References for Research Purposes

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.

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.”

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.

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.

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.

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).”

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, 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, 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 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 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, 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, 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 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, 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, 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.”

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, 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 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.”

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

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

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.”

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, 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.

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. 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.

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

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

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

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

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

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

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

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.

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.

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.

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.

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

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

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.”

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, 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.

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

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

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

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

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

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.”

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.

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.”

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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]

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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]

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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.”

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

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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]

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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]

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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]

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

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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.

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]

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

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

Ge HY, 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.

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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.”

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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]

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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.

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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.

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

Giamberardino MA, 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.”

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.

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.

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

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

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

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

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.”

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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.”

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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,]

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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]

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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]

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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."

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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.

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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.”

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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]

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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.”

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%.”

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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.

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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.

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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.

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]

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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]

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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.”

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(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.

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

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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.”

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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.

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.” [TrPs in the sternocleidomastoid muscle are known for ability to cause congestion. Other muscles may be part of the “cause and effect” spiral, and need to be checked as well, especially in cases of sleep apnea and known myofascial pain. DJS]

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.

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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.

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.

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]

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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.

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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.”

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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.”

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Imamura M, Hsing WT, Kaziyama H et al. 2007. Hyperalgesia of central origin in patients with severe osteoarthritis of the knee. J Musculoskel Pain 15 (Supp 13):25 item 40. [Myopain 2007 Poster] “There is a significant deficit in the PPT in all spinal levels studied. CS (central sensitization) needs to be addressed as part of the treatment.” [Central sensitization is often unacknowledged and untreated in osteoarthritis, as are co-existing MTPs. Peripheral pain can cause and maintain central sensitization, but the hypersensitive central nervous system must be treated to enable the peripheral areas to better respond to their treatment. DJS]

Imamura M, Kaziyama HHS, Hsing WT et al. 2007. Efficacy of a segmental neuromyotherapy approach to improve pain pressure threshold in patients with severe osteoarthritis of the knee. J Musculoskel Pain 15 (Supp 13):25 item 39. [Myopain 2007 Poster] “Segmental neuromyotherapy improved PPT immediately and after three months of treatment.” [Sclerodermal hyperalgesia of the supraspinous ligaments in addition to MTPs are often a vital yet unacknowledged and untreated component of osteoarthritic pain. DJS]

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Isomaa B. 2003. A major health hazard: the metabolic syndrome. Life Sci 73(19):2395-2411. “The metabolic syndrome seems to result from a collision between susceptible ‘thrifty genes’ and a society characterized by an increased prevalence of obesity and a sedentary lifestyle.” “The metabolic syndrome constitutes a major challenge for public health…since more than 40 million U.S. adults seem to be affected…. Lifestyle changes could have a profound influence on the syndrome and its development.”

Itoh K, Okada K. 2007. Influence of ovariectomy on development of delayed onset muscle soreness in female rates. J Musculoskel Pain 15 (Supp 13):26 item 42. [Myopain 2007 Poster] “In the present study, the muscle pain thresholds were influenced by the estrus cycle in the intact control female rates. The delay of development of muscular hyperalgesia was also detected in the OVX rats. These results suggest that the change of estrogen content might be a possible influence on the sensitivity of nociceptive process.” [This meshes well with other research that suggests that changes in estrogen may be involved in pain modulation. DJS]

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Jacobson PL, Mann JD. 2003. Evolving role of the neurologist in the diagnosis and treatment of chronic noncancer pain. Mayo Clin Proc. 78(1):80-84. “Informed regulatory agencies and professional organizations such as the American Academy of Neurology recognize the undertreatment of patients with CNP and provide clear recommendations to help neurologists in the ethical and effective treatment of patients with pain. Improved education of neurologists, other health care professionals, patients, and the media about evolving standards of pain care and therapy will produce a more supportive environment for the compassionate and ethical treatment of patients with CNP.”

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Jarrell J. 2007. Gynecological pain and the viscero-somatic connection. J Musculoskel Pain 15 (Supp 13):3 item 3. [Myopain 2007 Poster] “Myofascial dysfunction is common in the presence of endometriosis and visceral disease. There is an interesting relationship of the number of reported laparoscopies and the number of areas of myofascial dysfunction. This may reflect the severity of the visceral disease being treated at laparoscopy but also raises the possibility that laparoscopy may in some way exacerbate the viscero-somatic appreciation of pain physiology.”

Jarrell JF, Vilos GA, Allaire C et al. 2005. Consensus guidelines for the management of chronic pelvic pain. J Obstet Gynaecol Can. 27(8):781-826. Myofascial pain must be taken into account when looking for possible causes of chronic pelvic pain.

Jarrell J. 2004. Myofascial dysfunction in the pelvis. Curr Pain Headache Rep 8:452-456. Between 25% and 40% of all laparoscopy for pelvic pain finds no cause. Myofascial pain due to TrPs may be a significant and unrecognized cause of much pelvic pain.

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Association with psychiatric conditions and unexplained pain syndromes. J Gen Intern Med. 21 Suppl 3:S70-75. “Like other unexplained pain syndromes, frequent mastalgia is strongly associated with PTSD and other psychiatric conditions. Clinicians seeing patients with frequent mastalgia should inquire about anxiety, depression, alcohol misuse, and trauma history.” [Unfortunately, these patients were not evaluated for pectoral TrPs which may cause pain called mastalgia. DJS]

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Kapreli E, Vourazanis E, Strimpakos N. 2007. Neck pain causes respiratory dysfunction. Med Hypotheses [Oct 22 Epub ahead of print]. “The patient with neck pain presents a number of factors that could constitute a predisposition of leading to a respiratory dysfunction: (a) the decreased strength of deep neck flexors and extensors, (b) the hyperactivity and increased fatigability of superficial neck flexors, (c) the limitation of range of motion, (d) the decrease in proprioception and disturbances in neuromuscular control, (e) the existence of pain and (f) the psychosocial influence of dysfunction. The possible connection of neck pain and respiratory function could have a great impact on various clinical aspects, notably patient assessment, rehabilitation and pharmacological prescription.”

Kaput J, Perlina A, Hatipoglu B et al. 2007. Nutrigenomics: concepts and applications to pharmacogenomics and clinical medicine. Pharmacogenomics. 8(4):369-390. “The maintenance of health and the prevention and treatment of chronic diseases are influenced by naturally occurring chemicals in foods. In addition to supplying the substrates for producing energy, a large number of dietary chemicals are bioactive -- that is, they alter the regulation of biological processes and, either directly or indirectly, the expression of genetic information. Nutrients and bioactives may produce different physiological phenotypes among individuals because of genetic variability and not only alter health, but also disease initiation, progression and severity. The study and application of gene-nutrient interactions is called nutritional genomics or nutrigenomics. Nutrigenomic concepts, research strategies and clinical implementation are similar to and overlap those of pharmacogenomics, and both are fundamental to the treatment of disease and maintenance of optimal health.”

Kaput J, Rodriguez RL. 2004. Nutritional genomics: the next frontier in the post genomic era. Physiol Genomics. 16(2):166-177. “…dietary intervention based on knowledge of nutritional requirement, nutritional status, and genotype (i.e., ‘individualized nutrition’) can be used to prevent, mitigate, or cure chronic disease.”

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Karim MR, Fann AV, Gray RP et al. 2005. Enthesitis of biceps brachii short head and coracobrachialis at the coracoid process: a generator of shoulder and neck pain. Am J Phys Med Rehabil. 84(5):376-380. [This study used Marcaine and DepoMedrol for anterior shoulder pain and MPS, with a diagnosis of enthesitis. It would be interesting to know what would have happened if the patients had been examined for attachment trigger points and injected with procaine or lidocaine. A less toxic local anesthetic may often be effective for enthesiopathy caused by attachment trigger points. DJS]

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Kashikar-Zuck S, Lynch AM, Graham TB et al. 2007. Social functioning and peer relationships of adolescents with juvenile fibromyalgia syndrome. Arthritis Rheum. 57(3):474-480. “Adolescents with JPFS were perceived (by peer and self reports) as being more isolated and withdrawn and less popular. Adolescents with JPFS were less well liked, were selected less often as a best friend, and had fewer reciprocated friendships.” “Given the central role that peer relationships play in psychological development of children, and because peer rejection and isolation have been associated with subsequent adjustment problems, these findings are concerning.” [This is a significant study and indicates a great need for more attention to the support systems of adolescents with FM. DJS]

Kashikar-Zuck S, Vaught MH, Goldschneider KR et al. 2002. Depression, coping, and functional disability in juvenile primary fibromyalgia syndrome. J Pain 3(5):412-419. In this study, children with juvenile primary fibromyalgia syndrome (JPFS) and nonmalignant chronic back pain (CBP) were compared. “...both JPFS and CBP groups reported significant disruption in functional abilities and school attendance as a result of chronic pain.... The JPFS group had suffered from pain for significantly longer than the CBP group before being referred for specialty care... The JPFS group reported somewhat more school absences.”

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Kato K, Sullivan PF, Evengard B et al. 2006. Importance of genetic influences on chronic widespread pain. Arthritis Rheum. 54(5):1682-1686. “Individual differences in the likelihood of developing chronic widespread pain reflect modest genetic influences. There are no significant sex differences in the type or expression of the genes responsible for chronic widespread pain or in the magnitude of the relative importance of these influences on chronic widespread pain.”

Kato T, Rompre P, Montplaisir JY et al. 2001. Sleep bruxism: an oromotor activity secondary to micro-arousal. J Dent Res. 80(10):1940-1944. “A clear sequence of cortical to autonomic-cardiac activation precedes jaw motor activity in SB [sleep bruxism] patients. This suggests that SB is a powerful oromotor manifestation secondary to micro-arousal.” [This is contrary to the belief that jaw clenching and grinding is primarily caused by stress. It indicates that care providers should be checking sleep quality. DJS]

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Katz J, Cohen L, Schmid R, et al. 2003. Postoperative morphine use and hyperalgesia are reduced by preoperative but not intraoperative epidural analgesia: implications for preemptive analgesia and the prevention of central sensitization. Anesthesiology 98(6):144-1460.

Katz, N. P. 2000. MorphiDex (MS:DM) double-blind, multiple-dose studies in chronic pain patients. J Pain Symptom Manage 19(1 Suppl):S37-41.

Katz RS, Heard AR, Mills M et al. 2004. The prevalence and clinical impact of reported cognitive difficulties (fibrofog) in patients with rheumatic disease with and without fibromyalgia. J Clin Rheumatol. 10(2):53-58. “Memory decline and mental confusion were coupled more often in patients with FMS (50.9-8.8%). Patients with FMS with this combination of cognitive problems reported more pain (76.0-45.4%), stiffness (79.7-43.7%), fatigue (79.6-52.6%) and disturbed sleep (59.2-36.6%) compared with patients with FMS with memory problems alone. Patients with rheumatic disease substantially differ in cognitive vulnerability, with patients with FMS at considerably higher risk for cognitive difficulty. More importantly, the prevalence of a combined disturbance in memory and mental clarity is high and closely associated with the perception of increased illness severity and diminished mental health in FMS. That this linkage has the possibility of having a great deal to do with an important clinical variant of FMS underscores the need for greater clinical recognition of this underrecognized pattern and for further research.”

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Kawakita K, Itoh K, Okada K. 2007. Experimental model of trigger points using eccentric exercise. J Musculoskel Pain 15 (Supp 13):4 item 4. [Myopain 2007 Poster] “The tissue injuries and subsequent inflammation processes produced by the REC play an important role in the development of TrP, and ischemic condition could induce synaptic changes in the spinal cord. Sensitization of peripheral sensory could induce synaptic changes in the spinal cord. Sensitization of peripheral sensory receptors presumably polymodal receptors of the fascia and central sensitization might be a possible underlying mechanism of the TrP formation and referred pain phenomena.”

Kawakita K, Okada K. 2006. Mechanisms of action of acupuncture for chronic pain relief – polymodal receptors are the key candidates. Acupunct Med. 24 Suppl:S58-S66.

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Kaya A, Kamanii A, Ardicoglu O et al. 2009. Direct current therapy with/without lidocaine iontophoresis in myofascial pain syndrome. Bratisi Lek Listy 110(3):185-191. “Direct current therapy with/without lidocaine iontophoresis were determined to be effective treatment modalities in TrP management.” [It would be interesting to see how patients with more than a few TrPs reacted to this method of treatment. Is it possible to treat body-wide TrPs with this sort of therapy? DJS]

Kazennikov OV, Wiesendanger M. 2005. Goal synchronization of bimanual skills depends on proprioception. Neurosci Lett. [Epub ahead of print Jul 20] Proprioceptive feedback is necessary for the brain to monitor, correct and coordinate bimanual movements. [Proprioceptive dysfunction associated with myofascial TrPs may contribute to much more disability or dysfunction than is recognized.]

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Kempermann G, Neumann H. 2003. Neuroscience. Microglia: the enemy within? Science 302(5651):1689-1690. Microglia "...may be central players in repairing brain tissue and maintaining its integrity...and also...contribute to the rearrangement of neural connections and hence to the plasticity of normal brain tissue." [Microglia may be part of the cause and the cure of central sensitization. DJS]

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Khalsa PS. 2004. Biomechanics of musculoskeletal pain: dynamics of the neuromatrix. J Electromyogr Kinesiol. 14(1):109-120. “Mammals in general, and humans in particular, have evolved a highly sophisticated system of pain perception, which is characterized in humans by complementary but distinct neural processing of the intensity and location of a noxious stimulus, and a motivational/emotional or affective response to the stimulus. The peripheral and central neurons that comprise this system, which has been called the 'neuromatrix', dynamically (temporally) respond and adapt to noxious biomechanical stimuli. However, phenotypic variability of the neuromatrix can be large, which can result in a host of musculoskeletal conditions that are characterized by altered pain perception, which can and often does alter the course of the condition. This neural plasticity has been well recognized in the central nervous system, but it has only more recently become known that peripheral nociceptors also adapt to their altered extracellular matrix environment. This work reviews the biomechanics of pain focusing on the relevant stimulus that initiates responses by nociceptors to the cognitive perception of pain.” [It is becoming increasingly evident that each of us is indeed unique, including in response to medications and to just about everything else. One size does not fit all, and, especially in complex medical conditions, tailoring the medications and therapies to the individual is vital to success. DJS]

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Khasar SG, Green PG, Levine JD. 2005. Repeated sound stress enhances inflammatory pain in the rat. Pain 116(1-2):79-86. “Stress-induced enhancement of inflammatory hyperalgesia is associated with a change in mechanism by which bradykinin induces hyperalgesia, from being sympathetically mediated to being sympathetically independent. This sympathetic-independent enhancement of mechanical hyperalgesia is mediated by the stress-induced release of epinephrine from the adrenal medulla.”

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Khasar SG, Dina OA, Green PG et al. 2009. Sound stress-induced long-term enhancement of mechanical hyperalgesia in rats is maintained by sympathoadrenal catecholamines. J Pain. [Jul 1 Epub ahead of print]. “We present data showing mechanical hyperalgesia persisting for up to 28 days after exposure to sound stress, with evidence that the sympathoadrenal axis mediator epinephrine plays a major role. These findings could have clinical implications with regard to novel potential treatments for chronic widespread pain syndromes, such as fibromyalgia.” As many of us with FM know, noise can create a major stressor to the central nervous system. This article provides some proof, and an indication of how long the effects can last.

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Kobesova A, Lewit K. 2000. A case of a pathogenic active scar. Australas Chiropr Osteopathy. 9(1):17-19. Scars are like icebergs. Their surface is only a small indication of the amount of disruption that they can be causing. The example is an appendectomy scar in a person with abdominal and low back pain. Extensive and expensive testing remained negative, and the pain persisted. When the scar was treated with barrier release mobilizing the tissue and treating related TrPs, the symptoms were relieved.

Kobesova A, Morris CE, Lewit K et al. 2007. Twenty-year-old pathogenic “active” postsurgical scar: a case study of a patient with persistent right lower quadrant pain. J Manipulative Physiol Ther. 30(3):234-238. Even after decades without adequate diagnosis and treatment, trigger points in scar tissue may be effectively treated with tissue mobilization. [This gives pain patients hope, but also leads one to wonder how many people are living with unnecessary pain. DJS]

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Kuan TS, Chen JT, Chen SM, Chien CH, Hong CZ. 2002. Effect of botulinum toxin on endplate noise in myofascial trigger spots of rabbit skeletal muscle. Am J Phys Med Rehabil 81(7):512-20. This study confirms the association of excess acetylcholine in the motor endplates as part of the pathogenesis of myofascial trigger points.

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Kumar S, Ferrari R, Narayan Y. 2004. Electromyographic and kinematic exploration of whiplash-type rear impacts: effect of left offset impact. Spine J. 4(6):656-665. “When a rear impact is offset to the subject’s left, it results in not only increased electromyographic generation in both sternocleidomastoids, but the splenius capitis contralateral to the direction of impact offset also bears part of the force of the neck perturbation. Expecting or being aware of imminent impact also plays a role in reducing muscle responses in low-velocity offset rear impacts.” [It is an interesting reflection that while some researchers are working to understand the mechanisms of whiplash and thus benefiting patients and care providers, and perhaps preventing further injury, there are doctors (primarily under the pay and/or influence of insurance companies) who still refuse to believe whiplash exists. DJS]

Kumar S, Narayan Y, Amell T. 2002. An electromyographic study of low-velocity rear-end impacts. Spine 27(10):1044-1055. “Muscle responses were greater with higher levels of acceleration. Because the muscular component of the head-neck complex plays a central role in the abatement of higher acceleration levels, it may be a primary site of injury in the whiplash phenomenon.”

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Kung YY, Chen FP, Chaung HL et al. 2001. Evaluation of acupuncture effect to chronic myofascial pain syndrome in the cervical and upper back regions by the concept of Meridians. Acupunct Electrother Res. 26(3):195-202. “Acupuncture is a somewhat effective method for pain relief of patients with chronic MPS in the cervical and upper back regions. The effect of acupuncture with the concept of meridians on MPS is insidious and the duration of the relief is not long enough.”

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Kurland JE, Coyle WJ, Winkler A et al. 2006. Prevalence of irritable bowel syndrome and depression in fibromyalgia. Dig Dis Sci. 51(3):454-460. “The prevalence of IBS and depressive symptoms was higher in FM patients compared to the control population.”

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Kvale A, Skouen JS, Ljunggren, AE. 2003. Discriminative validity of the global physiotherapy examination-52 in patients with long lasting musculoskeletal pain versus healthy persons. J Musculoskel Pain 11(3):23-35. This study separated patients into subgroups, comparing healthy patients, patients with long-standing musculoskeletal pain, men and women. The physical therapy evaluations were separated into 5 domains: Posture, Respiration, Movement, Muscle and Skin. They found significant variations, especially in Movement and Muscle groups, and also differences dependent on gender and pain distribution.

Kwan CL, Diamant NE, Pope G et al. 2005. Abnormal forebrain activity in functional bowel disorder patients with chronic pain. Neurology 65(8):1268-1277. Abnormal brain responses in IBS may cause many sensory symptoms including pain, dysfunction and dysfunctional processing of visceromotor stimuli.

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