Falla D, Jull G, Edwards S et al. 2004.  Neuromuscular efficiency of the sternocleidomastoid and anterior scalene muscles in patients with chronic neck pain.  Disabil Rehabil. 26(12):712-717. “Reduced NME in the superficial cervical flexor muscles in patients with neck pain may be a measurable altered muscle strategy for dysfunction in other muscles.  This aberrant pattern of muscle activation appears to be most evident under conditions of low load.  NME, when measured at 25% MVC, may be a useful objective measure for future investigation of muscle dysfunction in patients with neck pain.”

Fang L., Wu J., Lin Q. et al. 2002. Calcium-calmodulin-dependent protein kinase II contributes to spinal cord central sensitization. J Neurosci 22(10):4196-4204.

Fannelli Jr., G. M. and I. M. Weiner.  1975. Species variations among primates in responses to drugs which alter the renal excretion of uric acid.  J Pharmacol Exp Ther 193(2):363-375.

Farella M., Michelotti A., Gargano A et al. 2002. Myofascial pain syndrome misdiagnosed as odontogenic pain: a case report.  Cranio 20(4):307-11.  When the cause of dental pain cannot be clearly identified, consider all possible causes of dental pain, including the nonodontogenic ones such as myofascial pain, before any irreversible dental procedures are considered.

Farina S, Casarotto M, Benelle M et al. 2004.  A randomized controlled study on the effect of two different treatments (FREMS AND TENS) in myofascial pain syndrome.  N Eura Medicophys. 40(4):293-301.  Both methods appeared effective for myofascial pain, although FREMS seemed better.

Farrell, J and G. O. Littlejohn. 1999. Pain, nature of task, and body part used in fibromyalgia syndrome. J Musculoskel Pain 7(1-2):279-284.

Fasmer, B. 1990. [Do antidepressive agents have analgesic effects?] Tidsskr Nor Laegeforen 110(18:2370-2. [Norwegian]

Fass R, Naliboff BD, Fass SS et al. 2007.  The effect of auditory stress on perception of intraesophageal acid in patients with gastroesophageal reflux disease.  Gastroenterology [Dec 7 Epub ahead of print].  “Acute auditory stress can exacerbate heartburn symptoms in GERD patients by enhancing perceptual response to intraesophageal acid exposure.  This greater perceptual response is associated with greater emotional responses to the stressor.”  [For those of us with FM amplification and GERD, auditory stress may be an even greater peril. DJS]

Faucett, J. A. 1994.  Depression in painful chronic disorders: the role of pain and conflict about pain.  J Pain Symptom Manage 9(8):520-526.

Faucett, J. A. and J. D. Levine.  1991.  The contributions of interpersonal conflict to chronic pain in the presence of absence of organic pathology.  Pain 44(1):35-43.

Feder KP, Majnemer A. 2007.  Handwriting development, competency and intervention.  Dev Med Child Neurol. 49(4):312-317.  “Poor handwriting may be related to intrinsic factors, which refer to the child’s actual handwriting capabilities, or extrinsic factors which are related to environmental or biomechanical components, or both.”  “There is evidence to indicate that handwriting difficulties do not resolve without intervention and affect between 10 and 30% of school-aged children.”  [Students with these problems should be evaluated for myofascial TrPs. DJS]    

Feinberg, B. I. and R. A. Feinberg. 1998. Persistent pain after total knee arthroplasty: treatment with manual  therapy and trigger point injections.  J Musculoskel Pain 6(4):85-95.  

Feldman, D. and A. Krishnan.  1995.  Estrogens in unexpected places: possible implications for researchers and consumers.  Environ Health Perspect 103 Suppl 7: 129-33.  

Feldman, R. D. and N. D. Schmidt.  1999.  Moderate dietary salt restriction increases vascular and systemic insulin resistance.  Am J Hypertens 12(6):643-7.

Feng B, La JH, Schwartz ES et al. 2012. Neural and neuro-immune mechanisms of visceral hypersensitivity in irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol. [Mar 8 Epub ahead of print]. "Irritable bowel syndrome (IBS) is characterized as 'functional' because a pathobiological cause is not readily apparent. Considerable evidence, however, documents that sensitizing pro-inflammatory and lipotoxic lipids, mast cells and their products, tryptases, enteroendocrine cells and mononuclear phagocytes and their receptors are increased in tissues of IBS patients with colorectal hypersensitivity. It is also clear from recordings in animals of the colorectal afferent innervation that afferents exhibit long-term changes in models of persistent colorectal hypersensitivity. Such changes in afferent excitability and responses to mechanical stimuli are consistent with relief of discomfort and pain in IBS patients, including relief of referred abdominal hypersensitivity, upon intra-rectal instillation of local anesthetic. In the aggregate, these experimental outcomes establish the importance of afferent drive in IBS, consistent with a larger literature with respect to other chronic conditions in which pain is a principal complaint (e.g., neuropathic pain, painful bladder syndrome, fibromyalgia). Accordingly, colorectal afferents and the environment in which these receptive endings reside constitute the focus of this review."

Feng J, Zhang Z, Li W et al. 2009.  Missense mutations in the MEFV gene are associated with fibromyalgia syndrome and correlate with elevated IL-1beta plasma levels.  PLoS One. 4(12):e8480.  “Since misregulation of IL-1beta expression has been predicted for patients with mutations in the MEFV gene, we conclude that patients heterozygous for rare missense variants of this gene may be predisposed to FMS, possibly triggered by environmental factors.”

Fenton BW, Palmieri P, Diantonio G et al. 2011. Application of patient-reported outcomes measurement information system to chronic pelvic pain. J Minim Invasive Gynecol. 18(2):189-193. "A total of 149 consecutive patients with chronic pelvic pain provided evaluable results....Pain-related and global PROMIS (Patient-Reported Outcomes Measurement Information System) scores were significantly worse than in the reference population..... The presence of myofascial pain was also associated with worse PROMIS scores.....Chronic pelvic pain is associated with impaired quality of life regardless of the diagnosis, including myofascial pain."

Fenton BW, Palmieri PA, Durner C et al. 2009.  Quantification of abdominal wall pain using pain pressure threshold algometry in patients with chronic pelvic pain.  Clin J Pain. 25(6):500-505.  Pressure algometry is a very useful tool for those who cannot palpate TrPs.  There was a 75% improvement in pressure point testing after treating abdominal wall TrPs.  The authors seem unaware of the explicit specifications of myofascial TrPs.  They also seem unaware that most chronic pelvic pain comes from TrPs in the pelvic floor and other related areas, although they are to be commended for their work confirming the ubiquity of abdominal wall TrPs.

Feraco P, Bacci A, Pedrabissi F et al. 2011. Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study. AJNR Am J Neuroradiol. [Jul 28 Epub ahead of print]. "The presence of elevated Glu/Cr levels in VLPFC strengthens the opinion that a complex neurophysiologic imbalance of different brain areas involved in pain processing underlies FM. These data may be useful in the diagnosis and development of more effective pharmacologic treatments."

Ferencik, M., M. Novak and J. Rovensky.  1998.  [Relation and interactions between the immune and neuroendocrine systems].  Bratisl Lek Listy 99(8-9):454-64 [Slovak].

Fernandez-de-las-Penas C. 2009. Interaction between trigger points and joint hypomobility: a clinical perspective. J Man Manip Ther. 17(2):74-77. "Reduction of joint mobility appears related to local muscles innervated from the segment, which suggests that muscle and joint impairments may be indivisible and related disorders in pain patients. …There is scientific evidence showing change in muscle sensitivity in muscle TrP after spinal manipulation, which suggests that clinicians should include treatment of joint hypomobility in the management of TrPs. Nevertheless, the order in which these muscle and joint impairments should be treated is not known and requires further investigation." [The intriguing hypotheses mentioned here did not include the possibility that muscle contracture caused by TrPs can torque the joint, provoking hypermobility in the opposite direction. It is to be hoped that more investigations on this interrelationship will be forthcoming. DJS]

Fernandez-de-Las-Penas C, Ortega-Santiago R, Cuandrado ML et al. 2010. Bilateral widespread mechanical pain hypersensitivity as a sign of central sensitization in patients with cluster headaches. Headache Nov 4 [Epub ahead of print] Pain hypersensitivity was global, including tibialis (calf muscle), in chronic headache patients. "Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with CH confirming the presence of central sensitization mechanisms in this headache condition." [Chronic headache, even from TrPs, can lead to a central sensitization state such as fibromyalgia. DJS]

Fernandez-de-las-Penas C, Perez-de-Heredia-Torres M, Miangolarra J. 2007.  Trigger point management in lateral epicondylalgia.  J Musculoskel Pain 15 (Supp 13):20 item 29.  [Myopain 2007 Poster]  “Referred pain from TrPs in these patients was causing the usual pain reported by patients with lateral epicondylalgia.  Muscle tension provoked by TrP taut band may play an important role in the genesis and relief of the pain commonly seen in lateral epicondylalgia.”

Fernandez de las Penas CF, Carnero JF, Page JCM. 2005.  Musculoskeletal disorders in mechanical neck pain: myofascial trigger points versus cervical joint dysfunction – a clinical study.  J Musculoskeletal Pain 13(1).  “There is a possible relationship between the presence of TrPs in the upper trapezius muscle and the presence of cervical dysfunctions at C3 and C4 vertebrae in patients suffering from mechanical neck pain.  However, it cannot be established as a cause-effect relationship.  Moreover, there is clinical evidence showing that joint dysfunctions can induce TrP activity, and that TrP activity can aggravate corresponding joint dysfunction.”

Fernandez-Lao C, Cantarero-Villanueva I, Fernanndez-de-Las-Penas C et al. 2010. Widespread Mechanical Pain Hypersensitivity as a Sign of Central Sensitization after Breast Cancer Surgery: Comparison between Mastectomy and Lumpectomy. Pain Med. [Dec 10 Epub ahead of print]. "The current study found widespread pressure pain hyperalgesia in women who received breast cancer surgery suggesting central spreading sensitization. The degree of central sensitization was similar between lumpectomy and mastectomy surgery."

Fernandez-Lao C, Cantarero-Villanueva I, Fernandez-de-Las-Penas C et al. 2010. Myofascial Trigger Points in Neck and Shoulder Muscles and Widespread Pressure Pain Hypersensitivity in Patients with Postmastectomy Pain: Evidence of Peripheral and Central Sensitization. Clin J Pain. [Sep 8 Epub ahead of print]. "Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with postmastectomy pain. In addition, the local and referred pain elicited by active TrPs reproduced neck and shoulder/axillary complaints in these patients. These results suggest peripheral and central sensitization in patients with postmastectomy pain." [Other research has found evidence of TrPs causing post-surgical pain. This also indicates that the TrPs are at least contributing, and possibly causing, the development of hypersensitivity in other areas. This is one way central sensitization can develop. DJS]

Fernández-Pérez AM, Villaverde-Gutiérrez C, Mora-Sánchez A et al. 2012. Muscle trigger points, pressure pain threshold, and cervical range of motion in patients with high level of disability related to acute whiplash injury. J Orthop Sports Phys Ther. 42(7):634-641. This study was created to..."analyze the differences in the prevalence of trigger points (TrPs) between patients with acute whiplash-associated disorders (WADs) and healthy controls, and to determine if widespread pressure hypersensitivity and reduced cervical range of motion are related to the presence of TrPs in patients with acute WADs....Patients had significantly lower PPTs (pressure pain threshold) in all tested locations and less active cervical range of motion than controls.... In the patient group, there were significant negative correlations between the number of active TrPs and PPT over the C5-C6 joints and cervical range of motion in flexion, extension, and rotation in both directions: the greater the number of active TrPs, the lower the bilateral PPT over the neck and the greater the cervical range of motion limitation....The local and referred pain elicited from active TrPs reproduced neck and shoulder pain patterns in individuals with acute WADs with higher levels of disability. Patients with acute WADs exhibited widespread pressure hypersensitivity and reduced cervical mobility. The number of active TrPs was related to higher neck pain intensity, the number of days since the accident, higher pressure pain hypersensitivity over the cervical spine, and reduced active cervical range of motion."

Fernstrom, J. D.  1994.  Dietary amino acids and brain function.  J Am Diet Assoc 94(1):71-77.

Ferranninni, E. A. Q. Galvan, A. Gastaldelli, S. Camastra, A. M. Sironi, E. Toschi, S. Baldi, S. Frascerra, F. Monzani, A. Antonelli, M. Nannipieri, A. Mari, G. Seghieri, and A. Natali. 1999. Insulin: New roles for an ancient hormone. Eur J Clin Invest 29(10):842-52.

Ferrari R. 2012. Quantitative assessment of the "inexplicability" of fibromyalgia patients: a pilot study of the fibromyalgia narrative of "medically unexplained" pain. Clin Rheumatol. [Jul 22 Epub ahead of print]. "Compared to other patients with chronic, widespread pain, fibromyalgia patients report a much greater degree of difficulty in understanding the cause of their pain and explaining the cause of their pain to others. This phenomenon may reflect the narrative of 'inexplicability' in fibromyalgia patients that distinguishes them from other widespread pain populations."

Ferrari R., H. Schrader and D. Obelieniene. 1999.  Prevalence of temporomandibular disorders associated with whiplash injury in Lithuania. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 87(6):653-7. 

Fetler L, Amigorena S. 2005.  Neuroscience.  Brain under surveillance: the microglia patrol.  Science 309(5733):392-393.  Opioids can activate pain inhibitory and facilitatory systems, but opioid-induced hyperalgesia may be prevented by strategies such as concomitant administration of NSAIDS or NMDA antagonists, use of combinations of opioids with different receptor selectivity, and other methods.

Field T, Hernandez-Reif M, Diego M et al. 2007.  Lower back pain and sleep disturbance are reduced following massage therapy.  J Bodywork Move Ther. 11, 141-145.  “…the massage therapy group, as compared to the relaxation group, reported experiencing less pain, depression, anxiety and sleep disturbance.  They also showed improved trunk and pain flexion performance.”

Field T, Diego M, Cullen C et al. 2002.  Fibromyalgia pain and substance P decrease and sleep improves after massage therapy.  J Clin Rheumatol. 8(2):72-76.  “Both groups showed a decrease in anxiety and depressed mood immediately after the first and last therapy sessions.  However, across the course of the study, only the massage therapy group reported an increase in the number of sleep hours and a decrease in their sleep movements.  In addition, substance P levels decreased, and the patients’ physicians assigned lower disease and pain ratings and rated fewer tender points in the massage therapy group.”

Filipovic V, Viskic-stalec N. 2006.  The mobility capabilities of persons with adolescent idiopathic scoliosis.  Spine. 31(19):2237-2242.  When there is a lack of normal mobility functions, especially with weak postural control mechanisms and proprioception, the body compensates and scoliosis can result.

Filos, K.S. and C.E.Vagianos. 1999. Pre-emptive analgesia: how important is it in clinical reality?  Eur Surg Res 31(2): 122-32.

Finckh A, Berner IC, Aubry-Rozier B et al. 2005.  A randomized controlled trial of dehydroepiandrosterone in postmenopausal women with fibromyalgia.  J Rheumatol 32(7):1336-1340.  This study did not find that taking DHEA brought about any useful changes.

Fink, G., B. Sumner, R. Rosie, H. Wilson and J. McQueen.  1999.  Androgen actions on central serotonin neurotransmission: relevance for mood, mental state and memory.  Behav Brain Res 105(1):53-68.

Fishbain, D. A., H. L. Rosomoff and R. S. Rosomoff. 1992.  Drug abuse, dependence, and addiction in chronic pain patients.  Clin J Pain 8(2):77-85.  

Fishbain, D. A., M. Goldberg, R. S. Rosomoff and H. Rosomoff.  1991.  Completed suicide in chronic pain.  Clin J Pain 7(1):29-36. 

Fischer, A. A. 1999. Treatment of myofascial pain. J Musculoskel Pain 7(1-2):131-142.

Fischer, A. A. 1999.  Algometry in diagnoses of musculoskeletal pain and evaluation of treatment outcome: an update. J Musculoskel Pain 6(1): 5-32.

Fischer, H. P., W. Eich and I. J. Russell.  1998.  A possible role for saliva as a diagnostic fluid in patients with chronic pain.  Semin Arthritis Rheum 27(6):348-59.

Fischer, A. A.  1988.  Documentation of myofascial trigger points.  Arch Phys Med Rehabil 69(4):286-91. 

Fishman SM. 2006.  The role of the pain psychologist, trigger point injections, reflex sympathetic dystrophy.  J Pain Palliat Care Pharmacother. 20(4):93-97.  “This feature presents information for patients in a question and answer format.  It is written to simulate actual questions that many pain patients ask and to provide answers in a context and language that most pain patients will comprehend.  Issues addressed in this issue are the role of the pain psychologist, trigger point injections, and reflex sympathetic dystrophy.”

Fitzcharles M.A., Boulos P. 2003.  Inaccuracy in the diagnosis of fibromyalgia syndrome: analysis of referrals.  Rheumatology (Oxford) 42(2):263-7.  “At the final evaluation the accuracy of the diagnosis regarding FM by either the referring physician or by the rheumatologist at the time of the initial visit was correct in 34% of patients.”  This finding may help explain the current high rates of FM and caution physicians to consider other diagnostic possibilities when addressing diffuse musculoskeletal pain.

Fitzcharles, M. A. and J. M. Esdaile. 1997. The overdiagnosis of fibromyalgia syndrome. Am J Med 103(1):44-50.

Fiz J, Duran M, Capella D et al. 2011. Cannabis use in patients with fibromyalgia: effect on symptoms relief and health-related quality of life. PLoS One. 6(4):e18440. "The use of cannabis was associated with beneficial effects on some FM symptoms. Further studies on the usefulness of cannabinoids in FM patients as well as cannabinoid system involvement in the pathophysiology of this condition are warranted."

Flanagan, D. E. , J. C. Vaile, G. W. Petley, V. M. Moore, I. F. Godsland, R. A. Cockington, J. S. Robinson and D. I. Phillips. 1999. The autonomic control of heart rate and insulin resistance in young adults. J Clin Endocrinol Metab 84(4):1263-7. 

Flanagan, D., P. Wood, R. Sherwin, K. Debrah and D. Kerr.  1998.  Gin and tonic and reactive hypoglycemia: what is important–the gin, the tonic, or both?  J Clin Endocrinol Metab 83(3):   796-800.

Flato, B., A. Aasland, I. H. Vandvik and O. Forre. 1997.  Outcome and predictive factors in children with chronic idiopathic musculoskeletal pain.  Clin Exp Rheumatol 15(5):567-577.  

Flax, B. J.  1995.  Myofascial pain syndomes–the great mimicker.  Bol Assoc Med P R 87(10-12):167-170.

Floyd, J. A. 1999. Sleep promotion in adults. Annu Rev Nurs Res 17:27-56.  

Foerster BR, Petrou M, Edden RA et al. 2011. Reduced insular gamma-aminobutyric acid in fibromyalgia. Arthritis Rheum. [Sep 13 Epub ahead of print]. "Diminished inhibitory neurotransmission resulting from lower concentrations of GABA within the right anterior insula may play a role in the pathophysiology of FM and other central pain syndromes."

Fogel RB, Triner J, White DP 2005.  The effect of sleep onset on upper airway muscle activity in patients with sleep apnoea versus controls.  J Physiol 564(Pt 2):549-562.  “Although CPAP eliminated differences in UAR (Upper Airway Resistance) during wakefulness and sleep, GGEMG genioglossus (activity) remained greater in the OSA patients.” [TrPs in the pharyngeal dilator muscles can significantly affect OSA.  Their previous work indicated tensor palatini muscle activity is high in OSA patients as well. DJS]

Ford, ES, Giles WH, Dietz WH. 2002. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA Jan16;287(3):356-9.  About 47 million US residents have the metabolic syndrome, according to 2000 census data.

Forman MB, Sutej PG, Jackson EK. 2011. Hypertension, tachycardia, and reversible cardiomyopathy temporally associated with milnacipran use. Tex Heart Inst J. 38(6):714-718. "Milnacipran is a dual and equipotent inhibitor of norepinephrine and serotonin uptake. It is frequently prescribed as therapy for fibromyalgia, and the drug has a good safety profile. Herein, we report the case of a 42-year-old woman with undefined connective-tissue disease and fibromyalgia who developed a severe and reversible cardiomyopathy while taking recommended doses of milnacipran. The cardiomyopathy was associated with a hyperadrenergic state manifested by tachycardia, hypertension, and elevated plasma catecholamine levels. The discontinuation of milnacipran and the initiation of anti-failure therapy resulted in complete resolution of the cardiomyopathy in 6 months. To our knowledge, this is the first report of milnacipran as a possible cause of catecholamine-induced cardiomyopathy."

Fornasari D. 2012. Pain mechanisms in patients with chronic pain. Clin Drug Investig. 32 Suppl 1:45-52. "The mechanisms involved in the development of chronic pain are varied and complex. Pain processes are plastic and unrelieved pain may lead to changes in the neural structure involved in pain generation. Nociceptive pain announces the presence of a potentially damaging stimulus that occurs when noxious stimuli activate primary afferent neurons. Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system resulting from trauma, infection, ischemia, cancer or other causes such as chemotherapy. The exact mechanisms involved in the pathophysiology of chronic pain are not well understood, but rapid and long-term changes are thought to occur in parts of the central nervous system that are involved in the transmission and modulation of pain following injury. Peripheral and central sensitization of sensory nerve fibres are the primary reasons for hypersensitivity to pain after injury, and mainly occur in inflammatory and neuropathic pain. During these processes the sensation of pain is enhanced as a result of changes in the environment, the nerve fibres and modifications of the functional properties and the genetic program of primary and secondary afferent neurons. Non-steroidal anti-inflammatory drugs and opioid analgesics are two of the most common classes of drugs used for the treatment of pain. Response to drug treatment shows significant inter-individual variability and can lead to side effects. The neurobiological mechanisms that cause pain may account for the different types of pain observed. Identification of these mechanisms may allow us to move from an empirical therapeutic approach to one that it is specifically targeted at the particular mechanisms of the type of pain experienced by an individual patient."

Forrest JB, Schmidt S. 2004.  Interstitial cystitis, chronic nonbacterial prostatitis and chronic pelvic pain syndrome in men: a common and frequently identical clinical entity.  J Urol. 172(6 Pt 2):2561-2562.  “Interstitial cystitis in males appears to be more common than historically reported.  Interstitial cystitis in males and patients with chronic pelvic pain syndrome and chronic nonbacterial prostatitis share many clinical findings.  A higher incidence of interstitial cystitis had been found in American Indian males of Cherokee descent and deserves further investigation.”

Fors EA, Landmark T, Bakke O. 2012. Contextual and time dependent pain in fibromyalgia: An explorative study. BMC Res Notes. 5(1):644. "Little is known about contextual effects on chronic pain, and how vulnerability factors influence pain in different contexts. We wanted to examine if fibromyalgia (FM) pain varied between two social contexts, i.e. at home versus in a doctor office, when it was measured the same day, and if pain was stable for 14 years when measured in similar contexts (doctor office). Our secondary aim was to explore if pain vulnerability factors varied in the two different contexts.....Pain and pain predictors seem to vary by contexts and time, with less pain at home than to a doctor the same day, but with unchanged pain in the same context after 14 years. Thus, contextual pain cues should be accounted for when pain is measured and treated, e.g. by focusing more on home-measured pain and by optimizing the doctor office context. This explorative study should be followed up by a larger full-scale study."

Forseth KO, Hafstrom I, Husby G et al. 2010. Comprehensive rehabilitation of patients with rheumatic diseases in a warm climate: a literature review. J Rehabil Med. 42(10):897-902. "In groups with mixed rheumatic diagnoses, low evidence was found for reduction of pain, activity limitation, global disease impact and improved health-related quality of life. No studies on psoriatic arthritis, osteoarthritis, fibromyalgia or osteoporosis were found.....Well-designed studies to validate and improve the low-to-moderate evidence found for the efficacy of comprehensive rehabilitation in a warm climate among patients with inflammatory rheumatic disease are greatly needed."

Forseth KO, Mengshoel AM. 2007.  Multidimensional therapy in warm climate for patients with fibromyalgia syndrome – a pilot study.  J Musculoskel Pain 15 (Supp 13):47 item 82.  [Myopain 2007 Poster]  “The multiple improvements indicate that multidimensional treatment in warm climate may have short and long lasting effect in patients with FMS.  Further controlled studies are needed to confirm these findings.”  [FM patients are heterogenous.  Some patients do better in warm dry climates and some do better in cold dry climates.  Some patients are both cold and heat sensitive, some are helped by humidity and others feel worse with humidity.  There are so many environmental variables that can affect a climate reactor that studies such as this may be very difficult to interpret.  DJS]

Forseth, K. O. , O. Forre and J. T. Gran. 1999. A 5.5 year prospective study of self-reported musculoskeletal pain and of fibromyalgia in a female population: significance and natural history. Clin Rheumatol 18(2):114-21.

Forseth, K. O. and J. T. Gran.  1992. The prevalence of fibromyalgia among women aged 20-49 years in Arendal, Norway.  Scand J Rheumatol 21(2):74-78.

Forst R, Ingenhorst A. 2005.  [Myofascial pain syndrome]  Internist [Oct 15 Epub ahead of print] [German]  “Untreated, the myofascial pain syndrome leads to a reduced extensibility of the involved muscle with consecutive decrease of the range of motion and development of a muscular imbalance resulting in a disturbance of complex movement and evolution of a chronic pain disease.  An early started and aimed therapy can prevent effectively the chronification.”

Fox AD, Kunins HV, Starrels JL. 2012. Which skills are associated with residents' sense of preparedness to manage chronic pain? J Opioid Manag. 8(5):328-336. "Few internal medicine residents felt prepared to manage CNMP. Our findings suggest that educational interventions to improve residents' preparedness to manage CNMP should target complex pain syndromes (e.g., fibromyalgia and neuropathic pain), safer opioid prescribing practices, and alternatives to opioid analgesics." [I strongly urge them to add myofascial trigger points and chronic myofascial pain to this list of pain sources. DJS]

Fox, A. W. and R. L. Davis.  1998.  Migraine chronobiology.  Headache 38(6):436-41.

Fraenkel, L., Y. Zhang, C. E. Chaisson, S. R. Evans, P. W. Wilson and D. T. Felson.  1998. The association of estrogen replacement therapy and the Raynaud phenomenon in postmenopausal women.  Ann Intern Med 129(3):208-11.

Fraenkel, L., Y. Zhang, C. E. Chaisson, H. R. Maricq, S. R. Evans, F. Brand, P. W. Wilson and D. T. Felson.  1999.  Different factors influencing the expression of Raynaud’s phenomenon in men and women.  Arthritis Rheum 42(2):306-10.

Fraga BP, Santos EB, Farias Neto JP et al. 2012. Signs and symptoms of temporomandibular dysfunction in fibromyalgic patients. J Craniofac Surg. 23(2):615-618. "The most common signs (A) and symptoms (B) reported by FM patients were (A) pain in the masticatory muscles (masseter, 80%; posterior digastric, 76.7%), pain in the temporomandibular joint (83.3%), and 33.3% and 28.3%, respectively, presented joint sounds when opening and closing the mouth; (B) headache (97%) and facial pain (81.7%). In regard to the classic triad for the diagnosis of the TMD, it was found that 35% of the FM patients presented, at the same time, pain, joint sounds, and alteration of the mandibular movements. It was verified that myofascial pain without limitation of mouth opening was the most prevalent diagnosis (47%) for the RDC subgroup I. For the subgroup II, the disk displacement with reduction was the most prevalent diagnosis (21.6%). For the subgroup III, 36.7% of the subjects presented osteoarthritis.....Thus, there is a high prevalence of signs and symptoms of TMD in FM patients, indicating the need for an integrated diagnosis and treatment of these patients, which suggest that the FM could be a medium- or long-term risk factor for the development of TMD." [It is of critical importance that research papers specify the criteria used for the identification of for myofascial trigger points. All of these symptoms can be caused by TrPs, including disc displacement and restricted mouth opening. Most patients with osteoarthritis also have TrPs. We need to shift the focus from FM (the central sensitization) to the cause of the central sensitization (TrPs) DJS].

Frampton M, Harvey RJ, Kirchner V. 2003.  Propentofylline for dementia.  Cochrane Database Syst Rev (2):CD002853.  This study is included on this website because this medication is being studied as a spinal glial cell modulator for central sensitization.  It crosses the blood-brain barrier.

Franco C, Bengtsson BA, Johannsson G. 2001.  Visceral obesity and the role of the somatotropic axis in the development of metabolic complications.  Growth Horm IGF 11:S97-S102.  “Several studies have described a range of metabolic disturbances associated with abdominal obesity, including glucose intolerance, hyperinsulinaemia, insulin resistance, hypertension and dyslipoproteinaemia, now widely known as the metabolic syndrome.  Several abnormalities in the hypothalamic-pituitary axis have been described associated with visceral obesity, suggesting a central neuroendocrine dysregulation including increased cortisol concentration and impaired gonadotropin and growth hormone (GH) secretion.”

Francois, P. P., K. T. Preissner, M. Herrmann, R. P. Haugland, P. Vaudaux, D. P. Lew and K. H. Krause.  1999.

Frank, E. M. 1999. Myofascial trigger point diagnostic criteria in the dog. J Musculoskel Pain 7(1-2):231-237.

Franssen JLM, Beersma B, Bron C. 2007.  Shoulder pain during swallowing: the use of surface electromyography as a valuable diagnostic and therapeutic tool in myofascial pain syndrome.  J Musculoskel Pain 15 (Supp 13):22 item 33.  [Myopain 2007 Poster]  “MPS should be considered as a possible cause of musculoskeletal complaints in neck or shoulder disorders.  Surface electromyography can be of great benefit in the process of differential diagnosis and may be illuminate non-physiological motor behavior, which is one of the perpetuating factors in MPS.  The knowledge of referred pain patterns may be helpful in identifying the muscle to be treated.”  [This is a very interesting study, as the MTPs were initiated due to use of endotracheal tube during surgery, and the referral pain pattern occurred during swallowing.  Having experienced TPM cascade from endotracheal intubation myself, I know how difficult this can be and how unaware most anesthesiologists and other medical team members are that this can occur.  DJS]

Fredheim OM, Kaasa S, Dale O et al. 2006.  Opioid switching from oral slow release morphine to oral methadone may improve pain control in chronic non-malignant pain: a nine-month follow-up study.  Palliat Med. 20(1):35-41.

Freedenfeld RN, Murray M, Fuchs PN et al. 2006.  Decreased pain and improved quality of life in fibromyalgia patients treated with olanzapine, an atypical neuroleptic.  Pain Pract. 6(2):112-118.  “In general, the data provide strong support that olanzapine can, in certain patients, improve symptoms associated with fibromyalgia in patients who have had limited success with other treatment modalities.”  There were significant side-effects that caused discontinuance of treatment in a number of patients.

Freitas, J. P. , P. Filipe, I. Emerit, P. Meunier, C. F. Manso and F. Guerra Rodrigo. 1996. Hyaluronic acid in progressive systemic sclerosis. Dermatology. 192(1):46-9.

Fricton, J. R. 2002. "Masticatory myofascial pain" an explanatory model of regional muscle pain syndromes. J Musculoskel Pain 10(1/2)131-150. The presence of myofascial trigger points should be explored in cases of masticatory pain.

Fricton, J. R.  1996.  Myofascial pain of the head and neck: diagnosis and management. J Back & Musculoskeletal Rehab 6:177-194.

Fricton JR, Kroening R, Haley D et al. 1985.  Myofascial pain syndrome of the head and neck: a review of clinical characteristics of 164 patients. Oral Surg Oral Med Oral Pathol. 60(6):615-623.  “Misdiagnosis or inadequate management of this disorder after onset may lead to development of a complex chronic pain syndrome.”  [This is a study of 164 patients, as true today as it was when it was written.  Far too many dentists have no knowledge of myofascial pain, and this lack of knowledge on their part results in far too many chronic pain patients.  DJS]

Fricton JR, Steenks MH. 1996.  [Diagnosis and treatment of myofascial pain] Ned Tijdschr Tandheelkd. 103(7):249-253.  [Dutch]  “MFP is frequently overlooked as a diagnosis because it is often accompanied by signs and symptoms in addition to pain….”   “The difficulty in managing MFP lies in the critical need to match the level of complexity of the management program with the complexity of the patient.  Failure to address the entire problem may lead to failure to resolve the pain and perpetuation of a chronic pain syndrome.”

Friedberg F, Williams DA, Collinge W. 2012. Lifestyle-oriented non-pharmacological treatments for fibromyalgia: a clinical overview and applications with home-based technologies. J Pain Res. 5:42535. Many of these treatments help and are cost-effective. [It is unfortunate that co-existing conditions such as myofascial trigger points, insulin resistance and other illnesses were not considered, although the study was basically aimed at controlling some common perpetuating factors. DJS]

Friederich HC, Schellberg D, Mueller K et al.  2004.  [Stress and autonomic dysregulation in patients with fibromyalgia syndrome.]  Schmerz [Epub May 12 ahead of print] [German]  This study indicates that the stress system in FMS patients is hyporeactive.

Friedman, D. P. 1990.  Perspectives on the medical use of drugs of abuse.  J Pain Symptom Manage 5(1 Suppl):S2-S5.

Friedman M, Gurpinar B, Lin HC et al. 2007.  Impact of treatment of gastroesophageal reflux on obstructive sleep apnea-hypopnea syndrome.  Ann Otol Rhinol Laryngol. 116(11):805-811.  “Treatment of GERD had a significant impact on the reduction of the apnea-hypopnea index, snoring, and daytime sleepiness.  Elimination of GERD should be part of a comprehensive treatment plan for patients with OSAHS.” 

Friedrich M, Hahne J, Wepner F. 2009.  A controlled examination of medical and psychosocial factors associated with low back pain in combination with widespread musculoskeletal pain.  Phys Ther. [Jun 18 Epub ahead of print].

Frieri M. 2003.  Identification of masqueraders of autoimmune disease in the office.  Allergy Asthma Proc 24(6):421-9. Fibromyalgia is included as one of the diseases that often masquerades as and may be misdiagnosed as an autoimmune disease.  [This may result in inappropriate medications and therapies. DJS]

Frokjaer JB, Andersen SD, Gale J et al. 2005.  An experimental study of viscero-visceral hyperalgesia using an ultrasound-based multimodal sensory testing approach.  Pain [Nov 15 Epub ahead of print]. “Central mechanisms can explain the remote hyperalgesia to mechanical visceral stimulation and the increase in referred pain areas.”

Frost J, Okun S, Vaughan T et al. 2011. Patient-reported Outcomes as a Source of Evidence in Off-Label Prescribing: Analysis of Data from PatientsLikeMe. J Med Internet Res. 13(1):e6. "Evaluating a new use for an existing drug can be expensive and time consuming. Providers and patients must all too often rely upon their own individual-level experience to inform clinical practice, which generates only anecdotal and unstructured data....In this work, we explored how a patient-centered online research platform could supplement traditional trials to create a richer understanding of medical products postmarket by efficiently aggregating structured patient-reported data. PatientsLikeMe is a tool for patients, researchers, and caregivers (currently 82,000 members across 11 condition-based communities) that helps users make treatment decisions, manage symptoms, and improve outcomes. Members enter demographic information, longitudinal treatment, symptoms, outcome data, and treatment evaluations. These are reflected back as longitudinal health profiles and aggregated reports. Over the last 3 years, patients have entered treatment histories and evaluations on thousands of medical products. These data may aid in evaluating the effectiveness and safety of some treatments more efficiently and over a longer period of time course than is feasible through traditional trials.....Patient-reported outcomes, like those entered within PatientsLikeMe, offer a unique real-time approach to understand utilization and performance of treatments across many conditions. These patient-reported data can provide a new source of evidence about secondary uses and potentially identify targets for treatments to be studied systematically in traditional efficacy trials."

Fruchwald-Schultes B, Kern W, Born J, et al.. 2001.  Hyperinsulinemia causes activation of the hypothalamus-pituitary-adrenal axis in humans.  Int J Obes Relat Metab Disord 25 Suppl 1:S38-40. Hyperinsulinemia acutely increases HPA secretory activity in healthy men.

Frye, J. 1997.  Homeopathy in office practice.  Prim Care 24(4):845-865.

Fuentes CT, Bastian AJ. 2009. Where is your arm?  Variations in proprioception across space and tasks. J Neurophysiol. [Oct 28 Epub ahead of print]  “The sense of limb position is crucial for movement control and environmental interactions.”  “In sum, we have uncovered fundamental aspects of proprioceptive processing, demonstrating both predictable biases that are dependent on joint configuration and independent of task as well as improved precision when integrating information across joints.”  [Patients with proprioceptive dysfunction, which can be associated with myofascial TrPs, vestibular dysfunction, eye inequalities, or brain injury, or a combination of all of them (which many FM and CMP patients have), may feel clumsy, but in actuality, it is a magnificent thing that some of us can walk across a room.  The endless compensation that goes on is often unnoticed and unremarked until a compensation mechanism fails, and we feel “clumsy.”  DJS]

Fugh-Berman, A. and J. M. Cott.  1999.  Dietary supplements and natural products as psychotherapeutic agents.  Psychosom Med 61(5):712-28.

Fujioka, M., K. Okuchi, K. I. Hiramatsu, T. Sakaki, S. Sakaguchi and Y. Ishii. 1997. Specific changes in human brain after hypoglycemic injury. Stroke 28(3):584-587.

Fukuda, K., Straus, S. E. , Hickie I., Sharpe, M. , Dobbins J, G., Komaroff A., and the ICFSSG.  1994. The Chronic Fatigue Syndrome: A Comprehensive Approach to Its Definition and Study. Ann Int Med 121(12)953-959.

Furnes B, Dysvik E. 2010. Dealing with grief related to loss by death and chronic pain: An integrated theoretical frame work. Part 1. Patient Prefer Adherence. 4:135-140. "Two main themes were formulated, 'relearning the world' and 'adaptation'. Between these themes a continuous movement emerged involving experience such as: 'despair and hope', 'lack of understanding and insight', 'meaning disruption and increased meaning', and 'bodily discomfort and reintegrated body'." "Grief as a distinctive experience means that health care must be aimed at each individual experience and situation." [This article explains why care providers and supporters of patients dealing with chronic pain situations need to understand the enormity of life disruption that a chronic pain state can bring.]

Furuta A, Suzuki Y, Honda M et al. 2011. Time-dependent changes in bladder function and plantar sensitivity in a rat model of fibromyalgia syndrome induced by hydrochloric acid injection into the gluteus. BJU Int. [Aug 2 Epub ahead of print]. "HCl injection (pH 4.0) into the gluteus can induce plantar hypersensitivity and urinary frequency (in the rat) for up to 2 weeks after the injection, suggesting that somatic (gluteus)-to-visceral (bladder) cross-sensitization might underlie bladder hypersensitivity in patients with FMS. Moreover, intervention at specific tender points outside the bladder could be effective in treating urinary frequency because lidocaine injection into the gluteus normalized bladder function in FMS rats for up to 2 weeks."

Ga H, Choi JH, Park CH et al. 2007.  Acupuncture needling versus lidocaine injection of trigger points in myofascial pain syndrome in elderly patients – a randomized trial.  Acupunct Med. 25(4):130-136.  “There was no significant difference between acupuncture needling and 0.5% lidocaine injection of trigger points for treating myofascial pain syndrome in elderly patients.”

Ga H, Koh HJ, Choi JH et al. 2007.  Intramuscular and nerve root stimulation vs. lidocaine injection to trigger points in myofascial pain syndrome.  J Rehabil Med. 39(5):374-378.  “In managing myofascial pain syndrome, after one month intramuscular stimulation resulted in more significant improvements in pain intensity, cervical range of motion and depression scales than did 0.5% lidocaine injection of trigger points.  Intramuscular stimulation is therefore recommended for myofascial pain syndrome.”

Gagliardi GS, Shah AP, Goldstein M et al. 2009.  The effect of zolpidem on the sleep arousal response to nocturnal esophageal acid exposure.  Clin Gastroenterol Hepatol. [May 5 Epub ahead of print].  “Zolpidem reduced the arousal response to nocturnal acid exposure and increased the duration of each esophageal acid reflux event in healthy individuals and patients with GERD.  Since nocturnal acid exposure was prolonged, hypnotic use by GERD patients could lead to increased risk for complicated disease.”

Gagliese, L. and R. Melzack.  1997.  Chronic pain in elderly people.  Pain 70(1):3-14.

Gagnon I, Swaine B, Friedman D et al. 2004.  Children show decreased dynamic balance after mild traumatic brain injury.  Arch Phys Med Rehabil 85(3):444-452.  Even mild traumatic brain injury can cause postural balance dysfunction in children 10 weeks after the injury.

Galic MA, Persinger MA. 2007.  Lagged association between geomagnetic activity and diminished nocturnal pain thresholds in mice.  Bioelectromagnetics [Jul 26 Epub ahead of print].  “If the geomagnetic activity was greater 3 days before a given hotplate trial, subjects tended to exhibit shorter response latencies, suggesting lower pain thresholds or less analgesia.  These results are supported by related experimental findings and suggest that natural variations in geomagnetic intensity may influence nociceptive behaviors in mice.”  [This study, although done in mice, may have implications for electromagnetic sensitivity observed in some FM patients.  DJS]

Galinier, M., J. Fourcade, N. Ley, S. Boveda, S. Solera, M. L. Solera, P. Massabuau, S. Elhabaj, J. M. Fauvel, P. Valdiguie and J. P. Bounhoure. 1999. [No title available] Arch Mal Coeur Vaiss 92(8):1105-9. [French] 

Gallagher L, McAuley J, Moseley GL. 2013. A randomized-controlled trial of using a book of metaphors to reconceptualize pain and decrease catastrophizing in people with chronic pain. Clin J Pain 29(1):20-25. In this randomized single-blind crossover controlled trial, a group of chronic pain patients were taught by giving them a booklet of metaphors and stories and a control group was given advice on how to manage pain according to cognitive behavior principles. Pain biology knowledge and catastrophizing were measured at intervals. The educational material provided by the metaphors and stories helped patients to reconceptualize pain and reduce catastrophizing, and gains were maintained for at least 3 months. Changes were replicated in the advice booklet group when they were crossed over to the booklet with metaphors and stories. There was no change in self-reported disability. Metaphor and story appears to be a preferred precursor to functional capacity interventions.

Gallagher, R. M.  1999.  Primary care and pain medicine.  A community solution to the public health problem of chronic pain.  Med Clin North Am 83(3):555-83,v.

Gallagher, R. M. and S. Verma.  1999.  Managing pain and comorbid depression: A public health challenge.  Semin Clin Neuropsychiatry 4(3):203-20.

Galland L. 2006.  Patient-centered care: antecedents, triggers and mediators.  Altern Ther Health Med. 12(4):62-70.  “Functional medicine is essentially patient centered, rather than disease centered.  A structure is presented for uniting a patient-centered approach to diagnosis and treatment with the fruits of modern clinical science (which evolved primarily to serve the prevailing model of disease-centered care).  The core scientific concepts of disease pathogenesis are antecedents, triggers, and mediators.  Antecedents are factors, genetic or acquired, that predispose to illness; triggers are factors that provoke the symptoms and signs of illness; and mediators are factors, biochemical or psychosocial, that contribute to pathological changes and dysfunctional responses.  Understanding the antecedents, triggers, and mediators that underlie illness or dysfunction in each patient permits therapy to be targeted to the needs of the individual.  The conventional diagnosis assigned to the patient may be of value in identifying plausible antecedents, triggers or mediators for each patient, but is not adequate by itself for the designing of patient-centered care.  Applying the model of person-centered diagnosis to patients facilitates the recognition of disturbances that are common in people with chronic illness.  Diet, nutrition, and exposure to environmental toxins play central roles in functional medicine because they may predispose to illness, provoke symptoms, and modulate the activity of biochemical mediators through a complex and diverse set of mechanisms.  Explaining those mechanisms is a key objective of the Textbook of Functional Medicine (from which this article is excerpted).  A patient's beliefs about health and illness are critically important for self-care and may influence both behavioral and physiological responses to illness.  Perceived self-efficacy is an important mediator of health and healing.  Enhancement of patients' self-efficacy through information, education, and the development of a collaborative relationship between patient and healer is a cardinal goal in all clinical encounters.”  [ I strongly recommend this textbook for any doctor who has patients with chronic illness.  It will help them get to the cause of some of the metabolic dysfunctions. DJS]

Galski, T., J. B. Williams and H. T. Ehle.  2000.  Effects of opioids on driving ability.  J Pain Symptom Manage 19(3):200-8.

Gamez-Nava, J. I., L. Gonzalez-Lopez, P. Davis and M. E. Suarez-Almazor.  1998.  Referral and diagnosis of common rheumatic diseases by primary care physicians.  Br J Rheumatol 37(11):1215-9.

Gamsa, A.  1990. Is emotional disturbance a precipitator or a consequence of chronic pain? Pain 42(2): 183-195.

Gansky SA, Plesh O. 2007.  Widespread pain and fibromyalgia in a biracial cohort of young women.  J Rheumatol. [Feb 1 Epub ahead of print]  These conditions are common, and there may be racial differences that seem to develop early.

Gao YJ, Ji RR. 2010. Chemokines, neuronal-glial interactions, and central processing of neuropathic pain. Pharmacol Ther. [Jan 28 Epub ahead of print]  “It has been increasingly recognized that spinal cord glial cells such as microglia and astrocytes play a critical role in the induction and maintenance of neuropathic pain by releasing powerful neuromodulators such as proinflammatory cytokines and chemokines. Recent evidence reveals chemokines as new players in pain control. In this article, we review evidence for chemokine modulation of pain via neuronal-glial interactions by focusing on the central role of two chemokines, CX3CL1 (fractalkine) and CCL2 (MCP-1), because they differentially regulate neuronal-glial interactions. Release of CX3CL1 from neurons is ideal to mediate neuronal-to-microglial signaling, since the sole receptor of this chemokine, CX3CR1, is expressed in spinal microglia and activation of the receptor leads to phosphorylation of p38 MAP kinase in microglia. Although CCL2 was implicated in neuronal-to-microglial signaling, a recent study shows a novel role of CCL2 in astroglial-to-neuronal signaling after nerve injury. In particular, CCL2 rapidly induces central sensitization by increasing the activity of NMDA receptors in dorsal horn neurons. Insights into the role of chemokines in neuronal-glial interactions after nerve injury will identify new targets for therapeutic intervention of neuropathic pain.”  

Gao YJ, Xu ZZ, Liu YC et al. 2009.  The c-Jun N-terminal kinase 1 (JNK1) in spinal astrocytes is required for the maintenance of bilateral mechanical allodynia under a persistent inflammatory pain condition.  Pain. [Dec 16 Epub ahead of print]  “Peripheral inflammation induces persistent central sensitization characterized by mechanical allodynia and heat hyperalgesia that are mediated by distinct mechanisms.”  “…we investigated the distinct role of spinal JNK in heat hyperalgesia, mechanical allodynia, and contralateral pain in an inflammatory pain model.”  “…our data suggest that spinal JNK, in particular HNK1, plays an important role in the maintenance of persistent inflammatory pain.  Our findings also reveal a unique role of JNK1 and astrocyte network in regulating tactile allodynia and contralateral pain.”  [This article is relevant as astrocytes (glial cells) are implicated in the development of the central sensitization of FM, and opposite side, contralateral) pain occurs in TrPs when the pain fields are expanding and central sensitization is developing.  Since we have recently found that FM patients have myofascial TrPs, TrPs are responsible for generating some FM pain and can of themselves maintain central sensitization, this is an important piece of the puzzle. DJS]

Gao YJ, Zhang L, Ji RR. 2010. Spinal injection of TNF-alpha-activated astrocytes produces persistent pain symptom mechanical allodynia by releasing monocyte chemoattractant protein-1. Glia. [Aug 24 Epub ahead of print]. "Accumulating evidence suggests that spinal astrocytes play an important role in the genesis of persistent pain, by increasing the activity of spinal cord nociceptive neurons, i.e., central sensitization.....We investigated whether and how spinal injection of activated astrocytes could produce mechanical allodynia, a cardinal feature of chronic pain, in....mice.....our results suggest that activated astrocytes are sufficient to produce persistent pain symptom in our mice...." [We can look forward to the development of astrocyte modulators to minimize central sensitization. DJS]

Garbuzenko E, Nagler A, Pickholtz D et al. 2002.  Human mast cells stimulate fibroblast proliferation, collagen synthesis and lattice contraction: a direct role for mast cells in skin fibrosis.  Clin Exp Allergy. 32(2):237-246.  This study indicates that co-existing allergies and the presence of more numerous mast cells may have a significant affect on scarring, formation of adhesions and fibrosis.  One of the two main mast cell mediators involved is histamine, one of the biochemicals produced during MTrP local twitch response.  Allergies may thus be interactive with other conditions in yet one more way.

Garcia,  J. and R. D. Altman. 1997 a.  Chronic pain states: invasive procedures. Semin Arthritis Rheum 27(3):156-160.  

--- 1997 b.  Chronic pain states: pathophysiology and medical therapy.  Semin Arth Rheum 27(1):1-16.  

Garcia R. Jr., and J. A. Arrington. 1996. The relationship between cervical whiplash and temporomandibular joint injuries: an MRI study.  Cranio 14(3):233-9. 

Garcia-Martinez AM, De Paz JA, Marquez S. 2011. Effects of an exercise program on self-esteem, self-concept and quality of life in women with fibromyalgia: a randomized controlled trial. Rheumatol Int. [Mar 27 Epub ahead of print]. "Compared to the control group, statistically significant improvements in self-esteem, self-concept, FIQ (Fibromyalgia Impact Questionnaire), physical functioning, role physical, bodily pain, vitality, role emotional, social functioning, mental health, isometric strength, muscular endurance and flexibility were evident in the exercise group at the end of treatment. Self-esteem and self-concept scores were correlated positively with role emotional, mental health and the mental component summary of SF-36 and were negatively correlated to FIQ scores. No significant correlation existed between self-esteem or self-concept and isometric strength, muscular endurance or flexibility. Our results highlight the need for a broader array of physical and mental outcomes and the importance of examining patient's perceptions in future research therapies." [Co-existing trigger points must be taken into consideration when constructing an exercising program. When TrPs are causing weakness in a muscle, you cannot strengthen it though exercise. DJS]

Gardner, J. R. and G. Sandhu.  1997.  The stigma and enigma of chronic non-malignant back pain (CNMBP) treated with long-term opioids (LTO).  Contemp Nurse 6(2):61-66. 

Garg A. 2006.  Adipose tissue dysfunction in obesity and lipodystrophy.  Clin Cornerstone 8 Suppl 4:S7-S13.  “Dysfunction of adipose tissue can result in insulin resistance and its metabolic complications in patients with excess body fat (obesity) or markedly reduced body fat (lipodystrophy).  Alterations in free fatty acid and adipocytokine release from adipose tissue may underlie metabolic complications.”   Adipose tissue is more than a mechanical perpetuating factor.

Garrett CG, Cohen SM. 2008. Otolaryngological perspective on patients with throat symptoms and laryngeal irritation.  Curr Gastroenterol Rep. 10(3):195-199.  Laryngeal reflux is an increasingly common condition.  Symptoms include an urge to clear the throat, sore throat, hoarseness, cough, and sensation of a foreign body in the throat.  It is usually treated with anti-reflux medication.  The article indicates that failure to consider other diagnoses may result in unnecessary treatment and diagnostic delay.  [TrPs in the laryngeal muscles are frequently irritated by reflux, and must be considered as part of treatment regimen.  They can also mimic other laryngeal conditions.  Symptoms including vocal dysfunctions may be considerably helped by TrP treatment, but the perpetuating factors must be removed as well. DJS]

Garrison RL, Breeding PC. 2003.  A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone.  Med Hypotheses 61(2):182-189.  Thyroid resistance may be a key perpetuating factor of FMS.

Garvey TA, Marks MR, Wiesel SW. 1989. A prospective, randomized, double-blind evaluation of trigger point injection therapy for low back pain.  Spine 14(9):962-964.  “Trigger point therapy seems to be a useful adjunct in treatment of low back strain. The injected substance apparently is not the critical factor, since direct mechanical stimulus to the trigger point seems to give symptomatic relief equal to that of treatment with various types of injected medication.”  [Chronic low back pain is often due to TrPs.   This has long been known but has not filtered down to the clinician level. DJS]

Gatchel RJ, Okifuji A. 2006.  Evidence-based scientific data documenting the treatment and cost effectiveness of comprehensive pain programs for chronic nonmalignant pain.  J Pain 7(11):779-793.   “This review clearly revealed that CPPs offer the most efficacious and cost effective treatment for persons with chronic pain, relative to a host of widely used conventional medical treatment.” [Chronic pain programs for patients with FMS and CMP must include care providers with the skills to diagnose and treat these conditions. DJS]

Gatts SK, Woollacott MH. 2006.  Neural mechanisms underlying balance improvement with short term Tai Chi training.  Aging Clin Exp Res. 18(1):7-19.  “TC (t’ai chi) enhanced neuromuscular responses controlling the ankle joint of the perturbed leg.  Fast, accurate neuromuscular activation is crucial for efficacious response to slips or trips.”

Gavish A., Winocur E., Ventura Y.S. et al. 2002.  Effects of stabilization splint therapy on pain during chewing in patients suffering from myofascial pain.  Patients with masticatory myofascial pain who used flat occlusal splints experienced less intense pain than the control patients. [Part of the reduction in pain may be due to TrPs becoming latent because of using the splint. DJS]

Ge HY. 2010. Prevalence of myofascial trigger points in fibromyalgia: the overlap of two common problems. Curr Pain Headache Rep. 14(5):339-345. Now that we have objective evidence of the reality of myofascial trigger points, it is becoming more apparent that they contribute to many chronic regional and widespread pain conditions. "Active MTrPs as tonic peripheral nociceptive input contribute tremendously to the initiation and maintenance of central sensitization, to the impairment of descending inhibition, to the increased excitability of motor units, and to the induction of sympathetic hyperactivity observed in FM. The considerable overlap of MTrPs and FM in pain characteristics and pathophysiology suggests that FM pain is largely due to MTrPs."

Ge HY, Arendt-Nielsen L. 2011. Latent myofascial trigger points. Curr Pain Headache Rep May 11 [Epub ahead of print] The treatment of latent TrPs may improve function, decrease sensitivity to pain, prevent the activation of those TrPs, and, if caught in time, may prevent the development of myofascial pain syndrome.

Ge HY, Fernandez-de-Las-Penas C, Yue SW. 2011. Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med. 6(1):13. "Referred pain is dependent on the sensitivity of myofascial trigger points. Active myofascial trigger points may play an important role in the transition from localized pain to generalized pain conditions via the enhanced central sensitization, decreased descending inhibition and dysfunctional motor control strategy."

Ge HY, Nie H, Madeleine P et al. 2009.  Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome.  Pain. [Oct 8 Epub ahead of print].  “The generalized hypersensitivity associated with fibromyalgia syndrome (FMS) may in part be driven by peripheral nociceptive sources.”  “Active MTrPs bilaterally in the upper trapezius muscle contribute to the neck and shoulder pain in FMS.  Active MTrPs may serve as one of the sources of noxious input leading to the sensitization of spinal and supraspinal pain pathways in FMS.”  [We are getting more confirmation that myofascial TrPs can be in some if not many instances at least one way that the central sensitization we know of as fibromyalgia is maintained.  To treat fibromyalgia adequately, co-existing myofascial TrPs MUST be treated.  Any doctor who treats fibromyalgia patients MUST know how to diagnose and treat patients with myofascial TrPs or they cannot justifiably take money to treat patients for these conditions.  DJS]

Ge HY, Fernandez-de-Las-Penas C, Madeleine P et al.  2008.  Topographical mapping and mechanical pain sensitivity of myofascial trigger points in the infraspinatus muscle.  Eur J Pain. [Jan 17 Epub ahead of print].  “There exists bilateral mechanical hyperalgesia in patients with unilateral shoulder pain.  Further, the association of multiple active MTPs with unilateral shoulder pain and the heterogeneity of mechanical pain sensitivity distribution suggest a crucial role of peripheral sensitization in chronic myofascial pain conditions.”

Ge HY, Serrao M, Anderson OK et al. 2007.  Increased H-reflex response induced by intramuscular electrical stimulation at trigger points.  J Musculoskel Pain 15 (Supp 13):22 item 34.  [Myopain 2007 Poster]  “The data suggest that there exists increased sensitivity of muscle spindle afferents at TrPs.”  This study indicates heightened H-reflex response at MTPs and gives additional data documenting the nature of the increased motor endplate sensitivity.

Ge HY, Wang Y, Fernandez-de-Las-Penas C et al. 2011. Reproduction of overall spontaneous pain pattern by manual stimulation of active myofascial trigger points in fibromyalgia patients. Arthritis Res Ther. 13(2):R48. "The overall spontaneous FM pain pattern can be reproduced by mechanical stimulation of active MTPs located in different muscles, suggesting that fibromyalgia pain is largely composed of pain arising from muscle pain and spasm. Targeting active MTPs and related perpetuating factors may be an important strategy in FM pain control." [More research is showing that one cannot treat FM without treating the pain generators, including myofascial TrPs. DJS]

Gear, R. W., C. Miaskowski, N. C. Gordon, S. M. Paul, P. H. Heller and J. D. Levine.  1999. The kappa opioid nalbuphine produces gender- and dose-dependent analgesia and antianalgesia in patients with postoperative pain.  Pain 83(2):339-45.   

Gear, R. W., C. Miaskowski, P. H. Heller, S. M. Paul, N. C. Gordon and J. D. Levine.  1997. Benzodiazepine mediated antagonism of opioid analgesia.  Pain 71(1):25-29.

Gear,  R. W., C. Miaskowski, N. C. Gordon,  S. M. Paul, P. H. Heller and J. D. Levine 1996.  Kappa-opioids produce significantly greater analgesia in women than in men.  Nat Med 2(11):1248-1250.

Gedalia, A., J. Press, M. Klein and D. Buskila. 1993. Joint hypermobility and fibromyalgia in schoolchildren. Ann Rheum Dis 52 (7):494-496.  

Geddes, B. J. and A. J. Summerlee. 1995. The emerging concept of relaxin as a centrally acting peptide hormone with hemodynamic actions. J Neuroendocrinol 7(6):411-417.

Geenen R, Jacobs JWG, Bijlsma JWJ. 2009.  A psychoneuroendocrine perspective on the management of fibromyalgia syndrome.  J Musculoskel Pain. 17(2):178-188.  “Essential aims in the tailored management of FMS are enhancement of functional capacity and quality of life, and symptomatic treatment of individual symptoms such as pain, distress, and sleep disturbances.  Patient education, pharmacological interventions with analgesics and antidepressants, cognitive-behavioral therapy, sleep hygiene training, and low-intensity physical exercise training are commonly employed in tailored management of FMS.  Our review suggests that favorable neuroendocrine changes are to be expected as part of a successful outcome of these therapeutic strategies.”

Geenen R, Jacobs JW. 2001.  Fibromyalgia: diagnosis, pathogenesis and treatment.  Curr Opin Anaesthesiol. 14(5):533-539.  “Fibromyalgia is a multifaceted problem.”  “…the objective in future evaluations should be to try to find the combined pharmacological or non-pharmacological treatment of choice for specific subgroups of patients.”

Geiss A, Rohleder N, Anton F. 2011. Evidence for an association between an enhanced reactivity of interleukin-6 levels and reduced glucocorticoid sensitivity in patients with fibromyalgia. Psychoneuroendocrinology. [Oct 13 Epub ahead of print]. "Whereas FMS patients were found not to differ from controls in cortisol awakening response, daytime profile of cortisol secretion and cortisol suppression after overnight DST, they did exhibit a reduced GC sensitivity of inflammatory cytokine production. PPT measurement did induce three times higher cortisol and four times higher IL-6 levels in FMS patients, but no change in their ACTH levels. The enhanced IL-6 reactivity after PPT measurement was accompanied by an increase in the severity of FMS patients' pain and fatigue ratings. The findings of the present study provide evidence for the pathophysiologic relevance of a disturbed glucocorticoid receptor (GR) function, rather than reduced cortisol levels for the maintenance of FMS core symptoms." [It would be interesting to have a companion study to see how many of these patients also had insulin resistance and thyroid resistance, as these are common coexisting conditions with FM. DJS]

Geletka BJ, O'Hearn MA, Courtney CA. 2012. Quantitative sensory testing changes in the successful management of chronic low back pain. J Man Manip Ther. 20(1):16-22. "Individuals with chronic low back pain (LBP) represent a significant percentage of patients in physical therapy practice. The clinical pattern often includes diffuse pain and a variety of sensory complaints, making categorization difficult and leading to diagnoses such as non-specific LBP. Objective measures of sensory changes through quantitative sensory testing may help identify central sensitization of nociceptive pathways in this population. Identification of these somatosensory changes may contribute to clinical decision making and patient management. The purpose of this case report is to present objective evaluation findings, including altered somatosensation, in a patient with a 2-year history of LBP, and to describe changes in function and quantitative sensory testing with successful management."

Gelfand , M. M . 2000.  Sexuality among older women. J Womens Health Gend Based Med   Suppl 1:S15-20.       

Gemignani F, Vitetta F, Brindani F et al. 2012. Painful polyneuropathy associated with restless legs syndrome. Clinical features and sensory profile. Sleep Med. [Oct 3 Epub ahead of print]. "RLS is frequently associated with painful polyneuropathy, in keeping with the hypothesis that its occurrence is favored by small fiber involvement. It represents a heterogeneous entity, differentiated in chronic and remitting-intermittent subtypes, possibly conditioned by indolent or aggressive neuropathy course and phenomena of central sensitization."

Gemmell C, Leathem JM. 2006.  A study investigating the effects of Tai Chi Chuan: individuals with traumatic brain injury compared to controls.  “Tai Chi provides short-term benefits after TBI, with rigorous outcome measurement needed to examine long-term benefits.”

Genazzani, A. R., A. Spinetti, R. Gallo and F. Bernardi.  1999.  Menopause and the central nervous system: intervention options.  Maturitas 31(2):103-10.

Gendreau M, Hufford MR, Stone AA. 2003.  Measuring clinical pain in chronic widespread pain: selected methodological issues.  Best Pract Res Clin Rheumatol 17(4):575-592.  “Patients pain reports can be systematically biased by a number of methodological factors.”

Genter, P. M. and E. Ipp.  1994.  Accuracy of plasma glucose measurements in the hypoglycemic range. Diabetes Care 17(6):595-598.  Any interpretation or comparison of critical clinical and research measurements of glucose in different settings take into account methodological differences, particularly in the hypoglycemic range. 

Gentili, A. and J. D. Edinger.  1999.  Sleep disorders in older people.  Aging (Milano) 11(3):137-41.

Gerbershagen HJ. 2013. [Transition from acute to chronic postsurgical pain: Physiology, risk factors and prevention.] Schmerz. [Feb 2 Epub ahead of print]. [Article in German] "Chronic postsurgical pain (CPSP) is defined as pain persisting for longer than 3 months postoperatively. The frequency of occurrence ranges from 5 % to 60 % in all types of surgery and 1-3 % of patients with CPSP will suffer from severe pain and pain-related interference with daily activities. The pathological mechanisms which lead to the development of CPSP are complex and have not yet been analyzed. Neuropathic pain after surgical nerve lesions has been reported. Many patients with CPSP, however, do not present with any neuropathic pain characteristics. Peripheral and central sensitization are the essential mechanisms of the development of pain chronicity in the postoperative period. As treatment of CPSP is demanding it is attempted to prevent central sensitization before CPSP develops." [It would be wise to assess each post-surgical patient for developing TrPs in a follow-up exam at least a month after surgery. DJS]

Gerdle B, Forsgren MF, Bengtsson A et al. 2013. Decreased muscle concentrations of ATP and PCR in the quadriceps muscle of fibromyalgia patients – A (31) P-MRS study. Eur J Pain. [Jan 30 Epub ahead of print]. "Alterations in intramuscular ATP, PCr and fat content in FMS probably reflect a combination of inactivity related to pain and dysfunction of muscle mitochondria." [OR, they may reflect the presence of co-existing TrPs. DJS]

Gerdle B, Grönlund C, Karlsson SJ et al. 2010. Altered neuromuscular control mechanisms of the trapezius muscle in fibromyalgia. BMC Musculoskelet Disord. 11:42. “For decades, the association between motor control strategies and chronic pain has been a topic for debate. One long held functional neuromuscular control mechanism is differential activation between regions within a single muscle. The aim of this study was to investigate differences in neuromuscular control, i.e. differential activation, between myalgic trapezius in fibromyalgia patients and healthy controls. METHODS: 27 fibromyalgia patients and 30 healthy controls performed 3 minutes bilateral shoulder elevations with different loads (0-4 Kg) with a high-density surface electromyographical (EMG) grid placed above the upper trapezius. Differential activation was quantified by the power spectral median frequency of the difference in EMG amplitude between the cranial and caudal parts of the upper trapezius. The average duration of the differential activation was described by the inverse of the median frequency of the differential activations. RESULTS: the median frequency of the differential activations was significantly lower, and the average duration of the differential activations significantly longer in fibromyalgia compared with controls at the two lowest load levels (0-1 Kg) (p < 0.04), but not at the two highest load levels (2 and 4 Kg). CONCLUSION: these findings illustrate a different neuromuscular control between fibromyalgia patients and healthy controls during a low load functional task, either sustaining or resulting from the chronic painful condition. The findings may have clinical relevance for rehabilitation strategies for fibromyalgia.”  [I believe that this article, although claiming to be about FM, actually deals with co-existing myofascial trigger points, known to cause the different EMG effects described.  Fibromyalgia is central nervous system sensitivity.  Until we get the researchers clear on these frequently co-existing but very different conditions, we will have misleading research with misleading conclusions. DJS]

Gerdle B, Ostlund N, Gronlund C et al. 2007.  Firing rate and conduction velocity of single motor units in the trapezius muscle in fibromyalgia patients and healthy controls.  J Electromyogr Kinesiol. [Apr 23 Epub ahead of print].  “CV (conduction velocity) was significantly higher in FM than in healthy controls; this might be due to alterations in histopathology and microcirculation.”  [It is unfortunate that patients were not screened for co-existing myofascial trigger points. DJS]

Germanowicz D, Lumertz MS, Martinez D et al. 2006.  Sleep disordered breathing concomitant with fibromyalgia syndrome.  J Bras Pneumol. 32(4):333-338.  “…the more than ten-fold higher proportion of fibromyalgia cases seen in this sample supports the hypothesis that there is an association between sleep disordered breathing and fibromyalgia syndrome.

Gerster, J. C. and A. Hadj-Djilani. 1984. Hearing and vestibular abnormalities in primary fibromyalgia syndrome. J Rheumatol 11(5):678-680.

Gervais Tougas G. 1999. The autonomic nervous system in functional bowel disorders. Can J Gastroenterol 13 Suppl A:15A-7A.  [ED, THIS NOTATION IS CORRECT]

Gerwin R. 2007.  Trigger points: a comprehensive hypothesis of trigger point formation.  J Musculoskel Pain 15 (Supp 13):12 item 14.  [Myopain 2007 Poster]  Dr. Gerwin’s hypothesis may fill in the missing elements in the formation of myofascial trigger points (MTPs).  We did not have an explanation for the excess release of acetylcholine, the excess release of calcium, and the excessive motor endplate noise, nor did we understand why the taut band forms.  These phenomenon could be explained by a dysfunctional ryanodine receptor calcium channel.  This dysfunctional ion channel could promote the excessive calcium release from the sarcoplasmic reticulum, resulting in persistent muscle fiber contraction.  Gates in the cell wall, like tiny airlocks in a space station, allow charged particles such as calcium, potassium and other minerals to flow in and out of the cell membrane and affect the interior metabolism of the cell.  The pathways are called ion channels.  An illness caused by dysfunction of the gate mechanism is called a channellopathy.   This important piece of the puzzle indicates that myofascial pain due to trigger points could be a channellopathy.  Dysfunctional mitochondria and/or second messenger dysfunction metabolically upstream could also be responsible or be associated with the ryanodine dysfunction. [I found this to be one of the most exciting revelations at the Myopain ‘07 Congress, offering great hope to those of us with myofascial pain.  This offers a whole new way of looking at myofascial pain, and perhaps a whole new way of treating it.  I hope researchers will take note and mobilize forces to investigate this. DJS]

Gerwin R. 2004.  Differential diagnosis of trigger points.  J Musculoskeletal Pain 12(3/4):23-28.   “Trigger points pain can have many different causes that must be identified and treated specifically.”

Gerwin, R. D. 1999.  Differential diagnosis of myofascial pain syndrome and fibromyalgia. J Musculoskel Pain 7(1-2):209-215.

Gerwin, R. D.  1999.  Myofascial pain syndromes from trigger points.  Pain 3:153-159. 

Gerwin, R. D.  1998.  Myofascial pain and fibromyalgia: Diagnosis and treatment.  J Back & Musculoskeletal Rehab 11:175-181.

Gerwin, R. D. and D. Duranleau. 1997. Ultrasound identification of the myofascial trigger point. Muscle Nerve 20:767-768. 

Gerwin, R. D.  1997.  Myofascial pain syndromes in the upper extremity.  J Hand Ther 10: 130-136.

Gerwin, R. D., S. Shannon, C. Z. Hong, D. Hubbard and R. Gevirtz.  1997.  Interrater reliability in myofascial trigger point examination.  Pain 69(1-2):65-73. 

Gerwin,  R. D. 1995.  A study of 96 subjects examined both for fibromyalgia and myofascial pain. J Musculoskel Pain 3(Suppl 1):121.(Abstract).  

Gerwin, R. D.  1991.  Myofascial aspects of low back pain.  Neurosurgery Clin North Am2(4):761-782.

Ghanbari A, Rahimijaberi A, Mohamadi M et al. 2012. The effect of trigger point management by positional release therapy on tension type headache. NeuroRehabilitation. 30(4):333-339. Both positional release therapy for trigger points and routine medical therapy were equally effective in treatment of tension type headache. [This could vary tremendously in regards to control of perpetuating factors, the skill of the practitioner, and the type of routine medical therapy, as we live in a world where even the recognition of trigger points is not routine. DJS]

Gharaibeh TM, Jadallah K, Jadayel FA. 2009.  Prevalence of temporomandibular disorders in patients with gastroesophageal reflux disease: a case controlled study.  J Oral Maxillofac Surg. [Dec 1 Epub ahead of print]   [Temporomandibular disorders often coexist with GERD.  It is unfortunate that patients were not checked for co-existing TrPs, as both of these conditions can be associated with TrPs and may be interactive.  It is to be hoped that future research will consider the affect of TrP-riddled chewing muscles on GERD, and the affect of acid fumes on throat and jaw muscle TrPs.   In the world of chronic pain, differential diagnosis must give way to interactive diagnoses, and doctors working in chronic pain must be so trained. DJS] 

Ghazan-Shahi S, Towheed T, Hopman W. 2012. Should rheumatologists retain ownership of fibromyalgia? A survey of Ontario rheumatologists. Clin Rheumatol. [May 2 Epub ahead of print]. "Key findings were: (1) 71 % believe that rheumatologists should not retain ownership of fibromyalgia, (2) 55 % believe that fibromyalgia is primarily a psychosomatic illness as opposed to a physical illness, (3) 89 % believe that the family physician should be the main care provider for these patients, and (4) rheumatologists who consider fibromyalgia to be a physical illness were also significantly more likely to believe that rheumatologists should retain ownership of this disease…and were more likely to continue managing these patients in their practice …. The majority of Ontario rheumatologists do not wish to retain ownership of fibromyalgia. However, most of them continue to manage these patients, even though they believe that the family physician should be the main care provider for patients with fibromyalgia. Rheumatologists may be providing care to these patients primarily because this care is not available to them from their primary care physicians."

Gheita TA, Ezzat Y, Sayed S et al. 2009.  Musculoskeletal manifestations in patients with malignant disease.  Clin Rheumatol. [Nov 8 Epub ahead of print].  “Musculoskeletal manifestations occurring during malignancies and following the treatment represent a significant percentage of symptoms and signs which may raise a clue to differential diagnosis.”

Ghione S, Del Seppia C, Mezzasalma L et al. 2004.  Human head exposure to a 37 Hz electromagnetic field: Effects on blood pressure, somatosensory perception, and related parameters. Bioelectromagnetics 25(3):167-175. Specific electromagnetic field exposure can alter pain sensitivity in human beings.

Giamberardino MA, Affaitati G, Costantini R. 2010. Visceral referred pain. J Musculoskel Pain. 18(4):403-410. "Visceral referred pain occurs in somatic areas neuromerically connected with the affected organs where secondary hyperalgesia takes place mostly in deep body wall tissues, extending to superficial layers in repeated/prolonged visceral processes. When two internal organs sharing part of their central sensory projection are affected, visceral pain and referred hyperalgesia from each organ are significantly enhanced ('viscero-visceral hyperalgesia'). In this case, treatment of one visceral condition significantly improves symptoms from the other. Referred phenomena are mainly sustained by central sensitization processes, involving viscero-somatic or viscero-visceral-somatic convergent neurons, as shown by electrophysiological studies in animal models. A contribution by viscero-somatic reflexes is also present, which would account for the trophic changes of deep body wall tissues that often accompany the hyperalgesia. The expression of visceral referred pain is reduced with the aging process, which renders diagnosis more difficult in the elderly, increasing the risks in life-threatening conditions. Some of the contributing mechanisms may include age-related impaired A-Delta fiber function and a reduction in the content and turnover of neurotransmitter systems involved in nociception..... Visceral referred pain and accompanying phenomena are being increasingly understood as regards their pathophysiology. This opens new avenues for treatment strategies that are more mechanism-based and not purely symptomatic."[As it is important to understand the concepts of viscero-somatic and somato-visceral referred pain, it is also important to understand how visceral pain can lead to central sensitization. As this article demonstrates, even advanced age can lead to referred visceral pain. DJS]

Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 25(2):185-198. "This article reviews the available published knowledge about the diagnosis, pathophysiology and treatment of myofascial pain syndromes from trigger points. Furthermore, epidemiologic data and clinical characteristics of these syndromes are described, including a detailed account of sensory changes that occur at both painful and nonpainful sites and their utility for diagnosis and differential diagnosis; the identification/diagnostic criteria available so far are critically reviewed. The key role played by myofascial trigger points as activating factors of pain symptoms in other algogenic conditions - headache, fibromyalgia and visceral disease - is also addressed. Current hypotheses on the pathophysiology of myofascial pain syndromes are presented, including mechanisms of formation and persistence of primary and secondary trigger points as well as mechanisms beyond referred pain and hyperalgesia from trigger points. Conventional and most recent therapeutic options for these syndromes are described, and their validity is discussed on the basis of results from clinical controlled studies."

Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Effects of Treatment of Myofascial Trigger Points on the Pain of Fibromyalgia. Curr Pain Headache Rep. [May 5 Epub ahead of print]. "FMS is mainly rooted in the central nervous system, while TrPs have a peripheral origin. However, the nociceptive impulses from TrPs may have significant impact on symptoms of FMS, probably by enhancing the level of central sensitization typical of this condition. Several attempts have been made to assess the effects of treatment of co-occurring TrPs in FMS. We report the outcomes of these studies showing that local extinction of TrPs in patients with fibromyalgia produces significant relief of FMS pain. Though further studies are needed, these findings suggest that assessment and treatment of concurrent TrPs in FMS should be systematically performed before any specific fibromyalgia therapy is undertaken."

Giamberardino, M. A., G. Affaitati, S. Iezzi and L. Vecchiet. 1999. Referred muscle pain and hyperalgesia from viscera. J Musculoskel Pain 7(1-2):61-69.

Giamberardino, M. A., K. J. Berkley, S. Iezzi, P. de Bigontina, and L. Vecchiet.  1997. Pain threshold variations in somatic wall tissues as a function of menstrual cycle, segmental site and tissue depth in non-dysmenorrhic women, dysmenorrhic women and men. Pain 71(2):187-97.

Giamberardino MA, Vecchiet J, Affaitati G et al. 2007.  Antioxidative treatment for muscle symptoms in chronic fatigue syndrome.  J Musculoskel Pain 15 (Supp 13):64 item 113.  [Myopain 2007 Poster]  “In CFS, prolonged treatment with Vitamin E produces parallel improvement of oxidative stress and muscle fatigue/hyperalgesia.  The results suggest an important pathophysiologic role for OS in the genesis of muscle symptoms in CFS.”

Gil, I. A., C. M. Barbosa, V. M. Pedro, K. C. Silverio, D. P. Goldfarb, V. Fusco and C. M. Navarro.  1998.  Multidisciplinary approach to chronic pain from myofascial pain dysfunction syndrome: a four-year experience at a Brazilian center.  Cranio 16(1):17-25.

Gill K. A., Woodroofe, M. N. 2002.  Effect of extracellular matrix components on the presentation of chemokines and migration of microglia and astrocytes cell lines.  Glia (Suppl 1):S43 [Abstract]. These researchers “conclude that the effect of chemokines is significantly influenced by the extracellular environment, and the composition of the ECM may be important in the design of therapeutic strategies for inflammatory conditions.”

Gilula MF. 2007.  Cranial electrotherapy stimulation and fibromyalgia.  Expert Rev Med Devices. 4(4):489-495.  “Future medicine for FM and related conditions may increasingly involve multimodality treatment that features CES as one significant part of the therapeutic regimen.  Future medicine may also include CES as an invaluable, cost-effective add-on to many facets of clinical pharmacology and medical therapeutics.”

Giovengo, S. L. , I. J. Russell and A. A. Larson.  1999. Increased concentrations of nerve growth factor (NGF) in cerebrospinal fluid of patients with fibromyalgia. J Rheumatol 26(7):1564-9.

Giske L, Bautz-Holter E, Sandvik L et al. 2009.  Relationship between pain and neuropathic symptoms in chronic musculoskeletal pain.  Pain Med. [Apr 22 Epub ahead of print].  “Our study demonstrates that neuropathic symptoms are prominent features of chronic musculoskeletal pain and are stable over time.  These symptoms were closely related to emotional distress and to the diagnosis of fibromyalgia.  The results lend support to the theory that neuropathic symptoms represent an underlying sensitization.”

Giske L, Vollestad NK, Mengshoel AM et al. 2007.  Attenuated adrenergic responses to exercise in women with fibromyalgia – a controlled study.  Eur J Pain. [Sep 7 Epub ahead of print]  “...the exercise was perceived as being more painful and strenuous in the FM group.  Muscle performance was altered with increased muscle activity during the exercise.  Women with FM showed an attenuated Adr (plasma adrenalin) response to repetitive isometric exercise.”

Gjesdal S, Bratberg E, Maeland JG. 2011. Gender differences in disability after sickness absence with musculoskeletal disorders: five-year prospective study of 37,942 women and 26,307 men. BMC Musculoskel Disord. 12:37. "Having children and working full time decreased the DP risk for both genders, whereas low socioeconomic status increased the risk similarly. There was a different age effect as more women obtained a DP (disability pension) below the age of 50. Increased female risk of chronicity remained for myalgia/fibromyalgia, back disorders and 'other/unspecified' after relevant adjustments, whereas men with neck disorders were at higher risk of chronicity." "When all sociodemographic and diagnostic variables were adjusted for, no gender difference remained, except for some diagnostic subgroups."

Glass JM. 2010. Cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain. 18(4):367-372. "Fibromyalgia syndrome (FMS) is characterized by chronic, widespread, musculoskeletal pain, but symptoms other than pain are common. Dyscognition is a term used to refer to subjective feelings and objective performance measures of cognitive dysfunction. In this paper, the evidence for dyscognition in FMS is reviewed. Dyscognition is a prevalent symptom among patients with FMS that can be very disruptive. Studies using self-report measures support patient reports of dyscognition, demonstrating perceived problems across a number of cognitive domains. Tests using performance-based measures of cognitive function also support patient reports of dyscognition. Furthermore, these tests have thus far revealed a pattern of impairment in working memory and attention/executive control as well as memory impairment. Dyscognition is a real and troubling symptom for many patients with fibromyalgia. However, the body of research on dyscognition in FMS is still quite small. More research is needed to understand the factors that contribute to dyscognition and treatment approaches that help with dyscognition and to understand the cognitive symptoms that are affected, including neuroimaging studies." "Although pain is the defining symptom, it is well known that other symptoms often accompany FMS, including fatigue, somatic complaints, mood disorders, and cognitive dysfunction. Researchers have used the term 'dyscognition' to refer to both self- reported cognitive problems and objective dysfunction seen on performance-based measures of cognition. Patients refer to the subjective experience of cognitive dysfunction as 'fibrofog,' and several studies point to the salience of this particular symptom. Memory and concentration problems are reported by many patients, following pain, stiffness, fatigue, and nonrestorative sleep as the most prevalent symptoms. When dyscognition problems are present, patients report that they are very disruptive." "Glass et al. found that FMS patients reported lower memory capacity, more negative change in memory, and more anxiety about memory performance than healthy age- and education-matched controls. Of interest was the fact that patients also reported more use of strategies to support memory while at the same time reporting lower self-efficacy over memory performance….Specifically, tests that focus on working memory and on executive control of attention, as well as tests of long-term verbal episodic and semantic memory, appear to be most likely to reveal dysfunction. Working memory is the ability to briefly store a small amount of information in mind while performing other mental operations….The evidence to date suggests that the aspect of working memory that is most affected in FMS is the ability to maintain attention or to manage the items in working memory, rather than with the simple storage of items for a brief period. Consistent with this view, FMS patients perform poorly on tests that involve attentional control and the ability to ignore distraction….suggest that FMS patients have a particular difficulty dealing with distraction or managing attention. This ability to manage distraction is part of a domain of cognitive abilities called executive function….In addition to working memory and attention control tests, several studies point to problems with memory function in FMS patients." "Dick et al. found that when pain was included as a covariate in their analyses, differences between FMS patients and controls became nonsignificant. These results suggest that the most important contributor to cognitive dysfunction in FMS is pain, but this is still very much a preliminary conclusion." [This article is a masterful presentation of what we know now about FM cognitive dysfunction. DJS]

Glass JM. 2009. Review of cognitive dysfunction in fibromyalgia: a convergence on working memory and attentional control impairments.  Rheum Dis Clin North Am. 35(2):299-311.  “Clinical and laboratory evidence confirm that dyscognition is a real and troubling symptom in fibromyalgia (FM), and that the cognitive mechanisms most affected in FM are working memory, episodic memory, and semantic memory.  Recent evidence provides further convergence on specific difficulty with attentional control.  Dyscognition in FM…does seem to be related to the level of pain.”  [Cognitive dysfunction is real in FM, and the need for adequate pain control is great. DJS]

Glass JM. 2006.  Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: new trends and future directions.  Curr Rheumatol Rep. 8(6):425-429.  “Fibromyalgia (FM) and chronic fatigue syndrome (CFS) patients often have memory and cognitive complaints.  Objective cognitive testing demonstrates long-term and working memory impairments.  In addition, CFS patients have slow information processing, and FM patients have impaired control of attention, perhaps due to chronic pain.  Neuroimaging studies demonstrate cerebral abnormalities and a pattern of increased neural recruitment during cognitive tasks.  Future work should focus on the specific neurocognitive systems involved in cognitive dysfunction in each syndrome.”

Glass JM, Williams DA, Fernandez-Sanchez ML et al. 2011. Executive Function in Chronic Pain Patients and Healthy Controls: Different Cortical Activation During Response Inhibition in Fibromyalgia. J Pain. [Sep 24 Epub ahead of print]. "Neural activation (fMRI) during response inhibition was measured in fibromyalgia patients and controls. FM patients show lower activation in the inhibition and attention networks and increased activation in other areas. Inhibition and pain perception may use overlapping networks: resources taken up by pain processing may be unavailable for other processes." The brain can be so occupied dealing with pain input that it can't handle other tasks. Multitasking can only go so far, especially if the brain is handling pain from multiple sources.

Gleberzon B, Stuber K. 2013. Frequency of use of diagnostic and manual therapeutic procedures of the spine taught at the Canadian Memorial Chiropractic Collage: preliminary survey of Ontario chiropractors. Part 1—practice characteristics and demographic profiles. J Can Chiropr Assoc 57(1):32-41. This study got a low response rate, but those responding reported highest use for "diversified technique" with specific trigger point therapy in second.

Gleditsch J. 1984.  [Trigger point therapy in functional and inflammatory diseases in the dento-oro-gnathic region]  Zahnarzt 28(11):863-869. [German]

Gleitz M, Hornig K. 2012. [Trigger points - Diagnosis and treatment concepts with special reference to extracorporeal shockwaves]. Orthopade. 41(2):113-125. [German] "The 70-year-old trigger point theory has experienced a growing scientific confirmation and clinical significance as a consequence of recent muscle pain research....The most effective conventional forms of treatment are aimed at a direct mechanical manipulation of the trigger point as are new forms of therapy with focused and radial shockwaves. By using high pressures the focused shockwaves in particular are suitable to provoke local and referred pain and thus simplify the trigger point diagnosis....Overall, the shockwave therapy on muscles represents a confirmation and extension of the existing trigger point therapy. It seems to be suitable for treating functional muscular disorders and myofascial pain syndromes within the locomotor system."

Gloth, F. M. 3^rd.  1996.  Concerns with chronic analgesic therapy in elderly patients.  Am J Med101(1A):19S-24S. 

Gluszek, J., L. Szczesniak, F. Banaszak, A. Tykarski and T. Rychlewski.  1999. [No title available].  Pol Arch Med Wewn 101(3):191-6 [Polish].

Goadsby PJ, Edvinsson L, Ekman R. 1992.  Cutaneous sensory stimulation leading to facial flushing and release of calcitonin gene-related peptide.  Cephalalgia. 12(1):53-56.  [This article may provide clues as to some of the mechanisms of some of the autonomic concomitants of specific TrPs. DJS]

Godfrey, R. G.  1996.  A guide to the understanding and use of tricyclic antidepressants in the overall management of fibromyalgia and other chronic pain syndromes. Arch Intern Med156(10):1047-1052. 

Goebel A. 2010. Immunoglobulin Responsive Chronic Pain. J Clin Immunol. [Apr 28 Epub ahead of print]. “Over the last 15 years, clinical and experimental data have emerged that suggest that peripheral and central, glial-mediated neuroimmune activation is both necessary and sufficient to sustain chronic pain. Immune modulation appears to be, therefore, a possible new therapeutic option.....  IVIG therapy may emerge as a novel treatment modality for refractory cases. However, before this drug can be confidently used by clinicians, important questions need to be answered concerning optimal treatment doses, duration of treatment, and its effect on function and quality of life.” [Other less invasive glial cell modulators such as topical pentoxifylline may be potential sources of calming down glial cells. DJS]

Gogas KR. 2005.  Glutamate-based therapeutic approaches: NR2B receptor antagonists.  Curr Opin Pharmacol Dec 20; [Epub ahead of print]  “...phosphorylation of the NR2B subunit (-containing NMDA receptor) could be responsible for the initiation and maintenance of the central sensitization seen in neuropathic pain states.” 

Gold AR, Dipalo F, Gold MS et al. 2004.  Inspiratory airflow dynamics during sleep in women with fibromyalgia.  Sleep 27(3):459-466.  “Inspiratory airflow limitation is a common inspiratory airflow pattern during sleep in women with fibromyalgia.  Our findings are compatible with the hypothesis that inspiratory flow limitation during sleep plays a role in the development of the functional somatic syndromes.”

Gold, D. R., S. Rogacz, N. Bock, T. D. Tosteson, T. M. Baum, F. E. Speizer and C. A. Czeisler. 1992.  Rotating shift work, sleep, and accidents related to sleepiness in hospital nurses.  Am JPublic Health 82(7):1011-4.  

Goldenberg DL, Burckhardt C, Crofford L. 2004.  Management of fibromyalgia syndrome.  JAMA 292(19):2388-2395.  “A number of commonly used FMS therapies, such as trigger point injections, have not been adequately evaluated.”  [This is a noteworthy quote, in so much as there are no such things as fibromyalgia trigger points and thus no FMS trigger point injections to be evaluated.  Myofascial trigger point injections, however, have been adequately evaluated.  It is fundamental that clinicians and researchers need to understand that there are no fibromyalgia trigger points, and that myofascial pain is not the same as fibromyalgia.  Until this happens, the research will be skewed and the conclusions reached not viable.  DJS]

Goldenberg DL, Burchkardt C, Crofford L. 2004.  JAMA 292(19):2388-2395.  “Despite the chronicity and complexity of FMS, there are pharmacological and nonpharmacological interventions available that have clinical benefit.”  [FMS is treatable,]

Goldenberg, DL. 1999.  Fibromyalgia syndrome a decade later: what have we learned?  Arch Intern Med 159(8):777-85.

Goldberg, G. M., R. D. Kerns and R. Rosenberg. 1993. Pain-relevant support as a buffer from depression among chronic pain patients low in instrumental activity. Clin J Pain 9(1):34-40.  

Goldberg, R. T., W. N. Pachas and D. Keith.  1999.  Relationship between traumatic events in childhood and chronic pain.  Disabil Rehabil 21(1):23-30.  

Goldberg, R. L. , J. P. Huff, M. E. Lenz, P. Glickman, R. Katz and E. J. Thonar.  1991. Elevated plasma levels of hyaluronate in patients with osteoarthritis and rheumatoid arthritis. Arthritis Rheum 34(7):799-807.

Goldstein, L. B., F. C. Last and V. M. Salerno.  1997.  Prevalence of hyperactive digastric muscles during swallowing as measured by electromyography in patients with myofascial pain dysfunction syndrome.  Funct Orthod 14(3):18-22.

Golinski, M. A. and D. M. Fill.  1995.  Preemptive analgesia.  CNRA 6(1):16-20.  

Gonzalez B, Baptista TM, Branco JC et al. 2013. Fibromyalgia: antecedent life events, disability, and causal attribution. Psychol Health Med. [Jan 17 Epub ahead of print]. "This study aimed to evaluate the relation of disability and physical and mental health status with potentially traumatic life events (PTLE) before the onset of fibromyalgia in women diagnosed with this syndrome. We also investigated causal attribution of fibromyalgia to a triggering event, physical or psychological in nature, and its relation with the health measures and the adverse life events….There were no statistically significant relations between the health measures (disability, physical and mental health, and pain) and the PTLE. The predominant attribution was to a physical event. There were no significant differences neither in the health measures across causal attribution status….nor in the PTLE not in childhood….There were significant differences across causal attribution status in the PTLE in childhood…., specifically between the group that made a psychological attribution and the group that made no attribution….with the former having a higher score of PTLE in childhood. The results raise questions about the importance of psychological aspects in the appraisal of the adverse events and its possible relation to the psychological functioning in women with fibromyalgia." [Many symptoms now attributed to FM may be due to co-existing conditions. FM is heterogeneous. DJS]

Gonzalez-Iglesias J, Cleland JA, Del Rosario Gutierrez-Vega M et al. 2011. Multimodal management of lateral epicondylalgia in rock climbers: a prospective case series. J Manipulative Physiol Ther. [Oct 20 Epub ahead of print]. [This is very interesting, as myofascial TrPs are often the cause of epicondylagia. The latter term is a description, and not a diagnosis. Since TrP dry needling and cervical spine manipulation were part of the therapies utilized, this has interesting ramifications. DJS]

Gonzalez-Perez LM, Infante-Cossio P, Granados-Nunez M et al. 2012. Treatment of temporomandibular myofascial pain with deep dry needling. Med Oral Patol Oral Cir Bucal. [May 1 Epub ahead of print]. "Although further studies are needed, our findings suggest that deep dry needling in the trigger point in the external pterygoid muscle can be effective in the management of patients with myofascial pain located in that muscle."

Gonzalez-Viejo MA, Avellanet M, Hernandez-Morcuende MI. 2005.  [A comparative study of fibromyalgia treatment: ultrasonography and physiotherapy versus sertraline treatment.]  Ann Readapt Med Phys.  [Epub ahead of print June 22] [French]  “Patients treated with sertraline had a better outcome in terms of pain, morning stiffness and sleep disorders, than the group treated with ultrasonography and physical therapy.”

Gordon, D. A.  1999.  Chronic widespread pain as a medico-legal issue.  Baillieres Best Pract Res Clin Rheumatol 13(3):531-43.  

Gordon, N. P., P. D. Cleary, C. E. Parker and C. A. Czeisler.  1986.  The prevalence and health impact of shiftwork.  Am J Public Health 76(10):1225-8. 

Gotlin, R. S., S. Hershkowitz, P. M. Juris, E. G. Gonzalez, W. N. Scott and J. N. Insall.  1994. Electrical stimulation effect on extensor lag and length of hospital stay after total knee arthroplasty.  Arch Phys Med Rehabil 75(9):957-959.

Goucke CR. 2001.  Australian management strategies for oral opioid use in non-malignant pain. Eur J Pain 5 Suppl A:99-101.

Govender C, Cassimjee N, Schoeman J et al. 2007.  Psychological characteristics of FMS patients.  J Musculoskel Pain 15 (Supp 13):55 item 98.  [Myopain 2007 Poster]  “The majority of subjects exhibited secure attachment and the results questions the existence of a single FMS-prone psychological profile.”

Gowans SE, Dehueck A. 2007.  Pool exercise for individuals with fibromyalgia.  Curr Opin Rheumatol. 19(2):168-173.  “Pool exercise can be an effective intervention for individuals with fibromyalgia.”  [One must be careful of the temperature of the pool and the type of exercise, especially if patients have co-existing myofascial TrPs. DJS]

Gowans SE, DeHueck A. 2004.  Effectiveness of exercise in management of fibromyalgia.  Curr Opin Rheumatol 16(2):138-42.  “Individuals with fibromyalgia also need to be able to access community exercise programs that are appropriate for them.  This may require community instructors to receive instruction on exercise prescription and progression for individuals with fibromyalgia.”  [ It is also vitally important that these individuals receive instruction on the dangers of repetitive exercise for individuals with co-existing CMP. DJS]

Graboski CL, Gray DS, Burnham RS. 2005.  Botulinum toxin A versus bupivacaine trigger point injections for the treatment of myofascial pain syndrome: a randomized double-blind crossover study.  Pain. 118(1-2):170-175.  “There was, however, no significant difference between the BTX A and 0.5% bupivacaine groups in duration or magnitude of pain relief, function, satisfaction or cost of care (cost of injectate excluded).  Considering the high cost of BTX A, bupivacvaine is deemed a more cost-effective injectate for MPS.”  [There are other options.  It would be interesting to study the use of procaine or lidocaine, which have been shown to be as effective as bupivicaine without being as toxic.  DJS]

Gracely RH, Geisser ME, Giesecke T et al. 2004.  Pain catastrophizing and neural responses to pain among persons with fibromyalgia.  Brain 127(Pt 4):835-843. [Epub ahead of print Feb 11]  “Catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain.  Activation associated with catastrophizing in motor areas of the brain may reflect expressive responses to pain that are associated with greater pain catastrophizing.”

Gracely R.H., Petzke F., Wolf J.M. et al. 2002.  Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum 46(5):1333-43.

Graff-Radford, S. B. , J. L. Reeves, R. L. Baker and D. Chiu. 1989. Effects of transcutaneous electrical nerve stimulation on myofascial pain and trigger point sensitivity. Pain 37(1):1-5.

Grafe, A., U. Wollina, B. Tebbe, H. Sprott, C. Uhlemann and G. Hein.  1999.  Fibromyalgia in lupus erythematosus.  Acta Derm Venereol 79(1):62-4.  

Graham, C. and M. R. Cook.  1999.  Human sleep in 60 Hz magnetic fields.  Bioelectro-magnetics 20(5):277-83.

Grant, J. A., L. Danielson, J. P. Rihoux and C. DeVos.  1999.  A double-blind, single-dose, crossover comparison of cetirizine, ebastine, epinastine, fexofenadine, terfenadine, and loratadine versus placebo: suppression of histamine-induced wheal and flare response for 24 h in. Allergy 54(7):700-7.

Grassi, W., R. De Angelis, G. Lapadula, G. Leardini and R. Scarpa.  1998.  Clinical diagnosis found in patients with Raynaud’s phenomenon: a multicenter study.  Rheumatol Int 18(1):17-20.

Grassi, W., P. Core, G. Corlino, F. Salaffi and C. Cervini. 1994. Capillary permeability in fibromyalgia.  J Rheumatol 21(7):1328-1331.

Graven-Nielsen, T., K. S. Aspegren, K. G. Henriksson, M. Bengtsson, J. Sorensen, A. Johnson, B. Gerdle and L. Arendt-Nielsen.  2000.  Ketamine reduces muscle pain, temporal summation, and referred pain in fibromyalgia patients.  Pain 85(3):483-491.

Greenblatt, D. J., J. S. Harmatz, L. L. von Moltke, B. L. Ehrenberg, L. Harrel, K. Corbett, M. Counihan, J. A. Graf, M. Darwish, P. Mertzanis, P. T. Martin, W. H. Cevallos and R. I. Shader.  1998. Comparative kinetics and dynamics of zaleplon, zolpidem, and placebo.  Clin Pharmacol Ther 64(5):553-61.

Greenburg, P.E., Leong, S. A., Birnbaum, H.G. et al. 2003.  The economic burden of depression with painful symptoms.  64 Suppl 7:17-23.  “When painful physical symptoms accompany the already debilitating psychiatric and behavioral symptoms of depression, the economic burden that ensues for patients and their employers increases considerably.  On purely economic grounds, more aggressive outreach may be warranted for patients with depression and comorbid pain to initiate treatment before symptoms are allowed to persist.”

Greenfield, S., M. A. Fitzcharles and J. M . Esdaile. 1992. Reactive fibromyalgia syndrome. Arthritis Rheum 35(6):678-681.

Greenlund, K. J., R. Valdez, M. L. Casper, S. Rith-Najarian and J. B. Croft.  1999.  Prevalence and correlates of the insulin resistance syndrome among Native Americans.  Diabetes Care22:441-447.

Greenman, Philip E.  1996. Principles of Manual Medicine. Baltimore MD: Williams and Wilkins. Griffiths, R. D., C. J. Hinds and R. A. Little.  1999.  Manipulating the metabolic response to injury.  Br Med Bull 55(1):181-95.

Greisen J, Juhl CB, Grofte T et al. 2001.  Acute pain induces insulin resistance in humans.  Anesthesiology. 95(3):573-4  “...pain relief in stress states is important for maintenance of normal glucose metabolism.”  [Chronic pain patients may also be predisposed to insulin resistance.  DJS]

Grichnik, K. P. and F. M. Ferrante.  1991.  The difference between acute and chronic pain.  Mt Sinai J Med 58(3):217-220.  

Grider JS, Harned ME, Sloan PA. 2010. Patient selection and trialing techniques utilizing low-dose intrathecal morphine for chronic nonmalignant pain: a report of two cases. J Opioid Manag. 6(5):371-376. "The administration of opioid analgesics via the intrathecal route is becoming more commonplace for a variety of chronic nonmalignant pathologic pain states. Despite this growing trend, there is very little information available to guide practitioners with regard to patient selection as well as intrathecal drug dosing paradigms. The authors describe the use of a protocol for patient selection, including pretrial preparation, as well as detailed very low-dose chronic intrathecal morphine dosing regimens to treat patients with refractory chronic nonmalignant pain."

Griep, E. N.,  J. W. Boersma, E. G. Lentjes, A. P. Prins, J. K. van der Korst and E. R. de Kloet. 1998. Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and low back pain.  J. Rheumatol 25(7):1374-81.

Griep, E. N., J. W. Boersma, and E. R. de Kloet. 1994. Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome.  J Rheumatol 21(11):2125-2130.

Griep, E. N. , J. W. Boersma, and E. R. de Kloet. 1993. Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromylgia syndrome. J Rheumatol 20(3):469-74.

Griffin, L. D. and S. H. Mellon.  1999.  Selective serotonin reuptake inhibitors directly alteractivity of neurosteroidogenic enzymes.  Proc Natl Acad Sci 96(23):13512-7.

Grigsby, J., N. L. Rosenberg and D. Busenbark. 1995. Chronic pain is associated with deficits in information processing. Percept Mot Skills 81(2):403-410.

Grigsby, J., N. L. Rosenberg and D. Busenbark.  1995.  Chronic pain is associated with deficits in information processing.  Percept Mot Skills 81(2):403-410.

Grip H, Sundelin G, Gerdle B et al. 2007.  Variations in the axis of motion during head repositioning – a comparison of subjects with whiplash-associated disorders or non-specific neck pain and healthy controls.  Clin Biomech [Jul 6 Epub ahead of print].   “Measuring variation in the axis of motion together with target performance gives objective measures on proprioceptive ability that are difficult to quantify by visual inspection.  Repositioning errors were in general small, suggesting it is not sufficient as a single measurement variable in a clinical situation, but should be measured in combination with other tests, such as range of motion.”  [Pain at the end of range of motion indicates the possibility of myofascial trigger points, and as MTrPs often have proprioceptor components, this study would have been better for including them.  DJS]

Grisart J, Masquelier E, Desmedt A et al. 2010. Behavioral and representational components of "hyperactivity" in fibromyalgia syndrome patients. J Musculoskel Pain. 18(3).226-234. This study looked at fibromyalgia patients' life before obvious clinical fibromyalgia occurred, to assess for hyperactivity. They used 24 patients with their significant others, and 24 healthy controls with their significant others. Patients were significantly higher in some types of past hyperactivity and current lessened activity. They did not differ significantly from controls in behavioral hyperactivity before FM except that they had less time resting and sleeping. The study was hampered by the lack of a clear definition of hyperactivity.

Grisart, J., Van der Linden M., Masquelier E. 2002. Controlled processes and automaticity in memory functioning in fibromyalgia patients: relation with emotional distress and hypervigilance. J Clin Exp Neuropsychol 24(8):994-1009.  “...memory functioning in fibromyalgia patients is related to their painful condition as a whole rather than to any particular patient’s characteristics.”

Grisart, J. M. and L. H. Plaghki.  1999.  Impaired selective attention in chronic pain patients.Eur J Pain 3(4):325-333.

Grontved, A., T. Brask, J. Kambskard and E. Hentzer.  1988.  Ginger root against seasickness.A controlled trial on the open sea.  Acta Otolarygol (Stockh) 105(1-2):45-49.

Grosshandler SL, Stratas NE, Toomey TC et al. 1985.  Chronic neck and shoulder pain.  Focusing on myofascial origins.  Postgrad Med. 77(3):149-151.  “Chronic neck and shoulder pain is a complex, multifactorial problem.  Often many months have passed since its onset.  During this time the patient may have seen many physicians and tried many medications, some with abuse potential.  Most patients are depressed and have lost their ability to cope with the stresses of daily life.  The goals of therapy are to enable patients to deal with the problem and to bring them to the point where pain is no longer the dominant factor in their lives.  For patients with chronic neck and shoulder pain of myofascial origin, this is accomplished with a multi-disciplinary approach that incorporates use of psychotherapeutic techniques, nonsteroidal anti-inflammatory medications, antidepressant drugs, trigger-point injection, and several physical therapy modalities.”

Grossman P, Tiefenthaler-Gilmer U, Raysz A et al. 2007.  Mindfulness training as an intervention for fibromyalgia: evidence of postintervention and 3-year follow-up benefits in well-being.  Psychother Psychosom. 76(4):226-233.  “…results indicate mindfulness intervention to be of potential long-term benefit for female fibromyalgia patients.”  

Grotenhermen F. 2005. Cannabinoids. Curr Drug Targets CNS Neurol Disord. 4(5):507-530.  “Cannabinoid receptors are distributed in the central nervous system and many peripheral tissues, including immune system, reproductive and gastrointestinal tracts, sympathetic ganglia, endocrine glands, arteries, lung and heart.”  “The current main focus of clinical research is their efficacy in chronic pain and neurological disorders.”

Gruber, D. M. and J. C. Huber.  1999.  Gender-specific medicine: the new profile of gynecology.Gynecol Endocrinol 13(1):1-6.

Grumbach, M. M. and R. J. Auchus.  1999.  Estrogen: consequences and implications of human mutations in synthesis and action.  C Clin Endocrinol Metab 84(12):4677-94.  

Grundy, S. M.  1999.  Hypertriglyceridemia, insulin resistance, and metabolic syndrome.  Am J Cardiol 83(9B):25F-29F.  

Gunn, C. C. 1996. The Gunn Approach to the Treatment of Chronic Pain. New York, New York: Churchill Livingstone

Gunter, H. H., H. J. Balks, U. Messner, M. Meffert, U. Nitsche, N. F. Rath and F. Degenhardt. 1999. [No title available. German].  Zentralbl Gynakol 121(8):357-66.

Haak T, Scott B. 2007.  The effect of Qigong on fibromyalgia (FMS): a controlled randomized study.  Disabil Rehabil.  [Jun 15 Epub ahead of print]  “…Qigong has positive and reliable effects regarding FMS.”  “…Qigong intervention could be a useful complement to medical treatment for subjects with FMS.”

Haanen, H. C. , H. T. Hoenderdos, L. K. van Romunde, W. C. Hop, C. Mallee, H. P. Terwiel and G. B. Hekster. 1991. Controlled trial of hypnotherapy  in the treatment of refractory fibromyalgia. J Rheumatol 18(1):72-75. 

Hader, N., D. Rimon, A. Kinarty and N. Lahat. 1991. Altered interleukin-2 secretion in patients with primary fibromyalgia syndrome. Arthritis Rheum 34(7):866-71.

Hagglund, K. J., W. E. Deuser, S. P. Buckelew, J. Hewett and D. R. Kay.  1994.  Weather, beliefs about weather, and disease severity among patients with fibromyalgia.  Arthritis Care Res7(3):130-135.

Hainaut, K. and J. Duchateau. 1992. Neuromuscular electrical stimulation and voluntary exercise. Sports Med 14(2):100-113.

Hadjistavropoulos, H. D., F. K. MacLeod and G. J. Asmundson.  1999.  Validation of the Chronic Pain Coping Inventory.  Pain 80(3):471-81.

Hakguder A, Birtane M, Gurcan S et al. 2003.  Efficacy of low level laser therapy in myofascial pain syndrome: An Algometric and thermographic evaluation.  Lasers Surg Med 33(5):339-343.  “LLLT seemed to be beneficial for pain in MPS...” documented by algometry and thermography.

Hakonarson H, Thornorsson A. 2001.  [Common causes of sleep disturbances in Icelandic children who undergo sleep studies.]  Laeknabladid 87(10):799-804.  [Icelandic]  “…both OSA and GER are common problems in children with sleep disturbances.  We conclude that sleep studies are important in the overall workup of children with sleep disturbances….”

Hall AM, Maher CG, Lam P et al. 2011. Tai chi exercise for treatment of pain and disability in people with persistent low back pain: A randomized controlled trial. Arthritis Care Res (Hoboken). 63(11):1576-1583. "Tai chi exercise reduced bothersomeness of back symptoms by 1.7 points on a 0-10 scale, reduced pain intensity by 1.3 points on a 0-10 scale, and improved self-report disability by 2.6 points on the 0-24 Roland-Morris Disability Questionnaire scale. The follow-up rate was >90% for all outcomes. These results were considered a worthwhile treatment effect by researchers and participants."

Hall, S.  1999.  Common pain scenarios.  Aust Fam Physician 28(1):31-5.

Hallberg, L. R. and S. G. Carlsson.  1998.  Anxiety and coping in patients with chronic work-related muscular pain and patients with fibromyalgia.  Eur J Pain 2(4):309-319.

Hamada H, Moriwaki K, Shiroyama K et al. 2000. Myofascial pain in patients with postthoracotomy pain syndrome.  Reg Anesth Pain Med. 25(3):302-305.  “Postthoracotomy pain may result, at least in part, from a nonneuropathic origin (myofascial pain).  It is recommended that each patient be examined in detail to determine whether there is a trigger point in a taut muscular band within the scapular region.  If found, this point is suggested as a good area for anesthetic injection.”

Hameed H, Hameed M, Christo PJ. 2010. The effect of morphine on glial cells as a potential therapeutic target for pharmacological development of analgesic drugs. Curr Pain Headache Rep.14(2):96-104. “Opioids have played a critical role in achieving pain relief in both modern and ancient medicine. Yet, their clinical use can be limited secondary to unwanted side effects such as tolerance, dependence, reward, and behavioral changes. Identification of glial-mediated mechanisms inducing opioid side effects include cytokine receptors, kappa-opioid receptors, N-methyl-D-aspartate receptors, and the recently elucidated Toll-like receptors. Newer agents targeting these receptors such as AV411, MK-801, AV333, and SLC022, and older agents used outside the United States or for other disease conditions, such as minocycline, pentoxifylline, and UV50488H, all show varied but promising profiles for providing significant relief from opioid side effects, while simultaneously potentiating opioid analgesia.”

Hameroff SR, Crago BR, Blitt CD et al. 1981.  Comparison of bupivacaine, etidocaine, and saline for trigger-point therapy.  Anesth Analg. 60(10):752-755.  “Injections of local anesthetics, saline, ‘dry needling’, or other stimuli at specific, tender loci (trigger or acupuncture points) are reportedly efficacious in treatment of chronic pain syndromes.”  “Trigger-point injections with bupivacaine and etidocaine were generally preferred over saline in several pain-tested categories.”  [There are other options.  It would be interesting to study the use of procaine or lidocaine, which have been shown to be as effective as bupivicaine without being as toxic.  DJS]

Hameroff, S. R., J. L. Weiss, J. C. Lerman, R. C. Cork, K. S. Watts, B. R. Crago, C. P. Neuman,J. R. Womble and T. P. Davis.  1984.  Doxepin’s effects on chronic pain and depression: acontrolled study.  J Clin Psychiatry 45(3 Pt2):47-53. 

Hamnes B, Hauge MI, Kjeken I et al. 2011. 'I have come here to learn how to cope with my illness, not to be cured': A Qualitative Study of Patient Expectations Prior to a One-Week Self-Management Program. Musculoskeletal Care. [Jul 20 Epub ahead of print]. "Self-management programs (SMPs) have been developed to help patients with chronic rheumatic diseases to manage their health problems. Patients' expectations prior to treatment are important determinants of outcomes, and should therefore be identified, to ensure that interventions meet the participants' needs. The aim of the present study was to determine participant expectations with respect to a one-week inpatient SMP for those with fibromyalgia (FM) and rheumatoid arthritis (RA).....The findings show that the participants expected the SMP to be a turning point towards a better future and to empower them to assume more responsibility for their own health and self-care. They also expected the SMP to facilitate acceptance, help them to gain new knowledge and be a forum in which to share their experience. Participants who were employed assumed that participation in the SMP would help to ensure that they would continue in their jobs.....This qualitative study indicated that identifying expectations prior to an SMP provides important information which has implications for the program's implementation. Additional themes, such as acceptance of the illness and management of work, should also be included in the programs and they should focus more on sharing experience."

Han L, Ma C, Liu Q et al. 2013. A subpopulation of nociceptors specifically linked to itch. Nat Neurosci 16(2):174-182. This team has found a new itch-specific type of neuron in mice. This is a big first step in developing itch-specific therapies that will stop itching that anti-histamines don't help.

Han HS, Suk K. 2005.  The function and integrity of the neurovascular unit rests upon the integration of the vascular and inflammatory cell systems.  Curr Neurovasc Res. 2(5):409-423.  “In an effort to understand the pathogenesis and find rational treatments against inflammatory disorders in brain, studies have been separately carried out using either endothelial cells or microglia.  Increased evidence, however, indicates that a crosstalk between these two cell types is important for the brain inflammation.” 

Han SC, Harrison P. 1997.  Myofascial pain syndrome and trigger-point management.  Reg Anesth 22(1):89-101.  “A multidisciplinary approach to treatment appears to be most beneficial and may include such modalities as trigger-point injections, dry needling, stretch and spray, and transcutaneous electrical nerve stimulation.”

Han, S. C. and P. Harrison.  1997.  Myofascial pain syndrome and trigger-point management.Reg Anesth 22(1):89-101.  

Han, Y., J. Wang, D. A. Fischman, H. F. Biller and I. Sanders.  1999.  Slow tonic muscle fibers in the thyroarytenoid muscles of human vocal folds; a possible specialization for speech. Anat Rec 256(2):146-57. 

Hanani M., T. Huang, P. Cherkas et al. 2002. Glial cell plasticity in sensory ganglia induced by nerve damage. Neuroscience 114(2):279. Changes in glial cells may contribute to neuropathic pain.

Handa, R., P. Aggarwal,  J. P. Wali, N. Wig and S. N. Dwivedi. 1998.  Fibromyalgia in Indian patients with SLE.  Lupus 7(7):475-8. 

Handwerker, H. O. , C. Forster and C. Kirchhoff. 1991. Discharge patterns of human C-fibers into used by itching and burning stimuli.  J Neurophysiol 66(1):307-15.

Hanna, J. L.  1995.  The power of dance: health and healing.  J Altern Complement Med 1(4): 323-31.

Hannonen, P., K. Malminiemi, U. Yli-Kerttula, R. Isomeri and P. Roponen.  1998. A randomized, double-blind, placebo-controlled study of moclobemide and amitriptyline in the treatment of fibromyalgia in females without psychiatric disorder.  Br J Rheumatol 37(12):1279-86.

Hansson E, Svensson H, Brorson H. 2012. Review of Dercum's disease and proposal of diagnostic criteria, diagnostic methods, classification and management. Orphanet J Rare Dis. 7(1):23. "We propose the minimal definition of Dercum's disease to be generalized overweight or obesity in combination with painful adipose tissue. The associated symptoms in Dercum's disease include obesity, fatty deposits, easy bruisability, sleep disturbances, impaired memory, depression, difficulty concentrating, anxiety, rapid heartbeat, shortness of breath, diabetes, bloating, constipation, fatigue, weakness and joint and muscle aches….The prevalence of Dercum's disease has not yet been exactly established. Aetiology: Proposed, but unconfirmed aetiologies include: nervous system dysfunction, mechanical pressure on nerves, adipose tissue dysfunction and trauma. Diagnosis and diagnostic methods: Diagnosis is based on clinical criteria and should be made by systematic physical examination and thorough exclusion of differential diagnoses. Advisably, the diagnosis should be made by a physician with a broad experience of patients with painful conditions and knowledge of family medicine, internal medicine or pain management. The diagnosis should only be made when the differential diagnoses have been excluded ….Differential diagnoses include: fibromyalgia, lipoedema, panniculitis, endocrine disorders, primary psychiatric disorders, multiple symmetric lipomatosis, familial multiple lipomatosis, and adipose tissue tumors….The following treatments have lead to some pain reduction in patients with Dercum's disease: Liposuction, analgesics, lidocaine, methotrexate and infliximab, interferon -2b, corticosteroids, calcium-channel modulators and rapid cycling hypobaric pressure. As none of the treatments have led to long lasting complete pain reduction and revolutionary results, we propose that Dercum's disease should be treated in multidisciplinary teams specialized in chronic pain. Prognosis: The pain in Dercum's disease seems to be relatively constant over time." [Dercum's may be mistaken for either FM or CMP, coexisting with insulin resistance. DJS]

Hanten WP, Olson SL, Butts NL et al. 2000.  Effectiveness of a home program of ischemic pressure followed by sustained stretch for treatment of myofascial trigger points.  Phys Ther. 80(10):997-1003.  “Myofascial trigger points (TPs) are found among patients who have neck and upper back pain.”  “A home program, consisting of ischemic pressure and sustained stretching, was shown to be effective in reducing TP sensitivity and pain intensity in individuals with neck and upper back pain.  The results of this study indicate that clinicians can treat myofascial TPs through monitoring of a home program of ischemic pressure and stretching.”  [This may provide some temporary relief, but no treatment of TrPs will be complete without identification and control of perpetuating factors. DJS]

Hao J, Ruel J, Coste B et al. 2013. Piezo-electrically driven mechanical stimulation of sensory neurons. Methods Mol Biol. 998:159-170. "Mechanotransduction, the conversion of a mechanical stimulus into a biological response, constitutes the basis of a variety of physiological functions such as the senses of touch, balance, proprioception, blood pressure, and hearing. In vertebrates, mechanosensation is mediated by mechanosensory neurons, whose cell bodies are located in trigeminal and dorsal root ganglia. Here, we describe an in vitro model of mechanotransduction that provides an opportunity to explore the properties of mechanosensitive channels in mammalian sensory neurons. The mechano-clamp method allows applying local force on plasma membrane of whole-cell patch-clamped sensory neurons. This technique uses a mechanical probe driven by a computer-assisted piezoelectric microstage to repeatedly stimulate sensory neurons with accurate control of stimulus strength, duration, and speed." [Considering the piezoelectrical properties of myofascia, this might prove interesting. DJS]

Hapidou, E. G.  and G. B. Rollman. 1998. Menstrual cycle modulation of tender points.  Pain 77(2):151-61

Harden RN, Revivo G, Song S et al. 2007.  A critical analysis of the tender points in fibromyalgia.  Pain Med. 8(2):147-156.  “There was a significant difference in the ‘algometric total score’ between patients with fibromyalgia and controls….”  “The points specified by the ACR were only modestly superior to sham points in making the diagnosis.”  [We clearly need a better definition of FM.  One is under development now. DJS]

Harden RN, Bruehl SP, Gass S, Niemiec C, Barbick B 2000. Signs and symptoms of the myofascial pain syndrome: a national survey of pain management providers.Clin J Pain 16(1):64-72. 

Harding, S. M. 1998. Sleep in fibromyalgia patients: subjective and objective findings. Am J Med Sci 315(6):367-376.

Hargrove JB, Bennett RM, Clauw DJ. 2012. Long-Term Outcomes in Fibromyalgia Patients Treated with Noninvasive Cortical Electrostimulation. Arch Phys Med Rehabil. [Apr 20 Epub ahead of print]. "Sixty-nine originally studied subjects were eligible, 39 of which were mailed surveys. There was a 64% survey return rate. The total FIQ score was 52.6 at baseline, 35.7 at end-of-study and 31.8 at follow-up….Subjects reported symptom improvements lasting at least two-years, with a reduction or elimination of medicine use and need to see physicians for FM….A high percentage of FM patients treated with RINCE (Reduced Impedance Noninvasive Cortical Electrostimulation) continued to experience worthwhile improvement at follow-up."

Hargrove JB, Bennett RM, Simons DG et al. 2012. A randomized placebo-controlled study of noninvasive cortical electrostimulation in the treatment of fibromyalgia patients. Pain Med. 13(1):115-124. " Noninvasive cortical electrostimulation in FM patients provided modest improvements in pain, TeP (tender points) measures, fatigue, and sleep; and the treatment was well tolerated. This form of therapy could potentially provide worthwhile adjunctive symptom relief for FM patients."

Hargrove JB, Bennett RM, Simons DG et al. 2010. Quantitative electroencephalographic abnormalities in fibromyalgia patients. Clin EEG Neurosci. 41(3):132-139. "There is increasing acceptance that pain in fibromyalgia (FM) is a result of dysfunctional sensory processing in the spinal cord and brain, and a number of recent imaging studies have demonstrated abnormal central mechanisms. The objective of this report is to statistically compare quantitative electroencephalogram (qEEG) measures in 85 FM patients with age and gender matched controls in a normative database....A consistent and significant negative correlation was found between pain severity and the magnitude of the EEG abnormalities. No relationship between EEG findings and medicine use was found. It is concluded that qEEG analysis reveals significant differences between FM patients compared to age and gender matched healthy controls in a normative database, and has the potential to be a clinically useful tool for assessing brain function in FM patients."

Harlow, B. L., L. B. Signorello, J. E. Hall, C. Dailey and A. L. Komaroff. 1998.  Reproductive correlates of chronic fatigue syndrome.  Am J Med 105(3A):94S-99S. 

Harrington MG, Chekmenev EY, Schepkin V et al. 2011. Sodium MRI in a rat migraine model and a NEURON simulation study support a role for sodium in migraine. Cephalalgia. [Aug 4 Epub ahead of print]. During a migraine-like state in rats, "...sodium rises to levels that increase neuronal excitability. We propose that rising sodium in CSF (cerebrospinal fluid) surrounding trigeminal nociceptors increases their excitability and causes pain and that rising sodium in vitreous humor increases retinal neuronal excitability and causes photosensitivity."

Harris, A. J.  1999.  Cortical origin of pathological pain.  Lancet 354(9188):1464-6.

Harris RE. 2010. Elevated excitatory neurotransmitter levels in the fibromyalgia brain. Arthritis Res Ther. 12(5):141. "Consistent brain imaging findings demonstrate that neurobiological factors may contribute to the pathology of 'central' pain states such as fibromyalgia (FM). Studies using proton magnetic resonance spectroscopy suggest that glutamate (Glu), a key excitatory neurotransmitter, may be present in higher concentrations within the brains of FM patients. This neurotransmitter imbalance is present in multiple brain regions that have been implicated in processing pain information. However, it is unknown if elevated Glu is acting at the synapse. New investigations are needed to investigate the molecular action of Glu in FM and to investigate these findings during treatment that modulates glutamatergic neurotransmission."

Harrison, D. E., R. Cailliet, D. D. Harrison, S. J. Troyanovich and S. O. Harrison.  1999. A review of biomechanics of the central nervous system–Part I: spinal canal deformations resulting from changes in posture.  J Manipulative Physiol Ther 22(4):227-34.

Hart, P., S. Townley, M. Grimbaldston et al. 2002. Mast cells, neuropeptides, histamine, and prostagladins in UV-induced systemic immunosuppression. Methods 28(1):79.  This article points out the direct correlation between dermal mast cell prevalence and susceptibility to UVB-induced systemic immunosuppression in mice. [Above normal counts of mast cells have been found in fibromyalgia patients.] The authors propose histamine and prostaglandin E2 are important in downstream immunosuppression.

Harty J, Soffe K, O'Toole G et al. 2005.  The role of hamstring tightness in plantar fasciitis.  Foot Ankle Int. 26(12):1089-1092.  [Hamstring tightness, such as that due to myofascial TrPs, could be a major unrecognized factor contributing to plantar fasciitis. DJS]

Harvey, A. G. and R. A. Bryant.  1999.  Predictors of acute stress following motor vehicle accidents.  J Trauma Stress 12(3):519-25.

Hashkes PJ, Friedland O, Jaber L et al. 2004.  Decreased pain threshold in children with growing pains.  J Rheumatol 31(3):610-613.  Growing pain may be indicative of developing fibromyalgia tender points, according to this research, but they did not check for co-existing myofascial TrPs.  Growing pains are often due to TrPs.  Research that takes them into account would be more valuable, because we can't know if the link between the tender points and the growing pains is coincidental.

Hassett AL, Epel E, Clauw DJ et al. 2012. Pain is associated with short leukocyte telomere length in women with fibromyalgia. J Pain. 13(10):959-969. "Telomere length, considered a measure of biological aging, is linked to morbidity and mortality. Psychosocial factors associated with shortened telomeres are also common in chronic pain; yet, little is known about telomere length in pain populations. Leukocyte telomere length was evaluated in 66 women with fibromyalgia and 22 healthy female controls....Our findings support a link between premature cellular aging and chronic pain. These preliminary data imply that chronic pain is a more serious condition than has typically been recognized in terms of bodily aging."

Hassett AL, Radvanski DC, Vaschillo EG et al. 2007.  A pilot study of the efficacy of heart rate variability (HRV) biofeedback in patients with fibromyalgia.  Appl Psychophysiol Biofeedback. [Jan 12 Epub ahead of print]  “These data suggest that HRV biofeedback may be a useful treatment for FM, perhaps mediated by autonomic changes.  While HRV effects were immediate, blood pressure, baroreflex, and therapeutic effects were delayed.  This is consistent with data on the relationship among stress, HPA axis activity, and brain function.”

Hauser W. 2005.  [Fibromyalgia in the legal procedures of the German Sozialgericht – psychosocial risk factors and predictors of health care utilization]  Psychother Psychosom Med Psychol. 55(2):72-78 [German]  “Former and current psychiatric disorders, biographic adverse experiences, duration of generalized pain, sex and social class had no substantial predictive value on the extensive health care utilization (number of doctors, pain-related hospital and rehabilitation stays and pain-related operations).”  [This is important, as other studies have indicated that some chronic conditions, such as fibromyalgia, can impact health care utilization. DJS]

Hauser W, Bohn D, Kuhn-Becker H et al. 2012. Is the association of self-reported childhood maltreatments and adult fibromyalgia syndrome attributable to depression? A case control study. Clin Exp Rheumatol. [Nov 6 Epub ahead of print]. Systematic reviews of case-control studies demonstrated an association between self-reported childhood sexual and physical abuse and fibromyalgia syndrome (FMS). We tested in a case-control study if the association of self-reported childhood maltreatments in childhood and in adult FMS-patients is attributable to depression....Reports of FMS-patients some on childhood maltreatments were biased by depressed mood. However, the difference in self-reported childhood sexual abuse between adult FMS-patients and population controls was not attributable to depression.

Hauser W, Kuhn-Becker H, von Wilmoswky H et al. 2011. Demographic and clinical features of patients with fibromyalgia syndrome of different settings: a gender comparison. Gend Med. 8(2):116-125. "A total of 1023 patients (885 female, 138 male) were included in the analysis..... We found no relevant gender differences in the clinical picture of FMS. The assumption of well-established gender differences in the clinical picture of FMS could not be supported."

Hauser W, Petzke F, Sommer C. 2010. Systematic review with met analysis: comparative efficacy and harms of duloxetine, milnacipran, and pregabalin in fibromyalgia syndrome. J Pain. [Apr 23 Epub ahead of print]. “Duloxetine (DLX), milnacipran (MLN), and pregabalin (PGB) are the only drugs licensed by the US Food and Drug Administration (FDA) for fibromyalgia syndrome (FMS). Evidence on the comparative benefits and harms is still accruing. .... Outcomes of interest were symptom reduction (pain, fatigue, sleep disturbance, depressed mood, reduced health-related quality of life), and adverse events. 17 studies with 7,739 patients met the inclusion criteria. The 3 drugs were superior to placebo except DLX for fatigue, MLN for sleep disturbance, and PGB for depressed mood. Adjusted indirect comparisons indicated no significant differences for 30% pain relief and dropout rates due to adverse events between the 3 drugs. Significant differences in average symptom reduction were found: DLX and PGB were superior to MLN in reduction of pain and sleep disturbances. DLX was superior to MLN and PGB in reducing depressed mood. MLN and PGB were superior to DLX in reducing fatigue. The risk of headache and nausea with DLX and MLN was higher compared with PGB. The risk of diarrhea was higher with DLX compared to MLN and PGB. There is evidence for the short-term (up to 6 months) efficacy of DLX, MLN, and PGB. Differences with regard to the occurrence of the key symptoms of FMS and to drug-specific adverse events may be relevant for the choice of medication. PERSPECTIVE: This article presents comparative data on the efficacy and harms of duloxetine, milnacipran, and pregabalin in fibromyalgia syndrome. The results can help clinicians in choosing medication since the 3 drugs have different effects on the key symptoms of fibromyalgia syndrome and differences in side effects, contraindications, and warnings.”

Hauser W, Petzke F, Uceyler N et al. 2010. Comparative efficacy and acceptability of amitriptyline, duloxetine and milnacipran in fibromyalgia syndrome: a systematic review with meta-analysis. Rheumatology (Oxford). [Nov 14 Epub ahead of print]. In adjusted indirect comparisons, AMT was superior to DLX and MLN in reduction of pain, sleep disturbances, fatigue and limitations of HRQOL. DLX was superior to MLN in reducing pain, sleep disturbances and limitations of HRQOL. MLN was superior to DLX in reducing fatigue. There were no significant differences in acceptability of the three drugs.....AMT cannot be regarded as the gold standard of FMS therapy with antidepressants because of the (major) methodological limitations of its trials."

Hauser W, Urrutia G, Tort S et al. 2013. Serotonin and noradrenaline reuptake inhibitors (SNRIs) for fibromyalgia syndrome. Cochrane Database Syst Rev. 1:CD010292. "The SNRIs duloxetine and milnacipran provided a small incremental benefit over placebo in reducing pain. The superiority of duloxetine and milnacipran over placebo in reducing fatigue and limitations of QOL (quality of life) was not substantial. Duloxetine and milnacipran were not superior to placebo in reducing sleep problems. The dropout rates due to adverse events were higher for duloxetine and milnacipran than for placebo. The most frequently reported symptoms leading to stopping medication were nausea, dry mouth, constipation, headache, somnolence/dizziness and insomnia. Rare complications of both drugs may include suicidality, liver damage, abnormal bleeding, elevated blood pressure and urinary hesitation."

Hautanen, A., K. Raikkonen and H. Adlercreutz. 1997. Associations between pituitary-adrenocortical function and abdominal obesity, hyperinsulinaemia and dyslipidaemia in normotensive males.  J Intern Med 241(6):451-61.

Havas M. 2006.  Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes and multiple sclerosis.  Electromagn Biol Med. 25(4):259-268.  “Several disorders, including asthma, ADD/ADHD, diabetes, multiple sclerosis, chronic fatigue, and fibromyalgia, are increasing at an alarming rate, as is electromagnetic pollution in the form of dirty electricity, ground current, and radio frequency radiation from wireless devices.  The connection between electromagnetic pollution and these disorders needs to be investigated and the percentage of people sensitive to this form of energy needs to be determined.”  [One might want to add CMP to this list, especially if FMS amplification is part of the picture. DJS]

Hawk, C., C. Long and A. Azad. 1997. Chiropractic care for women with chronic pelvic pain: a prospective single-group intervention study.  J Manip Physiol Ther 20 (2): 73-79.

Hayashi K, Ozaki N, Kawakita K et al. 2011. Involvement of NGF in the rat model of persistent muscle pain associated with taut band. J Pain. 12(10):1059-1068. In rats, the taut band associated with myofascial TrPs can be affected by the administration of nerve growth factor (NGF). Mice that received the NGF receptor (TrkA) inhibitor K252a had significantly decreased hyperalgesia related to taut bands. "...NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS."

Hayes, J. A.  1998.  TAC-TIC therapy: a non-pharmacological stroking intervention for premature infants.  Complement Ther Nurs Midwifery 4(1):25-7.  

Hayes SM, Myhal GC, Thornton JF et al. 2010. Fibromyalgia and the therapeutic relationship: where uncertainty meets attitude. Pain Res Manag. 15(6):385-391. "GPs reported insufficient knowledge and skill in diagnosing fibromyalgia, with not all believing it to be a diagnosable condition…. Twenty-three per cent of GPs and 12% of specialists characterized fibromyalgia patients as malingerers. They further reported a lack of knowledge and skill in treating fibromyalgia…., including the pain, sleep disorders and mood disorders related to the condition…. Specialists shared these challenges, although to a lesser degree ….. Attitudinal issues centered around frustration….and negative profiling of fibromyalgia patients….Findings revealed the presence of GP attitudinal and confidence challenges in caring for fibromyalgia patients. As care of fibromyalgia patients moves to general practices, these fundamental competencies must be addressed to assure that all patients receive the quality of care necessary to manage their disease and to empower physicians to be more professionally effective. As stated by one patient, 'why are we being penalized for having this disability?'" [As the information on central sensitization mounts, it is sad to see so much evidence that so few care providers in the trenches are reading it and understanding what they read. Patients do get penalized for the ignorance of their care providers, and thus the care providers are doing them harm, failing to providing care because they do not understand fibromyalgia (and other central sensitization states), or myofascial trigger points, two of the three most common causes of musculoskeletal pain. DJS]

Haythornthwaite, J. A., L. A. Menefee, L. J. Heinberg and M. R. Clark.  1998.  Pain coping strategies predict perceived control over pain.  Pain 77(1):33-9.

Haythornthwaite, J. A., L. A. Menefee, A. L. Quatrano-Piacentini and M. Pappagallo.  1998. Outcome of chronic opioid therapy for non-cancer pain.  J Pain Symptom Manage 15(3):185-94.

Haythornthwaite, J. A., M. T. Hegel and R. D. Kerns.  1991.  Development of a sleep diary for chronic pain patients.  J Pain Symptom Manage 6(2):65-72.

Haythornthwaite, J. A., W. J. Sieber and R. D. Kerns.  1991.  Depression and the chronic pain experience.  Pain 46(2):177-184. 

Heap, L. C., T. J. Peters and S. Wessely.  1999.  Vitamin B status in patients with chronic fatigue syndrome.  J R Soc Med 92(4):183-5.

Heath KM, Elovic EP. 2006.  Vitamin D deficiency: implications in the rehabilitation setting.  Am J Phys Med Rehabil. 85(11):916-923.  “Vitamin D deficiency should be included in the differential diagnosis in the evaluation of musculoskeletal pain complaints in the rehabilitation setting, and treatment of any identified deficiency should be considered a potentially important component of the treatment regimen.”

Hegarty D, Shorten G. 2012. Multivariate prognostic modeling of persistent pain following lumbar discectomy. Pain Physician. 15(5):421-434. "Persistent postsurgical pain (PPSP) affects between 10% and 50% of surgical patients, the development of which is a complex and poorly understood process. To date, most studies on PPSP have focused on specific surgical procedures where individuals do not suffer from chronic pain before the surgical intervention. Individuals who have a chronic nerve injury are likely to have established peripheral and central sensitization which may increase the risk of developing PPSP. Concurrent analyses of the possible factors contributing to the development of PPSP following lumbar discectomy have not been examined....We demonstrated that the occurrence of PPSP can be predicted using a small set of variables easily obtained at the preoperative visit. This is a prediction rule that could further optimize perioperative pain treatment and reduce attendant complications by allowing the preoperative classification of surgical patients according to their risk of developing PPSP."

Hein G., Franke S. 2002.  Are advanced glycation end-product-modified proteins of pathogenetic importance in fibromyalgia?  Rheumatology (Oxford) 41(10):1163-7.

Heinrich, S.  1991.  The role of physical therapy in craniofacial pain disorders: an adjunct to dental pain management.  Cranio 9(1):71-75.

Helfenstein, M. and D. Feldman.  2000.  The pervasiveness of the illness suffered by workersseeking compensation for disabling arm pain.  J Occup Environ Med 42(2):171-5.  

Heller, U., E. W. Becker, H. P. Zenner and P. A. Berg. 1998. [Incidence and clinical relevance of antibodies to phospholipids, serotonin and ganglioside in patients with sudden deafness and progressive inner ear hearing loss].   HNO 46(6):583-6. [German]

Hellstrom, O. , J. Bullington, G. Karlsson, P. Lindqvist and B. Mattsson. 1999. A phenomenological study of fibromyalgia.  Patient perspectives. Scand J Prim Health Care 17(1):11-6. 

Helme, R. D. , S. Gibson and Z. Khalil. 1990. Neural pathways in chronic pain. Med J Aust 153(7):400-406.

Helme, R. D. , G. O. Littlejohn and C. Weinstein. 1987. Neurogenic flare responses in chronic rheumatic pain syndromes. Clin Exp Neurol 23(1):91-94.  

Hemmeter, U., R. Kocher, D. Ladewig, M. Hatzinger, E. Seifritz, C. J. Lauer and E. Holsboer-Trachsler.  1995. [Sleep disorders in chronic pain and generalized tendomyopathy].  Schweiz Med Wochenschr 125(49):2391-7 [German] 

Henderson, D. J., B. S. Withington, J. A. Wilson and L. M. Morrison.  1999.  Perioperative dextromethorphan reduces postoperative pain after hysterectomy.  Anesth Analg 89(2):399-402.

Hendler, N. 1984. Depression caused by chronic pain. J Clin Psychiatry 45(3 pt 2):30-38.

Henriksson, C. and C.Burckhardt. 1996.  Impact of fibromyalgia on everyday life: a study of women in the  USA and Sweden. Disabil Rehabil 18(5):241-248.  

Henriksson, C., I. Gundmark , A. Bengtsson and A. C. Ek.  1992. Living with fibromyalgia. Consequences for everyday life. Clin J Pain 8(2):138-144.

Henriksson, C. M.1994. Longterm effects of fibromyalgia on everyday life. A study of 56 patients. Scand J Rheumatol 23(1):36-41.

Henriksson KG. 2009.  The fibromyalgia syndrome: translating science into clinical practice.  J Musculoskel Pain. 17(2):189-194.  “The biological part of FMS reflects a long-standing or permanent change in the function of the nociceptive nervous system that can be equated with a disease.  It is hoped that upgrading FMS from illness to disease will increase the awareness of FMS among health personnel.  This will in turn help patients with FMS to get correct diagnosis and treatment.”

Henriksson, K. G. 2001. Is fibromyalgia a central pain state? J Musculoskel Pain 10(1/2):45:57. "There is strong support for the notion that pain and allodynia/hyperalgesia in FMS have an organic cause. The hyperexcitability in the nociceptive nervous system is mainly due to changes in the CNS."  " The permanent changes constitute a disease. There are methods for objectively diagnosing this disease."  "Many causes could initiate and maintain the disease: e.g., long-standing local or regional musculoskeletal pain, changes in stress-regulating systems, hormonal changes, changes in serotonin metabolisms, and genetic factors."  [This includes chronic myofascial pain as a perpetuating factor of FMS.]

Henriksson, K. G. 1999. Muscle activity and chronic muscle pain. J Musculoskel Pain 7(1-2):101-109.

Henriksson, K. G.  1999.  Is fibromyalgia a distinct clinical entity?  Pain mechanisms in fibromyalgia syndrome.  A myologist’s view.  Baillieres Best Pract Res Clin Rheumatol 13(3):455-61. 

Henriksson KG, Sorensen J. 2002.  The promise of N-methyl-D-aspartate receptor antagonists in fibromyalgia.  Rheum Dis Clin North Am. 28(2):343-351.  “The combination of a weak opioid and an NMDA-receptor antagonist with few side effects is presently a promise for treatment of pain in a subgroup of patients with FM.”

Henriksson K. G., Sorensen J. 2002.  The promise of N-methyl-D-aspartate receptor antagonists in fibromyalgia. Rheum Dis Clin North Am 28(2):343-51. "The combination of a weak opioid and an NMDA-receptor antagonist with few side effects is presently a promise for treatment of pain in a subgroup of patients with FM."

Henriksson M, Henriksson J, Bergenius J. 2011. Gait initiation characteristics in elderly patients with unilateral vestibular impairment. Gait Posture. [Mar 28 Epub ahead of print]. "....chronically impaired vestibular function leads to a different strategy to create forward momentum to the body. In addition, there is evidence that vestibular patients have diminished postural stability, or alternatively a more cautious behavior, when initiating the second step."

Henriques DY, Cressman EK. 2012. Visuomotor adaptation and proprioceptive recalibration. J Mot Behav. 44(6):435-444. "Motor learning, in particular motor adaptation, is driven by information from multiple senses. For example, when arm control is faulty, vision, touch, and proprioception can all report on the arm's movements and help guide the adjustments necessary for correcting motor error. In recent years we have learned a lot about how the brain integrates information from multiple senses for the purpose of perception. However, less is known about how multisensory data guide motor learning. Most models of, and studies on, motor learning focus almost exclusively on the ensuing changes in motor performance without exploring the implications on sensory plasticity. Nor do they consider how discrepancies in sensory information (e.g., vision and proprioception) related to hand position may affect motor learning. Here, we discuss research from our lab and others that shows how motor learning paradigms affect proprioceptive estimates of hand position, and how even the mere discrepancy between visual and proprioceptive feedback can affect learning and plasticity. Our results suggest that sensorimotor learning mechanisms do not exclusively rely on motor plasticity and motor memory, and that sensory plasticity, in particular proprioceptive recalibration, plays a unique and important role in motor learning." [This is of importance, since most trigger points, and probably fibromyalgia, have proprioceptive components. DJS]

Henry R, Cahill CM, Wood g et al. 2012. Myofascial pain in patients waitlisted for total knee arthroplasty. Pain Res Manag 17(5):321-327. "Knee pain is one of the major sources of pain and disability in developed countries, particularly in aging populations, and is the primary indication for total knee arthroplasty (TKA) in patients with osteoarthritis (OA)....Following ethics approval, 25 participants were recruited from the wait list for elective unilateral primary TKA at the study centre. After providing informed consent, all participants were examined for the presence of active trigger points in the muscles surrounding the knee and received trigger point injections of bupivacaine. Assessments and trigger point injections were implemented on the first visit and at subsequent visits on weeks 1, 2, 4 and 8 ...Myofascial trigger points were identified in all participants. Trigger point injections significantly reduced pain intensity and pain interference, and improved mobility...All patients had trigger points in the vastus and gastrocnemius muscles, and 92% of patients experienced significant pain relief with trigger point injections at the first visit, indicating that a significant proportion of the OA knee pain was myofascial in origin. Further investigation is warranted to determine the prevalence of myofascial pain and whether treatment delays or prevents TKA."

Herald, J. and M.Pecenka. 1991.  Pain doctors: the real world of a pain practice.  An interview with Lawrence A. Funt. Dental Management March, 26-29.  

Heredia-Jimenez JM, Soto-Hermoso VM. 2013. Kinematics gait disorder in men with fibromyalgia. Rheumatol Int. [Jan 5 Epub ahead of print]. "We studied 12 male with fibromyalgia and 14 healthy men. Each participant of the study walked five trials along a 18.6-m walkway. Fibromyalgia patients completed a Spanish version of Fibromyalgia Impact Questionnaire. Significant differences between fibromyalgia and control groups were found in velocity, stride length, and cadence. Gait parameters of men affected by fibromyalgia were impaired when compared to those of healthy group due to bradykinesia. According to previous studies to assess gait variables in female patients, the male with fibromyalgia also showed lower values of velocity, cadence, and stride length than healthy group but not reported significant differences in swing, stance, single, or double support phase." [It would be interesting to check these men for co-existing TrPs, as TrPs usually co-exist with FM and some TrPs influence gait profoundly. DJS]

Hetrick DC, Ciol MA, Rothman I et al. 2003.  Musculoskeletal dysfunction in men with chronic pelvic pain syndrome type III: a case-control study.  J Urol. 170(3):828-831.  “Men with CPPS have more abnormal pelvic floor muscular findings compared with a group of men without pain.  Abnormalities of the pelvic muscles may contribute to this pain syndrome.”

Heyes, M. P., K. Saito and S. P. Markey. 1992. Human macrophages convert L-tryptophan into the neurotoxin quinolinic acid. Biochem J 283(Pt. 3):633-635.

Hickey C, Thomas B. 2011. Delirium secondary to pregabalin. Gen Hosp Psychiatry. [Dec 14 Epub ahead of print]. "Fibromyalgia is a common and disabling disease, and treatment can be challenging. More recently, pregabalin has been approved to treat pain associated with fibromyalgia. ...Several case reports have documented delirium secondary to pregabalin, usually in older patients with multiple medical comorbidities and concurrent medications. We describe a case of delirium in a young patient without significant medical problems and in the absence of other potentially causal medications. In this case, pregabalin appears to be the single causal etiology for delirium. We recommend clinicians to consider the causal role it may play in any patient who presents with delirium."

Hicks GE, Morone N, Weiner DK. 2009. Degenerative lumbar disc and facet disease in older adults: prevalence and clinical correlates. Spine. 34(12):1301-1306. "Results demonstrated that the presence of degenerative disc and facet pathology in older adults is ubiquitous, regardless of clinical status, with greater than 90% demonstrating some level of degeneration. Higher radiographic severity scores were associated with the presence of CLBP. In fact, presence of severe disc pathology was associated with 2-fold greater odds of having CLBP. But, radiographic severity of disc and facet disease was not associated with pain severity among those with CLBP." "From a research perspective, radiographic evaluation of spinal pathology provides additional information about older adults with CLBP compared to pain-free individuals, but its clinical utility for diagnostic purposes is still in question." [Spine generated pain no longer means surgery. It has been noted in many other research articles that pain in the elderly is undertreated. If facet or interlaminary injection can provide relief to some of these patients, more of their brain would be freed from pain processing. Aside from the humanitarian reasons, which are considerable, the economic considerations are huge. Some patients might regain a significant increase of mental and physical function. Some might be able to stay in their own homes longer, and some might be considerably less disabled. Insurance companies and lawyers, as well as doctors, take note. DJS]

Hicks. R. A., D. DeHaro, G. Inman and G. J. Hicks. 1999. Consistency of hand use and sleep problems. Percept Mot Skills 89(1):49-56.

Hill Jr., C. S.  1996.  Government regulatory influences on opioid prescribing and their impact on the treatment of pain of nonmalignant origin.  J Pain Symptom Manage 11(5):287-298.

Hill Jr., C. S.  1995. When will adequate pain treatment be the norm?  JAMA 274 (23):1881-2. 

Hill, C. S. Jr. 1992 The intractable pain treatment act of Texas. Tex Med 88(2):70-72.

Hitchcock, L. S., B. R. Ferrell and M. McCaffery. 1994 The experience of chronic non-malignant pain J Pain Sympt Manage 9(5):312-318.

Ho KY, Tan KH. 2006.  Botulinum toxin A for myofascial trigger point injection: a qualitative systematic review.  [Oct 26 Epub ahead of print] Eur J Pain.  This database study concluded that evidence does not support the use of BTA injections for TrPs.  [Many variables could have influenced this conclusion.  TrP injections must be used wisely.  BTA injections are experimental, should be restricted to those patients who temporarily respond to TrP injections with local anesthetics.  Perpetuating factors must still be brought under control.  The clinician performing the injections must scrupulously practice sound technique, including palpation for TrPs, proper positioning of the patient and slow range of motion stretches as part of the procedure.  Clinicians who give trigger point injections must be trained and experienced.  Looking at photos of possible TrP sites and giving the injections as if they were flu shots is not appropriate and can significantly skew a paper study such as this. DJS]

Ho, M. and J. J. Belch.  1998.  Raynaud’s phenomenon: state of the art in 1998.  Scand JRheumatol 27(5):319-22.  

Hobson, J. A., R. Stickgold and E. F. Pace-Schott.  1998.  The neuropsychology of REM sleep dreaming.  NeuroReport 9(3):R1-R14. 

Hocking G, Cousins MJ. 2003.  Ketamine in chronic pain management: an evidence-based review.  Anesth Analg 97(6):1730-1739.  This review indicates evidence of increase of fibromyalgia pain relief, endurance, and decreased trigger point tenderness [one must assume that tender points are meant] with ketamine therapy, but with a narrow therapeutic window.  Perhaps other NMDA inhibitors such as dextromethorphan might have beneficial effect without the narrow therapeutic window, and/or might be used to enhance opioid treatment.

Hodgson, M. J. and H. M. Kipen.  1999.  Gulf War illnesses: causation and treatment.  J Occup Environ Med 41(6):443-52.

Hoffman D. 2011. Understanding Multisymptom Presentations in Chronic Pelvic Pain: The Inter-relationships between the Viscera and Myofascial Pelvic Floor Dysfunction. Curr Pain Headache Rep. [Jul 8 Epub ahead of print]. "Patients presenting with chronic pelvic pain frequently complain of multiple symptoms that appear to involve more than one organ system, creating diagnostic confusion. The multisymptom presentation of chronic pelvic pain has been frequently described. This article describes four proposed explanations for the clinical observation of multisymptom presentations of patients with chronic pelvic pain. These include the concepts of viscerovisceral convergence; viscerosomatic convergence; hypertonicity of pelvic floor muscles creating visceral symptoms along with somatovisceral convergence; and central sensitization with expansion of receptive fields."

Hoffman DL, Dukes EM. 2007.  The health status burden of people with fibromyalgia: a review of studies that assessed health status with the SF-36 or the SF-12.  Int J Clin Pract. [Nov 24 Epub ahead of print].  “FM groups had similar or significantly lower (poorer) physical and mental health status scores compared to those with rheumatoid arthritis, osteoarthritis, osteoporosis, systemic lupus erythematosus, myofascial pain syndrome, primary Sjogren’s syndrome and others.  FM groups scored significantly lower than the pain condition groups mentioned above on domains of bodily pain and vitality.”  “People with FM had an overall health status burden that was greater in magnitude compared to people with other specific pain conditions that are widely accepted as impairing.”  [What does this indicate about those patients with FM AND CMP (and perhaps multiple other conditions)? DJS]

Hoffmann RG, Kotchen JM, Kotchen TA et al. 2010. Temporomandibular Disorders and Associated Clinical Comorbidities. Clin J Pain. [Dec 20 Epub ahead of print]. "The TMJD (temporomandibular joint and muscle disorders) -affected individuals were on average 41 years of age and predominantly female (90%). Nearly 60% of both men and women reported recent pain of moderate-to-severe intensity with a quarter of them indicating interference or termination of work-related activities. In the case-control comparison, a higher frequency of headaches, allergies, depression, fatigue, degenerative arthritis, fibromyalgia, autoimmune disorders, sleep apnea, and gastrointestinal complaints were prevalent among those affected with TMJD. Many of the associated comorbid conditions were over 6 times more likely to occur after TMJD was diagnosed. Among a wide array of treatments used (46 listed), the most effective relief for most affected individuals (91%) was the use of thermal therapies-hot/cold packs to the jaw area or hot baths. Nearly 40% of individuals affected with TMJD patients reported one or more surgical procedures and nearly all were treated with one or many different medications. Results of these treatments were generally equivocal. Although potentially limited to the most severe TMJD affected individuals, the survey results provide a comprehensive dataset describing the clinical manifestations of TMJD….The data provide evidence that TMJD represent a spectrum of disorders with varying pathophysiologies, clinical manifestations, and associated comorbid conditions. The findings underscore the complex nature of TMJD, the need for more extensive interdisciplinary basic and clinical research, and the development of outcome-based strategies to more effectively diagnose, prevent, and treat these chronic, debilitating conditions." [It is unfortunate that these patients were not assessed for co-existing myofascial trigger points, which can cause TMJD, are treatable, and are often components of other co-morbidities as well. DJS]

Hojsted, J., A. Alban, K. Hagild and J. Erikson.  1999.  Utilization of health care system by chronic pain patients who applied for disability pensions.  Pain 82(3):275-82.

Holick MF. 2004.  Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.  Am J Clin Nutr 79(3):362-371. "Vitamin D deficiency is often misdiagnosed as fibromyalgia." 

Holla JF, van der Leeden M, Peter WF et al. 2012. Proprioception, laxity, muscle strength and activity limitations in early symptomatic knee osteoarthritis: Results from the CHECK cohort. J Rehabil Med. [Aug 29 Epub ahead of print]. "The results of the present study support the theory that in the absence of adequate proprioceptive input, lower muscle strength affects a patient's level of activities to a greater degree than in the presence of adequate proprioceptive input."

Hollister, L. E.  2000.  An approach to the medical marijuana controversy.  Drug Alcohol Depend 58(1-2):3-7.  

Holman AJ, Neradilek MB, Dryland DD et al. 2010. Patient-derived determinants for participation in placebo-controlled clinical trials for fibromyalgia. Curr Pain Headache Rep. 14(6):470-476. "Perspectives of patients with fibromyalgia influence their likelihood of participating in randomized placebo-controlled trials and potentially clash with current, well-established methodology of randomized controlled trial design. Mandates to use only acetaminophen for breakthrough pain and that require discontinuation of concomitant medications, especially in studies lacking an active comparator arm, could bias a trial cohort to thereby reduce the generalizability of study findings and conclusions. This study evaluates factors affecting willingness to participate in such clinical trials, including the impact of altruism, payment, study duration, forced discontinuation of specific medications, and subject demographics for patients seen by rheumatologists proficient and avidly interested in treating fibromyalgia." [This casts yet another shadow on current fibromyalgia research. DJS]

Holst H, Arendt-Nielsen L, Mosbech H et al. 2011. Increased capsaicin-induced secondary hyperalgesia in patients with multiple chemical sensitivity. Clin J Pain. 27(2):156-162. "Temporal summation was increased in MCS patients compared with controls.... Further, in patients with comorbidity of fibromyalgia, pain and chronic fatigue, pain continued after end stimulation, and the stimulus response function was enhanced compared with patients without comorbidity, and significant to controls....This is the first study to show facilitated pain processing in MCS and EC (eczema patients with airway symptoms from odorous chemicals) patients with the most abnormal responses in MCS."

Holsten, F. and B. Bjorvatn.  1997. [Phototherapy.  An alternative for seasonal affective disordersor sleep disorders.  Tidsskr Nor Laegeforen 117(17):2484-2488 [Norwegian].

Holland, N. W. and E. B. Gonzalez.  1998.  Soft tissue problems in older adults.  Clin Geriatr Med 14(3):601-11.

Holtedahl R. 2010. [Pregabalin for fibromyalgia – can we rely on the pharmaceutical industry?] Tidsskr Nor Laegeforen 130(10):1032-1036. [Norwegian] “Negative results were seldom mentioned in the abstracts, and secondary endpoints were reported incompletely. All 19 reviews referred to one or more of the clinical trials, and were generally limited to describing main results. Interpretation. Recommendations for pregabalin in treatment of patients with fibromyalgia are based on rather weak evidence. Until trials independent of industry-funding are published, the role of pregabalin in treatment of fibromyalgia remains unclear.”  

Holton KF, Taren DL, Bennett RM et al. 2010. The excitotoxin elimination diet: a novel dietary intervention for fibromyalgia patients. International Myopain Society Eighth Clinical Meeting Oct 3-7, 2010. Toledo, Spain. Abstract No. 47. "Results suggest that the excitotoxin elimination diet, with wider food choices than a living foods diet, can significantly improve symptoms in patients with FM. Future large scale testing of the dietary intervention is warranted." [This is exciting research on a preventable perpetuating factor for both fibromyalgia and myofascial pain. Do you have aspartame, MSG and other excitotoxins in your pantry? DJS]

Holton KF, Taren DL, Thomson CA et al. 2012. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol [July 4 Epub ahead of print]. "To examine the effects of a challenge with monosodium glutamate (MSG) as compared to placebo on the symptoms of fibromyalgia (FM), in participants who initially experienced >30% remission of symptoms on an excitotoxin elimination diet....The MSG challenge, as compared to placebo, resulted in a significant return of symptoms (total symptom score.... These findings suggest that dietary glutamate may be contributing to FM symptoms in some patients. Future research on the role of dietary excitotoxins in FM is warranted." [Patients who routinely ingest aspartame, MSG and other excitotoxins take note. Diet is a perpetuating factor you can control. DJS]

Holzberg, A. D., M. E. Robinson, M. E. Geisser and H. A. Gremillion.  1996.  The effects of depression and chronic pain on psychosocial and physical functioning.  Clin J Pain 12(2):118-125.  

Homann D, Louzada FM, Goes SM. 2013. Acylated ghrelin: A potential marker for fibromyalgia? Eur J Pain. [Mar 8 Epub ahead of print]. "Fibromyalgia is characterized by chronic widespread pain and sleep disturbances. Overweight and obesity, which lead to metabolic changes, are additional comorbidities that are rarely explored, although they are highly prevalent in patients with fibromyalgia....These findings indicate that the decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity."

Homko, C. J. , E. Sivan, E. A. Reece and G. Boden. 1999. Fuel metabolism during pregnancy. Semin Reprod Endocrinol 17(2):119-25.

Hong C. 2004.  Myofascial pain therapy.  J Musculoskeletal Pain 12(3/4):37-43.  “Myofascial pain should be appropriately treated to inactivate TrPs completely and to avoid recurrence permanently.”  This is a good overview of common options in the treatment of TrPs. 

Hong CZ. 2000.  Specific sequential myofascial trigger point therapy in the treatment of a patient with myofascial pain syndrome associated with reflex sympathetic dystrophy: commentary.  Australas Chiropr Osteopathy 9(1):7-11.

Hong CZ. 2002. New trends in myofascial pain syndrome.  Zhonghua Yi Xue Za Zhi 65(11):501-512.  This is a good overview of current findings in myofascial medicine.

Hong CZ. 2006.  Treatment of myofascial pain syndrome.  Curr Pain Headache Rep. 10(5):345-349.   “Effective MTrP therapies include manual therapies, physical therapy modalities, dry needling, or MTrP injection.  It is also important to eliminate any perpetuating factors and provide adequate education and home programs to patients so that recurrent or chronic pain can be avoided.”

Hong C-Z. 2002.  New trends in myofascial pain syndrome. Zhonghua Yi Xue Za Zhi (Taipei) 65(11):501-12.  Review article. “The pathogenesis of [myofascial trigger points] MTrPs appears to be related to the integration in the spinal cord (formation of MTrP circuits) in response to the disturbance of the nerve endings and abnormal contractile mechanism at multiple dysfunctional endplates.”

Hong, C-Z. 1999. Current research on myofascial trigger points-pathophysiological studies. J Musculoskel Pain 7(1-2):121-129.

Hong C-Z and T-C Hsueh. 1996. “The difference in pain relief after trigger point injections in myofascial pain in patients with and without fibromyalgia.” Arch Phys Med Rehabil 77:1161-1166.

Hong, C-Z, and  J. Yu. 1998. Spontaneous electrical activity of rabbit trigger after transection of spinal cord and peripheral nerve. J Musculoskel Pain 6(4):45-58.

Hong, C. Z. and D. G. Simons.  1998.  Pathophysiologic and electrophysiologic mechanisms of myofascial trigger points.  Arch Phys Med Rehabil 79(7):863-72.

Hong, C. Z., T. S. Kuan, J. T. Chen and S. M. Chen.  1997.  Referred pain elicited by palpitation and by needling of myofascial trigger points: a comparison.  Arch Phys Med Rehabil 78(9):957-960.

Hong, C. Z.  1996.  Pathophysiology of myofascial trigger point.  J Formos Med Assoc 92(2):93-104.

Hoog SL, Cheng Y, Elpers J et al. 2013. Duloxetine and pregnancy outcomes: safety surveillance findings. Int J Med Sci. 10(4):413-419. "While limitations of these data are recognized, the information available to date from these two data sources suggest that the frequency of abnormal outcomes reported in duloxetine pregnancy cases is generally consistent with the historic control rates in the general population." [This study was financed by Eli Lilly and Company, manufacturers of duloxetine]

Hooper MM, Stellato TA, Hallowell PT et al. 2006.  Musculoskeletal findings in obese subjects before and after weight loss following bariatric surgery.  Int J Obes (Lond) [Apr 25 Epub ahead of print]  “There was a higher frequency of multiple MSK (musculoskeletal) complaints, including non-weight-bearing sites compared to historical controls, before surgery, which decreased significantly at most sites following weight loss and physical activity.  These benefits may improve further, as weight loss may continue for up to 24 months.  The benefits seen with weight loss indicate that prevention and treatment of obesity can improve MSK health and function.”   [Obesity can be a major perpetuating factor.  DJS]

Hopman-Rock, M., F. W. Kraaimaat, E. Odding and J. W. Bijlsma.  1998.  Coping with pain in the hip or knee in relation to physical disability in community-living elderly people.  Arthritis Care Res 11(4):243-52.

Hopwood, M. B. and S. E. Abram.  1994.  Factors associated with failure of trigger point injections.  Clin J Pain 10:227-234. 

Horne,. J. and L. Reyner. 1999. Vehicle accidents related to sleep: a review. Occup Environ Med 56(5):289-94. 

Horning, M. R.  1997. Chronic opioids: a reassessment.  Alaska Med 39(4):103-110.  

Horowits, R. 1999.  The physiological role of titin in striated muscle.  Rev Physiol Biochem Pharmacol 138:57-96.

Horowitz L, Sarkin JM. 1992.  Video display terminal operation: a potential risk in the etiology and maintenance of temporomandibular disorders.  Cranio. 10(1):43-50.  “TMD (temporomandibular disorder) is associated with numerous risk factors that commonly initiate sympathetic nervous system and stress hormone response mechanisms resulting in muscle spasms, trigger point formation, and pain in the head and neck.”

Horven, S., T. C. Stiles, A. Holst and T. Moen. 1992. HLA antigens in primary fibromyalgia syndrome.  J. Rheumatol 19(8):1269-70.

Hoseini SS, Hoseini M, Gharibzadeh S. 2005.  Sprouting phenomenon, a new model for the role of A-beta fibers in wind up.  Med Hypotheses [Dec 12 Epub ahead of print]  “In this study, we have proposed a new model for the role of Abeta fibers in wind up, through sprouting of nerve fibers in the dorsal horn of spinal cord.  We named it “sprouting phenomenon”.  It has been reported that in some clinical hyperalgesic states induced by peripheral injury or inflammation, wind up may aggravate the pain.  Studies have indicated the presence of …fibromyalgia syndrome….  According to sprouting phenomenon, it seems that some clinical interventions can be assessed to alleviate post-inflammatory pains: (1) immediate and complete relief of inflammation by anti-inflammatory agents to prevent repetitive excitation of C-fibers and subsequent morphological changes of dorsal horn laminae; (2) using local anesthetics in order to prevent pain signal transmission; (3) prevention of sprouting by intrathecal injection of some anti-proliferation agents; (4) using NMDA or NK1 receptor antagonists to prevent central mechanism of wind up.”  “Future clinical studies are needed…”

Hou C.R., Chung K.C., Chen J.T. et al. 2002.  Effects of a calcium channel blocker on electrical activity in myofascial Trigger spots in rabbits.  Am J Phys Med Rehabil 81(5):342-9.  Calcium channel blockers are effective inhibitors of myofascial trigger point spontaneous electrical activity.

Hou C.R., Tsai L.C., Cheng K.F. et al. 2002.  Immediate effects of various physical therapeutic modalities on cervical myofascial pain and trigger-point sensitivity.  Arch Phys Med Rehabil 83(10):1406-14.  “Results suggest that therapeutic combinations such as hot pack plus active ROM and stretch with spray, hot pack plus active ROM and stretch with spray as well as TENS, and hot pack plus active ROM and interferential current as well as myofascial release technique, are most effective for releasing MtrP pain and increasing cervical ROM.”

Houtmeyers, E., R. Gosselink, G. Gayan-Ramirez and M. Decramer.  1999.  Effects of drugs on mucus clearance.  Eur Respir J 14(2):452-67.

Howard KJ, Mayer TG, Neblett R et al. 2010. Fibromyalgia Syndrome in Chronic Disabling Occupational Musculoskeletal Disorders: Prevalence, Risk Factors, and Post treatment Outcomes. J Occup Environ Med. [Nov 30 Epub ahead of print]. "OBJECTIVE: To identify the prevalence, risk factors, and treatment outcomes of patients with chronic disabling occupational musculoskeletal disorders (CDOMD) who met criteria for fibromyalgia....The CDOMD patients with fibromyalgia reported higher-level psychosocial distress. Women with fibromyalgia were 9.6 times less likely to return to work 1-year post treatment and, of those who did, were 4.3 times less likely to retain work....Of this cohort, 23.2% patients met criteria for fibromyalgia. Patients with fibromyalgia were found to show greater psychosocial distress and significantly poorer rates of work return and work retention 1-year post rehabilitation."

Howell ER. 2012. Conservative management of a 31 year old male with left sided low back and leg pain: a case report. J Can Chiropr Assoc. 56(3):225-232. "This case study reported the conservative management of a patient presenting with left sided low back and leg pain diagnosed as a left sided L5-S1 disc prolapse/herniation....A 31-year-old male recreational worker presented with left sided low back and leg pain for the previous 3-4 months that was exacerbated by prolonged sitting....The plan of management included interferential current, soft tissue trigger point and myofascial therapy, lateral recumbent manual low velocity, low amplitude traction mobilizations and pelvic blocking as necessary. Home care included heat, icing, neural mobilizations, repeated extension exercises, stretching, core muscle strengthening, as well as the avoidance of prolonged sitting and using a low back support in his work chair. The patient responded well after the first visit and his leg and back pain were almost completely resolved by the third visit....Conservative chiropractic care appears to reduce pain and improve mobility in this case of a L5-S1 disc herniation. Active rehabilitative treatment strategies are recommended before surgical referral."

Hoyle JA, Marras WS, Sheedy JE et al. 2010. Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. J Electromyogr Kinesiol. [Jun 25 Epub ahead of print]. "Musculoskeletal complaint rates are high among those performing low-level static exertions (LLSEs), such as computer users." "It was hypothesized that myofascial trigger point (MTrP) development might be one causal mechanism to help explain these complaints and that static postural and visual demands may be contributing factors." "…MTrPs developed after one hour of continuous typing, despite the stress condition." "Findings suggest that MTrPs may be one causal pathway for pain during LLSEs and both postural and visual demands may play a role in muscle activation patterns, perhaps attributing to MTrP development and resultant discomfort."

Hrebicek J, Janout V, Malincilova J, Horakova D, Cizek L. Detection of insulin resistance by simple quantitative insulin sensitivity check index QUICKI for epidemiological assessment and prevention.  J Clin Endocrinol Metab Jan;87(1):144-7.  

Hrycaj P, Stratz T, Mennet P et al. 1996.  Pathogenetic aspects of responsiveness to ondansetron (5-hydroxytryptamine type 3 receptor antagonist) in patients with primary fibromyalgia syndrome — a preliminary study.  J Rheumatol 23(8):1418-1423.  “Ondansetron appears to be an effective drug in about 50% of patients with FM.  There may be two subsets of patients with FM that differ clinically and pathogenetically with regard to the disturbance in the 5-HT-3R system."

Hsieh C.Y., Hong C. Z., Adams A. H., Platt K. J. , Danielson C. D. , Hoehler F. K., and Tobis JS 2000. Interexaminer reliability of the palpation of trigger points in the trunk and lower limb muscles. Arch Phys Med Rehabil  81(3):258-64

Hsieh LF, Hong CZ, Chern SH et al. 2009.  Efficacy and side effects of diclofenac patch in treatment of patients with myofascial pain syndrome of the upper trapezius.  J Pain Symptom Manage. [Oct 10 Epub ahead of print].  “This study demonstrates that the diclofenac sodium patch was superior to the control patch in terms of reducing pain and improving functional outcomes, and did not result in significant adverse effects.”  [This may be a helpful option for patients with one or a small cluster of TrPs DJS]

Hsieh YL, Kao MJ, Kuan TS et al. 2007.  Dry needling to a key myofascial trigger point may reduce the irritability of satellite MTrPs.  Am J Phys Med Rehabil. 86(5):397-403.  “This study supports the concept that activity in a primary MTrP leads to the development of activity in satellite MTrPs and the suggested spinal cord mechanism responsible for this phenomenon.”

Hsieh YL, Yang SA, Yang CC et al. 2012. Dry needling at myofascial trigger spots of rabbit skeletal muscles modulates the biochemicals associated with pain, inflammation, and hypoxia. Evid Based Complement Alternat Med. 2012:342165. "Dry needling at the MTrSs modulates various biochemicals associated with pain, inflammation, and hypoxia in a dose-dependent manner."

Hsin ST, Yin YC, Juan CH et al. 2002.  Myofascial pain syndrome induced by malpositioning during surgery – a case report.  Acta Anaesthesiol Sin. 40(1):37-41.  “It is a real challenge to the anesthesiologists to differentiate brachial plexus injury (BPI) from myofascial pain syndrome (MPS).  The possibility of MPS should be suspected in a patient with complaints of pain and dysfunction of the upper arm immediately after surgery.  Here we report a case of gallstone with cervical ankylosing spondylitis who sustained myofascial pain syndrome immediately after open cholecystectomy.  We utilized dry needle stimulation to deactivate the trigger point of the pectoris minor muscle and stretching the muscle to relieve the muscle pain after the diagnosis was made.  The patient completely recovered 2 weeks later.”

Hsu J.C., Lee Y.S.., Chang C.N. et al. 2002.  Sleep deprivation affects nitric oxide synthesis and glial reactions in the rat hippocampus. Glia (Suppl 1):S51 [Abstract].

Hsueh, T. C., S. Yu, T. S. Kuan and C. Z. Hong.  1998.  Association of active myofascial trigger points and cervical disc lesions.  J Formos Med Assoc 97(3):174-180.

Hsueh, T-C. , P. T. Cheng, T. S. Kuan and C-Z Hong. 1997. The immediate effectiveness of electrical nerve stimulation and electrical muscle stimulation on myofascial trigger points.  1997. Am J Phys Med Rehabil 76(6):471-476.

Hu, F. B., M. J. Stampfer, J. E. Manson, E. Rimm, G. A. Colditz, F. E. Speizer, C. H. Hennekens and W. C. Willett.  1999.  Dietary protein and risk of ischemic heart disease in women.  Am J Clin Nutr 70(2):221-7.  

Huang TT, Yang LH, Liu CY. 2011. Reducing the fear of falling among community-dwelling elderly adults through cognitive-behavioral strategies and intense Tai Chi exercise: a randomized controlled trial. J Adv Nurs. Jan 7 [Epub ahead of print]. "The results of this trial suggest that the cognitive-behavioral intervention with Tai Chi exercise helped community-dwelling elderly adults to enhance their mobility, to manage their fear of falling and to increase their quality of life." [It has been my personal experience that t'ai chi chuan, at least the Yang long form I practice, helps even younger patients with mobility and balance. DJS]

Huang YT, Lin SY, Neoh CA et al. 2011. Dry needling for myofascial pain: prognostic factors. J Altern Complement Med. 17(8):755-762. "Dry needling is an effective treatment for reducing pain and pain interference. However, long pain duration, high pain intensity, poor quality of sleep, and repetitive stress are associated with poor outcomes. Treatment outcome depends not only on the dry needling protocol, but also on disease characteristics and patient demographic profile." [Outcome would also depend on the proper identification of the myofascial trigger points involved, as well as the training and skill of the practitioner. DJS]

Hubbard, D. R. and G. M. Berkoff.  1993.  Myofascial trigger points show spontaneous needle EMG activity.  Spine 18(13):1803-7.  Sustained spontaneous EMG activity was found in the 1-2 mm nidus of all TrPs, and was absent in non-TrPs.

Hubbell, S. L. and M. Thomas.  1985.  Postpartum cervical myofascial pain syndrome: review of four patients.  Obstet Gynecol 65(3 Suppl):56S-57S.

Hudson J.I., Mangweth B., Pope H.G. et al.  Family study of affective spectrum disorder.  Arch Gen Psychiatry.  This study suggests that some disorders such as ADHD, IBS, migraine, OC, PTSD, fibromyalgia and other conditions may share a genetic predisposition, as these conditions are often found clustered in families.

Hudson, N., M. A. Fitzcharles, M. Cohen, M. R. Starr and J. M. Esdaile.  1998.  The association of soft-tissue rheumatism and hypermobility.  Br J Rheumatol 37(4):382-6.  

Hudson, N., M. R. Starr, J. M. Esdaile and M. A. Fitzcharles. 1995. Diagnostic associations with hypermobility in rheumatology patients. Br J Rheumatol 34(12):1157-1161.

Hudson, T.  2000.  Fibrocystic breasts.  Women’s Health Update.  Townsend Letter for Doctors & Patients Jan:142-3.

Huggins T, Boras AL, Gleberzon BJ et al. 2012. Clinical effectiveness of the activator adjusting instrument in the management of musculoskeletal disorders: a systematic review of the literature. J Can Chiropr Assoc. 56(1):49-57. "This systematic review of eight clinical trials involving the use of the AAI found reported benefits to patients with a spinal pain and trigger points, although the clinical trials reviewed suffered from many methodological limitations, including small sample size, relatively brief follow-up period and lack of control or sham treatment groups."

Hughes G, Martinez C, Myon E et al. 2005.  The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice.  Arthritis Rheum. 54(1):177-183.  “Being diagnosed as having FM may help patients cope with some symptoms, but the diagnosis has a limited impact on health care resource use in the longer term, possibly because there is little effective treatment.”  [This could also be because insurance companies do not cover nor many health care resources provide effective treatment regiments. DJS]

Huppe A, Brockow T, Raspe H. 2004.  [Chronic widespread pain and tender points in low back pain: a population-based study].  Z Rheumatol 63(1):76-83.  [German]  These researchers did not find fibromyalgia to be a common and significant factor in low back pain. 

Hurtig IM, Raak RI, Kendall SA, Gerdle B, Wahren LK. Quantitative sensory testing in fibromyalgia patients and in healthy subjects: identification of subgroups. Clin J Pain Dec:17(4):316-22,2001.  There are distinct subgroups of FMS patients that have different cold pain thresholds. These groups have differences in sleep quality, pain intensity, and number of tender points.

Hwang M, Kang YK, Shin JY et al. 2005.  Referred pain pattern of the abductor pollicis longus muscle. Am J Phys Med Rehabil. 84(8):593-597.  “Referred pain patterns of the abductor pollicis longus resemble pain experienced in de Quervain’s tenosynovitis.  Thus, identification of the abductor pollicis longus trigger point should be considered in pain of the radial aspect of the wrist and thumb, especially when no other neurologic abnormalities or inflammatory conditions are present.”

Hwang M, Kang YK, Kim DH. 2005.  Referred pain pattern of the pronator quadratus muscle.  Pain [Epub ahead of print June 16^th]  This paper describes two main pain patterns of pronator quadratus myofascial trigger points.