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Patients &
trained Companions

Doctors & Other
Care Providers



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

annotated by Devin J. Starlanyl



References for Research Purposes

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NOTE:  New Nomenclature

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

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



Facco E, Ceccherelli F. 2005.  Myofascial pain mimicking radicular syndromes.  Acta Neurochir 92:147-150.  “Myofascial pain is very often underscored and misunderstood in clinical practice.  In many cases the localization of myofascial pain may resemble other diseases, such as radicular syndromes and even diseases of internal organs.  When vertebral abnormalities are present on CT or MRI, it should be checked whether the cause of pain is radicular, myofascial, or both.  On the other hand, the conventional approach to painful disorders may lead to errors and wrong diagnosis, depending on several factors: a) pain is often considered a symptom of an organic disease; b) the diagnosis is usually directed towards the structural cause of pain only; c) the functional components of the suffering patient are underscored; d) the site of pain may introduce some bias.”


Faerber L, Drechsler S, Ladenburger S et al. 2007.  The neuronal 5-HT(3) receptor network after 20 years of research – evolving concepts in management of pain and inflammation.  Eur J Pharmacol. 560(1):1-8.

Fais A, Cacace E, Corda M et al. 2012. Purine metabolites in fibromyalgia syndrome. Clin Biochem. [Sep 18 Epub ahead of print]. "Study results suggest that purines, in particular adenosine and inosine, may be involved in pain transmission in fibromyalgia."

Falla D, Andersen H, Danneskiold-Samsoe B et al. 2009.  Adaptations of upper trapezius muscle activity during sustained contractions in women with fibromyalgia.  J Electromyogr Kinesiol. [Aug 12 Epub ahead of print].  “The results indicate that muscle pain prevents the adaptation of upper trapezius activity during sustained contractions as observed in non-painful conditions, which may induce overuse of similar muscle compartments with fatigue.”  [This study may actually have been done on co-existing myofascial TrPs in the trapezius muscle.  It may also be showcasing the increasing interaction of these 2 conditions. DJS]


Falla D, Bilenkij G, Jull G. 2004.  Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task.  Spine 29(13):1436-1440.  “Patients with neck pain demonstrated greater activation of accessory neck muscles during a repetitive upper limb task compared to asymptomatic controls.”

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.”

Fallon N, Li X, Chiu Y et al. 2015. Altered cortical processing of observed pain in fibromyalgia syndrome patients. J Pain. [May 12 Epub ahead of print.] "FMS patients demonstrate increased activations for pain and non-pain pictures. The findings suggest that even innocuous, everyday visual stimuli with somatic connotations may challenge the emotional state of FMS patients. Our study points towards the importance of cognitive-emotional therapeutic approaches for the treatment of FMS."

Fan YH, Lin AT, Lu SH et al. 2014. Non-bladder conditions in female Taiwanese patients with interstitial cystitis/hypersensitive bladder syndrome. Int J Urol. [Apr 13 Epub ahead of print.] "Interstitial cystitis/hypersensitive bladder syndrome patients are more likely to have multiple non-bladder conditions. These conditions correlate with the severity of interstitial cystitis/hypersensitive bladder syndrome symptoms."

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.

Farajidavar A, Gharibzadeh S, Towhidkhah F et al. 2006.  A cybernetic view on wind-up.  Med Hypotheses [Mar 21 Epub ahead of print]  “Wind-up may aggravate the pain in clinical hyperalgesic situations such as post-surgical states, some neuropathic pains, fibromyalgia syndrome, and post-herpetic neuralgia.  [This work was based on wind-up in Abeta fibers, and other wind-up studies have been based on afferent C-fibers. DJS]

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.

Faro M, Saez-Francas N, Castro-Marrero J et al. 2014. [Impact of fibromyalgia in the chronic fatigue syndrome.] Med Clin (Barc). [Jan 2 Epub ahead of print.] [Article in Spanish] "Different studies have showed association of the chronic fatigue syndrome (CFS) with other pathologies, including fibromyalgia (FM)….We included 980 CFS patients (mean age: 48±9 years; 91% women). Fibromyalgia was present in 528 patients (54%). The level of fatigue… and pain … was higher in FM patients. Patients with CFS and FM had more prevalence of sleep-related phenomena. The percentage of patients and the degree of severity of cognitive symptoms, neurological and autonomic dysfunction was higher in FM patients…. FM patients scored higher on the fatigue impact scale … and showed worse results in the quality of life questionnaire….FM (patients have) co-morbidity (with) worse clinical parameters, fatigue and the perception of quality of life (than) in CFS patients."

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]

Fass, R, Quan SF, O’Connor GT et al. 2005.  Predictors of heartburn during sleep in a large prospective cohort study.  Chest 127:1658-1666.  “Heartburn during sleep is very common in the general population.  Reports of this type of symptom of GERD are strongly associated with increased BMI, carbonated soft drink consumption, snoring and daytime sleepiness, insomnia, hypertension, asthma, and usage of benzodiazepines.  Overall, heartburn during sleep may be associated with sleep complaints and excessive daytime sleepiness.”

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.

Fava A, Plastino M, Cristiano D et al. 2013. Insulin resistance possible risk factor for cognitive impairment in fibromyalgic patients. Metab Brain Dis. [Jul 28 Epub ahead of print]. "The results of this study suggest that IR (insulin resistance) may represent a risk factor for memory impairment in fibromyalgic patients." [We have found IR to be a common interactive co-existing condition with both FM and CMP, and mentioned it as a cause of cognitive deficits in "Fibromyalgia and Chronic Myofascial Pain: A Survival Guide". DJS]

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.”

Feng J, Zhang Z, Wu X et al. 2013. Discovery of potential new gene variants and inflammatory cytokine associations with fibromyalgia syndrome by whole genome sequencing. PLoS One. [June 10 Epub ahead of print]. This is an article on the complete exome sequencing on a subset of fibromyalgia patients from 150 nuclear families. Their conclusions "…implicate an inflammatory basis for FMS, as well as specific cytokine dysregulation, in at least 35% of our FMS cohort. "Among 9 patients bearing more than one of the variants we have described, 4 had onset of symptoms between the ages of 10 and 18. The subset with the C11orf40 mutation had elevated plasma levels of the inflammatory cytokine, IL-12, compared with unaffected controls or FMS patients with the wild-type allele." [We do not know if these patients had co-existing inflammatory processes, but in that one subset of FM patients they did find 35% with inflammatory findings. Linda Watkins' team also found pro-inflammatory cytokines elevated in FM, but that was considered a prelude to fractalkine and interthecal (dural tube) glial cell activation. DJS]

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].

Ferguson AR, Crown ED, Grau JW. 2006.  Nociceptive plasticity inhibits adaptive learning in the spinal cord.  Neuroscience [May 5 Epub ahead of print]  “Recent data suggest links between the learning deficit and the sensitization of pain circuits associated with inflammation or injury (central sensitization).”  “Central sensitization enhances reactivity to mechanical stimulation (allodynia) and depends on the N-methyl-d-aspartate receptor (NMDAR)."

Fernández-Carnero J, La Touche R, Ortega-Santiago R et al. 2010. Short-term effects of dry needling of active myofascial trigger points in the masseter muscle in patients with temporomandibular disorders. J Orofac Pain. 24(1):106-112. “The application of dry needling into active TrPs in the masseter muscle induced significant increases in PPT (pressure pain threshold) levels and maximal jaw opening when compared to the sham dry needling in patients with myofascial TMD.”  [Treatment of related TrPs can significantly ease symptoms of TMJ, including pain and jaw restriction. It is essential that treatment be as prompt as possible to avoid unequal tension on the discs of the jaw. DJS]

Fernandez-Carnero J, Ge HY, Kimura Y.  2010. Increased spontaneous electrical activity at a latent myofascial trigger point after nociceptive stimulation of another latent trigger point. Clin J. Pain 26(2):138-143.  This groundbreaking paper shows how activity at a latent TrP in the infraspinus muscle may increase sensitivity and activity of a TrP in the forearm.  This study demonstrates both the formation of satellite TrPs and TrP cascades, showing a sensory connection between distant TrPs.  It also shows a decrease in sensitivity of the forearm TrP after the shoulder TrP was successfully treated.  [This is a critical paper. I hope it quiets critics who disbelieve in the formation of satellite TrPs and TrP cascades. Thank you, authors.  DJS]

Fernandez-Carnero J, Fernandez-de-Las-Penas C, de la Liave-Rincon AI et al. 2007.  Prevalence of and referred pain from myofascial trigger points in the forearm muscles in patients with lateral epicondylalgia.  Clin J Pain. 23(4):353-360.  “Lower PPT (pressure pain threshold) and larger referred pain patterns suggest that peripheral and central sensitization exists in LE (lateral epicondamgia).”

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. 2010. New evidence for trigger point involvement in tension-type headaches. J Musculoskel Pain. 18(4):354-360. "Tension-type headache (TTH) is the most common form of headache and its chronic form (chronic tension-type headache (CTTH)) is one of the most neglected and difficult headaches to treat. TTH is an overarching syndrome of 'featureless' headaches characterized by nothing but pain in the head….The term 'tension-type' has been chosen by the International Headache Society (ICHD-II) to offer a new heading underlining the uncertain pathogenesis, but indicating that some form of muscle tension may play a role….Hyperalgesic and allodynic responses support the role of both peripheral and central mechanisms in the development of the clinical picture of CTTH. In fact, it is suggested that central sensitization, a reduction in inhibitory pain mechanisms, and peripheral sensitization of muscle nociceptors are mechanisms involved in perceived pain in CTTH….Subjects who develop TTH have showed normal tenderness scores and pressure pain threshold levels before the beginning of the symptoms, which suggests that the mechanical hypersensitivity is rather a consequence than a risk factor for the development of TTH." "Previous studies have found that TTH patients described their head pain as pressing, tightening, or soreness. Dull and tight heaviness are also pain quality features of TTH attacks. These pain features resemble the descriptions of clinically referred pain elicited by TrPs as described by Simons et al." "Recent clinical studies have clearly demonstrated the relevance of active TrPs in CTTH. In fact, recent studies have described the referred pain elicited from two extra-ocular muscles, i.e., superior oblique and lateral rectus in patients with CTTH."

Fernandez-de-las-Penas C, Alonso-Blanco C, Del Amo-Perez A et al. 2007.  Trigger points in the masticatory muscles in subjects presenting with ankylosing spondylitis.  J Musculoskel Pain. 15(3):39-47.  “Trigger points in the masticatory muscles were more conspicuous in AS subjects than in HNCs.  Patients showed a reduced active mouth opening and cervical flexion-extension motion than matched HNCs.  The AS subjects with lesser mouth opening showed a greater occiput-to-wall distance and a greater number of TrPs in the masticatory muscles.”

Fernandez-de-Las-Penas C, Alonso-Blanco C, Luz Cuadrado M et al. 2006.  Myofascial trigger points in the suboccipital muscles in episodic tension-type headache.  Man Ther. 11(3):225-230.   

Fernandez-de-Las-Penas C, Alonso-Blanco C, Miangolarra JC. 2006.  Myofascial trigger points in subjects presenting with mechanical neck pain: a blinded, controlled study.  Man Ther. [Jun 10 Epub ahead of print]  “Active TrPs were more frequent in patients presenting with mechanical neck pain than in healthy subjects.”

Fernández-de-Las-Peñas C, Ambite-Quesada S, Gil-Crujera A et al. 2012. Catechol-O-Methyltransferase Val158Met Polymorphism Influences Anxiety, Depression, and Disability, but not Pressure Pain Sensitivity, in Women with Fibromyalgia Syndrome. J Pain. [Sep 28 Epub ahead of print]. "Our aim was to assess the relationship of the Val158 Met polymorphism to pain, anxiety, depression, functional ability, and pressure pain sensitivity in women with fibromyalgia (FMS).... This study suggests that the Val158Met COMT polymorphism modulated some psychological variables but not pressure pain sensitivity in FMS because women with FMS carrying the Met/Met genotype exhibit higher disability, depression, and anxiety than but similar PPTs to those with Val/Met and Val/Val genotypes. This study provides further evidence of potential genetic factors that predispose women with FMS to exhibit the disease more severely."

Fernandez-de-las-Penas C, Carratala-Tejada M, Luna-Oliva L et al. 2006.  The immediate effect of hamstring muscle stretching in subjects’ trigger points in the masseter muscle.  J Musculoskel Pain 14(3):27-35.  “The present study demonstrated an increase in active mouth opening and a decrease in TrP sensitivity in the masseter muscle in response to the stretch of the hamstring muscles.”  Treatment, and constriction, in the myofascia of one area can significantly alter the myofascia in another area, even long distance.

Fernandez-de-las-Penas C, Cleland JA, Cuadrado ML et al. 2008.  Predictor variables for identifying patients with chronic tension-type headache who are likely to achieve short-term success with muscle trigger point therapy.  Cephalalgia. 28(3):264-275.  “The present CPR (clinical prediction rule) provides the potential to identify CTTH (chronic tension-type headache) patients who are likely to experience short-term and 1-month follow-up success...” with manual TrP therapy.

Fernandez-de-Las-Penas C, Cleland JA, Palomeque-Del-Cerro L et al. 2010. Development of a clinical prediction rule for identifying women with tension-type headache who are likely to achieve short-term success with joint mobilization and muscle trigger point therapy. Headache Nov 4 [Epub ahead of print] The current clinical prediction rule may allow clinicians to make an a priori identification of women with TTH who are likely to experience short-term self-report improvement with a multimodal session including joint mobilization and TrP therapies."

Fernandez-de-Las-Penas C, Cleland JA, Ortega-Santiago R et al. 2010. Central sensitization does not identify patients with carpal tunnel syndrome who are likely to achieve short-term success with physical therapy. Exp Brain Res. 207(1-2):85-94. "The aim of the current study was to identify whether hyperexcitability of the central nervous system is a prognostic factor for individuals with carpal tunnel syndrome (CTS) likely to experience rapid and clinical self-reported improvement following a physical therapy program including soft tissue mobilization and nerve slider neurodynamic interventions.... The physical therapy sessions included both soft tissue mobilization directed at the anatomical sites of potential median nerve entrapment and a passive nerve slider neurodynamic technique targeted to the median nerve.... Our results support that widespread central sensitization may not be present in women with CTS who are likely to achieve a successful outcome with physical therapy."

Fernandez-de-Las-Penas C, Courtney CA. 2014. Clinical reasoning for manual therapy management of tension type and cervicogenic headache. J Man Manip Ther. 22(1):44-50. "In recent years, there has been an increasing knowledge in the pathogenesis and better management of chronic headaches. Current scientific evidence supports the role of manual therapies in the management of tension type and cervicogenic headache, but the results are still conflicting. These inconsistent results can be related to the fact that maybe not all manual therapies are appropriate for all types of headaches; or maybe not all patients with headache will benefit from manual therapies. There are preliminary data suggesting that patients with a lower degree of sensitization will benefit to a greater extent from manual therapies, although more studies are needed. In fact, there is evidence demonstrating the presence of peripheral and central sensitization in chronic headaches, particularly in tension type. Clinical management of patients with headache needs to extend beyond local tissue-based pathology, to incorporate strategies directed at normalizing central nervous system sensitivity. In such a scenario, this paper exposes some examples of manual therapies for tension type and cervicogenic headache, based on a nociceptive pain rationale, for modulating central nervous system hypersensitivity: trigger point therapy, joint mobilization, joint manipulation, exercise, and cognitive pain approaches."

Fernandez-de-Las-Penas C, Cuadrado M, Arendt-Nielsen L et al. 2007.  Myofascial trigger points and sensitization: an updated pain model for tension-type headache.  Cephalalgia [Mar 14 Epub ahead of print]   “Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles.  In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.”

Fernandez-de-las-Penas C, Cuadrado M, Pareja J. 2007.  Referred pain from extra-ocular muscle trigger points in chronic headache.  J Musculoskel Pain 15 (Supp 13):19 item 27.  [Myopain 2007 Poster]   “Nociceptive inputs from the extra-ocular muscles may provoke a continuous afferent bombardment to the trigeminal nerve nucleus caudalis in CTTH (chronic tension-type headache).  The prolonged nociceptive activation by such muscle inputs might contribute to central sensitization.”  [This exciting research indicates that even constant pain from facial muscles around the eye could be enough to contribute to body-wide central nervous system sensitization. DJS]

Fernandez-de-Las-Penas C, Cuadrado M, Pareja J. 2006.  Myofascial trigger points, neck mobility and forward head posture in unilateral migraine.  Cephalalgia. 26(9):1061-1070.  “Active TrPs located ipsilateral to migraine headaches might be a contributing factor in the initiation or perpetuation of migraine.”

Fernandez de las Penas C, Cuadrado ML, Gerwin RD et al. 2005.  Referred pain from the trochlear region in tension-type headache: a myofascial trigger point from the superior oblique muscle.  Headache. 45(6):731-737.  “This pain was perceived as a deep ache located at the retro-orbital region, sometimes extending to the supra-orbital region or the homo-lateral forehead.  Pain intensity was greater in CTTH (chronic tension-type headache) patients than in ETTH (episodic tension-type headache) patients or control subjects (P<.001)...  MTrPs in the SOM (superior oblique muscle) may evoke a typical referred pain pattern in patients with TTH (tension-type headache).  The presence of a myofascial disorder in the trochlear region might contribute to the pathogenesis of TTH.”  [It is with gratitude that I post this confirmation of the extrinsic eye TrPs mentioned in my books, and I hope to see much more work from this excellent team. DJS]

Fernandez-de-las-Penas C, Cuadrado ML, Arendt-Nielsen L et al. 2007.  A pain model for tension type headache based on muscle trigger points.  J Musculoskel Pain 15 (Supp 13):20 item 30.  [Myopain 2007 Poster]  “Our studies suggest that TTH (tension-type headache) can be explained by referred pain from active TrPs in neck-shoulder muscles.  Since chemical mediators most likely are released by active TrPs, nociceptive inputs from these TrPs may lead to increased afferent barrage into the trigeminal nucleus caudalis.  This updated pain model proposes that TrPs may be primary hyperalgesic zones, while referred pain areas in the head could be viewed as secondary hyperalgesic zones.”

Fernandez-de-las-Penas C, Cuadrado ML, Pareja JA. 2007. Muscle atrophy of the suboccipital muscles associated with active trigger points in chronic tension type headache.  J Musculoskel Pain 15 (Supp 13):19 item 28.  [Myopain 2007 Poster]  “Muscle atrophy in the RCPmin, but not in the RCPmaj, was associated to active TrPs in the suboccipital muscles in CTTH.  Nociceptive inputs originated in active TrPs might contribute to a greater muscle atrophy of the involved muscles.”  [This study is interesting in that it suggests that pain from MTPs could contribute to muscle atrophy.  As MTPs can cause nerve entrapment and blood vessel entrapment, this would be logical. DJS]

Fernandez-de-las-Penas C, De-la-Llave-Rincon A, Miangolarra J. 2007.  Uncommon referred pain from scalene muscle trigger points in chronic tension type headache.  J Musculoskel Pain 15 (Supp 13):21 item 31.  [Myopain 2007 Poster]  “Nine CTTH (chronic tension type headache) patients had an uncommon referred pain pattern from scalene muscle TrPs, so these headache patients may need examination for scalene TrPs.  It is known that CTH show sensitization of central pathways, which may provoke larger referred pain areas of active muscle TrPs.  Further, there are examples of neurologically related exceptional pain patterns in other muscles [e.g. the soleus].”  [I believe that this is not so uncommon, and I have seen it several times before, but it may be more common in patients with CMP and central sensitization. DJS]

Fernandez-de-Las-Penas C, Dommerholt J. 2014. Myofascial trigger points: peripheral or central phenomenon? Curr Rheumatol Rep. 16(1):395. "Trigger points (TrP) are hyperirritable spots in a taut band of a skeletal muscle, which usually have referred pain. There is controversy over whether TrP are a peripheral or central nervous system phenomenon. Referred pain, the most characteristic sign of TrP, is a central phenomenon initiated and activated by peripheral sensitization, whereby the peripheral nociceptive input from the muscle can sensitize dorsal horn neurons that were previously silent. TrP are a peripheral source of nociception, and act as ongoing nociceptive stimuli contributing to pain propagation and widespread pain. Several studies support the hypothesis that TrP can induce central sensitization, and appropriate TrP treatment reduces central sensitization. In contrast, preliminary evidence suggests that central sensitization can also promote TrP activity, although further studies are needed. Proper TrP management may prevent and reverse the development of pain propagation in chronic pain conditions, because inactivation of TrP attenuates central sensitization."

Fernandez-de-las-Penas C, Fernandez-Carnero J, Miangolarra J. 2007.  Multifidus muscle trigger point management and stabilizing exercises in low back pain.  J Musculoskel Pain 15 (Supp 13):21 item 32.  [Myopain 2007 Poster]  “In some CLBP (chronic low back pain) patients, it would be necessary to treat lumbar multifidus TrPs before starting a stability exercise program because it includes voluntary contraction of this muscle.  Nociceptive barrage originated in active TrPs could act as a contributing factor for muscle inhibition.”  [Multifidi, especially with nerve entrapment, is exceedingly common in patients with CMP and central sensitization.   Treatment of the nerve pain is before the TPM will increase the efficacy of the TPM treatment. DJS]

Fernandez-de-las-Penas C, Fernandez-Mayoralas DM, Ortega-Santiago R et al. 2011. Referred pain from myofascial trigger points in head, neck and shoulder muscles reproduces head pain features in children with chronic tension type headache. J Headache Pain. 12(1):35-43. TrPs are a common cause of chronic tension type headaches in children. [Pediatricians must become aware of this fact, and be trained in diagnosis and treatment of TrPs. DJS]

Fernandez-de-Las-Penas C, Galan-Del-Rio F, Alonso-Blanco C et al. 2010. Referred pain from muscle trigger points in the masticatory and neck-shoulder musculature in women with temporomandibular disorders. J Pain. [May 20 Epub ahead of print]. “The current study showed the existence of multiple active muscle TrPs in the masticatory and neck-shoulder muscles in women with myofascial TMD pain. The local and referred pain elicited from active TrPs reproduced pain complaints in these patients. Further, referred pain areas were larger in TMD pain patients than in healthy controls. The results are also in accordance with the notion of peripheral and central sensitization mechanisms in patients with myofascial TMD.” [Another paper showing the association of TrPs and the central sensitization of FM. DJS]

Fernandez-de-Las-Penas C, Ge HY, Arendt-Nielsen L et al. 2006.  Referred pain from trapezius muscle trigger points shares similar characteristics with chronic tension type headache.  Eur J Pain. [Aug 17 Epub ahead of print]  Patients with chronic tension type headache may have spatial summation of perceived pain and mechanical pain, with referral pain characteristics of myofascial TrPs.

Fernandez-de-las-Penas C, Grobli C, Ortega-Santiago R et al. 2012. Referred pain from myofascial trigger points in head, neck, shoulder, and arm muscles reproduces pain symptoms in blue-collar (manual) and white-collar (office) workers. Clin J Pain. 28(6):511-518. "Blue-collar and white-collar workers exhibited a similar number of TrPs in the upper quadrant musculature. The referred pain elicited by active TrPs reproduced the overall pain pattern. The distribution of TrPs was not significantly different between groups. Clinicians should examine for the presence of muscle TrPs in blue-collar and white-collar workers." [TrPs are common in people no matter what type of work they do. DJS]

Fernández-de-Las-Peñas C, Madeleine P, Martínez-Perez A. 2010. Pressure pain sensitivity topographical maps reveal bilateral hyperalgesia of the hands in patients with unilateral carpal tunnel syndrome. Arthritis Care Res (Hoboken). [Mar 16 Epub ahead of print]. “Our findings revealed bilateral generalized pressure pain hyperalgesia in unilateral CTS (carpal tunnel syndrome) since lower PPT (pressure pain threshold) levels were found in all the points. The pressure pain hyperalgesia was not uniformly distributed since PPTs were lower in points over the proximal phalanx of the fingers and the thenar eminency as compared to those points located over the distal phalanx of the fingers. The decrease in PPT levels was associated with the intensity and the duration of the pain symptoms supporting a role of both peripheral and central sensitization mechanisms in this pain condition.”  [TrPs are frequently the cause of symptoms described as “carpal tunnel.”  It is essential to find the cause of the pain and treat that as soon as possible, so that surgery can be avoided. 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, Ortega-Santiago R, Ortíz-Gutierrez R et al. 2014. Widespread Pressure Pain Hypersensitivity in Patients with Multiple Sclerosis with and Without Pain as Sign of Central Sensitization. Clin J Pain. [Feb 12 Epub ahead of print.] "Our study found widespread pressure pain hyperalgesia in individuals with MS as compared to healthy controls. No differences existed between MS patients with pain and those without pain in the presence of widespread pressure sensitivity. Current results suggest that MS is associated with sensory hyper-excitability of the central nervous system or dysfunction in endogenous pain modulatory systems."

Fernandez-de-Las-Penas C, Penacoba-Puente C, Cigaran-Mendez M et al. 2014. Has catechol-O-methyltransferase genotype (Val158Met) an influence on endocrine, sympathetic nervous and humoral immune systems in women with fibromyalgia syndrome? Clin J Pain. 30(3):199-204. "Stress can play an important role in etiology of fibromyalgia syndrome (FMS) by activating the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system (SNS), and altering the immune system. The current study examined the influence of catechol-O-methyltransferase (COMT) Val158Met genotypes on salivary markers of HPA axis (cortisol), SNS (α-amylase), and immune (IgA) systems in women with FMS….The results suggest that women with FMS with the Met/Met genotype exhibit greater disturbed activity of the SNS and humoral immune system. These results provide initial evidence of a link between Val158Met polymorphism and dysfunctions in the SNS and humoral immune system in women with FMS."

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, Russell AS. 2014. Perceived injustice in fibromyalgia and rheumatoid arthritis. Clin Rheumatol. [Mar 4 Epub ahead of print.] "Fibromyalgia is associated with a higher level of perceived injustice than is seen with rheumatoid arthritis. This difference appears to be associated with higher levels of pain reported by fibromyalgia patients, and therefore may not be specific to the diagnosis. Prospective studies may help to resolve this issue."

Ferrari R, Russell AS. 2013. A questionnaire using the Modified 2010 American College of Rheumatology criteria for fibromyalgia: specificity and sensitivity in clinical practice. J Rheumatol. [Jul 1 Epub ahead of print]. "The Modified ACR (American College of Rheumatology) 2010 criteria questionnaire can be used in primary care as a tool to assist physicians in the diagnosis of FM with high specificity and sensitivity. Calculating the total score on a Modified ACR 2010 criteria questionnaire, and setting the value of > 13 as the cutoff for a diagnosis of FM appears to be the most effective approach. The Modified ACR 2010 criteria may reduce the need for rheumatology referral simply for the diagnosis of FM."

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. Massage therapy research review. Complement Ther Clin Pract. 2014 [Aug 1 Epub ahead of print.] "When moderate and light pressure massage have been compared in laboratory studies, moderate pressure massage reduced depression, anxiety and heart rate, and it altered EEG patterns, as in a relaxation response. Moderate pressure massage has also led to increased vagal activity and decreased cortisol levels. Functional magnetic resonance imaging data have suggested that moderate pressure massage was represented in several brain regions including the amygdala, the hypothalamus and the anterior cingulate cortex, all areas involved in stress and emotion regulation. Further research is needed to identify underlying neurophysiological and biochemical mechanisms associated with moderate pressure massage."

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.

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.”

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.”

Fields RD, Araque A, Johansen-Berg H et al. 2013. Glial Biology in Learning and Cognition. Neuroscientist. 2013 Oct 11. [Epub ahead of print] "Neurons are exquisitely specialized for rapid electrical transmission of signals, but some properties of glial cells, which do not communicate with electrical impulses, are well suited for participating in complex cognitive functions requiring broad spatial integration and long-term temporal regulation. Astrocytes, microglia, and oligodendrocytes all have biological properties that could influence learning and cognition. Myelination by oligodendrocytes increases conduction velocity, affecting spike timing and oscillations in neuronal activity. Astrocytes can modulate synaptic transmission and may couple multiple neurons and synapses into functional assemblies. Microglia can remove synapses in an activity-dependent manner altering neural networks. Incorporating glia into a bicellular mechanism of nervous system function may help answer long-standing questions concerning the cellular mechanisms of learning and cognition."

Figueroa J. 2007.  Multidrug therapy including gamma hydroxybuterate as used in the treatment of fibromyalgia and associated anxiety, depression and post traumatic stress disorder.  J Musculoskel Pain 15 (Supp 13):46 item 80.  [Myopain 2007 Poster]  “GHB, when used in a CMTM, can benefit FMS but also anxiety, depression and PTSD.”


Figueroa J, Kobus B. 2007. Tizanidine and tender point pain.  J Musculoskel Pain 15 (Supp 13):46 item 79.  [Myopain 2007 Poster]  “Of the 22 patients, 21 observed a decrease in sleep duration, latency and fragmentation.  Fatigue also decreased.  All 22 patients had a significant decrease in TeP pain [i.e. a mean decrease of 2.09] which was continuous and sustained [mean of 11.9 months].”  “These data suggest combination therapy of tizanidine with analgesic/anti-inflammatory agents benefit sleep and additionally result in reduced TeP pain.”

Fikree A, Aktar R, Grahame R. 2015. Functional gastrointestinal disorders are associated with the joint hypermobility syndrome in secondary care: a case-control study. Neurogastroenterol Motil. 27(4):569-579. "JHS (joint hypermobility syndrome) is significantly associated with FGID functional gastrointestinal disorders, and this subgroup of patients has increased comorbidity and decreased QOL (quality of life). Further research is required to understand the pathophysiological basis of this association."

Fikree A, Grahame R, Aktar R et al. 2014. A Prospective Evaluation of Undiagnosed Joint Hypermobility Syndrome in Patients with Gastrointestinal Symptoms. Clin Gastroenterol Hepatol. [Jan 15 Epub ahead of print.] "Many upper and lower GI symptoms increased with increasing severity of JHS phenotype. Upper GI symptoms were dependent on autonomic and chronic pain factors. JHS is common in GI clinics, with increased burden of upper GI and extraintestinal symptoms and poorer quality of life. Recognition of JHS will facilitate multidisciplinary management of GI and extra-GI manifestations."

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.

Fillingim RB, Bruehl S Dworkin RH et al. 2014. The ACTTION-American Pain Society Pain Taxonomy (AAPT): An Evidence-Based and Multidimensional Approach to Classifying Chronic Pain Conditions. J Pain. 15(3):241-249. "Current approaches to classification of chronic pain conditions suffer from the absence of a systematically implemented and evidence-based taxonomy. Moreover, existing diagnostic approaches typically fail to incorporate available knowledge regarding the biopsychosocial mechanisms contributing to pain conditions. To address these gaps, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) public-private partnership with the U.S. Food and Drug Administration and the American Pain Society (APS) have joined together to develop an evidence-based chronic pain classification system called the ACTTION-APS Pain Taxonomy. This paper describes the outcome of an ACTTION-APS consensus meeting, at which experts agreed on a structure for this new taxonomy of chronic pain conditions. Several major issues around which discussion revolved are presented and summarized, and the structure of the taxonomy is presented. ACTTION-APS Pain Taxonomy will include the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors. In coming months, expert working groups will apply this taxonomy to clusters of chronic pain conditions, thereby developing a set of diagnostic criteria that have been consistently and systematically implemented across nearly all common chronic pain conditions. It is anticipated that the availability of this evidence-based and mechanistic approach to pain classification will be of substantial benefit to chronic pain research and treatment….The ACTTION-APS Pain Taxonomy is an evidence-based chronic pain classification system designed to classify chronic pain along the following dimensions: 1) core diagnostic criteria; 2) common features; 3) common medical comorbidities; 4) neurobiological, psychosocial, and functional consequences; and 5) putative neurobiological and psychosocial mechanisms, risk factors, and protective factors."

Fillingim RB, Gear RW. 2004.  Sex differences in opioid analgesia: clinical and experimental findings. Eur J Pain 8(5):413-425.

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.

Finan PH, Zautra AJ, Davis MC et al. 2010. COMT moderates the relation of daily maladaptive coping and pain in fibromyalgia. Pain. [Dec 2 Epub ahead of print]. "Forty-five women with fibromyalgia (FM) engaged in a 30-day electronic diary assessment, recording daily ratings of pain and 2 forms of maladaptive coping: pain catastrophizing and pain attention. Participants were genotyped for the val(158)met single nucleotide polymorphism (rs4680) in the catechol-O-methyltransferase (COMT) gene. COMT genotype moderated the daily relations of both maladaptive coping processes and pain. FM women with the homozygous met/met genotype evidenced more pain on days when pain catastrophizing was elevated relative to heterozygous and homozygous val(158) carriers. FM women with the homozygous met/met genotype evidenced more pain on days when pain attention was elevated relative to those with the homozygous val/val genotype. Evidence is presented to suggest that these are independent effects. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process, which has been previously characterized in a sample of postoperative shoulder pain patients. Further, the findings advance our understanding of the role of COMT in FM, suggesting that genetic variation in the val(158)met polymorphism may affect FM pain through pathways of pain-related cognition. This study examined 2 forms of maladaptive coping: pain catastrophizing and pain attention. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process and suggest that genetic variation in the val(158)met polymorphism may affect fibromyalgia pain through pathways of pain-related cognition."

Finan PH, Zautra AJ, Davis MC et al. 2010. Genetic influences on the dynamics of pain and affect in fibromyalgia. Health Psychol. 29(2):134-142. “This finding supports a role for catecholamines in positive affective reactivity to FM pain. A gene x experience interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele maintained greater positive affect despite elevations in daily pain than those homozygous for the asn allele. This finding may be explained by the asp allele's role in reward processing. …Together, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.” [We are honing in on some of the genetic combinations that may be involved in subsets of FM central sensitization. DJS]

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.

Fine PG. 1987. Myofascial trigger point pain in children.  J Pediatr. 111(4):547-548. 

Fine PG, Milano R, Hare BD. 1988.  The effects of myofascial trigger point injections are naloxone reversible.  Pain. 32(1):15-20.  “These results demonstrate a naloxone-reversible mechanism in TPI (trigger point injection) therapy.  This suggests an endogenous opioids system as a mediator for the decreased pain and improved physical findings following injection...” of TrPs with local anesthetic.

Fine, PG. 1987.  Myofascial trigger point pain in children.  J Pediatr.111(4):547-548.  This article is noteworthy in that it misidentified myofascial pain syndrome as part of fibromyalgia.  This is too common a mistake.  It does encourage early diagnosis and treatment, but to do that doctors will have to know which condition – or both – are involved.

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.

Fink-Miller EL, Long DM, Gross RT. 2014. Comparing Chronic Pain Treatment Seekers in Primary Care versus Tertiary Care Settings. J Am Board Fam Med. 27(5):594-601. "Patients frequently seek treatment for chronic nonmalignant pain in primary care settings. Compared with physicians who have completed extensive specialization (e.g., fellowships) in pain management, primary care physicians receive much less formal training in managing chronic pain. While chronic pain represents a complicated condition in its own right, the recent increase in opioid prescriptions further muddles treatment….This study sought to determine whether patients with chronic pain in primary care reported less pain, fewer psychological variables related to pain, and lower risk of medication misuse/abuse compared with those in tertiary care….Findings suggest that primary care patients with chronic pain were similar to those in tertiary care on a host of indices and reported more severe pain. There were no significant group differences for risk of medication misuse or abuse…. It seems that primary care physicians care for a complicated group of patients with chronic pain that rivals the complexity of those seen in specialized tertiary care pain management facilities." Free Article

Firmani M, Miralles R, Casassus R. 2014. Effect of lidocaine patches on upper trapezius EMG activity and pain intensity in patients with myofascial trigger points: A randomized clinical study. Acta Odontol Scand. 1-9. "These clinical and EMG results support the use of 5% lidocaine patches for treating patients with MTrP of the upper trapezius muscle."

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

Fischer AA. 1987.  Reliability of the pressure algometer as a measure of myofascial trigger point sensitivity.  Pain. 28(3):411-414.

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 SG, Collins S, Boogaard S et al. 2013. Intravenous magnesium for chronic complex regional pain syndrome type 1 (CRPS-1). Pain Med. [Jul 25 Epub ahead of print]. "Administration of the physiological competitive N-methyl-D-aspartate receptor antagonist magnesium in chronic CRPS (chronic regional pain syndrome) provides insufficient benefit over placebo. Future research should focus on patients with acute CRPS and early signs and symptoms of central sensitization."

Fishbain DA 1, Cole B, Lewis JE et al. 2014. What is the evidence that neuropathic pain is present in chronic low back pain and soft tissue syndromes? An evidence-based structured review. Pain Med. 15(1):4-15. "There is consistent evidence by all methods that NP (neuropathic pain) is present in CLBP and STS. Reported prevalence percentages by all methods are substantial. This has significant implications for the treatment of CLBP and STS."

Fishbain DA, Lewis JE, Cole B et al. 2006.  Lidocaine 5% patch: an open-label naturalistic chronic pain treatment trial and prediction of response.  Pain Med. 7(2):135-142.  This article shows some parameters in predicting the use of lidocaine patch response.  [There is also the necessity to locate the main pain generators.  If someone has a spinal abnormality instigating the TrPs or central sensitization, an articular area that is causing a TrP cascade or central sensitization, or one or two primary TrPs that are setting off others, then the lidocaine patch(es) could be very helpful.  If there are TrPs all over, or diffuse pain with no specific instigator that has been found, the patch may not be a good choice.  One to three patches may be used, and only for 12 hours at a time, with a 12 hour break.  The patient may have to make the choice of being able to sleep, if pain is causing unrestorative sleep or wakefulness, or being able to function during the day. DJS]

Fishbain DA, Cutler RB, Rosomoff HL et al.  2000.  Clonazepam open clinical treatment trial for myofascial syndrome associated chronic pain.  Pain Med. 1(4):332-339.  Clonazepam may help some myofascial pain.

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

Fishbain DA, Lewis JE, Cole B et al. 2006.  Lidocaine 5% patch: an open-label naturalistic chronic pain treatment trial and prediction of response.  Pain Med. 7(2):135-142.  This article shows some parameters in predicting the use of lidocaine patch response.  [There is also the necessity to locate the main pain generators.  If someone has a spinal abnormality instigating the TrPs or central sensitization, an articular area that is causing a TrP cascade or central sensitization, or one or two primary TrPs that are setting off others, then the lidocaine patch(es) could be very helpful.  If there are TrPs all over, or diffuse pain with no specific instigator that has been found, the patch may not be a good choice.  One to three patches may be used, and only for 12 hours at a time, with a 12 hour break.  The patient may have to make the choice of being able to sleep, if pain is causing unrestorative sleep or wakefulness, or being able to function during the day. DJS]

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.  

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.”

Fishman SM, Mahajan G, Jung SW et al. 2002.  The trilateral opioid contract.  Bridging the pain clinic and the primary care physician through the opioid contract.  J Pain Symptom Manage. 24(3):335-344. “We have extended the traditional use of opioid contracts to involve the primary care physician (PCP).  The PCP was asked to collaborate with the pain specialist’s decision to use opioids by cosigning an opioid contract.  Explicit in the agreement was the understanding that the primary care physician would assume prescribing the refills for these medications once the opioid regimen had become stabilized.  In all cases in which a contract was completed, the patient successfully stabilized on an appropriate opioid regimen and then discharged to the care of the PCP for long-term opioid treatment.  The opioid contract made an effective tool for networking specialty and primary care services in…chronic opioid therapy.”  [Too often the physician is neglected as part of the contract, and very often the pain is vastly undertreated.]

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.

Fitzcharles MA, Shir Y Ablin JN et al. 2013. Classification and Clinical Diagnosis of Fibromyalgia Syndrome: Recommendations of Recent Evidence-Based Interdisciplinary Guidelines. Evid Based Complement Alternat Med. 2013:528952. "Guidelines from three continents showed remarkable consistency regarding the clinical concept of FMS, acknowledging that FMS is neither a distinct rheumatic nor mental disorder, but rather a cluster of symptoms, not explained by another somatic disease. While FMS remains an integral part of rheumatology, it is not an exclusive rheumatic condition and spans a broad range of medical disciplines."

Fitzcharles MA, Ste-Marie PA, Goldenberg DL et al. 2013. Canadian Pain Society and Canadian Rheumatology Association recommendations for rational care of persons with fibromyalgia. A summary report. J Rheumatol. [Jul 1 Epub ahead of print]. "These guidelines should provide the health community with reassurance for the global care of patients with FM with the aim of improving patient outcome by reducing symptoms and maintaining function."

Fitzcharles MA, Ste-Marie PA, Goldenberg DL et al. 2013. Canadian guidelines for the diagnosis and management of fibromyalgia syndrome: executive summary. Pain Res Manag. 18(3):119-126.

Fitzcharles MA, Ste-Marie PA, Shir Y et al. 2014. Management of fibromyalgia in older adults. Drugs Aging. 31(10):711-719. "Although the focus symptom of FM is generalized body pain, patients may also experience sleep and mood disturbance, fatigue, and other somatic symptoms leading to the concept of a polysymptomatic condition. In view of prevalent other comorbidities in older patients, FM may be overlooked and management may be neglected, thereby contributing to poor well-being. Pertinent to the older patient is to ensure that the diagnosis of FM is correct and that other conditions are not misdiagnosed as FM. Wherever possible, treatment strategies should emphasize non-pharmacologic interventions that encompass healthy lifestyle habits, with attention to adequate physical activity in particular. Drug treatments should be tailored to the individual needs of the patient, with knowledge that they may offer only a modest effect, but with caution to ensure that adverse effects do not overshadow therapeutic effects."

Fitzgerald MP, Kotarinos R. 2003.  Rehabilitation of the short pelvic floor. I: Background and patient evaluation.  Int Urogynecol J Pelvic Floor Dysfunct. 14(4):261-268. (See next entry)

Fitzgerald MP, Kotarinos R. 2003.  Rehabilitation of the short pelvic floor. II: Treatment of the patient with the short pelvic floor.  Int Urogynecol J Pelvic Floor Dysfunct. 14(4):269-275.  These articles provide options for patient care and help for the diagnoses and treatment of many common but often misdiagnosed pelvic and lower abdominal pain cases.  Care providers are reminded that myofascial TrPs can cause dysfunction such as muscle weakness as well as pain, and many cases of bladder and bowel dysfunction, vulvodynia, and similar ailments may be greatly relieved by TrP treatment.

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."

Flammer J, Konieczka K, Flammer AJ. 2013. The primary vascular dysregulation syndrome: implications for eye diseases. EPMA J. 4(1):14. "Subjects with PVD (primary vascular dysregulation) tend to suffer more often from tinnitus, muscle cramps, migraine with aura and silent myocardial ischaemic and are at greater risk for altitude sickness. While the main cause of vascular dysregulation is vascular endotheliopathy, dysfunction of the autonomic nervous system is also involved. In contrast, SVD occurs in the context of other diseases such as multiple sclerosis, retrobulbar neuritis, rheumatoid arthritis, fibromyalgia and giant cell arteritis. Taking into consideration the high prevalence of PVD in the population and potentially linked pathologies, in the current article, the authors provide recommendations on how to effectively promote the field in order to create innovative diagnostic tools to predict the pathology and develop more efficient treatment approaches tailored to the person."

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.

Fleckenstein J, Zaps D, Ruger LJ et al. 2010. Discrepancy between prevalence and perceived effectiveness of treatment methods in myofascial pain syndrome: Results of a cross-sectional, nationwide survey. BMC Musculoskel Disord. 11(1):32. “Myofascial pain is a common dysfunction with a lifetime prevalence affecting up to 85% of the general population. Current guidelines for the management of myofascial pain are not available. In this study we investigated how physicians on the basis of prescription behavior evaluate the effectiveness of treatment options in their management of myofascial pain…..Effectiveness ratings of the various treatment options between specialties were widely variant. 54.3% of all physicians characterized the available treatment options as insufficient.” “Myofascial pain was estimated a prevalent condition. Despite a variety of commonly prescribed treatments, the moderate effectiveness ratings and the frequent characterizations of the available treatments as insufficient suggest an urgent need for clinical research to establish evidence-based guidelines for the treatment of myofascial pain syndrome.” [We are approaching a stage where the medical community is beginning to recognize that myofascial pain is terribly important across a wide range of medical fields, knowledge of individual TrPs is vital before one can hope to manage complex CMP, it takes a long time to learn TrPs, and the number of care providers trained in myofascial medicine is woefully low.  DJs]

Fleischmann R. 2007.  Primer: establishing a clinical trial unit – regulations and infrastructure.  Nat Clin Pract Rheumatol. 3(4):234-239.  [This comprehensive review would be very helpful for physicians interested in doing a clinical trial. DJS]


Fleury B. 2000.  [Pharyngeal musculature and obstructive sleep apnea syndromes]  Rev Mal Respir. 17 Suppl 3:S15-20. [French]  “The caliber of the pharynx at the soft palate depends on the action of the tensor veli, the palatoglossus, the palatopharyngeus and the uvula muscles.  At the lingual level, the action of the genioglossus and the geniohyoideus predominate.  These different muscle groups contract in coordination before the diaphragm contracts.  Their activity is diminished and disorganized during sleep.  These muscles appear to have a histological composition adapted to short duration intense contractions making them vulnerable to fatigue.  In apneic patients, these muscles are solicited constantly.  Muscular lesions related to overwork have been suggested.”  [Muscle tension can affect sleep apnea.  Myofascial TrPs can affect muscle tension.  Therefore, myofascial TrPs can affect sleep apnea. DJS]

Florian H, Young Jr. J, Haig G et al. 2007.  Pregabalin is effective for the long-term treatment of pain associated with fibromyalgia syndrome: a 1-year, open-label study.  J Musculoskel Pain 15 (Supp 13):47 item 81.  [Myopain 2007 Poster]  “Pregabalin administered for up to 1 year was associated with improvements in FMS-related pain.  Pregabalin was generally well tolerated.”

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]

Fogelman Y, Kent J. 2014. Efficacy of dry needling for treatment of myofascial pain syndrome. J Back Musculoskelet Rehabil. Oct 15. [Epub ahead of print] "Myofascial pain is a major cause of musculoskeletal regional pain. Myofascial pain, which is a high-prevalence but eminently treatable condition, is almost universally underdiagnosed by physicians and undertreated by physical therapy modalities Large numbers of patients can be left suffering in chronic pain for years. Dry needling, also referred to as Intramuscular Stimulation, is a method in the arsenal of pain management which has been known for almost 200 years in Western medicine, yet has been almost completely ignored. With the increase in research in this field over the past two decades, there are many high-quality studies that demonstrate dry needling to be an effective and safe method for the treatment of myofascial pain when diagnosed and treated by adequately-trained physicians or physical therapists. This article provides an overview of recent literature regarding the treatment of myofascial pain syndrome, evidence for the efficacy of dry needling as a central component of its management, and a glimpse at developments in recent imaging methods to aid in the treatment of these problems."

Fong A, Schug SA. 2014. Pathophysiology of pain: a practical primer. Plast Reconstr Surg. 134(4 Suppl 2):8S-14S. "The experience of pain is a subjective one and more than a simple sensation. Pain is commonly defined as an unpleasant sensory and emotional experience due to actual or potential tissue damage or described in such terms. Pain may be broadly classified into physiological and pathological pain. Nociceptive and inflammatory pains are physiological pain states, as they are protective and adaptive, whereas pathological pain is nonprotective and maladaptive. Nociception is the result of suprathreshold stimulation of peripheral nociceptors. Inflammatory pain follows release of various chemical mediators after tissue injury including surgery leading to peripheral sensitization. Nociceptive input is then transmitted to the spinal cord via primary afferents. Modulation of the nociceptive input occurs in the dorsal horn of the spinal cord, influenced by descending inhibitory systems. Central sensitization is a neuromodulatory change that results in the development of secondary hyperalgesia. The modulated nociceptive input then travels up the ascending tracts, mainly via the spinothalamic tract to the thalamus and subsequently to the higher centers of the brain. Pathological pain such as neuropathic pain and central nervous system dysfunctional pain are the result of neuroplasticity of the peripheral and central nervous system. Abnormal ectopic firing of neurons in the absence of a stimulus, increased neuronal hypersensitivity, changes within ion channels, and even alteration in gene expression and changes in the cortical representation are involved in the pathogenesis of these pain states. The development of persistent postsurgical pain is an example for this complex process."

Fontaine KR, Conn L, Clauw DJ. 2010. Effects of lifestyle physical activity on perceived symptoms and physical function in adults with fibromyalgia: results of a randomized trial.  Arthritis Res Ther. 12(2):R55. “Although exercise is therapeutic for adults with fibromyalgia (FM), its symptoms often create obstacles that discourage exercise…. Accumulating 30 minutes of [exercise] throughout the day produces clinically relevant changes in perceived physical function and pain in previously minimally active adults with FM.”  [Exercise must be carefully tailored to the patient’s tolerance, with care given to co-existing conditions such as chronic myofascial pain.  Exercise is a treatment that is free, independent of care-providers, dosage can be personally titrated, and, if done carefully, has limited side-effects.  Patients may have to start at a low dosage and proceed slowly, but one must start and one must proceed.  Exercise benefits are not gained by watching exercise tapes. 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 Res 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.”

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 A, Laffray S, Pizzoccaro A et al. 2014. T-type calcium channels in chronic pain: mouse models and specific blockers. Pflugers Arch. 466(4):707-717. "Pain is a quite frequent complaint accompanying numerous pathologies. Among these pathological cases, neuropathies are retrieved with identified etiologies (chemotherapies, diabetes, surgeries…) and also more diffuse syndromes such as fibromyalgia. More broadly, pain is one of the first consequences of the majority of inherited diseases. Despite its importance for the quality of life, current pain management is limited to drugs that are either old or with a limited efficacy or that possess a bad benefit/risk ratio. As no new pharmacological concept has led to new analgesics in the last decades, the discovery of medications is needed, and to this aim the identification of new druggable targets in pain transmission is a first step. Therefore, studies of ion channels in pain pathways are extremely active. This is particularly true with ion channels in peripheral sensory neurons in dorsal root ganglia (DRG) known now to express unique sets of these channels. Moreover, both spinal and supraspinal levels are clearly important in pain modulation. Among these ion channels, we and others revealed the important role of low voltage-gated calcium channels in cellular excitability in different steps of the pain pathways. These channels, by being activated nearby resting membrane potential have biophysical characteristics suited to facilitate action potential generation and rhythmicity. In this review, we will review the current knowledge on the role of these channels in the perception and modulation of pain."

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

Frange C, Hirotsu C, Hachul H et al. 2014. Fibromyalgia and sleep in animal models: a current overview and future directions. Curr Pain Headache Rep.18(8):434. "Sleep disorders are highly prevalent in patients with fibromyalgia (FM). Many of the daytime symptoms, such as chronic pain and fatigue, may be related to the non-restorative sleep patterns associated with the disease. Pain influences the sleep process and sleep disturbances decrease the pain threshold in a reciprocal framework. Thus, understanding the link between sleep and FM has become an important research topic in basic science. Therefore, in the current review we connect these topics and provide some insights into the cyclic relationship between sleep and pain, which has been addressed mainly in animal models. Additionally, we highlight the urgent need for sleep studies in FM animal models, which might improve the knowledge base and accelerate advances in this field."

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]

Franken P, Chollet D, Tafti M. 2001.  The homeostatic regulation of sleep need is under genetic control.  Jour of Neuroscience 21(8):2610-2621.

Fredheim OM, Borchgrevink PC, Klepstad P et al. 2007.  Long term methadone for chronic pain: a pilot study of pharmacokinetic aspects. Eur J Pain. 11(6):599-604.  This study showed that a 3-day switch from morphine to methadone, followed by a week-long titration period, is a pharmaceutically sound way of moving chronic non-malignant pain patients from morphine to methadone.


Fredheim OM, Borchgrevink PC, Klepstad P et al. 2006.  Long term methadone for chronic pain: a pilot study of pharmacokinetic aspects.  [Nov 16 Epub ahead of print] Eur J Pain  “...a 3-day opioid switch from morphine to methadone followed by a one week titration seems pharmacologically sound.”  These patients had chronic non-malignant pain.  Methadone serum concentrations did not change significantly from dose titration through 9 months therapy.

Fredheim OM, Borchgrevink PC, Mahic M et al. 2013. A pharmacoepidemiological cohort study of subjects starting strong opioids for nonmalignant pain: A study from the Norwegian Prescription Database. Pain. [Sep 24 Epub ahead of print]. "Clinical studies of short duration have demonstrated that strong opioids improve pain control in selected patients with chronic nonmalignant pain. However, high discontinuation rates and dose escalation during long-term treatment have been indicated. The aim of the present study was to determine discontinuation rates, dose escalation, and patterns of co-medication with benzodiazepines. The Norwegian Prescription Database provides complete national data at an individual level on dispensed drugs. A complete national cohort of new users of strong opioids was followed up for 5 years after initiation of therapy with strong opioids. Of the 17,248 persons who were new users of strong opioids in 2005, 7229 were dispensed a second prescription within 70 days and were assumed to be intended long-term users. A total of 1233 persons in the study cohort were still on opioid therapy 5years later. This equals 24% of the study cohort who were still alive. Of the participants, 21% decreased their annual opioid dose by 25% or more, whereas 21% kept a stable dose (±24%) and 34% more than doubled their opioid dose from the first to the fifth year. High annual doses of opioids were associated with high annual doses of benzodiazepines at the end of follow-up. It is an issue of major concern that large dose escalation is common during long-term treatment, and that that high doses of opioids are associated with high doses of benzodiazepines. These findings make it necessary to question whether the appropriate patient population receives long-term opioid treatment." [Benzodiazepines reduce the efficiency of opioids for pain control. Are doctors not aware of this? 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.

Fredheim OM, Kaasa S, Fayers P et al. 2008.  Chronic non-malignant pain patients report as poor health-related quality of life as palliative cancer patients.  Acta Anaesthesiol Scand. 52(1):143-148.


Fredheim OM, Kaasa S, Fayers P et al. 2007.  Chronic non-malignant pain patients report as poor health-related quality of life as palliative cancer patients.  Acta Anaesthesiol Scand. [Nov 13 Epub ahead of print].  “CNMP patients admitted to multidisciplinary pain centres report significantly reduced HRQoL, in addition to severe pain.  They consider their HRQoL to be as poor as HRQoL reported from dying cancer patients and substantially poorer than national norms.”  [This leaves one to wonder about the ethics of having a substantial group of patients, those with chronic non-cancer pain, with a quality of life lower than terminal cancer patients.  How can any system allow this situation, and what will it take to improve it?  DJS]

Fredheim OM, Mahic M, Skurtveit S et al. 2014. Chronic pain and use of opioids: A population-based pharmacoepidemiological study from the Norwegian prescription database and the Nord-Trondelag health study. Pain. [Mar 15 Epub ahead of print.] "The study showed that most people having chronic nonmalignant pain are not using opioids, even if the pain is strong or very strong. However, the vast majority of patients with persistent opioid use report strong or very strong pain in spite of opioid treatment." [This should not be interpreted to mean that opioids do not help chronic pain. In this increasingly wary culture, many chronic pain patients are denied access to adequate opioid pain medications. Opioids should not be used as the only treatment, but can be a logical part of the management of some chronic pain treatment plans. Efforts also must be made to treat the cause of the pain, such as myofascial trigger points, and the perpetuating factors of that cause. Doctors and other care providers who are involved in any pain management must be trained in the diagnosis and treatment of the most common cause of musculoskeletal pain; myofascial trigger points. DJS]

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.

Freeman MD, Nystrom A, Centeno C. 2009.  Chronic whiplash and central sensitization; an evaluation of the role of a myofascial trigger point in pain modulation.  J Brachial Plex Peripher Nerve Inj. 4:2.  “Conclusion: the present data suggest that myofascial trigger points serve to perpetuate lowered pain thresholds in uninjured tissues.”   [This study indicates that TrPs perpetuate central sensitization (FM).  The effects of TrP treatment on lowered pain thresholds were temporary, perhaps because the perpetuating factors and follow-up treatment did not occur.  The authors contemplated surgical removal or ablation of TrPs, which is not logical considering the physiology of TrP formation, and it is hoped that the authors will study the Travell and Simons texts and current research before continuing to treat myofascial pain.  Trauma, including surgery, can be an initiator and perpetuator of TrPs and could promote further chronic pain. DJS]


Fregni F, Gimenes R, Valle AC et al. 2006.  A randomized, sham-controlled, proof of principle study of transcranial direct current stimulation for the treatment of pain in fibromyalgia.  Arthritis Rheum. 54(12):3988-3998.  “Our findings provide initial evidence of a beneficial effect of tDCS in fibromyalgia, thus encouraging further trials.”


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]

Fries E, Hesse J, Hellhammer J et al. 2005.  A new view on hypocortisolism.  Psychoneuroendocrinology [Epub ahead of print June 8].  “Low cortisol levels have been observed in patients with different stress-related disorders such as chronic fatigue syndrome, fibromyalgia, and post-traumatic stress disorder.  We propose that the phenomenon of hypocortisolism may occur after a prolonged period of hyperactivity of the hypothalamic-pituitary-adrenal axis due to chronic stress as illustrated in an animal model.  Despite symptoms such as pain, fatigue and high stress sensitivity, hypocortisolism may also have beneficial effects on the organism.”

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.

Fruth SJ. 2006.  Differential diagnosis and treatment in a patient with posterior upper thoracic pain. Phys Ther. 86(2):254-268.  “This case suggests that CV/CT mobilizations and active TrP release may have been beneficial in reducing pain and restoring function in this patient.”  This case is interesting in that myofascial dysfunction occurred after a 35-year old man had been on the  bleachers at a hockey game for 3 hours. Two days later he had pain in the right scapular area and spine that increased during the next 6 weeks. He had considerable pain, lost some function and range of motion and had difficulty sleeping due to movement-triggered pain. He was subjected to weeks of physical therapy including spine mobilization, and given many expensive radiological tests. After months of this, trigger points were found in multiple area muscles. After 4 weeks of specific treatment the patient had full return to function. [How much pain is needless, and how much time and other resources are wasted, because we do not have care providers who are adequately trained in the diagnosis and treatment of myofascial TrPs? DJS]

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.

Fulle S., Mecocci P., Fano G., Vecchiet I., Vecchini A., Racciotti D., Cherubini A., Pizzigallo E., Vecchiet, Senin U., Beal M.F. 2000.  Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome. Free Radic Biol Med 29(12):1252-9. Patients with chronic fatigue syndrome have differences in muscle membranes, fluidity and fatty acid composition compared to patients with fibromyalgia and healthy patients.


Furlan AD, Sandoval JA, Mailis-Gagnon A et al. 2006.  Opioids for chronic non-cancer pain: a meta-analysis of effectiveness and side effects.  CMAJ 174(11):1589-1594.  “Weak and strong opioids outperformed placebo for pain and function in all types of CNCP.  Other drugs produced better functional outcomes than opioids, whereas for pain relief they were outperformed only by strong opioids.  Despite the relative shortness of the trials, more than one-third of the participants abandoned treatment.”   This study included patients with fibromyalgia.  “Among the side effects for opioids, only constipation and nausea were clinically and statistically significant.”

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. 2014. The Gut Microbiome and the Brain. J Med Food. 17(12):1261-1272. "The human gut microbiome impacts human brain health in numerous ways: (1) Structural bacterial components such as lipopolysaccharides provide low-grade tonic stimulation of the innate immune system. Excessive stimulation due to bacterial dysbiosis, small intestinal bacterial overgrowth, or increased intestinal permeability may produce systemic and/or central nervous system inflammation. (2) Bacterial proteins may cross-react with human antigens to stimulate dysfunctional responses of the adaptive immune system. (3) Bacterial enzymes may produce neurotoxic metabolites such as D-lactic acid and ammonia. Even beneficial metabolites such as short-chain fatty acids may exert neurotoxicity. (4) Gut microbes can produce hormones and neurotransmitters that are identical to those produced by humans. Bacterial receptors for these hormones influence microbial growth and virulence. (5) Gut bacteria directly stimulate afferent neurons of the enteric nervous system to send signals to the brain via the vagus nerve. Through these varied mechanisms, gut microbes shape the architecture of sleep and stress reactivity of the hypothalamic-pituitary-adrenal axis. They influence memory, mood, and cognition and are clinically and therapeutically relevant to a range of disorders, including alcoholism, chronic fatigue syndrome, fibromyalgia, and restless legs syndrome. Their role in multiple sclerosis and the neurologic manifestations of celiac disease is being studied. Nutritional tools for altering the gut microbiome therapeutically include changes in diet, probiotics, and prebiotics."

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.

Gambi F, DeBerardis D, Sepede G et al. 2005.  Cannabinoid receptors and their relationships with neuropsychiatric disorders.  Int J Immunopathol Pharmacol. 18(1):15-20.  “The endocannabinoids may represent the first members of a new class of neuromodulators that are not stored in cell vesicles, but rather synthesized by the cell on demand.  The endogenous cannabinoid system could play a central role in several neuropsychiatric disorders and is also involved in other conditions such as pain, spasticity and neuroprotection.”


Gandhi R, Ryals JM, Wright DE. 2004.  Neurotrophin-3 reverses chronic mechanical hyperalgesia induced by intramuscular acid injection.  J Neurosci. 24(42):9405-9413.  “NT-3 (neurotrophine-3) may suppress events that lead to secondary hyperalgesia triggered by insult to muscle afferents.”


Gangi, S. and O. Johansson. 2000. A theoretical model based on mast cells and histamine to explain the recent proclaimed sensitivity to electric and/or magnetic fields in humans. Med Hypos 54(4):663-671. Electromagnetic energy can activate mast cells, a type of connective tissue cell, causing the release of a number of informational substances including hyaluronic acid, vasoactive intestinal polypeptide (VIP, a substance which has been implicated in keeping our HPA-axis in the "fight or flight" stress mode), histamine (which can add to swelling, itching, pain, allergic manifestations and hypersensitivity,) and cause other cells to release somatostatin (which can enhance sensations of inflammation and light sensitivity).

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.

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.  “...mast cells have a direct and potentiating role in skin remodeling and fibrosis.”  [Excess histamine in the system, from allergy, fibromyalgia imbalance, myofascial TrP twitch response, and/or other reasons may directly affect the formation of adhesion and scar tissue.  DJS]

Garcia,  J. and R. D. Altman. 1997
a.  Chronic pain states: invasive procedures. Semin Arthritis Rheum 27(3):156-160.  
b.  Chronic pain states: pathophysiology and medical therapy.  Semin Arth Rheum 27(1):1-16.  

Garcia JJ, Ortega E. 2014. Soluble fractalkine in the plasma of fibromyalgia patients. An Acad Bras Cienc. Dec 9;0:0. [Epub ahead of print.] "Fibromyalgia is a form of non-articular rheumatism in which inflammatory cytokines seem to be involved. However, there is still no analytical specific diagnostic criterion for this disease. The aim was to examine a possible role of fractalkine as a biomarker in fibromyalgia. Plasma levels of soluble fractalkine were compared between women diagnosed with fibromyalgia (n=17) and healthy women (n=10) as controls. Fractalkine released by monocytes was also evaluated. Fibromyalgia patients showed lower plasma fractalkine than healthy women. Since most inflammatory pathologies show elevated plasma levels of soluble fractalkine, the results may contribute towards a differential diagnosis for fibromyalgia." Free Article

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]

Garrido-Maraver J, Cordero MD, Oropesa-Avila M et al. 2014. Clinical applications of coenzyme Q. Front Biosci (Landmark Ed). 19:619-33. "Coenzyme Q (Co Q or ubiquinone) was known for its key role in mitochondrial bioenergetics as electron and proton carrier; later studies demonstrated its presence in other cellular membranes and in blood plasma, and extensively investigated its antioxidant role. These two functions constitute the basis for supporting the clinical indication of Co Q. Furthermore, recent data indicate that Co Q affects expression of genes involved in human cell signaling, metabolism and transport and some of the effects of Co Q supplementation may be due to this property. Co Q deficiencies are due to autosomal recessive mutations, mitochondrial diseases, ageing-related oxidative stress and carcinogenesis processes, and also a secondary effect of statin treatment. Many neurodegenerative disorders, diabetes, cancer, fibromyalgia, muscular and cardiovascular diseases have been associated with low Co Q levels. Co Q treatment does not cause serious adverse effects in humans and new formulations have been developed that increase Co Q absorption and tissue distribution. Oral Co Q treatment is a frequent mitochondrial energizer and antioxidant strategy in many diseases that may provide a significant symptomatic benefit."

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]

Garza-Villarreal EA, Wilson AD, Vase L et al. 2014. Music reduces pain and increases functional mobility in fibromyalgia. Front Psychol. 5:90. "Twenty-two FM patients were passively exposed to (1) self-chosen, relaxing, pleasant music, and to (2) a control auditory condition (pink noise). They rated pain and performed the "timed-up & go task (TUG)" to measure functional mobility after each auditory condition. Listening to relaxing, pleasant, self-chosen music reduced pain and increased functional mobility significantly in our FM patients. The music-induced analgesia was significantly correlated with the TUG scores; thereby suggesting that the reduction in pain unpleasantness increased functional mobility. Notably, this mobility improvement was obtained with music played prior to the motor task (not during), therefore the effect cannot be explained merely by motor entrainment to a fast rhythm. Cognitive and emotional mechanisms seem to be central to music-induced analgesia. Our findings encourage the use of music as a treatment adjuvant to reduce chronic pain in FM and increase functional mobility thereby reducing the risk of disability."

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, Arendt-Nielsen L. 2006.  Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain.  Clin Neurophysiol.  [May 29 Epub ahead of print]  Myofascial pain can cause sympathetic system facilitation, and this sensitization factor must be considered when determining evaluation and treatment.

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, 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, Monterde S, Graven-Nielsen T et al. 2014. Latent myofascial trigger points are associated with an increased intramuscular electromyographic activity during synergistic muscle activation. J Pain. 15(2):181-7. "The aim of this study was to evaluate intramuscular muscle activity from a latent myofascial trigger point (MTP) in a synergistic muscle during isometric muscle contraction. Intramuscular activity was recorded with an intramuscular electromyographic (EMG) needle inserted into a latent MTP or a non-MTP in upper trapezius at rest and during isometric shoulder abduction at 90° performed at 25% of maximum voluntary contraction in 15 healthy subjects. Surface EMGs were recorded from the middle deltoid muscle, upper-, middle-, and lower- parts of the trapezius muscle. Maximal pain intensity and referred pain induced by EMG needle insertion and maximal pain intensity during contraction were recorded on a visual analogue scale (VAS). The results showed that higher VAS scores were observed following needle insertion and during muscle contraction for latent MTPs than non-MTPs…. The intramuscular EMG activity in the upper trapezius muscle was significantly higher at rest and during shoulder abduction at latent MTPs compared with non-MTPs…. This study provides evidence that latent MTPs are associated with increased intramuscular, but not surface, EMG amplitude of synergist activation. The increased amplitude of synergistic muscle activation may result in incoherent muscle activation pattern of synergists inducing spatial development of new MTPs and the progress to active MTPs." [This study shows one way in which TrPs can develop satellite TrPs, and myofascial trigger point pain and dysfunction can spread to muscles recruited by TrP-weakened muscles to help them. The newly recruited muscles, now also overworked doing tasks they were not designed to do, then need other muscles to help them perform their tasks. This can lead to the false impression of the presence of a progressive illness. DJS]

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, 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, Danneskiold-Samsoe B et al. 2009.  The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points.  J Pain. [Nov 13 Epub ahead of print]  “The current study provides first evidence that pain from active MTrPs at TP sites mimics fibromyalgia pain.  MTrPs may relate to generalized increased sensitivity in FMS due to central sensitization.”  “…This article underlies the importance of active MTrPs in FMS patients.  Most of the TP sites in FMS are MTrPs.  Active MTrPs may serve as a peripheral generator of fibromyalgia pain and inactivation of active MTrPs may thus be an alternative for the treatment of FMS.”  [It is very good to have such fine research confirm that TrPs themselves can be the cause or maintainer of much FM pain, and that one cannot adequately treat FM without being able to diagnose and treat co-existing TrPs. DJS]

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, Garcia CO, Molina JF et al. 2000.  Fibromyalgia syndrome: experience in a pediatric rheumatology clinic.  Clin Exp Rheumatol 18(3):415-419.

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.”

Geib RW, Roberts BL, Li H et al. 2013. Using posturography to assess expertise among tai chi practitioners – biomed. Biomed Sci Instrum. 49:195-200. "While standing, participants performed a series of movements from the Tai Chi for Arthritis form based on Sun style (commencement, open/close, single whip and wave hands in cloud). Master trainers and senior trainers were considered experts; all others were considered non-experts. Body sway was assessed....While standing, the experts displayed statistically greater displacement excursion and velocity when performing commencement and wave hands in clouds forms. The results of this pilot study indicated that posturography may be a useful method to assess the quality of Tai Chi movements and potentially link the expertise of Tai Chi practitioners to changes in health related outcomes."

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.

Geranton SM, Tochiki KK. 2015. Regulation of gene expression and pain states by epigenetic mechanisms. Prog Mol Biol Transl Sci. 131:147-183. "The induction of inflammatory or neuropathic pain states is known to involve molecular activity in the spinal superficial dorsal horn and dorsal root ganglia, including intracellular signaling events which lead to changes in gene expression. These changes ultimately cause alterations in macromolecular synthesis, synaptic transmission, and structural architecture which support central sensitization, a process required for the establishment of long-term pain states. Epigenetic mechanisms are essential for long-term synaptic plasticity and modulation of gene expression. This is because epigenetic modifications are known to regulate gene transcription by aiding the physical relaxation or condensation of chromatin. These processes are therefore potential regulators of the molecular changes underlying permanent pain states. A handful of studies have emerged in the field of pain epigenetics; however, the field is still very much in its infancy. This chapter draws upon other specialties which have extensively investigated epigenetic mechanisms, such as learning and memory and oncology. After defining epigenetics as well as the recent field of "neuroepigenetics" and the main molecular mechanisms involved, this chapter describes the role of these mechanisms in the synaptic plasticity seen in learning and memory, and addresses those epigenetic mechanisms that have been linked with the development of acute and prolonged pain states. Finally, the idea that long-lasting epigenetic modifications could contribute to the transition from acute to chronic pain states by supporting maladaptive molecular changes is discussed."

Gerber LH, Shah J, Rosenberger W et al. 2015. Dry Needling Alters Trigger Points in the Upper Trapezius Muscle and Reduces Pain in Subjects With Chronic Myofascial Pain. PM R. [Feb 4 Epub ahead of print.] "Dry needling reduces pain and changes MTrP status. Change in trigger point status is associated with a statistically and clinically significant reduction in pain. Reduction of pain is associated with improved mood, function, and level of disability."

Gerber LH, Sikdar S, Armstrong K et al. 2013. A Systematic Comparison Between Subjects with No Pain and Pain Associated with Active Myofascial Trigger Points. PM R. 5(11):931-938. "We evaluated adults with MPS and active (painful) MTrPs and those without pain. Subjects in the "Active" ('A') group had at least one active MTrP with spontaneous pain which was persistent, lasted more than 3 months and had characteristic pain on palpation. Subjects in the "No pain" ('Np') group had no spontaneous pain. However, some had discomfort on MTrP palpation (latent MTrP) while others in the Np group had no discomfort on palpation of nodules or had no nodules….Each participant underwent range of motion (ROM) measurement, 10-point manual muscle test, and manual and algometric palpation. The latter determined the pain/pressure threshold using an algometer of 4 pre-determined anatomical sites along the upper trapezius. Participants rated pain using a verbal analogue scale (0-10); completed the Brief Pain Inventory and Oswestry Disability Scale (ODS), which included a sleep sub-scale; Short Form 36(SF36) and the Profile of Mood States (POMS)….There were 24 in the 'A' group (mean 36yrs, 16 women) and 26 in the 'Np' group (mean 26yrs, 12 women). Subjects in group 'A' differed from 'Np' in number of latent MTrPs…; asymmetrical cervical ROM…; in all pain reports…; algometry…; POMS…; SF36…and ODS….A systematic musculoskeletal evaluation of people with MPS reliably distinguishes them from subjects with no pain. The two groups are significantly different in their physical findings and self-reports of pain, sleep disturbance, disability, health status and mood. These findings support the view that a "local" pain syndrome has significant associations with mood, health-related quality of life and function."

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, Ghafouri B, Ernberg M et al. 2014. Chronic musculoskeletal pain: review of mechanisms and biochemical biomarkers as assessed by the microdialysis technique. J Pain Res.7:313-326. "These results indicate that peripheral muscle alterations are parts of the activated pain mechanisms in common chronic pain conditions. Muscle alterations have been reported in fibromyalgia syndrome and chronic widespread pain, but more studies are needed before definite conclusions can be drawn. For other substances, results are inconclusive across studies and patient groups."

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, Larsson B, Forsberg F et al. 2013. Chronic Widespread Pain: Increased Glutamate and Lactate Concentrations in the Trapezius Muscle and Plasma. Clin J Pain. [Jul 24 Epub ahead of print]. "The present study supports the suggestion that aspects of pain and central alterations in CWP/FM are influenced by peripheral tissue alterations."

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. 2013. Are peripheral pain generators important in fibromyalgia and chronic widespread pain? Pain Medicine. 14:777-778. "Pain is not a simple sensation, and is rarely the result of a disorder in one system only. It is complex, involving multiple interactions. CWPS and FM cannot be considered to be solely a disorder of central pain modulation, and perhaps not even primarily so. Pain is the outcome of a complex interplay between the central modulation and peripheral pain input. That balance between inhibition and facilitation of incoming pain impulses determines the pain that we experience, as shown when descending pain modulation shifts from inhibition to facilitation following sustained isometric contraction sufficient to cause muscle nociception in FM patients."

Gerwin R. 2012. Botulinum Toxin Treatment of Myofascial Pain: A Critical Review of the Literature. Curr Pain Headache Rep. [Jul 10 Epub ahead of print]. "This is a review of literature relevant to the treatment of myofascial pain syndrome by botulinum injections. The objective is to critically review the studies to see if they are appropriately designed, conducted, and interpreted to provide guidance in the management of myofascial pain. The intent is to better understand the mixed results that these studies have provided. A search was made utilizing PubMed for literature relevant to the use of botulinum toxin in the treatment of myofascial pain. All identifiable series were reviewed, including open label, single-blinded and double-blinded studies, randomized and controlled, or not. In general, small case series of only a few patients were not included unless they made a relevant point and there were no available randomized studies or larger studies.... Problems that were common to the studies were robust placebo responders, incomplete treatment of a regional myofascial pain syndrome, inappropriate or confounding control populations or treatments, and inappropriate time periods for assessment of outcomes, or misinterpretation of the time-frame of action of botulinum toxin. The studies of the effect of botulinum toxin treatment of myofascial trigger points have had mixed results. However, few studies have been designed to avoid many of the pitfalls associated with a trial of botulinum toxin treatment of trigger points. Better-designed studies may give results that can be used to guide practice based on reliable evidence. At the present time, one must conclude that the available evidence is insufficient to guide clinical practice."

Gerwin R. 2010. Myofascial pain syndrome: here we are; where must we go? J Musculoskel Pain. 18(4):329-347.

"MPS was first defined clinically by Janet Travell, MD, and later by David Simons, MD. Pain neurophysiology has only recently provided the basis for understanding the sensorimotor manifestations of MPS. This article reviews the current state of knowledge concerning MPS. MPS is a form of myalgia characterized by local regions of muscle hardness and tenderness that cause referred pain. The signature feature is the trigger point, a tender, taut band of muscle that can be painful spontaneously or when stimulated. The active trigger point has identifiable pathophysiologic changes. Levels of substance P, calcitonin gene related peptide, bradykinin, and assorted cytokines, are elevated, indicating a chemical inflammation. Trigger point milieu pH is low, about pH 5, consistent with hypoxia and ischemia. Persistent, low-amplitude, high-frequency electrical discharges that look like endplate potentials characteristic. The taut band can be visualized using high definition ultrasonograpy and magnetic resonance sonography. Central scanning. The role of MPS in headache and pelvic pain has been extensively studied in the last few years. Although great progress has been made, studies are still needed to substantiate the energy crisis hypothesis of trigger point formation, to understand the nature of sustained muscle contraction that forms the taut band and of referred pain in humans, and to develop a more rationale and effective treatment."
"Nociceptive activity from TrPs activates spinal cord dorsal horn neurons and sensitizes the central nervous system, causing central sensitization, hyperalgesia, and referred pain. Muscle weakness without atrophy occurs due to TrP-induced motor inhibition. Restricted range of motion occurs because of the shortening of the contracted taut band, and perhaps because of pain. The range of motion in hypermobile individuals must be interpreted cautiously, because it can appear to be normal, but can still be restricted. Impaired reciprocal inhibition results in co-contraction of agonists and antagonists, thus interfering with fine motor control and coordination. Autonomic disturbances can accompany TrP activation leading to changes in skin temperature and color, piloerection (goosebumps), and lacrimation (tearing)….The clinically evident progression from a non-tender taut band to a tender taut band suggests that the first change in muscle is the development of the contracted, taut group of muscle fibers that can become painful when sufficiently stressed."
"Myofascial pain syndrome presents as acute and chronic muscle pain….It may be regional or widespread. It may be accompanied by a sensory component of parasthesias or dysesthesias. MPS may persist long after the initiating cause of pain has resolved. Thus, myofascial pain can be complex." "Muscles harboring a TrP are often weak. Weakness in affected muscles occurs without atrophy, and is not neuropathic or myopathic. It is rapidly reversible immediately on inactivation of the TrP, suggesting that it is caused by the inhibition of muscle action….a TrP in one muscle can inhibit effort or contractile force in another muscle." "The TrP causes a disordered recruitment of muscles that work together to produce an action." "Reciprocal inhibition, whereby contraction of one muscle is inhibited by the contraction of its antagonist muscle, is reduced or absent when the activated muscle contains a TrP. The lack of reciprocal inhibition causes co-contraction that reduces the quality of movement and leads to clumsiness and an incoordination of fine movement." "The range of motion around a joint moved by muscles with TrPs is often limited. The end range may be painful, but limitation of the range may be painless unless the patient is pushed to move beyond comfort. Limitation of range of motion is not a reliable indicator of the presence of a TrP in persons who are hypermobile…. Changes in spatial distribution also occur with muscle contraction, the changes correlating with the duration of contraction. This suggests that a more long-lasting nociceptive irritant like a TrP would also cause a functional spatial reorganization of muscle activity….The TrP is a tender focus in muscle, the region of tenderness always located on the taut band. The region of greatest hardness is usually also the region of greatest tenderness. A tender TrP always means that there is hyperalgesia or allodynia."
"Miniature endplate potentials are thought to be the result of spontaneous release of acetylcholine from motor nerve potentials….It is now clear that motor endplates are more widely distributed throughout the muscle than just the endplate zone….A greater endplate activity and consequently greater focal muscle sarcomere compression can be thought of as being associated with greater local muscle injury and local release of nociceptive substances." "It is likely that TrPs are first formed as latent TrPs and then become tender as muscle is activated. Latent TrPs exist without spontaneous pain. Furthermore, TrP tenderness does not occur except in regions of muscle hardness, but regions of muscle hardness occur without local or referred pain. Hence, muscle hardness or the taut band that occurs in the absence of pain may be the first abnormality, and the active TrP is a more activated TrP." "Current thinking in keeping with the expanded integrated hypothesis of the TrP is that localized ischemia is associated with the acute development and maintenance of the TrP. Localized ischemia results from capillary compression within the taut band. In turn, the release of vasodilating substances such as calcitonin gene-related peptide (CGRP) and substance P leads to localized non-inflammatory edema that further compresses capillaries. The initial change in the muscle associated with the TrP seems to be a motor abnormality, the development of the taut band."
"Sympathetic modulation of the SEA is the most important concept because of the important role the sympathetic nervous system plays in maintaining the abnormal electrical activity at the TrP. A post-synaptic muscle dysfunction that increases intracellular calcium concentration through a leaky ryanidine receptor calcium channel on the sarcoplasmic reticulum membrane or through adrenergic-mediated second-messenger systems involving protein kinase C and cyclic adenosine monophosphate (cAMP), initiating actin-myosin interaction, may also result in muscle fibril contraction….Calcium channel activity is important in the generation of TrP endplate noise…." "The association of endplate noise and the trigger zone has led to the suggestion that the trigger zone is where the endplate zone is located and that is in mid-belly of the muscle. However, the muscle mid-belly is not always obvious and depends on the specific anatomy of the muscle." "The myofascial trigger zone or region is hypoxic, a region of severe oxygen desaturation at the core surrounded by a region of increased oxygenation, consistent with capillary compression and ischemia. The core is ischemic and the surrounding zone hyperemic. Temperature studies of the trigger zone showed an increase in temperature in the TrP region, consistent with a hyperemic outer area but inconsistent with a hypoxic trigger zone core." "TrP tenderness is associated with central sensitization and hypersensitivity, as is the case with other tissues….Central sensitization is the mechanism through which referred pain occurs….One of the consequences of central sensitization is the activation of otherwise ineffective (sometimes called 'sleeping') synaptic connections from one afferent nerve fiber to many recipient nociceptive neurons. A single dorsal horn neuron will thus respond to a larger pool of afferent fiber connections, thereby greatly expanding its receptive field." "The most common referred pain patterns are within the same or adjacent spinal segments as that of the primary sensory nerve. Thus, TrPs in muscles innervated predominantly by the C5 nerve root refer pain largely to the C5 dermatome and myotome, overlapping into the C4 and C6 innervated areas. Because muscle innervation is relatively constant, segmental referred pain patterns tend to be relatively constant from one person to another….The activation of latent TrPs in one muscle results in increased motor activity in a distant muscle latent TrP in the same segmental level." "The segmental spread of referred pain can also be bilateral." "In summary, central sensitization and widespread pain referral is clinically important because individuals who have had seemingly local injury producing persistent pain can develop extraordinarily widespread pain with hyperalgesia or allodynia that appears to involve most of the body." "The proposal discussed herein is that muscle overuse, or bio-mechanical stress, is the cause of the TrP….Supramaximal muscle contraction or overloaded eccentric contraction can damage muscle and lead to pain, including delayed onset muscle soreness. Repetitive strain is a variant of muscle overload and is thought to have the same effect….The maintenance of fixed positions for long periods of time and sustained contraction of muscle as a result of emotional stress (anxiety, fear, and depression) are also thought to produce muscle overuse….There has long been a concern about the overlap of FMS and MPS, a concern now resolved with the understanding that FMS is a central pain disorder and MPS has a major central hypersensitization component. Therefore, it is not surprising that there are TrPs at many if not all of the sites selected for tender point assessment in FMS and that TrPs present as a comorbid finding in FMS can contribute to pain in FMS. Thus, the concurrence of the two conditions in individual patients with clinical pain syndromes is to be expected. Nearly one-quarter of patients with chronic cervical myofascial pain met the criteria for FMS. An earlier study found that 75 percent of subjects with FMS had clinically significant MPS. TrPs may be a peripheral pain generator initiating or sustaining FMS, or may occur secondarily to the development of central sensitization in FMS. No study has looked at the effect of treating TrPs on comorbid FMS."
"….the hyperirritable "nodule" does not have to be a palpable nodule at all. However, the taut band is a constant finding in active and latent TrPs, and is the only consistent objective finding on physical examination." "Dommerholt and Gerwin (unpublished data) found that identification of a taut band, tenderness of the taut band, and reproduction of the patient's pain were sufficient to guide effective treatment and presented this concept at the International Myopain Congress in Italy in 1998." [This is the International Myopain President's Address from the Myopain Congress 2010, and it is dedicated to David G. Simons MD. I believe Dr. Simons is very proud of it. It is strongly suggested that interested readers obtain the whole article from Journal of Musculoskeletal Pain. In my opinion, this is the best summary of myofascial medicine available. DJS]

Gerwin RD. 2014. Diagnosis of Myofascial Pain Syndrome. Phys Med Rehabil Clin N Am. 25(2):341-355. "Myofascial pain is one of the most common causes of pain. The diagnosis of myofascial pain syndrome (MPS) is made by muscle palpation. The source of the pain in MPS is the myofascial trigger point, a very localized region of tender, contracted muscle that is readily identified by palpation. The trigger point has well-described electrophysiologic properties and is associated with a derangement of the local biochemical milieu of the muscle. A proper diagnosis of MPS includes evaluation of muscle as a cause of pain, and assessment of associated conditions that have an impact on MPS."

Gerwin RD. 2013. Chronic Pain Perspectives: Diagnosing fibromyalgia and myofascial pain syndrome: A guide. J Fam Pract. 62(12 Suppl 1):S19-25. "The instruments and physical exam techniques described here will help you to diagnose these 2 common soft-tissue pain conditions."

Gerwin RD. 2010. Fibromyalgia Tender Points at Examination Sites Specified by the American College of Rheumatology Criteria Are Almost Universally Myofascial Trigger Points. Curr Pain Headache Rep. [Oct 27 Epub ahead of print]. [Until FM researchers realize that most of the symptoms they are describing as fibromyalgia-related are actually caused by myofascial trigger points, their conclusions are suspect and resources are being wasted. DJS]

Gerwin RD. 1997.  Myofascial pain syndromes in the upper extremity.  J Hand Ther. 10(2):130-136.  “Myofascial pain syndromes of the upper extremity are common causes of pain that may follow trauma and are associated with acute or chronic musculoskeletal stress.  The syndromes are characterized by the presence of the myofascial trigger point, a physical finding that is reliably identified by palpation.  Local and referred pain are hallmarks of the syndrome, and the referred pain patterns may mimic such conditions as radiculopathy and nerve entrapment syndromes.  Treatment is directed toward inactivating the myofascial trigger point, correcting underlying perpetuating factors, and restoring the normal relationships between the muscles of the affected functional motor units.”


Gerwin RD. 1994. Neurobiology of the myofascial trigger point. Baillieres Clin Rheumatol. 8(4):747-762.  “The clinical phenomenon of the MTrP is accessible to any clinician who takes the time to learn to palpate skeletal muscle gently and carefully, and who is willing to learn the functional anatomy necessary to understand the regional spread of MTrPs through functional muscle units (Travell and Simons, 1992).”  “…researchers in the field of pain have given us an understanding of the basis for the hyperalgesia, allodynia and the previously difficult-to-understand finding of referred pain zones that we see daily in our patients.”

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 RD. 2005.  A review of myofascial pain and fibromyalgia—factors that promote their persistence.  Acupunct Med. 23(3):121-134.  Fibromyalgia and myofascial pain are common and different conditions, although they may occur in the same patient.  “Fibromyalgia is a chronic, widespread muscle tenderness syndrome, associated with central sensitization.  It is often accompanied by chronic sleep disturbance and fatigue, visceral pain syndromes like irritable bowel syndrome and interstitial cystitis.  Myofascial pain syndrome is an overuse or muscle stress syndrome characterized by the presence of trigger points in muscle.”  It is important to uncover the cause of chronic muscle pain so that treatment will be effective.  “Chronic myalgia may not improve until underlying precipitating or perpetuating factor(s) are themselves managed.”  These causes may include structural and metabolic conditions.  If the underlying  conditions are brought under control, the chronic myalgia may resolve.

Gerwin RD, Dommerholt J, Shah JP. 2004.  An Expansion of Simons’ integrated hypothesis of trigger point formation.  Curr Pain Headache Rep 8:468-475.  This paper further expounds on the mechanism of TrP formation explained in Simons Travell and Simons 1999 in the light of new research.  Individual irritating substances released at the motor endplate have been sampled during the TrP twitch response and subjected to microanalysis.  This research further substantiates the release of muscle damaging biochemicals and a significant drop in pH at the TrP site.  The pH drop alone is sufficient to cause a change in the nociceptive milieu, and the addition of proinflammatory mediators such as substance P, bradykinin and cytokines may additionally aggravate this change.  The continual pain barrage can affect central nervous system plasticity, resulting in hyperalgesia and allodynia as well as referred pain.

Gerwin RD. 1993.  The management of myofascial pain syndromes.  Jour Musculoskel Pain 1(3/4):83-94.  “MPS is a condition which is treatable by eliminating the specific trigger points that are the immediate cause of pain, and correcting those factors that predispose to recurrence.”

Gerwin RD. 1994.  Neurobiology of the myofascial trigger point. Bailliere’s Clin Rheumatology 8(4):747-762.  “Myofascial pain is pain of muscle origin, although the central feature, a painful trigger point, can also be found in skin, tendon, periosteum and ligament.  The properties of MPS that define it clinically and differentiate it from other painful muscle conditions are: (a) the exquisitely tender trigger point in a taut band of muscle; (b) the restriction of range of motion related to the taut band; (c) a local twitch of the taut band within muscle when physically stimulated; (d) the appearance of zones of referred pain; and (e) the development of satellite trigger points within the zones of referred pain.”

Gerwin RD. 2001.  Classification, epidemiology and natural history of myofascial pain syndrome.  Curr Pain Headache Rep 5(5):412-420.  Myofascial pain can be primary or secondary to another condition.  When it becomes chronic myofascial pain, it can become generalized, but according to this respected author [he is a master of treating myofascial pain – DJS], does not turn into fibromyalgia.  It is treatable, but the perpetuating factors must be treated.  This includes mechanical factors such as structural asymmetry and posture as well as metabolic, toxic or infectious perpetuators.

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.

Gesquiere-Dando A, Attarian S, Maues de Paula A et al. 2015. Fibromyalgia-like symptoms associated with irritable bowel syndrome: A challenging diagnosis of late-onset Pompe disease. Muscle Nerve. [Feb 20 Epub ahead of print.] This report from France: "Late-onset Pompe disease (LOPD) is a rare autosomal recessive disorder, which usually presents as a limb-girdle myopathy with early respiratory involvement….We report 2 sisters with an uncommon presentation of LOPD characterized by fibromyalgia-like pain associated with irritable bowel syndrome….In both sisters, clinical examination was normal and had remained stable for 10 years. The serum creatine kinase level was mildly elevated. Several muscle biopsies showed slight non-specific myopathic abnormalities. A dried blood spot test indicated acid maltase deficiency. The diagnosis of LOPD was confirmed genetically. Both sisters subsequently developed proximal muscle weakness after pregnancy and started enzyme replacement therapy. Under treatment, gastrointestinal symptoms improved, but pain persisted….Clinicians should be aware of this atypical presentation of LOPD to enable earlier diagnosis and treatment." [Everything isn't FM and CMP. You may have those conditions AND others that perpetuate them. Keep looking for perpetuating factors. Some of them may be "rare" because they are not being diagnosed. For those who suspect, Google Pompe disease, or LOPD. DJS]

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] 

Ghavidel-Parsa B, Amir Maafi A, Aarabi Y. 2014. Correlation of invalidation with symptom severity and health status in fibromyalgia. Rheumatology (Oxford). [Sep 8 Epub ahead of print.] "Invalidation is a new construct in health psychology, especially in diseases with inherently invisible symptoms such as FM. It can potentially affect both the quality of life and disease severity in patients with FM. This study aimed to investigate the correlation of illness invalidation with health status and symptom severity in FM….The current study revealed that active negative social responses and the source of invalidation are important in predicting symptom severity and quality of life in FM."

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.”

Gheita TA, Sayed S, Gheita HA et al. 2014. Vitamin D status in rheumatoid arthritis patients: relation to clinical manifestations, disease activity, quality of life and fibromyalgia syndrome. Int J Rheum Dis. Oct 7. [Epub ahead of print] "Special attention is required regarding vitamin D levels in RA patients with FMS and decreased QoL. Vitamin D should be corrected and supplementation considered among the RA management armamentarium."

Ghibellini G, Brancati F, Castori M 2015. Neurodevelopmental attributes of joint hypermobility syndrome/Ehlers-Danlos syndrome, hypermobility type: Update and perspectives. Am J Med Genet C Semin Med Genet. [Feb 5 Epub ahead of print.] "In the last decade, increasing attention has been devoted to the extra-articular and extra-cutaneous manifestations of joint hypermobility syndrome, also termed Ehlers-Danlos syndrome, hypermobility type (i.e., JHS/EDS-HT). Despite the fact that the current diagnostic criteria for both disorders remain focused on joint hypermobility, musculoskeletal pain and skin changes, medical practice and research have started investigating a wide spectrum of visceral, neurological and developmental complications, which represent major burdens for affected individuals. In particular, children with generalized joint hypermobility often present with various neurodevelopmental issues and can be referred for neurological consultation. It is common that investigations in these patients yield negative or inconsistent results, eventually leading to the exclusion of any structural neurological or muscle disorder. In the context of specialized clinics for connective tissue disorders, a clear relationship between generalized joint hypermobility and a characteristic neurodevelopmental profile affecting coordination is emerging. The clinical features of these patients tend to overlap with those of developmental coordination disorder and can be associated with learning and other disabilities. Physical and psychological consequences of these additional difficulties add to the chief manifestations of the pre-existing connective tissue disorder, affecting the well-being and development of children and their families. In this review, particular attention is devoted to the nature of the link between joint hypermobility, coordination difficulties and neurodevelopmental issues in children."

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.

Ghizzani A, Di Sabatino V Suman AL et al. 2014. Pain Symptoms in Fibromyalgia Patients with and without Provoked Vulvodynia. Pain Res Treat. [Jan 29 Epub ahead of print.] "The study reveals that increased vulvar pain excitability may occur in FMS patients independently of the presence of coital pain. Results suggest that coital pain develops in patients with higher FMS symptoms severity due to the cooperative effects of peripheral and central sensitization mechanisms."

Giacomelli C, Talarico R, Bombardieri S et al. 2013. The interaction between autoimmune diseases and fibromyalgia: risk, disease course and management. Expert Rev Clin Immunol. 9(11):1069-1076. "Fibromyalgia (FM) is a common non-autoimmune rheumatologic disease with a wide range of symptoms that worsen the clinical status of patients. Several authors have tried to identify a putative autoimmune biomarker but, unfortunately, without positive results. Moreover, the altered pain perception characteristic of FM patients is similar in other autoimmune rheumatologic and non-rheumatologic diseases, in fact the pain in FM is not strictly tied to an organic disease; the perception and the severity of it are comparable with those of autoimmune conditions, for example, the polymyalgia rheumatica. In this review, we focus on the FM comorbidities, especially related to autoimmune rheumatologic and non-rheumatologic conditions". [This review from Italy clarifies, once again, that fibromyalgia is not itself an auto-immune disease, but can co-exist with auto-immune diseases. The pain of FM is as severe as many autoimmune illnesses. They do not grasp the trigger point generation of the "FM" pain and dysfunction, and that trigger points can generate pain and dysfunction in any illness. DJS]

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.”

Giannoccaro MP, Donadio V, Incensi A et al. 2013. Small nerve fiber involvement in patients referred for fibromyalgia. Muscle Nerve. [Dec 28 Epub ahead of print.] "Fibromyalgia (FM) is a chronic syndrome characterized by widespread pain often accompanied by other symptoms suggestive of neuropathic pain. We evaluated patients for small fiber neuropathy (SFN) who were referred for fibromyalgia (FM). Methods: We studied 20 consecutive subjects with primary FM. Patients underwent neurological examination, nerve conduction studies, and skin biopsies from distal leg and thigh. Results: Electrodiagnostic studies were normal in all patients. SFN was diagnosed in 6 patients by reduced epidermal nerve fiber density. These patients also showed abnormalities of both adrenergic and cholinergic fibers….A subset of FM subjects have SFN, which may contribute to their sensory and autonomic symptoms. Skin biopsy should be considered in the diagnostic work-up of FM."

Giesecke T, Gracely RH, Williams DA et al. 2005.  The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort.  Arthritis Rheum. 52(5):1577-1584.  This study suggests a parallel but different sensory matrix for pain and for depression.  In a patient with both pain and depression, treating the depression alone is not adequate.  The pain must also be treated.   

Giesecke T, Williams DA, Harris RE et al. 2003. Subgrouping of fibromyalgia patients on the basis of pressure-pain thresholds and psychological factors. Arthritis Rheum 48 (10):2916-2922.  The authors separate FMS subsets based on several factors.

Giggins OM, Persson UM, Caulfield, B. 2013. Biofeedback in rehabilitation J Neuroeng Rehabil. [June 18 2013 Epub ahead of print]. [This is a review of the use of many types of biofeedback now being used in many conditions, including fibromyalgia. DJS]

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.

Gilbert JW, Vogt M, Windsor RE et al. 2014. Vestibular dysfunction in patients with chronic pain or underlying neurologic disorders. J Am Osteopath Assoc. 114(3):172-178. "Individuals with vestibular dysfunction are at increased risk for falling. In addition, vestibular dysfunction is associated with chronic pain, which could present a serious public health concern as approximately 43% of US adults have chronic pain." Using a retrospective review of records, the authors found that: "Patients being treated with medications for chronic, noncancer pain or other underlying neurologic disorders may have a higher-than-average incidence of vestibular dysfunction. Baseline assessment and monitoring of the vestibular apparatus may be indicated for these patients.

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.

Girschick HJ, Morbach H, Tappe D. 2009. Treatment of Lyme borreliosis. Arthritis Res Ther. 11(6):258. “Borrelia burgdorferi sensu lato is the causative agent of Lyme borreliosis in humans. This inflammatory disease can affect the skin, the peripheral and central nervous system, the musculoskeletal and cardiovascular system and rarely the eyes. Early stages are directly associated with viable bacteria at the site of inflammation. The pathogen-host interaction is complex and has been elucidated only in part. B. burgdorferi is highly susceptible to antibiotic treatment and the majority of patients profit from this treatment. Some patients develop chronic persistent disease despite repeated antibiotics. Whether this is a sequel of pathogen persistence or a status of chronic auto-inflammation, auto-immunity or a form of fibromyalgia is highly debated. Since vaccination is not available, prevention of a tick bite or chemoprophylaxis is important. If the infection is manifest, then treatment strategies should target not only the pathogen by using antibiotics but also the chronic inflammation by using anti-inflammatory drugs.”

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, Park DC, Minear M et al. 2005.  Memory beliefs and function in fibromyalgia patients.  J Psychosom Res. 58(3):263-269.  “Among the patients, perceived capacity, achievement motivation, and self-efficacy were significantly correlated with objective memory performance on a recall task.”


Glass JM, Lyden AK, Petzke F et al. 2004.  The effect of brief exercise cessation on pain, fatigue, and mood symptom development in healthy, fit individuals.  J Psychosom Res. 57(4):391-398.  “A subset of subjects developed symptoms of pain, fatigue, and mood changes after exercise deprivation.  This cohort was different from the individuals who did not develop symptoms in baseline measures of HPA axis, immune, and autonomic function.  We speculate that a subset of healthy individuals who have hypoactive function of the biological stress response systems unknowingly exercise regularly to augment the function of these systems and suppress symptoms.  These individuals may be at risk for developing chronic multisymptom illnesses when a ‘stressor’ leads to lifestyle changes that disrupt regular exercise.”


Glass JM, Lyden AK, Petzke F et al. 2004.  The effect of brief exercise cessation on pain, fatigue, and mood symptom development in healthy, fit individuals.  J Psychosom Res 57(4):391-398.  “A subset of subjects developed symptoms of pain, fatigue, mood changes after exercise deprivation.  This cohort was different from the individuals who did not develop symptoms in baseline measures of HPA axis, immune, and autonomic function.  We speculate that a subset of healthy individuals who have hypoactive function of the biological stress response systems unknowingly exercise regularly to augment the function of these systems and suppress symptoms.  These individuals may be at risk for developing chronic multisymptom illnesses when a 'stress' leads to lifestyle changes that disrupt regular exercise.”

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. 3rd.  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]


Gockel U, Tolle T. 2007.  Fibromyalgic vs. neuropathic pain.  J Musculoskel Pain 15 (Supp 13):48 item 83.  [Myopain 2007 Poster]  “The pain experienced subjectively by FMS patients is conspicuously greater than that experienced by other patients with typical neuropathic complaints.  Furthermore, this pain is associated with more severe co-morbidities such as depression/anxiety and sleep disturbance.”

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]

Goes SM, Leite N, de Souza RM. 2014. [Gait characteristics of women with fibromyalgia: a premature aging pattern]. Rev Bras Reumatol. 54(5):335-341. [Article in Portuguese] "There was no difference in walking speed, stride length, cadence, hip, knee and ankle joints range of motion between groups, except the pelvic rotation, in which the fibromyalgia group showed greater rotation…and between pelvic obliquity and greater trochanter pain…in the fibromyalgia group….Middle-aged women with fibromyalgia showed gait pattern resemblances to elderly women, which is characterized by reduced lower limb ROM, stride length and walking speed." Free Article [Since we know that FM does not cause these things, and chronic myofascial pain does, it is likely that the conclusion is erroneous and that the premature aging gait pattern was due to treatable myofascial trigger points. DJS]

Goesling J, Brummett CM, Meraj TS et al. 2015. Associations between Pain, Current Tobacco Smoking, Depression, and Fibromyalgia Status among Treatment-Seeking Chronic Pain Patients. Pain Med. [Mar 20 Epub ahead of print.] "Current smoking and positive fibromyalgia status were associated with greater pain and impairment among chronic pain patients, possibly as a function of depression. Although FM+ smokers report the most negative clinical symptomatology (i.e., high pain, greater interference), smoking does not appear to have a unique association with pain or functioning in FM+ patients, rather the effect is additive. The 38.7% smoking rate in FM+ patients is high, suggesting FM+ smokers present a significant clinical challenge."

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.

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.  

Gollwitzer H, Opitz G, Gerdesmeyer L et al. 2014. [Greater trochanteric pain syndrome.] Orthopade. 43(1):105-118. [Article in German] Greater trochanteric pain is one of the common complaints in orthopedics. Frequent diagnoses include myofascial pain, trochanteric bursitis, tendinosis and rupture of the gluteus medius and minimus tendon, and external snapping hip. Furthermore, nerve entrapment like the piriformis syndrome must be considered in the differential diagnosis. This article summarizes essential diagnostic and therapeutic steps in greater trochanteric pain syndrome. Careful clinical evaluation, complemented with specific imaging studies and diagnostic infiltrations allows determination of the underlying pathology in most cases. Thereafter, specific nonsurgical treatment is indicated, with success rates of more than 90 %. Resistant cases and tendon ruptures may require surgical intervention, which can provide significant pain relief and functional improvement in most cases.

Gonzalez B, Baptista TM, Branco JC et al. 2014. Fibromyalgia characterization in a psychosocial approach. Psychol Health Med. 25:1-6. "This study aimed to characterize a group of women diagnosed with fibromyalgia, evaluating the relationship between personality and psychopathology, health status (disability, physical health, mental health, and pain), and potentially traumatic life events (PTLE) before the onset of the syndrome. The disability caused by fibromyalgia, physical and mental health status, pain, PTLE in childhood and in the course of life, and personality were assessed in a sample of 50 women with fibromyalgia, age 25-70 years ….. A multiple correspondence analysis with all the variables identified two types of profiles and a K-Means cluster analysis confirmed two groups of patients: cluster 1 (n = 36), with better health and less psychopathological problems, named 'Better adjustment' and cluster 2 (n = 14), with less health and more personality problems, named 'Disorder and disability.' Pertaining to personality only, a K-Means cluster analysis replicated the three classic personality profiles (normal, neurotic, and psychopathological) identified in chronic pain patients; and the normal profile was the more prevalent (n = 22). The results enhance the importance of recognizing the heterogeneity of fibromyalgia population and the great closeness between personality and physical health, with the PTLE having a less important role than expected."

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. 2015. Deep dry needling of trigger points located in the lateral pterygoid muscle: Efficacy and safety of treatment for management of myofascial pain and temporomandibular dysfunction. Med Oral Patol Oral Cir Bucal. [Feb 7 Epub ahead of print.] This study from Spain attempted to discover "…whether deep dry needling (DDN) of trigger points (TPs) in the lateral pterygoid muscle (LPM) would significantly reduce pain and improve function, compared with methocarbamol/paracetamol medication…." They found that "…DDN of TPs in the LPM showed better efficacy in reducing pain and improving maximum mouth opening, laterality, and protrusion movements compared with methocarbamol/paracetamol treatment. No adverse events were observed with respect to DDN." Free Article

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-Roldan AM, Munoz MA, Cifre I et al. 2013. Altered psychophysiological responses to the view of others' pain and anger faces in fibromyalgia patients. J Pain. [Apr 25 Epub ahead of print]. "Our findings suggest that brain and cardiac activity elicited by viewing facial expressions of pain and anger in others is altered in fibromyalgia patients. This cognitive bias toward negative emotions could be used in clinical settings as a psychobiological marker during the assessment and treatment of fibromyalgia."

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 DB, Loeser JD, Tauben D et al. 2013. Development of the KnowPain-12 Pain Management Knowledge Survey. Clin J Pain. [Oct 16 Epub ahead of print.] "The purpose of this study was to develop a brief knowledge survey about chronic non-cancer pain that could be used as a reliable and valid measure of a provider's pain management knowledge…. This study used a cross-sectional study design. A group of pain experts used a systematic consensus approach to reduce the previously validated KnowPain-50 to 12 questions (2 items per original six domains). A purposive sampling of pain specialists and health professionals generated from public lists and pain societies was invited to complete the KnowPain-12 online survey. Between April 4 and September 16, 2012, 846 respondents completed the survey…..Respondents included registered nurses (34%), physicians (23%), advanced practice registered nurses (14%), and other allied health professionals and students. Twenty-six percent of the total sample self-identified as "pain specialist". Pain specialists selected the most correct response to the knowledge assessment items more often than did those who did not identify as pain specialists, with the exception of one item. KnowPain-12 demonstrated adequate internal consistency reliability…. Total scores across all 12 items were significantly higher….among pain specialists compared to respondents who did not self-identify as pain specialists…..The psychometric properties of the KnowPain-12 support its potential as an instrument for measuring provider pain management knowledge. The ability to assess pain management knowledge with a brief measure will be useful for developing future research studies and specific pain management knowledge intervention approaches for health care providers."

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. 

Gorenberg M, Schwartz K. 2013. Imaging-guided hyperstimulation analgesia in low back pain. J Pain Res. 6:487-491. "Low back pain in patients with myofascial pain syndrome is characterized by painful active myofascial trigger points (ATPs) in muscles. This article reviews a novel, noninvasive modality that combines simultaneous imaging and treatment, thus taking advantage of the electrodermal information available from imaged ATPs to deliver localized neurostimulation, to stimulate peripheral nerve endings…. and in turn, to release endogenous endorphins. 'Hyperstimulation analgesia' with localized, intense, low-rate electrical pulses applied to painful ATPs was found to be effective in 95% patients with chronic nonspecific low back pain, in a clinical validation study."

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.

Gottrup H, Juhl G, Kristensen AD et al. 2004.  Chronic oral gabapentin reduces elements of central sensitization in human functional hyperalgesia. Anesthesiology 101(6):1400-1408.

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]

Gowing LR, Ali RL, Christie P et al. 1998.  Therapeutic use of cannabis: clarifying the debate.  Drug Alcohol Rev. 17(4):445-452.  “The debate regarding therapeutic use of cannabis is being confused by a lack of distinction between therapeutic and social use of cannabis.”  “At present the evidence is limited, it mostly relates to the use of synthetic cannabinoids, and much of it fails to compare cannabis with the best therapies available for the conditions of interest.”  “There is sufficient evidence of potential therapeutic benefit to justify the facilitation of further research.”

Gowri V, Krolikowski A. 2001.  Chronic pelvic pain. Laparoscopic and cystoscopic findings.  Saudi Med J. 22(9):769-770.  [Another study that failed to include myofascial TrPs in the differential diagnosis. 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.

Gracely RH, Petzke F, Wolf JM, Clauw DJ.2002. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum 46(5):1333-43. "Supports the hypothesis that FM is characterized by cortical or subcortical augmentation of pain processing."

Graff-Radford SB. 2004.  Myofascial pain: diagnosis and management.  Curr Pain Headache Rep. 8(6):463-467. “Clinical understanding and management of myofascial pain is overlooked frequently when dealing with pain.  Myofascial pain is defined as pain or autonomic phenomena referred from active trigger points, with associated dysfunction.”  “Myofascial pain is poorly understood, which results too often in under diagnosis and poor management.  The pathogenesis likely has a central mechanism with peripheral clinical manifestations.  The therapy for myofascial pain requires enhancing central inhibition through pharmacology or behavioral techniques and simultaneously reducing peripheral inputs through physical therapies including exercises and trigger point-specific therapy.”

Graff-Radford SB. 2001.  Regional myofascial pain syndrome and headache: principles of diagnosis and management.  Curr pain Headache Rep. 5(4):376-381.

Graff-Radford SB. 2004.  Myofascial pain: diagnosis and management.  Curr Pain Headache Rep. 8(6):463-467.  “Clinical understanding and management of myofascial pain is overlooked frequently when dealing with pain.”

Graff-Radford SB. 2004.  Myofascial pain: diagnosis and management.  Curr Pain Headache Rep. 8(6):463-467.  Myofascial pain is an often-neglected and treatable as a component of patients’ pain.

Graff-Radford SB, Bassiur JP. 2014. Temporomandibular Disorders and Headaches. Neurol Clin. 32(2):525-537. "Headache and temporomandibular disorders should be treated together but separately. If there is marked limitation of opening, imaging of the joint may be necessary. The treatment should then include education regarding limiting jaw function, appliance therapy, instruction in jaw posture, and stretching exercises, as well as medications to reduce inflammation and relax the muscles. The use of physical therapies, such as spray and stretch and trigger point injections, is helpful if there is myofascial pain."

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.

Grahmann PH, Jackson KC 2nd, Lipman AG. 2004.  Clinician beliefs about opioid use and barriers in chronic nonmalignant pain.  J Pain Palliat Care Pharmacother. 18(2):7-28.  “There is increasing acceptance of opioids for most of the listed types of chronic nonmalignant pain, but the acceptance varies by types of pain syndromes.”

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.

Grape HE, Solbrække KN, Kirkevold M et al. 2014. Staying Healthy From Fibromyalgia Is Ongoing Hard Work. Qual Health Res. [Nov 11 Epub ahead of print.] "Fibromyalgia syndrome (FMS) is a chronic musculoskeletal pain condition. Although studies have reported that some patients can become healthy again, little is known about what they tell about their lives after having FMS. In this study, we interviewed eight Norwegian women who had all recovered from FMS about their experiences when ill and subsequently being healthy. Inspired by narrative methods, we then conducted a thematic narrative analysis. The findings indicate that although women reported that life was better than before, they also reported investing considerable effort in remaining healthy. When ill, they struggled to maintain the routines of everyday life. Being healthy again, they put great effort into avoiding illness through diet, exercise, and relaxation. In conclusion, remaining healthy requires ongoing hard work to maintain the body, as well as profound changes in everyday life. At the same time, the narratives show continuity in the informants' self-presentation as hard-working women."

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. 2007.  The interaction of musculoskeletal pain and motor control.  J Musculoskel Pain 15 (Supp 13):10 item 12.  [Myopain 2007 Poster]  “The functional adaptation to muscle pain may also involve increased muscle activity reflecting compensatory muscle coordination.  Such adaptation in motor function might evoke overload of other muscle groups and as such play a role in the persistence, amplification and spread of pain, and interventions should take this aspect into consideration.”


Graven-Nielsen T, Mense S, Arendt-Nielsen L. 2004.  Painful and non-painful pressure sensations from human skeletal muscle.  Exp Brain Res. [Epub ahead of print]  Specific nerve fiber contributions to peripheral pain.

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.

Greaves MW, Wall PD. 1996.  Pathophysiology of itching.  Lancet 348(9032):938-940.  There is a strong central nervous system component to some forms of itch, and the neurotransmitter histamine is frequently involved.  [The connection between itch and pain is involved and still being explored. DJS]


Greco R, Gasperi V, Maccarrone M et al. 2010. The endocannabinoid system and migraine.  Exp Neurol. [Mar 27 Epub ahead of print]. “The recently discovered endocannabinoid system (ECS), which includes endocannabinoids and the proteins that metabolize and bind them, has been implicated in multiple regulatory functions both in health and disease. Several studies have suggested that ECS is centrally and peripherally involved in the processing of pain signals. This finding is corroborated by the evidences that endocannabinoids inhibit, through a cannabinoid type-1 receptor (CB1R)-dependent retrograde mechanism, the release of neurotransmitters controlling nociceptive inputs and that the levels of these lipids are high in those regions (such as sensory terminals, skin, dorsal root ganglia) known to be involved in transmission and modulation of pain signals. In this review we shall describe experimental and clinical data that, intriguingly, demonstrate the link between endocannabinoids and migraine, a neurovascular disorder characterized by recurrent episodic headaches and caused by abnormal processing of sensory information due to peripheral and/or central sensitization. Although the exact ECS-dependent mechanisms underlying migraine are not fully understood, the available results strongly suggest that activation of ECS could represent a promising therapeutical tool for reducing both the physiological and inflammatory components of pain that are likely involved in migraine attacks.”  [This is yet another paper describing the connection between defects in the endocannabinoid system and central sensitization states such as migraine and fibromyalgia. DJS]


Green CR, Anderson KO, Baker TA et al. 2003.  The unequal burden of pain: confronting racial and ethnic disparities in pain.  Pain Med. 4(3):277-294.  “Racial and ethnic disparities in pain perception, assessment, and treatment were found in all settings (i.e., postoperative, emergency room) and across all types of pain (i.e., acute, cancer, chronic nonmalignant, and experimental).  The literature suggests that the sources of pain disparities among racial and ethnic minorities are complex, involving patient (e.g., patient/health care provider communication, attitudes), health care provider (e.g., decision making), and health care system (e.g., access to pain medication) factors.  There is a need for improved training for health care providers and educational interventions for patients.”  [People of color often seem to be treated as invisible people, just like people with invisible illness.  The combination may cause untold and needless misery. DJS]


Green CR, Anderson KO, Baker TA et al. 2003.  The unequal burden of pain: confronting racial and ethnic disparities in pain.  Pain Med. 4(3):277-294.  There are complex variables in the sources of pain disparity among ethnic and racial groups.  Some of this pain is unnecessary and can be remedied.


Green JS, Stanforth PR, Rankinen T et al. 2004.  The effects of exercise training on abdominal visceral fat, body composition, and indicators of the metabolic syndrome in postmenopausal women with and without estrogen replacement therapy: the HERITAGE family study.  Metabolism 53(9):1192-1196.  Exercise did not improve the Metabolic Syndrome status of these study participants.

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.

Grieve R, Barnett S, Coghill N et al. 2013. Myofascial trigger point therapy for triceps surae dysfunction: A case series. Man Ther. [June 4 Epub ahead of print]. Four women and 6 men with triceps surae dysfunction ("triceps surae" is an anatomical term for the combination of gastrocnemius and soleus muscles) were evaluated for myofascial trigger points. All participants had active and latent myofascial TrPs on assessment. A program of trigger point pressure release, self-TrP release and home stretching was instituted. Ankle dorsiflexion, pain scale, function scale improve, and improvement was still evident 6 weeks later. "This case series suggests that a brief course of multimodal MTrP therapy would be helpful for some patients with sub-acute or chronic calf pain."

Grieve R, Cranston A, Henderson A et al. 2013. The immediate effect of triceps surae myofascial trigger point therapy on restricted active ankle joint dorsiflexion in recreational runners: A crossover randomized controlled trial. J Bodyw Mov Ther. 17(4):453-461. "To investigate the immediate effect on restricted active ankle joint dorsiflexion range of motion (ROM), after a single intervention of myofascial trigger point (MTrP) therapy on latent triceps surae MTrPs in recreational runners"….a crossover randomized controlled trial was conducted on: "Twenty-two recreational runners (11 men and 11 women…with a restricted active ankle joint dorsiflexion and presence of latent MTrPs….Participants were screened for a restriction in active ankle dorsiflexion in either knee flexion (soleus) or knee extension (gastrocnemius) and the presence of latent MTrPs. Participants were randomly allocated a week apart to both the intervention (combined pressure release and 10 s passive stretch) and the control condition….A clinically meaningful and statistically significant increase in ankle ROM in the intervention compared to the control group was achieved, for the soleus…and the gastrocnemius…."

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.


Grobli C, Dejung B. 2003. [Non-medical therapy of myofascial pain] Schmertz 17(6):475-480. Specific manual therapy is effective for low back trigger point pain.  Connective tissue adhesions that may form in the regions of TrPs as a result of localized edema may be key areas involved in myofascial pain.  They deserve prompt and thorough attention. [German]

Grobli C, Dejung B. 2003. [No Title Given] Schmertz 17(6):475-480. Specific manual therapy is effective for low back trigger point pain. [German]

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.  

Gruneberg C, Bloem BR, Honegger F et al.  2004.  The influence of artificially increased hip and trunk stiffness on balance control in man.  Exp Brain Res.  [Epub May 12  ahead of print].  Trunk and hip stiffness increases the possibility of falling. This has implications for people with restricted range of motion due to myofascial TrPs.


Gryfe Saperia NJ, Swartzman LC. 2011. Openness to psychological explanations and treatment among people with Fibromyalgia versus Rheumatoid Arthritis. Psychol Health. [Jul 26 Epub ahead of print]. "The classic perspective in the psychosomatic literature is that patients with medically unexplained syndromes do not acknowledge psychologically-based causes for their conditions and will not engage in psychological treatments. These assumptions were tested by contrasting the illness models and reported treatment experiences of individuals with fibromyalgia (FM), a syndrome with a currently unknown organic origin, with those of individuals with rheumatoid arthritis (RA), a 'legitimate' (i.e. organic) condition.... Contrary to prediction, compared to patients with RA, patients with FM were more likely to endorse psychological causes for their condition and reported having used more psychological management approaches. Moreover, patients with FM considered psychological approaches to be more effective than narcotics....These findings indicate that patients with FM do not react defensively to the implication of psychogenic causes. Rather, as a group, they tend to acknowledge both the psychosocial influences on and the effectiveness of psychological management approaches for their condition." [The study is interesting, although some of the wording is unfortunate and one can only guess the authors intent. They should be aware, however, that FM is organic, although different causes may institute the biochemical cascades that result in central sensitization. It might be interesting if co-existing TrPs were included in this mix, as they maintain most cases of central sensitization. First, however, one must have researchers and patients aware of these co-existent and ubiquitous pain generators. For now, much research focuses on the pain amplifier, FM, instead. DJS]

Guan H, Koceja DM. 2011. Effects of long-term tai chi practice on balance and h-reflex characteristics. Am J Chin Med. 39(2):251-260. "The findings of this study support the positive effects of Tai Chi exercise on balance control under different conditions."

Guarda-Mardini L, Stecco A, Stecco C et al. 2012. Myofascial pain of the jaw muscles; comparison of short-term effectiveness of botulinum toxin injections and fascial manipulation technique. Cranio 30(2):95-102. As a comparison of single session botulinum injections and multiple session fascial manipulation: "The two treatments seem to be almost equally effective, fascial manipulation being slightly superior to reduce subjective pain perception, and botulinum toxin injections being slightly superior to increase jaw range of motion. Differences between the two treatment protocols aw to changes in the outcome parameters at the three-months follow-up were not relevant clinically."

Guedj E, Cammilleri S, Colavolpe C et al. 2007.  Predictive value of brain perfusion SPECT for ketamine response in hyperalgesic fibromyalgia.  Eur J Nucl Med Mol Imaging. [Mar 13 Epub ahead of print.  “Brain perfusion SPECT may predict response to ketamine in hyperalgesic FM patients.”


Guerineau M, Labat JJ, Sibert L et al. 2010. [Treatment of the musculoskeletal component of chronic pelvic and perineal pain]. Prog Urol. 20(12):1103-1110. [French] "The management of patients with chronic pelvic and perineal pain requires preliminary clinical analysis designed to identify trigger points responsible for myofascial pain, pelvic floor muscle tension, and lumbar-pelvic-hip instability. Physiotherapy must be initiated early in the course of the disease by therapists trained in these recent techniques. Botulinum toxin injections have been shown to be effective in piriformis syndrome, but a review of the literature indicates more controversial results in the other chronic pelvic and perineal pain syndromes." [This paper was based on a review of the literature, which reflects the general lack of understanding and knowledge of myofascial TrPs, their ubiquity and their clinical significance. Faulty research begets faulty research. DJS]

Guermazi M, Ghroubi S, Sellami M et al. 2008.  [Fibromyalgia prevalence in Tunisia  Tunis Med. 86(9):806-811.  [French]  “FM prevalence in Tunisia is estimated at least at 8.27%.”

Guerrero-Romero F., Rodriguez-Moran M. 2002.  Low serum magnesium levels and metabolic syndrome.  Acta Diabetol 39(4):209-13.  “This study reveals a strong relationship between decreased serum magnesium and MS.”

Gui MS, Pedroni CR, Aquino LM et al. 2013. Facial pain associated with fibromyalgia can be marked by abnormal neuromuscular control: A cross-sectional study. Phys Ther. [Apr 18 Epub ahead of print]. "Altered neuromuscular control in masticatory muscles may be correlated with perceived facial pain in patients with FMS." [This altered neuromuscular control is probably due to co-existing trigger points. FM researchers must learn to recognize TrPs. DJS]

Guilleminault C, Huang YS, Kirisoglu C et al. 2005.  Is obstructive sleep apnea syndrome a neurological disorder?  A continuous positive airway pressure follow-up study.  Ann Neurol. 58(6):880-887.  “Obstructive sleep apnea syndrome involves abnormal upper airway sensory input, which may be responsible for the development of apneas and hypopneas.  These neurological lesions are persistent despite nasal CPAP treatment.”  Even with relatively successful CPAP treatment for obstructive sleep apnea, heightened pharyngeal sensation persists.


Guilleminault C, Kirisoglu C, Poyares D et al. 2006.  Upper airway resistance syndrome: a long-term outcome study.  J Psychiatr Res. 40(3):273-279.   “Many UARS patients remained untreated following initial evaluation. Worsening of symptoms of insomnia, fatigue and depressive mood were seen with absence of treatment of UARS.”  Sleep studies must include evaluation for UARS, and patients diagnosed with UARS must be treated successfully.  CPAP therapy often is the most efficient treatment.


Guilleminault C, Lee JH, Chan A. 2005.  Pediatric obstructive sleep apnea syndrome.  Arch Pediatr Adolesc. 159(8):775-785.  Pediatric OSA is not uncommon and needs to be considered in the differential diagnosis.  Orthodontic treatment, CPAP and other options may be preferable to adenotonsillectomy.


Gul K, Onal SA. 2009.  [Comparison of non-invasive and invasive techniques in the treatment of patients with myofascial pain syndrome.]  Agri. 21(3):104-112. [Turkish]  Botulinum toxin-A injection provided better pain control when compared to trigger point injection with lidocaine and non-invasive techniques including TENS (transcutaneous electrical nerve stimulation) and laser treatments.”


Gulec H, Sayar K, Yazici Gulec M. 2007.  [The relationship between psychological factors and health care-seeking behavior in fibromyalgia patients]  Turk Psikiyatri Derg. 18(1):22-30 [Turkish].  “The rate of psychiatric and medical history is not related to the FMS syndrome.  Expectations and a normalizing attribution style may contribute to help-seeking behavior for FMS.

Gulick DT, Palombaro K, Lattanzi JB. 2011. Effect of ischemic pressure using a Backnobber II device on discomfort associated with myofascial trigger points. J Bodyw Mov Ther 15(3):319-325. The patients in this study had two TrPs in the upper back. For these patients with limited TrPs, the therapy tool was effective in reducing TrP irritability.


Gullacksen AC, Lidbeck J. 2004.  The life adjustment process in chronic pain: psychosocial assessment and clinical implications.  Pain Res. Manag. 9(3):145-153.

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.

Gunthert E.A. 2002. [no title]  Urologe A 41(6):602-10. [German]  This article refers to urogenital symptoms due to myofascial pain as the result of psychologically-induced muscular tension and classifies it as a somatization disorder.  This is not consistent with the facts concerning the physiological basis of myofascial trigger points as we know them.  The author implies that because the symptoms cannot be “...proven by laboratory tests or common technical diagnostic methods...” they are somatization disorders.  Patients should not pay for their care provider’s lack of myofascial TrP diagnostic training.


Gupta A, McBeth J, Macfarlane GJ et al. 2006.  Pain thresholds and tender point counts as predictors of new chronic widespread pain in psychologically distressed subjects.  Ann Rheum Dis. [Sep 29 Epub ahead of print]   Subjects who are psychologically distressed but without chronic pain are not at increased risk of its development.  Low pain-threshold is probably a secondary result of chronic widespread pain and not a primary condition.

Gupta A, Rapkin AJ, Gill Z et al. 2015. Disease-Related Differences in Resting State Networks: A Comparison between Localized Provoked Vulvodynia, Irritable Bowel Syndrome, and Healthy Control Subjects. Pain. [Feb 12 Epub ahead of print.] "Localized provoked vulvodynia (LPVD) affects approximately 16% of the female population, but biological mechanisms underlying symptoms remain unknown. Like in other, often comorbid, chronic pain disorders, altered sensory processing and modulation of pain, including central sensitization, dysregulation of endogenous pain modulatory systems, and attentional enhancement of pain perception have been implicated….The current findings indicate LPVD subjects have alterations in the intrinsic connectivity of regions comprising the sensorimotor, salience, and default mode networks. Although shared brain mechanisms between different chronic pain disorders have been postulated, the current findings suggest some alterations in functional connectivity may show disease specificity."

Gupta V, Tiwari S, Agarwal CG. 2006.  Effect of short-term cigarette smoking on insulin resistance and lipid profile in asymptomatic adults.  Indian J Physiol Pharmacol. 50(3):285-290.  “It appears that smokers are prone to develop hyperinsulenemia, hyperglycemia and the metabolic syndrome.”   Another indication that smoking is a perpetuating factor for many ailments, including those which can be perpetuating factors of FMS and CMP.


Gur A, Sarac AJ, Cevik R et al. 2004.  Efficacy of 904 nm gallium arsenide low level laser therapy in the management of chronic myofascial pain in the neck: a double-blind and randomize-controlled trial.  Lasers Surg Med. 35(3):229.  Short-term LLLT may be useful to reduce pain and raise quality of life in patients with cervical MPS.

Gur A, Cevik R, Nas K et al.  2004.  Cortisol and hypothalamic-pituitary-gonadal axis hormones in follicular-phase women with fibromyalgia and chronic fatigue syndrome and effect of depressive symptoms on these hormones.  Arthritis Res Ther. 6(3):R232-238.

Gur, A., M. Karakoe, K. Nas et al. 2002. Effects of low power laser and low dose amitriptyline therapy on clinical symptoms and quality of life in fibromyalgia: a single-blind, placebo-controlled trial. Rheumatol Int 22(5):188-93. Active low-power gallium-arsenide laser therapy and/or amitriptyline therapy may be effective for fibromyalgia patients.

Gurbuzler L, Unanir, Yelken K et al. 2013. Voice disorder in patients with fibromyalgia. Auris Nasus Larynx [May 30 Epub ahead of print]. Thirty fibromyalgia patients were analyzed with laryngostroboscopy, acoustic analysis, aerodynamic measurements and perceptual analysis and compared to control subjects. [The authors concluded that FM impairs voice quality in patient self-evaluation or clinical evaluation, but they did not assess for co-existing TrPs that can cause these same results. It would help greatly if patients had assessment for area TrPs in future studies. DJS]

Gurer G, Sendur OF, Ay C. 2005.  Serum lipid profile in fibromyalgia women.  Clin Rheumatol. [Oct 1 Epub ahead of print]  “In the FM group, we could not find a significant correlation between the serum lipid profile values and the FM parameters (p>0.05).”  [This research confirms the research of Dr. Salih Ozgocmen and his team.  They found that in patients with both fibromyalgia and chronic myofascial pain who had high lipid profiles, the high lipid profile was related to the myofascial pain component and not the fibromyalgia. DJS]


Gursoy S, Erdal E, Sezgin M et al. 2007.  Which genotype of MAO gene that the patients have are likely to be most susceptible to the symptoms of fibromyalgia?  Rheumatol Int.  [Sep 20 Epub ahead of print]  “It seems plausible to say that MAOA-dependent metabolism of the biological amines may be partly related to high-activated MAO-A, allele 3, in the occurrence of FS among Turkish population.”


Gursoy, S., Erdal, E., Herken, H., et al.  Significance of catechol-O-methyltransferase gene polymorphism in fibromyalgia syndrome.  Rheumatol Int 23(3):104-7.  [This research may have implications in the treatment of FMS, as well as genetic tendency to develop FMS.  It indicates that the metabolism of catechol drugs in FMS patients may be different. DJS]


Gurvich C, Maller JJ, Lithgow B et al. 2013. Vestibular insights into cognition and psychiatry. Brain Res. [Sep 6 Epub ahead of print]. "...emerging research suggests the vestibular system can be considered a potential window for exploring brain function beyond that of maintenance of balance, and into areas of cognitive, affective and psychiatric symptomology. Given the paucity of biological and diagnostic markers in psychiatry, novel avenues to explore brain function in psychiatric disorders are of particular interest and warrant further exploration."

Gusi N, Tomas-Carus P, Hakkinen A et al. 2006.  Exercise in waist-high warm water decreases pain and improves health-related quality of life and strength in the lower extremities in women with fibromyalgia.  Arthritis Rheum. 55(1):66-73.  “The therapy relieved pain and improved HRQOL (health-related quality of life) and muscle strength in the lower limbs at low velocity in patients with initial low muscle strength and high number of tender points.  Most of these improvements were maintained long term.”

Gustafsson M, Ekholm J, Ohman A.  2004.  From shame to respect: musculoskeletal pain patients’ experience of a rehabilitation programme, a qualitative study.  J Rehabil Med. 36(3):97-103.

Gustaw K. 2000.  Myofascial pain syndrome in farmers – a comprehensive approach to treatment.  Ann Agric Environ Med 7(2):95-99.  “The MPS syndrome was found to be relatively common in Polish farmers and formed 12.7% of all chronic pain syndromes diagnosed in the Institute of Agricultural Medicine during 18 months.”

Gutierrez-Reyes G, Lopez-Ortal P, Sixtos S et al. 2006.  Effect of pentoxifylline on levels of pro-inflammatory cytokines during chronic hepatitis C.  Scand J Immunol 63(6):461-467.  Pentoxifylline may be helpful in controlling cytokine storms such as may occur in hepatitis C.  [And FMS, and avian influenza. DJS]

Guttu RL, Page DG, Laskin DM. 1990.  Delayed healing of muscle after injection of bupivicaine and steroid.  Ann Dent 49(1):5-8.  “Bupivicaine produces more tissue reaction than procaine and that the addition of steroid to bupivicaine increases the initial tissue damage and prolongs the healing phase.”  [Some physicians still use bupivicaine (Marcaine) for TrP injections, although research shows that procaine or lidocaine are much less toxic and more useful for these injections. DJS]

Guven H, Cilliler AE, Comoglu SS. 2012. Cutaneous allodynia in patients with episodic migraine. Neurol Sci. [Nov 23 Epub ahead of print]. "The results of present study revealed that cutaneous allodynia was rather frequent in episodic migraine, particularly in patients having longer disease duration. Higher frequency of allodynia in women and its association with menstrually related migraine may be related to the effects of hormonal factors on cutaneous pain thresholds and central sensitization. Association of nausea and phonophobia with allodynia may be interpreted as the common pathways are shared in the development of these symptoms."

Guymer EK, Clauw DJ.2002  Treatment of fatigue in fibromyalgia.  Rheum Dis Clin North Am 2002 28(2):367-78. "Clearly, fatigue is a large and challenging problem for those suffering from fibromyalgia.  It adds greatly to the morbidity and disability associated with the disease.  In the management of this specific symptom in fibromyalgia, attention should first be focused on identifying comorbidities that may be present and contribute to fatigue.  As with other symptoms of fibromyalgia, education is a critical component of management.  Easier access to well designed nonpharmacologic therapies is essential, because these treatments are underutilized in clinical practice at present."

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. 

Hackshaw KV, Rodriguez-Saona L, Plans M et al. 2013. A bloodspot-based diagnostic test for fibromyalgia syndrome and related disorders. Analyst. [Apr 17 Epub ahead of print]. "The aim of this study was to investigate the ability of a rapid biomarker-based method for diagnosis of fibromyalgia syndrome (FM) using mid-infrared microspectroscopy (IRMS) to differentiate patients with FM from those with osteoarthritis (OA) and rheumatoid arthritis (RA), and to identify molecular species associated with the spectral patterns….Metabolomic analysis revealed that RA and OA groups were metabolically similar, whereas biochemical differences were identified in the FM that were quite distinctive from those found in the other two groups. Both IRMS and metabolomic analysis identified changes in tryptophan catabolism pathway that differentiated patients with FM from those with RA or OA."

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.

Hagen, NA.  2004.  A multi-centre open-label, dose-escalation study of intramuscular tetrodoroxin for severe cancer pain.  Second Joint Scientific Meeting of the American Pain Society and the Canadian Pain Society.  May 6-9.  Vancouver, B.C.

Hagenfeld D, Schulz T, Ehling P et al. 2010. Depolarization of the membrane potential by hyaluronan. J Cell Biochem. 111(4):858-864. "Depolarization of the plasma membrane by hyaluronan (hyaluronic acid) represents an additional pathway of signal transduction to the classical CD44 signal transduction pathway, which links the extracellular matrix to intracellular metabolism." [This research meshes well with the studies we did on geloid masses inpatients with FM and CMP, and indicates that patients with FM and CMP may need to be very careful using any product with hyaluronic acid. That is a component in many cosmetics, body lotions, and anti-aging formulas. DJS]

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….”

Haliloglu S, Carlioglu A, Akdeniz D et al. 2014. Fibromyalgia in patients with other rheumatic diseases: prevalence and relationship with disease activity. Rheumatol Int. [Mar 4 Epub ahead of print.] "Concomitant FM is a common clinical problem in rheumatologic diseases, and its recognition is important for the optimal management of these diseases. Increased pain, physical limitations, and fatigue may be interpreted as increased activity of these diseases, and a common treatment option is the prescription of higher doses of biologic agents or corticosteroids. Considerations of the FM component in the management of rheumatologic diseases increase the likelihood of the success of the treatment."

Haliloglu S, Carlioglu A, Sahiner E et al. 2014. Mean platelet volume in patients with fibromyalgia. Z Rheumatol. [Feb 20 Epub ahead of print.] "These results suggest that an early atherosclerosis marker, mean platelet volume, is elevated in patients with fibromyalgia. This indicates increased platelet activation and therefore a higher risk of future cardiovascular disease."

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 D, Jones S, Iverson D. 2011. Disease awareness advertising - women's intentions following exposure. Aust Fam Physician. 40(3):143-147. "In Australia, where direct to consumer advertising of prescription medicines is prohibited, pharmaceutical companies can sponsor disease awareness advertising targeting consumers. This study examined the impact of disease awareness advertising exposure on older women's reported behavioral intentions….Women were approached in a shopping centre and randomly assigned mock advertisements for two health conditions. Disease information and sponsors were manipulated….Two hundred and forty-one women responded to 466 advertisements. Almost half reported an intention to ask their doctor for a prescription or referral as a result of seeing the advertisement, but more reported they would talk to their doctor and ask about treatments and tests. Participants were more likely to report an intention to ask for prescriptions if they perceived the health condition to be severe and themselves susceptible or if they had viewed advertisements containing limited information on the disease….Disease awareness advertising may stimulate demand for prescription medicine products. This has serious implications for general practitioners and regulators." [Australia sets a fine example for the rest of the world in this, as in other areas such as gun control. Now if we would only follow. DJS]

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.”

Hamaue Y, Nakano J, Sekino Y et al. 2013. Immobilization-induced hypersensitivity associated with spinal cord sensitization during cast immobilization and after cast removal in rats. J Physiol Sci. [Jul 2 Epub ahead of print]. "This study examined mechanical and thermal hypersensitivity in the rat hind paw during cast immobilization of the hind limbs for 4 or 8 weeks and following cast removal. Blood flow, skin temperature, and volume of the rat hind paw were assessed in order to determine peripheral circulation of the hind limbs. Sensitization was analyzed by measuring the expression of the calcitonin gene-related peptide (CGRP) in the spinal dorsal horn following cast immobilization. Two weeks post immobilization, mechanical and thermal sensitivities increased significantly in all rats; however, peripheral circulation was not affected by immobilization. Cast immobilization for 8 weeks induced more serious hypersensitivity compared to cast immobilization for 4 weeks. Moreover, CGRP expression in the deeper lamina layer of the spinal dorsal horn increased in the rats immobilized for 8 weeks but not in those immobilized for 4 weeks. These findings suggest that immobilization-induced hypersensitivity develops during the immobilization period without affecting peripheral circulation. Our results also highlight the possibility that prolonged immobilization induces central sensitization in the spinal cord." [Although trigger points were not mentioned in this study, prolonged immobility in humans can cause trigger points that can cause the central sensitization noted here in rats. The omission points to the need for more TrP training among researchers. DJS]

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."

Hampson JP, Reed BD, Clauw DJ et al. 2013. Augmented Central Pain Processing in Vulvodynia. J Pain. pii: S1526-5900(13)00805-5. "Vulvodynia (VVD) is a chronic pain disorder wherein women display sensitivity to evoked stimuli at the vulva and/or spontaneous vulvar pain. Our previous work suggests generalized hyperalgesia in this population; however, little is known about central neurobiological factors that may influence pain in VVD…..The presence of augmented brain responses to pressure stimuli remote from the vulva was observed in vulvodynia patients. These findings may guide treatment decisions for better response, as brain mechanisms may be a factor in some VVD patients." [Researchers must learn to consider the causes of the pain, including trigger points, and the causes of hyperalgesia (or FM). DJS]

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 J, Waddington G, Adams R et al. 2013. Ability to discriminate movements at multiple joints around the body: global or site-specific. Percept Mot Skills. 116(1):59-68. This finding extends a previous report of non-significantly correlated proprioception test scores at two lower limb sites, and the findings taken together suggest that rather than proprioception being a global, general ability, sensitivity to the proprioception that underlies movement control is site-specific. [This proprioceptive dysfunction may relate to TrPs. DJS]

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 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.

Handa T, Fukuda K, Ichinohe T. 2013. Effect of Combination of Trigger Point Injection and Stellate Ganglion Block on Non-odontogenic Mandibular Molar Pain Referred from Masseter Muscle: A Case Report. Bull Tokyo Dent Coll. 54(3):171-175. "We report a case of myofascial pain syndrome (MPS), manifested as nonodontogenic mandibular molar pain referred from the masseter muscle, relieved by a combination of trigger point injection (TPI) and stellate ganglion block (SGB). The patient was a 32-year-old woman who had experienced cold hypersensitivity in the right third mandibular molar 2 months prior to visiting our department. Subsequently, she had visited a family dentist and undergone pulpectomy under local anesthesia. She eventually visited our clinic because there was no marked change in her symptoms. On the first visit, no tooth abnormality was found and the patient was neither anxious nor depressive. Tender points were found in the right masseter and temporal muscles during muscle palpation. Referred pain radiating to the right mandibular molars was observed when pressure was applied to the central portion of the right masseter muscle. As a result, we diagnosed MPS based on evidence of nonodontogenic tooth pain caused by referred pain from the masseter muscle. We performed TPI with 2% lidocaine hydrochloride to the tender point in the masseter muscle. Although the visual analog scale (VAS) pain score dropped from 97 to 36, complete pain relief was not achieved. The TPI was effective for approximately 7 hrs, after which severe throbbing pain returned. The sustained nature of the tooth pain suggested that it was sympathetic nerve-dependent. Subsequently, we performed SGB, resulting in a reduction in the VAS pain score from 90 to 32. Therefore, we performed another TPI and the VAS pain score dropped to 0. We continued SGB and TPI for the next 3 days and the symptoms disappeared. Thus, a combination of TPI and SGB controlled MPS manifested as masseter muscle-mediated nonodontogenic tooth pain."

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.

Hansraj KK. 2014. Assessment of stresses in the cervical spine caused by posture and position of the head. Surg Technol Int. 25:277-279. "Billions of people are using cell phone devices on the planet, essentially in poor posture. The purpose of this study is to assess the forces incrementally seen by the cervical spine as the head is tilted forward, into worsening posture. This data is also necessary for cervical spine surgeons to understand in the reconstruction of the neck." The study from New York Spine Surgery & Rehabilitation Medicine again validated information on the head-forward position as a perpetuating factor for pain and dysfunction. With the head erect in a healthy position, it places a weight of about 10 pounds on your straight spine. This is the weight the spine is designed to hold comfortably. When the head is tilted downward even 2 to 3 inches, it causes the stress on the spine to the equivalent of 27 pounds of weight. The more you tilt your head, such as to look down at a laptop or other device, the greater the weight of stress on your head. The use of electronic devices has developed a medical condition, called "tech neck".

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

Hassett AL, Hilliard PE, Goesling J et al. 2013. Reports of chronic pain in childhood and adolescence among patients at a tertiary care pain clinic. J Pain. 14(11):1390-1397. "Although chronic pain in childhood can last into adulthood, few studies have evaluated the characteristics of adults with chronic pain who report childhood chronic pain. Thus, 1,045 new patients…at an academic tertiary care pain clinic were prospectively evaluated using validated self-report questionnaires. Patients also responded to questions about childhood pain. We found that almost 17%…of adult chronic pain patients reported a history of chronic pain in childhood or adolescence, with close to 80% indicating that the pain in childhood continues today. Adults reporting childhood chronic pain were predominantly female (68%), commonly reported widespread pain (85%), and had almost 3 times the odds of meeting survey criteria for fibromyalgia….than those denying childhood chronic pain. Similarly, those with childhood pain had twice the odds of having biological relatives with chronic pain….and almost 3 times the odds of having relatives with psychiatric illness….. Lastly, compared to patients who did not report childhood chronic pain, those who did were more likely to use neuropathic descriptors for their pain…, have slightly worse functional status…, and have increased anxiety….Our study revealed that 1 in 6 adult pain patients reported pain that dated back to childhood or adolescence. In such patients, evidence suggested that their pain was more likely to be widespread, neuropathic in nature, and accompanied by psychological comorbidities and decreased functional status." [This is logical. The longer one has had pain, especially pain that often is accompanied by lack of understanding on the part of medical and nonmedical care providers and is insufficiently addressed, and the more genetic factors involved the more chance of developing pain that would lead one to a tertiary pain facility eventually. This paper offers some fascinating insights in chronic pain, and in the treatment of pain and dysfunction, of lack thereof, in early years. We must change this pattern and prevent chronicity by identifying and treating trigger points and other pain generators as soon as possible. DJS]

Haq SA, Darmawan J, Islam MN et al. 2005.  Prevalence of rheumatic diseases and associated outcomes in rural and urban communities in Bangladesh: a COPCORD study.  J Rheumatol. 32(2):348-353.  “Fibromyalgia is a common cause of morbidity, disability, and work loss in rural and urban communities of Bangladesh.”  [Fibromyalgia syndrome occurs worldwide, irrespective of race, socioeconomic class, or other variables. DJS]

Harbeck B, Sufke S, Harten P et al. 2013. High prevalence of fibromyalgia-associated symptoms in patients with hypothalamic-pituitary disorders. Clin Exp Rheumatol. [Epub ahead of print.] "Our data suggest that patients with hypothalamic-pituitary disorders may be at increased risk of developing fibromyalgia-associated symptoms."

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. 

Harrell JS, Chiou-Tan FY, Zhang H et al. 2009.  Procedure-oriented sectional anatomy of the shoulder.  J Comput Assist Tomogr. 33(5):814-817.  “This paper provides anatomically accurate schematics of the shoulder anatomy relevant to needle procedures.”  “The schematics allow for safer and more accurate non-image-guided needle procedures in the shoulder region.”

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."

Harris RE, Sundgren PC, Craig AD et al. 2009.  Elevated insular glutamate in fibromyalgia is associated with experimental pain.  Arthritis Rheum. 60(10):3146-3152.


Harris RE, Clauw DJ, Scott DJ et al. 2007.  Decreased central mu-opioid receptor availability in fibromyalgia.  J Neurosci. 27(37):10000-10006.  Positron emission tomography indicates that FM patients have a decreased mu-opioid binding potential in several areas of the brain associated with pain modulation.  This altered endogenous opioid activity may explain why it takes a greater amount of opioids for some FM patients to produce the same amount of pain control.


Harris RE, Clauw DJ. 2006.  How do we know fibromyalgia is “real?”  Curr Pain Headache Rep

(10):403-407.  There is now “overwhelming data” that indicate FMS is real, with genetic predisposition.  Functional magnetic resonance imaging (fMRI) and single photon emission computed tomography (SPECT) show significant difference between FMS patients and others.  It is not a psychological, functional or “somatic” disorder.  A variation in the gene that encodes the enzyme catechol-O-methyl transferase, significantly affects pain sensitivity and pain-related emotions and feelings.  This enzyme also is related to development of TMJD.  The pain is real, and it can be shown by radiological studies. 

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 FX. 2009.  Cytoskeletal forces produced by extremely low-frequency electric fields acting on extracellular glycoproteins.  [Jul 10 Epub ahead of print].  This article may explain one of the mechanisms by which microcurrent and other electroceutical devices can create changes in the cellular matrix.

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.

Hartmann D, Sarton J. 2014. Chronic pelvic floor dysfunction. Best Pract Res Clin Obstet Gynaecol. [Jul 17 Epub ahead of print.] "The successful treatment of women with vestibulodynia and its associated chronic pelvic floor dysfunctions requires interventions that address a broad field of possible pain contributors. Pelvic floor muscle hypertonicity was implicated in the mid-1990s as a trigger of major chronic vulvar pain. Painful bladder syndrome, irritable bowel syndrome, fibromyalgia, and temporomandibular jaw disorder are known common comorbidities that can cause a host of associated muscular, visceral, bony, and fascial dysfunctions. It appears that normalizing all of those disorders plays a pivotal role in reducing complaints of chronic vulvar pain and sexual dysfunction. Though the studies have yet to prove a specific protocol, physical therapists trained in pelvic dysfunction are reporting success with restoring tissue normalcy and reducing vulvar and sexual pain. A review of pelvic anatomy and common findings are presented along with suggested physical therapy management."

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, Burgmer M, Kollner V et al. 2013. [Fibromyalgia syndrome as a psychosomatic disorder - Diagnosis and therapy according to current evidence-based guidelines. Z Psychosom Med Psychother. 59(2):32-152. [German]. [The lead author is a known "debunker" of fibromyalgia. He seems unaware or disregarding of the research dismissing the usefulness of terms such as "somatoform" or the inappropriate use of "psychosomatic" in relation to fibromyalgia. As research piles up about the importance of peripheral pain driving the central sensitization of FM, these authors remain oblivious. They also seem unaware of the works as from Drs. Feng J, Zhang Z, Wu X et al. 2013, or Oaklander AL, Herzog ZD, Downs H et al 2013. The team also seems unaware of the medical vow, "Do no harm", as in my opinion, by publishing this erroneous article, they certainly are. DJS]

Hauser W, Galek A, Erbsloh-Moller B et al. 2013. Posttraumatic stress disorder in fibromyalgia syndrome: Prevalence, temporal relationship between posttraumatic stress and fibromyalgia symptoms, and impact on clinical outcome. Pain. [Apr 2 Epub ahead of print]. "FMS and PTSD are linked in several ways: PTSD is a potential risk factor of FMS and vice versa. FMS and PTSD are comorbid conditions because they are associated with common antecedent traumatic experiences." [This paper highlights another set of interactive diagnoses. DJS]

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. This article has several case studies and anecdotal inforamtin on sick building syndrome remediation by Graham/Stetzer filters to reduce dirty electricity, that is, electrical fields from wires and electrical devices causing sick building syndrome. This article infers that the increase in rates of disorders such as fibromyalgia, asthma, chronic fatigue, MS, ADD/ADHD, and diabetes might have a contributor in rising "electromagnetic pollution in the form of dirty electricity, ground current, and radio frequency from wireless devices," and urges that more research be done on this and on finding the number of people who are affected.

Hawk C, Long CR, Rowell RM et al. 2005.  A randomized trial investigating a chiropractic manual placebo: a novel design using standardized forces in the delivery of active and control treatments.  J Altern Complement Med. 11(1):109-117.  “Patients in the control group were not successfully blinded; however, patients’ perceptions of treatment group assignment did not significantly affect outcomes.   The clinically significant improvement in both groups, independent of patient or clinician expectations, suggests the presence of therapeutic factors common to both groups, other than biomechanical force.  Further studies examining other aspects of the clinical encounter, considered separately from biomechanical force, are warranted before arbitrarily designating any intervention as a ‘placebo’.”

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.

Hawkes TD, Manselle W, Woollacott MH. 2014. Tai Chi and meditation-plus-exercise benefit neural substrates of executive function: a cross-sectional, controlled study. J Complement Integr Med. Oct 8. [Epub ahead of print] "Our results suggest long-term Tai Chi practice, and meditation plus exercise may benefit the neural substrates of executive function."

Hawkins JL, Denson JE, Miley DR et al. 2015. Nicotine stimulates expression of proteins implicated in peripheral and central sensitization. Neuroscience. [Jan 28 Epub ahead of print.] "Our findings demonstrate that prolonged systemic administration of nicotine promotes sustained behavioral and cellular changes in the expression of key proteins in the spinal trigeminal nucleus and trigeminal ganglion implicated in the development and maintenance of peripheral and central sensitization."

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."

Hayden RJ, Louis DS, Doro C. 2005.  Fibromyalgia and myofascial pain syndromes and the workers’ compensation environment: an update.  Clin Occup Environ Med. 5(2):455-469.  “Controversy exists as to whether fibromyalgia and myofascial pain syndromes represent a specific pathology or are merely terms to describe clinical conditions that provide patients with the reassurance that their symptoms are real and help clinicians with therapeutic direction.  In the occupational health setting, this uncertainty can lead to significant difficulty in determining short- and long-term disability and assigning culpability to an individual’s work environment.”

Hayes AG, Arendt-Nielsen L, Tate S. 2014. Multiple mechanisms have been tested in pain – how can we improve the chances of success? Curr Opin Pharmacol. 14C:11-17. "Recent advances in understanding the pathophysiology of pain have led to a wealth of molecular targets for novel analgesic drugs and many clinical drug trials. There have been successes, like the gabapentinoids for neuropathic pain and calcium channel blockers for otherwise intractable pain states; and drugs which show promise in clinical trials, like nerve growth factor inhibitors and p38 kinase inhibitors. Unfortunately there have also been a number of failures. We suggest factors which might predispose to success, for example some clinical precedence for the mechanism in pain or a genetic link for the mechanism, for example a mutation linked to a pain syndrome. We also stress the importance of demonstrating molecular target engagement with a novel compound and suggest pain biomarkers which can be used for mechanistic drug profiling."

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. 

He D, Veiersted KB, Hostmark AT et al. 2004.  Effect of acupuncture treatment on chronic neck and shoulder pain in sedentary female workers: a 6-month and 3-year follow-up study.  Pain 109(3):299-307.  “Adequate acupuncture treatment may reduce chronic pain in the neck and shoulders and related headache.  The effect lasted for 3 years.”

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.

Henrich CF, Ramulu PY, Akpek EK. 2014. Association of dry eye and inflammatory systemic diseases in a tertiary care-based sample. Cornea. 33(8):819-825."Systemic inflammatory diseases are frequently associated with dry eye in patients evaluated at a tertiary academic center. Diagnostic evaluations may help uncover previously undiagnosed significant conditions in about one-third of tested patients."

Henriksen M, Lund H, Christensen R et al. 2009.  Relationships between the fibromyalgia impact questionnaire, tender point count, and muscle strength in female patients with fibromyalgia: a cohort study.  Arthritis Rheum. 61(6):732-739.  “…reduced knee muscle strength appears to be a common objective abnormality in FM that is independent of measurements of disease activity.”  [ It would be helpful if co-existing TrPs were evaluated, as muscle weakness occurs with TrPs even before pain.  Muscle weakness noted in this study could be due to co-existing TrPs. DJS]

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 CM, Liedberg GM, Gerdle B. 2005.  Women with fibromyalgia: work and rehabilitation.  Disabil Rehabil. 27(12):685-694.  “The total life situation, other commitments, type of work tasks, the ability to influence the work situation, and the physical and psychosocial work environment are important factors in determining whether a person can remain in a work role.  More knowledge is needed about how to adjust work conditions for people with partial work ability to the benefit of society and the individual.”

Henriksson CM. 1995.  Living with continuous muscular pain — patient perspectives.  Part I: Encounters and consequences.  Scand J Caring Sci 9(2):67-76.  “The contradiction between the patients’ perception of illness and the lack of objective findings is stressful.  The women feel rejected, misunderstood, and disbelieved, which prevents them from dealing with their situation constructively.  Long investigation periods provoke anxiety, and confirmation of the diagnosis is a relief.  Daily routines are disrupted, conflicts between life roles lead to additional stress and the women experience loss of ability to perform valued activities, lack of physical fitness and loss of future opportunities.  Patients need early and adequate information and the consequences of the condition must be acknowledged and taken into consideration if secondary economic and psychosocial consequences are to be minimized.”

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 L. 2015. Chiropractic management of postpartum pubic symphysis diastasis: A case report. J Can Chiropr Assoc. 59(1):30-36. "This case report describes the chiropractic management of a 30-year-old female patient with severe postpartum pelvic pain secondary to pubic symphysis diastasis. No literature was found on the chiropractic management of postpartum symphysis pubis diastasis. The existing literature concerning chiropractic care for symphysis pubis dysfunction during pregnancy is limited and indicates a potential benefit. Separation of the pubic symphysis may include ligamentous injury to the sacroiliac joints and may lead to chronic pain. Pubic symphysis separation of 17 millimeters was present on digital radiograph. Management consisted of chiropractic adjustments, trigger point release, electrical stimulation, moist heat, sacroiliac belt, and specific stabilizing exercises. The patient's pain improved immediately following treatment on the initial visit. Pain was reduced from 8/10 VAS at the first visit to 2/10 at the fourth visit. She was able to resume normal activities and reached a final pain level of 1/10. The diastasis was reduced by 7 millimeters at 14-weeks post radiograph for a final separation of just under 10 millimeters. Collaboration between obstetricians, midwives and chiropractors may be warranted." Free PMC Article

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.

Hillstrom HJ, Buckland MA, Slevin CM et al. 2013. Effect of shoe flexibility on plantar loading in children learning to walk. J Am Podiatr Med Assoc. 103(4):297-305. This study from the Motion Analysis Laboratory of New York Rehabilitation Department, Hospital for Special Surgery, suggests that increased shoe flexibility helps foot health. "This mechanical feedback may enhance proprioception, which is a desirable attribute for children learning to walk." [Good for adults, too. DJS]

Hirsch JK, Sirois FM. 2014. Hope and fatigue in chronic illness: The role of perceived stress. J Health Psychol. [Mar 26 Epub ahead of print.] "Fatigue is a debilitating symptom of chronic illness that is deleteriously affected by perceived stress, a process particularly relevant to inflammatory disease. Hopefulness, a goal-based motivational construct, may beneficially influence stress and fatigue, yet little research has examined these associations. We assessed the relation between hope and fatigue, and the mediating effect of stress, in individuals with fibromyalgia, arthritis, and inflammatory bowel disease. Co-varying age, sex, and pain, stress partially mediated the association between hope and fatigue; those with greater hope reported less stress and consequent fatigue. Therapeutically, bolstering hope may allow proactive management of stressors, resulting in less fatigue." [Hope often comes with identifying the causes of the fatigue and treating them, and the focus should be towards this goal. DJS]

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.

Hiyama S, Ono T, Ishiwata Y et al. 2003.  Effects of experimental nasal obstruction on human masseter and suprahyoid muscle activities during sleep.  Angle Orthod. 73(2):151-157.  “Nasal obstruction could modulate the activities of the masseter and suprahyoid muscles during sleep.”  Activity of the suprahyoid muscles tended to increase significantly and the masseter tended to decrease significantly with nasal obstruction during sleep.  [This could affect TrPs, and also CPAP therapy for co-existing sleep apnea.  For the latter, it may indicate need for automatically adjusting CPAP set to maximum high equal to that of the sleep study need of the patient, rather than standard CPAP in some patients. DJS]

Holman AJ, Neiman RA, Ettlinger RE. 2004. Preliminary efficacy of the dopamine agonist, pramipexole for fibromyalgia: the first, open label, multicenter experience. J Musculoskel Pain 12(1):69-74. Dopamine agonists may be promising pharmaceutical agents for the treatment of  FMS.

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.

Hocking MJ. 2013. Exploring the central modulation hypothesis: do ancient memory mechanisms underlie the pathophysiology of trigger points? Curr Pain Headache Rep. 17(7):347. The author proposes that central nervous system-maintained global changes in alpha-motorneuron function, resulting from sustained plateau polarization, rather than local dysfunction of the motor endplate, underlie the pathogenesis of TrPs.

Hodges PW, Mellor R, Crossley K et al. 2009.  Pain induced by injection of hypertonic saline into the infrapatellar fat pad and effect on coordination of the quadriceps muscles.  Arthritis Rheum. 61(1):70-77.  “…alterations in coordination of knee muscle activity can be caused by pain, even when it is of nonmuscle origin.  Treatment of pain is therefore important to facilitate performance of the quadriceps muscles, which are essential for locomotor and functional tasks as well as for knee stability.”  [Although this article does not specifically site TrPs as part of this connection, they are involved.  DJS]

Hodges PW, Sapsford R, Pengel LH. 2007.  Postural and respiratory functions of the pelvic floor muscles.  Neurourol Urodyn. 26(3):362-371.  “This study provides evidence that the PFM (pelvic floor muscles) contribute to both postural and respiratory functions.”  [Although this article does not specifically site TrPs as part of this connection, they are involved.  Releasing the pelvic floor tightness, which is often caused by TrPs, may indirectly aid posture and respiration. DJS]

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

Hoeger Bement MK, Weyer AD, Yoon T et al. 2014. Corticomotor excitability during a noxious stimulus before and after exercise in women with fibromyalgia. J Clin Neurophysiol. 31(1):94-98. "The purposes of this study were to assess corticomotor excitability in people with fibromyalgia during a noxious stimulus before and after fatiguing exercise and examine associations with pain perception. Fifteen women with fibromyalgia completed three sessions: one familiarization and two experimental. The experimental sessions were randomized and involved measurement of pain perception and motor evoked potentials before and after (1) quiet rest and (2) isometric contraction of the elbow flexor muscles. Motor evoked potential amplitude of brachioradialis muscle was measured following transcranial magnetic stimulation delivered before, during, and after a noxious mechanical stimulus. After quiet rest, there was no change in pain perception. After the submaximal contraction, there was considerable variability in the pain response. Based on the changes in the experimental pain, subjects were divided into three groups (increase, decrease, and no change in pain). There was an interaction between pain response and the pain-induced change in motor evoked potentials. Those individuals who had an increase in motor evoked potentials during the pain test had an increase in pain after exercise. Thus, women with fibromyalgia were classified based on their pain response to exercise, and this response was associated with the change in corticomotor excitability during the application of a noxious stimulus."

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.

Holey LA, Dixon J. 2014. Connective tissue manipulation: A review of theory and clinical evidence. J Bodyw Move Ther. 18:112-118. "Connective tissue manipulation or connective tissue massage (bindegewebsmassage) is a manual reflex therapy in that it is applied with the therapist's hands which are in contact with the patient's skin. The assessment of the patient and the clinical decision-making that directs treatment is based on a theoretical model that assumes a reflex effect on the autonomic nervous system which is induced by manipulating the fascial layers within and beneath the skin to stimulate cutaneo-visceral reflexes. This paper reviews the literature and current research findings to establish the theoretical framework for CTM and the evidence for its clinical effects. The rationale for the principles of treatment is discussed and the evidence for the clinical effectiveness assessed through an analytical review of the clinical research." [This paper indicates to me that CTM would be an excellent therapy option for chronic myofascial pain. If fibromyalgia central sensitization were also involved, therapy would, as always, require modification. DJS]

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].

Holman AJ, Myers RR. 2005.  A randomized, double-blind, placebo-controlled trial of pramipexole, a dopamine agonist, in patients with fibromyalgia receiving concomitant medications.  Arthritis Rheum. 52(8):2495-2505.  “In a subset of patients with fibromyalgia, approximately 50% of whom required narcotic analgesia and/or were disabled, treatment with pramipexole improved scores on assessments of pain, fatigue, function, and global status, and was safe and well-tolerated.”

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, Louzeda FM, Goes SM et al. 2013. Acylated ghrelin: a potential marker for fibromyalgia? Eur J Pain. 17(8):1216-1224. The findings in this study indicate that decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity. [These patients were not assessed for co-existing insulin resistance, which may relate to the ghrelin finding. DJS]

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

Homma M, Ishikawa H, Kiuchi T. 2014. Association of physicians' illness perception of fibromyalgia with frustration and resistance to accepting patients: a cross-sectional study. Clin Rheumatol. [Aug 3 Epub ahead of print.] "The aim of this study was to elucidate whether physicians' illness perceptions correlate with their frustration or resistance to accepting patients with fibromyalgia (FM). In this cross-sectional postal survey, questionnaires were sent to member physicians of the Japan College of Rheumatology and Japan Rheumatism Foundation. Measures collected included the Brief Illness Perception Questionnaire with Causal Attribution, the Illness Invalidation Inventory, and the Difficult Doctor-Patient Relationship Questionnaire (DDPRQ-10). Multiple logistic regression was performed to examine associations between the DDPRQ-10 and resistance to accepting patients with FM for treatment. We analyzed data from 233 physicians who had experience in consulting with patients with FM. Only 44.2 % answered that they wanted to accept additional patients with FM. Physicians' frustration was associated with difficulty controlling symptoms, patients' emotional responses, and causal attribution of FM to patient internal factors. Conversely, lower levels of frustration were associated with causal attributions to biological factors and uncontrollable external factors. However, the 'difficult patient' perception did not correlate with resistance to accepting patients with FM. Difficulty controlling symptoms with treatment was the one factor common to both physicians' frustration and resistance to accepting patients with FM. Physicians may hesitate to accept patients with FM not because of the stigmatic image of the 'difficult patient,' but instead because of the difficulty in controlling the symptoms of FM. Thus, to improve the quality of consultation, physicians must continuously receive new information about the treatments and causes of FM."

Hong CZ. 2013. Needling therapy for myofascial pain control. Evid Based Complement Alternat Med. [Aug 26 Epub ahead of print]. Needling in this context includes all therapies that include the use of a needle for penetration for medication injection or mechanical stimulation by needle alone (dry needling), including acupuncture and superficial needling. This paper specifically deals with needling for myofascial pain due to trigger points, and is written by a myofascial specialist who originally trained with David G. Simons. It touches on two review articles and seven original research papers. The use of the multiple insertion technique of dry needling is highlighted, as it can provide fast and efficient immediate pain control. During the injection, the needle is moved in and out, as it is positioned in different directions to find and treat multiple loci in the area. The author has modified this Travell-Boggs technique using a very fast method recommended by David Simons that avoids much of the muscle fiber damage due to side movement of the needle or the needle grab by the muscle. The immediate pain relief from multiple needle insertion is due to effects on the descending pain inhibitory system. A local twitch response (LTR) or the muscle grabbing of the needle (De-Qi effect) can signal the successful needle contact with each sensitive locus. It is important to find as many as possible to obtain maximum relief of pain. Needling key trigger points can inhibit satellite trigger point irritability and minimize central sensitization, so it is important to discover which trigger points are primary or "key."

Hong CZ. 1996.  Pathophysiology of myofascial trigger point.  J Formos Med Assoc. 95(2):93-104.  “Myofascial trigger point is a sensitive spot in a palpable taut band of skeletal muscle fibers.  Two important clinical characteristics of trigger points, referred pain and local twitch response, can be elicited by mechanical stimulation (palpation or needling).  The trigger point is usually activated by acute or chronic injury to a muscle, tendon, ligament, joint, disc or nerve.  Recent human and animal studies have suggested that the pathogenesis of either referred pain or local twitch response is related to integration in the spinal cord.  It has been proposed that there are multiple sensitive loci in a trigger point region.  A sensitive locus may contain one or more sensitized nociceptive nerve endings.  Mechanical stimulation of a sensitive locus can elicit a local twitch response which is frequently associated with characteristic referred pain.  Theoretically, sensitive loci can be found in any site of a skeletal muscle, but is usually distributed with highest concentration near the endplate region where a trigger point is frequently found.  The trigger point is a common pathogenic pathway of muscle pain from different causes.”

Hong CZ. 1994.  Lidocaine injection versus dry needling to myofascial trigger point.  The importance of the local twitch response.  Am J Phys Med Rehabil. 73(4):256-263.  “This study was designed to investigate the effects of injection with a local anesthetic agent or dry needling into a myofascial trigger point (TrP) of the upper trapezius muscle in 58 patients.  Trigger point injections with 0.5% lidocaine were given to 26 patients (Group I), and dry needling was performed on TrPs in 15 patients (Group II).  Local twitch responses (LTRs) were elicited during multiple needle insertions in both Groups I and II.  In another 17 patients, no LTR was elicited during TrP injection with lidocaine (9 patients, group Ia) or dry needling (8 patients, group IIa).  Improvement was assessed by measuring the subjective pain intensity, the pain threshold of the TrP and the range of motion of the cervical spine.  Significant improvement occurred immediately after injection into the patients in both group I and group II.  In Groups Ia and Ib, there was little change in pain, tenderness or tightness after injection.  Within 2-8 h after injection or dry needling, soreness (different from patients’ original myofascial pain) developed in 42% of the patients in group I and in 100% of the patients in group II.  Patients treated with dry needling had postinjection soreness of significantly greater intensity and longer duration than those treated with lidocaine injection.  The author concludes that it is essential to elicit LTRs during injection to obtain an immediately desirable effect.  TrP injection with 0.5% lidocaine is recommended, because it reduces the intensity and duration of postinjection soreness compared with that produced by dry needling.”

Hong CZ. 1994.  Persistence of local twitch response with loss of conduction to and from the spinal cord.  Arch Phys Med Rehabil. 75(1):12-16.  “These findings indicate that the transmission of LTR (local twitch response) depends mainly on the central nervous system with a possible minor degree of local transmission.”

Hong CZ. 1996.  Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil. 77(11):1161-1166.  “Two weeks after injection, the degree of improvement in PT (pain threshold) or ROM (range of motion) (but not PI (pain intensity)) was not significantly different between two groups.  Post-injection soreness (different from myofascial pain) was more severe, developed sooner, and lasted longer in Group 1 than in Group 2.  Conclusion: Trigger point injection is a valuable procedure for pain relief for patients in both groups.  Patients with FMS are likely to experience significant but delayed and attenuated pain relief following injection of their active TrPs compared to myofascial pain patients with similar TrPs but without FMS.  aAlso, FMS patients are likely to experience significantly more post-injection soreness for a longer period of time.”

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 CZ. 1994.  Lidocaine injection versus dry needling to myofascial trigger point.  The importance of the local twitch response.  Am J Phys Med Rehabil 73(4):256-263.  “Lidocaine reduces the intensity and duration of postinjection soreness compared with that produced by dry needling.”  [This is important to remember for patients who also have the central sensitization of FMS.  The pain of dry needling may needlessly further sensitize the central nervous system in some patients with both FMS and TrPs. DJS]


Hong CZ. 2002.  New trends in myofascial pain syndrome.  Zhonghua Yi Xue Za Zhi 65(11):501-512.  Myofascial TrP therapies include “...stretch, massage, thermotherapy, electrotherapy, laser therapy, MTrP injection, dry needling, and acupuncture.”  [Dry needling is not recommended if the patient also has central sensitization such as fibromyalgia. DJS]


Hong CZ. 1994.  Lidocaine injection versus dry needling to myofascial trigger point.  The importance of the local twitch response.  Am J Phys Med Rehabil 73(4):256-263.  “Patients treated with dry needling had post-injection soreness of significantly greater intensity and longer duration than those treated with lidocaine injection.  It is essential to elicit LTRs during injection to obtain an immediately desirable effect.  TrP injection with 0.5% lidocaine is recommended, because it reduces the intensity and duration of post-injection soreness compared with that produced by dry needling.”

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.

Horwitz S, Stewart A. 2015. An exploratory study to determine the relationship between cervical dysfunction and perimenstrual migraines. Physiother Can. 67(1):30-38. "Subjects with perimenstrual migraines were compared with controls on the basis of neck stiffness, trigger points, posture, range of motion, muscle strength, neural mobility and assessment of cervical joint mobility." There may be an association, according to these results, and more studies are needed.

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…”

Hotamisligil GS. 2003.  Inflammatory pathways and insulin action.  Int J Obes Relat Metab Disord. 27 Suppl 3:S53-55.  “Obesity and type 2 diabetes are associated with a state of abnormal inflammatory response.  The state of chronic inflammation typical of obesity and type 2 diabetes occurs at metabolically relevant sites, such as the liver, muscle, and most interestingly, adipose tissues.  Interference with these pathways improves or alleviates insulin resistance.  The abnormal production of tumor necrosis factor alpha (TNF-alpha) in obesity is a paradigm for the metabolic significance of this inflammatory response.  When TNF-alpha activity is blocked in obesity, either biochemically or genetically, the result is improved insulin sensitivity.” 


Hotamisligil GS. 2003.  Inflammatory pathways and insulin action.  Int J Obes Relat Metab Disord. 27 Suppl 3:S53-55.  “Obesity and type 2 diabetes are associated with a state of abnormal inflammatory response.  The state of chronic inflammation typical of obesity and type 2 diabetes occurs at metabolically relevant sites, such as the liver, muscle, and most interestingly, adipose tissues. …interference with these pathways improve or alleviate insulin resistance.  Recent years have seen a critical progress in this respect by the identification of several downstream mediators and signaling pathways, which provide the crosstalk between inflammatory and metabolic signaling.”

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.”

Hou, C-R,  K-C Chung, J-T Chen. 1991. The effect of calcium channel blocker on spontaneous potentials of trigger points in rabbits: Clin J of Biomed Eng 18(3):143-149.


Houle S, Descarreaux M. 2009. Conservative care of temporomandibular joint disorder in a 35-year-old patient with spinal muscular atrophy type III: a case study.  J Chiropr Med. 8(4):187-192.  “Chiropractic care was provided and included TMJ mobilization, myofascial therapy, trigger point therapy, and light spinal mobilizations of the upper cervical vertebrae.  Final evaluation of TMJ range of motion showed active opening of 12 mm with absence of pain and muscle tenderness of the jaw.  Conclusion: This case suggests that a patient with musculoskeletal disorders related to underlying neurodegenerative pathologies may benefit from chiropractic management adapted to their condition.  In the present case, chiropractic treatment of the TMJ represented a viable, low-cost approach with limited adverse effects compared with surgery.”   [Noninvasive successful therapy is always to be preferred.   Treatment included trigger point therapy and myofascial therapy.   Much surgery could be avoided by the prompt and successful treatment of TrPs. DJS]

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 CC, Liu SY et al. 2014. Remote dose-dependent effects of dry needling at distant myofascial trigger spots of rabbit skeletal muscles on reduction of substance p levels of proximal muscle and spinal cords. Biomed Res Int. 2014:982121. This remote effect of dry needling involves the reduction of SP levels in proximal muscle and spinal superficial laminaes, which may be closely associated with the control of myofascial pain. Free Article

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].

Hsu RY, Bariteau J. 2013. Management of ankle fractures. R I Med J. 96(5):23-27. "Ankle fractures are a common injury across all age groups. Management may be operative or nonoperative, depending on the severity of the injury and the patient's overall health and functional status. Although imaging defines the nature of the fracture, a careful history and physical also helps determine the patient's plan of care. Initial management is focused on adequate alignment and safe immobilization of the injury. Definitive management must provide anatomic alignment of the joint as well as consideration of the surrounding soft tissues. Rehabilitation after either operative or nonoperative treatment aims at restoring range of motion, strength, proprioception, and function." [Often it is the imagery that is treated—the MRI, X-ray or whatever, rather than the patient. The soft tissue is immobilized (and usually untreated) while the bone is in a cast. We must remember the importance of soft tissue. DJS]

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 CY, Chen YL, Li AH et al. 2014. Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons. Neuroinflammation. 11(1):7. This study in rats found that injecting minocycline, a specific inhibitor of microglial activation, provided pain relief in rats with induced central sensitization.

Huang JT, Chen HY, Hong CZ et al. 2014. Lumbar facet injection for the treatment of chronic piriformis myofascial pain syndrome: 52 case studies. Patient Prefer Adherence. 8:1105-1111. "It is important to identify the possible cause of piriformis myofascial pain syndrome. If this pain is related to lumbar facet lesions, lumbar facet joint injection can immediately suppress piriformis myofascial pain symptoms. This effectiveness may last for at least 6 months in most patients. This study further supports the importance of eliminating the underlying etiological lesion for complete and effective relief of myofascial pain syndrome." Iglesias-Gonzalez JJ, Munoz-García MT, Rodrigues-de-Souza DP et al. 2013. Pain Med. 14(12):1964-1970. Myofascial trigger points, pain, disability, and sleep quality in patients with chronic nonspecific low back pain. Forty-two patients with nonspecific LBP (50% women), aged 23-55 years old, and 42 age- and sex-matched controls participated…. TrPs were bilaterally explored within the quadratus lumborum, iliocostalis lumborum, psoas, piriformis, gluteus minimus, and gluteus medius muscles in a blinded design. TrPs were considered active if the subject recognized the local and referred pain as familiar symptoms, and TrPs were considered latent if the pain was not recognized as a familiar symptom…. The local and referred pain elicited by active TrPs in the back and hip muscles contributes to pain symptoms in nonspecific LBP. Patients had higher disability and worse sleep quality than controls. The number of active TrPs was associated with pain intensity and sleep quality. It is possible that a complex interaction among these factors is present in patients with nonspecific LBP.

Huang QM, Liu L. 2014. Wet needling of myofascial trigger points in abdominal muscles for treatment of primary dysmenorrhoea. Acupunct Med. 32(4):346-349. "Primary dysmenorrhoea was significantly reduced 1 year after wet needling to MTrPs in the abdominal region and home stretching exercises, justifying further research with controlled trials."

Huang QM, Lv JJ, Ruanshi QM et al. 2015. Spontaneous electrical activities at myofascial trigger points at different stages of recovery from injury in a rat model. Acupunct Med. [May 13 Epub ahead of print.] "Background: Spontaneous electrical activity (SEA) is a feature of myofascial trigger points (MTrPs), which can either be latent or active. However, SEA at different stages of recovery from MTrPs remains unclear....Conclusions: Increasing recovery periods following a MTrP modeling intervention in rats are characterized by different frequencies and amplitudes of SEA from TBs (taut bands)."

Huang QM, Ye G, Zhao ZY et al. 2013. Myoelectrical activity and muscle morphology in a rat model of myofascial trigger points induced by blunt trauma to the vastus medialis. Acupunct Med. 31(1):65-73. "A total of 24 male SD rats were randomly divided into a control group (group A) and model group (group B). A blunt striking injury and eccentric exercise were applied to the vastus medialis (VM) of rats in group B for 8 weeks. Later, the palpable taut band (TB), local twitch response, myoelectrical activities and morphology in the two groups were examined….An average of 2.5 (30/12) palpable TBs were detected in the VM in group B compared with none in group A. The MTrPs had two types of abnormal potential. Their amplitudes were significantly higher than those in the control group…but their durations showed no significant differences. A series of reflex contractions appeared in groups A and B in response to external stimulation to the ear. Their amplitude and duration in group B were significantly lower than those in group A. A series of lower fibrillation potentials repeatedly occurred in model MTrPs in group B. The morphology of MTrPs showed abnormal muscle fibres with large round or ellipse shapes in cross-section and enlarged tapering shapes in longitudinal section….Active MTrPs can be provoked by repeated blunt injury. Active MTrPs are a group of muscle fibres with abnormal shapes and abnormal myoelectrical potentials. External stimulation provokes low-voltage responses in MTrPs, which is different from the response of normal muscle fibres.

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.

Huber J, Lisiñski P, Polowczyk A. 2013. Reinvestigation of the dysfunction in neck and shoulder girdle muscles as the reason of cervicogenic headache among office workers. Disabil Rehabil. 35(10):793-802. This study from Poland investigated: "Dysfunction of cervical and shoulder girdle muscles as reason of cervicogenic headache (CEH) was reinvestigated with clinical and neurophysiological studies….Forty office workers were randomized into two groups to verify efficiency of supervised kinesiotherapy (N = 20) aimed with improvement of muscle's activity and headache symptoms releasing. Headache intensity was evaluated with visual analog scale (VAS), range of cervical movement (ROM) with goniometer, trigger points (TrPs) incidence with palpation and muscle's strength with Lovett's scale. Reaction of patients for muscle's elongation was also evaluated. Surface electromyographical recordings were bilaterally analyzed at rest (rEMG) and during maximal contraction (mcEMG)….Deficits of cervical flexion and muscles strength were found in all patients. TrPs occurred predominantly in painful trapezius muscle. Incidence of trigger points coexisted with intensity of CEH. Results indicated on muscles dysfunction which improved only after supervised therapy. Positive correlations between increase in rEMG amplitudes and high VAS scores, high-amplitude rEMG recordings incidence and increased number of TrPs were found. Negative correlation was detected between amplitude in mcEMG and amplitude of rEMG recordings…Dysfunction of trapezius muscle was most responsible for CEH etiology. Proposed algorithm of kinesiotherapy was effective as complementary method of the CEH patients' treatment."

Huber R, Ghilardi MF, Massimini M et al.  2004.  Local sleep and learning.  Nature 430(6995):78-81. The amount of slow-wave activity in right brain areas can help consolidate new learning.  It is important for medical teams to help FMS patients regain deep level sleep.

Hudson JI, Arnold LM, Bradley LA et al. 2009.  What makes patients with fibromyalgia feel better?  Correlations between patient global impression of improvement and changes in clinical symptoms and function: a pooled analysis of four randomized placebo-controlled trials of duloxetine.  J Rheumatol. 36(11):2517-2522.  “In addition to pain reduction, what makes patients with FM feel better may include improvement in fatigue, physical functioning, mood, and impact on daily living.  An assessment of these domains may be important in clinical trials of FM and in the management of patients with FM.”

Hudson JL, Arnold LM, Keck PE et al. 2004.  Family study of fibromyalgia and affective spectrum disorder.  Biol Psychiatry 56(11):884-891.  This study found that FMS was associated with the other medical and psychiatric disorders that are proposed to be grouped as affective spectrum disorder.  [Since FMS does not cover a homogenous group, lumping it as such with a group of medical and psychiatric disorders could add to the confusion. DJS]

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]

Hughes KH. 1998. Painful rib syndrome. A variant of myofascial pain syndrome. AAOHN J. 46(3):115-120.

Humphreys BK, Kenin S, Hubbard BB et al. 2003.  Investigation of connective tissue attachments to the cervical spinal dura mater.  Clin Anat. 16(2):152-159.  Common but previously unremarked connective tissue attachments originating from the nuchal ligament and rectus capitis posterior minor muscle to the dura may play a significant role in neck pain.

Hunter C, Dubois M, Zou S et al. 2009.  A new muscle pain detection device to diagnose muscles a source of back and/or neck pain.  Pain Med. [Dec 16 Epub ahead of print].  “…a Muscle Pain Detection Device (MPDD) has been developed.  A muscle is stimulated and painful muscles are precisely detected, allowing distinctions between primary and referred muscle pain as well as distinguishing other functional muscle pain thought to cause MPS.”  “Using the MPDD appears to be more valid and potentially more reliable than palpation to identify muscles causing regional pain that could benefit from injections.”  [It might be useful and effective to teach palpation skills in medical, dental and other health care schools. DJS]

Huntley AH, Srbely JZ, Zettel JL. 2015. Experimentally induced central sensitization in the cervical spine evokes postural stiffening strategies in healthy young adults. Gait Posture. [Jan 24 Epub ahead of print.] "Dysequilibrium of cervicogenic origin can result from pain and injury to cervical paraspinal tissues post-whiplash; however, the specific physiological mechanisms still remain unclear. Central sensitization is a neuradaptive process which has been clinically associated with conditions of chronic pain and hypersensitivity. Strong links have been demonstrated between pain hypersensitivity and postural deficits post-whiplash; however, the precise mechanisms are still poorly understood. The purpose of this study was to explore the mechanisms of cervicogenic disequilibrium by investigating the effect of experimentally induced central sensitization in the cervical spine on postural stability in young healthy adults." The results of this study suggest that the body stiffens in reaction to sensitizing spinal stimulation. "Future studies need to further explore this relationship in clinical (whiplash, chronic pain) populations." [This stiffening may be part of the formation of myofascial trigger points. 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.

Huskey AM, Thomas CC, Waddell JA. 2013. Occurrence of milnacipran-associated morbilliform rash and serotonin toxicity. Ann Pharmacother. 47(7-8):e32. "A 57-year-old white female presented to the emergency department because of a full-body morbilliform rash, which appeared 9 days after initiation of milnacipran 50 mg twice daily. In the emergency department the patient's vital signs were: heart rate 121 beats/min, blood pressure 180/100 mm Hg, and temperature 38.9 °C. The patient reported diarrhea, nausea, dizziness, restlessness, and increased muscle pain. Her history included recurrent breast cancer first diagnosed in 1999, hypertension, fibromyalgia, depression, osteopenia, gastroesophageal reflux disease, insomnia, and endometriosis. Her home medications included milnacipran, fluoxetine, alprazolam, zolpidem, zoledronic acid, anastrozole, doxepin, ranitidine, levocetirizine, doxazosin, tramadol, vitamin D, and ferrous gluconate. The patient's increased heart rate, blood pressure, and temperature, as well as restlessness, self-reported diarrhea and nausea, and self-reported increase in muscle pain, indicated serotonin toxicity. Milnacipran, fluoxetine, and tramadol were discontinued, while doxepin was continued. Treatment consisted of acetaminophen, diphenhydramine, methylprednisolone, promethazine, and hydralazine 10 mg intravenously. The following morning all vital signs were within normal limits and the patient's diarrhea, nausea, dizziness, restlessness, and muscle pain resolved. She was discharged the following morning. The rash had resolved after day 2 of hospital discharge, which was the fourth day after discontinuation of milnacipran….It is important to increase awareness of the possibility of developing morbilliform rash and serotonin toxicity with milnacipran therapy, as both conditions can be associated with poor outcomes if not detected early and treated appropriately."

Hussain SA, Al-Khalifa II, Jasim NA et al. 2010. Adjuvant use of melatonin for treatment of fibromyalgia. J Pineal Res. [Dec 16 Epub ahead of print]. "Using melatonin (3mg or 5mg/day) in combination with 20 mg/day fluoxetine resulted in significant reduction in both total and different components of FIQ score compared to the pretreatment values. In conclusion, administration of melatonin, alone or in a combination with fluoxetine, was effective in the treatment of patients with FMS."

Huysmans MA, Hoozemans MJ, van der Beek AJ et al. 2007.  Fatigue effects of tracking performance and muscle activity.  [Jan 5 Epub ahead of print] J Electromyogr Kinesiol.

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 16th]  This paper describes two main pain patterns of pronator quadratus myofascial trigger points.

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