and Trigger
Points for
Care Providers



in Spanish

in Dutch


Myofascial Pain

Fibromyalgia Subsets

Health Care
Providers Bibliography

References for




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

annotated by Devin J. Starlanyl



References for Research Purposes

A-C       D-E

F-H       I-K

L-N       O-R


On This Page
W  X  Y  Z

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).


Wadiche JI, Jahr CE. 2005.  Patterned expression of Purkinje cell glutamate transporters controls synaptic plasticity.  Nat Neurosci. [Sept 4 Epub ahead of print]  “Neuronal uptake sites must be overwhelmed by glutamate to activate perisynaptic metabotropic glutamate receptors.  Regional differences in glutamate transporter expression affect the degree of metabotropic glutamate receptor activation and therefore regulate synaptic plasticity.”

Wagner B, Kagan-HAllet KS, Russell IJ. 2003.  Concomitant presentation of adermatopathic dermatomyositis, statin myopathy, fibromyalgia syndrome, piriformis muscle myofascial pain syndrome, and diabetic neuropathy.  J Muscoloskel Pain 11(2):25-30.  This interesting case study details how complex chronic pain diagnosis and treatment can be and teaches a good lesson why it is very important not to ascribe all chronic pain symptoms to one syndrome.  It takes knowledge, care and time to optimize the quality of life of a patient with multiple conditions.

Wagner JS, Chandran A, DiBonaventura M et al. 2013. The costs associated with sleep symptoms among patients with fibromyalgia. Expert Rev Pharmacoecon Outcomes Res. 13(1):131-139. "Among the FM population, sleep symptoms were prevalent and associated with higher direct and indirect costs, suggesting improved management may have long-term cost savings." [This leads one to wonder why Xyrem is not approved for deep-sleep-deprived patients with FM. DJS]

Wagner JS, Dibonaventura MD, Chandran AB et al. 2012. The association of sleep difficulties with health-related quality of life among patients with fibromyalgia. BMC Musculoskel Disord. 13(1):199. "Among the FM population, sleep difficulty symptoms were independently associated with clinically-meaningful decrements in mental and physical HRQoL (health-related quality of life). These results suggest that greater emphasis in the treatment of sleep difficulty symptoms among the FM population may be warranted."

Wagner, J., M. L. Wagner and W. A. Hening. 1998. Beyond benzodiazepines: alternative pharmacologic agents for the treatment of insomnia. Ann Pharmacother 32(6):680-91.

Wagner, M. L., A. S. Walters, R. G. Coleman, W. A. Hening, K. Grasing and S. Choroverty. 1996. Randomized, double blind, placebo-controlled study of clonidine in restless legs syndrome. Sleep 19(1):52-58.

Walen H.R., Cronan T.A., Server E.R. et al. 2002. Subgroups of fibromyalgia patients: evidence for heterogeneity and an examination of differential effects following a community-based intervention.  J Musculoskel Pain 10(3):9-32.

Walitt B, Roebuck-Spencer T, Esposito G et al. 2007.  The effects of multidisciplinary therapy on positron emission tomography of the brain in fibromyalgia: a pilot study.  Rheumatol Int. [Jul 20 Epub ahead of print].  “An increase in limbic metabolism was noted with concomitant symptomatic improvement, suggesting that the limbic system attenuates FM symptoms.”

Walitt B, Roebuck-Spencer T, Esposito G et al. 2007.  The effects of multidisciplinary therapy on positron emission tomography of the brain in fibromyalgia: a pilot study.  Rheumatol Int. [Jul 20 Epub ahead of print].  “This pilot study sought to determine if alterations in regional brain metabolism from baseline occur in FM after undergoing a multidisciplinary therapeutic regimen.”  “A clinical improvement was noted with treatment.”  “An increase in limbic metabolism was noted with concomitant symptomatic improvement, suggesting that the limbic system attenuates FM symptoms.”

Walker E.A., Keegan D., Gardner G. et al. 1997. Psychosocial factors in fibromyalgia compared with rheumatoid arthritis: II.  Sexual, physical and emotional abuse and neglect.  Psychosom Med 59:572-7.  “Although childhood maltreatment was found to be a general risk factor for fibromyalgia, particular forms of maltreatment (e.g. sexual abuse per se) did not have specific effects... Fibromyalgia seems to be associated with increased risk of victimization, particularly adult physical abuse.”

Walker, E. A., W. J. Katon, D. Keegan, G. Gardner and M. Sullivan. 1997. Predictors of physician frustration in the care of patients with rheumatological complaints. Gen Hosp Psychiatry 19(5):315-23. .

Walker, E. A., D. Keegan, G. Gardner, M. Sullivan, D. Bernstein and W. J. Katon. 1997.Psychosocial factors in fibromyalgia compared with rheumatoid arthritis: II. Sexual, physical, and emotional abuse and neglect. Psychosom Med 59(6):572-577.

Walker, E. A., J. Unutzer and W. J. Katon. 1998. Understanding and caring for the distressed patient with multiple medically unexplained symptoms. J Am Board Fam Pract 11(5):347-56.

Walker, J. M., A. G. Hohmann, W. J. Martin, N. M. Strangman, S. M. Huang and K. Tsou.1999. The neurobiology of cannabinoid analgesia. Life Sci 65(6-7):665-73.

Walker LS, Sherman AL, Bruehl S et al. 2012. Functional abdominal pain patient subtypes in childhood predict functional gastrointestinal disorders with chronic pain and psychiatric comorbidities in adolescence and adulthood. Pain. [Jun 19 Epub ahead of print]. "Although pediatric functional abdominal pain (FAP) has been linked to abdominal pain later in life, childhood predictors of long-term outcomes have not been identified. This study evaluated whether distinct FAP profiles based on patterns of pain and adaptation in childhood could be identified and whether these profiles predicted differences in clinical outcomes and central sensitization (wind-up) on average 9 years later. In 843 pediatric FAP patients, cluster analysis was used to identify subgroups at initial FAP evaluation based on profiles of pain severity, gastrointestinal (GI) and non-GI symptoms, pain threat appraisal, pain coping efficacy, catastrophizing, negative affect, and activity impairment. Three profiles were identified: high pain dysfunctional, high pain adaptive, and low pain adaptive....Pediatric patients with the high pain adaptive profile had baseline pain severity comparable to that of the high pain dysfunctional profile, but had outcomes as favorable as the low pain adaptive profile. In laboratory pain testing at follow-up, high pain dysfunctional patients showed significantly greater thermal wind-up than low pain adaptive patients, suggesting that a subgroup of FAP patients has outcomes consistent with widespread effects of heightened central sensitization." [It would have been valuable if these patients had been assessed for co-existing trigger points often causing abdominal pain and dysfunction. It is hoped that future studies would include this important parameter. DJS]

Wallace D. 2007.  Bipolar illness with complaints of chronic musculoskeletal pain is a form of pseudofibromyalgia.  J Musculoskel Pain 15 (Supp 13):59 item 105.  [Myopain 2007 Poster]  “Bipolar illness may be associated with a form of chronic musculoskeletal pain complaints which is not FMS.  Studies into the role that neurotransmitters play in bipolar patients with complaints of musculoskeletal discomfort deserves further exploration.”  [This study suggests that patients diagnosed with FM and bipolar disorder may not have FM at all, but may have another condition entirely. DJS]

Wallace DJ, Hallegua DA. 2004.  Fibromyalgia: the gastrointestinal link.  Curr Pain Headache Rep. 8(5):364-368.  30% to 70% of FMS patients have IBS.

Wallace DJ. 2006.  Is there a role for cytokine based therapies in fibromyalgia?  Curr Pharm Des. 12(1):17-22.  “A review of the fibromyalgia literature and related studies suggest that IL-1, IL-6 and IL-8 are dysregulated in the syndrome.  Therapies directed against these cytokines may be of potential importance in the management of fibromyalgia.”

Wallace, D. J. 1997. The fibromyalgia syndrome. Ann Med 29(1):9-21.

Wallace, D. J. 1990. Genitourinary manifestations of fibrositis; An increased association with the female urethral syndrome. J Rheumatol 17(2):238-9.

Wallace M, Moulin DE, Rauck RL et al. 2009.  Long-term safety, tolerability, and efficacy of OROS hydromorphone in patients with chronic pain.  J Opioid Manag. 5(2):97-105.  “Once-daily OROS hydromorphone is an osmotically driven, controlled-release preparation that may be particularly well suited to long-term use, because it provides consistent plasma concentrations and sustained around-the-clock analgesia.  In this study, the benefits of OROS hydromorphone attained in short-term studies were maintained in the long-term when daily administration was continued.”

Wallden M. 2013. The primal nature of core function: In rehabilitation & performance conditioning. J Bodyw Mov Ther. 17(2):239-248. "In this editorial, what is understood of the definition and function of the human core is discussed; presented in the context of evolution and holistic human modeling. It appears likely from this understanding of neural phenomena such as central sensitization, neural facilitation/inhibition, tonic and phasic motoneuron excitatory thresholds and viscerosomatic convergence that, very simply, for effective core function, optimal visceral function is a pre-requisite and may be a commonly overlooked aspect of patient rehabilitation. Furthermore, not only is core function key for optimal expression of forces through the appendicular skeleton, but since it is the tonic motoneurons most readily inhibited by nociceptive (including viscerosomatic) phenomena, this will likely affect the tonic components of peripheral musculature directly; impairing both local motor control and performance at peripheral joints." [Core muscle dysfunctions are often at the base of peripheral muscle symptoms. The peripheral muscles try to compensate when the core is weakened by trigger points, causing the peripheral muscles to become overloaded and develop their own trigger points (and the pain and dysfunction they cause). Too often this valuable insight is ignored. DJS]

Walsh, J. K. and C. L. Engelhardt. 1999. The direct economic costs of insomnia in the United States for 1995. Sleep Suppl 2:S386-93.

Walter A, Rigaud J, Labat JJ. 2010. [Irritable bowel syndrome, levator ani syndrome, proctalgia fugax and chronic pelvic and perineal pain.] Prag Urol 20(12):995-1002. [French] These conditions are frequently found together, and may have related initiating and perpetuating factors. [Myofascial trigger points, vertebral disorders, imbalances of neuromodulators, leaky gut, and central sensitization are some of the interactive factors mentioned in this article. DJS]

Walter, B., D. Vaitl and R. Frank. 1998. Affective distress in fibromyalgia syndrome is associated with pain severity. Z Rheumatol 57 Suppl 2:101-4.

Walters, A. S., D. L. Picchietti, B. L. Ehrenberg and M. L. Wagner. 1994. Restless legs syndrome in childhood and adolescence. Pediatr Neurol 11(3):241-5.

Walters A. S. 1995. Toward a better definition of the restless legs syndrome. The International Restless Legs Syndrome Study Group. Mov Disord 10(5):634-642.

Walz, F. 1987. [Whiplash, of the cervical vertebrae in traffic: bio mechanical and expert-opinion aspects]. Schweiz Med Wochenschr 117(16):619-623. [German]

Wang C. 2012. Role of tai chi in the treatment of rheumatologic diseases. Curr Rheumatol Rep. 14(6):598-603. "Rheumatologic diseases (e.g., fibromyalgia, osteoarthritis, and rheumatoid arthritis) consist of a complex interplay between biologic and psychological aspects, resulting in therapeutically challenging chronic conditions to control. Encouraging evidence suggests that Tai Chi, a multi-component Chinese mind-body exercise, has multiple benefits for patients with a variety of chronic disorders, particularly those with musculoskeletal conditions. Thus, Tai Chi may modulate complex factors and improve health outcomes in patients with chronic rheumatologic conditions. As a form of physical exercise, Tai Chi enhances cardiovascular fitness, muscular strength, balance, and physical function. It also appears to be associated with reduced stress, anxiety, and depression, as well as improved quality of life. Thus, Tai Chi can be safely recommended to patients with fibromyalgia, osteoarthritis, and rheumatoid arthritis as a complementary and alternative medical approach to improve patient well-being."

Wang C. 2011. Tai chi and rheumatic diseases. Rheum Dis Clin North Am. 37(1):19-32. "Tai chi is a complex multicomponent mind-body exercise. Many studies have provided evidence that tai chi benefits patients with a variety of chronic disorders. This form of mind-body exercise enhances cardiovascular fitness, muscular strength, balance, and physical function and seems to be associated with reduced stress, anxiety, and depression and improved quality of life. Thus, despite certain limitations in the evidence, tai chi can be recommended to patients with osteoarthritis, rheumatoid arthritis, and fibromyalgia as a complementary and alternative medical approach."

Wang C, Ge HY, Ibarra JM et al. 2012. Spatial Pain Propagation over Time Following Painful Glutamate Activation of Latent Myofascial Trigger Points in Humans. J Pain. [Apr 25 Epub ahead of print]. "The aim of this present study was to test the hypothesis that tonic nociceptive stimulation of latent myofascial trigger points (MTPs) may induce a spatially enlarged area of pressure pain hyperalgesia….This study shows that MTPs are associated with an early occurrence of a locally enlarged area of pressure hyperalgesia associated with spreading central sensitization. Inactivation of MTPs may prevent spatial pain propagation."

Wang CF, Chen M, Lin MT et al. 2006.  Teres minor tendonitis manifested with chronic myofascial pain syndrome in the scapular muscles: a case report.  J Musculoskeletal Pain 14(1):39-43.

Wang CF, Pancaro C, Gerner P et al. 2011. Prolonged Suppression of Postincisional Pain by a Slow-release Formulation of Lidocaine. Anesthesiology. 114(1):135-149. "Postoperative pain can occur despite nerve blocks during the surgical period. Here we tested Xybrex (Orthocon, Inc., Irvington, NY), a slow-release formulation of lidocaine that blocks rat sciatic nerve for 1-2 days, for its ability to suppress postincisional pain…..Implants of slow-release lidocaine formulations are most effective against postincisional pain when placed at the ipsilateral nerve innervating the area of incision. Contralateral nerve implants are somewhat less effective, probably acting by releasing lidocaine into the systemic circulation. There appears to be a differential role of central sensitization between postincisional allodynia and hyperalgesia." [Although this study was done in rats, it may have important ramifications in preventing one cause of central sensitization in humans. DJS]

Wang H, Kohno T, Amaya F et al. 2005.  Bradykinin produces pain hypersensitivity of potentiating spinal cord glutamatergic synaptic transmission.  J Neurosci. 25(35):7986-7992.   “...bradykinin is released in the spinal cord in response to nociceptor inputs and acts as a synaptic neuromodulator, potentiating glutamatergic synaptic transmission to produce pain hypersensitivity.”

Wang, K., R. McCarter, J. Wright, J. Beverly and R. Ramirez-Mitchell. 1993. Viscoelasticity of the sarcomere matrix of skeletal muscles. The titin-myosin composite filament is a dual-stage molecular spring. Biophys J 64(4):1161-77.

Wang, K. 1984. Cytoskeletal matrix in striated muscle: the role of titin, nebulin and intermediate filaments. Adv Exp Med Biol 170:285-305.

Wang LM, Suthana NA, Chaudhury D et al. 2005.  Melatonin inhibits hippocampal long-term potentiation.  Eur J Neurosci. 22(9):2231-2237.

Wang YH, Chen SM, Kuan TS et al. 2007.  Therapeutic effect of kinesio TM taping on the myofascial pain syndrome in upper trapezius muscle.  J Musculoskel Pain 15 (Supp 13):40 item 70.  [Myopain 2007 Poster]

Wang YH, Yin MJ, Fan ZZ et al. 2013. Hyperexcitability to electrical stimulation and accelerated muscle fatigability of taut bands in rats. Acupunct Med. [Dec 6 Epub ahead of print.] The taut bands associated with myofascial trigger points were, in this study, more excitable to electrical stimulation in rats, and significantly less resistant to fatigue than healthy muscle fibers.

Wang YT, Taylor L, Pearl M et al. 2004.  Effects of Tai Chi exercise on physical and mental health of college students.  Am J Chin Med. 32(3):453-459. “Tai Chi exercise had positive effects on the self-assessed physical and mental health of college students.”

Wang YX, Pettus M, Gao D et al. 2000.  Effects of intrathecal administration of ziconotide, a selective neuronal N-type calcium channel blocker, on mechanical allodynia and heat hyperalgesia in a rat model of postoperative pain.  Pain. 84(2-3):151-158.  This study done on a cone shell biochemical indicates that it may be an effective pain reliever more potent than morphine.  [There are many researchers looking at different types of pain relief, but it will take time to evaluate them.  Some may eventually be useful for myofascial pain or fibromyalgia, and it can give patients hope to know that there are many alternatives for symptom relief “in the pipeline.”  DJS]  


Ware M, Beaulieu P. 2005.  Cannabinoids for the treatment of pain: an update on recent clinical trials.  Pain Res Manag. 10 Suppl A:27A-30A.  “The potential for cannabinoid therapy for chronic pain states is encouraging.  Clinicians working in pain management should be aware of the options becoming available from the cannabinoid class of medications.”

Warner, E., al-N. Keshavjee, R. Shupak and A. Bellini. 1997. Rheumatic symptoms following adjuvant therapy for breast cancer. Am J Clin Oncol 20(3):322-326.

Warnock, J. K., J. C. Bundren and D. W. Morris. 1999. Female hypoactive sexual disorder: case studies of physiologic androgen replacement. J Sex Marital Ther 25(3):175-82.

Warren JW, Clauw DJ. 2012. Functional Somatic Syndromes: Sensitivities and Specificities of Self-Reports of Physician Diagnosis. Psychosom Med. [Oct 15 Epub ahead of print]. "Self-report of physician diagnosis did not identify most of the three most venerable functional somatic syndromes, IBS, FM, and, especially, CFS; nor did it identify substantial minorities of individuals with panic disorder and migraine. Self-report of physician diagnosis was particularly poor in recognizing persons with multiple syndromes. The insensitivity of this diagnostic test has effects on not only prevalence and incidence estimates but also correlates, comorbidities, and case recruitment. To reveal individuals with these syndromes, singly or together, queries of symptoms, not diagnoses, are necessary."

Wasilewska J, Kaczmarski M. 2004.  Sleep-related breathing disorders in small children with nocturnal acid gastroesophageal reflux.  Rocz Akad Med Bialymst. 49:98-102.  “Higher number of apnea/hypopnea during REM sleep was found in children with nocturnal gastroesophageal reflux.”

Wasner, G., K. Heckmann, C. Maier and R. Baron. 1999. Vascular abnormalities in acute reflex sympathetic dystrophy (CRPS I): complete inhibition of sympathetic nerve activity with recovery. Arch Neurol 56(5):613-20.

Watkin H. 2004.  Back pain – an integrated approach in primary care.  Acupunct Med. 22(4):203-206.  “For chronic back pain, exercise, pain management programs, non-steroidal anti-inflammatory and analgesic drugs and trigger point and ligament injections are also recommended.  There appears to be increasing evidence in favor of the use of acupuncture.  Acupuncture appears to be useful to treat back pain, but patients should probably be advised to take advantage of any pain relief obtained to maintain or increase their activity.”

Watkins LR, Hutchinson MR, Johnston IN et al. 2005.  Glia: novel counter-regulators of opioid analgesia.  Trends Neurosci. [Oct 20 Epub ahead of print]  During the past four years the glial cell has been found to have the ability to contribute to opioid intolerance and also to interfere with opioid analgesia.  Glial cells are “important contributors to the creation of enhanced pain states via the release of neuroexcitatory substances.  New data suggest that glia also release neuroexcitatory substances in response to morphine, thereby opposing its effects.  Controlling glial activation could therefore increase the clinical utility of analgesic drugs.”  [This may be why many patients with FMS need higher amounts of opioids to achieve the same affects.  The use of a glial cell moderator such as topical pentoxifylline may be helpful until we can find  ways to interrupt the glial cell activation pathways. DJS].

Watkins LR, Maier SF. 2002.  Beyond neurons: evidence that immune and glial cells contribute to pathological pain states.  Physiol Rev 82(4):981-1011.  Chronic pain states with grossly abnormal sensory processing can result following a peripheral nerve injury, infection or inflammation.  Activated immune and glial cells release biochemicals that can induce chronic pain states.  These include proinflammatory cytokines such as tumor necrosis factor and interleukins 1 and 6.  “..all nerves and neurons regardless of modality or function are likely affected by immune and glial activation…”

Watkins LR, Milligan ED, Maier SF. 2003.  Glial proinflammatory cytokines mediate exaggerated pain states: implications for clinical pain.  Adv Exp Med Biol 521:1-21.  “…drugs that target glia and the chemical substances that these glia release are predicted to be powerful remedies for pain problems in people.”

Watson, C. P. 1994. Topical capsaicin as an adjuvant analgesic. J Pain Symptom Manage 9(7):425-433.

Watson NF, Buchwald D, Goldberg J et al. 2010. Is Chiari-I Malformation Associated with Fibromyalgia? Neurosurgery. [Nov 30 Epub ahead of print]. "Most patients with FM do not have CIM pathology. Future studies should focus on dynamic neuroimaging of craniocervical neuroanatomy in patients with FM." [We know that TrPs, and even turning the head, can narrow the canal. Surgery should never be done lightly. DJS]

Watson NF, Buchwald D, Goldberg J et al. 2009.  Neurologic signs and symptoms in fibromyalgia.  Arthritis Rheum. 60(9):2839-2844.  “This blinded, controlled study demonstrated neurologic physical examination findings in persons with FM.  The FM group had more neurologic symptoms than did the controls, with moderate correlation between symptoms and signs.  These findings have implications for the medical evaluation of patients with FM.”  [Co-existing conditions were not taken into account, so it may be likely that at least some if not most of these symptoms, such as numbness and tingling and gait disturbance, were in actuality due to co-existing myofascial TrPs. DJS]

Watt-Watson JH, Graydon JE. 1989.  Sickness impact profile: a measure of dysfunction with chronic pain patients.  J Pain Symptom Manage. 4(3):152-156.  “Although chronic pain may affect all facets of a patient’s life, there is no generally accepted method of measuring the extent of the disability experienced.  The SIP scores indicated severe disruption in daily activities and relationships for this sample.  Significant correlations between the SIP and visual analogue scales measuring coping adequacy and activity levels were interesting and warrant further study.”

Waxman, J. and S. M. Zatzkis. 1986. Fibromyalgia and menopause: examination of the relationship. Postgrad Med 80(4):165-7, 170-1.

Waylonis, G. W. and R. H. Perkins. 1994. Post-traumatic fibromyalgia. A long-term follow-up. Am J Phys Med Rehabil.

Waylonis, G. W. and W. Heck. 1992. Fibromyalgia syndrome. New associations. Am J Phys Med Rehabil 71(6):343-8.

Weaver SA, Janal MN, Aktan N et al. 2010. Sex differences in plasma prolactin response to tryptophan in chronic fatigue syndrome patients with and without comorbid fibromyalgia. J Womens Health [Apr 12 Epub ahead of print]. “Abstract Background: Some think chronic fatigue syndrome (CFS) and fibromyalgia (FM) are variants of the same illness process. This would imply that CFS patients with and without comorbid FM have similar biological underpinnings. To test this, we compared serotonergic-based responses, plasma prolactin (PRL), and self-reported measures of fatigue to intravenous infusion of tryptophan among patients with CFS alone, CFS + FM, and healthy controls.....Conclusions: These results indicate that women with CFS alone have upregulated serotonergic tone that is not seen in those with comorbid FM. The lack of effect in men suggests a mechanism that might explain, in part, the increased prevalence of CFS in women. The data support the interpretation that CFS in women is a different illness from FM”.

Weber, C. 1998. [NMDA-receptor antagonist in pain therapy]. Anasthesiol Intensivmed Notfallmed Schmerzther 33(8):475-83 [German].

Weber RK, Jaspersen D, Keerl R et al. 2004. [Gastroesophageal reflux disease and chronic sinusitis]  Laryngorhinootologie 83(3):189-195.  German]  This article indicates that there may be a connection between GERD and chronic sinusitis, and this should be further studied.  [Since GERD is common in FMS patients, and other research indicates that chronic sinusitis may be due to an immune response to fungi, this is very interesting.  DJS]

Weed ND. 1983.  When shoulder pain isn’t bursitis.  The myofascial pain syndrome.  Postgrad Med. 74(3):97-98, 101-102, 104.  “Pain in the shoulder girdle and the arm is often referred pain from a remote trigger point, i.e., the myofascial pain syndrome.  Once initiated, this definite disease entity perpetuates itself through various feedback loops.  Treatment consists of interrupting the pain cycle.  Local block of the trigger point with 1% lidocaine (Xylocaine), to which a short- or long-acting steroid may or may not be added, has proved to be most effective.”

Wehr, T. A . 1998. Effect of seasonal changes in day length on human neuroendocrine function. Horm Res 49(3-4):118-24.

Wehr, T. A. 1997. Melatonin and seasonal rhythms. J Biol Rhythms 12(6):518-27.

Wehr, T. A, D. A. Sack and N. E. Rosenthal. 1987. Seasonal affective disorder with summer depression and winter hypomania. Am J Psychiatry 144(12):1602-3.

Wei GX, Xu T, Fan FM et al. 2013. Can tai chi reshape the brain? A brain morphometry study. PLoS One. 8(4):e61038. "These findings indicate that long-term TCC (t'ai chi chuan) practice could induce regional structural change and also suggest TCC might share similar patterns of neural correlates with meditation and aerobic exercise."

Weibel, L., M. Follenius and G. Brandenberger. 1999. Biologic rhythms: their changes in night-shift workers. Presse Med 28(5):252-8. [French]

Weifen W, Muheremu A, Chaohui C et al. 2013. Effectiveness of tai chi practice for non-specific chronic low back pain on retired athletes: a Randomized controlled study. J Musculoskel Pain 21(1):37-45. "Tai chi has better efficacy than certain other sports on the treatment of non-specific chronic LBP."

Weigent, D. A., L. A. Bradley, J. E. Blalock and G. S. Alarcon. 1998. Current concepts in the pathophysiology of abnormal pain perception in fibromyalgia. Am J Med Sci 315 (6): 405-412.

Weijenborg PW, Bredenoord AJ. 2013. How reflux causes symptoms: Reflux perception in gastroesophageal reflux disease. Best Pract Res Clin Gastroenterol. 27(3):353-364. Gastroesophageal reflux occurs in everyone, but in the vast majority of the population it remains asymptomatic. This review considers factors affecting symptomology of GERD, including central sensitization, leaky gut, enzymatic factors, acidity, and genetic tendencies, as well as treatments.

Weimer MB, Macey TA, Nicolaidis C et al. 2013. Sex differences in the medical care of VA patients with chronic non-cancer pain. [Epub ahead of print]. Female VA patients moderate to severe chronic non-cancer pain are more likely to be diagnosed with two or more conditions. These more often included fibromyalgia, low back pain, inflammatory bowel disease, migraines, neck or joint pain, and/or arthritis. "After adjustment for demographic characteristics, pain diagnoses, mental health diagnoses, substance use disorders, and medical comorbidity, women had lower odds of being prescribed chronic opioid therapy…greater odds of visiting an emergency department for a pain related complaint… and greater odds of receiving physical therapy….Primary are utilization was not significantly different between sexes."

Weinberg, J. S., D. L. Freed, J. Sadock, M. Handler, J. H. Wisoff and F. J. Epstein. 1998. Headache and Chiari I malformation in the pediatric population. Pediatr Neurosurg 29(1):14-18.

Weiner DK. 2007.  Office management of chronic pain in the elderly.  Am J Med. 120(4):306-315.   “While common, chronic pain is not a normal part of aging, and it should be treated with an emphasis on improved physical function and quality of life.” 

Weiner DK, Sakamoto S, Perera S et al. 2006. Chronic low back pain in older adults: prevalence, reliability, and validity of physical examination findings. J Am Geriatr Soc. 54(1):11-20. "Biomechanical and soft tissue pathologies are common in older adults with CLBP, and many can be assessed reliably using a brief physical examination. Their recognition may save unnecessary healthcare expenditure and patient suffering." {This is a truly remarkable and comprehensive study, and is a must-read for any care provider diagnosing and treating chronic low back pain. The information needed to do the job correctly is in here. The experience, you must provide. DJS]

Weiner DK, Schmader KE. 2006.  Postherpetic pain: more than sensory neuralgia?  Pain Med. 7(3):243-249.  “Myofascial pathology was diagnosed by the presence of taut bands and trigger points in the affected myotome.  Upon successful treatment of the myofascial pain with nonpharmacologic modalities (e.g., physical therapy, trigger point injections, dry needling, and/or percutaneous electrical nerve stimulation), all patients reported symptomatic improvement, and four out of five were able to significantly reduce or discontinue their opioids.  Postherpetic pain is traditionally conceptualized as a purely sensory phenomenon.  Identification of the intrusion of a myofascial component may be worthwhile, both from the standpoint of enhanced pain relief and reduction in the need for oral analgesics.  Formal exploration of this phenomenon is needed.”  [Post-herpetic neuralgia often responds to Neurontin, but may also be helped by frequency specific microcurrent and other TrP-successful treatments. DJS]

Weiner, S. R. 1983. Growing pains. Am Fam Physician 27(1):189-191.

Weinstock LB, Fern SE, Duntley SP. 2007.  Restless legs syndrome in patients with irritable bowel syndrome: response to small intestinal bacterial overgrowth therapy.  Dig Dis Sci. [Oct 13 Epub ahead of print].  “This study suggests that SIBO associated with IBS may be a factor in some RLS patients and SIBO therapy provides long-term RLS improvement.”  [Small intestinal bacterial overgrowth can be responsible for more than gut problems.  One must be careful in addressing this issue with antibiotics, as this kills off all the good bacteria that are useful and can give the fungi a chance for a growth spurt.  What is needed is a replenishment of the healthy gut environment and healthy gut species that we need for digestion and good health. DJS]

Weinstock, M. 1997. Does prenatal stress impair coping and regulation of hypothalamic-pituitary-adrenal axis? Neurosci Biobehav Rev 21(1):1-10.

Weir PT, Harlan GA, Nkoy FL et al. 2006.  The incidence of fibromyalgia and its associated comorbidities: a population-based retrospective cohort study based on International Classification of Diseases, 9th Revision codes.  J Clin Rheumatol. 12(3):124-128.  “Females were 1.64 times more likely than males to have fibromyalgia.  Patients with fibromyalgia were 2.14 to 7.05 times more likely to have one or more of the following comorbid conditions: depression, anxiety, headache, irritable bowel syndrome, chronic fatigue syndrome, systemic lupus erythematosus, and rheumatoid arthritis.  Females are more likely to be diagnosed with fibromyalgia than males, although to a substantially smaller degree than previously reported, and there are strong associations for comorbid conditions that are commonly thought to be associated with fibromyalgia.”  [This is interesting in that the researchers found that the percentages of women and men FMS patients are much closer than other studies have indicated.  DJS]

Weiss, D. J. , T. Kreck and R. K. Albert. 1998. Dyspnea resulting from fibromyalgia. Chest 113(1):246-249.

Weiss S, Winkelmann A, Duschek S. 2013. Recognition of facially expressed emotions in patients with fibromyalgia syndrome. Behav Med. 39(4):146-154. "Thirty-five FMS patients and 35 healthy controls accomplished a face recognition task. Additionally, pain severity, alexithymia, depression, anxiety, psychiatric co-morbidity and medication use were assessed. The patients displayed reduced task performance in terms of more misclassifications of emotional expressions than controls. Pain severity, alexithymia, depression and anxiety were inversely related to recognition performance, with pain severity accounting for the largest portion of test score variance. Psychiatric co-morbidity and medication had no impact on performance. The study documented impaired emotion recognition in FMS, which may contribute to the interpersonal difficulties and reduced social functioning related to this condition."

Weiss TJ. 2007.  The influence of the diagnosis on the disease process in fibromyalgia syndrome.  J Musculoskel Pain 15 (Supp 13):60 item 106.  [Myopain 2007 Poster]  “Diagnosis and information about self-help alone improves the short- and middle-term prognosis in fibromyalgia.  This effect is less marked than the outcome of a multimodal therapy program.”  Multimodal program included short term psychotherapy, physical therapy, physiotherapy, education, nutritional changes, self-help and low-dose amitriptyline.

Weiss TJ, Freynhagen R, Glockel U et al. 2007.  Fibromyalgia vs neuropathic pain.  J Musculoskel Pain (suppl 13):40 item 83. “The pain experienced subjectively by FM patients is conspicuously greater than that experienced by other patients with typical neuropathic complaints.  Furthermore, this pain is associated with more severe co-morbidities such as depression/anxiety and sleep disturbance.”

Weissbecker I, Floyd A, Dedert E et al. 2005.  Childhood trauma and diurnal cortisol disruption in fibromyalgia syndrome.  Psychoneuroendocrinology [Nov 4 Epub ahead of print].  “These findings suggest that severe traumatic experiences in childhood may be a factor of adult neuroendocrine dysregulation among fibromyalgia sufferers.  Trauma history should be evaluated and psychosocial intervention may be indicated as a component of treatment for fibromyalgia.”

Weissman, D. E. 1993. Doctors, opioids, and the law: the effect of controlled substances regulations on cancer pain management. Semin Oncol 20(2 Suppl 1):53-58.

Wellen KE, Hotamisligil GS. 2003.  Obesity-induced inflammatory changes in adipose tissue.  J Clin Invest. 112(12):1785-1788.  “Obesity is associated with a state of chronic, low-grade inflammation.  Obese adipose tissue is characterized by macrophage infiltration and that these macrophages are an important source of inflammation in this tissue.  These studies prompt consideration of new models to include a major role for macrophages in the molecular changes that occur in adipose tissue in obesity.”  [Obesity may be common in chronic pain states for more reasons than lack of exercise.  Fat cells may interact with other mechanisms present in chronic pain. DJS]

Wells-Federman C, Arnstein P, Caudill-Slosberg M. 2003. Comparing patients with fibromyalgia and chronic low back pain participating in an outpatient cognitive-behavioral treatment program.  J Musculoskel Pain 11(3):5-12.  Both sets of patients experienced similar and long-lasting (up to a year) improvements in mood, disability, pain and self-efficacy.

Wen YR, Tan PH, Cheng JK et al. 2011. Microglia: a promising target for treating neuropathic and postoperative pain, and morphine tolerance. J Formos Med Assoc. 110(8):487-494. "...targeting microglial signaling might lead to more effective treatments for devastating chronic pain after diabetic neuropathy, viral infection, cancer, and major surgeries, partly via improving the analgesic efficacy of opioids."

Wentz KA, Lindberg C, Hallberg LR. 2004. Psychological functioning in women with fibromyalgia: a grounded theory study.  Health Care Women Int. 25(8):702-729.  This study revealed a core concept identity with “unprotected self.”  The women showed a pattern of developing helpfulness beyond their limits as adults, and this resulted in reduction of cognitive function and increased pain.

Wepner F, Scheuer R, Schuetz-Wieser B et al. 2014. Effects of vitamin D on patients with fibromyalgia syndrome: A randomized placebo-controlled trial. Pain. 155(2):261-268. "The role of calcifediol in the perception of chronic pain is a widely discussed subject. Low serum levels of calcifediol are especially common in patients with severe pain and fibromyalgia syndrome (FMS). We lack evidence of the role of vitamin D supplementation in these patients. To our knowledge, no randomized controlled trial has been published on the subject. Thirty women with FMS according to the 1990 and 2010 American College of Rheumatology criteria, with serum calcifediol levels <32ng/mL (80nmol/L), were randomized to treatment group (TG) or control group (CG). The goal was to achieve serum calcifediol levels between 32 and 48ng/mL for 20weeks via oral supplementation with cholecalciferol. The CG received placebo medication. Re-evaluation was performed in both groups after a further 24weeks without cholecalciferol supplementation. The main hypothesis was that high levels of serum calcifediol should result in a reduction of pain (visual analog scale score). Additional variables were evaluated using the Short Form Health Survey 36, the Hospital Anxiety and Depression Scale, the Fibromyalgia Impact Questionnaire, and the Somatization subscale of Symptom Checklist-90-Revised. A marked reduction in pain was noted over the treatment period in TG: a 2 (groups)×4 (time points) variance analysis showed a significant group effect in visual analog scale scores. This also was correlated with scores on the physical role functioning scale of the Short Form Health Survey 36. Optimization of calcifediol levels in FMS had a positive effect on the perception of pain. This economical therapy with a low side effect profile may well be considered in patients with FMS. However, further studies with larger patient numbers are needed to prove the hypothesis."

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

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

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

Wesson, D. R., W. Ling and D. E. Smith. 1993. Prescription of opioids for treatment of pain in patients with addictive disease. J Pain Sympt Manage 8(5):289-96.

Westgaard RH, Jensen C, Berg K et al. 1994.  [Occupational and individual risk factors of muscular pain] Tidsskr Nor Laegeforen.  114(8):922-927. [Norwegian]  “Occupational exposure to muscle load should be described by three factors to indicate health risks: level, repetitiveness and duration.  When interventions are carried out to reduce the risk of occupational musculoskeletal complaints, it is necessary to consider psychosocial and individual constitutional factors in addition to the three factors constituting the occupational exposure to muscle load.”

Westley, B. R., S. J. Clayton, M. R. Daws, C.A. Molloy and F. E. May. 1998. Interactions between the oestrogen and insulin-like growth factor signalling pathways in the control of breast epithelial cell proliferation. Biochem Soc Symp 63:35-44.

Wetter, D. W., T. B. Young, M. C. Fiore, J. B. McClure, C. A. de Moor and T. B. Baker. 1999.Gender differences in response to nicotine replacement therapy: objective and subjective indexes of tobacco withdrawal. Exp Clin Psychopharacol 7(2):135-44.

Wetzel, M. S., D. M. Eisenberg and T. J. Kaptchuk. 1998. Courses involving complementary and alternative medicine at US medical schools. JAMA 280(9):784-7.

Wheatley, D. 1999. Hypericum in seasonal affective disorder (SAD). Curr Med Res Opin15(1):33-7.

Wheeler AH. 2004.  Myofascial pain disorders: theory to therapy.  Drugs. 64(1):45-62.  “Forty-four million Americans are estimated to have myofascial pain….”  “Muscles with activity or injury-related pain are usually abnormally shortened with increased tone and tension.  In addition, myofascial pain disorders are characterized by the presence of tender, firm nodules called trigger points.”  “Most experts believe that appropriate treatment should be directed at the trigger point to restore normal muscle length and proper biomechanical orientation of myofascial elements, followed by treatment that includes strengthening and stretching of the affected muscle.”

Wheeler AH. 2004.  Myofascial pain disorders: theory to therapy.  Drugs 64(1):45-62.  “Forty-four million Americans are estimated to have myofascial pain…”  [This number might rise substantially if care providers were trained to recognize myofascial pain due to TrPs. DJS]

Wheeler, A. H., P. Goolkasian and S. S. Gretz. 1998. A randomized, double-blind, prospective pilot study of botulinum toxin injection for refractory, unilateral, cervicothoracic, paraspinal, myofascial pain syndrome. Spine 23(15):1662-6.

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


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


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


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


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

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

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

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

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

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

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

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

White S, Siebold C. 2008.  Walk a mile in my shoes: an auto-ethnographic study.  Contemp Nurse. 30(1):57-58. “‘Walk a mile in my shoes’.  It is written in the form of a letter to health professionals such as doctors and nurses in order that they may better understand the lives of chronic non-malignant pain sufferers with a view to improving the care they provide when these patients are admitted to hospital.  Issues identified include struggling with unremitting pain, loss of relationships and a fulfilling social life, as well as dealing with suspicion, labeling and stigmatizing by nurses and the community at large.”

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

Whyte Ferguson L. 2014. Adult Idiopathic scoliosis: The tethered spine. J Bodyw Mov Ther. 18(1):99-111. "This article reports on an observational and treatment study using three case histories to describe common patterns of muscle and fascial asymmetry in adults with idiopathic scoliosis (IS) who have significant scoliotic curvatures that were not surgically corrected and who have chronic pain. Rather than being located in the paraspinal muscles, the myofascial trigger points (TrPs) apparently responsible for the pain were located at some distance from the spine, yet referred pain to locations throughout the thoracolumbar spine. Asymmetries in these muscles appear to tether the spine in such a way that they contribute to scoliotic curvatures. Evaluation also showed that each of these individuals had major ligamentous laxity and this may also have contributed to development of scoliotic curvatures. Treatment focused on release of TrPs found to refer pain into the spine, release of related fascia, and correction of related joint dysfunction. Treatment resulted in substantial relief of longstanding chronic pain. Treatment thus validated the diagnostic hypothesis that myofascial and fascial asymmetries were to some extent responsible for pain in adults with significant scoliotic curvatures. Treatment of these patterns of TrPs and muscle and fascial asymmetries and related joint dysfunction was also effective in relieving pain in each of these individuals after they were injured in auto accidents. Treatment of myofascial TrPs and asymmetrical fascial tension along with treatment of accompanying joint dysfunction is proposed as an effective approach to treating both chronic and acute pain in adults with scoliosis that has not been surgically corrected."

Wick JY, Zanni GR. 2010. Tiptoeing around gait disorders: multiple presentations, many causes. Consult Pharm. 25(11):724-737. "Walking appears to be a simple innate ability, but it is an extraordinarily complex process involving three major afferent systems (visual, proprioception, and vestibular). Humans' unique gait is established around age seven. Velocity and step-length change with age, but the overall package we call "gait" remains stable. Age is the single most important factor in changing gait, with some normal changes expected. Gait disorders, beyond what are normal age-related changes, are common among elders. At 60 years of age, 15% of elders have gait problems, increasing to 82% for those 85 years of age and older. Abnormal gait movement can be broadly defined as hyperkinetic (too much movement) and hypokinetic (too little movement). Gait disorders are classified into lowest level (affecting one afferent system), middle level (more afferent system involvement), and highest level (characterized by planning deficits) disorders. Gait disturbances may be a manifestation of underlying conditions or may be drug-induced. To treat gait disorders appropriately, clinicians must review the patient's disease progression, medication status, and environmental conditions. Physical therapy, medication changes, and, rarely, surgery can help improve gait." [Patient education is also a vital component of physical retraining and therapy, and possible TrPs must also be taken into consideration when confronting gait irregularities. DJS]

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


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


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


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


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


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


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

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

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

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

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

Wilbarger JL, Cook DB. 2011. Multisensory hypersensitivity in women with fibromyalgia: implications for well being and intervention. Arch Phys Med Rehabil. 92(4):653-656. "The FM group reported significantly increased sensory sensitivities to both somatic (tactile) and nonsomatic (e.g., auditory and olfactory) sensory stimuli compared with the RA and control groups. The RA and control groups did not differ in reported hypersensitivities."


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

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

Wilke WS, Gota CE, Muzina DJ. 2010. Fibromyalgia and bipolar disorder: a potential problem? Bipolar Disord. 12(5):514-520. "We report a high prevalence of positive testing for bipolar disorder in this fibromyalgia cohort. Clinical data and questionnaire instruments other than nonspecific high depression severity failed to identify these patients. Since the norepinephrine serotonin reuptake inhibitors duloxetine and milnacipran have been recently approved by the U.S. Food and Drug Administration for the treatment of fibromyalgia, and because patients with bipolar disorder may experience destabilization of mood when treated with such agents, patients with fibromyalgia should be systematically screened for bipolar disorder prior to treatment."

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

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

Williams DA, Clauw DJ, Glass JM. 2011. Perceived cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain. 19(2):66-75. "In general, perceived dyscognition in FMS was most strongly associated with fatigue and mood. Pain was uniquely associated with perceived language deficits, and sleep was uniquely associated with aspects of dyscognition involving memory. Somewhat unexpected, pain was not related to attention or concentration….These data suggest that perceived dyscognition is a multi-faceted clinical concern in individuals with FMS. When assessed, dyscognition should reflect the multi-dimensionality of the symptom in order to be valid. Treatments aimed at dyscognition should similarly consider the importance of addressing multiple types of dyscognition in order to be considered effective." Many tests that measure cognitive dysfunction in patients with FM do not have the specific sensitivity required.

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

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

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

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

Willigenburg NW, Kingma I, Hoozemans MJ et al. 2013. Precision control of trunk movement in low back pain patients. Hum Mov Sci. [Feb 19 Epub ahead of print]. "Motor control is challenged in tasks with high precision demands. In such tasks, signal-dependent neuromuscular noise causes errors and proprioceptive feedback is required for optimal performance. Pain may affect proprioception, muscle activation patterns and resulting kinematics. Therefore, we investigated precision control of trunk movement in 18 low back pain (LBP) patients and 13 healthy control subjects. …These results suggest that reduced precision in LBP patients might be explained by proprioceptive deficits. Ratios of antagonistic over agonistic muscle activation were similar between groups. Tracking errors increased trunk inclination, but no significant relation between tracking error and agonistic muscle activation was found. Tracking errors did not decrease when antagonistic muscle activation increased, so, neither healthy subjects nor LBP patients appear to counteract trunk movement errors by increasing co-contraction."

Wilsey BL, Fishman SM, Casamalhuapa C et al. 2010. Computerized Progress Notes for Chronic Pain Patients Receiving Opioids; the Prescription Opioid Documentation System (PODS). Pain Med. 11(11):1707-1717. "The Prescription Opioid Documentation and Surveillance (PODS) System PODS fulfills medicolegal requirements for documentation and provides a systematic means of determining outcomes. This process facilitates the determination of the appropriate intervals between clinic visits by stratifying patients into high, moderate, and low risk."

Wilson Arboleda BM, Frederick AL. 2008.  Considerations for maintenance of postural alignment for voice production.  J Voice. 22(1):90-99.  “Specific exercises with emphasis on altering the alignment of the cervical and thoracic spine are presented with suggestions for their use in the clinic.”  [Posture affects voice, and the relationship of one muscle to the next in the laryngeal and surrounding areas can have profound implications for vocal success.  It is unfortunate that researchers in this field often lack knowledge of TrPs and their ability to cause contractures in muscles and/or muscle weakness.  If they understood TrPs, in my opinion, they could work magic with their patients.  Such magic has been done by practitioners such as Dr. Lawrence Funt.  It needs to be done by others as well.  DJS]

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

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

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

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

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

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

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

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

Winkelmann A, Perrot S, Schaefer C et al. 2011. Impact of fibromyalgia severity on health economic costs: results from a European cross-sectional study. Appl Health Econ Health Policy. 9(2):125-136. "FM imposes a significant economic burden on society. Consistent with other studies, FM subjects were found to have substantial costs, over 75% of which were driven by indirect costs from lost productivity. These costs increased as FM severity increased, resulting in a more than 200% difference in cost between mild and severe FM. Overall FM costs were similar between France and Germany; although lost productivity accounted for a higher proportion of costs in France."

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

Wisner, K. L. and Z. N. Stowe. 1997. Psychology of postpartum mood disorders. Semin Reprod Endocrinol 15(1):77-89.

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

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

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


Wolfe F, Clauw DJ, Fitzcharles MA et al. 2010. The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care Res (Hoboken). 62(5):600-610. “Objective: To develop simple, practical criteria for clinical diagnosis of fibromyalgia that are suitable for use in primary and specialty care and that do not require a tender point examination, and to provide a severity scale for characteristic fibromyalgia symptoms.” “This simple clinical case definition of fibromyalgia correctly classifies 88.1% of cases classified by the ACR classification criteria, and does not require a physical or tender point examination.” [The old criteria for FM clinical study patients, counting tender points, is irrelevant to the central sensitization of FM and we do need new criteria based on new understanding.   It is most unfortunate that some of the specific symptoms included in the new criteria actually are not part of FM at all. They are most probably due to co-existing conditions such as chronic myofascial pain. Until researchers and clinicians understand that symptoms such as numbness and tingling are due to myofascial nerve entrapment or some other co-existing condition and not FM, we are not going to have consistent research with meaningful conclusions.  FM research will continue to be flawed, based on faulty assumptions and faulty criteria. How do we get FM researchers to read TrP research?  DJS]


Wolfe F, Hassett AL, Walitt B et al. 2010. Mortality in fibromyalgia: An 8,186 patient study over 35 years. Arthritis Care Res (Hoboken). [Jul 26 Epub ahead of print]. "Mortality does not appear to be increased in patients diagnosed with fibromyalgia, but the risk of death from suicide and accidents was increased."

Wolfe F, Simons DG, Fricton J et al. 1992.  The fibromyalgia and myofascial pain syndromes: a preliminary study of tender points and trigger points in persons with fibromyalgia, myofascial pain syndrome and no disease.  J Rheumatol. 19(6):944-951.


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

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

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

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

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

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

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

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

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

Wolfe, F., K. Ross., J. Anderson, I. J. Russell and L. Hebert. 1995. The prevalence and characteristics of fibromyalgia in the general population. Arth Rheum 38(1):19-28.

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

Wolfe F, Walitt B. 2013. Culture, science and the changing nature of fibromyalgia. Nat Rev Rheumatol. [Jul 2 Epub ahead of print]. [The lead author is a known "debunker" of the reality of FM. These authors would have us believe that the fibromyalgia diagnoses are harmful to patients, in spite of research to the contrary. They also infer that FM is a mythical entity that is supported only because of those who would benefit from it, such as pharmaceutical companies and patient organizations. This flies in the face of research that the central sensitization of FM is caused by peripheral pain generators, and other research specifying genetic links, biochemical and skin differences, and other objective changes of FM. The research is there to be examined. It is left to the reader to decide why such an experienced and well-known researcher such as Dr. Wolfe ignores it. DJS]

Wolfe F, Walitt BT, Katz RS et al. 2012. Longitudinal patterns of analgesic and central acting drug use and associated effectiveness in fibromyalgia. Eur J Pain. [Nov 21 Epub ahead of print]. "We describe the changing pattern of analgesic and new central acting drug (NCAD) use (pregabalin, duloxetine, milnacipran) in fibromyalgia and measure NCAD effectiveness in clinical practice....There is a changing pattern of drug treatment in fibromyalgia, consisting mostly of decreased NSAID and amitriptyline use and an increase in NCAD. Drug costs are substantially higher because of NCAD use, but we found no evidence of clinical benefit for NCAD compared with prior therapy.

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

Woller SA, Hook MA. 2013. Opioid administration following spinal cord injury: Implications for pain and locomotor recovery. Exp Neurol. [Mar 15 Epub ahead of print]. "Approximately one-third of people with a spinal cord injury (SCI) will experience persistent neuropathic pain following injury. This pain negatively affects quality of life and is difficult to treat. Opioids are among the most effective drug treatments, and are commonly prescribed, but experimental evidence suggests that opioid treatment in the acute phase of injury can attenuate recovery of locomotor function. In fact, spinal cord injury and opioid administration share several common features (e.g. central sensitization, excitotoxicity, aberrant glial activation) that have been linked to impaired recovery of function, as well as the development of pain. Despite these effects, the interactions between opioid use and spinal cord injury have not been fully explored. A review of the literature, described here, suggests that caution is warranted when administering opioids after SCI. Opioid administration may synergistically contribute to the pathology of SCI to increase the development of pain, decrease locomotor recovery, and leave individuals at risk for infection. Considering these negative implications, it is important that guidelines are established for the use of opioids following spinal cord and other central nervous system injuries."

Wong CS, Wong SH. 2012. A new look at trigger point injections. Anesthesiol Res Pract [Epub Sept 29, 2011.] This article is a new look at TrP injections, from the perception of nerve entrapment and associated TrPs. "The advent of ultrasound technology in the non-invasive real-time imaging of soft-tissues sheds new light on visualization of trigger points, explaining the effect of trigger point injection by blockade of peripheral nerves, and minimizing the complications of blind injection." [Although the specific ultrasound technique required is expensive and limited to universities and other research settings, it may be helpful in exact placement of pudendal nerve entrapment and other deep injections, such as the iliopsoas. DJS]

Wong SH, Ji T, Hong Y et al. 2012. Foot forces induced through tai chi push-hand exercises. J Appl Biomech. [Aug 23 Epub ahead of print]. "This study indicates that push-hand exercises generate lower vertical forces than those induced by walking, bouncing, jumping and Tai Chi gait, and that the greatest plantar force is located in the toe area which may have an important application in balance training particularly for older adults."

Wood PB. 2010. Neuroimaging in fibromyalgia syndrome. J Musculoskel Pain. 18(4):387-392. "Fibromyalgia is associated with a variety of brain abnormalities demonstrable by neuroimaging that correlate with patients' symptoms. Future neuroimaging studies that take into account distinguishing characteristics among different populations of FMS patients may help to improve approaches to treatment and provide insight as to the pathophysiology of symptoms in addition to chronic widespread pain."


Wood PB, Ledbetter CR, Patterson JC 2nd. 2009.  Changes in hippocampal metabolites after effective treatment for fibromyalgia: a case study. Clin J Pain. 25(9):810-814.


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

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

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

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

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

Woolf CJ. 2010. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. [Oct 18 Epub ahead of print]. "Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, after-sensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification."

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

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

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

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

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

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

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

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

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

Wuytack F, Miller P. 2011. The lived experience of fibromyalgia in female patients, a phenomenological study. Chiropr Man Therap. 19(1):22. "Fibromyalgia pervaded all aspects of life. Four main themes arose from data analysis, namely; the impact of fibromyalgia on patients' occupational and personal life, the impact on their future and aspects of social interaction. Nearly all participants had stopped working, giving rise to feelings of uselessness and loss of identity. Leisure activities were also greatly affected. Fibromyalgia was said to alter family bonds, some of which were reinforced, others were broken. The diagnosis was seen as a relief, marking an end to a period of uncertainty. Participants reported ambivalence in interaction. Despite some positive encounters, frustration arising from perceived incomprehension dominated. Consequently patients preferred not to share their experiences.... The study revealed the negative impact of fibromyalgia on patients' lives as comprising of great complexity and individuality. Several implications for health care practitioners can be extrapolated, including the need of a more efficient diagnostic process and increased education about the fibromyalgia experience. Further studies are required to better clarify the multifaceted nature of living with the condition."

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

Xie X, Ye C. 1997.  [Clinical analysis of 120 patients with fibromyalgia]  Hunan Yi Ke Da Xue Xue Bao. 22(2):167-170. [Chinese]  [There is a basic problem here in that the trigger point is “…regarded as an important ophysical sign…” of fibromyalgia when in fact, it has absolutely nothing to do with fibromyalgia and everything to do with myofascial pain.  Researchers, and clinicians, must learn that there is a significant difference between the two conditions.  DJS]

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

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

Xie L, Kang H, Xu Q et al. 2013. Sleep drives metabolite clearance from the adult brain. Science. 2013 Oct 18;342(6156):373-7. "The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system."

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

Xu YM, Ge HY, Arendt-Nielsen L. 2010. Sustained nociceptive mechanical stimulation of latent myofascial trigger point induces central sensitization in healthy subjects. J Pain. [May 5 Epub ahead of print]. “The aim of the study is to test if sustained nociceptive mechanical stimulation (SNMS) of latent myofascial trigger points (MTrPs) induces widespread mechanical hyperalgesia.” “Painful stimulation of latent MTrPs can initiate widespread central sensitization. Muscle cramps contribute to the induction of local and referred pain. Perspective: This study shows that MTrPs are one of the important peripheral pain generators and initiators for central sensitization. Therapeutic methods for decreasing the sensitivity and motor-unit excitability of MTrPs may prevent the development of muscle cramps and thus decrease local and referred pain.” [Another fine piece of research that I wish FM researchers would read. DJS]

Yacoub HA, Johnson WG, Souayah N. 2010. Serotonin syndrome after administration of milnacipran for fibromyalgia. Neurology. 74(8):699-700. Several of the new medications touted for FM run the risk of causing or contributing to potentially fatal serotonin syndrome in at least some patients. This is one of them. DJS]

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

Yalgin S, Unalan H, Oztezcan S et al. 2010. Experimental study on static ultrasound [high-power pain threshold ultrasound] application: potential adverse effects on rats. J Musculoskel Pain. 18(3). This study indicates that this mode of therapy has potential to break up myofascial TrPs without tissue damage, at least in rats. The same static ultrasound parameters used were that being used on humans in some countries. (It is to be hoped that humans being treated by this method will have blood testing to indicate if tissue damage is occurring, and that we can have some research in this area, as the treatment has been shown to be effective. Perpetuating factors would still require control. DJS)

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

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

Yamagucchi A, Ogino Y, Iwakoshi C et al. 2012. [Trigger point therapy for myofascial pain in cancer patients (second report)-analysis results of special-use-results surveillance by neovitacain® injection] Gan To Kagaku Ryoho 39(4):605-611. [Japanese] "Injection of trigger points on both sides of the spine in cancer patients relieved musculoskeletal pain of cancer patients." [This study was financed by Vitacain pharmaceuticals and had no comparison done with other local anesthetics. There was no comparison between this medication and plain local anesthetic, so we can't tell if there was any improvement in the treatment over trigger point injection with procaine or Xylocaine. DJS]

Yan JH, Guo YZ, Yao HM et al. 2013. Effects of tai chi in patients with chronic obstructive pulmonary disease: preliminary evidence. PLoS One. 8(4):e61806. "Findings suggest that TC may provide an effective alternative means to achieve results similar to those reported following participation in pulmonary rehabilitation programs. Further studies are needed to substantiate the preliminary findings and investigate the long-term effects of TC." [Anything that inhibits oxygen from reaching the soft tissue can be an initiating or perpetuating factor to the development of trigger points. T'ai chi may be helpful preventative medicine. DJS]

Yang CM, Chen NC, Shen HC et al. 2012. Guideline of neuropathic pain treatment and dilemma from neurological point of view. Acta Neurol Taiwan. 21(3):136-144. "Neuropathic pain is a complicated symptomatic disease as migraine in recent years. Not because the pain character differed from the nociceptive inflammatory symptoms but because of its complexity of mechanisms. Though peripheral sensitization, ectopic discharge, central sensitization, central re-organization and loss of inhibition play part of roles in mechanisms, however, based on this mechanistic treatment, the outcome still disappointed physicians and patients, exampled as central post-stroke central pain (CPSP). The pain reduction is far less than the expectation from patients and physician's under-treatment frequently occur due to the fear of adverse effects or off-label use of these anti-neuropathic pain drugs. Therefore, a multidisciplinary procedure including non-pharmacological management, rehabilitation program, careful explanation, stepwise pain reduction, daily diary record, and tailored individual planning for medications are helpful in treating this kind of sufferers. Pharmacological treatment is the mainstream in post-herpetic neuralgia (PHN), diabetic peripheral neuropathic pain (DPNP), central post-stroke pain (CPSP), trigeminal neuralgia (TN), complex regional pain syndrome (CRPS), cancer pain, failed back syndrome etc, while polypharmacy is still the major prescriptions facing such kind of miserable patients. The tricyclic antidepressants (TCA), gamma-aminobutyric acid (GABA), voltage-dependent calcium channel blockers, selective non-epinephrine reuptake inhibitor (SNRI), opioid or morphine etc, are still evidence-based medicines (EBM) but with different outcome for individuals."

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

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

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

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

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

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

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

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

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

Yeh GY, Mietus JE, Peng CK et al. 2007. Enhancement of sleep stability with Tai Chi exercise in chronic heart failure: preliminary findings using an ECG-based spectrogram method.  Sleep Med. [Aug 2 Epub ahead of print]  “Tai Chi exercise may enhance sleep stability in patients with chronic heart failure.  This sleep effect may have a beneficial impact on blood pressure, arrhythmogenesis and quality of life.”  [T’ai chi could be very beneficial to patients with FM as well as those with CHF, as it impacts both sleep quality and blood pressure, as well as improving balance and other effects shown in other studies. DJS]

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

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

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

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

Yemisci OU, Cosar SN, Oztop P et al. 2010. Spondylodiscitis associated with multiple level involvement and negative microbiological tests: an unusual case. Spine. [Apr 15 Epub ahead of print]. Spondylodiscitis, an infection of the intervertebral disc space, vertebral bodies, or the paraspinal epidural space can be a serious disease because of diagnostic delay and inadequate treatment. METHODS: A previously healthy, 52-year-old man was presented to our outpatient clinic with a complaint of acute, atraumatic onset of severe back pain for more than 1 month. Initially, he was misdiagnosed at another clinic as myofascial pain and treated with nonsteroidal antiinflammatories and physical therapy, which he did not benefit from. He never complained of fever; however, laboratory tests revealed raised erythrocyte sedimentation values, increased C-reactive protein values but normal leukocyte count. Thoracal and lumbal plain radiographs were nonspecific. Magnetic resonance imaging demonstrated increased signal intensity in vertebral bodies and intervertebral disc space through T12-L4 and in the paravertebral musculature at L2-L3 with contrast enhancement. Blood cultures and computed tomography-guided needle biopsy and cultures were negative. RESULTS.: The patient was treated with oral amoxicillin and clavulanate and responded very well clinically; however, imaging examinations were repeated up to 6 months because of multilevel involvement. Follow-up magnetic resonance imaging findings at 3 months and 6 months showed decreased signal intensity, and luckily, there was no evidence of vertebral destruction. CONCLUSION: Diagnosis of spondylodiscitis could be challenging and commonly missed; however, it should always be included in the differential diagnoses of back pain in the middle aged and healthy population. [Myofascial TrPs are great mimics and can cause many symptoms, but they don’t cause all symptoms.  Part of the workup must include a thorough history and exam for TrP criteria, and a check for perpetuating factors.  When I doubt, check it out.  DJS]

Yigit S, Inanir A, Tekcan A et al. 2013. Association between fibromyalgia syndrome and polymorphism of the IL-4 gene in a Turkish population. Gene.. [May 2 Epub ahead of print]. "Our findings suggest that there is an association of IL-4 gene 70bp VNTR polymorphism with susceptibility of a person for development of FM. As a result, further studies are necessary to determine whether IL-4 may be a genetic marker for FM in the Turkish population."

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

Yokota S, Kikuchi M, Miyamae T. 2013. Juvenile fibromyalgia: Guidance for its management. Pediatr Int. [June 13 Epub ahead of print]. In Japan, the exact number of children with FM is unknown. Pediatric rheumatologists see children with a wide variety of musculoskeletal conditions. This provides guidelines for diagnosis and treatment. [It is not known if this paper differentiates between myofascial trigger points and FM. DJS]

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

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

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

Younger J, Noor N, McCue R et al. 2013. Low-dose naltrexone for the treatment of fibromyalgia: Findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels. Arthritis Rheum. 65(2):529-538. "The preliminary evidence continues to show that low-dose naltrexone has a specific and clinically beneficial impact on fibromyalgia pain. The medication is widely available, inexpensive, safe, and well-tolerated. Parallel-group randomized controlled trials are needed to fully determine the efficacy of the medication."

Younger JW, Shen YF, Goddard G et al. 2010. Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems. Pain. [Mar 15 Epub ahead of print]. “Myofascial pain of the temporomandibular region (M-TMD) is a common, but poorly understood chronic disorder. It is unknown whether the condition is a peripheral problem, or a disorder of the central nervous system (CNS). To investigate possible CNS substrates of M-TMD, we compared the brain morphology of 15 women with M-TMD to that of 15 age- and gender-matched healthy controls. High-resolution structural brain and brainstem scans were carried out using magnetic resonance imaging (MRI), and data were analyzed using a voxel-based morphometry approach. The M-TMD group evidenced decreased or increased gray matter volume compared to controls in several areas of the trigeminothalamocortical pathway, including brainstem trigeminal sensory nuclei, the thalamus, and the primary somatosensory cortex. In addition, M-TMD individuals showed increased gray matter volume compared to controls in limbic regions such as the posterior putamen, globus pallidus, and anterior insula. Within the M-TMD group, jaw pain, pain tolerance, and pain duration were differentially associated with brain and brainstem gray matter volume. Self-reported pain severity was associated with increased gray matter in the rostral anterior cingulate cortex and posterior cingulate. Sensitivity to pressure algometry was associated with decreased gray matter in the pons, corresponding to the trigeminal sensory nuclei. Longer pain duration was associated with greater gray matter in the posterior cingulate, hippocampus, midbrain, and cerebellum. The pattern of gray matter abnormality found in M-TMD individuals suggests the involvement of trigeminal and limbic system dysregulation, as well as potential somatotopic reorganization in the putamen, thalamus, and somatosensory cortex.” [It is a wonder to me that the authors believe that myofascial pain is poorly understood. Perhaps if they were familiar with the texts on myofascial pain due to trigger points, they would not be so confused.  It is interesting that they have found CNS involvement in their myofascia pain patients, which indicates that the patients probably have the central sensitization of FM as well as what they call myofascial pain, but their criteria is not carefully specified. DJS]

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

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

Yuan SL, Berssaneti AA, Marques AP. 2013. Effects of Shiatsu in the Management of Fibromyalgia Symptoms: A Controlled Pilot Study. J Manipulative Physiol Ther. [Jul 4 Epub ahead of print]. "This pilot study showed the potential of Shiatsu in the improvement of pain intensity, pressure pain threshold, sleep quality, and symptoms impact on health of patients with fibromyalgia."

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

Yun DJ, Choi HN, Oh GS. 2013. A case of postural orthostatic tachycardia syndrome associated with migraine and fibromyalgia. Korean J Pain. 26(3):303-306. "Postural orthostatic tachycardia syndrome (POTS) refers to the presence of orthostatic intolerance with a heart rate (HR) increment of 30 beats per minute (bpm) or an absolute HR of 120 bpm or more. There are sporadic reports of the autonomic nervous system dysfunction in migraine and fibromyalgia. We report a case of POTS associated with migraine and fibromyalgia. The patient was managed with multidisciplinary therapies involving medication, education, and exercise which resulted in symptomatic improvement. We also review the literature on the association between POTS, migraine, and fibromyalgia."

Yun MJ, Kang DM, Lee KH et al. 2013. Multiple chemical sensitivity caused by exposure to ignition coal fumes: a case report. Ann Occup Environ Med. 25(1):32. "Since 2011, a 55-year-old woman had experienced edema, myalgia, and other symptoms when she smelled ignition coal near her workplace. She had been diagnosed with fibromyalgia syndrome (FMS) and was treated, with no improvement of symptoms. Since then, she showed the same symptoms after exposure to city gas, the smell of burning, and exhaust gas. To avoid triggering substances, she moved to a new house and used an air purifier. She quit her job in November 2012. After visiting our hospital, she underwent a differential diagnosis for FMS, chronic fatigue syndrome, and somatization disorder….She was educated about the disease and to avoid triggering substances. She received ongoing treatment for her symptoms….This case showed that symptoms began after smelling ignition coal. After that, her triggers were increased such as the smell of city gas, burning, and exhaust gas. This case is the first reported in Korea of MCS due to environmental exposure after ruling out other diseases."

Yunus MB. 2012. The prevalence of fibromyalgia in other chronic pain conditions. Pain Res Treat. 2012:584573. "An important recent recognition is an increased prevalence of FMS in other chronic pain conditions with structural pathology; for example, rheumatoid arthritis, systemic lupus, ankylosing spondylitis, osteoarthritis, diabetes mellitus, and inflammatory bowel disease. Diagnosis and proper management of FMS among these diseases are of crucial importance so that unwarranted use of such medications as corticosteroids can be avoided, since FMS often occurs when RA or SLE is relatively mild."

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

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

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

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

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

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

Yunus, M. B. , F. X. Hussey and J. C. Aldag. 1993. Antinuclear antibodies and connective tissue disease features in fibromyalgia syndrome: a controlled study. J. Rheumatol 20(9):1557-60.

Yunus, M. B. , J. W. Dailey, J. C. Aldag, A. T. Masi and P. C. Jobe. 1992. Plasma tryptophan and other amino acids in primary fibromyalgia: a controlled study. 1992. J Rheumatol 19(1):90-4.

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

Zamanillo D, Romero L, Merlos M et al. 2013. Sigma 1 receptor: A new therapeutic target for pain. Eur J Pharmacol. [Mar 13 Epub ahead of print]. "Sigma 1 receptor... is a unique ligand-regulated molecular chaperone located mainly in the endoplasmic reticulum and the plasma membrane. (Sigma 1) receptor is activated under stress or pathological conditions and interacts with several neurotransmitter receptors and ion channels to modulate their function. The effects reported preclinically with (Sigma 1) receptor ligands are consistent with a role for (Sigma 1) receptor in central sensitization and pain hypersensitivity and suggest a potential therapeutic use of (Sigma 1) receptor antagonists for the management of neuropathic pain as monotherapy. Moreover, data support their use in opioid adjuvant therapy: combination of (Sigma 1) receptor antagonists and opioids results in potentiation of opioid analgesia, without significant increases in opioid-related unwanted effects. Results from clinical trials using selective (Sigma 1) receptor antagonists in several pain conditions are eagerly awaited to ascertain the potential of (Sigma 1) receptor modulation in pain therapy."

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

Zammurrad S, Munir W, Farooqi. 2013. Disease activity score in rheumatoid arthritis with or without secondary fibromyalgia. J Coll Physicians Surg Pak. 23(6):413-417. "DAS-28 (disease activity score) is a useful tool for assessing rheumatoid arthritis disease status in outpatient setting; however, increased disease activity must be assessed for possible co-existence of fibromyalgia which can spuriously give high DAS value and adversely affect treatment decision."

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

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

Zeidan F, Martucci KT, Kraft RA et al. 2011. Brain mechanisms supporting the modulation of pain by mindfulness meditation. J Neurosci 31(14):5540-5548. Some parts of the brain are activated by meditation, and others are quieted. This study indicates that with mindfulness meditation, we can change our perception of the pain we have, to the point that it will not bother us as much.

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

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

Zettel-Watson L, Rakovski CC, Levine B et al. 2010. Impact of employment and caregiving roles on the well-being of people with fibromyalgia syndrome. J Musculoskel Pain. 19(1):8-17. This study showed that in adults who are middle aged or older, fibromyalgia patients who were involved in home, work and community relationships had a higher quality of life than those who did not have fibromyalgia. The FM patients had significantly higher pain and fatigue levels and yet functioned better if they could maintain multiple roles in life.

Zhang JF, Wu YC, Mi YQ. 2009. [Observation on therapeutic effect of acupuncture at pain points for treatment of myofascial pain syndrome] Zhongguo Zhen Jiu. 29(9):717-720. [Chinese]

Zhang L, Berta T, Xu ZZ et al. 2010. TNF-alpha contributes to spinal cord synaptic plasticity and inflammatory pain: Distinct role of TNF receptor subtypes 1 and 2. Pain. [Dec 13 Epub ahead of print]. "Tumor necrosis factor-alpha (TNF-alpha) is a key proinflammatory cytokine…. Our findings support a central role of TNF-alpha in regulating synaptic plasticity (central sensitization) and inflammatory pain via both TNFR1 and TNFR2. Our data also uncover a unique role of TNFR2 in mediating early-phase inflammatory pain. TNF-alpha is shown to play a critical role in regulating spinal cord synaptic plasticity and central sensitization, and TNFR1 and TNFR2 play a distinct role in regulating different phases of inflammatory pain."

Zhang RX, Ren K, Dubner R. 2013. Osteoarthritis pain mechanisms: basic studies in animal models. Osteoarthritis Cartilage. 21(9):1308-1315. This study, from the Center for Integrative Medicine, School of Medicine, University of Maryland, was done in rats, but may hold clues pertaining to human osteoarthritic development. "Conditioned place preference tests demonstrate that OA pain induces aversive behaviors, suggesting the involvement of brain. During OA, brain functional connectivity is enhanced, but at present it is unclear how this change is related to OA pain….Animal studies demonstrate that peripheral and central sensitization contributes to OA pain, involving inflammatory cytokines, neuropeptides, and a variety of chemical mediators. Interestingly, brainstem descending facilitation of 5-HT/5-HT3 receptors plays a role in OA pain."

Zhang T, Adatia A, Zarin W et al. 2010. The efficacy of botulinum toxin type A in managing chronic musculoskeletal pain: a systematic review and meta analysis. Inflammopharmacology. [Nov 13 Epub ahead of print]. "Botulinum toxin type A (BoNTA) is a neurotoxin that acts by inhibiting the release of neurotransmitters acetylcholine at neuromuscular junctions, thus reducing muscular contractions. Recent evidence suggests that BoNTA can reduce nociceptive activities of sensory neurons in animal models by inhibiting release of certain neuropeptides.....In our meta-analysis; BoNTA had a small to moderate analgesic effect in chronic musculoskeletal pain conditions. It was particularly effective in plantar fasciitis, tennis elbow, and back pain, but not in whiplash or shoulder pain patients. However, more evidence is required before definitive conclusions can be drawn. On the other hand, there is convincing evidence that BoNTA lacks strong analgesic effects in patients with myofascial pain syndrome. A general dose-dependent and temporal response with BoNTA injections was also observed.

Zhao Y, Sun P, Watson P et al. 2010. Comparison of Medication Adherence and Healthcare Costs between Duloxetine and Pregabalin Initiators among Patients with Fibromyalgia. Pain Pract. [Aug 26 Epub ahead of print]. "Fibromyalgia patients on duloxetine had significantly higher medication adherence, but significantly lower direct healthcare costs than those on pregabalin." [Note: the investigation came out of Eli Lilly and Company.]

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

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

Zhou Q, Zhang B, Verne GN. 2009. Intestinal membrane permeability and hypersensitivity in the irritable bowel syndrome. Pain 146(1-2):41-46.  This research confirmed intestinal permeability in a subset of IBS-with-diarrhea patients.  The severity of leaky gut was directly associated with severity in pain and central sensitization of the gut.

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

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

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

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

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

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

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

Zink W, Sinner B, Zausig Y et al. 2007.  [Myotoxicity of local anaesthetics: experimental myth or clinical truth?]  Anaesthesist. 56(2):118-127.  “Intramuscular injections of local anaesthetic agents regularly result in reversible muscle damage, with a dose-dependent extent of the lesions.  All local anaesthetic agents that have been examined are myotoxic, whereby procaine produces the least and bupivacaine the most severe muscle injury.”

Zioni T, Buskila D, Aricha-Tamir B et al. 2011. Pregnancy outcome in patients with fibromyalgia syndrome. J Matern Fetal Neonatal Med. [Feb 1 Epub ahead of print]. "FMS is an independent risk factor for intrauterine growth restriction. Nevertheless, it is associated with lower rates of preterm deliveries."

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

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

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

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

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

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

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

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

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

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

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