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

annotated by Devin J. Starlanyl

 

 

References for Research Purposes

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NOTE:  New Nomenclature

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

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

 

 

Oaklander AL, Herzog ZD, Downs H et al. 2013. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain. [Jun 5 Epub ahead of print.] "Fibromyalgia is a common, disabling syndrome that includes chronic widespread pain plus other diverse symptoms….In contrast, small-fiber polyneuropathy (SFPN), despite causing similar symptoms, is definitely a disease caused by dysfunction and degeneration of peripheral small-fiber neurons…..41% of skin biopsies from fibromyalgia subjects vs. 3% of biopsies from control subjects were diagnostic for SFPN, and MNSI (Michigan Neuropathy Screening Instrument) and UENS (Utah Early Neuropathy Scale) scores were higher among fibromyalgia than control subjects…. Abnormal AFT (Autonomic Function Testing) was equally prevalent suggesting that fibromyalgia-associated SFPN is primarily somatic. Blood tests from all 13 fibromyalgia subjects with SFPN-diagnostic skin biopsies provided insights into etiologies. All glucose tolerance tests were normal, but eight subjects had dysimmune markers, 2 had hepatitis C serologies, and one family had apparent genetic causality. These findings suggest that some patients with chronic pain labeled as "fibromyalgia" have unrecognized small-fiber polyneuropathy, a distinct disease that can be objectively tested for an sometimes definitively treated."

Oberklaid F, Amos D, Liu C et al. 1997.  “Growing pains”: clinical and behavioral correlates in a community sample.  J Dev Behav Pediatr 18(2):102-106.  Parents consider children with growing pains to have different behavioral and temperamental profiles than healthy children.  [There is no acknowledgement in this study that the presence of chronic pain could contribute to the behavior problems, rather than the reverse. DJS]

Oberkalaid, F., D. Amos, C. Liu, F. Jarman, A. Sanson and M. Prior. 1997. "Growing pains": clinical and behavioral correaltes in a community sample. J Dev Behav Pediatr 18(2):102-106.

O'Brien EM, Waxenberg LB, Atchison JW et al. 2010. Negative mood mediates the effect of poor sleep on pain among chronic pain patients. Clin J Pain. 26(4):310-319. “These findings suggest that addressing negative mood directly, or by addressing sleep disturbances in chronic pain patients, may have a beneficial impact on patients' pain. As sleep disturbance may be causing negative mood, treating the sleep disturbance may also be beneficial among chronic pain patients. Negative mood may perpetuate the impact of sleep disturbances on pain, possibly through increased arousal or disruptions in diurnal patterns.”

O’Brien EM, Staud RM, Hassinger AD et al. 2009.  Patient-centered perspective on treatment outcomes in chronic pain.  Pain Med. [Sep 1 Epub ahead of print].  “Results highlight the importance of assessing the patient’s view of successful outcome.  Both fibromyalgia and back pain patients appear to have stringent criteria for success that existing treatments are often unlikely to meet.  Comparison across groups indicated fibromyalgia patients have higher than usual levels of pain, fatigue, distress, and interference.  Interestingly, fibromyalgia patients also require greater changes across domains in order to consider treatment successful, despite rating higher levels of pain, fatigue, distress, and interference as successful.  Recognizing patients’ success criteria and treatment expectations encourages discussion and development of individualized treatment goals, and wider implementation of individualized treatment for chronic-pain populations is encouraged.”

O'Brien EM, Waxenberg LB, Atchison JW et al. 2011. Intraindividual Variability in Daily Sleep and Pain Ratings among Chronic Pain Patients: Bidirectional Association and the Role of Negative Mood. Clin J Pain. [Mar 16 Epub ahead of print]. "These findings suggest that addressing sleep is important in the treatment of individuals with chronic pain."

Ocana M, Cendan CM, Cobos EJ et al. 2004.  Potassium channels and pain: present realities and future opportunities.  Eur J Pharmacol. 500(1-3):203-219.  New potassium channel openers may be useful in treatment of acute and chronic pain.

Ochs L. 2006.  The low energy feedback system (LENS): Theory, background, and introduction.  J Neurother 10(2/3):5-40.  Concepts, operations and history of this electrical neurofeedback system.

Ochs, L. 1999. Fibromyalgia as a phantom phenomenon: research considerations. BiofeedbackFall:13-15.

Oestreicher, M. K., J. Desmeules, V. Piguet, A. F. Allaz and P. Dayer. 1998. [Genetic and environmental effects of neuromodulation and the antinociceptive effect of dextromethorphan].Schweiz Med Wochenschr 128(6):212-215 [French].

Offenbacher M, Stucki G. 2000. Physical therapy in the treatment of fibromyalgia. Scand J Rheumatol 113: 78-85. "Trigger point injection may reduce pain originating in concomitant trigger points in selected fibromyalgia patients. Massage may reduce muscle tension and may be prescribed as an adjunct with other therapeutic interventions. Acupuncture may reduce pain and increase pain threshold. Biofeedback may positively influence subjective and objective disease measures. TENS may reduce localized musculoskeletal pain in fibromyalgia. … Accordingly. a multidisciplinary approach combining these therapies in a well balanced program may be the most promising strategy and is currently recommended in the treatment of fibromyalgia."

Offenbaecher, M., B. Bondy, S. de Jonge, K. Glatzeder, M. Kruger, P. Schoeps and M. Ackenheil. 1999. Possible association of fibromyalgia with a polymorphism in the serotonin transporter gene regulatory region. Arthritis Rheum 42(11):2482-8.

Offenbaecher M, Kohls N, Toussaint LL et al. 2013. Spiritual needs in patients suffering from fibromyalgia. Evid Based Complement Alternat Med. [Nov 20 Epub ahead of print.] "Using a set of standardized questionnaires (i.e., Spiritual Needs Questionnaire, Fibromyalgia Impact Questionnaire, SF-36's Quality of Life, Brief Multidimensional Life Satisfaction Scale, etc.), we enrolled 141 patients (95% women, mean age 58 ± 10 years). Here, needs for inner peace and giving/generativity scored the highest, while existential needs and religious needs scored lowest. Particularly inner peace needs and existential needs correlated with different domains of reduced mental health, particularly with anxiety, the intention to escape from illness, and psychosocial restrictions. Thirty-eight percent of the patients stated needs to be forgiven and nearly half to forgive someone from their past life. Therefore, the specific spiritual needs of patients with chronic diseases should be addressed in clinical care in order to identify potential therapeutic avenues to support and stabilize their psychoemotional situation."

Ofluoglu D, Gunduz OH, Kul-Panza E et al. 2005.  Hypermobility in women with fibromyalgia syndrome.  Clin Rheumatol. [Oct 16 Epub ahead of print]  “Hypermobility syndrome is more common in women with FS than in those in the control group.  Therefore, the relationship between hypermobility and FS should be taken into consideration in the diagnosis and follow-up of women, especially those with widespread pain.”

Oh S, Kim HK, Kwak J et al. 2013. Causes of hand tingling in visual display terminal workers. Ann Rehabil Med. 37(2):221-228. "To offer the basic data about the causes and distribution of hand tingling, symptoms and physical findings, and pressure pain threshold in desk workers… Five physiatrists participated in the screening test composed of history and physical examination. A total of 876 desk workers were evaluated and of them 37 subjects with hand tingling were selected. For further analyzing, detailed history taking and meticulous physical examination were taken. Pressure pain threshold (PPT) at the infraspinatus, upper trapezius, flexor carpi radialis, rhomboideus, and flexor pollicis longus were examined. PPT measurements were repeated three times with two minute intervals by a pressure algometer. Electrodiagnostic study was done to detect potential neurologic abnormalities….THE CAUSES OF HAND TINGLING IN ORDER OF FREQUENCY WERE: myofascial pain syndrome, 68%; cervical radiculopathy, 27%; rotator cuff syndrome, 11%; tenosynovitis, 8%; and carpal tunnel syndrome, 5%. The location of trigger points in the myofascial pain syndrome, which were proven to evoke a tingling sensation to the hand in order of frequency were: infraspinatus, 65.4%; upper trapezius, 57.7%; flexor carpi radialis, 38.5%; rhomboideus 15.4%; and flexor pollicis longus 11.5%. The PPT of the affected side was significantly lower than that of the unaffected side in myofascial pain syndrome (p<0.05)…The most common cause of hand tingling in desk workers was myofascial pain syndrome rather than carpal tunnel syndrome. Common trigger points to evoke hand tingling were in the infraspinatus and upper trapezius."

Oh TH, Hoskin TL, Luedtke CA et al. 2012. Predictors of clinical outcome in fibromyalgia after a brief interdisciplinary fibromyalgia treatment program: single center experience. PM R. 4(4):257-263. "Patients with younger age, more years of education (with college or graduate degree), higher baseline FIQ depression score, lower tender point count, and absent abuse history experience greater benefit from a brief fibromyalgia treatment program." [The Mayo Clinic has such a program, and generated this research. It is not known if patients are taught about co-existing myofascial trigger points at this clinic. DJS]

Ohayon MM. 2005.  Prevalence and correlates of nonrestorative sleep complaints.  Arch Intern Med. 165(1):35-41.  “Nonrestorative sleep is a frequent symptom in the general population, but its prevalence largely varies between countries.  Nonrestorative sleep affected more frequently the active classes of the population and caused greater daytime impairment than difficulty initiating or maintaining sleep.”

Ohmori A, Iranami H, Fujii K et al. 2013. Myofascial involvement of supra- and infraspinatus muscles contributes to ipsilateral shoulder pain after muscle-sparing thoracotomy and video-assisted thoracic surgery. J Cardiothorac Vasc Anesth. 27(6):1310-1314. "This study examined the hypothesis that ipsilateral upper extremity elevation for muscle-sparing thoracotomy procedures contributes to the postoperative shoulder pain….These results supported the hypothesis that myofascial involvement contributed, to some extent, to shoulder pain after muscle-sparing thoracotomy with ipsilateral upper extremity elevation."

Ohsawa M, Yamamoto S, Ono H. 2014. Contribution of the sensitization of supraspinal nociceptive transmission in chronic pain. Yakugaku Zasshi. 134(3):387-395. "Central sensitization in the spinal cord is well known to be involved in chronic pain. Recent investigations indicated that the protein expressions involving the synaptic plasticity are changed in several brain areas under a chronic pain condition. These changes in supraspinal neural function might cause the emotional and memory dysfunction. It is also possible that these changes are involved in the chronic pain. Indeed, since the improvement of spinal and peripheral sensitization showed limited relief in the neuropathic pain, the sensitization of supraspinal nociceptive transmission might be involved in the expression of chronic pain. We recently found that intra-thalamic treatment with excitatory neurotransmitter glutamate caused hyperalgesia, which is mediated by the stimulation of glutamate N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Moreover, intracerebroventricular treatment with gabapentin, a calcium channel alpha2delta-1 subunit blocker, attenuated the hyperalgesia in the nerve-injury model of mice. These results suggest that the sensitization of supraspinal nociceptive transmission is involved in neuropathic pain. It is also indicated that neuropathic pain is resulted from the activations of spinal glial cells. Likewise, the supraspinal glial activation was observed in the neuropathic pain. Therefore, the sensitization of supraspinal nociceptive transmission might be important for a chronic pain. In this review, we would like to discuss the possible involvement of the supraspinal sensitization in neuropathic pain and in its application for the curative treatment in chronic pain." Free Article.

Ohta H, Oka H, Usui C et al. 2012. A randomized, double-blind, multicenter, placebo-controlled phase III trial to evaluate the efficacy and safety of pregabalin in Japanese patients with fibromyalgia. Arthritis Res Ther. 14(5):R217. "This trial demonstrated that pregabalin, at doses of up to 450 mg/day, was effective for the symptomatic relief of pain in Japanese patients with fibromyalgia. Pregabalin also improved measures of sleep and functioning and was well tolerated. These data indicate that pregabalin is an effective treatment option for the relief of pain and sleep problems in Japanese patients with fibromyalgia."

Okifuji A, Donaldson GW, Barck L et al. 2010. Relationship between fibromyalgia and obesity in pain, function, mood, and sleep. J Pain. [Jun 8 Epub ahead of print]. "Fibromyalgia syndrome (FMS) is a prevalent and disabling chronic pain disorder.… A total of 215 FMS patients completed a set of self-report inventories to assess FMS-related symptoms and underwent the tender point (TP) examination, physical performance testing, and 7-day home sleep assessment. Forty-seven percent of our sample was obese and an additional 30% was overweight. Obesity was related significantly to greater pain sensitivity to TP palpation particularly in the lower body areas, reduced physical strength and lower-body flexibility, shorter sleep duration, and greater restlessness during sleep….The results suggest that obesity may aggregate FMS and weight management may need to be incorporated into treatments."

Okifuji, A., D. C. Turk and J. J. Sherman. 2000. Evaluation of the relationship between depression and fibromyalgia syndrome: what aren’t all patients depressed?  J Rheumatol 27(1):212-9.

Okifuji, A., D. C. Turk, J. D. Sinclair, T. W. Starz and D. A. Marcus. 1997. A standardized manual tender point survey. I. Development and determination of a threshold point for the identification of positive tender points in fibromyalgia syndrome. J Rheumatol 24(2):377-383.

Okumus M, Ceceli E, Tuncay F et al. 2010. The relationship between serum trace elements, vitamin B12, folic acid and clinical parameters in patients with myofascial pain syndrome. J Back Musculoskel Rehabil. 23(4):187-191. "Serum levels of zinc...were significantly decreased in patients with MPS. VAS, total myalgic and BDI scores of patients were significantly higher than the control group....Association between TMS and magnesium, vitamin B12 levels was found statistically significant. BDI (Beck Depression Inventory) score correlated significantly with the serum zinc level...and VAS (Visual Analogue Scale) in patients with MPS....According to the results of this study, it was asserted that trace elements, vitamins may play an important role in the pathophysiology of MPS and psychological factors may also have additional effect."

Okumus M, Gokoglu F, Kocaoglu S et al. 2006. Muscle performance in patients with fibromyalgia. Singapore Med J. 47(9):752-756. "Our results indicate that osteoporotic patients with FMS have impairment in strength of lumbar and abdominal muscles an in measurement of chest expansion. Further studies are needed to investigate the mechanism of reduced muscle performance and the effects of aerobic exercise in this patient group." [As FM patients have TrPs and TrPs in the indicated muscles and other respiratory muscles can profoundly affect breathing, it perhaps would be wise to discover if the difference in muscle performance was due to co-existing TrPs. DJS]

Okumus M, Koybası M, Tuncay F et al. 2013. Fibromyalgia syndrome: is it related to vitamin D deficiency in premenopausal female patients? Pain Manag Nurs. 14(4):e156-163. "In conclusion, the results of this study indicate that deficiency of vitamin D is not more common in premenopausal female patients with FM than in control subjects without FM. However, the association between pain and vitamin D levels in FM patients emphasizes that hypovitaminosis of vitamin D in the FM syndrome may have an augmenting impact on pain intensity and functional status. Future studies are needed to show the effect of vitamin D supplementation in the reduction of pain intensity and disability in patients suffering from this chronic condition."

Okuyama-Tamura M, Mikuna M, Kojima I. 2003.  Modulation of the human glucocorticoid receptor function by antidepressant compounds.  Neurosci Lett 342(3):206-210.  This article explains how antidepressants, but not tranquilizers, affect the glucocorticoid receptors indirectly, affecting the hyperactivity of the HPA axis (common in FMS).

Olea, N., F. Olea-Serrano, P. Lardelli-Claret, A. Rivas and A. Barba-Navarro. 1999. Inadvertent exposure to xenoestrogens in children. Toxicol Ind Health 15(1-2):151-8.

Olin, R. R. Klein and P. A. Berg. 1998. A randomized double-blind 16-week study of ritanserin in fibromyalgia syndrome: clinical outcome and analysis of autoantibodies to serotonin, gangliosides, and phospholipids. Clin Rheumatol 17(2):89-94.

Olin, R. 1995. [Fibromyalgia. A neuro-immuno-endocrinologic syndrome]? Lakartidnigen 92(8):755-8, 761-3.[Swedish].

Oliveira P, Costa ME. 2009.  Interrelationships of adult attachment orientations, health status and worrying among fibromyalgia patients.  J Health Psychol. 14(8):1184-1195.

Oliveira-Campelo NM, de Melo CA, Alburquerque-Sendín F et al. 2013. Short- and Medium-Term Effects of Manual Therapy on Cervical Active Range of Motion and Pressure Pain Sensitivity in Latent Myofascial Pain of the Upper Trapezius Muscle: A Randomized Controlled Trial. J Manipulative Physiol Ther. [Jun 11 Epub ahead of print]. "Manual techniques on upper trapezius with latent trigger point seemed to improve the cervical range of motion and the pressure pain sensitivity. These effects persist after 1 week in the IC (ischemic compression) group."

Oliven A, Odeh M. 2006.  Effect of positional changes of anatomic structure on upper airway dilating muscle shortening during electro- and chemostimulation.  J Appl Physiol 101(3):745-751.   “...positional alterations of anatomic structures in the neck have a dramatic effect on the magnitude of shortening of the activated GG (genioglossus) and GH (geniohyoid), which may reduce substantially their ability to protect pharyngeal patency.”  [TrPs in some muscles may affect upper airway function. DJS]

Oliver K, Cronan TA. 2005.  Correlates of physical activity among women with fibromyalgia syndrome.  Ann Behav Med. 29(1):44-53.  "...self-efficacy may play a critical role in both the present and long-term PA of women with FMS.”

Olsen MN, Sherry DD, Boyne K et al. 2013. Relationship between sleep and pain in adolescents with juvenile primary fibromyalgia syndrome. SLEEP 36(4):509-516. Although perceived sleep quality improved in adolescents with JPFS after treatment, objective measures did not. Our findings do not suggest exercise therapy for pain improves sleep by reducing ADS (alpha-delta sleep), nor do they support causal relationships between ADS and chronic pain or subjective sleep quality.

Olsen, N. J. and J. H. Park. 1998. Skeletal muscle abnormalities in patients with fibromyalgia. Am J Med Sci 315(6):351-358.

Olsen RV, Andersen HH, Moller HG et al. 2014. Somatosensory and vasomotor manifestations of individual and combined stimulation of TRPM8 and TRPA1 using topical L-menthol and trans-cinnamaldehyde in healthy volunteers. Eur J Pain. [Mar 25 Epub ahead of print.] "This study elucidates the potential of L-menthol as a counter-irritant to secondary neurogenic inflammation and provides evidence of an intricate interplay between cold receptors TRPA1 and TRPM8, warranting further investigation of the neural coding of cold pain perception."

Olsen Y, Daumit GL. 2004.  Opioid prescribing for chronic nonmalignant pain in primary care: challenges and solutions.  Adv Psychosom Med 25:138-150.

Omoigui S. 2007.  The biochemical origin of pain – proposing a new law of pain: the origin of all pain is inflammation and the inflammatory response.  Part 1 of 3 – A unifying law of pain.  Med Hypotheses. [Jan 18 Epub ahead of print]

Onal SA. 2006.  [Adjuvant analgesics in pain management.]  Agri. 18(4):10-23. [Turkish]

Oncu J, Basoglu F, Kuran B. 2013. A comparison of impact of fatigue on cognitive, physical, and psychosocial status in patients with fibromyalgia and rheumatoid arthritis. Rheumatol Int. [Jul 24 Epub ahead of print]. This study from turkey found "Fatigue has different impacts on QoL (quality of life) in FM and RA, respectively. Together with pain, fatigue leads FM patients to see disease as having worse health in terms of mental function, whereas it leads to poor health in terms of physical function in RA."

O’Neill, A. B., S. J. Morgan and J. D. Brioni. 1998. Histological and behavioral protection by(-)-nicotine against quinolinic acid-induced neurodegeneration in the hippocampus. NeurobiolLearn Mem 69(1):46-64.

Orellana C, Gratacos J, Galisteo C et al. 2009.  Sexual dysfunction in patients with fibromyalgia.  Curr Rheumatol Rep. 11(6):437-442.  “Several studies have investigated sexual function in patients with fibromyalgia (FM).  All reports agree that sexual function seems frequently impaired in this condition.  This dysfunction is usually severe and may affect all domains of sexuality.  Given the complexity of factors involved in human sexual function and the intricacy of the physiopathology of FM, many factors and mechanisms have been implicated.  Per our literature review, depression may be the main contributing factor to FM-related sexual dysfunction.  However, prospective studies are needed, as reports have lacked sufficient quality to draw definitive conclusions.  Recognition of sexual dysfunction and its inclusion in multidisciplinary management are needed to improve quality of life for patients with FM.”  [It is greatly to be hoped that future research will consider that much of these symptoms attributed to FM are actually due to co-existing TrPs, well-documented as causing sexual dysfunction in both male and female patients.  DJS]

Orenstein, S. R. 1994. The prone alternative. Pediatrics 94(1):104-5.

Orenstein, S. R., H. H. Magill and P. Brooks. 1987. Thickening of infant feedings for therapy of gastroesophageal reflux. J Pediatr 110(2):181-6.

Orenstein, S. R. and P. F. Whitington. 1983. Positioning for prevention of infant gastroesophageal reflux. J Pediatr 103(4):534-7.

Orenstein, S. R., P. F. Whitington and D. M. Orenstein. 1983. The infant seat as treatment for gastroesophageal reflux. N Engl J Med 309(13):760-3.

Orlandi AC, Ventura C, Gallinaro AL et al. 2012. Improvement in pain, fatigue, and subjective sleep quality through sleep hygiene tips in patients with fibromyalgia. Rev Bras Reumatol. 52(5):672-678. "The sleep hygiene instructions allowed changing the patients' behavior, which resulted in pain and fatigue improvement, increased subjective quality of sleep, in addition to facilitating falling asleep after waking up in the middle of the night."

Ormandy L. 1994. Scapulocostal syndrome.  Va Med Q. 121(2):105-108.  Much deep pain in the scapular region may be helped by “...infiltrating a trigger point in the subscapularis region of the medical aspect of the scapular spine (root of the scapular spine) with a mixture of 2cc plain 1% lidocaine hydrochloride...plus 1 cc beta-methasone sodium phosphate and acetate suspension...followed by physical therapy exercises.  190 patients (43.19%) received one block, 175 (39.77%) received two blocks, and 75 (17.04%) received three blocks.  Upon completion of treatment, 97.7% of the patients were relieved of their discomfort and returned to their original occupation.”  [Since this was published, one must wonder how many patients with similar symptoms have been subjected to unnecessary surgery.  DJS]

Orr, R. D. and G. Isaac. 1992. Religious variables are infrequently reported in clinical research.Fam Med 24(8):602-606.

Orr WC. 2005.  Therapeutic options in the treatment of nighttime gastroesophageal reflux.  Digestion 72(4):229-238.  “Approximately three quarters of individuals who suffer from gastroesophageal reflux disease (GERD) experience its symptoms at night.  Nighttime GERD symptoms disturb sleep and diminish quality of life more so than daytime symptoms.  Nighttime gastroesophageal reflux is common in individuals with respiratory disorders such as sleep apnea and asthma, and may affect the severity and the frequency of these disorders.  The treatments of choice for nighttime GERD symptoms are proton pump inhibitors (PPIs) due to their efficacy in relieving daytime and nighttime GERD symptoms and controlling acid secretion.”

Orr WC, Heading R, Johnson LF et al. 2004.  Review article: sleep and its relationship to gastro-oesophageal reflux.  Aliment Pharmacol Ther 20 Suppl 9:39-46.  “Obstructive sleep apnea syndrome and obesity seem to predispose patients to nocturnal GERD.  Recognition and treatment of night-time GERD are important because it can be associated with decreased quality of life (including sleep disruption) and increased risk of serious oesophageal and respiratory complications.”

Orstavik K, Norheim I, Jorum E. 2006.  Pain and small-fiber neuropathy in patients with hypothyroidism.  Neurology 67(5):786-791.  “Some patients treated for hypothyroidism have symptoms and findings compatible with small-fiber neuropathy or ‘hyperphenomena’ indicating central sensitization.”  This is another study showing a link between FMS and hypothyroid.

Ortancil O, Sanli A, Eryuksel R et al. 2010. Association between serum ferritin level and fibromyalgia syndrome. Eur J Clin Nutr. [Jan 20 Epub ahead of print]  “Iron is essential for a number of enzymes involved in neurotransmitter synthesis. Analysis of cerebrospinal fluid in fibromyalgia syndrome (FMS) has shown a reduction in the concentration of biogenic amine metabolites, including dopamine, norepinephrine and serotonin…. A total of 46 patients with primary FMS participated in this case-control study, and 46 healthy females who were age matched to the patients were used as the control group….Our study implicates a possible association between FM and decreased ferritin level, even for ferritin in normal ranges. We suggest that iron as a cofactor in serotonin and dopamine production may have a role in the etiology of FMS.”  [Decreased muscle ferritin level is also a perpetuating factor for TrPs, and TrPs often maintain FM central sensitization. One must be careful, however, as increased iron in post-menopausal women can increase cholesterol levels. For people with multiple co-existing interactive conditions it is not easy. DJS]

Ortega-Santiago R, de-la-Llave-Rincon AI, Laguarta-Val S et al. 2012. [Neurophysiological advances in carpal tunnel syndrome: process of central sensitization or local neuropathy]. Rev Neurol. 54(8):490-496. [Spanish] "Several studies…support the presence of a complex process of peripheral and central sensitization in patients with CTS which may constitute a negative prognosis factor for the management of these patients….The advances in neurosciences in the last years support the presence of peripheral and central sensitization mechanisms in CTS. These mechanisms justify the necessity of conceptual changes and in the management, both conservative and surgical, of this syndrome. Additionally, central sensitization can also play a relevant role in the prognosis of CTS since it can constitute a negative prognosis factor for its treatment.

Osborne NJ, Gatt IT. 2010. Management of shoulder injuries using dry needling in elite volleyball players. Acupunct Med. 28(1):42-45. “These case reports describe the short-term benefits of dry needling in shoulder injuries in four international female volleyball athletes during a month-long intense competitive phase, using both replicable subjective and objective measures. Dry needling of scapulohumeral muscles was carried out. Range of movement, strength and pain were assessed before and after treatment, with a functional assessment of pain immediately after playing and overhead activity, using the short form McGill Pain Questionnaire. All scores were improved post-treatment and athletes were able to continue overhead activities. Previous studies have suggested that myofascial trigger points may cause significant functional weakness and reduced range of motion, with referred pain. Trigger point dry needling has been successful in treating athletes with myofascial pain and impingement symptoms but with only subjective improvement and not during a competitive phase. These cases support the use of dry needling in elite athletes during a competitive phase with short-term pain relief and improved function in shoulder injuries. It may help maintain rotator cuff balance and strength, reducing further pain and injury.”  [Although this study was done on volleyball players, it can be extrapolated to professional sports.  Considering the amount of money involved with athletes and the invasiveness, expense and sometimes career-limiting effect of surgery, it is certainly in the interest of the insurance companies to become proficient in the field of myofascial pain.  Right now the reimbursement system doesn’t cover many myofascial treatments, but does cover the surgery, and this must be changed. Many rotator cuff and other soft tissue injuries could be treated effectively and risk of further injury minimized if the trigger points were treated. DJS] 

O’Shaughnessy, T. 1994. Craniomandibular/temporomandibular/cervical implications of a forced hyper-extension/hyper-flexion episode (ie., whiplash). Funct Orthod 11(2):5-10, 12.

Ostensen, M., A. Rugelsjoen and S. H. Wigers. 1997. The effect of reproductive events and alterations of sex hormone levels on the symptoms of fibromyalgia. Scand J Rheumatol 26(5):355-360.

Otadi K, Hadian MR, Talebian S et al. 2013. The effect of myofascial neck pain on postural control: visual deprivation. J Back Musculoskelet Rehabil. 26(4):375-380. "Our results showed that myofascial neck pain syndrome might be one of the disturbing factors on standing balance."

Otani K, Kikuchi S. 2005.  [Block treatment for low back pain-Technical note.]  Clin Calcium 15(3):437-441. [Japanese]  Trigger point block is one of the common procedures discussed in this paper on low back pain.

Otis J, Rothman M. 2006.  A Phase III study to assess the clinical utility of low-dose fentanyl transdermal system in patients with chronic nonmalignant pain.  Curr Med Res Opin. 22(8):1493-1501.  This lower-dose fentanyl may be of benefit to opioid-naive patients and the elderly.  It had a beneficial therapeutic effectiveness with a lessened drop out rate.

Ouyang A, Wrzos HF. 2006.  Contribution of gender to pathophysiology and clinical presentation of IBS: should management be different in women?  Am J Gastroenterol. 101 Suppl 3:S602-609.

Overlie, I., M. H. Moen, L. Morkrid, J. S. Skjaeraasen, and A. Holte.1999. The endocrine transition around menopause-a five-year prospective study with profiles of gonadotropins, estrogens, androgens, and SHBG among healthy women. Acta Obstet Gynecol Scand 78(7):643-7.

Ozcan U, Cao Q, Yilmaz E et al. 2004.  Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes.  Science 306(5695):457-461.

Ozel HE, Ozkiris M, Gencer ZK et al. 2013. Audiovestibular functions in noninsulin-dependent diabetes mellitus. Acta Otolaryngol. [Oct 16 Epub ahead of print]. "This study supports the proposition that vestibular dysfunction and sensorineural hearing loss (SNHL) may be considered among the complications due to noninsulin-dependent diabetes mellitus (NIDDM)….Hearing thresholds in all frequencies (except at 500 Hz for bone conduction) and SRS values were statistically significant in patients with NIDDM and control subjects, but there was no statistically significant difference according to the duration of the disease. Statistically significant alterations were present in VFT in patients with NIDDM compared with the control subjects."

Ozer D, Senbursa G, Baltaci G et al. 2009. The effect on neuromuscular stability, performance, multi-joint coordination and proprioception of barefoot, taping or preventative bracing. Foot (Edinb). 19(4):205-210. “… bracing and taping may play an important role in preventing injury or rehabilitation of the injured ankle by improving concentric and eccentric coordination, proprioception with the ability of reproducing motion in closed kinetic chain while decreasing vertical jump performance. No superiority of brace over tape or vice versa was found in this study.”

Ozgocmen S, Kaya A, Gulkesen A et al. 2006.  Comparison of pain threshold, health and functional status of females with fibromyalgia and multiple sclerosis: a pilot study.  Int J Psych Clin Pract. 10(3):160-165.  FMS and MS share many psychosocial and clinical features.  Controlling chronic pain, fatigue, social and emotional reactions and disability are important in both conditions.

 

Ozgocmen, Salih. 2005.  New strategies in evaluation of therapeutic efficacy in fibromyalgia syndrome.  Current Pharmaceutical Design [November Epub ahead of print].  “The use of multiple outcome variables reflecting the complexity of FM and co-morbid syndromes makes it difficult to evaluate the efficacy or effectiveness of the treatment in clinical trials.  Additionally, researchers inevitably rely on patients’ self-reported outcome data, which is prone to error and bias.”  “Clinicians and researchers now have various highly validated and adequate outcome domains to assess FM symptoms and new researches continue to add new valuable domains.  Nevertheless the current problem is to conclude which treatment works best for whom and which are the outcome domains suitable for FM patients or patients’ subgroups with different prominent features.  Standardized and appropriate core outcome domains for FM clinical trails will encourage more complete investigations, relevant outcome reporting and well-designed multicenter trials.”

 

Ozgocmen S, Ozyurt H, Sogut S et al. 2005.  Current concepts in the pathophysiology of fibromyalgia: the potential role of oxidative stress and nitric oxide.  Rheumatol Int. [Nov 20 Epub ahead of print]  “Researches on genetics, biogenic amines, neurotransmitters, hypothalamic-pituitary-adrenal axis hormones, oxidative stress, and mechanisms of pain modulation, central sensitization, and autonomic functions in FM revealed various abnormalities indicating that multiple factors and mechanisms are involved in the pathogenesis of FM.  Oxidative stress and nitric oxide may play an important role in FM pathophysiology; however, it is still not clear whether oxidative stress abnormalities documented in FM are the cause or the effect.  This should encourage further researches evaluating the potential role of oxidative stress and nitric oxide in the pathophysiology of FM and the efficacy of antioxidant treatments (omega-3 and –6 fatty acids, vitamins and others) in double blind and placebo controlled trials.”

Ozgocmen S, Ozyurt H., Sogut S et al. 2005.  Antioxidant status, lipid peroxidation, and nitric oxide in fibromyalgia: etiologic and therapeutic concerns.  Rheumatol Int. Nov 10:1-10.  [Epub ahead of print]  This article offers several possible therapeutic avenues for fibromyalgia treatment by indicating possible metabolic subsets.

Ozgocmen, S., Yoldas, T., Kamanli, A. et al. 2003.  Auditory P300 event related potentials and serotonin reuptake inhibitor treatment in patients with fibromyalgia.  Ann Rheum Dis 62(6):551-5.  P300 amplitude components of auditory event potentials, as measured by scalp electrodes, are associated with attention allocation, information and cognitive processing, and maintenance of working memory.  In fibromyalgia patients, P300 amplitudes are reduced.

Ozgocmen, S, Ardicoglu O, Lipid Profile in Patients with Fibromyalgia and Myofascial Pain Syndromes, Yonsei Medical Journal 41(5):541-545, 2000. Significant changes to the lipid profile seems to be part of the myofascial component rather than the fibromyalgia component when these conditions occur together.

Ozkan F, Cakir Ozkan N, Ekorkmaz U. 2011. Trigger point injection therapy in the management of myofascial temporomandibular pain. Agri 23(3):119-125. "Myofascial pain is the most common temporomandibular disorder.....Our results indicate that trigger point injection therapy combined with splint therapy is effective in the management of myofascial TMD pain. " Further research is needed. [One must be careful with splint use in TrPs, as immobility is a perpetuating factor of TrPs. One needs to treat all the TrPs affecting the TMJ, including the soleus. Unless one knows all TrPs, one may not know to check the calf for TrPs that can affect the jaw. DJS]

Oztürk O, Tek M, Seven H. 2012. Temporomandibular disorders in scuba divers - an increased risk during diving certification training. J Craniofac Surg. 23(6):1825-1829. The design and fit of a mouthpiece on SCUBA can increase the risk of developing TMJD and TrPs as the diver is constantly struggling to attain mouthpiece stability.

Pace JB, Nagle D. 1976.  Piriform syndrome. West J Med. 124(6):435-439.  Piriformis TrPs are often mistaken as discogenic pain, causing unnecessary pain, cost and delay of adequate treatment.  Symptoms can include female dyspareunia, low back pain and hip pain radiating down the leg, and muscle weakness.

 

Pachas WN, Bekken KN. 2007.  Development of fibromyalgia syndrome following traumatic brain injury.  J Musculoskel Pain 15 (Supp 13):56 item 100.  [Myopain 2007 Poster]  “In all patients there was a clear relationship between the time of their TBI (traumatic brain injury) and subsequent FMS.”   “The factors involved in TBI as the cause or as an initiating factor of FMS are unknown.  Our data suggest that there might be a connection between these disorders.”

 

Pachas WN, Bekken KN. 2007.  The role of memantine in the treatment of the memory dysfunction of patients with fibromyalgia syndrome.  J Musculoskel Pain 15 (Supp 13):42 item 73.  [Myopain 2007 Poster]  “Memantine improves memory and function in patients with Alzheimer’s.  The possibility that FMS patients may also benefit was explored in this trial.”  “Sixteen patients were treated with memantine, 3 patients did not improve.  The other patients had moderate to excellent response, some were able to return to work and most felt marked improvement in the quality of life.  Neuropsychological testing reflected some of these changes.”  “Memantine is an N-methyl-D-aspartic acid receptor antagonist.”  “Some of the patients on this trial had a remarkable improvement in their memory and could not function without it.  However, double-blind placebo-controlled studies should define the value of memantine in FMS.”

Packard C., Nunn A., Hobbs R. et al. 2002.  High density lipoprotein: guardian of the vascular system?  Int J Clin Pract 56(10):761-71.  “Patients with low HDL-C levels often have central obesity, insulin resistance and other features of the metabolic syndrome.  This syndrome is both increasingly common and strongly implicated in the growing worldwide epidemic of type 2 diabetes . . . . Although current guidelines are beginning to recognize the protective role of HDL-C level in preventing coronary events, HDL-C should be adopted soon as a target for intervention in its own right.”

Padamsee M, Mehta N, White GE. 1987.  Trigger point injection: a neglected modality in the treatment of TMJ dysfunction.  J Pedod. 12(1):72-92.

Pagotto U, Marsicano G, Cota D et al. 2005.  The emerging role of the endocannabinoid system in endocrine regulation and energy balance.  Endocr Rev. [Nov 23 Epub ahead of print]   [The role of the endocannabinoid system includes the modulation of all the endocrine hypothalamic-peripheral endocrine axes, control of reproduction and sexual behavior, control of appetite and energy balance and other  metabolic areas that are often imbalanced in FMS. DJS]

Painter JT, Crofford LJ, Talbert J. 2013. Geographic variation of chronic opioid use in fibromyalgia. Clin Ther. 35(3):303-311. "Opioid use for the treatment of chronic nonmalignant pain has increased drastically over the past decade. Although no evidence of efficacy exists supporting the treatment of fibromyalgia (FM) with chronic opioid therapy, a large number of patients are receiving this therapy....Geographic variation in chronic opioid use among patients with FM exists at rates similar to those seen in other studies examining opioid use. This large level of geographic variation suggests that the prescribing decision is not based solely on physician-patient interaction but also on contextual and structural factors at the state level. The level of physician and condition prevalence suggest that information dissemination and peer-to-peer interaction may play a key role in adopting evidence-based medicine for the treatment of patients suffering from FM and related conditions. Level of diagnosis prevalence as a predictor of evidence-based practice has not been reported in the literature and is an important contribution to research on geographic variation."

Paira, S. O. 1994. Fibromyalgia associated with female and urethral syndrome. Clin Rheumatol 13(1):88-89.

Paiva ES, Deodhar A, Jones KD, Bennett R. 2002. Impaired growth hormone secretion in fibromyalgia patients: Evidence for augmented hypothalamic somatostatin tone.  Arthritis Rheum 46(5):1344-50. "Because pyridostigmine is known to reduce somatostatin tone, it is surmised that the defective GH response to exercise in FM patients probably results from increased levels of somatostatin, a hypothalamic hormone that inhibits GH secretion."

 

Pal JS, Desai J, Bajwa Z. 2007.  Superior oblique muscle deinnervation: implications for differential innervation of myofascial trigger points.  J Musculoskel Pain 15 (Supp 13):66 item 117.  [Myopain 2007 Poster]  “SOM (superior oblique muscle) TrPs may be a cause, as opposed to a consequence, of headache.”  “Eye movement disorders increase risk for headache due to awkward head tilts and double vision.”

Palestini P, Calvi C, Conforti E et al. 2003.  Compositional changes in lipid microdomains of air-blood barrier plasma membranes in pulmonary interstitial edema.  J Appl Physiol 95(4):1446-1452.

Palm HG, Laufer C, von Luebken F et al. 2010. [Do meniscus injuries affect postural stability?] Orthopade. [Jan 20 Epub ahead of print]. [German]  Background: Meniscal lesions are known to cause a loss of proprioception, which plays an important role in the regulation of postural stability.  This study showed that in spite of  “…the presence of an arthroscopically confirmed meniscal lesion, none of the stability indexes that we calculated revealed significant differences in postural stability between the injured and uninjured sides…..It was surprising to note that the loss of proprioception in patients with meniscus injuries did not influence postural stability. Patients with functional knee instability must therefore be examined for the presence of further injuries because a meniscal lesion alone cannot explain instability symptoms.” [It is suggested the authors look for myofascial trigger points in the regions of the meniscal lesions in future research, as TrP are often associated with proprioceptor dysfunction. DJS]

Palomino RA, Nicassio PM, Greenberg MA et al. 2007.  Helplessness and loss as mediators between pain and depressive symptoms in fibromyalgia.  Pain. [Feb 28 Epub ahead of print]  “The findings confirm the importance of helplessness and demonstrate that the cognitive meaning of having FM plays a more central role in predicting depressive symptomatology than illness-related stressors, such as pain or disability.”

Palstam A, Gard G, Mannerkorpi K. 2013. Factors promoting sustainable work in women with fibromyalgia. Disabil Rehabil. [Jan 22 Epub ahead of print]. "Promoting factors for work were identified, involving individual and environmental factors. These working women with FM had developed advanced well-functioning strategies to enhance their work ability. The development of such strategies should be supported by health-care professionals as well as employers to promote sustainable work in women with FM… Working women with FM appear to have developed advanced well-functioning individual strategies to enhance their work ability. The development of individual strategies should be supported by health-care professionals as well as employers to promote sustainable work and health in women with FM."

Pang, S. F., L. Li, E. A. Ayre, C. S. Pang, P. P. Lee, R. K. Xu, P. H. Chow, Z. H. Yu and S. Y. Shiu. 1998. Neuroendocrinology of melatonin in reproduction: recent developments. J Chem Neuroanat 14(3-4):157-66.

Panton L, Simonavice E, Williams K et al. 2012. Effects of Class IV Laser Therapy on Fibromyalgia Impact and Function in Women with Fibromyalgia. J Altern Complement Med. [Nov 23 Epub ahead of print]. "This study provides evidence that LHT (laser heat therapy) may be a beneficial modality for women with FM in order to improve pain and upper body range of motion, ultimately reducing the impact of FM."

Panton LB, Kingsley JD, Toole T et al. 2006.  A comparison of physical functional performance and strength in women with fibromyalgia, age- and weight-matched controls, and older women who are healthy.  Phys Ther. 86(11):1479-1488.  “This study demonstrated that women with FM and older women who are healthy have similar lower-body strength and functionality, potentially enhancing the risk for premature age-associated disability.”

Paolisso, G., M. R. Tagliamonte, M. R. Rizzo and D. Giugliano. 1999. Advancing age and insulin resistance: new facts about an ancient history. Eur J Clin Invest 29(9):758-769.

Pappagallo, M. and L. J. Heinberg. 1997. Ethical issues in the management of chronic nonmalignant pain. Semin Neurol 17(3):203-211.

Pappagallo, M. 1998. Aggressive pharmacologic treatment of pain. Rheum Dis Clin North Am25(1):193-213, vii.

Papageorgiou AC, Silman AJ, Macfarlane GJ. 2002.  Chronic widespread pain in the population: a seven year follow up study.  Ann Rheum Dis. 61(12):1071-1074.  “Pain, once established, is likely to persist (or recur) especially if accompanied by other somatic symptoms and older age.”

Papageorgiou AC, Silman AJ, Macfarlane GJ. 2002.  Chronic widespread pain in the population: a seven-year follow up study.  Ann Rheum Dis 61(12):1071-1074.  “The proportion of subjects from a general population sample changing from CWP to no pain, or vice versa, over a seven year period was very low. This suggests that pain, once established, is likely to persist (or recur) especially if accompanied by other somatic symptoms and older age.”

Papazisis G, Tzachanis D. 2014. Pregabalin's abuse potential: a mini review focusing on the pharmacological profile. Int J Clin Pharmacol Ther. [May 21 Epub ahead of print.] "Pregabalin is approved for the treatment of partial epilepsy; generalized anxiety disorder; peripheral and central neuropathic pain and fibromyalgia. Its prescribing is rapidly increasing and total sales of the drug worldwide reached 4.6 billion US$ in 2012. Since entering widespread clinical use, reports of pregabalin abuse appeared more often, usually involving individuals with a history of abuse of other medications. The purpose of this mini review is to present available published data signaling pregabalin's abuse liability reflecting on the pharmacological characteristics that might enable this agent to trigger addictive behaviors."

Paradies, G., F. M. Ruggiero and P. Dinoi. 1991.  The influence of hypothyroidism on the transport of phosphate and on the lipid composition in rat-liver mitochondria.  Biochim Biophys Acta 1070(1):180-186.

Park AJ, Paraiso MF. 2009.  Successful use of botulinum toxin type A in the treatment of refractory postoperative dyspareunia.  Obstet Gynecol. 114(2 Pt 2):484-487.  “Refractory dyspareunia presents a challenging therapeutic dilemma.  Case: A woman with defecatory dysfunction and dysparenuria presented with stage 2 prolapse.  She underwent laparoscopic and vaginal pelvic floor reconstruction with excision of endometriosis.  The patient experienced increased dysparenuria and de novo vaginismus postoperatively that were refractory to trigger point injections, physical therapy, and medical and surgical management.  She underwent botulinum toxin type A injections into her levator ani muscles, which allowed her to have sexual intercourse again after 2 years of apareunia with no recurrence of pain for 12 months.  Conclusion: Injecting botulinum toxin into the levator ani muscles shows promise for postoperative patients who develop vaginismus and do not respond to conservative therapy.”  [Men and women with sexual dysfunction must be assessed for myofascial TrPs in the pelvic floor, including perineum, plus low abdominal wall and rectal and vaginal TrPs.   There is so much unnecessary misery (and cost) due to lack of training on the part of practitioners. DJS] 

Park AJ, Paraiso MF. 2009.  Successful use of botulinum toxin type a in the treatment of refractory postoperative dyspareunia.  Obstet Gynecol. 114(2 Pt 2):484-487.  [This is one more indication of pain on intercourse caused by trigger points.  Perhaps much of this could be prevented by TrP injections of topical anesthetic along the surgical incision sites, as recommended in the myofascial texts.  DJS]

Park CH, Huh BK, Lee SH et al. 2011. Efficacy of oblique fluoroscopic approach for stellate ganglion block. J Musculoskel Pain. 19(2):101-104. "The C7 oblique approach SGB (stellate ganglion block) showed the same SGB effects compared with the C7 anterior approach SGB, and did not cause hoarseness. We concluded that the C7 oblique approach SGB may be a beneficial method for patients." Spinal pathology is a frequent perpetuating factor for TrPs in CMP. It is good to have the safest options for controlling spinal pain. DJS]

Park CH, Lee YW, Kim YC et al. 2012. Treatment experience of pulsed radiofrequency under ultrasound guided to the trapezius muscle at myofascial pain syndrome - a case report. Korean J Pain. 25(1):52-54. "Trigger point injection treatment is an effective and widely applied treatment for myofascial pain syndrome. The trapezius muscle frequently causes myofascial pain in neck area. We herein report a case in which direct pulsed radio frequency (RF) treatment was applied to the trapezius muscle. .... RF treatment produced continuous pain relief when the effective duration of trigger point injection was temporary in myofascial pain."

Park HJ, Moon DE. 2010. Pharmacologic management of chronic pain. Korean J Pain. 23(2):99-108. "This article provides a mechanism- and evidence-based approach to improve the outcome for pharmacologic management of chronic pain. The usual approach to treat mild to moderate pain is to start with a nonopioid analgesic. If this is inadequate, and if there is an element of sleep deprivation, then it is reasonable to add an antidepressant with analgesic qualities. If there is a component of neuropathic pain or fibromyalgia, then a trial with one of the gabapentinoids is appropriate. If these steps are inadequate, then an opioid analgesic may be added. For moderate to severe pain, one would initiate an earlier trial of a long term opioid. Skeletal muscle relaxants and topicals may also be appropriate as single agents or in combination. Meanwhile, the steps of pharmacologic treatments for neuropathic pain include (1) certain antidepressants (tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors), calcium channel alpha(2)-delta ligands (gabapentin and pregabalin) and topical lidocaine, (2) opioid analgesics and tramadol (for first-line use in selected clinical circumstances) and (3) certain other antidepressant and antiepileptic medications (topical capsaicin, mexiletine, and N-methyl-d-aspartate receptor antagonists). It is essential to have a thorough understanding about the different pain mechanisms of chronic pain and evidence-based multi-mechanistic treatment. It is also essential to increase the individualization of treatment."

Park, J. H., P. Phothiamat, C. T. Oates, M. Hernanz-Schulman and N. J. Olsen. 1998.  Use of P-31 magnetic resonance spectroscopy to detect metabolic abnormalities in muscles of patients with fibromyalgia.  Arth Rheum 41(3):406-413.

Park JM, Kim CK, Lee HC et al. 2013. Antiallodynic effects of vitamin C and vitamin E in chronic post-ischemia pain rat model. Korean J Anesthesiol. 65(5):442-448. The authors of this study in rats concluded: "The reduced phosphorylated NR1 and ERK levels indicate that vitamins C and E inhibit the modulation of spinal cord neuropathic pain processing. Co-administration of vitamins C and E had a greater antiallodynic effect."

Park SC, Kim KH. 2012. Effect of adding cervical facet joint injections in a multimodal treatment program for long-standing cervical myofascial pain syndrome with referral pain patterns of cervical facet joint syndrome. J Anesth. [May 31 Epub ahead of print]. Addition of therapeutic CFJ (cervical facet joint) injections to a multimodal treatment program is a useful therapeutic modality for patients, especially young patients, suffering from long-standing MPS with referral pain of CFJ syndrome.

Park TJ, Comer C, Carol A et al. 2003.  Somatosensory organization and behavior in naked mole-rats: I - Peripheral structures, innervation, and selective lack of neuropeptides associated with thermoregulation and pain.  J Comp Neurol 465(1):104-20.  The naked mole-rat may be a lab model for fibromyalgia. 

Parr, T. 1996.  Insulin exposure controls the rate of mammalian aging.  Mech Ageing Dev 88(1-2):75-82.

Parrott, Tom. 1999.  Using opioid analgesics to manage chronic noncancer pain in primary care.  J Am Board Fam Pract 12:293-306.

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.

Pasisson TS, Graven-Neilsen T. 2012. Experimental pelvic pain facilitates pain provocation tests and causes regional hyperalgesia. Pain. 153(11):2233-2240. This study showed that an extra-articular sacroiliac joint structure (the long posterior sacroiliac ligament) can hold pain receptors that can cause referred pain and regional hyperalgesia that is sensitive to manual pain provocation testing.

Pasquali R, Vicennati V. 2000.  The abdominal obesity phenotype and insulin resistance are associated with abnormalities of the hypothalamic-pituitary-adrenal axis in humans.  Horm Metab Res 32(11-12):521-525.

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.”

Passik SD, Kirsh KL, Whitcomb L et al. 2004.  A new tool to assess and document pain outcomes in chronic pain patients receiving opioid therapy.  Clin Ther 26(4):552-561.  “In this study, the PADT appeared to be a useful tool for clinicians to guide the evaluation of several important outcomes during opioid therapy and provide a simple means of documenting patient care.”

Pastore A, Lanna M, Lombardo N et al. 2013. Intravenous infusion of magnesium sulphate during subarachnoid anesthesia in hip surgery and its effect on postoperative analgesia: our experience. Transl Med UniSa. 5:18-21. "Magnesium sulphate is the drug of choice in case of eclampsia, and pre-eclampsia (for the risk of evolution in eclampsia). According to the most recent findings, this drug has also analgesic properties: its use as an adjunct to analgesia is based on a non-competitive antagonism towards the NMDA receptor and on the blocking of calcium channels: these properties prevent the mechanisms of central sensitization due to nociceptive stimulation of peripheral nerves." [This study suggests that magnesium sulphate might prevent the development of central sensitization.] [Other studies show that once central sensitization has developed, magnesium sulphate will not reverse central sensitization. See: Pain Med. 2013 Jul 25. [Epub ahead of print] Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Fischer SG, Collins S, Boogaard S et al. DJS]

Pastore EA, Katzman WB. 2012. Recognizing Myofascial Pelvic Pain in the Female Patient with Chronic Pelvic Pain. J Obstet Gynecol Neonatal Nurs. 2012 Aug 3. [Epub ahead of print] "Myofascial pelvic pain (MFPP) is a major component of chronic pelvic pain (CPP) and often is not properly identified by health care providers. The hallmark diagnostic indicator of MFPP is myofascial trigger points in the pelvic floor musculature that refer pain to adjacent sites. Effective treatments are available to reduce MFPP, including myofascial trigger point release, biofeedback, and electrical stimulation. An interdisciplinary team is essential for identifying and successfully treating MFPP."

Patel SB, Kumar SK. 2012. Myofascial pain secondary to medication-induced bruxism. J Am Dent Assoc. 143(10):e67-69.

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]

Paul TM , Hoo JS, Chae J et al. 2012. Central Hypersensitivity in Patients with Subacromial Impingement Syndrome. Arch Phys Med Rehabil. [Jul 9 Epub ahead of print]. "This study provides further evidence that SIS (secondary hyperalgesia) patients have significantly lower PPTs (pain-pressure thresholds) than controls in both local and distal areas from their affected arm consistent with primary and secondary hyperalgesia, respectively. Data suggest the presence of central sensitization among subjects with chronic SIS."

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.

Pavlou M, Quinn C, Murray K et al. 2010. The effect of repeated visual motion stimuli on visual dependence and postural control in normal subjects. Gait Posture. [Dec 6 Epub ahead of print]. "Patients with vestibular dysfunction, migraine and/or anxiety may experience visual vertigo (VV), whereby symptoms are provoked by disorienting visual environments (e.g., supermarkets). Patients with VV over rely on vision for balance (i.e., visually dependent). Visual vertigo significantly improves when vestibular rehabilitation incorporates exposure to optokinetic stimulation (OKS). However, whether OKS exposure induces a reduction in visual dependency is unknown. This study investigated this issue by measuring visual dependency before and after repeated OKS exposure. Twenty-six healthy subjects (10 males; mean age 29.8 years, range 20-42 years) were randomly allocated into an OKS group who underwent graded OKS exposure for five consecutive days, or a no intervention control group. Assessment included the 'Rod and Frame' and 'Rod and Disc' tests where subjects set the subjective visual vertical in darkness, facing a tilted luminous frame or luminous rotating disc, respectively. Postural sway measures were obtained with eyes open, closed and facing the rotating disc. Results showed significant reductions in subjective vertical tilt with the frame and rotating disc for the OKS group only.... Total sway path and mean deviation induced by the rotating stimulus decreased significantly only for the OKS group (p<0.01), as did the Kinetic Quotient (disc rotation/eyes open sway path ratio; p=0.04). The Romberg Quotient (eyes closed/eyes open ratio) showed no change. Findings suggest visual dependency, both at a perceptual and a postural level, can be reduced with short-term graded OKS exposure in healthy subjects. This has important implications for treatment of patients with VV and balance disorders."

Paxton SE. 2011. Perioperative care of the patient with fibromyalgia. AORN J. 93(3):380-389.

Payne P, Crane-Godreau MA. 2012. Meditative movement for depression and anxiety. Front Psychiatry. 4:71. This review from Dartmouth "…focuses on Meditative Movement (MM) and its effects on anxiety, depression, and other affective states. MM is a term identifying forms of exercise that use movement in conjunction with meditative attention to body sensations, including proprioception, interoception, and kinesthesis. MM includes the traditional Chinese methods of Qigong (Chi Kung) and Taijiquan (Tai Chi), some forms of Yoga, and other Asian practices, as well as Western Somatic practices; however this review focuses primarily on Qigong and Taijiquan…. Results suggest that MM may be at least as effective as conventional exercise or other interventions in ameliorating anxiety and depression; however, study quality is generally poor and there are many confounding factors. This makes it difficult to draw definitive conclusions at this time. We suggest, however, that more research is warranted, and we offer specific suggestions for ensuring high-quality and productive future studies."

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]

Pedrelli A, Stecco C, Day JA. 2009. treating patellar tendinopathy with fascial manipulation. J Bodyw Mov Ther 13(1):73-80. Trigger points in quadriceps muscles can cause kneecap pain with motor incoordination. Fascial manipulation technique of the quadriceps may relieve kneecap pain and dysfunction, and thus the focus of therapy may need to be the anterior thigh.

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

Pelin Z, Karadeniz D, Ozturk L et al. 2003.  The role of mean inspiratory effort on daytime sleepiness.  Eur Respir J 21(4):688-694.  “The data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.”

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.

Peng PW. 2012. Tai Chi and Chronic Pain. Reg Anesth Pain Med. [May 17 Epub ahead of print]. Most tai chi studies were found to be of low quality. "Only 5 pain conditions were reviewed: osteoarthritis, fibromyalgia, rheumatoid arthritis, low back pain, and headache. Of these, Tai Chi seems to be an effective intervention in osteoarthritis, low back pain, and fibromyalgia."

Peng PW, Castano ED. 2005.  Survey of chronic pain practice by anesthesiologists in Canada.  Can J Anaesth. 52(4):383-389.  “While 38% of responding anesthesiologists were involved in CPP (chronic pain practice), in the majority of cases, this accounted for less than 20% of their clinical time.  Thirty percent of those involved in CPP had previous training in pain management.  The types of CPP included nerve blocks (84%) and pharmacological treatment (60%) in non-cancer pain (85%) and cancer pain (50%) patients.”  “Approximately one-third of anesthesiologists surveyed incorporate chronic pain in their practice and their pattern of practice is widely diversified.”  Only 30% of these anesthesiologists had previous training in chronic pain management.  Trigger point injections were responsible for 70% of this work.  [One must wonder how many of the patients had proper placement and range of motion stretching for their injections, and how much was done to identify and control the perpetuating factors–both minimal and necessary parts of proper treatment of TrPs. DJS]

Peng ZF. 2008.  [Comparison between western trigger point of acupuncture and traditional acupoints]  Zhongguo Zhen Jiu. 28(5):349-352.  “Trigger point theory as the soul of western acupuncture is very similar to acupoint theory of traditional acupuncture and moxibustion science.  After comparison, it is found that over 92% of trigger points (235/255) is corresponding to acupoints in anatomy, and the local pain treated by 79.5% acupoints are similar to corresponding myofascial trigger point.  Both of them can induce similar linear propagation of needling response, with complete uniform or basically complete uniform of 76%, and a part uniform of 14%; next, both of them can treat symptoms of internal organs such as diarrhea, constipation, dysmenorrheal, etc.  Therefore, they are very similar in anatomic location, clinical indications, and the linear propagation of needling response induced by acupuncture, etc.

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.

Penrod JR, Bernatsky S, Adam V et al.  2004.  Health services costs and their determinants in women with fibromyalgia.  J Rheumatol. 31(7):1391-1398.  Women with FMS use a high level of both conventional and complementary medical services.  Although there are significant direct costs associated with FMS, 70% of the economic burden on the patient is indirect, and often unrecognized.

Perea G, Navarrete M, Araque A. 2009.  Tripartite synapses: astrocytes process and control synaptic information.  Trends Neurosci. 32(8):421-431.  This explanation of a three part synaptic system of information flow between pre- and post-synaptic neurons, astrocytes (glial cells) is elegant.  The astrocytes not only respond to synaptic transmission but regulate it.  [Astrocytes are the controllers of neural plasticity, including the central sensitization of FM. DJS]  Contrasting to the old view of neuron dominance of information exchange in the central nervous system, the emerging view indicates that the synaptic activity is a coordinated effort by both the glial and the neurons. 

 

Perea G, Araque A. 2005.  Glial calcium signaling and neuron-glia communication.  Cell Calcium [ Aug 13 Epub ahead of print]  “There is a new concept of the synaptic physiology - ‘the tripartite synapse’, where astrocytes exchange information with the pre- and post-synaptic elements and participate as dynamic regulatory elements in neurotransmission.  The control of the Ca(2+) excitability in astrocytes is a key element in this loop of information exchange.  The ability of astrocytes to respond to neuronal activity and discriminate between the activity of different synapses, the modulation of the astrocytic cellular excitability by the synaptic activity, and the expression of cellular intrinsic properties indicate that astrocytes are endowed with cellular computational characteristics that process synaptic information.”

Peres JF, Goncalves AL, Peres MF. 2009.  Psychological trauma in chronic pain: implications of PTSD for fibromyalgia and headache disorders.  Curr Pain Headache Rep. 13(5):350-357.  “The association of traumatic exposures with posttraumatic stress disorder (PTSD) and other mental health conditions is well known.  Patients with chronic pain, particularly headache disorders and fibromyalgia (FM), associated with psychological traumas need a special management strategy.  Diagnosis of headache disorders and FM in traumatized patients and collecting the clinical history of a traumatic event or diagnosing PTSD in chronic pain patients is of great importance.  Psychotherapy and pharmacotherapeutic options should be started on patients with comorbid PTSD and headache disorders and/or FM.”  [This article would have been well-served if the authors had included myofascial TrPs as part of the picture, as they so obviously are.  Recent research abound in which headaches are part of myofascial pain rather than FM. DJS]

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.

Perez-de-Heredia-Torres M, Martínez-Piedrola RM et al. 2013. Bilateral deficits in fine motor control ability and manual dexterity in women with fibromyalgia syndrome. Exp Brain Res. [Jan 26 Epub ahead of print]. "Our findings revealed bilateral deficits in fine motor control ability and manual dexterity in patients with FMS without symptoms in the upper extremity. These deficits are not related to the clinical features of the symptoms supporting an underlying central mechanism of altered motor control." [These patients should be assessed for the presence of latent TrPs, as they are known (or should be) to co-exist with FM, and can cause deficits in fine motor control and manual dexterity. DJS]

Perez-Palomares S, Olivan-Blazquez B, Magallon-Botaya R et al. 2010. Percutaneous electrical nerve stimulation versus dry needling: effectiveness in the treatment of chronic low back pain. J Musculoskel Pain. 18(1). “At least one TrP was found in all patients, most commonly situated in the quadratus lumborum muscle [97.6 percent]. The improvement achieved for both treatment groups was similar in all the measured variables, although the DN (dry needling) group carried out fewer sessions than the PENS (percutaneous electrical nerve stimulation) group.”  [The term “chronic low back pain” is a description, not a diagnosis, and our reimbursement system must be set up to reflect this.  Quadratus lumborum TrPs are potentially disabling and can cause tremendous amount of pain and dysfunction, and must be part of the assessment for causes of chronic low back pain.  DJS]

Pergolizzi J, Ahlbeck K, Aldington D et al. 2013. The development of chronic pain: physiological CHANGE necessitates a multidisciplinary approach to treatment. Curr Med Res Opin. [Jul 3 Epub ahead of print]. "Chronic pain is currently under-diagnosed and under-treated, partly because doctors' training in pain management is often inadequate. This situation looks certain to become worse with the rapidly increasing elderly population unless there is a wider adoption of best pain management practice. This paper reviews current knowledge of the development of chronic pain and the multidisciplinary team approach to pain therapy. The individual topics covered include nociceptive and neuropathic pain, peripheral sensitization, central sensitization, the definition and diagnosis of chronic pain, the biopsychosocial model of pain and the multidisciplinary approach to pain management. This last section includes an example of the implementation of a multidisciplinary approach in Belgium and describes the various benefits it offers; for example, the early multidimensional diagnosis of chronic pain and rapid initiation of evidence-based therapy based on an individual treatment plan. The patient also receives continuity of care, while pain relief is accompanied by improvements in physical functioning, quality of life and emotional stress. Other benefits include decreases in catastrophizing, self-reported patient disability, and depression. Improved training in pain management is clearly needed, starting with the undergraduate medical curriculum, and this review is intended to encourage further study by those who manage patients with chronic pain."

Pergolizzi JV Jr, Raffa RB, Taylor R Jr. 2014. Treating Acute Pain in Light of the Chronification of Pain. Pain Manag Nurs. 15(1):380-390. "The progression of acute to chronic pain, also known as pain chronification, remains incompletely understood. Biologic factors involved in this transition include central sensitization, neuroplastic changes, altered pain modulation, and changes to the "neuromatrix." Chronic pain may involve irreversible pathophysiologic changes, so interrupting the cascade of events that allows acute pain to advance to chronic pain is of crucial importance. This involves recognition and prompt treatment of acute pain, better awareness and application of evidence-based guidelines on pain management by all clinicians (not just pain specialists), and patient education. By interrupting nociceptive input in acute pain conditions, it might be possible to prevent transition to chronic pain syndromes."

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.

Perrot S. 2012. If fibromyalgia did not exist, we should have invented it. A short history of a controversial syndrome. Reumatismo. 64(4):186-193. "Fibromyalgia is a recent disease, and some physicians remain doubtful about its reality. The history of fibromyalgia is a story of controversies: the fight between subjectivity and cartesianism, and between old mind and body concepts. Fibromyalgia represents the emblematic condition of unexplained medical symptoms, far from well-defined diseases with objective biomarkers. In this review we will follow the fibromyalgia story along the ages and sciences to better understand this complex pain disorder, between soma and psyche, and between medicine and psycho-sociology and to demonstrate that fibromyalgia exists; we have not invented it."

Perrot S, Choy E, Petersel D et al. 2012. Survey of physician experiences and perceptions about the diagnosis and treatment of fibromyalgia. BMC Health Serv Res. 12(1):356. "Fibromyalgia (FM) is a condition characterized by widespread pain and is estimated to affect 0.5-5% of the general population. Historically, it has been classified as a rheumatologic disorder, but patients consult physicians from a variety of specialties in seeking diagnosis and ultimately treatment. Patients report considerable delay in receiving a diagnosis after initial presentation, suggesting diagnosis and management of FM might be a challenge to physicians....A questionnaire survey of 1622 physicians in six European countries, Mexico and South Korea was conducted. Specialties surveyed included primary care physicians (PCPs; n=809) and equal numbers of rheumatologists, neurologists, psychiatrists and pain specialists. The sample included experienced doctors, with an expected clinical caseload for their specialty. Most (>80%) had seen a patient with FM in the last 2 years. Overall, 53% of physicians reported difficulty with diagnosing FM, 54% reported their training in FM was inadequate, and 32% considered themselves not knowledgeable about FM. Awareness of American College of Rheumatology classification criteria ranged from 32% for psychiatrists to 83% for rheumatologists. Sixty-four percent agreed patients found it difficult to communicate FM symptoms, and 79% said they needed to spend more time to identify FM. Thirty-eight percent were not confident in recognizing the symptoms of FM, and 48% were not confident in differentiating FM from conditions with similar symptoms. Thirty-seven percent were not confident developing an FM treatment plan, and 37% were not confident managing FM patients long-term. In general, rheumatologists reported least difficulties/greatest confidence, and PCPs and psychiatrists reported greatest difficulties/least confidence....Diagnosis and managing FM is challenging for physicians, especially PCPs and psychiatrists, but other specialties, including rheumatologists, also express difficulties. Improved training in FM and initiatives to improve patient-doctor communication are needed and may help the management of this condition. [This free article is available on the Internet, and confirms what many patients know all too well. DJS]

Perrot S, Schaefer C, Knight T et al. 2012. Societal and individual burden of illness among fibromyalgia patients in France: Association between disease severity and OMERACT core domains. BMC Musculoskel Disord. 13(1):22. "In a sample of 88 patients with FM from France, we found that FM poses a substantial economic and human burden on patients and society. FM severity level was significantly associated with patients' health status and core symptom domains."

Perruccio AV, Power JD, Badley EM. 2007.  The relative impact of 13 chronic conditions across three different outcomes.  J Epidemiol Community Health 61(12):1056-1061.  “At the individual level, fibromyalgia/chronic fatigue syndrome and cancer, and to a lesser extent stroke and heart disease, were associated with an increased risk of both activity limitations and a self-rated health status of fair or poor…”  “Differences in the ranking of individual risks and population attributable fractions for different disease and outcomes are substantial.  This needs to be taken into account when setting priorities, as interventions may need to be targeted to different conditions depending on which aspects of health are being considered, and whether the focus is on individuals, such as in clinical care, or improving the health of the population.”

 

Perry CP. 2001.  Current concepts of pelvic congestion and chronic pelvic pain.  JSLS 5(2):105-110.  Pelvic congestion is a common contributor of pelvic pain.  Although recognized in the United Kingdom, it is controversial in the United States. [This paper refers to it as a condition, but it is a symptom.  The causes of pelvic congestion include blood and lymph vessel entrapment by myofascial TrPs, and this cause is treatable.  DJS]

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.”

Petra AI, Panagiotidou S, Stewart JM et al. 2014. Spectrum of mast cell activation disorders. Expert Rev Clin Immunol. [May 1 Epub ahead of print.] "Mast cell (MC) activation disorders present with multiple symptoms including flushing, pruritus, hypotension, gastrointestinal complaints, irritability, headaches, concentration/memory loss and neuropsychiatric issues. These disorders are classified as: cutaneous and systemic mastocytosis with a c-kit mutation and clonal MC activation disorder, allergies, urticarias and inflammatory disorders and mast cell activation syndrome (MCAS), idiopathic urticaria and angioedema. MCs are activated by IgE, but also by cytokines, environmental, food, infectious, drug and stress triggers, leading to secretion of multiple mediators. The symptom profile and comorbidities associated with these disorders, such as chronic fatigue syndrome and fibromyalgia, are confusing. We propose the use of the term 'spectrum' and highlight the main symptoms, useful diagnostic tests and treatment approaches." [These interactive conditions may be much more common than now suspected. DJS]

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.

Pfau DB, Rolke R, Nickel R et al. 2009.  Somatosensory profiles in subgroups of patients with myogenic temporomandibular disorders and fibromyalgia syndrome.  [Sep 18 Epub ahead of print]

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.

Piao S, He Y, Yuan F. 1998.  [The effects of transcutaneous electrical stimulation during sleep on obstructive sleep apnea]  Zhonghua Jie He He Hu Xi Za Zhi 21(8):492-493. [Chinese]  “TES is a conservative but effective treatment in patients with obstructive sleep apnea syndrome, although it failed to improve central sleep apnea.”

 

Picavet HS, Hoeymans N.  2004.  Health related quality of life in multiple musculoskeletal disease SF-36 and EQ-5D in the DMC3 study.  Ann Rheum Dis. 63(6):723-729.  This study included patients with osteoarthritis, fibromyalgia, rheumatoid arthritis and osteoporosis.  “The co-existence of musculoskeletal diseases should be taken into account in research and clinical practice because of its high prevalence and its substantial impact on health related quality of life.”

Picelli A, Ledro G, Turrina A et al. 2011. effects of myofascial technique in patients with subacute whiplash associated disorders: a pilot study. Eur J Phys Rehabil Med 47(4):561-568. "Myofascial techniques may be useful for improving treatment of subacute whiplash associated disorders also reducing their economic burden."

Pieczenik SR, Neustadt J. 2007.  Mitochondrial dysfunction and molecular pathways of disease.  Exp Mol Pathol. [Jan 17 Epub ahead of print]  This study proposes that many conditions, including fibromyalgia, have “...underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mt DNA) damage, resulting in mitochondrial dysfunction.. Antioxidant therapies hold promise for improving mitochondrial performance.”  The authors suggest that clinicians consider testing urinary organic acids to determine how best to treat these patients.

 

Pielsticker A, Haag G, Zaudig M et al. 2005.  Impairment of pain inhibition in chronic tension-type headache.  Pain [Sep 30 Epub ahead of print].  These findings suggest that patients with CTTH (chronic tension type headache) suffer from deficient DNIC (diffuse noxious inhibitory controls)-like pain inhibitory mechanisms in a similar manner, as do patients with anatomically generalized chronic pain like fibromyalgia.”

 

Pierrynowski MR, Tiidus PM, Galea V. 2005.  Women with fibromyalgia walk with an altered muscle synergy.  Gait Posture 22(3):210-218.  “Results show that FS (fibromyalgia syndrome) and CV (control volunteers) walk with externally similar stride lengths, times and velocities, and joint angles and ground reaction forces but they use internally different muscle recruitment patterns.  Specifically, FS preferentially power gait using their hip flexors instead of their ankle plantar flexors.”  [This may cause a tendency to develop myofascial TrPs in specific muscles, or may enhance certain muscle fatigue. DJS]

Pierson MJ. 2011. Changes in temporomandibular joint dysfunction symptoms following massage therapy: a case report. Int J Ther Massage Bodywork. 4(4):37-47. "Ten 45-minute massage therapy treatments were administered over a five-week period. The client's progress was monitored by an initial, midway, and final assessment, using range of motion testing, personal interview, an orthopedic test, and postural analysis.....The client participated in a home care routine consisting of stretches, self-massage, postural training, a proprioception exercise, and hydrotherapy.....Results include an increase in maximal opening from 3.1 cm to 3.8 cm, an overall increase in neck range of motion, a decrease in muscle hypertonicity using the Wendy Nickel's Scale, a decrease in pain from 7/10 to 3/10 on a numerical pain scale, and a decline in stress. [TMJD is often due to TrPs, and this combination of therapies deserves further study. DJS]

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.”

Pimentel MJ, Gui MS, Reimao R et al. 2014. Sleep quality and facial pain in fibromyalgia syndrome. Cranio. [Jul 16 Epub ahead of print.] "Fibromyalgia patients experience intense facial pain in addition to poor sleep and high disabilities. TMD and FMS association do not appear to worsen this condition; however, facial pain intensity was correlated with low sleep quality." [These patients were not assessed for co-existing CMP. DJS]

Pinals RS, Hassett AL. 2013. Reconceptualizing John F. Kennedy's Chronic Low Back Pain. Reg Anesth Pain Med. [Jul 29 Epub ahead of print]. "When the medical records for John Fitzgerald Kennedy were made public, it became clear that the 35th President of the United States suffered greatly from a series of medical illnesses from the time he was a toddler until his assassination in November of 1963. Aside from having Addison disease, no condition seemed to cause him more distress than did his chronic low back pain. A number of surgical procedures to address the presumed structural cause of the pain resulted in little relief and increased disability. Later, a conservative program, including trigger point injections and exercises, provided modest benefit. Herein, the mechanisms underlying his pain are evaluated based on more contemporary pain research. This reconceptualizing of John Fitzgerald Kennedy's pain could serve as a model for other cases where the main cause of the pain is presumed to be located in the periphery."

Pincus T, Castrejón I, Bergman MJ et al. 2012. Treat-to-target: not as simple as it appears. Clin Exp Rheumatol. [Oct 16 Epub ahead of print]. "Treat-to-target as a strategy for rheumatoid arthritis (RA) is now widely advocated based on strong evidence. Nonetheless, implementation of treat-to-target raises caveats, as is the case with all clinical care strategies. The target of remission or even low disease activity does not apply to all individual patients, some of whom are affected by concomitant fibromyalgia, other comorbidities, joint damage, and/or who simply prefer to maintain current status and avoid risks of more aggressive therapies. No single universal 'target' measure or index exists for all individual RA patients. An emphasis in most studies on radiographic progression, rather than physical function or mortality, as the most important outcome to document the value of treat-to-target may be inappropriate. Many reports imply that the only limitation to treating all RA patients with biological agents involves costs, ignoring effective results in most patients with methotrexate and other disease-modifying anti-rheumatic drugs (DMARDs) and adverse events associated with biological agents. Indeed, the best outcomes in reported RA clinical trials result from tight control with DMARDs, rather than from biological agents, as does better overall status of RA patients at this time compared to previous decades. Pharmacoeconomic reports may ignore that RA patients are older, less educated, and have more comorbidities than the general population, as well as critical differences in patient status according to the gross domestic product of different countries. While treating to a target of remission or low disease activity, including with biological agents, is appropriate for many patients, awareness of these concerns could improve implementation of treat-to-target for optimal care of all RA patients." [Many patients have RA, FM and CMP and other conditions as well. Improvement of one condition often improves quality of life, although it may not affect the radiological images. Clinicians must learn to treat the patients and not the diagnostic images. DJS]

Pinquart M, Shen Y. 2010. Depressive Symptoms in Children and Adolescents with Chronic Physical Illness: An Updated Meta-Analysis. J Pediatr Psychol. [Nov 18 Epub ahead of print]. "Pediatricians and others working with children with chronic illnesses should screen children with chronic physical illness for symptoms of psychological distress and make appropriate referrals for mental health services, when needed."[All co-existing conditions should be screened for, and psychologists must be aware that co-existing conditions such as vestibular dysfunction, fibromyalgia and myofascial pain may have some symptoms that may be mistaken for psychological. Lack of support for chronic invisible illnesses can often lead to psychological distress. DJS]

Pinto Fiamengui LM, Freitas de Carvalho JJ, Cunha CO et al. 2013. The influence of myofascial temporomandibular disorder pain on the pressure pain threshold of women during a migraine attack. J Orofac Pain. 27(4):343-349. Thirty-four women between the ages of 18-60 were separated into a group with migraine and one with migraine and myofascial pain, that later category being assumed as the same as temporomandibular pain. The pressure pain threshold (PPT) on the masseter, anterior temporalis, and Achilles tendon were taken by algometer when the patients were pain free, and during a migraine. "Results: Significantly lower PPT values were found during the migraine attack, especially for women with concomitant myofascial pain, regardless of the side of the reported pain. Conclusion: Migraine attack is associated with a significant reduction in PPT values of masticatory muscles, which appears to be influenced by the presence of myofascial TMD pain." [Dentists, and psychologists, must become aware of pain and dysfunction-generating TrPs that can occur over the whole body, so that they cease the confusing use of "myofascial pain" as synonymous with TMJD. DJS]

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.”

Pitcher GM, Ritchie J, Henry JL. 2013. Peripheral neuropathy induces cutaneous hypersensitivity in chronically spinalized rats. Pain Med. 14(7):1057-1071. "Our findings demonstrate an aberrant peripheral/spinal mechanism that induces and maintains thermal and to a greater degree tactile cutaneous hypersensitivity in the cuff model of neuropathic pain, and raise the prospect that altered peripheral/spinal nociceptive mechanisms in humans with peripheral neuropathy may have a pathologically relevant role in both inducing and sustaining neuropathic pain."

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.

Plazier M, Dekelver I, Vanneste S et al. 2013. Occipital nerve stimulation in fibromyalgia: A double-blind placebo-controlled pilot study with a six-month follow-up. Neuromodulation. [Oct 7 Epub ahead of print]. "The goal of this study is to evaluate the effectiveness of occipital nerve stimulation (ONS) as a surgical treatment for fibromyalgia in a placebo-controlled design….Eleven patients were selected based on the American College of Rheumatology-90 criteria and implanted with an occipital nerve trial-lead stimulator. Baseline scores for pain, mood, and fatigue were acquired, and patients were randomized in a ten-week double-blinded crossover design with placebo and effective subsensory threshold stimulation (no paresthesias). After finalizing the trial, nine patients were implanted permanently; evaluation was performed prior to surgery and at six months after surgery for pain, fatigue, and mood of the number of trigger points and overall morbidity. Significant results were found during the trial for a decrease in pain intensity (39.74%) on visual analogue scale …and pain catastrophizing scale (PCS) during effective stimulation. A total of 9/11 patients responded to trial treatment; however, in two patients, this might be a placebo effect, recognizable due to the study design. Six months after permanent implantation, pain intensity remained decreased (44.01%) on VAS…. Besides the VAS, significant changes were noted for PCS, fatigue (modified fatigue impact scale), the number of trigger points, and overall morbidity (fibromyalgia impact questionnaire). There were no serious adverse events. Our data strongly suggest that ONS is beneficial in the treatment of fibromyalgia. The beneficial effects are stable at six months after permanent implantation. Subsensory threshold stimulation is feasible in designing a placebo-controlled trial." [Although the authors recognize the importance of the "trigger point count", they fail to recognize the trigger points as the actual generators of pain and dysfunction. Perhaps if the trigger points had been treated and perpetuating factors identified and controlled, the surgery would not have been necessary. Then again, the surgery might have taken care of some of the perpetuating factors. We will not know, because the authors did not understand the role of the trigger points. DJS]

Plazier M, Ost J, Stassijns G et al. 2014. Pain characteristics in fibromyalgia: understanding the multiple dimensions of pain. Clin Rheumatol. [Jul 22 Epub ahead of print.] "Fibromyalgia is a common disease with a high economic burden. The etiology of this disease remains unclear, as there are no specific abnormalities on clinical or technical examinations. Evidence suggests that central pain sensitization at the brain pain matrix might be involved. Understanding the pain characteristics of this disease is of importance both for diagnosis and treatment. … We were able to define pain characteristics in this group of patients. The reciprocal effects of mood and fatigue on pain experience could be identified within the data; catastrophizing scores show a high correlation with overall life quality and pain experience. We have performed a cluster analysis on the fibromyalgia patients, based on the four main principal components defining the overall disease burden. Mood explained most of the variance in symptoms, followed by mental health state, fatigue, and catastrophizing. Three clusters of patients could be revealed by these components. Clusters: 1) high scores on mood disorders, pain, and decreased mental health, 2) high scores on fatigue and physical health, and 3) a mixture of these two groups. This data suggest that different subgroups of fibromyalgia patients could be identified and based on that, treatment strategies and results might be adapted."

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).”

Pogatzki-Zahn EM, Englbrecht JS, Schug SA. 2009.  Acute pain management in patients with fibromyalgia and other diffuse chronic pain syndromes.  Curr Opin Anaesthesiol. [Jul 13 Epub ahead of print].  Adequate pain management of acute pain is of vital necessity for patients with the central sensitization of FM.  [It is also of vital necessity for others to help prevent FM central sensitization. DJS]

Polat A, Ekinci O, Terzioglu B et al. 2011. Treatment of lateral epicondylitis using betahistine dihydrochloride. J Musculoskel Pain. 19(4):201-206. The description of lateral epicondylitis is often given to pain in the area caused by myofascial TrPs, and TrP twitch causes excess histamine at the motor endplate. Betahistadine is a histamine agonist. Interesting. DJS]

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 D, Spath M. 2001.  [What helps in back pain? Guideline for symptomatic therapy] MMW Fortschr Med. 143(18):26-29. [German]  “Both in acute and chronic, unspecific back pain, the myofascial pain syndrome resulting in muscular dysbalance is a major factor.  For the differential diagnosis, however, consideration must always be given to concomitant symptoms (neurological deficits, general symptoms, signs of osteopathy).  Pathophysiologically, the active trigger point corresponds to a contraction in the muscle fibers that forms in the region of the a neuromuscular endplate, and leads, via biochemical processes, to the stimulation of mesochymal nociceptors.  Symptomatic treatment of acute and chronic back pain may be broken down into a) physical measures, b) local therapeutic regimens, and c) systemic pharmacotherapy.  As medication, non-steroidal anti-inflammatory drugs, non-opioid analgesics, opioids analgesics, muscle relaxants, and antidepressives are available, and are dose-matched to the severity and stage of the condition.  The spectrum of therapeutic options is outlined.”

 

Pongratz DE, Spath M. 1998.  [Myofascial pain syndrome – frequent occurrence and often misdiagnosed]  Fortschr Med. 116(27):24-29.  “The difference between trigger points (MPS) and tender points (fibromyalgia) is of central importance – not merely in a linguistic sense.  Knowledge of the signs and symptoms typically associated with a trigger point often obviates the need for time-consuming and expensive technical diagnostic measures.  The assumption that many cases of unspecific complaints affecting the musculoskeletal system may be ascribed to MPS makes clear the scope for the saving of costs.”

 

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 DE, Spath M. 1998.  [Myofascial pain syndrome – frequent occurrence and often misdiagnosed].  Fortschr Med 116(27):24-9.[German]

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.

Ponikau JU, Sherris DA, Weaver A et al. 2005.  Treatment of chronic rhinosinusitis with intranasal amphotericin B: a randomized, placebo-controlled, double-blind pilot trial.  J Allergy Clin Immunol. 115(1):125-131.  “Intranasal amphotericin B reduced inflammatory mucosal thickening on both CT scan and nasal endoscopy and decreased the levels of intranasal markers for eosinophilic inflammation in patients with CRS.”  Ampho B nasal spray may be an effective and relatively safe treatment for chronic fungal sinusitis.

Pontari M, Giusto L. 2013. New developments in the diagnosis and treatment of chronic prostatitis/chronic pelvic pain syndrome. Curr Opin Urol. 23(6):565-569. "Symptoms in men with chronic prostatitis/CPPS appear to cluster into a group with primarily pelvic or localized disease, and a group with more systemic symptoms. Several other chronic pain conditions can be associated with chronic prostatitis/CPPS, including irritable bowel syndrome, fibromyalgia, and chronic fatigue syndrome. Markers of neurologic inflammation and autoimmune disease parallel changes in symptoms after treatment. Treatment options include new alpha-blockers, psychological intervention, and prostate-directed therapy. The areas of acupuncture and pelvic floor physical therapy/myofascial release have received increased recent attention and appear to be good options in these patients. Future therapy may include antibodies to mediators of neurogenic inflammation and even treatment of bacteria in the bowel….The diagnosis of chronic prostatitis/CPPS must include conditions traditionally outside the scope of urologic practice but important for the care of men with chronic pelvic pain. The treatment is best done using multiple simultaneous therapies aimed at the different aspects of the condition."

Ponte CD, Johnson-Tribino J. 2005.  Attitudes and knowledge about pain: an assessment of West Virginia family physicians.  Fam Med. 37(7):477-480.  “Chronic nonmalignant pain and assessing pain in the elderly are problematic for many physician providers.  Perceived regulatory scrutiny does impact physician prescribing of opioids for patients in pain.  The majority of respondents felt that their formal medical training did not prepare them to effectively manage pain.”

Porcelli MJ. 2004.  Why are our patients still in pain? Finding a balance in treating patients for nonmalignant pain.  J Am Osteopath Assoc. 104(2):73-75, 66.  “Are physicians doing patients harm by allowing them to remain in chronic pain?  Conversely, are physicians doing patients harm by supporting a dependence on pain-relieving medication that allows normal functions of daily life? There is a delicate balance that each physician must find in the context of his or her practice of medicine.”

Portenoy, R. K., V. Dole, H. Joseph, J. Lowinson, C. Rice, S. Segal and B. L. Richman. 1997.  Pain management and chemical dependency.  Evolving perspectives.  JAMA 278(7):592-593.

Portenoy, R. K. 1996.  Opioid therapy for chronic nonmalignant pain: a review of the critical issues.  J Pain Symptom Manage 11(4):203-217.

Portenoy RK. 2000.  Current pharmacotherapy of chronic pain.  J Pain Symptom Manage 19(1 Suppl):S16-S20.  “The combination of opioids and other drugs, such as an N-methyl-D-aspartate-receptor antagonist, may improve the balance between analgesia and adverse effects.”

 

Portenoy RK, Ugarte C, Fuller I et al. 2004.  Population-based survey of pain in the United States: differences among white, African American, and Hispanic subjects.  J Pain 5(6):317-328.  “Neither race nor ethnicity predicted disabling pain, but the minorities had more characteristics identified as predictors.  The data suggest that race and ethnicity contribute to clinical diversity, but socioeconomic disadvantage is the more important predictor of disabling pain.  Race and ethnicity influence the presentation and treatment of chronic pain.  Pain was highly prevalent across groups, and there were racial and ethnic differences in pain experience and treatment preferences.”

 

Porter FL, Grunau RE, Anand KJ. 1999.  Long-term effects of pain in infants.  J Dev Behav Pediatr 20(4):253-261.  Inadequate pain control in infancy may contribute to central sensitization.

 

Porter FL, Wolf CM, Miller JP. 1999.  Procedural pain in newborn infants: the influence of intensity and development.  Pediatrics 104(1):e13.  “Newborn and developing infants show increased magnitude physiologic and behavioral responses to increasingly invasive procedures, demonstrating that even very prematurely born infants respond to pain and differentiate stimulus intensity.  The best approach may be one of universal precaution to provide pain management systematically to reduce the acute and long-term impact of early procedural pain, development, stimulus intensity, pain response.”

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.

Potenzieri C, Undem BJ. 2011. Basic mechanisms of itch. Clin Exp Allergy. [Jun 6. doi: 10.1111/j.1365-2222.2011.03791.x. Epub ahead of print]. "Studies have demonstrated that both peripheral and central sensitization to pruritogenic stimuli occur during chronic itch."

Potter M, Schafer S, Gonzalez-Mendez E et al. 2001.  Opioids for chronic nonmalignant pain.  Attitudes and practices of primary care physicians in the UCSF/Stanford Collaborative Research Network.  University of California, San Francisco.  J Fam Pract 50(2):145-151.  “Primary care physicians are willing to prescribe schedule III opioids as needed, but many are unwilling to use schedule II opioids around the clock for CNMP.  Individual prescribing practices vary widely among primary care physicians.  Concerns about physical dependence, tolerance, and addiction are barriers to the prescription of opioids by primary care physicians for patients with CNMP.”

Potts J, Payne RE. 2007.  Prostatitis: infection, neuromuscular disorder, or pain syndrome?  Proper patient classification is key.  Cleve Clin J Med. 74 Suppl 3:S63-71. “Prostatitis is a broad term used to describe inflammation of the prostate that may be associated with a myriad of lower urinary tract symptoms of sexual discomfort and dysfunction.”  “Prostatitis is classified into four categories, including acute and chronic bacterial forms, a chronic abacterial form, and an asymptomatic form.”  “Chronic abacterial prostatitis (also known as chronic pelvic pain syndrome) is both the most prevalent form and also the least understood and the most challenging to evaluate and treat.  This form of prostatitis may respond to non-prostate-centered treatment strategies such as physical therapy, myofascial trigger point release, and relaxation techniques. Because the various forms of prostatitis call for vastly different treatment approaches, appropriate evaluation, testing, and differential diagnosis are crucial to effective management.”

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.

Prados G, Miro E, Martínez MP et al. 2013. Fibromyalgia: gender differences and sleep-disordered breathing. Clin Exp Rheumatol. 31(6 Suppl 79):102-110. "Alterations in sleep respiratory patterns were more highly prevalent in male than in female FM patients. More so in male FM patients, the alterations in sleep patterns, non-refreshing sleep, and other FM-related symptoms observed in this population might be part of a primary sleep-disordered breathing."

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.

Prehm P. 2013. Curcumin analogue identified as hyaluronan export inhibitor by virtual docking to the ABC transporter MRP5. Food Chem Toxicol. 62:76-81. Hyaluronan (hyaluronic acid) is produced in excess in many disease states, including metastatic cancers, inflammation, or insufficient blood flow (such as the energy crisis in trigger point areas). Fibroblasts are the most common type of connective tissue cell, and they form hyaluronic acid. Fibroblasts synthesize the extra cellular matrix, collagen, and stroma, which make up the connective tissue framework. Fibroblasts play a critical role in cellular healing. The multidrug resistance associated protein 5 (MRPS 5) transports the hyaluronic acid from the fibroblasts. MRPS 5 is inhibited by the plant phenols curcumin or xanthohumol. The best plant phenol to inhibit hyaluronic acid is hylin. Hylin is found in natural curcumin extracts, such as turmeric. "Since curcumin itself is unstable under physiological conditions, the active component for many cell biological and pharmaceutical effects of natural curcumin preparations could be that hylin that acts by hylauronan inhibition." [This research meshes well with the studies we did on geloid masses in patients with FM and CMP, and indicates that patients with FM and CMP may need to be very careful using any product with hyaluronic acid. HA is a component in many cosmetics, body lotions, and anti-aging formulas. DJS]

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 DD, Staud R. 2005.  Neurobiology of fibromyalgia syndrome.  J Rheumatol Suppl. 75:22-28.  “Accumulating evidence suggests that fibromyalgia syndrome (FM) pain is maintained by tonic impulse input from deep tissues, such as muscle and joints, in combination with central sensitization mechanisms.  This nociceptive input may originate in peripheral tissues (trauma and infection) resulting in hyperalgesia/allodynia and/or central sensitization.  Such alterations of relevant pain mechanisms may lead to long term neuroplastic changes that exceed the antinociceptive capabilities of affected individuals, resulting in ever-increasing pain sensitivity and dysfunction.  Future research needs to address the important role of abnormal nociception and/or antinociception for chronic pain in FM.”

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.

Prince PB, Rapaport AM, Sheftell FD et al. 2004.  The effect of weather on headache.  Headache 44(6):596-602.  This study supports the influence of weather changes on headache.

Prist V, De Wilde VA, Masquelier E. 2012. Ann Phys Rehabil Med 55(3):174-189. This case report presents a 49-year old woman suffering from widespread pain since 2002. Her gait pattern included hip adduction, flexed hips and knees and bilateral equines hip deformity. She was diagnosed by several clinicians, but each had a different idea of what she had: fibromyalgia with dystonia, CNS injury, Little's disease, intramedullary spinal cord tumor, or multiple sclerosis. The authors conclude that the logical diagnosis is fibromyalgia with dystonia; the dystonia being due to generalized analgesic protective attitude. [The patient was not assessed for myofascial trigger points. If she had been, by someone well-trained in myofascial medicine, the diagnosis might have been different. Other diagnoses may be involved, and central sensitization is certainly part of this patient's cause of misery, but as to what the cause behind the descriptions are, the TrP assessment and postural analysis must be done to complete the picture. DJS].

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

Proctor SL, Estroff TW, Empting LD et al. 2012. Prevalence of Substance Use and Psychiatric Disorders in a Highly Select Chronic Pain Population. J Addict Med. [Nov 5 Epub ahead of print]. "Certain populations of patients with complex nociceptive, neuropathic, and myofascial pain syndromes may have a lower prevalence of substance use disorders than the general population. They also have concurrent psychiatric disorders, which should be evaluated and treated concomitantly as part of their chronic pain treatment. Despite the low prevalence of substance use disorders, these patients must be continuously monitored for abuse, misuse, and diversion of their medication. The low prevalence may be attributable to the severity of their illness, the patients' inability to achieve pain relief and obtain pain medications easily, and their persistence in pursuing accurate diagnoses and treatment. A major limitation of this study was that it relied on self-report and there were no urine drug screens to report."

Proske U, Gandevia SC. 2012. The proprioceptive senses: their roles in signaling body shape, body position and movement, and muscle force. Physiol Rev. 92(4):1651-1697. Proprioceptive senses "...include the senses of position and movement of our limbs and trunk, the sense of effort, the sense of force, and the sense of heaviness. Receptors involved in proprioception are located in skin, muscles, and joints. Information about limb position and movement is not generated by individual receptors, but by populations of afferents. Afferent signals generated during a movement are processed to code for endpoint position of a limb. The afferent input is referred to a central body map to determine the location of the limbs in space. Experimental phantom limbs, produced by blocking peripheral nerves, have shown that motor areas in the brain are able to generate conscious sensations of limb displacement and movement in the absence of any sensory input. In the normal limb tendon organs and possibly also muscle spindles contribute to the senses of force and heaviness. Exercise can disturb proprioception, and this has implications for musculoskeletal injuries. Proprioceptive senses, particularly of limb position and movement, deteriorate with age and are associated with an increased risk of falls in the elderly. [Trigger points can cause proprioceptive dysfunction, so this information is very important. DJS]

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]

Pujol J, Lopez-Sola M, Ortiz H et al. 2009.  Mapping brain response to pain in fibromyalgia patients using temporal analysis of FMRI.  PloS ONE. 4(4):e5224. “The results suggest that data-driven fMRI assessments may complement conventional neuroimaging for characterizing pain responses and that enhancement of brain activation in fibromyalgia patients may be particularly relevant in emotion-related regions.”

Pujol J, Macia D, Garcia-Fontanals. 2014. The contribution of sensory system functional connectivity reduction to clinical pain in fibromyalgia. Pain. [May 2 Epub ahead of print.] "The results confirm previous research demonstrating abnormal functional connectivity in fibromyalgia and show that alterations at different levels of sensory processing may contribute to account for clinical pain. Importantly, reduced functional connectivity extended beyond the somatosensory domain and implicated visual and auditory sensory modalities. Overall, this study suggests that a general weakening of sensory integration underlies clinical pain in fibromyalgia."

Punjabi NM, Shahar E, Redline S et al. 2004.  Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study.  Am J Epidemiol. 160(6):521-530.  “Sleep-related hypoxemia was also associated with glucose intolerance independently of age, gender, body mass and waist circumference.  The results of this study suggest that SDB is independently associated with glucose intolerance and insulin resistance and lead to type 2 diabetes mellitus.”

Puretic MB, Demarin V. 2012. Neuroplasticity mechanisms in the pathophysiology of chronic pain. Clin Croat. 51(3):425-429. "Chronic pain is a widespread healthcare problem with great impact on mental health, professional and family life of the patient. It can be a consequence of many disorders; however, its pathogenesis has not yet been fully understood. Neuroplasticity is the ability of the nervous system to adapt to different changes and it is present throughout life, not only in prenatal period, infancy and childhood. However, in the pathophysiology of chronic pain, neuroplasticity shows its 'dark side'. Due to the central sensitization process, noxious stimuli can produce chronic pain or misinterpretation of non-noxious stimuli (secondary hyperalgesia and allodynia). These changes occur at the level of brain cortex as well at peripheral nerves and receptors. This review summarizes a significant portion of literature dealing with neuroplasticity processes in well known chronic pain conditions such as migraine, chronic posttraumatic headache, low back pain, fibromyalgia, and others." [This review from Croatia is well-thought-out and well-done. It is to be hoped that in the future, these researchers will include papers dealing with central sensitization generating TrPs in their research. 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.

Przekop P, Haviland MG, Morton KR et al. 2010. Correlates of Perceived Pain-Related Restrictions among Women with Fibromyalgia. Pain Med. 11(11):1698-1706. "Women with fibromyalgia reporting the more severe pain-related restrictions were those who had experienced trauma accompanied by physical pain, were older, less educated, more depressed, more hostile, had high BMI (body mass index) scores, and had been treated for fibromyalgia in the last 12 months. Predictors in women with osteoarthritis were age, BMI, treatment in the last 12 months, experience of a major life stressor, and greater depression symptom severity. ....In both groups, age, BMI, treatment in the last 12 months, and depression predicted pain-related restrictions. Experience of a traumatic event with physical pain was the strongest predictor in the fibromyalgia group. These findings may be useful in constructing novel treatments and prevention strategies for pain-related morbidity in fibromyalgia patients." [One can always tell when the researchers are psychologist and/or psychiatrists. The BMI is usually an indication of co-existing insulin resistance, and one can only suspect that the hostility and depression have a lot to do with the failure of the doctors to address the myofascial trigger points causing the symptoms and maintaining central sensitization. DJS]

Przekop P, Haviland MG, Zhao Y et al. 2012. Self-reported physical health, mental health, and comorbid diseases among women with irritable bowel syndrome, fibromyalgia, or both compared with healthy control respondents. J Am Osteopath Assoc. 112(11):726-735. "Physicians often encounter patients with functional pain disorders such as irritable bowel syndrome (IBS), fibromyalgia (FM), and their co-occurrence.... Respondents with IBS reported fewer traumatic and major life stressors and better health (ratings and comorbidity data) than respondents with FM or respondents with IBS plus FM. Overall, respondents with both diseases reported the worst stressors and physical-mental health profiles and reported more diagnosed medical, pain, and psychiatric comorbidities....The results revealed statistically significant, relatively large differences in perceptions of quality of life measures and health profiles among the respondents in the control group and the 3 clinical groups."

Queiroz LP. 2013. Worldwide epidemiology of fibromyalgia. Curr Pain Headache Rep. 17(8):356. "This article reviews the prevalence and incidence studies done in the general population, in several countries/continents, the prevalence of FM in special groups/settings, the association of FM with some sociodemographic characteristics of the population, and the comorbidity of FM with others' disorders, especially with headaches."

Queme F, Taguchi T, Mizumura K et al. 2013. Muscular Heat and Mechanical Pain Sensitivity After Lengthening Contractions in Humans and Animals. J Pain. [Sep 21 Epub ahead of print]. "Mechanical sensitivity of muscle nociceptors was previously shown to increase 2 days after lengthening contractions (LC), but heat sensitivity was not different despite nerve growth factor (NGF) being upregulated in the muscle during delayed-onset muscle soreness (DOMS). The discrepancy of these results and lack of other reports drove us to assess the heat sensitivity during DOMS in humans and to evaluate the effect of NGF on the heat response of muscle C-fibers. Pressure pain thresholds and pain intensity scores to intramuscular injection of isotonic saline at 48°C and capsaicin were recorded in humans after inducing DOMS. The response of single unmyelinated afferents to mechanical and heat stimulations applied to their receptive field was recorded from muscle-nerve preparations in vitro. In humans, pressure pain thresholds were reduced but heat and capsaicin pain responses were not increased during DOMS. In rats, the mechanical but not the heat sensitivity of muscle C-fibers was increased in the LC group. NGF applied to the receptive field facilitated the heat sensitivity relative to the control. The absence of facilitated heat sensitivity after LC, despite the NGF sensitization, may be explained if the NGF concentration produced after LC is not sufficient to sensitize nociceptor response to heat….This article presents new findings on the basic mechanisms underlying hyperalgesia during DOMS, which is a useful model to study myofascial pain syndrome, and the role of NGF on muscular nociception. This might be useful in the search for new pharmacologic targets and therapeutic approaches."

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 BP, Sturzenegger M, Di Stefano G. 1995.  Long-term outcome after whiplash injury.  A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings.  Medicine 74(5):281-297.  “Symptomatic patients were older, had higher incidence of rotated or inclined head position at the time of impact, had higher prevalence of pretraumatic headache, showed higher intensity of initial neck pain and headache, complained of a greater number of symptoms, had a higher incidence of symptoms of radicular deficit and higher average scores on a multiple symptom analysis, and displayed more degenerative signs on X-ray.  Symptomatic patients scored higher with regard to impaired well-being and performed worse on tasks of attentional functioning and showed more concern with regard to long-term suffering and disability.”

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].

Ragab A, Clement P, Vincken W. 2004.  Objective assessment of lower airway involvement in chronic rhinosinusitis.  Am J Rhinol. 18(1):15-21.  Sixty percent of chronic rhinosinusitis patients have lower airway involvement, 24 % had asthma and 36% had small airway disease.  These may often be unsuspected.

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.”

Rahman W, Dickenson AH. 2013. Voltage gated sodium and calcium channel blockers for the treatment of chronic inflammatory pain. Neurosci Lett. [Aug 11 Epub ahead of print]. "The inflammatory response is a natural response of the body that occurs immediately following tissue damage, which may be due to injury, infection or disease. The acute inflammatory response is an essential mechanism that promotes healing and a key aspect is the ensuing pain, which warns the subject to protect the site of injury. Thus, it is common to see a zone of primary sensitization as well as consequential central sensitization that generally, is maintained by a peripheral drive from the zone of tissue injury. Inflammation associated with chronic pain states, such as rheumatoid and osteoarthritis, cancer and migraine etc. is deleterious to health and often debilitating for the patient. Thus there is a large unmet clinical need. The mechanisms underlying both acute and chronic inflammatory pain are extensive and complex, involving a diversity of cell types, receptors and proteins. Among these the contribution of voltage gated sodium and calcium channels on peripheral nociceptors is critical for nociceptive transmission beyond the peripheral transducers and changes in their distribution, accumulation, clustering and functional activities have been linked to both inflammatory and neuropathic pain. The latter has been the main area for trials and use of drugs that modulate ion channels such as carbamazepine and gabapentin, but given the large peripheral drive that follows tissue damage, there is a clear rationale for blocking voltage gated sodium and calcium channels in these pain states. It has been hypothesized that pain of inflammatory origin may evolve into a condition that resembles neuropathic pain, but mixed pains such as low back pain and cancer pain often include elements of both pain states. This review considers the therapeutic potential for sodium and calcium channel blockers for the treatment of chronic inflammatory pain states." [This paper confirms the role of peripheral pain generation in initiating the central sensitization state. It is very interesting, considering the idea that trigger points may be associated with a calcium channelopathy. DJS]

Rahn EJ, Guzman-Karlsson MC, David Sweatt J. 2013. Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: Implications for pain and memory. Neurobiol Learn Mem. [Jun 22 Epub ahead of print]. "Sensitization is a form of non-associative conditioning in which amplification of behavioral responses can occur following presentation of an aversive or noxious stimulus. Understanding the cellular and molecular underpinnings of sensitization has been an overarching theme spanning the field of learning and memory as well as that of pain research. In this review we examine how sensitization, both in the context of learning as well as pain processing, shares evolutionarily conserved behavioral, cellular/synaptic, and epigenetic mechanisms across phyla. First, we characterize the behavioral phenomenon of sensitization both in invertebrates and vertebrates. Particular emphasis is placed on long-term sensitization (LTS) of withdrawal reflexes in Aplysia following aversive stimulation or injury, although additional invertebrate models are also covered. In the context of vertebrates, sensitization of mammalian hyperarousal in a model of post-traumatic stress disorder (PTSD), as well as mammalian models of inflammatory and neuropathic pain is characterized. Second, we investigate the cellular and synaptic mechanisms underlying these behaviors. We focus our discussion on serotonin-mediated long-term facilitation (LTF) and axotomy-mediated long-term hyperexcitability (LTH) in reduced Aplysia systems, as well as mammalian spinal plasticity mechanisms of central sensitization. Third, we explore recent evidence implicating epigenetic mechanisms in learning- and pain-related sensitization. This review illustrates the fundamental and functional overlay of the learning and memory field with the pain field which argues for homologous persistent plasticity mechanisms in response to sensitizing stimuli or injury across phyla."

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.”

Rainey CE. 2013. The use of trigger point dry needling and intramuscular electrical stimulation for a subject with chronic low back pain: a case report. Int J Sports Phys Ther 8(2):145-161. The subject of this case report is a 30 year old female on active military duty, who developed low back and right posteriolateral hip pain after a lumbar flexion injury from picking up a barbell. Exam revealed a multi-segmental flexion movement pattern dysfunction, with TrPs in the right gluteus maximus and medius. Dry needling of the trigger points and intramuscular stimulation coupled with a home program of core stability exercises helped the patient return to full military duty without pain.

Rainsford KD. 2006.  Influenza (“Bird Flu”), inflammation and anti-inflammatory/analgesic drugs.  Inflammopharmacology 14(1-2):2-9.  This study is related to fibromyalgia in that avian flu may cause a pro-inflammatory cytokine storm to kill its victims, and FMS patients may already be in a cytokine storm, or at least at a high level of pro-inflammatory cytokine activity.  A number of potential medications are listed, among which are pentoxifylline, macrolide antibiotics, reservatrol, flavenoids and EPA.  [Reduced anti-inflammatory cytokines may also be part of the problem.  (See Uceyler N et al 2006 et al.)  Statins are also mentioned, but there is concern due to their potential adverse affects on co-existing myofascial TrPs.]

Rainville P, Bushnell MC, Duncan GH. 2001.  Representation of acute and persistent pain in the human CNS: potential implications for chemical intolerance.  Ann N Y Acad Sci. 933:130-141.  CNS neuroplasticity involved in chronic pain may share similarities with environmental chemical sensitivity.

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]

Rakovski C, Zettel-Watson L, Rutledge D. 2012. Association of employment and working conditions with physical and mental health symptoms for people with fibromyalgia. Disabil Rehabil. [Feb 12 Epub ahead of print]. "Work modifications could allow more people with FM to remain employed and alleviate symptoms. Persons with FM should be counseled to consider what elements of their work may lead to symptom exacerbation." [To do these modifications adequately, one must take into consideration the peripheral pain generators that are causing and/or maintaining the central sensitization of FM. Controlling the perpetuating factors of the peripheral pain generators can substantially help in the management of FM. DJS]

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

Ramanathan S, Panksepp J, Johnson B. 2012. Is Fibromyalgia An Endocrine/Endorphin Deficit Disorder? Is Low Dose Naltrexone a New Treatment Option? Psychosomatics. [Apr 3 Epub ahead of print].

 

Ramirez BG, Blazquez C, Gomez del Pulgar T et al. 2005.  Prevention of Alzheimer’s disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation.  J Neurosci. 25(8):1904-1913.  “Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo.  Intracerebroventricular administration of the synthetic cannabinoid WIN55,212-2 to rats prevent betaA-induced microglial activation, cognitive impairment, and loss of neuronal markers.  Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.  [This may have relevance in the treatment of cognitive deficits in fibromyalgia. DJS]

 

Rao SG. 2002.  The neuropharmacology of centrally-acting analgesic medications in fibromyalgia.  Rheum Dis Clin North Am 28(2):235-259.  “FMS consists of more than just chronic pain, and the question of how sleep abnormalities, depression, fatigues, and so forth tie into disordered pain processing is being researched actively.  Future research focusing on how the various manifestations of FMS related to one another undoubtedly will lead to a more rational targeting of drugs in this complex disorder.”

Raouf R, Quick K, Wood JN. 2010. Pain as a channelopathy. J Clin Invest. 120(11):3745-3752. "Mendelian heritable pain disorders have provided insights into human pain mechanisms and suggested new analgesic drug targets. Interestingly, many of the heritable monogenic pain disorders have been mapped to mutations in genes encoding ion channels. Studies in transgenic mice have also implicated many ion channels in damage sensing and pain modulation. It seems likely that aberrant peripheral or central ion channel activity underlies or initiates many pathological pain conditions. Understanding the mechanistic basis of ion channel malfunction in terms of trafficking, localization, biophysics, and consequences for neurotransmission is a potential route to new pain therapies." [This is interesting in that the most likely current hypothesis for the cause of myofascial TrPs is a calcium channelopathy. DJS]

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 KG, Janal MN, Nayak S et al. 2006.  Psychiatric comorbidities in a community sample of women with fibromyalgia.  Pain [May 12 Epub ahead of print]  “Prior studies of care-seeking fibromyalgia (FM) patients often report that they have an elevated risk of psychiatric disorders, but biased sampling may distort true risk.”  “Although risk of current MDD was nearly 3-fold higher in community women with than without FM, the groups had similar risk of lifetime MDD.  Risk of lifetime anxiety disorders, particularly obsessive compulsive disorder and post-traumatic stress disorder, was approximately 5-fold higher among women with FM.  Overall, this study found a community prevalence for FM among women that replicates prior North American studies and revealed that FM may be even more prevalent among racial minority women.  These community-based data also indicate that the relationship between MDD and FM may be more complicated than previously thought, and call for an increased focus on anxiety disorders in FM.”

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.

Rauck R, Busch M, Marriott T. 2013. Effectiveness of a heated lidocaine/tetracaine topical patch for pain associated with myofascial trigger points: results of an open-label pilot study. Pain Pract. 13(7):533-538. This study was done on patients with up to three myofascial trigger points. They found that: "The heated lidocaine/tetracaine patch has potential utility as a noninvasive pharmacologic approach for managing MTP pain. Further studies are warranted." [For those of us with hundreds of trigger points, this still might be useful for the worst TrPs. Please do not try this at home. The patches were designed to release the topical anesthetic slowly. As of now, the patches contain warnings not to use them with heat, as a much higher amount of lidocaine could enter the body much more rapidly, and could have systemic effects on blood pressure and other systems. DJS]

Ravera S, Bianco B, Cugnoli C et al. 2009.  Sinusoidal ELF magnetic fields affect acetyl cholinesterase activity in cerebellum synaptosomal membranes.  Bioelectromagnetics. [Dec 29 Epub ahead of print].  [This article is of interest in that Simons’ Integrated Hypothesis of myofascial TrP formation includes the excess amount of acetylcholine produced at the motor endplate.  Anything, even these magnetic fields that affect the metabolism of acetylcholine, might then impact TrPs and their ability to heal. DJS]

Rayegani S, Bahrami M, Samadi B et al. 2011. Comparison of the effects of low energy laser and ultrasound in treatment of shoulder myofascial pain syndrome: a randomized single-blinded clinical trial. Eur J Phys Rehabil Med. 47(3):381-389. "Myofascial pain syndrome (MPS) is one of the most prevalent musculoskeletal diseases. MPS impaired quality of life in the patients. There is a lot of controversy about different treatment options which include medical treatments, physical therapy, injections, ultrasound and laser.... This study introduces laser as one of the preferred treatments of myofascial pain syndrome in shoulder." [It is a sad commentary on the state of medical care that most care providers are unaware that this common cause of musculoskeletal pain even exists. DJS]

Rayhan RU, Ravindran MK, Baraniuk JN. 2013. Migraine in gulf war illness and chronic fatigue syndrome: prevalence, potential mechanisms, and evaluation. Front Physiol. 4:181. "The high prevalence of migraine in CFS (chronic fatigue syndrome) was confirmed and extended to GWI (gulf war illness) subjects. GWI and CFS may share dysfunctional central pathophysiological pathways that contribute to migraine and subjective symptoms. The high migraine prevalence warrants the inclusion of a structured headache evaluation in GWI and CFS subjects, and treatment when present."

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.

Ready LB, Kozody R, Barsa JE et al. 1983.  Trigger point injections vs. jet injection in the treatment of myofascial pain.  Pain. 15(2):201-206.  “Trigger point injections using dilute solutions of local anesthetic agents have proved effective for many patients with myofascial pain.  The treatment itself, however, can produce severe pain and may occasionally be associated with complications.  It was determined in this study that a local anesthetic solution administered by jet injection in the area of myofascial trigger points was capable of providing short-term pain relief equal to conventional trigger point injections using a hypodermic needle and syringe.  The jet injector system produced significantly less pain during treatment than conventional trigger point injections and therefore was preferred by most subjects having the opportunity to compare both forms of treatment.”

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]

Reed BD, Harlow SD, Sen A et al. 2012. Relationship between vulvodynia and chronic comorbid pain conditions. Obstet Gynecol. 120(1):145-151. "To estimate the relationship among the presence of vulvodynia, fibromyalgia, interstitial cystitis, and irritable bowel syndrome. Validated questionnaire-based screening tests for the four pain conditions were completed by women with and without vulvodynia who were participating in the Michigan Woman to Woman Health Study, a longitudinal population-based survey in southeastern Michigan. Weighted population-based estimates of the prevalence and characteristics of participants with these chronic comorbid pain conditions were calculated using regression analyses....Chronic pain conditions are common, and a subgroup of women with vulvodynia is more likely than those without vulvodynia to have one or more of the three other chronic pain conditions evaluated. [It is most unfortunate that myofascial trigger points, one of the main co-existing conditions of vulvodynia as well as one of the main causes, was not included in this study. DJS]

Reeh ES, elDeeb ME. 1991.  Referred pain of muscular origin resembling endodontic involvement.  Case report. Oral Surg Oral Med Oral Pathol. 71(2):223-227.  “Referred pain is common in the orofacial region and can cause considerable difficulties in diagnosis.  Referred pain is defined as pain that is referred to a part of the body other than the site of origin, and as a result, severe pain may arise without an associated causative lesion.  A muscular trigger point that resembled a tooth with endodontic involvement is discussed.” 

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.

Rehm SE, Koroschetz J, Gockel U et al. 2010. A cross-sectional survey of 3035 patients with fibromyalgia: subgroups of patients with typical comorbidities and sensory symptom profiles.

Rheumatology (Oxford). [Mar 17 Epub ahead of print]. “Patients with FM…present with a variety of pain qualities, sensory abnormalities and additional comorbidities. The aim was to identify clinically distinguishable subgroups of patients….Clinically relevant sensory abnormalities (strongly, very strongly present) included pressure pain (58%), prickling (33%), burning (30%) and thermal hypersensitivity (24%). Pain attacks were complained by 40% of patients. Moderate to severe comorbid depression occurred in 66% of patients. Only approximately 30% of the patients had optimal sleep. A hierarchical cluster analysis using descriptors of sensory abnormalities as well as the extent of comorbidities revealed five distinct subgroups of patients showing a characteristic clinical profile. Four subgroups of patients suffer from severe sensory disturbances in various combinations but lack pronounced comorbidities. In one subgroup, however, severe comorbidities dominate the clinical picture. ….The results of this study indicate that FM patients can be classified on the basis of their sensory symptoms and comorbidities by the use of a patient-reported questionnaire. Subgrouping of patients with FM may be used for future research and to tailor optimal treatment strategies for the appropriate patient.”

 

Reich JW, Johnson LM, Zautra AJ et al. 2006.  Uncertainty of illness relationships with mental health and coping processes in fibromyalgia patients.  J Behav Med. [May 6 Epub ahead of print]   “Fibromyalgia syndrome (FMS) is a chronic musculoskeletal pain condition poorly understood in terms of etiology and treatment by both physicians and patients. This condition of ‘uncertainty of illness’ was examined as a variable involved in the adjustment of FMS patients, relating it to their depression, anxiety, affect and coping styles.”  “Both cross-sectional and more dynamic longitudinal analyses showed that illness uncertainty was significantly associated with anxiety, negative affect, and avoidant and passive coping. Its positive relationship with depression was eliminated when a control variable, pain helplessness, was included as a covariate. Longitudinally, illness uncertainty interacted with interpersonally stressful daily events in predicting reports of reduced positive affect, suggesting that illness uncertainty acts as a risk factor for affective disturbances during stressful times.” 

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.”

Reichling DB, Levine JD. 2009.  Critical role of nociceptors plasticity in chronic pain.  Trends Neurosci. [Sep 23 Epub ahead of print]  “The transition from acute to chronic pain states might be the most important challenge in research to improve clinical treatment of debilitating pain.  We describe a recently identified mechanism of neuronal plasticity in primary afferent nociceptive nerve fibers (nociceptors) by which an acute inflammatory insult or environmental stressor can trigger long-lasting hypersensitivity of nociceptors to inflammatory cytokines.  This phenomenon, ‘hyperalgesic priming’, depends on the epsilon isoform of protein kinase C (PKCvarepsilon) and a switch in intracellular signaling pathways that mediate cytokine-induced nociceptor hyperexcitability.  We discuss the impact of this discovery on our understanding of, and ultimately our ability to treat, a variety of enigmatic and debilitating pain conditions, including those associated with repetitive injury and generalized pain conditions, such as fibromyalgia.”

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.

Reiestad F, Kulkarni J. 2013. Role of myofascial trigger points in post-amputation pain: causation and management. Prosthet Orthot Int. 37(2):120-123. "Identification of myofascial trigger points in amputation stumps and their role in post-amputation pain, followed by appropriate intervention is an important facet of management of this complex chronic pain. Clinical relevance Myofascial trigger points in amputation stumps can lead to ongoing chronic post-amputation pain and our results indicate that identification and intervention of these trigger points does lead to notable resolution of this pain."

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.

Reimann F, Cox JJ, Belfer I et al. 2010 March 8 Proc Natl Acad Sci USA [Epub ahead of print.]  The gene SCN9A has been shown to be responsible for several pain disorders in human beings.  This study shows that a nucleotide polymorphism in this gene is also part of central sensitization through C-fiber activation.

Reisenauer SJ. 2012. A needle in the neck: trigger point injections as headache management in the emergency department. Adv Emerg Nurs J. 34(4):350-356. "A review of recent research suggests that the use of trigger point injections is successful in relieving the acute pain of musculoskeletal headaches. Patients with the chief complaint of headache commonly present to the emergency department (ED) and are often treated with multiple intravenous medications including narcotics....This article will address the problems of intravenous medication therapy and discuss the benefits of trigger point therapy as management for musculoskeletal headaches specifically in the ED. In addition, discussion aims to provide tools for the nurse practitioner to integrate this skill into clinical practice."

Reisine S, Fifield J, Walsh S et al. 2004.  Employment and quality of life outcomes among women with fibromyalgia compared to healthy controls.  Women Health 39(4):1-19.  “Employed women report better quality of life than those not employed, but only for the physical dimension of quality of life.  The findings regarding MCS [Mental Component Summary Scores] are intriguing in that women with FMS are not very different from controls and that employment has little effect on the mental health component of quality of life.”

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

Relph N, Herrington L, Tyson S. 2013. The effects of ACL injury on knee proprioception: a meta-analysis. Physiotherapy. [Dec 4 Epub ahead of print.] ACL injuries may cause knee proprioception deficits compared to uninjured knees and control groups. Although differences were statistically significant, the clinical significance of findings can be questioned. Clinical practitioners using joint position sense or threshold to detect passive motion techniques need to consider the reliability and validity of data provided. [This study indicates to me that there may be trigger points in the ACL affecting proprioception. DJS]

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.

Renan-Ordine R, Alburquerque-Sendi N F, Rodrigues de Souza DP et al. 2011. Effectiveness of myofascial trigger point manual therapy combined with a self-stretching protocol for the management of plantar heel pain: a randomized controlled trial. J Orthop Sports Phys Ther. 41(2):43-50. A self-stretching program coupled with bodywork on TrPs was far superior to self-stretching alone in the relief of plantar heel pain.

Reuben SS, Reuben SS. 2007.  Chronic pain after surgery: what can we do to prevent it?  Curr Pain Headache Rep. 11(1):5-13.  “Effective preventative analgesic techniques may be useful in reducing not only acute pain but also chronic postsurgical pain and disability.  This review examines the efficacy of using a variety of analgesic techniques aimed at preventing or reducing chronic pain after surgery.”

 

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.

 

Reyes Del Paso GA, Garrido S, Pulgar A et al. 2011. Autonomic cardiovascular control and responses to experimental pain stimulation in fibromyalgia syndrome. J Psychosom Res. 70(2):125-134. "The data suggest impaired autonomic cardiovascular regulation in FMS in terms of reduced sympathetic and parasympathetic influences, as well as blunted sympathetic reactivity to acute stress. The association between baroreflex function and pain experience reflects the pain inhibition mediated by the baroreceptor system. Given the reduced baroreflex sensitivity in FMS, one may assume deficient ascending pain inhibition arising from the cardiovascular system, which may contribute to the exaggerated pain sensitivity of FMS."

Reyes Del Paso GA, Pulgar A, Duschek S et al. 2011. Cognitive impairment in fibromyalgia syndrome: The impact of cardiovascular regulation, pain, emotional disorders and medication. Eur J Pain. [Dec 19 Epub ahead of print]. "Thirty-five patients with FMS and 29 matched healthy controls completed a neuropsychological test measuring attention and arithmetic processing. As possible factors underlying the expected cognitive impairment, clinical pain intensity, co-morbid depression and anxiety disorders, sleep complaints, medication use, as well as blood pressure parameters were investigated. The patients' test performance was substantially reduced, particularly in terms of lower speed of cognitive processing and restricted improvement of performance in the course of the task. While the extent of depression, anxiety, fatigue and sleep complaints was unrelated to test performance, better performance was observed in patients showing lower pain ratings and those using opiate medication. The data corroborate the presence of substantial cognitive impairment in FMS. While the experience of chronic pain is crucial in mediating the deficits, co-morbid depression, anxiety, fatigue and sleep complaints play only a subordinate role. In the control group, but not in the patients, blood pressure was inversely associated with mental performance. This finding is in line with the well known cognitive impairment in hypertension. The lack of this association in FMS confirms previous research showing aberrances in the interaction between blood pressure and central nervous function in the affected patients."

Reynolds MD. 1981.  Myofascial trigger point syndromes in the practice of rheumatology.  Arch Phys Med Rehabil. 62(3):111-114.  “Pain referred from a muscle can mimic both pain from a joint and radicular pain associated with disease of spinal joints, leading to mistakes in diagnosis and in treatment.  When articular disease is present, it predisposes to myofascial trigger point (TP) syndromes.  With arthritis, TPs in muscles may result from decreased mobility with prolonged shortening of muscles, from abnormal mechanical stress on muscles and from stimuli arising in diseased joints.  During examination for signs of myofascial disorders, the numbers of tender points and of local twitch responses in women with rheumatoid arthritis were twice those found in women free of any rheumatic illness.  It is important to consider this high frequency of myofascial syndromes in persons with arthritis when treating pain or weakness which could be due to the muscles rather than the joints.  Conversely, it has been proposed, on theoretical and clinical grounds, that muscular TPs can cause joint disease.  This hypothesis has important implications for the treatment of arthritis.”  [Studies are linking TrPs with arthritic conditions, and have been doing so for some time.  They are going unnoticed.  ALL arthritis patients need assessment of co-existing TrPs to relieve them of unnecessary symptom burden. DJS]

 

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

 

Rha DW, Shin JC, Kim YK et al. 2011. Detecting local twitch responses of myofascial trigger points in the lower back muscles using ultrasonography. Arch Phys Med Rehabil. [Aug 11 Epub ahead of print]. "These findings suggest that ultrasonography was useful for detecting LTRs (local twitch responses) of MTrPs, especially for LTRs in the deep muscles. Ultrasound guidance may improve the therapeutic efficacy of trigger point injection for treating MTrPs in the deep muscles."

Rhodin A, Gronbladh L, Nilsson LH et al. 2005.  Methadone treatment of chronic non-malignant pain and opioid dependence – A long-term follow-up.  Eur J Pain [Epub ahead of print June 20]  “A structured methadone program can be used for treating chronic pain patients with opioid dependence improving pain relief and quality of life.  However, side effects and serious adverse events may limit the beneficial effects of the method.”

Rhudy JL, Martin SL, Terry EL et al. 2012. Using multilevel growth curve modeling to examine emotional modulation of temporal summation of pain (TS-pain) and the nociceptive flexion reflex (TS-NFR). Pain. [Aug 21 Epub ahead of print]. "Emotion can modulate pain and spinal nociception, and correlational data suggest that cognitive-emotional processes can facilitate wind-up-like phenomena (i.e., temporal summation of pain)....These results imply that, at least in healthy humans, within-subject changes in emotions do not promote central sensitization via amplification of temporal summation. However, future studies are needed to determine whether these findings generalize to clinical populations (e.g., chronic pain)."

Ribeiro LS, Proietti FA. 2004.  Interrelations between fibromyalgia, thyroid autoantibodies, and depression.  J Rheumatol. 31(10):2036-2040.  This study “...suggests an association between FMS and thyroid immunity.”

 

Ribel-Madsen S, Christgau S, Gronemann St et al. 2007.  Urinary markers of altered collagen metabolism in fibromyalgia patients.  Scand J Rheumatol. 36(6):470-477.  Altered collagen markers were found in FM patients, but their significance is unclear.

 

Ribel-Madsen S, Gronemann ST, Bartels EM et al. 2005.  Collagen structure in skin from fibromyalgia patients.  Int J Tissue React. 27(3):75-82. “There are some differences between the amino acid composition of skin proteins in fibromyalgia patients compared with controls.  The amount of collagen may be lower in skin from fibromyalgia patients, and collagen packing in the endoneurium may be less dense.”  [This research may hold a clue to why the skin of FMS patients reacts so differently than the skin of healthy people. DJS]

 

Ricci NA, Aratani MC, Dona F et al. 2010. [A systematic review about the effects of the vestibular rehabilitation in middle-age and older adults.] Rev Bras Fisioter.14(5):361-371. [Portuguese] "The studies included in this review provide evidence for the positive effects of VR (vestibular rehabilitation) in elderly and middle-aged adults with vestibular disturbances."[Vestibular dysfunction is a frequent co-existing condition in patients with FM and CMP. DJS]

Rich BA. 1997.  A legacy of silence: bioethics and the culture of pain.  J Med Humanit. 18(4):233-259. “This article takes bioethicists to task for failing to recognize the undertreatment of pain as a major ethical, and not merely a clinical, failing of the medical profession.”  Yet “for over 20 years the medical literature has carefully documented the undertreatment of all types of pain by physicians.” [At last, it is not just the patients who are asking why. DJS]

 

Rich BA. 1997.  A legacy of silence: bioethics and the culture of pain.  J Med Humanit. 18(4):233-259.  “For over 20 years the medical literature has carefully documented the undertreatment of all types of pain by physicians.  During this same period, as the field of bioethics came of age, the phenomenon of undertreated pain received almost no attention from the bioethics literature.  This article takes bioethicists to task for failing to recognize the undertreatment of pain as a major ethical, and not merely a clinical, failing of the medical profession.  The factors contributing to undertreated pain in the clinical setting are considered, as well as the hazards posed by recent failures to address ethically questionable clinical practices.”

Richards JR, Richards IN, Ozery G et al. 2010. Droperidol Analgesia for Opioid-Tolerant Patients. J Emerg Med. [Sep 10 Epub ahead of print]. "Patients with acute and chronic pain syndromes such as migraine headache, fibromyalgia, and sickle cell disease represent a significant portion of emergency department (ED) visits. Certain patients may have tolerance to opioid analgesics and often require large doses and prolonged time in the ED to achieve satisfactory pain mitigation. Droperidol is a unique drug that has been successfully used not only as an analgesic adjuvant for the past 30 years, but also for treatment of nausea/vomiting, psychosis, agitation, sedation, and vertigo....Droperidol has myriad pharmacologic properties that may explain its efficacy as an analgesic, including: histamine antagonist, muscarinic and nicotinic cholinergic antagonist, anticholinesterase activity, sodium channel blockade similar to lidocaine, and ...opiate receptor potentiation.....Droperidol is an important adjuvant for patients who are tolerant to opioid analgesics."

Richardson K, Gonzalez Y, Crow H et al. 2012. The effect of oral motor exercises on patients with myofascial pain of masticatory system. Case series report. NY State Dent J. 78(1):32-37. "The following case series report explores the impact of oral motor exercises on the management of myofascial pain when used in conjunction with other treatment modalities. Oral motor exercises are used by speech-language pathologists to improve the strength, range of movement and coordination of the oral musculature during non-speech movements. The findings of this case series report suggest an opportunity exists for collaboration between speech-language pathologists and the 'traditional' TMD team." [It will be a new world when the speech-language pathologists discover TrPs. DJS]

Rico-Villademoros F, Calandre EP, Rodriguez-Lopez CM et al. Sexual functioning in women and men with fibromyalgia. J Sex Med. [Oct 24 Epub ahead of print]. "Our results show that sexual dysfunction is common in patients with fibromyalgia. The disease seems to deeply affect all dimensions of sexual functioning in both females and males." [Since myofascial TrPs occur in patients with FM, and these patients were not assessed for pelvic floor and other TrPs that can cause sexual dysfunction, it is suspected that at least the majority of these symptoms could be caused by co-existing TrPs. DJS]

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.

Riemann BL, Lephart SM. 2002.  The sensorimotor system, part II: the role of proprioception in motor control and functional joint stability.  J Athl Train. 37(1):80-84.  “Although controversy remains over the precise contributions of specific mechanoreceptors, proprioception as a whole is an essential component to controlling activation of the dynamic restraints and motor control.”

 

Riering K, Rewerts C, Zieglgansberger W. 2004.  Analgesic effects of 5-HT3 receptor antagonists. Scand J Rheumatol Suppl. (119):19-23.  Tropisetron and other selective 5-HT3 receptor antagonists have promise in the treatment of FMS.

 

Rigaud J, Delavierre D, Sibert L et al. 2010. [General principles of the diagnostic approach to chronic postoperative pelvic and perineal pain.] Prog Urol 20(12:1139-1144.[French] "The aetieological and diagnostic assessment of chronic postoperative pelvic and perineal pain requires a detailed clinical analysis based on examination of the scars and analysis of the clinical signs of muscle and nerve lesions..... A test block of a nerve or trigger point is the main test performed to determine the level of the lesion responsible for pain. " [Trigger points again as the pain generator. When will the medical world get it? DJS]

Rigaud J, Delavierre D, Sibert L et al. 2010. [Management of chronic pelvic and perineal pain after suburethral tape placement for urinary incontinence.] Prog Urol. 20(12):1166-1174. [French] The role of suburethral tape in the pathogenesis of pain is essentially based on the fact that pain occurs immediately or over the days following (suburethral surgical) tape placement. The clinical features are usually fairly nonspecific, with pelvic myofascial pain, possibly associated with direct or indirect nerve lesions (obturator nerve or pudendal nerve). Local infiltration of anaesthetic along the tape is performed for diagnostic purposes to confirm the aetiology of the pain and can also have a temporary therapeutic efficacy. Surgical removal of the tape was performed with satisfactory intermediate-term results in about two out of three cases....The frequency of chronic pelvic and perineal pain following suburethral tape placement appears to be underestimated. The diagnostic approach is based on complete clinical examination and infiltration along the tape and any nerves involved. Surgical removal of the tape provides the best intermediate-term analgesic results."

Rigberg DA, Gelabert H. 2009.  The management of thoracic outlet syndrome in teenaged patients.  Ann Vasc Surg. 23(3):335-340.  A significant number of teenaged patients with thoracic outlet syndrome can be helped by TrP injection and other TrP therapy.  [Much surgery can be prevented if TRP therapy and control of perpetuating factors is done promptly and thoroughly. DJS]

Riley GP, Harrall RL, Constant CR et al. 1996.  Prevalence and possible pathological significance of calcium phosphate salt accumulation in tendon matrix degeneration.  Ann Rheum Dis. 55(2):109-115.

Riley JL 3rd, Cruz-Almeida Y, King CD et al. 2013. Age and race effects on pain sensitivity and modulation among middle-aged and older adults. J Pain. [Nov 13 Epub ahead of print.] "This study tested the effects of aging and race on responses to noxious stimuli using a wide range of stimulus modalities. The participants were 53 non-Hispanic Blacks and 138 non-Hispanic White adults, ages 45 to 76. The participants completed a single 3-hour sensory testing session where responses to thermal, mechanical, and cold stimuli were assessed. The results suggest that there are selected age differences, with the older group less sensitive to warm and painful heat stimuli than middle-aged participants, particularly at the knee. This site effect supports the hypothesis that the greatest decrement in pain sensitivity associated with aging occurs in the lower extremities. In addition, there were several instances where age and race effects were compounded, resulting in greater race differences in pain sensitivity among the older participants. Overall, the data suggest that previously reported race differences in pain sensitivity emerged in our older samples, and this study contributes new findings in that these differences may increase with age in non-Hispanic Blacks for temporal summation and both heat and cold immersion tolerance. We have added to the aging and pain literature by reporting several small to moderate differences in responses to heat stimuli between middle and older age adults."

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

Rios R, Zautra AJ. 2011. Socioeconomic disparities in pain: the role of economic hardship and daily financial worry. Health Psychol. 30(1):58-66. "Economic hardship was associated not only with greater exposure to daily financial worries but also with greater vulnerability to pain on days when daily financial worries were experienced."

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.

Rivera J, Rejas J, Esteve-Vives J et al. 2009. Resource utilization and health care costs in patients diagnosed with fibromyalgia in Spain. Clin Exp Rheumatol. 27(5 Suppl 56):S39-45. “Fibromyalgia (FM) patients have been regarded as great utilizers of health resources, with important related costs. The aim of this study is to describe health care resource utilization and related costs of FM from the perspective of the National Health System in Spain….During the year 2006 the mean total cost per patient per year was 9,982 Euros, of which 3,245.8 (32.5%) corresponded to health care costs and 6,736.2 (67.5%) to indirect costs attributable to productivity losses. Non-drug therapies accounted for the largest proportion of the health care costs, three times greater than the drug treatment. Patients with higher total costs showed the greatest disease involvement. The variables associated to the total health care costs were functional capacity, depression, comorbidities and age. Patients with permanent working disability were the greatest resource utilizers….. FM patients with higher costs show the greatest disease involvement. Direct and indirect costs are well correlated to disease severity. The indirect costs account for most of the economic burden of FM and approximately double the health care costs. Patients with permanent working disability present more severe disease and generate greater health care costs.”

Rivera J, Rejas-Gutiérrez J, Vallejo MA et al. 2012. Prospective study of the use of healthcare resources and economic costs in patients with fibromyalgia after treatment in routine medical practice. Clin Exp Rheumatol. [Aug 4 Epub ahead of print]. "Treated patients with FM in daily practice improved their clinical status and were accompanied by a significant reduction in the cost of the illness. The extra cost of drugs is substantially compensated for by less use of other healthcare resources and fewer days off work."

Rivera J, Vallejo MA, Esteve-Vives J. 2012. Drug prescription strategies in the treatment of patients with fibromyalgia. Reumatol Clin. [May 17 Epub ahead of print]. [Article in English, Spanish]. "The introduction of anticonvulsants or antidepressants, in an isolated or combined form, produces a significant clinical improvement in FM patients. The most effective drug strategy is the introduction of both drugs at the same time. The least effective strategy is not to change the number of drug prescriptions."

Rivner MH. 2001.  The neurophysiology of myofascial pain syndrome.  Curr Pain Headache Rep. 5(5):432-440.

Roach S, Sorenson E, Headley B et al. 2012. The prevalence of myofascial trigger points in the hip in patellofemoral pain patients. Arch Phys Med Rehabil Nov 2 [Epub ahead of print] Patients with pain in the front of the knee have a much greater prevalence of trigger points bilaterally in the gluteus medius and quadratus lumborum muscles. They also had less hip abduction strength which TrP release therapy was not sufficient to increase.

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.

Robinson de Senna B, Marques LS, Franca JP et al. 2009.  Condyle-disk-fossa position and relationship to clinical signs and symptoms of temporomandibular disorders in women.  Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 108(3):e117-124.

Robinson ME, Craggs JG, Price DD et al. 2010. Gray Matter Volumes of Pain-Related Brain Areas are Decreased in Fibromyalgia Syndrome. J Pain. [Dec 9 Epub ahead of print]. "Fibromyalgia (FM) is a chronic, widespread musculoskeletal pain disorder that is very prevalent in the general population (approximately 5%). Accumulating evidence suggests that FM is associated with central pain processing abnormalities, i.e., central sensitization. Several previous studies of chronic pain patients, including FM, have shown gray matter atrophy of brain areas associated with sensory and affective pain processing. These findings, however, have not been confirmed in all FM studies. In this study, we investigated gray matter volumes of brain areas associated with pain-related areas of FM patients identified by functional brain imaging…. Using a more stringent analysis than other VBM (voxel-based morphometric) studies, we provide evidence for decreased gray matter volumes in a number of pain-related brain areas in FM. Although the mechanisms for these gray matter changes are presently unclear, they may contribute to some of the core features of this chronic disorder including affective disturbances and chronic widespread pain….Increasing evidence supports the association of chronic pain with accelerated gray matter atrophy in pain disorders like low back pain, IBS, and FM syndrome. However, cause-effect relationships between chronic pain and decreased gray matter volumes have not been established yet and will require future prospective studies."

Robinson RL, Kroenke K, Williams DA et al. 2013. Longitudinal observation of treatment patterns and outcomes for patients with fibromyalgia: 12-month findings from the REFLECTIONS study. Pain Med. [June 11 Epub ahead of print]. This was a study using data from 1700 patients based on subjective inventories by patients on pregabalin (12%) duloxetine (15.5%), minilcipran (7.9%) or tricyclic antidepressants (3.9%). The focus was on "unique drugs for fibromyalgia" with over 75% of the patients taking over two or more medications, but not necessarily those medications. Duloxene and minilcipran patients had fewer outpatient visits than the others, and patients reported satisfaction with their treatment and "their fibromyalgia medication". [Bold lettering is theirs.] In the conclusions, ALL of the fibromyalgia patients had "modest improvements, high resources, and medication use, and were satisfied with the care they received." Authors admitted that it was difficult to tell the difference among the groups of patients due to the "high rates of drub discontinuation and concomitant medication over the 12 month period" of the study. The study was financed by Eli Lilly and Company. [This study is included in annotated references because it is easy to see how it could be misconstrued and perhaps misused. When quoting studies, often the sponsors of the studies and their relation to the medications are not given. DJS]

Robinson RLS, Jones ML. 2006.  In search of pharmacoeconomic evaluation for fibromyalgia treatments: a review.  Expert Opin Pharmacother. 7(8):1027-1039.  This article mentions the significant disability, complexity and economic costs of FMS, and stresses the lack of cost/benefit medical studies on remedies for FMS and that patients may try “...multiple pharmacological and non-pharmacological therapies with questionable efficacy.”  One must take into consideration any biases, intentional or unintentional, built in to research articles, but readers may not always be aware of the source of the research.  This paper was financed by a pharmaceutical company and written by its scientists. 

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 CB, Sanchez TG. 2012. [Efficacy of myofascial trigger point deactivation for tinnitus control] [Portuguese] Braz J Otorhinolaryngol 78(6):21-26. "Besides medical and audiological investigation, patients with tinnitus should also be checked for: 1) presence of myofascial pain surrounding the ear; 2) laterality between both symptoms; 3) initial decrease of tinnitus during muscle palpation. Treating this specific subgroup of tinnitus patients with myofascial trigger point release may provide better results than others described so far. [There must also be an understanding that bilateral TrPs can be interacting with tinnitus, and that TrPs in the areas of the neck and surrounding tissues may also contribute to tinnitus. DJS]

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.

Rodero B, Casanueva B, Garcia-Campayo J et al. 2010. Stages of chronicity in fibromyalgia and pain catastrophising: a cross-sectional study. BMC Musculoskel Disord. 11(1):251. "Fibromyalgia (FM) is a prevalent and disabling disorder characterized by widespread pain and other symptoms such as insomnia, fatigue and depression.... The present research examined the relationship among pain, catastrophic thinking and FM impact, as a function of stage of chronicity.... These findings provide preliminary evidence that stage of chronicity is an important moderator of psychological vulnerability for FM impact and should be taken into account by tailoring psychological interventions." [One can always tell when the researchers are psychologist and/or psychiatrists. The researchers must address the myofascial trigger points causing the symptoms and maintaining central sensitization. The lack of myofascial training in medical community is the greatest catastrophe of all. DJS]

Rodham K, Rance N, Blake D. 2010. A qualitative exploration of carers' and 'patients' experiences of fibromyalgia: one illness, different perspectives. Musculoskeletal Care. [Mar 15 Epub ahead of print]. “This study aimed to explore the lived experiences of both those with FMS and their spousal carers…. . An overriding theme running throughout was loss of identity, which fed into a sense of isolation. Participants reported feeling isolated from: healthcare professionals, whom they felt they had to convince that they had something 'real', and from friends and family because the unpredictability of their symptoms meant that they were less able to plan ahead and often had to pull out of arranged outings. They also felt isolated from their identity because they no longer recognized the person that they once were, and struggled to recognize the person that they had become. As a consequence, the people with FMS and their carers were both engaged in a process of reassessing who they were, now that FMS had become such a large part of their lives. This sense of isolation was evidenced for the carers as well as the people with FMS….”

Rodrigo L, Blanco I, Bobes J et al. 2013. Clinical impact of a gluten-free diet on health-related quality of life in seven fibromyalgia syndrome patients with associated celiac disease. BMC Gastroenterol. 13(1):157. "Celiac disease (CD) is an autoimmune disorder, characterized by the presence of gastrointestinal and multisystem symptoms, which occasionally mimic those of Irritable Bowel Syndrome (IBS) and Fibromyalgia Syndrome (FMS). To assess the effectiveness of a Gluten-Free Diet (GFD) in seven adult female screening-detected CD subjects, categorized as severe IBS and FMS patients….Results of this pilot study show that the adherence to a GFD by CD-related IBS/FMS patients can simultaneously improve CD and IBS/FMS symptoms, and indicate the merit of further research on a larger cohort."

Rodrigo L, Blanco I, Bobes J et al. 2013. Remarkable prevalence of celiac disease in patients with irritable bowel syndrome plus fibromyalgia in comparison with those with isolated irritable bowel syndrome: a case-finding study. Arthritis Res Ther. 15(6):R201. "The findings of this screening indicate that a non-negligible percentage of IBS/FMS patients are CD patients, who can improve symptoms and possibly prevent long-term CD-related complications with a strict lifelong GFD."

Rodreguez-Andreu J, Ibanez-Bosch R, Portero-Vasquez A et al. 2009.  Cognitive impairment in patients with fibromyalgia syndrome as assessed by the Mini-Mental State Examination.  BMC Musculoskeletal Disord. 10(1):162.  “Compared with the population reference value, patients with FMS showed high frequency of cognitive impairment.”

Rodreguez MA, Afari N, Buchwald DS. 2009.  Evidence for overlap between urological and noneurological unexplained clinical conditions.  J Urol. 182(5):2123-2131.  “The literature suggests considerable comorbidity between urological and noneurological unexplained clinical conditions.  The most robust evidence for overlap was for irritable bowel syndrome and urological unexplained syndromes with some estimates of up to 79% comorbidity between chronic pelvic pain and symptoms of irritable bowel syndrome.”  [Unfortunately, myofascial pain was not considered in this article, and much of the FM-relationship could be from co-existing myofascial TrPs.  Other research certainly indicates that the pelvic symptoms stem from co-existing TrPs and not from FM, which highlights the dangers of ignoring the contributions of the TrPs as well as the TrPs themselves. DJS]

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]

Rodriguez-Fernandez AL, Garrido-Santofimia V, Gueita-Rodriguez J et al. 2011. Effects of burst-type transcutaneous electrical nerve stimulation on cervical range of motion and latent myofascial trigger point pain sensitivity. Arch Phys Med Rehabil. 92(9):1353-1358. "A 10-minute application of burst-type TENS (transcutaneous electrical nerve stimulation) increases in a small but statistically significant manner the RPPT (referred pressure pain threshold) over upper trapezius latent MTrPs and the ipsilateral cervical range of motion."

Roehrs TA. 2009. Does effective management of sleep disorders improve pain symptoms? Drugs. 69 Suppl 2:5-11. “Co-morbid insomnia is a much more frequent problem than primary insomnia. In co-morbid insomnia, management of the underlying disease can improve sleep difficulty. Conversely, treating the sleep disorder may also improve the co-morbid condition. For example, patients with painful chronic illnesses are more likely to experience sleep disturbance than patients with non-painful illnesses. Moreover, there is evidence that insomnia further exacerbates pain in these illnesses. This suggests that a reciprocal relationship exists between pain and sleep, and that intervention targeted primarily at insomnia may improve pain. Treatment options for sleep disorders in the context of pain that have been assessed include cognitive behavioral therapy for insomnia and various pharmacological therapies. In randomized clinical trials, cognitive behavioral therapy significantly improved insomnia secondary to chronic pain compared with control therapy, but pain was only improved in patients in whom it was associated with pain disorders other than fibromyalgia. Of the pharmacological agents studied (zopiclone, zolpidem and triazolam), only triazolam improved both sleep and pain to a greater extent than placebo. Overall, clinical data supporting a cause-effect relationship between insomnia and pain are preliminary and are limited to several small trials. Further investigation is required to clarify the extent of the link between insomnia and pain and whether successfully managing insomnia secondary to pain improves pain symptoms. Areas of particular interest include investigation of the effect of sleep agents on analgesia and the effect of analgesics on sleep.”

Roehrs T, Diederichs C, Gillis M et al. 2012. Nocturnal sleep, daytime sleepiness and fatigue in fibromyalgia patients compared to rheumatoid arthritis patients and healthy controls: A preliminary study. Sleep Med. [Nov 10 Epub ahead of print]. "Women with FM have similar nocturnal sleep disturbance as those with RA (rheumatoid arthritis), but FM patients report greater self-rated daytime sleepiness and fatigue than RA and HC, which did not correspond to the relatively low level of objectively determined daytime sleepiness of FM patients. These findings suggest a generalized hyperarousal state in FM."

Roehrs T, Hyde M, Blaisdell B et al. 2006.  Sleep loss and REM sleep loss are hyperalgesic.  Sleep. 29(2):145-151.  “...the loss of four hours of sleep and specific REM sleep loss are hyperalgesic the following day.  Pharmacologic treatments and clinical conditions that reduce sleep and REM sleep time may increase pain.”

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.

Rogalski MJ, Kellogg-Spadt S, Hoffmann AR et al. 2010. Int Unrogynecol j PPelvic Floor Dysfunct [Epub ahead of print] Retrospective chart review of vaginal diazepam suppository in high-tone pelvic floor dysfunction.  Diazepam suppositories can be a helpful accessory treatment for tight pelvic floor muscles.  [This supports use of topical diazepam or carisoprodol used inside the vagina and/or rectum as an adjunct treatment for pelvic floor muscles tightened by TrPs. DJS]

 

Rogge N. 2003.  [Generalized muscle pain in a 67-year-old patient.  Myalgia/myogitis in therapy with Zocor]  Schweiz Rundsch Med Prax. 92(20):965-968. [German]

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.

Romanello S, Spiri D, Mancuzzi E et al. 2013 Association between childhood migraine and history of infantile colic. JAMA. 309(15):1607-1612. Infant with colic have a grater chance of developing migraines between 6 and 18 years old. The association between these types of pain is yet unknown to these researchers. [Janet Travell long ago documented that trigger points causing colic can be relieved by vapocoolant spray, and other researchers have documented the connection of trigger point cause or contribution to migraines. The great Czech doctor Karel Lewit MD has observed that colic is an early indication that trigger points will develop later, and that migraines (and menstrual pain) are adolescent signs that trigger points will be part of the diagnoses. Perhaps that is the connection for which these researchers search, and perhaps early detection and treatment of the TrPs would prevent chronic myofascial pain from developing. It certainly would be worth trying. DJS]

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

Romano, T. J. 1990. Clinical experiences with post-traumatic fibromyalgia syndrome. WV Med J 86(5):198-202.

Romero-Zurita A, Carbonell-Baeza A, Aparicio VA et al. 2012. Effectiveness of a tai-chi training and detraining on functional capacity, symptomatology and psychological outcomes in women with fibromyalgia. Evid Based Complement Alternat Med. 2012:614196 [May 9 Epub ahead of print]. "A 28-week Tai-Chi intervention showed improvements on pain, functional capacity, symptomatology and psychological outcomes in female FM patients."

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.”

Roosink M, Renzenbrink GJ, Buitenweg JR et al. 2010. Somatosensory Symptoms and Signs and Conditioned Pain Modulation in Chronic Post-Stroke Shoulder Pain. J Pain. [Dec 16 Epub ahead of print]. "Persistent shoulder pain is a common complication after stroke. Its etiology and underlying mechanisms are not well understood and treatment is generally unsatisfactory. The objective of this study was to assess the role of central sensitization and disinhibition in chronic stroke patients with chronic PSSP (n = 19), pain-free stroke patients (n = 29), and healthy controls (n = 23)….. Sensory abnormalities were more frequently observed and more severe in patients with PSSP, including positive signs such as allodynia at the affected side and generalized hyperalgesia at the unaffected side. CPM was similar in stroke patients and healthy controls. This study showed that chronic PSSP was associated with several positive and negative somatosensory signs, implicating a role for central sensitization and possibly for disinhibition. Since the causal relationship remains unclear, and may be related to either neuroplasticity induced by ongoing nociception as well as to the neuropathic brain lesion, prospective studies are warranted….The assessment of somatosensory symptoms and signs and endogenous pain modulation demonstrated a role for central sensitization and possibly for disinhibition in chronic PSSP. Prevention and treatment of PSSP could benefit from a more detailed analysis of both peripheral and central pain mechanisms." [It would be interesting to check these patients for those TrPs that cause shoulder pain. It is very likely that there are treatable myofascial components to post-stroke pain. DJS]

Roost M, Nilsson P. 2002.  [Sleep disorders — a public health problem.  Potential risk factor in the development of type 2 diabetes, hypertension, dyslipidemia and premature aging]  Lakartidningen 99(3):154-157. [Swedish]  “Sleep disorders may play a primary role in the pathophysiology of cardiovascular disease.  This has recently been documented in association with metabolic disturbances and impaired insulin action following experimental sleep deprivation.  Sleep disorders may finally prove to be part of the pathophysiological chain linking adverse psychosocial stress with the metabolic syndrome, and ultimately premature aging and early mortality.”

Rosado-Pérez J, Santiago-Osorio E, Ortiz R et al. 2012. Tai chi diminishes oxidative stress in Mexican older adults. J Nutr Health Aging. 16(7):642-646. "...the daily practice of Tai Chi is useful for reducing OxS (oxidative stress) in healthy older adults."

Rosenbaum TY. 2009.  Musculoskeletal pain and sexual function in women.  J Sex Med. [Sep 14 Epub ahead of print]  “Musculoskeletal pain (MP) that is not essentially genitally based often interferes with sex as well yet is not considered a distinct sexual dysfunction.  MP is generally addressed by physiatrists, orthopedists, and rheumatologists who are not traditionally trained in sexual medicine, and therefore, the sexual concerns of women with MP often go unaddressed.”  “Lack of mobility and MP can restrict intercourse and limit sexual activity, and gender differences are noted in response to pain.  Sexual and relationship counseling should be offered as a component of rehabilitative treatment.  Physical therapists are uniquely qualified to provide treatment to address functional activities of daily living, including sexual intercourse, and offer advice for modifications in positioning.”

Rosenbaum TY. 2009.  Musculoskeletal pain and sexual function in women.  J Sex Med. [Sep 14 Epub ahead of print].  “Lack of mobility and MP (musculoskeletal pain) can restrict intercourse and limit sexual activity, and gender differences are noted in response to pain.  Sexual and relationship counseling should be offered as a component of rehabilitative treatment.  Physical therapists are uniquely qualified to provide treatment to address functional activities of daily living, including sexual intercourse, and offer advice for modifications in positioning.”  [Future studies will be greatly enhanced if myofascial trigger point assessment and remediation would be included. DJS]

 

Rosenblum A, Joseph H, Fong C et al. 2003.  Prevalence and characteristics of chronic pain among chemically dependent patients in methadone maintenance and residential treatment facilities.  JAMA 289(18):2370-2378.  “Chronic severe pain is prevalent among patients in substance abuse treatment, especially MMTP patients.  Pain is associated with functional impairment and correlates of pain vary with the population.  Substance abuse treatment programs need to develop comprehensive and structured pain management programs.”

Rosengren SM, Colebatch JG. 2010. Vestibular evoked myogenic potentials are intact in cervical dystonia. Mov Disord. [Oct 19 Epub ahead of print]. "Vestibular dysfunction has been reported in patients with cervical dystonia (CD), but it is still unclear whether the abnormalities occur as part of the CD syndrome or whether they arise from the abnormal posture and movement of the head..... Both cervical and ocular VEMPs (vestibular-evoked myogenic potentials) were present in the majority of patients and controls..... Our results showed that VEMPs can be reliably recorded from both the neck and extraocular muscles in patients with CD, even after long disease or treatment durations, and provide evidence for intact short-latency vestibular reflexes in CD. " [FM, TrPs and vestibular dysfunction ar often interactive co-existing conditions. DJS]

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

Rosenhall, U., G. Johansson and G. Orndahl. 1987. Neuroaudiological findings in primary fibromyalgia with dysesthesia. Scand J Rehabil Med 19(4):147-152.

Rosenkranz JA, Venheim ER, Padival M. 2010. Chronic stress causes amygdala hyperexcitability in rodents. Biol Psychiatry. [Apr 6 Epub ahead of print]. “Chronic stress is a major health concern, often leading to depression, anxiety, or when severe enough, posttraumatic stress disorder. While many studies demonstrate that the amygdala is hyperresponsive in patients with these disorders, the cellular neurophysiological effects of chronic stress on the systems that underlie psychiatric disorders, such as the amygdala, are relatively unknown.... These data demonstrate a specific channelopathy that occurs in the amygdala (in rats) after chronic stress. This enhanced excitability of amygdala neurons after chronic stress may explain the observed hyperresponsiveness of the amygdala in patients with posttraumatic stress disorder and may facilitate the emergence of depression or anxiety in other patients.” [This study is of interest in that chronic stress can initiate TrPs, and TrPs may of themselves be a calcium channelopathy. DJs]

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.

Rosomoff, H.L., Rosomoff, R.S. 1999. Low back pain.  Evaluation and management in the primary care setting. Med Clin North Am 83(3):643-62. LBP is not a surgical problem [<1% of cases] needing orthopedic, neuro-surgical, or neurological attention.

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 DM, Morcelli MH, Marques NR et al. 2014. Antagonist coactivation of trunk stabilizer muscles during Pilates exercises. J Bodyw Mov Ther. 18:34-41. Pilates practitioners must be aware that some of their strategies could make some patients worse. One must be aware of compensatory muscle recruitment and other adjustments the body has made. [This is often due to trigger points.] "This suggests that the exercises of Skilled Modern Pilates only should be performed after appropriate learning and correct execution of all principles, mainly the Centering Principle."

Rossi S, della Volpe R, Ginanneschi 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.  “Early sensory processing at cortical level is changed during tonic muscle pain, mainly for those components which may be theoretically involved in proprioceptive afferent elaboration.  These changes are likely not due to subconscious or voluntary motor strategies of the subjects in the frame of a self-protective aversive reaction towards the noxious stimulus.”

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.

Roussel NA, Nijs J, Meeus M et al. 2013. Central Sensitization and Altered Central Pain Processing in Chronic Low Back Pain: Fact or Myth? Clin J Pain. 29(7):625-638. "Results of studies examining the responsiveness to various stimuli in patients with chronic LBP (low back pain) are conflicting. Some studies in patients with chronic LBP have demonstrated exaggerated pain responses after sensory stimulation of locations outside the painful region, while other studies report no differences between patients and healthy subjects. Studies examining the integrity of the endogenous pain inhibitory systems report unaltered activity of this descending inhibitory system. In contrast, studies analyzing brain structure and function in relation to (experimentally induced) pain provide preliminary evidence for altered central nociceptive processing in patients with chronic LBP. Finally, also psychosocial characteristics, such as inappropriate beliefs about pain, pain catastrophizing, and/or depression may contribute to the mechanisms of central sensitization. …It tempting to speculate that ongoing nociception is associated with cortical and subcortical reorganization and may play an important role in the process of the chronification of LBP. Future prospective research should explore to what extent these changes are reversible and if this reversibility is associated with improved functioning of patients."

Roussou E, Ciurtin C. 2012. Clinical overlap between fibromyalgia tender points and enthesitis sites in patients with spondyloarthritis who present with inflammatory back pain. Clin Exp Rheumatol. [Aug 30 Epub ahead of print]. "To assess the extent of coexistence of inflammatory back pain (IBP) with fibromyalgia (FM) features in patients with spondyloarthritis (SpA), and to assess the degree of overlap of FM tender points (TeP) and enthesitis sites (ES) in patients with SpA.....One third of patients with IBP fulfilled the criteria for FM. There is a significant degree of overlap between FM TeP and ES in patients with IBP.[Since many patients with FM have trigger points, and trigger points in the attachment areas cause enthesitis and enthesis, it would be helpful to know what percentage of these patients had TrPs and if the contracture from TrPs might cause the inflammation. DJS]

Rowbotham MC, Twilling L, Davies P et al. 2003.  Oral opioid therapy for chronic peripheral and central neuropathic pain.  New England Jour Med 348:1223-1232.

Rowe AH, Xiao Y, Rowe MP et al. 2013. Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin. Science. 342(6157):441-446. "Painful venoms are used to deter predators. Pain itself, however, can signal damage and thus serves an important adaptive function. Evolution to reduce general pain responses, although valuable for preying on venomous species, is rare, likely because it comes with the risk of reduced response to tissue damage. Bark scorpions capitalize on the protective pain pathway of predators by inflicting intensely painful stings. However, grasshopper mice regularly attack and consume bark scorpions, grooming only briefly when stung. Bark scorpion venom induces pain in many mammals (house mice, rats, humans) by activating the voltage-gated Na(+) channel Nav1.7, but has no effect on Nav1.8. Grasshopper mice Nav1.8 has amino acid variants that bind bark scorpion toxins and inhibit Na(+) currents, blocking action potential propagation and inducing analgesia. Thus, grasshopper mice have solved the predator-pain problem by using a toxin bound to a nontarget channel to block transmission of the pain signals the venom itself is initiating."

Rowe PC, Fontaine KR, Violand RL. 2013. Neuromuscular strain as a contributor to cognitive and other symptoms in chronic fatigue syndrome: hypothesis and conceptual model. Front Physiol. 4:115. "Individuals with chronic fatigue syndrome (CFS) have heightened sensitivity and increased symptoms following various physiologic challenges, such as orthostatic stress, physical exercise, and cognitive challenges. Similar heightened sensitivity to the same stressors in fibromyalgia (FM) has led investigators to propose that these findings reflect a state of central sensitivity. A large body of evidence supports the concept of central sensitivity in FM. A more modest literature provides partial support for this model in CFS, particularly with regard to pain. Nonetheless, fatigue and cognitive dysfunction have not been explained by the central sensitivity data thus far. Peripheral factors have attracted attention recently as contributors to central sensitivity. Work by Brieg, Sunderland, and others has emphasized the ability of the nervous system to undergo accommodative changes in length in response to the range of limb and trunk movements carried out during daily activity. If that ability to elongate is impaired-due to movement restrictions in tissues adjacent to nerves, or due to swelling or adhesions within the nerve itself-the result is an increase in mechanical tension within the nerve. This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through a variety of mechanisms. These include mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides. Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we use the more general term "neuromuscular strain." In our clinical work, we have found that neuromuscular restrictions are common in CFS, and that many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination. In this paper we submit that neuromuscular strain is a previously unappreciated peripheral source of sensitizing input to the nervous system, and that it contributes to the pathogenesis of CFS symptoms, including cognitive dysfunction." [This is an interesting paper indicating that perhaps trigger points may be common in CFS, as they are in FM. DJS]

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."

Rra ML, Angst F, Beck T et al. 2012. Horticultural therapy for patients with chronic musculoskeletal pain: results of a pilot study. Altern Ther Health Med. 18(2):44-50. "Seventy-nine patients with chronic musculoskeletal pain (fibromyalgia or chronic, nonspecific back pain) participated in the study….The addition of horticultural therapy to a pain management program improved participants' physical and mental health and their coping ability with respect to chronic musculoskeletal pain."

Ruaro JA, Frez AR, Ruaro MB et al. 2014. Low-level laser therapy to treat fibromyalgia. Lasers Med Sci. [May 7 Epub ahead of print.] "LLLT provided relief from fibromyalgia symptoms in patients and should be further investigated as a therapeutic tool for management in fibromyalgia."

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 Moral R, Rodriguez Salvador J, Perula L et al. 2006.  [Problems and solutions in health care for chronic diseases. A qualitative study with patients and doctors.] Aten Primaria 38(9):483-489. [Spanish]  “To tackle prevalent chronic problems requires, in the view of doctors and patients, important modifications that are related mainly to the kind of relationship between the two, with new clinical responsibilities and certain organizational care delivery features.”  Presently, chronic illness is frustrating to patients and care givers.  Suggestions are given to remedy this.

Ruiz-Párraga GT, López-Martínez AE, Gómez-Pérez L. 2012. Factor structure and psychometric properties of the resilience scale in a Spanish chronic musculoskeletal pain sample. J Pain. 13(11):1090-1098. "This article presents the first resilience questionnaire (RS-18) for chronic pain patients. The instrument obtained shows good reliability and validity. The results provide health-care professionals and researchers with a measure of resilience in chronic pain patients that excludes items related to functional disability."

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.”

Ruscheweyh R, Sandkuhler J. 2005.  Opioids and central sensitization: II.  Induction and reversal of hyperalgesia. Eur J Pain 9(2):149-152.  “Opioids are powerful analgesics when used to treat acute pain and some forms of chronic pain.  In addition, opioids can preempt some forms of central sensitization.”   This paper reviews evidence that opioids may also induce and also perhaps reverse some forms of central sensitization.

 

Rush SM, Christensen JC, Johnson CH. 2000.  Biomechanics of the first ray.  Part II: Metatarsus primus varus as a cause of hypermobility.  A three-dimensional kinematic analysis in a cadaver model.  J Foot Ankle Surg 39(2):68-77.  [Tightness of foot muscles, such as that due to myofascial TrPs, could be a major and unrecognized cause of foot hypermobility. DJS]

Rusiecki, RS. 1998.  Chest pain as result of temporomandibular disorder (TMD). Gen Dent46(4):352-5.

Russell AL, McCarty MF. 2000.  DL-phenylalanine markedly potentiates opiate analgesia – an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system.  Med Hypotheses 55(4):283-288.

Russell IJ. 2011. Future perspectives in generalized musculoskeletal pain syndromes. Best Pract Res Clin Rheumatol. 25(2):321-331. "This article describes contemporary controversies regarding two categories of soft-tissue pain (STP) - chronic widespread pain and fibromyalgia syndrome.... STP classification divides relevant painful conditions into three subgroups, depending on the extent of body involvement (localized, regional and generalized). Fibromyalgia syndrome, in the generalized STP category, is distinguished from other types of chronic widespread pain by virtue of its greater severity. During the past 20 years, the diagnosis of fibromyalgia was based on a research classification (1990 American College of Rheumatology Research Classification Criteria (1990 ACR RCC)) that requires a history of chronic widespread pain and the examination finding of widespread mechanical allodynia. A new approach (2010 American College of Rheumatology Fibromyalgia Diagnostic Criteria (2010 ACR FDC)), validated for clinical use, still requires a history of chronic widespread pain, but the examination is replaced by a historical assessment of co-morbid symptom severity. The populations identified by the two criteria are similar but not identical. Misuse of the new criteria could expand fibromyalgia from 2 to 10% of the general population. Avoidance of the term 'fibromyalgia' could return it to the obscurity from whence it came, leaving a much larger problem in its stead."

Russell IJ. 2004.  Developments in the fibromyalgia syndrome.  J Musculoskeletal Pain 12(3/4):47-57.   “The FMS is no longer unknown to the medical practitioner.  This new status requires practical diagnostic criteria validated for use in community care, a common nomenclature, a better understand of pathogenesis, and effective treatment modalities.  Remarkably, there is dramatic progress in all of these areas.”  This excellent overview provides reasons for identifying subgroups of FMS, some new and promising medications, and the need for training and clarification on several issues.

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

Russell IJ, Holman AJ, Swick TJ et al. 2011. Sodium oxybate reduces pain, fatigue and sleep disturbance and improves functionality in fibromyalgia: results from a 14-week, randomized, double-blind, placebo-controlled study. Pain. [Mar 10 Epub ahead of print]. "These results expand the evidence from previous clinical trials suggesting that SXB is effective and safe in FM. This study expands evidence from previous trials that sodium oxybate provides safe, effective treatment for multiple symptoms experienced by patients with fibromyalgia."

 

Russell IJ, Larson AA. 2009.  Neurophysiopathogenesis of fibromyalgia syndrome: a unified hypothesis.  Rheum Dis Clin North Am. 35(2):421-435.  “The characteristic presenting complaint of patients with fibromyalgia syndrome (FMS) is chronic widespread allodynia.  Research findings support the view that FMS is an understandable and treatable neuropathophysiologic disorder.  The pain of FMS is often accompanied by one or more other manifestations, such as affective moods, cognitive insecurity, autonomic dysfunction, or irritable bowel or bladder.  Growing evidence suggests that this is a familial disorder with many underlying genetic associations.  New findings from brain imaging and polysomnography imply that FMS may be a disorder of premature neurologic aging.  A conceptual model at the molecular level is proposed to explain many of the observed features of FMS.  The model can also explain anticipated responses to FDA approved pharmacologic therapies.”  [It is unknown at this time as to how much of the irritable bladder and bowel and autonomic dysfunction and other symptoms often attributed to FM may in actuality be due to co-existing TrPs.  This model is very interesting, and as genetic research and epigenetic research unfolds, those of us with FM can look forward to more answers. DJS]

 

Russell IJ, Crofford LJ, Leon T et al. 2009.  The effects of pregabalin on sleep disturbance symptoms among individuals with fibromyalgia syndrome.  Sleep Med. [Apr 30 Epub ahead of print].  “These data demonstrate improvement in FM-related sleep dysfunction with pregabalin therapy.  The majority of this benefit was a direct effect of pregabalin on the patients’ insomnia, while the remainder occurred through the drug’s analgesic activity.”

 

Russell IJ, Mease P, Smith T et al. 2007.  The safety and efficacy of duloxetine for the treatment of fibromyalgia syndrome in patients with or without major depressive disorder: results from a 6-month randomized, double-blind, placebo-controlled, fixed-dosed trial.  J Musculoskel Pain 15 (Supp 13):58 item 103.  [Myopain 2007 Poster]  “DLX60 (duloxetine 60 mg) and DLX120 mg/d are efficacious and safe treatment options for pain associated with FMS, whether or not MDD (major depressive disorder) is present.”

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, 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.

Ruster M, Franke S, Spath M et al. 2005.  Detection of elevated N(epsilon)-carboxymethyllysine levels in muscular tissue and in serum of patients with fibromyalgia.  Scand J Rheumatol. 34(6):460-463.  “Both mechanisms may contribute to the development, perpetuation, and spreading of pain characteristic in FM patients.”

 

Rustoen T, Wahl AK, Hanestad BR et al. 2005.  Age and the experience of chronic pain: differences in health and quality of life among younger, middle-aged and older adults.  Clin J Pain 21(6):513-523.  “The prevalence rates for chronic pain do vary with age and the middle-aged group may be a high-risk group of patients with chronic pain.”  [This may indicate that chronic pain precursors such as individual TrPs and developing initiators of FMS such as lack of restorative sleep are not being diagnosed and adequately treated.  We may be seeing a lack of medical training as a major perpetuating factor of chronic pain. DJS]

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.

Rutledge DN, Mouttapa M, Wood PB. 2009.  Symptom clusters in fibromyalgia: potential utility in patient assessment and treatment evaluation.  Nurs Res. 58(5):359-367.  “In this well-educated, primarily Caucasian sample, morning stiffness, fatigue, and not feeling rested in the morning were the symptoms with the highest severity scores.”  “The findings support the heterogeneity of the FM experience and the presence of symptom clusters within the greater spectrum of symptoms comprising the FM syndrome.  These observations suggest the possibility of tailoring interventions based upon individual patient symptomatology.”  [This article did not consider the co-existing TrPs, so many of the symptoms ascribed to FM may actually be due to TrPs.  DJS]

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.


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