can result in harm to the patients.

Moldofsky H. 2007.  The assessment and significance of the sleep/waking brain in patients with chronic widespread musculoskeletal pain and fatigue syndromes.  J Musculoskel Pain 15 (Supp 13):4 item 5.  [Myopain 2007 Poster]  “Psychophysiological studies demonstrate that total, partial and rapid eye movement [REM] sleep deprivations decrease pain threshold.  Pain stimuli disturb sleep, and non-painful stimuli [e.g. noise] that disrupt sleep [e.g. slow wave sleep] cause unrefreshing sleep, myalgia and fatigue.”  “In clinical studies of FMS and chronic fatigue syndrome, unrefreshing sleep is associated with frequent periodic electroencephalogram arousals from sleep, i.e. the cyclical alternating pattern, sleep apneas, and periodic limb movements.”  “Preliminary studies of novel treatments that aim to facilitate restorative sleep suggest a rationale for better management of FMS and related illnesses.”  [This information indicates that many sleep dysfunctions are interactive with FM and other disorders.]

Moldofsky, H. 2002. Management of sleep disorders in fibromyalgia.  Rheum Dis Clin North Am 28(2):353-65. "In summary, the treatment of patients with FM requires a proper assessment of the reason for the unrefreshing sleep, which is an important component of the FM syndrome."

Mueller HH, Donaldson CC, Nelson DV, Layman M. 2001.  Treatment of fibromyalgia incorporating EEG-Driven stimulation: A clinical outcomes study.  J Clin Psychol 57(7):933-52. "Electroencephalograph (EEG)-driven stimulation or EDS. Patients were initially treated with EDS until they reported noticeable improvements in mental clarity, mood, and sleep.  Self-reported pain, then, having changed from vaguely diffuse to more specifically localized, was treated with very modest amounts of physically oriented therapies."

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Muller W, Fiebich BL, Stratz T. 2006.  New treatment options using 5-HT3 receptor antagonists in rheumatic diseases.  Curr Top Med Chem. 6(18):2035-2042.  “Clinical trials have provided evidence of pain reduction in a subgroup of fibromyalgia syndrome and, moreover, have demonstrated that tropisetron injected locally for insertion tendinoses and myofascial syndromes with associated trigger points leads to an alleviation of pain that is comparable to injections with the combination of corticosteroids and local anesthetics.”

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Muller-Ehrenberg H, Thorwesten L. 2007.  Frequency and importance of trigger points in the case of sports-related shoulder pain.  J Musculoskel Pain 15 (Supp 13):33 item 55.  [Myopain 2007 Poster]  “Trigger points [TrPs] can often be diagnosed when patients complain about sports-related shoulder pain, and they contribute considerably to the symptoms.  Including the examination for TrP will therefore broaden the understanding of the cause of shoulder pain.”

Muller-Ehrenberg H, Thorwesten L. 2007.  Improvement of sports-related shoulder pain after treatment of trigger points using focused extracorporeal shock wave therapy regarding static and dynamic force development, pain relief and sensomotoric performance.  J Musculoskel Pain 15 (Supp 13):33 item 56.  [Myopain 2007 Poster]  “The treatment of trigger points using focused ESWT (extracorporeal shock wave therapy) significantly improves the pain symptoms as well as the performance of athletes suffering from acute or chronic shoulder pain.”  This study used piezoelectric shock waves, with significant reduction in pain and return to healthier movement.

Muls, E and G Vansant. 1999.  Clinical approaches to healthier diet modifications.  Acta Cardiol 54(3):159-61.

Munguia-Izquierdo D, Legaz-Arrese A. 2007. Exercise in warm water decreases pain and improves cognitive function in middle-aged women with fibromyalgia.  Clin Exp Rheumatol. 25(6):823-830.  “An exercise therapy three times per week for 16 weeks in a warm-water pool is an adequate treatment to decrease the pain and severity of FM well as to improve cognitive function in previously unfit women with FM and heightened painful symptomatology.”

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Myers T. 2007. Treatment approaches for three shoulder “tethers.”   J Bodywork Movement Ther 1(11):3-8.  This excellent article offers an in depth look at three common “sticking points” in the shoulder complex (subclavious, pectoralis minor, and teres minor) and how to treat them.

Nabekura T, Morishima S, Cover T.L. et al. 2003.  Recovery from lactacidosis-induced glial cell swelling with aid of exogenous anion channels.  Glia 41(3):247-59. Cerebral edema associated with lactacidosis or head trauma may be associated with swelling in astrocytes, and may be treated by introducing anion channel activity. [This may be relevant to some of the cerebral swelling and cognitive dysfunction noted in fibromyalgia. DJS]

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Naschitz JE, Rozenbaum M, Fields MC et al. 2005.  Cardiovascular reactivity in fibromyalgia: evidence for pathogenic heterogeneity.  J Rheumatol. 32(2):335-339.  “Patients with FM represent a heterogenous group with respect to their pattern of cardiovascular reactivity.”

Naschitz JE, Rosner I, Rozenbaum M et al. 2003.  The head-up tilt test with haemodynamic instability score in diagnosing chronic fatigue syndrome.  QJM 96(2):133-142.  The particular dysautonomia in CFS is different from that occurring in fibromyalgia and other illnesses, and this difference can be measured with objective testing.

Naschitz JE, Rozenbaum M, Rosner I, Sabo E, Priselac RM, Shaviv N, Ahdoot A, Ahdoot M, Gaitini L, Eldar S, Yeshurun D. 2001. Cardiovascular response to upright tilt in fibromyalgia differs from that in chronic fatigue syndrome.  J Rheumatol 28(6):1356-60.

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Niddam DM, Chan RC, Lee SH et al. 2007.  Central modulation of pain evoked from myofascial trigger point.  Clin J Pain. 23(5):440-448.  “Low-intensity low-frequency electrostimulation delivered within a myofascial trigger point (MTP) has been used as intervention to deactivate MTPs.”  “The applied intervention most likely involves supraspinal pain control mechanisms related to both antinociception and regulation of pain affect.”

Niddim DM, Chan Rc, Lee SH et al. 2008.  Central representation of hyperalgesia from myofascial trigger point.  NeuroImage. 39:1299-1306.  Using functional MRI, imaging regions that are dysfunctional in FM patients, researchers used a needle electrode or pressure to stimulate MTPs.  Both stimulations produced a higher pain response than normal controls, with “significantly enhanced somatosensory activity (SI, SII, inferior pareital, mid insula) and limbic (anterior insula) activity and suppressed right dorsal hippocampal activity in patients compared with controls.”  The results show that the hyperalgesic state in MTP patients is associated with abnormal brain activity in the areas that process stimulus activity and negative affect.  [This study indicates that MTPs may contribute significantly to central sensitization. DJS]

Nielsen LA, Henriksson KG. 2007.  Pathophysiological mechanisms in chronic musculoskeletal pain (fibromyalgia): the role of central and peripheral sensitization and pain disinhibition.  Best Pract Res Clin Rheumatol. 21(3):465-480.  “In FMS there is strong scientific support for the statement that the biological part of the syndrome is a longstanding or permanent change in the function of the nociceptive nervous system that can be equated with a disease.”  “FMS may be the far end of a continuum that starts with chronic localized/regional musculoskeletal pain and ends with widespread chronic disabling pain.”

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Nilsen KB, Sand T, Westgaard RH et al. 2007.  Autonomic activation and pain in response to low-grade mental stress in fibromyalgia and shoulder/neck pain patients.  Eur J Pain. [Jan 13 Epub ahead of print]  [This study might have yielded more information if the subjects had been checked for co-existing shoulder and neck myofascial trigger points. DJS]

Nilsen KB, Westgaard RH, Stovner LJ et al. 2005.  Pain induced by low-grade stress in patients with fibromyalgia and chronic shoulder/neck pain, relation to surface electromyography. Eur J Pain [Nov 18 Epub ahead of print].  “Muscular activity did not explain the pain which developed during the stressful task for either group. Pain lasted longer during recovery in both FMS and SNP (shoulder/neck pain) patients compared to healthy controls, possibly a result of disease-related sensitization in pain pathways."  [These patients were not screened for co-existing myofascial pain. DJS]

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Partanen JV, Ojala TA, Arokoski JP. 2009.  Myofascial syndrome and pain: a neurophysiological approach.  Pathophysiology. [Jun 3 Epub ahead of print].  This study indicates that TrPs are related to muscle spindles in the taut bands.

Partonen, T. 1999.  Melatonin-dependent infertility.  Med Hypotheses 52(3):269-70.

Pascarelli, E. F. and J. J. Kella. 1993.  Soft-tissue injuries related to the use of the computer keyboard.  A clinical study of 53 severely injured persons.  J Occup Med 35(5):522-532.

Pasquini, J. M. and A. M. Adamo. 1994. Thyroid hormones and the central nervous system.Dev Neurosci 16(1-2):1-8.

Passard A, Attal N, Benadhira R et al. 2007.  Effects of unilateral repetitive transcranial magnetic stimulation of the motor cortex on chronic widespread pain in fibromyalgia.  Brain. 130(Pt 10):2661-2670.  “…unilateral rTMS of the motor cortex induces a long-lasting decrease in chronic widespread pain and may therefore constitute an effective alternative analgesic treatment for fibromyalgia.”

Patkar AA, Masand PS, Krulewicz S et al. 2007.  A randomized, controlled trial of controlled release paroxetine in fibromyalgia.  Am J Med. 120(5):448-454.  “Paroxetine controlled release appears to be well-tolerated and improves the overall symptomatology in patients with fibromyalgia without current mood or anxiety disorders.  However, its effect on pain measures seems to be less robust.”

Patucchi, E, Fatati G, Puxeddu A. et al. 2003.  [Prevalence of fibromyalgia in diabetes mellitus and obesity.]  Recenti Prog Med 94(4):163-5.  [Italian] This study indicates that the association between obesity, diabetes mellitus and fibromyalgia is a significant one.  [Perhaps as common perpetuating factors for FMS? DJS]

Paulson, M., A. Norberg, E. Danielson. 2002. Men living with fibromyalgia-type pain: experiences as patients in the Swedish health care system. J Adv Nurs 40(1):87-95. Men with chronic diffuse pain waited a long time to be referred to a specialty clinic.  If the staff was interested and well-trained, the men experienced well-being in spite of the recognition that there was no cure. Lack of respect from the staff caused the patients to feel neglected, even if they had otherwise adequate care.

Payne RJ, Kost KM, Frenkiel S, et al. 2006.  Otolaryngeal inflammation assessed using the reflux finding score in obstructive sleep apnea. 134(5):836-842.  Laryngeal inflammation is prevalent among OSA patients and correlates with laryngeal sensory dysfunction, attenuation of the LAR (laryngeal adductor reflex), and apnea severity.  [GERD may activate laryngeal TrPs. DJS]

Pedretti, Lorraine Williams, ed. April 1996. Occupational Therapy: Practice Skills for PhysicalDisfunction. Mosby-Year Book. Chap. 21. Pope-Davis, S. A.

Pellegrino, M. J., G. W. Waylonis and A. Sommer. 1989. Familial occurrence of primaryfibromyalgia. Arch Phys Med Rehabil 70(1):61-63.

Pellegrino, M. J., D. Van Fossen, C. Gordon, J. M. Ryan and G.W. Waylonis. 1989.

Pennacchio, E. A., J. Borg-Stein and D. A. Keith. 1998. The incidence of pain in the muscles of mastication in patients with fibromyalgia. J Mass Dent Soc 47(3):8-12.

Peres M, Zukerman E, Senne Soares et al. 2004. Cerebrospinal fluid glutamate levels in chronic migraine.  Cephalalgia 24(9):735-739.  This study indicates that patients with both FMS and migraines may have a more severe central sensitization process than patients with FMS who do not have migraines.  The headache intensity of the chronic migraine patients correlated with cerebrospinal glutamate levels.

Perneger, T. V., P. K. Whelton and M. J. Klag. Risk of kidney failure associated with the use ofacetominophen, aspirin, and nonsteroidal anti-inflammatory drugs. N Engl J Med 331(25):1675-9.

Perry, F., P. H. Heller, J. Kamiya and J. D. Levine. 1989. Altered autonomic function in patients with arthritis or with chronic myofascial pain. Pain 39(1):77-84.

Persinger, M. A., S. G. Tiller and S. A. Koren. 1999. Background sound pressure fluctuations(5DB) from overhead ventilation systems increase subjective fatigue of university students during three-hour lectures. Percept Mot Skills 88(2):451-6.

Pert, C. B., H. E. Dreher and M. R. Ruff. 1998. The psychosomatic network: foundations of mind-body medicine. Altern Ther Health Med 4(4):30-41.

Peters A, Schweiger U, Fruhwald-Schultes B et al. 2002.  The neuroendocrine control of glucose allocation.  Exp Clin Endocrinol Diabetes 110(5):199-211.  “The concept of glucose allocation presented here challenges the common opinion of ‘blood glucose’ being the main parameter controlled.  The concept of glucose allocation would predict that weight gain — with abundance of glucose in muscle and fat — increases feedback to the brain (via hyperleptinemia) which in turn results in HPA-axis and SNS overdrive, impaired insulin secretion, and insulin resistance.  HPA-axis overdrive would account for metabolic abnormalities such as central adiposity, hyperglycemia, dyslipidemia, and hypertension that are well known clinical aspects of the metabolic syndrome.  This novel viewpoint of ‘brain glucose’ control may shed new light on the pathogenesis of the metabolic syndrome and type 2 diabetes.”

Petzke F, Harris RE, Williams DA et al. 2005.  Differences in unpleasantness induced by experimental pressure pain between patients with fibromyalgia and healthy controls.  Eur J Pain 9(3):325-335.  “Patients with FM unexpectedly display less relative unpleasantness than healthy controls in response to random noxious pressure stimuli.  These results are consistent with the concept that chronic pain may reduce the relative unpleasantness of evoked pain sensations.”  Sensitivity to pain and pain tolerance are different.  Patients may have hyperalgesia, a heightened sensitivity toward pain, but still have a greater tolerance to pain.  This difference has not been specified in most previous research.

Peyron, R., L. Garcia-Larrea, M. C. Gregoire, N. Costes, P. Convers, F. Lavenne, F. Mauguiere, D. Michel and B. Laurent. 1999. Haemodynamic brain responses to acute pain in humans:sensory and attentional networks. Brain 122(Pt 9):1765-1780. .

Pezet, S. B. Ont niente, G. Grannec and B. Calvino. 1999. Chronic pain is associated with increased TrkA immunoreactivity in spinoreticular neurons. J Neurosci 19(13):5482-92.

Phillips, S.M. and B.B. Sherwin. 1992. Effects of estrogen on memory function in surgically menopausal women. Psychoneuroendocrinology 17(5):485-95.

Phillips, S. M. and B. B. Sherwin. 1992. Variations in memory function and sex steroid hormones across the menstrual cycle. Psychoneuroendocrinology 17(5):497-506.

Pimentel M, Park S, Mirocha J et al. 2006.  The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial.  Ann Intern Med. 145(8):557-563.  “Rifaximin [Xifaxan] improves IBS symptoms for up to 10 weeks after the discontinuation of therapy.”

Pioro-Boisset, M., J. M. Esdaile and M. A. Fitzcharles. 1996. Alternative medicine use in fibromyalgia syndrome. Arth Care Res 9(1):13-17.

Piotrowski, C. 1997. Hypoglycemia as a mitigating factor in vehicular accidents. Perceptual Motor Skills 84(3 pt 2):1241-1242.

Pipereit K, Bock O, Vercher JL. 2006.  The contribution of proprioceptive feedback to sensorimotor adaptation.  Exp Brain Res. [Mar 10 Epub ahead of print]  “Intact proprioception is needed for mechanical but not for visual adaptation, which implies that the underlying mechanisms are at least partly distinct.”

Pittman, D. M. and M. J. Belgrade. 1997. Complex regional pain syndrome. Am Fam Physician56(9):2265-70, 2275-6.

Pizzigallo, E., D. Racciatti and J. Vecchiet.1999. Clinical and path of physiological aspects of chronic fatigue syndrome. J Musculoskel Pain 7(1-2):217-224.

Ploghaus, A., I. Tracey, J. S. Gati, S. Clare, R. S. Menon, P. M. Matthews and J. N. Rawlings.1999. Dissociating pain from its anticipation in the human brain. Science 284(5422):1979-81.

Plotnikoff GA. 2003.  Food as medicine – cost-effective health care?  The example of omega-3 fatty acids.  Minn Med 86(11):41-5.  This very interesting article notes that the US spends over half of the amount of money spent on pharmaceuticals in the world, yet our health care is not the best in many areas.  It proposes that it is in the best interest to look first at non-pharmaceutical methods to promote health, such as healthy food. 

Plotnikoff GA, Quigley JM. 2003.  Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain.  Mayo Clin Proc 78(12):1463-1470.  This study showed that vitamin D deficiency was present in 93% of consecutive patients with nonspecific muscle pain, no matter the season.

Plotsky, O. M. 1998. Stress system plasticity: neural adaptations to neonatal pain and stress. J Musculoskel Pain 6(3):57-60.

Plouffe, L. Jr., and J. A. Simon. 1998. Androgens effects on the central nervous system in the post menopausal woman. Semin Reprod Endocrinol 16(2):135-43.

Poelmans J, Feenstra L, Tack J. 2005.  The role of (duodeno)gastroesophagopharyngeal reflux in unexplained excessive throat phlegm.  Dig Dis Sci. 50(5):824-832.  “Unexplained excessive throat phlegm is a sign suggestive of GER and GEPR, and unexplained yellow throat phlegm a sign suggestive of duodenogastroesophagopharyngeal reflux (DGEPR).”

Polkinghorn, B. S. 1998. Treatment of cervical disc protrusions via instrumental chiropractic adjustment. J Manipulative Physiol Ther 21(2):114-121.

Pokorny, J. 1996. [Mechanisms of neuroplasticity]. Cesk Fysiol 45(1):21-28 [Czech].

Pongratz DE, Vorgerd M, Schoser BGH. 2004.  Scientific aspects and clinical signs of muscle pain.  J Musculoskeletal Pain 12(3/4):121-128.  This article highlights painful muscle disorders, including the myopathological aspects of inflammatory and metabolic conditions.  Exercise intolerance is a common symptom of many of them, due to their impact on muscle energy metabolism.  MPS due to TrPs is a more common cause of muscle pain, with morphological changes noted as contraction discs often located in the motor endplate area.  [Due to the localized energy depletion of these states, including TrPs, it is logical that the impact of TrPs would be especially devastating in a patient who had a co-existing condition that already depleted the energy state, such as the mitochondrial ATP affect of FMS.  DJS]

Pongratz, D. E, and M. Spath. 1997.  Morphologic aspects of muscle pain syndromes: a critical review. Myofascial pain–update in diagnosis and treatment.  Phys Med Rehab Clin North Am 8(1): 55-68.

Porter, F. L., R. E. Grunau and K. J. Anand. 1999.  Long-term effects of pain in infants.  J Dev Behav Pediatr 20(4):253-61.

Porter, F. L., C. M. Wolf and J. P. Miller. 1999. Procedural pain in newborn infants: the influence of intensity and development.  Pediatrics 104(1):e13.

Porter, R. J., B. S. Lunn, L. L. Walker, J. M. Gray, C. G. Ballard and J. T. O'Brien JT 2000.  Cognitive Deficit Induced by Acute Tryptophan Depletion in Patients With Alzheimer's Disease.  Am J Psychiatry. 157(4):638-640.

Post, L. F., J. Blustein, E. Gordon and N. N. Dubler. 1996. Pain: ethics, culture, and informed consent to relief. J Law Med & Ethics 24(4):348-59.

Potts JM. 2009.  Nonpharmacological approaches for the treatment of urological chronic pelvic pain syndromes in men.  Curr Urol Rep. 10(4):289-294.  “Chronic nonbacterial prostatitis, or urological chronic pelvic pain syndrome (UCPPS), remains a common and often challenging disorder to evaluate and treat.  Employing a more holistic approach, including urological therapy, physical therapy, and psychosocial perspectives, may be more appropriate for most patients.  Growing evidence supports the use of biofeedback, myofascial trigger point release, prescribed exercise regimens, relaxation techniques, and supportive counseling to treat men with UCPPS.”  [What is causing the pain?  As the work by Dr. Ragi Doggweiler-Wiygul explains, “nonbacterial Prostatitis” may often be a way the non-myofascial trained practitioner describes pain caused by some myofascial TrPs.  DJS]

Potvin S, Larouche A, Normand E et al. 2009.  DRD3 Ser9Gly polymorphism is related to thermal pain perception and modulation in chronic widespread pain patients and healthy controls.  J Pain. [May 21 Epub ahead of print].  “This experimental study is the first to relate DNIC (diffuse noxious inhibitory controls) and TPTs (thermal pain thresholds) to a functional polymorphism of limbic dopamine-D3 receptors.  As lowered pain thresholds and deficient pain inhibition are two core features of fibromyalgia, these preliminary results may help identify a subgroup of FM patients who require closer medical attention.”

Poulletier de Gannes F., Lagroye I., Haro E et al. 2002. Effects of radio frequencies emitted by mobile phone on CNS cell cultures.  Glia (Suppl 1):S51-52 [Abstract]. Mobile phones at 900 MHz could induce CNS response on the cellular level.

Prasanna, A. 1993. Myofascial pain as postoperative complication. J Pain Sympt Manage8(7):450-451.

Prateepavanich, P., V. Kupniratsaikul and T. Charoensak. 1999. The relationship between myofascial trigger points of gastrocnemius muscle and nocturnal calf cramps. J Med Assoc Thai82(5):451-9.

Prato, F. S., J. J. Carson, K. P. Ossenkopp, and M. Kavaliers. 1995. Possible mechanisms by which extremely low frequency magnetic fields affect opioid function. FASEB J 9(9):807-14.

Press, J., M. Phillip, L. Neumann, R. Barak, Y. Segev, M. Abu-Shakra and D. Buskila. Normal melatonin levels in patients with fibromyalgia syndrome. J Rheumatol 25(3):551-555.

Preuss HG, Bagchi D, Bagchi M. 2002.  Protective effects of a novel niacin-bound chromium complex and a grape seed proanthocyanidin extract on advancing age and various aspects of syndrome X.  Ann N Y Acad Sci. 957:250-259.  Chronium or grape seed supplementation may be helpful to control insulin resistance and age-related conditions.

Prevalence of mitral valve prolapse in primary fibromyalgia: a pilot investigation.  Arch Phys Med Rehabil 70(7):541-543.

Price DD, Zhou Q, Moshiree B et al. 2006.  Peripheral and central contributions to hyperalgesia in irritable bowel syndrome.  J Pain 7(8):529-535.  “Pain in irritable bowel syndrome is likely to be at least partly maintained by peripheral impulse input from the colon/rectum and central sensitization.”  Central sensitization contributes to IBS and is at least partly maintained by peripheral pain stimuli and is in this way similar to FMS.

Price, D. D., G. N. Verne. 2002. Brain mechanisms of persistent pain states. J Musculoskel Pain 10(1/2):73-83. Central sensitization involves increased activity in the same areas and along the same paths as acute pain, but there are additional areas involved, and some of these may be part of psychological factors that occur in chronic pain.

Procacci, P., M. Maresca and P. Gepetti. 1999. Neurogenic inflammation and muscle pain. J Musculoskel Pain 7(1-2):5-12.

Proudfoot CJ, Garry EM, Cottrell DF et al. 2006. Analgesia mediated by the TRPM8 cold receptor in chronic neuropathic pain.  Curr Biol. 16(16):1591-1605.  A synthetic with the same properties as mint oil may be an effective analgesic for some chronic pain when applied topically.

Przeklasa-Muszynska A, Nosek-Kozdra K, Muszynski T et al. 2006.  [Preemptive analgesia in postoperative pain for children in otolaryngological department]  Przegl Lek. 63(11):1168-1172. [Polish]  “Although much more about the safe and effective management of pain in children is now known, this knowledge has not been widely or effectively translated into routine clinical practice.” [This is very disturbing as inadequate acute pain management can predispose to chronic pain. DJS]

Putignano, P., G. A. Kaltsas, M. A. Satta and A. B. Grossman. 1998. The effects of anti-convulsant drugs on adrenal function. Horm Metab Res 30(6-7):389-97.

Quintner J, Buchanan D, Cohen M et al. 2003.  Signification and pain: a semiotic reading of fibromyalgia.  Theor Med Bioeth 24(4):345-354.  These authors contend that fibromyalgia does not exist.  I wonder if they have read any of the articles in this reference section.  While some researchers are zeroing in on causes and treatments options for patients with fibromyalgia, there are still a few who spend their time creating fodder for lawyers bent on denying benefits and care to patients with this condition.  They are part of the problem instead of part of the solution and seem determined to ignore the ever-mounting evidence that fibromyalgia is real and very treatable, and thus deny early interventions that may in many cases help prevent full-blown fibromyalgia from developing.

Rachlin, E. S. ed. 1994. Myofascial Pain and Fibromyalgia Trigger Point Management Mosby: St. Louis. Radanov, B. P., I. Bicik, J. Dvorak, J Antinnes, G. K. von Schulthess and A. Buck. 1999.Relation between neuropsychological and neuroimaging findings in patients with late whiplash syndrome. J Neurol Neurosurg Psychiatry 66(4):485-9.

Radanov, B. P., S. Begre, M. Sturzeneggar and K. F. Augustiny. 1996. Course of psychological variables in whiplash injury--a 2-year follow-up with age, gender and education pair-matched patients. Pain 64(3):429-434.

Radhakrishnan R, Sluka KA. 2009.  Increased glutamate and decreased glycine release in the rostral ventromedial medulla during induction of a pre-clinical model of chronic widespread muscle pain.  Neurosci Lett. 457(3):141-145.  “We hypothesize that increased release of excitatory neurotransmitters in the RVM (rostroventromedial medulla) drives the release of excitatory neurotransmitters in the spinal cord, central sensitization and the consequent hyperalgesia.”

Rafols, A., J. A. Garcia Vicente, M. Farre and M. Mas. 1999. [Dextromethorphan-induced sexual dysfunction]. Aten Primaria 24(8):495-7 [Spanish].

Raghavendra V, Tanga FY, DeLeo JA. 2004.  Complete Freunds adjuvant-induced peripheral inflammation evokes glial activation and proinflammatory cytokine expression in the CNS.  Eur J Neurosci 20(2):467-473.  Proinflammatory cytokines can result from hyperactivation of glial cells, producing central sensitization.

Raghavendra V, Tanga FY, DeLeo JA. 2004.  Attenuation of morphine tolerance, withdrawal-induced hyperalgesia, and associated spinal inflammatory immune responses by propentofylline in rats.  Neuropsychopharmacology 29(2):327-334.  This study indicates that propentopylline, a glial cell modulator and anti-inflammatory agent, can restore the analgesic efficacy of morpihine.  “These results further support the hypothesis that spinal glia and proinflammatory cytokines contribute to the mechanisms of morphine tolerance and associated abnormal pain sensitivity.”

Raikkonen K., Matthews K.A., Kuller L.H. 2002.  The relationship between psychological risk attributes and the metabolic syndrome in healthy women: Antecedent or consequence?  Metabolism 51(12):1573-1577.  “The metabolic syndrome is an important risk factor for major chronic diseases in women....Psychological risk factors affect the development of the metabolic syndrome.  The association between anger and the metabolic syndrome is reciprocal.  Reduction in the level of psychological distress may prevent the development of the metabolic syndrome in women.”

Raison CL, Capuron L, Miller AH. 2005.  Cytokines sing the blues: inflammation and the pathogenesis of depression.  Trends Immunol. [Nov 26 Epub ahead of print]  “Depression might be a behavioral byproduct of early adaptive advantages conferred by genes that promote inflammation.  These findings suggest that targeting proinflammatory cytokines and their signaling pathways might represent a novel strategy to treat depression.”  [This may be a helpful treatment strategy for patients with both depression and FMS. DJS]

Raloff, J. 2000. More Waters Test Positive for Drugs. Sci News157(14):212.

Raphael, J., J. Southall, G. Treharne et al. 2002. Efficacy and adverse effects of intravenous lignocaine therapy in fibromyalgia syndrome. BMC Musculoskel Disord 3(1):21. IV lidocaine may be a safe and beneficial therapy for fibromyalgia.

Raphael K.G., Natelson B.H., Janal M.N. et al. 2002.  A community-based survey of fibromyalgia-like pain complaints following the World Trade Center terrorist attacks.  Pain 100(1-2):131-9.  “The failure to detect a significant increase in symptoms consistent with a diagnosis of fibromyalgia and the failure of new onsets of such symptoms to be accounted for by exposure to major stressors or prior depressive symptoms suggests that these hypothesized risk factors are unlikely to be of major importance in the pathogenesis of fibromyalgia.”

Rashiq, S. and B. S. Galer. 1999. Proximal myofascial dysfunction in complex regional pain syndrome: a retrospective prevalence study. Clin J Pain 15(2):151-3.

Rask-Anderson, H., A. Kinnefors and R. B. Illing. 1999. On a novel type of neuron with proposed mechanoreceptor function in the human round window membrane–animmunohistochemical study. Rev Laryngol Otol Rhinol (Bord) 120(3):203-7.

Rasmussen, D. D., B. M. Boldt, C. W. Wilkinson, S. M. Yellon and A. M. Matsumoto. 1999.Daily melatonin administration at middle age suppresses male rat visceral fat, plasma leptin, and plasma insulin to youthful levels. Endocrinology 140(2):1009-12.

Rea, T., J. Russo, W. Katon, R. L. Ashley and D. Buchwald. 1999. A prospective study of tender points and fibromyalgia during and after an acute viral infection. Arch Intern Med159(8):865-707.

Reddy J.M., Joyce C., Zaneveld L.J. 1980.  Role of hyaluronidase in fertilization: The antifertility activity of Myocristin, a nontoxic hyaluronidase inhibitor. J Androl 1(1):28-32.  Excess hyaluronic acid may be a factor in infertility.

Redondo JR, Justo CM, Moraleda FV et al. 2004.  Long-term efficacy of therapy in patients with fibromyalgia: A physical exercise-based program and a cognitive-behavioral approach. Arthritis Rheum 51(2):184-192.  This study showed that “improvement in self-efficacy and physical fitness are not associated with improvement in clinical manifestations.”

Redwine L, Hauger RL, Gilin JC et al. 2000.  Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans.  J Clin Endocrinol Metab 85(10:3597-3603.  There is an association between sleep stages and IL-6 levels.  Populations with increased REM and relative loss of deep sleep [some FMS patients may fall in this category.  DJS] have elevated nighttime concentrations of IL-6.  This may signify increased inflammatory disease risk.  [It also may be a cause for chronic pain – see Focus on Pain 2003.  DJS]

Reece PH, Wyatt M, O’Flynn P. 1999.  Dercum’s disease (adiposis dolorosa).  J Laryngol Otol. 113(2):174-176.  Dercum’s disease, also called lipomtosis dolorosa and a variety of other names, is characterized by progressively painful fatty deposits.  There is at least 3 months pain in fatty deposits, and may be excessive fatigue, obesity, and mental disturbances including confusional states.  It is rare, but may be misdiagnosed as FM, or it may co-exist with FM and some of the confusional states and other symptoms may be due to co-existing conditions.  DJS]

Refshauge, K.M., Kilbreath, S.L., Raymond, J. 2003.  Deficits in detection of inversion and eversion movements among subjects with recurrent ankle sprains.  J Orthop Sports Phys Ther 33(4):166-173; discussion 173-6.  “Perception of passive inversion and eversion movements imposed at the ankle was impaired in subjects with recurrent ankle sprains.”  [This may have implications for spread of TrPs, involving, among other things, TrP proprioception dysfunction. DJS]

Regland, B., M. Andersson, L. Abrahamsson, J. Bagby, L. E. Dyrehag and C. G. Gottfries. 1997.Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scand J Rheumatol 26(4):301-307.

Reich JW, Olmsted ME, van Puymbroeck CM. 2006.  Illness uncertainty, partner caregiver burden and support, and relationship satisfaction in fibromyalgia and osteoarthritis patients.  Arthritis Rheum. 55(1):86-93.  “Partner caregiver burden was related to lower levels of partner supportiveness for the FMS dyads, but not for the OA dyads.”  “The results suggest that uncertainty of illness is a prominent feature affecting patients with FMS in their relationships with their partners.”

Reichmann H, Schaefer J. 2004.  Painful myopathies – metabolism of muscle cells and metabolic myopathies.  J Musculoskeletal Pain 12(3/4):75-83.   Types of myalgia considered in this article include causes of focal muscle pain such as restless leg syndrome and neurogenic pain, causes of diffuse muscle pain such as FMS, paroxysmal muscle pain such as contractures (which may be caused by TrPs) and exercise-induced muscle pain.  This excellent article on myopathies makes several points which are relevant to FMS or TrPs.  There is a clear and detailed explanation of energy metabolism in muscle mitochondria.  There is a clear explanation of muscle pain pathogenesis in myopathies.  Tissue pH importance, now found to be lowered at the TrP local twitch response (Shah et al 2005) is highlighted.   Muscle soreness caused by mechanical microrupture of the sarcomeric structures described in the article may happen in over-vigorous physical therapy, especially in patients with the combination of FMS and TrPs.  The article describes the hypersensitivity of FMS patients to normal mechanical stimuli.  A central nervous system disease may cause secondary myalgia due to spasticity or rigidity.  [Patients with chronic myofascial pain complex may have muscle tightness to the point of pain.]  Contractures are described briefly as never occurring at rest, but only after repetitive muscle contractions.  [Patients with chronic myofascial pain complex can have muscles in permanent contracture.  The muscles do not seem to be able to relax.  DJS] Disturbances in muscle metabolism can cause contractures, and among these are channelopathies.  [It has been proposed that myofascial TrPs are a type of channelopathy.  DJS] “All patients with a defect in glucose metabolism should have a protein-rich diet.”  Patients must learn to avoid overuse of their muscles, and “avoid endurance exercise with abnormalities of aerobic metabolism and to avoid brief intensive exercise with disturbances of anaerobic metabolism.”

Reid, G. J., B. A. Lang and P. J. McGrath. 1997. Primary juvenile fibromyalgia: psychological adjustment, family functioning, coping and functional disability. Arth Rheum 40(4):752-760.

Reid, W. D. and G. Dechman. 1995.  Considerations when testing and training the respiratory muscles.  Phys Ther 75(11):971-82.

Reidenberg, M. M. and R. K. Portenoy. 1994. The need for an open mind about the treatment of nonmalignant pain. Clin Pharmacol Ther 55(4):367-369.

Reiffenberger, D. H. and L. H. Amundson. 1996. Fibromyalgia syndrome: a review. Am Fam Physician 53(5):1698-712.

Reilich P, Fheodoroff K, Kern U et al. 2004.  Consensus statement: botulinum toxin in myofascial pain.  J Neurol 251(Suppl 1):1/36-1/38.  Botulinum toxin is suitable for patients with myofascial TrPs who have poor clinical outcomes after at least a month of physical therapy, including dry needling and medications.  Two techniques are explained.  It must be used with caution, and only as part of multimodal therapy.

Reilly, P. A. 1999. The differential diagnosis of generalized pain. Baillieres Best Pract ResClin Rheumatol 13(3):391-401.

Reitinger, A., H. Radner, H. Tilscher, M. Hanna, A. Windischand W. Feigl. 1996. [Morphologic study of trigger points.] Manuelle Medizin 34:256-262. [German]

Remesar, X., I Rafecas, J. A. Fernandez-Lopez and M. Alemany. 1997. Is leptin an insulin counter-regulatory hormone? FEBS Lett 402(1):9-11.

Reusch, J. 2002. Current concepts in insulin resistance, type 2 diabetes mellitus, and the metabolic syndrome. Am J Cardiol 90(Suppl 1):19. Insulin resistance plays a critical role in the development of cardiovascular disease. Nitric oxide-mediated vasodilation is impaired in insulin resistance. Insulin resistance may be moderated by the use of insulin sensitizing medications. 

Reynolds, M. D. 1984. Myofascial trigger points in persistent posttraumatic shoulder pain. South Med J 77(10):1277-1280.

Ridgway, K. 1999. Acupuncture as a treatment modality for back problems. Vet Clin North Am Equine Pract 15(1):211-21.

Riedel, W., H. Layka and G. Neeck. 1998. Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 57 Suppl 2:81-7.

Ring, J., B. Eberlein-Konig and H. Behrendt. 1999. "Eco-syndrome" ("Multiple Chemical Sensitivity"–MCS). Zentralbl Hyg Umweltmed 202(2-4):207-18.

Riskowski JL, Mikesky AE, Bahamonde RE et al. 2005.  Proprioception, gain kinematics, and rate of leading during walking: are they related?  J Musculoskelet Neuronal Interact. 5(4):379-387.

Ristow, M., M. Vorgerd, M. Mohlig, H. Schatz and A. Pfeiffer. 1997. Deficiency ofphosphofructo-1-kinase/muscle subtype in humans impairs insulin secretion and causes insulin resistance. J Clin Invest 100(11):2833-2841.

Rivera, J., A. de Diego, M. Trinchet and A. Garcia Monforte. 1997. Fibromyalgia-associated hepatitis C virus infection. Br J Rheumatol 36(9):981-985.

Robbins, W. R., P. S. Staats, J. Levine, H. L. Fields, R. W. Allen, J. N. Campbell and M. Pappagallo. 1998. Treatment of intractable pain with topical large-dose capsaicin: preliminary report. Anesth Analg 86(3):597-83.

Roberts, B. L. 1997. Soft tissue manipulation: neuromuscular and muscle energy techniques. J Neurosci Nurs 29(2):123-7.

Roberts, T. B. 1999. Do entheogen-induced mystical experiences boost the immune system? Psychedelics, peak experiences, and wellness. Adv Mind Body Med 15(2):139-47.

Robitaille, R., A. Castonguy, I. Rousse et al. 2002.  Glial cells are determinant of synaptic activity.  Glia (Suppl 1):S9 [Abstract].  This research indicates “that perisynaptic glial cells modulate sybaptic efficacy in a frequent dependent manner.

Rocca, P. V. 1999. Fibromyalgia: how disabling? Del Med Jrl 71(6): 263-5.

Rocha CA, Sanchez TG. 2007.  Myofascial trigger points: another way of modulating tinnitus.  Prog Brain Res. 166:209-214.  “Tinnitus is a multifaceted symptom that may have many causes…”  “Tinnitus can often be modulated by different kinds of stimuli.”  “In 56% of patients with tinnitus and MTPs, the tinnitus could be modulated by applying digital compression of such points, mainly those of the masseter muscle.”  “Compression of MTPs was most effective in patients who have had chronic pain earlier in the examined areas.”  [As tinnitus can be severe enough to cause suicidal ideation, disrupting lives significantly, it is ironic that some patients can be helped so easily, yet are not.  DJS]

Roche, H. M. 1999. Dietary carbohydrates and triacylglycerol metabolism. Proc Nutr Soc58(1):201-7.

Rodriguez EM, Blazquez JL, Pastor FE et al. 2005.  Hypothalamic tanycytes: a key component of brain-endocrine interaction.  Int Rev Cytol. 247:89-164.  “Tanycytes are bipolar cells bridging the cerebrospinal fluid (CSF) to the portal capillaries and may link the CSF to neuroendocrine events.  During the perinatal period a subpopulation of radial glial cells differentiates into tanycytes...”  There are four populations of tanycytes, and each subtype expresses important “...functional molecules, such as glucose and glutamate transpoters; a series of receptors for neuropeptide and peripheral hormones; secretory molecules  such as transforming growth factors, prostaglandin E(2), and the specific protein P85; and proteins of the endocytic pathways.”  “The discovery in tanycytes of new functional molecules is opening a new field of research.  Thus, thyroxine deiodinase type II, an enzyme generating triiodothyronine T(3) from thyroxine, appears to be exclusively expressed by tanycytes, suggesting that these cells are the main source of brain T(3).”  [Other types of tanycytes are involved in glucose, and the patients who are thyroid resistant also seem to be insulin resistant. This may be a clue to why some FMS patients are T4-resistant and insulin resistant. DJS]

Roehrs T, Roth T. 2005.  Sleep and pain: interaction of two vital functions.  Semin Neurol 25(1):106-116.  “The pain sleep nexus has been modeled in healthy pain-free subjects and the studies have demonstrated the bidirectionality of the sleep-pain relation.  ...treatment must focus on alleviation of both the pain and sleep disturbance.”

Roelofs J, Sluiter JK, Frings-Dresen MH et al. 2007.  Fear of movement and (re)injury in chronic musculoskeletal pain: evidence for an invariant two-factor model of the Tampa Scale for Kinesiophobia across pain diagnoses and Dutch, Swedish and Canadian samples.  Pain. [Feb 19 Epub ahead of print]  [This study does not take into consideration that restriction of movement may be due to co-existing myofascial trigger points that cause pain at the end of range of motion.  Until psychologists, psychiatrists, and indeed all health care professionals are trained in the awareness of myofascial medicine, papers like this will be, at best, incomplete, and, at worst, lead to erroneous conclusions. DJS]

Rogers, N., C. van den Heuvel, and D. Dawson. 1997. Effect of melatonin and corticosteroid on in vitro cellular immune function in humans. J Pineal Res 22(2): 75-80.

Rogozhin AA, Devlikamova FI. 2007.  Inactivation of trigger points could significantly reduce radicular pain.  J Musculoskel Pain 15 (Supp 13):35 item 59.  [Myopain 2007 Poster]  “It is difficult to distinguish between radicular and MPS because trigger points [TrPs] are widely present in patients with radiculopathy.”  “We can suppose that radicular pain in patients with acute radiculopathy partly could be caused by activation of TrPs.  Inactivation of TrPs in patients with radiculopathy never leads to complete pain relief but could be useful in patients with prolonged time course of disease.”  [The patient must be treated, rather than the radiography.  This means that soft tissue problems such as MTPs must be treated rather than the current focus on the skeletal system and discs alone.  DJS.]

Roizenblatt S, Fregni F, Gimenez R et al. 2007.  Site-specific effects of transcranial direct current stimulation on sleep and pain in fibromyalgia: a randomized, sham-controlled study.  Pain Pract. 7(4):297-306.  “Our findings suggest that one possible mechanism to explain the therapeutic effects of tDCS in fibromyalgia is via sleep modulation that is specific to modulation of primary M1 (motor cortex) activity.”

Roizenblatt, S., S. Tufik, J. Goldenberg, L. R. Pinto, M. P. Hilario and D. Feldman. 1997. Juvenile fibromyalgia; clinical and polysomnographic aspects. J Rheumatol 24 (3): 579-585.

Rolland JF, DeLuca A, Burdi R et al. 2006.  Overactivity of exercise-sensitive cation channels and their impaired modulation by IGF-1 in mdx native muscle fibers: beneficial effect of pentoxifylline.  Neurobiol Dis.  [Sep 27 Epub ahead of print]  Pentoxifylline may be helpful in some channelopathies.

Romano, T. J. 1991. Fibromyalgia in children: diagnosis and treatment. W V Med J 87 (3):112-114.

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Rooks DS. 2007.  Fibromyalgia treatment update. Curr Opin Rheumatol. 19(2):111-117.  “Treatment goals should include the improvement of symptoms, primarily pain and sleep, and the promotion of positive health behaviors with the aim of improving physical function and emotional well-being.”

Rosenhall, U., G. Johansson and G. Orndahl. 1996. Otoneurologic and audiologic findings in fibromyalgia. Scan J Rehabil Med 28(4):225-232.

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Roskos SE, Keenum AJ, Newman LM et al. 2007.  Literacy demands and formatting characteristics of opioid contracts in chronic nonmalignant pain management.  J Pain [Mar 21 Epub ahead of print]   “Most OCs contained not only sophisticated medical language but multisyllable, nonmedical terms and vocabulary not used in typical everyday conversation.”  Opioid contracts must be understandable and clear, and this is not the case.

Rosmond, R., E. Eriksson and P. Bjorntorp. 1999. Personality disorders in relation to anthropometric, endocrine and metabolic factors. J Endocrinol Invest 22(4):279-88.

Rossetti, L., D. Massillon, N. Barzilai, P. Vuguin, W. Chen, M. Hawkins, J. Wu and J. Wang.1997. Short term effects of leptin on hepatic gluconeogenesis and in vivo insulin action. J Biol Chem 272(44):27758-63.

Rossi S, della Volpe R, Giananneschi F et al. 2003.  Early somatosensory processing during tonic muscle pain in humans: relation to loss of proprioception and motor ‘defensive’ strategies. Clin Neurophysiol 114(7):1351-1358.  Contractured, painful muscles can cause early sensory processing at the cortical level. This may be part of the mechanism of proprioception dysfunction in myofascial TrPs.

Rossini M, Di Munno O, Valentini G et al. 2007.  Double-blind, multicenter trial comparing acetyl l-carnitine with placebo in the treatment of fibromyalgia patients.  Clin Exp Rheumatol. 25(2):182-188.  “LAC (acetyl l-carnitine) may be of benefit in patients with FMS, providing improvement in pain as well as the general and mental health of these patients.”

Rossy, L. A., S. P. Buckelew, N. Dorr, K. J. Hagglund, J. F. Thayer, M. J. McIntosh, J. E. Hewett and J. C. Johnson. 1999. A meta-analysis of fibromyalgia treatment interventions. Ann Behav Med 21(2):180-91.

Roth, R. S., K. Horowitz and J. E. Bachman. 1998. Chronic myofascial pain: knowledge of diagnosis and satisfaction with treatment. Arch Phys Med Rehabil 79(8):966-70.

Roth, T. and S. Ancoli-Israel. 1999. Daytime consequences and correlates of insomnia in the United States: results of the 1991 National Sleep Foundation Survey. II. Sleep 22 Suppl 2:S354-8.

Roy-Byrne P, Smith WR, Goldberg J et al. 2004.  Post-traumatic stress disorder among patients with chronic pain and chronic fatigue.  Psychol Med 34(2):363-368.  "Optimal clinical care for patients with FMS should include an assessment of trauma in general, and PTSD in particular."

Rubenstein, S. 1990. The osteopathy alternative. East West Dec:45-49.

Rubic B. 2002.  The biofield hypothesis: its biophysical basis and role in medicine.  J Altern Complement Med 8(6):703-717.  “This paper provides a scientific foundation for the biofield: the complex extremely weak electromagnetic field of the organism hypothesized to involve electromagnetic bioinformation for regulating homeodynamics.”  This hypothesis may relate to the benefits of acupuncture, bioelectromagnetic and other complementary medicine methods.

Rudin NJ. 2003.  Evaluation of treatments for myofascial pain syndrome and fibromyalgia.  Curr Pain Headache Rep 7(6):433-442.  As the title suggests, this is a general evaluation of these conditions, although the author mentions early that there is a question of whether either of these conditions exist. Treatment options are discussed without mention of perpetuating factors, and they often are the chief clue to the tailoring of specific remedial work and treatment regimens.

Care is taken to note that treatments must be carefully tailored to the needs of the individual patient.  What is effective for some may not fill the needs of others, and some types of therapies require specific attention to protocol for success, and as the author states, no single therapeutic regimen will be successful on every patient.  There are many fine points to this article, but it is unfortunate that the difference between hypothyroid and thyroid-resistant states was not specified, and that the dismissal of guaifenesin was based on a single flawed study.

Ruhl A. 2005. Glial cells in the gut. Neurogastroenterol Motil. 17(6):777-790.  “The enteric nervous system is composed of both neurons and glia.  Recent evidence indicates that enteric glia—which vastly outnumber enteric neurons—are actively involved in the control of gastrointestinal functions: they contain neurotransmitter precursors, have the machinery for uptake and degradation of neuroligands, and express neurotransmitter-receptors which makes them well suited as intermediaries in enteric neurotransmission and information processing in the ENS.  Novel data further suggest that enteric glia have an important role in maintaining the integrity of the mucosal barrier of the gut.  Finally, enteric glia may also serve as a link between the nervous and immune systems of the gut as indicated by their potential to synthesize cytokines, present antigen and respond to inflammatory insults.”  “...it is predictable that enteric glia are involved in the etiopathogenesis of various pathological processes in the gut.”

Ruiz-Saez M, Fernandez-de-las-Penas C, Blanco CR et al. 2007.  Changes in pressure pain sensitivity in latent myofascial trigger points in the upper trapezius muscle after a cervical spine manipulation in pain-free subjects.  J Manipulative Physiol Ther. 30(8):578-583.  “Our results suggest that a cervical spine manipulation directed at the C3 through C4 segment induced changes in pressure pain sensitivity in latent MTrPs in the upper trapezius muscle.  Different therapeutic mechanism, either segmental or central, may be involved at the same time.”

Rulh A. 2005. Glial cells in the gut.  Neurogastroenterol Motil 17(6):777-790.  [This may have relevance to central sensitization in both FMS and IBS. DJS]

Ruotolo G., Howard B.V. 2002.  Dyslipidemia of the metabolic syndrome.  Curr Cardio Rep 4(6):494-500. “...these lipoprotein defects contribute largely to the increased cardiovascular disease risk in individuals with insulin resistance.”

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Russell IJ. 2003.  Dissecting the Mechanisms of Soft Tissue Pain. J Muscoloskel Pain 11(2):1-2.  In this editorial, Dr. Russell stresses that he believes the importance of identifying subgroups of FMS patients will become much more important in deciding the most effective treatment options.  [I agree with this totally and urge clinicians to take under consideration initiating factors and perpetuating factors when developing FMS treatment regimens.  DJS]

Russell IJ. 2003.  Depression and soft tissue pain.  J Musculoskel Pain 11(1):1-3.  “The old arguments that depression is the cause of low back pain or of pain in patients with fibromyalgia are clearly lame from multiple unsupported parades, but it is fair to say that the resilience of the human spirit becomes less elastic in the presence of chronic pain.”

Russell, IJ. 1999.  Is fibromyalgia a distinct clinical entity?  The clinical investigator’s evidence.  Baillieres Best Pract Res Clin Rheumatol 13(3):445-54.

Russell, IJ. 1999.  Reliability of clinical assessment measures for the classification of myofascial pain syndrome.  J Musculoskel Pain 7(1-2):309-324.

Russell, IJ. 1999.  The reliability of algometry in the assessment of patients with fibromyalgia syndrome.  J Musculoskel Pain 6(1): 139-152. 

Russell, IJ, JE Michalek, YK Kang and AB Richards. 1999. Reduction of morning stiffness and improvement in physical function in fibromyalgia syndrome patients treated subligually with low doses of human interferon-alpha.  J Interferon Cytokine Res 19(8):961-8.

Russell, IJ , GA Vapriao, JE Michalek, FE Craig, YK Kang and AB Richards. 1999.  Lymphocyte markers and natural killer cell activity in fibromyalgia syndrome: effects of low-dose, subligually use of human interferon-alpha.  J Interferon Cytokine Res 19(8):969-78.

Russell, IJ. 1998.  Advances in fibromyalgia: possible role for central neurochemicals.  Am J Med Sci 315(6):377-384.

Russell, IJ, JE Michalek, JD Fletchas, and GE Abraham. 1995. Treatment of fibromyalgia syndrome with Super Malic; a randomized, double blind, placebo controlled, crossover pilot study.  J Rheumatol 22(5):953-958.

Russo, C. M. and W. G. Brose. 1998. Chronic pain. Annu Rev Med 49:123-33.

Rusy, L. M., S. A. Harvey and D. J. Beste. 1999. Pediatric fibromyalgia and dizziness: evaluation of vestibular function. J Dev Behav Pediatr 20(4):211-5.

Ryabow S. I. 2002.  Extracellular space volume changes in the cerebral cortex evoked by repetitive peripheral stimulation.  Glia (Suppl 1):S59 [Abstract].

Ryan E, Malboeuf CM, Barnard M et al. 2006.   Cyclooxygenase-2 Inhibition attenuates antibody responses against human papillomavirus-like particles.  J Immunol 177:7811-7819.  Some common over-the counter and other pain medications might weaken vaccines.  Vaccines are give to produce a response of antibodies.  Any COX inhibitor, such as aspirin, Advil, Celebrex, etc., may attenuate this.  In people with compromised immune systems, the effect may be even more pronounced.