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

annotated by Devin J. Starlanyl

 

 

References for Research Purposes

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NOTE:  New Nomenclature

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

 
The abbreviation for myofascial trigger point, "TrP," was replaced by "MTP" for a brief period of time.  It has been returned to "TrP."  The change was due to the author's work on the next edition of Travell and Simons' Trigger Point Manual, and reflects the changing nature of being on the threshold of developments.
 
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 TrPs and chronic myofascial pain (CMP) due to TrPs.  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.

 

Falcao DM, Sales L, Leite JR et al. 2008.  Cognitive behavioral therapy for the treatment of fibromyalgia syndrome: a randomized controlled trial.  J Musculoskel Pain. 16(3):133-140.  The psychological aspects of chronic pain seems to respond positively to cognitive behavior therapy.

 

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.”

 

Fatoye F, Palmer S, Macmillan F et al. 2008.  Proprioception and muscle torque deficits in children with hypermobility syndrome.  Rheumatology (Oxford). [Dec 16 Epub ahead of print].  [This study has some fatal flaws.  Hypermobility syndrome is common in children with growing pains, which includes those with myofascial trigger points.  The ropy bands of TrPs may indeed be the body’s attempt to stabilize the hypermobile joints.  The proprioceptive impairment noted in this study could be due to those very same myofascial trigger points, and the proposed   “...muscle strengthening...” would only worsen these TrPs, causing further muscle dysfunction, weakness and pain.  It is to be hoped that these authors learn about myofascial TrPs before a bad situation becomes worse.  DJS]

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

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

Faure A, Reynolds SM, Richard JM et al. 2008.  Mesolimbic dopamine in desire and dread: enabling motivation to be generated by localized glutamate in nucleus accumbens.  J Neurosci 28(28):7184-4192.  Reactions to dopamine deficiency seem to be exceedingly site-specific in the part of the brain called the nucleus accumbens, and the same amount injected in different areas of this part can generate appetite or fear.

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 FM 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.”

Filatova E, Latysheva N, Kurenkov A. 2008.  Evidence of persistent central sensitization in chronic headaches: a multi-method study.  J Headache Pain [Aug 9 Epub ahead of print].  “CS is persistent and prevalent in patients with various types of chronic headache.  CS levels are unrelated to the predominant side of pain, disease duration or depression.  Neither is CS related to the headache type, suggesting similar mechanisms of headache chronification and chronicity maintaining and possibly explaining clinical similarity of various forms of chronic headache.”

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 FM-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 FM.  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.”

Fourie WJ. 2008.  Considering wider myofascial involvement as a possible contributor to upper extremity dysfunction following treatment for primary breast cancer.  J Bodywork Move Ther. 12(4):349-355.  “Breast cancer treatment results in tissues losing their shearing and gliding ability.  Mapped restrictive tissue gliding clearly shows wider than reported restrictions.  This pattern needs further research and investigation.”  Breast cancer patients may find significant symptom relief from treatment of co-existing myofascial trigger points.

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.

Franklin DW, Burdet E, Tee KP et al. 2008.  CNS learns stable, accurate, and efficient movements using a simple algorithm.  J Neurosci. 28(44):11165-11173.  The algorithm proposed in this article may be very useful in understanding how the dysfunctional musculoskeletal system with proprioceptive concomitants in patients with chronic myofascial pain and the dysfunctional brain in FM can combine to cause exceptional difficulties for movement in patients with both of these conditions.  DJS]

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.

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.” 

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

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

Friedberg F, Sohl SJ, Halperin PJ. 2008.  Teaching medical students about medically unexplained illnesses: a preliminary study.  Med Teach. [May 20 Epub ahead of print].  “A relatively brief exposure to factual information on specific medically unexplained illnesses was associated with more favorable attitudes toward CFS in fourth year medical students. Conclusion: This type of instruction may lead to potentially more receptive professional attitudes toward providing care to these underserved patients.”  You can’t see the pain, or the fatigue.  Medical students are much more receptive to patients with “invisible illnesses” if they are trained in their reality.

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

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

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

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

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

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

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

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

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

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

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

 

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

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.”

Gadalla T. 2008.  Association of comorbid mood disorders and chronic illness with disability and quality of life in Ontario, Canada.  Chronic Dis Can. 28(4):148-154.  “Health care providers are urged to proactively screen chronically ill patients for mood disorders, particularly among the subgroups found to have elevated risk for these disorders.”

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

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

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

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

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

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

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

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

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

 

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

 

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

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

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

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

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

Garbuzenko E., Nagler A, Pickholtz D et al. 2002. Human mast cells stimulate fibroblast proliferation, collagen synthesis and lattice contraction: a direct role for mast cells in skin fibrosis.  “...mast cells have a direct and potentiating role in skin remodeling and fibrosis.”  [Excess histamine in the system, from allergy, fibromyalgia imbalance, myofascial TrP twitch response, and/or other reasons may directly affect the formation of adhesion and scar tissue.  DJS]

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

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

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

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

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

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 FM.

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 FM and CMP must include care providers with the skills to diagnose and treat these conditions. DJS]

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

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

Ge HY, 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. 12(7):859-865.  Patients who have shoulder pain on one side actually have mechanical hypersensitivity on both sides.  Also, this study indicates that peripheral sensitization plays a significant role in chronic pain conditions.  The study also showed that the locations of TrPs correspond to the locations of pressure pain thresholds.

 

Ge HY, Zhang Y, Boudreau S et al. 2008.  Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points.  Exp Brain Res. 187(4):623-629.  “These results suggest that latent MTrPs (myofascial trigger points) could be involved in the genesis of muscle cramps.”

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.

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

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

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

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

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

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

Geenen R, Jacobs 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.”

Geisser ME, Strader Donnell C, Petzke F et al. 2008.  Comorbid somatic symptoms and functional status in patients with fibromyalgia and chronic fatigue syndrome: sensory amplification as a common mechanism.  Psychosomatics 49(3):235-242.  “Sensory amplification may be an underlying pathophysiologic mechanism in these disorders that is relatively independent of depression and depressive symptoms.”

Geisser ME, Glass JM, Rajcevska LD et al. 2008.  A psychophysical study of auditory and pressure sensitivity in patients with fibromyalgia and healthy controls.  J Pain. 9(5):417-422.  “Muscle tenderness is the hallmark of FM, but the findings of this study and others suggest that persons with FM display sensitivity to a number of sensory stimuli.  These findings suggest that FM is associated with a global central nervous system augmentation of sensory information.  These findings may also help to explain why persons with FM display a number of comorbid physical symptoms other than pain.”  [As suspected and noted in my books and on the website handouts, the sensory amplification of FM does not stop with pain.  This means that the autonomic and proprioceptive symptoms of co-existing MTPS, such as dizziness, for example, may be greatly amplified.  Care providers and patients must be made aware of this to avoid expensive and possibly unnecessary testing and procedures. DJS]

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

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

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

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

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

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

Gerdle B, Ostlund N, Gronlund C et al. 2008.  Firing rate and conduction velocity of single motor units in the trapezius muscle in fibromyalgia patients and healthy controls.  J Electromyogr Kinesiol. 18(5):707-716.  “CV (conduction velocity) was significantly higher in FM than in healthy controls; this might be due to alterations in histopathology and microcirculation.”  [These might also be due to co-existing myofascial TrPs, as this has already been shown in other studies.  DJS]

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

Gerson LB, Fass R. 2008.  A systematic review of the definitions, prevalence, and response to treatment of nocturnal gastroesophageal reflux disease.  Clin Gastroenterol Hepatol.  [Dec 3 Epub ahead of print].  “Nocturnal GERD is common and is associated with adverse sleep parameters.  It can be effectively managed with medical and surgical therapy.”  [I disagree.  There is a subset of patients with GERD, especially those with FM and CMP, who may not be adequately managed by medical and surgical therapy.  I am one of those patients.  DJS]

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

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

Gerwin R. 2008.  The taut band and other mysteries of the trigger point: An examination of the mechanisms relevant to the development and maintenance of the trigger point.  J Musculoskel Pain 16(1-2):115-121.  Dr. Gerwin’s hypothesis may fill in the missing elements in the formation of myofascial trigger points (MTPs).  We did not have an explanation for the excess release of acetylcholine, the excess release of calcium, and the excessive motor endplate noise, nor did we understand why the taut band forms.  These phenomenon could be explained by a dysfunctional ryanodine receptor calcium channel.  This dysfunctional ion channel could promote the excessive calcium release from the sarcoplasmic reticulum, resulting in persistent muscle fiber contraction.  Gates in the cell wall, like tiny airlocks in a space station, allow charged particles such as calcium, potassium and other minerals to flow in and out of the cell membrane and affect the interior metabolism of the cell.  The pathways are called ion channels.  An illness caused by dysfunction of the gate mechanism is called a channellopathy.   This important piece of the puzzle indicates that myofascial pain due to trigger points could be a channellopathy.  Dysfunctional mitochondria and/or second messenger dysfunction metabolically upstream could also be responsible or be associated with the ryanodine dysfunction. [I found this to be one of the most exciting revelations at the Myopain ‘07 Congress, offering great hope to those of us with myofascial pain.  This offers a whole new way of looking at myofascial pain, and perhaps a whole new way of treating it.  I hope researchers will take note and mobilize forces to investigate this. DJS]

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

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

conditions are brought under control, the chronic myalgia may resolve.

 

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

Geudj E, Cammilleri S, Niboyet J et al. 2008.  Clinical correlate of brain SPECT perfusion abnormalities in fibromyalgia.  J Mucl Med. [Oct 16 Epub ahead of print].  “These results show that brain perfusion abnormalities in patients with fibromyalgia are correlated with the clinical severity of the disease.”

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 FM subsets based on several factors.

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

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

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

Giordano J, Schatman ME, Benedikter R. 2008.  Pain care for a global community – Part 2.  Pract Pain Manag. 8(7):65-69.   Although this article is about the global undertreatment of chronic pain, the authors acknowledge a sad fact:  “...the inadequacy of chronic pain treatment in the United States has been well documented, particularly with regard to the inappropriate exercise (i.e., under-use and/or incorrect/excessive use) of various diagnostic and therapeutic technologies, and a failure to provide integrative treatment approaches that address psycho-social, as well as biological, aspects of pain.”  [ I spend a lot of my time trying to help people who cannot find doctors who can diagnose and treat fibromyalgia and chronic myofascial pain all over the world, but mostly in the USA.  Most hospital physical therapy departments don’t understand myofascial trigger points.  This is a good article.  I hope that some day we will see adequate and comprehensive pain care in the USA as well as throughout the world.  DJS]

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, 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. 2008.  Fibromyalgia and cognition.  J Clin Psychiatry. 69 Suppl 2:20-24.  “Patients with fibromyalgia frequently complain of cognitive problems or ‘fibrofog’.  The existence of these symptoms has been confirmed by studies of the incident of cognitive problems in fibromyalgia patients and by the results of objective tests of metamemory, working memory, semantic memory, everyday attention, task switching, and selective attention.  The results of these tests show that fibromyalgia patients have impairments in working, episodic, and semantic memory that mimic about 20 years of aging.  These patients have particular difficulty with memory when tasks are complex and their attention is divided.  Cognitive symptoms in these patients may be exacerbated by the presence of depression, anxiety, sleep problems, endocrine disturbances, and pain, but the relationship of these factors to cognitive problems in fibromyalgia patients is unclear.  Standardized tests and treatment have not yet been established for cognitive problems in fibromyalgia patients.”

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.”

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

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

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 FM patients is conspicuously greater than that experienced by other patients with typical neuropathic complaints.  Furthermore, this pain is associated with more severe co-morbidities such as depression/anxiety and sleep disturbance.”

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

Goebal A, Buhner S, Schedel R et al. 2008.  Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome.  Rheumatology [Jun 7 Epub ahead of print]  Intestinal permeability is significantly increased in both FM and CRPS patients.  [It would be interesting to check what factors these patients had in common, such as medications. DJS]

Goebel A, Buhner S, Schedel R et al. 2008.  Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome.  Rheumatology (Oxford). 47(8):1223-1227.  FM patients in this study showed significant increased intestinal permeability.  [I have observed that permeable gut is a common interactive diagnoses associated with FM.  It is to be hoped that further research will be done concerning the possibility of intestinal permeability as an initiating factor of central sensitization, and even more hope that there will be more focus on healing permeable gut as an integral part of FM treatment.  DJS]

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

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

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

Goldenberg DL, Burckhardt C, Crofford L. 2004.  Management of fibromyalgia syndrome.  JAMA 292(19):2388-2395.  “A number of commonly used FM 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 FM 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 FM, there are pharmacological and nonpharmacological interventions available that have clinical benefit.”  [FM is treatable,]

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

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

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

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

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

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

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

Goodchild CS, Kolosov A, Tucker AP et al. 2008.  Combination therapy with flupirtine and opioids: studies in rat pain models.  Pain Med. 9(7):928-938.  “Flupirtine increases morphine antinociception without causing an increase in sedation.  Flupirtine should be investigated as an adjunct analgesic with opioids for the management of patients with pain states involving central sensitization.”  [Other available opioid “boosters” such as dextromethorphan and pherngan need to be looked at closely as well. DJS]

Goon JA, Aini AH, Musalmah M et al. 2009.  Effect of tai chi exercise on DNA damage, antioxidant enzymes, and oxidative stress in middle-age adults.  J Phys Act Health. 6(1):43-54.  “Regular tai chi exercise stimulated endogenous antioxidant enzymes and reduced oxidative damage markers.”

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

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

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

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

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

Govender C, Cassimjee N, Schoeman J et al. 2007.  Psychological characteristics of FM 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 FM-prone psychological profile.”

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

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

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

 

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

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

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

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

 

Gracovetsky, S. 2008.  Is the lumbodorsal fascia necessary?  J Bodywork Move Ther. 12(3):194-197.  “The role of the lumbodorsal fascia is generally neglected in spine biomechanics.  Yet it is perhaps with most important structure insuring the integrity of the spinal machinery.  The viscoelastic property of its collagen has a direct impact on the way the muscles are used and forces are channeled from the ground to the upper extremities.  As a controller of the forces distribution between muscles and fascia, lordosis is the prime candidate for rehabilitation in the event of injury.”  [An ounce of prevention is worth a pound of cure. DJS]

 

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

 

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

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

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

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

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

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

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

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

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

 

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

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

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Grinnell F. 2008.  Fibroblast mechanics in three-dimensional collagen matrices.  J Bodywork Move Ther. 12(3):191-193.  “Fascia provides mechanical support and frameworks for the other tissues of the body.  Type 1 collagen is the major protein component of fascia, and fibroblasts are the cell type primarily responsible for its biosynthesis and remodeling.  Research on fibroblasts interacting with collagen matrices provides new insights regarding how cell-matrix tension state and growth factor specificity regulate cell migration and matrix remodeling.”

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

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

 

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

  

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

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

 

Grodin MA, Piwowarczyk L, Fulker D et al. 2008.  Treating survivors of torture and refugee trauma: a preliminary case series using qigong and t’ai chi.  J Altern Comp Med 14(7):801-806.  This limited study found qigong and t’ai chi effective for torture survivors.  With the caveat that there are many kinds of qigong and t’ai chi, this suggests to me that these practices may also be helpful for the survivors of the torture of chronic pain.  I have found them most helpful.  DJS]

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

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

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

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

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

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

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

 

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.”

 

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

 

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

 

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

 

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

 

Gulec H. 2008.  Normalizing attributions may contribute to non-help-seeking behavior in people with fibromyalgia syndrome.  Psychosomatics 49(3):212-217.  Some attempts to “normalize” help-seeking behavior can backfire in tertiary care FM patients, leading to a self-perception of helplessness and hopelessness over symptoms, with subsequent lack of attempts to seek help for symptom control.

 

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

 

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

 

Gunduz B, Bayazit YA, Celenk F et al. 2008.  Absence of contralateral suppression of transiently evoked otoacoustic emissions in fibromyalgia syndrome.  J Laryngol Otol. [Mar 4 Epub ahead of print].  “The mechanisms related to contralateral suppression of transiently evoked otoacoustic emissions seem dysfunctional in fibromyalgia syndrome.”  Patients with FM had audio test results equal to control patients on pure tones, but there was a dysfunction in FM patients with transiently evoked otoacoustic emissions.  [This study indicates again that there is more to FM than pain. DJS] 

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

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

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

 

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

 

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

 

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

 

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

 

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

 

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 FM, as well as genetic tendency to develop FM.  It indicates that the metabolism of catechol drugs in FM patients may be different. DJS]

 

Gusi N, Tomas-Carus P. 2008.  Cost-utility of an 8-month aquatic training for women with fibromyalgia: a randomized controlled trial.  Arthritis Res Ther. 10(1):R24.  “The addition of an aquatic exercise program to the usual care for fibromyalgia in women is cost-effective in terms of both health care costs and societal costs.  However, the characteristics of facilities (distance from the patients’ homes and number of patients that can be accommodated per session) are major determinants to consider before investing in such a program.”  [Care must be taken to remember that all aquatic therapy programs are not the same, nor are all FM patients.  After individualized assessment, some FM patients may benefit from some aquatic programs, and this is another treatment option that may be considered if there is a nearby facility with a pool at the proper temperature and instructors that understand the ramifications of FM and exercise plus any co-existing conditions.  The additional plus to this study is that this treatment is shown as a cost-effective option.  It must be noted that the aquatic programs for arthritis may not be suitable for FM patients either in water temperature or exercise, especially if there are co-existing MTPs.  Co-existing MTPs also complicate therapy for arthritis patients. DJS]

 

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

 

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

 

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

 

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

Hamilton NA, Affleck G, Tennen H et al. 2008.  Fibromyalgia: the role of sleep in affect and in negative event reactivity and recovery.  Health Psychol. 27(4):490-497.  The amount of pain and the affect on quality of life was significantly impacted on the amount and quality of sleep the night before. Sleep duration and sleep quality affected the mood, stress reactivity and stress recovery of the patient the next day.  “Furthermore, the effects of inadequate sleep on negative affect were cumulative.  In addition, an inadequate amount of sleep prevented affective recovery from days with a high number of negative events....These results lend support to the hypothesis that sleep is a component of allostatic load and has an upstream role in daily functioning.”

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

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

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

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

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

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

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

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

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

Hansen A, Bi P, Nitschke M et al. 2008.  The effect of heat waves on mental health in a temperate Australian city.  Environ Health Perspect. 116(10):1369-1375.  “Conclusion: Our results suggest that episodes of extreme heat pose a salient risk to the health and well-being of the mentally ill.  Relevance to clinical or professional practice: Improvements in the management and care of the mentally ill need to be addressed to avoid an increase in psychiatric morbidity and mortality as heat waves become more frequent.”  [ This study is interesting, and I would like to see more work done on the effects on chronic pain by extreme weather changes, ionic winds, and other phenomena that will become more prevalent with climate change.  DJS]   

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

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

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

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

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

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

Haroutiunian S, Rosen G, Shouval R et al. 2008.  Open-label, add-on study of tetrahydrocannabinol for chronic nonmalignant pain.  J Pain Plliat Care Pharmacother. 22(3):213-217.  “Cannabinoids have been used for pain relief for centuries and recent studies have investigated their analgesic and anti-inflammatory mechanisms, as well as clinical efficacy, in treating chronic pain.  We report an open-label study addressed to evaluate the effect and adverse events of orally administered Delta-9-tetrahydrocannabinol (Delta-9-THC) in 13 patients with chronic nonmalignant pain (CNMP) unresponsive to conventional pharmacotherapy.  The effect of the treatment was assessed on an eight-item HRQoL questionnaire.  Five out of 13 patients reported adequate response to the treatment while eight patients reported inadequate or no response.  Seven patients did not experience any adverse events (AEs), six patients reported AEs, two of which discontinued the treatment.  We conclude that oral THC may be a valuable therapeutic option for selected patients with CNMP that are unresponsive to previous treatments, though further research is warranted to characterize those patients.”  [It is interesting that other studies have indicated a dysfunctional endocannabinoid system in FM patients.  A study using cannabinoids on patients with FM, TrPs and both CMP and central sensitization (Stage II CMP) might be very useful.  See McPartland JM on the cannabinoid/TrP connection.  DJS]  

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

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

 

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

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

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

Hart FX. 2008.  The mechanical transduction of physiological strength electric fields.  Bioelectromagnetics [Mar 31 Epub ahead of print].  This article explains how physiological strength electrical fields produce torque on the glycoproteins, which then signal the cytoskeleton and transmit the signals throughout the interior of the cell.  This may be part of a network of orchestrated transduction mechanisms including the opening and closing of ion channels in the cellular membranes.  [This process may explain one way electromedical devices can change cellular biophysics and biochemistry.  This could be very important for those of us with altered metabolisms.  One medical hypothesis mentions myofascial trigger points as a result of an ion channel dysfunction.  DJS]

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

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

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

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

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

Hauser W, Thieme K, Turk DC. 2009.  Guidelines on the management of fibromyalgia syndrome – a systematic review.  Eur J Pain [Mar 3 Epub ahead of print].  This article illustrates the problems that can occur even with the best researchers if the studies that they review are flawed.  In this overview, in the table on page 5, trigger point injections are included (as they have been in some of the articles assessed) as treatment for fibromyalgia.  Since trigger points are not part of fibromyalgia, it indicates that a lot of clinicians doing research don’t understand the very basic differences between myofascial pain due to trigger points and fibromyalgia, and the conclusions they reach are therefore suspect. DJS]

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Hendi A, Dorsher PT, Rizzo TD Jr et al. 2009.  Subcutaneous trigger point causing radiating postsurgical pain.  Arch Dermatol. 145(1):52-54.  “Surgeons and pain management specialists should be aware of this potential cause of immediate postoperative pain to prevent unnecessary medical or surgical interventions in the postoperative period.”  [They might assess pre-surgical patients for possible TrPs “to prevent unnecessary medical or surgical interventions.” DJS]

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

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

 

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

 

Henriksson KG, 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 FM 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 FM.]

 

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

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

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

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

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

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

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

Heredia Jimenez JM, Aparicio Garcia-Molina VA, Porres Foulquie JM et al. 2009.  Spatial-temporal parameters of gait in women with fibromyalgia.  Clin Rheumatol. [Jan 24 Epub ahead of print].  “Gait parameters of women affected by FM were severely impaired when compared to those of healthy women.  Different factors such as lack of physical activity, bradikinesia, overweight, fatigue and pain together with a lower isometric force in the legs can be responsible for the alterations in gait and poorer life quality of women with FM.”  [It is very likely that these gait abnormalities are due to the presence of co-existing soft tissue dysfunctions including TrPs.  It would have been valuable to assess these patients for co-existing TrPs, as their role in gait abnormalities has been carefully documented.  DJS]

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

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

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

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

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

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

Hilliard MJ, Martinez KM, Janssen I et al. 2008.  Lateral balance factors predict future falls in community-living older adults.  Arch Phys Med Rehabil. 89(9):1708-1713.  “The findings identify new predictor variables for risk of falling that underscore the importance of dynamic balance recovery performance through ML stepping in relation to neuromusculoskeletal factors contributing to lateral balance stability.  The results also highlight focused risk factors for falling that are amenable to clinical interventions for enhancing lateral balance function and preventing falls.”  [Any study on falls that fails to incorporate an assessment for relevant myofascial TrPs is failing in its purpose.  The presence of myofascial TrPs are a major risk factor for falls.  DJS]

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

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

 

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

 

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.”  [Could nasal obstruction cause or contribute to TrPs? DJS]

 

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 IK, Goldschneider KR, Kashikar-Zuck S et al. 2008.  Healthcare utilization and indirect burden among families of pediatric patients with chronic pain.  J Musculoskel Pain. 16(3):155-164.  Preliminary findings suggest that prompt involvement with a multidisciplinary outpatient treatment program may reduce significant direct and indirect costs of pediatric chronic pain patients.

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

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

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

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

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

Hoffman 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]

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

Holick MF, Chen TC, Lu Z et al. 2007.  Vitamin D and skin physiology: A d-lightful stody.  J Bone Miner Res 22 (Suppl 2): V-28-33.  This article indicates that it is extremely difficult to get adequate vitamin D from dietary sources.  Even foods normally high in this vitamin are variable.  For example, wild caught salmon have between 75% and 90% more vitamin D(3) than farmed salmon. [Now that the importance and relative commonality of vitamin D insufficiency is being accepted, use of light on skin and supplementation can be critical for patients with chronic pain. DJS]  

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

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

Holman AJ. 2008.  Positional cervical spinal cord compression and fibromyalgia: a novel comorbidity with important diagnostic and treatment implications.  J Pain. [May 20 Epub ahead of print].  Co-existing cervical cord compression may exist with FM.  [Much of this may be due to co-existing myofascial trigger points, and can be treated noninvasively. DJS]  

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

Holman AJ. 2009.  Impulse control disorder behaviors associated with pramipexole used to treat fibromyalgia.  J Gambl Stud. [Feb 25 Epub ahead of print].  “Objective: Compulsivity has been associated with use of dopamine agonists used to treat Parkinson’s disease (PD).  Increasing use of these agents to treat fibromyalgia (FM) raises concern for this unexpected toxicity in a new group of patients.  This is the first report of compulsive gambling and shopping among patients taking dopamine agonists for treatment of FM.”  “While biologic aspects of PD and FM differ considerably, compulsive gambling and shopping have become important, yet unexpected concern related to use of dopamine agonists for patients with FM and their treating clinicians.”

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

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

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

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

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

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

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

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

Hong 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 FM.  The pain of dry needling may needlessly further sensitize the central nervous system in some patients with both FM and TrPs. DJS]

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

Hsu HC, Hong CZ. 2008.  Floating kidney with chronic myofascial pain syndrome in the abdominal muscles as the major clinical manifestation: a case report.  J Musculoskel Pain. 16(3):199-204.  “Myofascial pain syndrome in the abdominal muscles may be caused by a floating kidney.  Treating an underlying pathological lesion is important when attempting to eliminate TrPs.”  When myofascial trigger point pain recurs after adequate treatment, the perpetuating factor(s) must be found and brought under control.

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

 

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

 

Ibanez-Garcia J, Alburquerque-Sendin F, Rodriguez-Blanco C et al. 2008.  Changes in masseter muscle trigger points following strain-counterstrain or neuro-muscular technique.  J Bodywork Move Ther. 13(1):3-10.  “Our results suggest that neuromuscular or strain-counterstrain technique might be employed in the management of latent MTrPs in the masseter muscle.”

 

Igaz P, Novak I, Lazaar E et al. 2001.  Bidirectional communication between histamine and cytokines.  Inflamm Res. 50(3):123-128.  “Histamine plays fundamental roles in numerous immune reactions.  In addition to its well-characterized effects in the acute inflammatory and allergic responses, histamine also influences the expression and actions of several cytokines.  Because antihistamines are widely used in the treatment of various human diseases, this complex interaction could have general medical relevance too.”

Ignatowski TA, Spengler RN. 2004.  Tumor necrosis factor-alpha quantification and expression by insitu hybridization.  Methods Mol Biol 196:85-96.  Antidepressants may work as pain relievers by inhibiting production of the inflammatory protein tumor necrosis factor in the brain.

Iguchi M., Katoh Y., Koike H. et al. 2002.  Randomized trial of trigger point injection for renal colic.  Int J Urol 9(9):475-479.  “Trigger point injection, in our experience, is an easy, safe and effective method for the amelioration of renal colic."

Ikeda H, Murase K. 2004.  Glial nitric oxide-mediated long-term presynaptic facilitation revealed by optical imaging in rat spinal dorsal horn.  J Neurosci. 24(44):9888-9896.  “Activity-dependent LTP of nociceptive afferent synaptic transmission the spinal cord is believed to underlie central sensitization after inflammation nerve injury. This glial NO-mediated control of presynaptic excitation may contribute to the induction at least in part.”

Ilbuldu E, Cakmak A, Disci R et al. 2004. Comparison of laser, dry needling, and placebo laser treatments in myofascial pain syndrome.  Photomed Laser Surg. 22(4):306-311.  “Laser therapy could be useful as a treatment modality in myofascial pain syndrome because of its noninvasiveness, ease, and short-term application.”

Ilkjaer, S., J. Dirks, J. Brennum, M. Wernberg and J. B. Dahl.  1997.  Effect of systemicN-methyl-D-aspartate receptor antagonist (dextromethorphan) on primary and secondary hyperalgesia in humans.  Br J Anaesth 79(5):600-605.

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]

Imamura, S.T., T.Y. Lin, M.J. Yriyrits, S.S. Fischer, R.J. Azze, L. A. Rosgano and R. Mahar. 1997. The importance of myofascial pain syndrome in reflex sympathetic dystrophy. Phys Med Rehab Clinics of North Am 8:207-211.

Imbierowicz K., Egle U.T. 2003.  Childhood adversities in patients with fibromyalgia and somatoform pain disorder.  Eur J Pain 7(2):113-9.  This study in primary FM found that “The FM patients show the highest score of childhood adversities.  In addition to sexual and physical maltreatment, the FM patients more frequently reported a poor emotional relationship with both parents, a lack of physical affection, experiences of the parent’s physical quarrels, as well as alcohol or other problems of addiction in the mother, separation, and a poor financial situation before the age of 7.”

Inanici F, Yunus MB. 2004.  History of fibromyalgia: past to present.  Curr Pain Headache Rep. 8(5):369-378.  ”Fibromyalgia syndrome (FM) is now a recognized clinical entity causing chronic and disabling pain.” 

Ingber DE. 2008.  Tensegrity and mechanotransduction.  J Bodywork Move Ther. 12(3):198-200.  This interesting article explains the malleability of the human body, and how external forces such as massage and other intentional bodywork can create ripple effects of movement on a cellular level, creating deep changes in the tissues via the mechanotransduction process.

Ingber, R. S.  1989.  Iliopsoas myofascial dysfunction: a treatable cause of “failed” low back syndrome.  Arch Phys Med Rehabil 70(5):382-6.  

Ingebrigtsen, T., B.  Romner, K. Waterloo and J. H. Trumpy. 1996. [Minor head injuries in sport. Occurrence, management, sequelae and prevention.] Tidsskr Nor Laegeforen 116(30):3594-3597. [Norwegian].

Ingman T, Nieminen T, Hurmerinta K. 2004.  Cephalometric comparison of pharyngeal changes in subjects with upper airway resistance syndrome or obstructive sleep apnoea in upright and supine positions.  Eur J Orthod 26(3):321-326.  “The present results suggest that OSA patients are prone to significant narrowing of their oropharyngeal, but not of their naso- or hypopharyngeal, airways in the supine position.  Thus, treatment of OSA and UARS patients should mainly be aimed at preventing further oropharyngeal airway narrowing as a result of supine-dependent sleep.”

 

Innes KE, Selfe TK, Taylor AG. 2008.  Menopause, the metabolic syndrome, and mind-body therapies.  Menopause. [Apr 17 Epub ahead of print].  This paper explains the rise in the occurrence of insulin resistance during menopause as well as the link between insulin resistance and cardiovascular disease, mood dysfunction, and sleep dysfunction.

Innes, K. E. and J. H. Wimsatt.  1999.  Pregnancy-induced hypertension and insulin resistance: evidence for a connection.  Acta Obstet Gynecol Scand 78(4):263-84.

Inoue K, Tsuda M, Koizumi S. 2004.  Chronic pain and microglia: the role of ATP.  Novartis Found Symp. 261:55-64.

Inturrisi, C. E., W. A. Colburn, R. F. Kaiko, R. W. Houde and K. M. Foley.  1987. Pharmacokinetics and pharmacodynamics of methadone in patients with chronic pain.  Clin Pharmacol Ther 41(4):392-401.

Ionescu-Tirgoviste, C.  1998.  Proposal for a new classification of diabetes mellitus. Rom J Intern Med 36(1-2):121-34. 

Irwin MR, Olmstead R, Oxman MN. 2007.  Augmenting immune responses to varicella zoster virus in older adults: a randomized, controlled trial of tai chi.  J Am Geriatr Soc. 55(4):511-517.  “Tai Chi augments resting levels of VZV-specific CMI and boosts VZV-CMI of the varicella vaccine.”  Regular practice of t’ai chi boosted cell-mediated immunity in immunized patients.

Irwin, M., J. McClintick, C. Costlow, M. Fortner, J. White and J. C. Gillin. 1996. Partial night sleep deprivation reduces natural killer and cellular immune responses in humans.  FASEB J10(5):643-653.

Irwin RS, Madison JM. 2000.  Anatomical diagnostic protocol in evaluating chronic cough with specific reference to gastroesophageal reflux disease.  Am J Med. 108 Suppl 4a:126S-130S.  “Gastroesophageal reflux disease (GERD), along with postnasal drip syndrome (PNDS) and asthma, is one of the three most common causes of chronic cough in all age groups.  When GERD is the cause of chronic cough, there may be no gastrointestinal (GI) symptoms up to 75% of the time, and, in these cases, the term ‘silent GERD’ is used.”

Irwin RW, Zuhosky JP, Sullivan WJ et al. 2007.  Industrial medicine and acute musculoskeletal rehabilitation.  4. Interventional procedures for work-related cervical spine conditions.  Arch Phys Med Rehabil. 88(3 Suppl 1):S18-S21.  An overview, including myofascial pain.

 

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.”

Israel HA, Ward JD. Horrell B, et al. 2003.  Oral and maxillofacial surgery in patients with chronic orofacial pain.  J Oral Maxillofac Surg 61(6):662-7.  “Misdiagnosis and multiple failed treatments were common in these patients with chronic orofacial pain ..... surgical treatment was rarely indicated as a treatment for pain relief ..... and it exacerbated and perpetuated pain symptoms in some of them.”

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, Hirota S, Katsumi Y et al. 2008.  Trigger point acupuncture for treatment of knee osteoarthritis – a preliminary RCT for a pragmatic trial.  Acupunct Med. 26(1):17-26.  “These results suggest that trigger point acupuncture therapy may be more effective for osteoarthritis of the knee in some elderly patients than standard acupuncture therapy.”  [This study may indicate that treating the associated myofascial trigger points results in more effective therapy of osteoarthritis of the knee. DJS]

 

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]

 

Itoh K, Katsumi Y, Hirota S et al. 2006.  Effects of trigger point acupuncture on chronic low back pain in elderly patients – a sham-controlled randomized trial.  Acupunct Med. 24(1):5-12.  “These results suggest that trigger point acupuncture may have greater short term effects on low back pain in elderly patients than sham acupuncture.”

Itoh, Y, T Igarashi, N Tatsuma, T Imai, J Yoshida, M Tsuchiya, M Murakami and Y Fukunaga. 1999.  [Autoimmune fatigue syndrome and fibromyalgia syndrome.]  Nippon Ika Daigaku Zasshi 66(4):239-44.

Ivanichev GA, Kuznetsova EA. 2007.  [Evoked potentials in patients with myofascial pain syndrome in the late residual period of natal cervical trauma.]  Zh Nevrol Psikhiatr Im S S Korsakova 107(4):49-53. [Russian]  Specific audio testing indicates that dysfunction in the somatosensory pathway of the brainstem is common in patients with cervical spine birth trauma, “...being most significant in patients with severe myofascial pain syndrome.”

Iverson L. 2004.  GABA pharmacology–what prospects for the future?  Biochem Pharmacol 68(8):1537-1540.  Gaboxadol (THIP) is one of the new non-benzodiazepine hypnotics that acts on GABA A receptors.  This type of medication shows promise as a more specific type of sleep medication.

 

Iwama H, Akama Y. 2000.  The superiority of water-diluted 0.25% to neat 1% lidocaine for trigger-point injections in myofascial pain syndrome: a prospective, randomized, double-blinded trial.  Anesth Analg 91(2):408-409.  “Trigger-point injection with a mixture of commercially available 1% lidocaine in sterile distilled water at a ratio of 1:3 compared with 1% lidocaine alone resulted in better efficacy and less injection pain.”  [Travell and Simons also reported better effects with diluted local anesthetic. DJS]

Iwasaka, M., Ueno, S. 2003.  Detection of intracellular macromolecule behavior under strong magnetic fields by linearly polarized light.  Bioelectromagnetics 24(8):564-70.  Strong static magnetic fields caused behavioral changes in cell components that corresponded to changes in polarized light.  The intracellular macromolecular arrangement may be affected by these fields.

Izquierdo-Alvarez S, Bocos-Terraz JP, Bancalero-Flores JL et al. 2008.  Is there an association between fibromyalgia and below-normal levels of urinary cortisol?  BMC Res Notes. 1:134.  “Our study confirms that women with FM have significantly lower urinary cortisol levels than healthy women.”

 

Jackman RP, Purvis JM, Mallett BS. 2008.  Chronic nonmalignant pain in primary care. Am Fam Physician. 78(10):1155-1162.

 

Jackson MJ. 2005.  Use of microdialysis to study interstitial nitric oxide and other reactive oxygen and nitrogen species in skeletal muscle.  Methods Enzymol. 396:514-525.

 

Jacob L, Jacob T, Jacob B. 2007.  Escitaloproan for fibromyalgia and multiple chemical sensitivity syndrome: Tolerable efficacy.  J Musculoskel Pain 15(Suppl 13):50. item 87.  Escitalopran (Lexapro) seems to help FM pain even if patients don't have MCS, and it appears to be well tolerated and have few side-effects. 

 

Jacobson BC, Somers SC, Fuchs CS et al. 2006.  Body-mass index and symptoms of gastroesophageal reflux in women.  N Engl J Med. 354(22):2340-2348.  “BMI is associated with symptoms of gastroesophageal reflux disease in both normal-weight and overweight women.  Even moderate weight gain among persons of normal weight may cause or exacerbate symptoms of reflux.”  [Obesity, or even overweight, may be an important perpetuating factor for GERD, which itself is an important perpetuating factor for sleep apnea, fibromyalgia and some myofascial TrPs.  DJS]

 

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. “The neurologist has become increasingly involved in the multidisciplinary treatment of patients with chronic noncancer pain. 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."

 

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.”

Jacobsen, S., I.S. Petersen and B. Danneskiold-Samsoe. 1993.Clinical features in patients with chronic muscle pain-with special reference to fibromyalgia. Scand J Rheumatol 22(2):69-76. 

Jacobsen, S. and B. Danneskiold-Samsoe. 1992. Dynamic muscular endurance in primary fibromyalgia compared with chronic myofascial pain syndrome. Arch Phys Med Rehab 73(2):170-173.

Jacobsen, S., M. Hoyer-Madsen, B. Danneskiold-Samsoe and A. Wiik. 1990.  Screening for autoantibodies in patients with primary fibromyalgia syndrome and a matched controlled group. APMIS 98(7):655-8.

Jacobsen, S. 1998.  Physical biodynamics and performance capacities of muscle in patients with fibromyalgia syndrome.  Z Rheumatol Suppl 57 (2):43-6.

Jain AK, Carruthers BM, van de Sande MI, Barron SR, Donaldson CCS, Dunne JV, Gingrich E, Heffez DS, Leung FYK, Malone DG, Romano TJ, Russell IJ, Saul D, Seibel DG.  2003.  Fibromyalgia syndrome: Canadian clinical working case definition, diagnostic and treatment protocols – a consensus document.  J Musculoskel Pain 11(4):3-107.

James G., Butt A.M. 2002.  P2Y and P2X purinoceptor medicated Ca (2+) signaling in glial cell pathology in the central nervous system.  Eur J Pharmacol 447(2-3):247-60.  This research suggests that ATP is a primary glial cell signal molecule in response to central nervous system injury, and that the named receptors are involved with this response.

Jamison, J.  1999.  Stress: the chiropractic patients’ self-perceptions.  J Manipulative Physiol Ther 22(6):395-8.

Jamison, R. N.  1996.  Comprehensive pretreatment and outcome assessment for chronic opioid therapy in nonmalignant pain.  J Pain Symptom Manage 11(4):231-241.  

Jamison, R. N., K. O. Anderson and M. A. Slater.  1995.  Weather changes and pain: perceived influence of local climate on pain complaint in chronic pain patients.  Pain 61(2):309-315.

Jamison, R. N., K. O. Anderson, C. Peeters-Asdourian and F. M. Ferrante.  1994.  Survey of opioid use in chronic nonmalignant pain patients.  Reg Anesth 19(4):225-230. 

Jan, J. E., M. B. Connolly, D. Hamilton, R. D. Freeman and M. Laudon.  1999.  Melatonin treatment of non-epileptic myoclonus in children.  Dev Med Child Neurol 41(4):255-9.

Janal MN, Ciccone DS, Natelson BH. 2006.  Sub-typing CFS patients on the basis of ‘minor’ symptoms.  Biol Psychol.  [Feb 9 Epub ahead of print]  “In 161 women meeting 1994 criteria for CFS, principal components analysis of the ten ‘minor’ symptoms of CFS produced three factors interpreted to indicate musculoskeletal, infectious and neurological subtypes.  Extreme scores on one or more of these factors characterized about 2/3 of the sample.”  “Results suggest that subtypes of CFS may be identified from reports of the minor diagnostic symptoms, and that these subtypes demonstrate construct validity.”

Janig, W., H. Blumberg, R. A. Boas et al. 1991.  The reflex sympathetic dystrophy syndrome: consensus statement and general recommendations for diagnosis and clinical research.  In Bond, M. R., J. E. Charleton and C. J. Woolf (eds): Proceedings of the VI th World Congress on Pain. Elsevier, Amsterdam, 1991, pp. 373-376.

Jankovic D, van Zundert A. 2006.  The frozen shoulder syndrome.  Description of a new technique and five case reports using the subscapular nerve block and subscapularis trigger point infiltration.  Acta Anaesthesiol Belg. 57(2):137-143.

Jansson C, Nordenstedt H, Wallander MA et al. 2009.  A population-based study showing an association between gastroesophageal reflux disease and sleep problems.  Clin Gastroenterol Hepatol. [Mar 12 Epub ahead of print].  “A large, population-based study indicates a link between sleep problems and gastroesophageal reflux disease that might be bi-directional.”   [This is a very good example of interactive diagnoses.  Also, both FM and TrPs can be interactive with both sleep problems and GERD.   Working on any one of these conditions may help the others, and each of them may worsen the others. DJS]

Jaracz J, Rybakowski J. 2005.  [Depression and pain: novel clinical, neurobiological and psychopharmacological data]  Psychiatr Pol. 39(5):937-950.  [Polish]  “In the pathogenesis of both depression and pain symptoms, an important role has been attributed to disturbances of serotonergic and noradrenergic neurotransmission as well as to neuropeptides such as opioids and substance P.  In mood regulation as well as in the perception and emotional dimension of pain stimuli, such brain structures as the amygdala, anterior cingulate cortex and prefrontal cortex are of main significance.  The action of antidepressant drugs results in a normalization of the activity of those neurotransmitter systems an brain structures.  It was found that dual action antidepressants (i.e., influencing both serotonergic and noradrenergic system) such as tricyclic antidepressants and new generation drugs (venlafaxine, milnacipram, duloxetine, mirtazapine) exert a stronger antidepressant effect and possess a broader therapeutic spectrum, including also an effect on pain symptoms.” 

Jarrell J. 2008.  Gynecological pain and the viscero-somatic connection.  J Musculoskel Pain 16(1-2):21-27.  “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.   

Jason LA, Taylor RR, Kennedy CL. 2000.  Chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities in a community-based sample of persons with chronic fatigue syndrome-like symptoms.  Psychosom Med. 62(5):655-663.  “People with CFS, MCS or FM endure significant disability in terms of physical, occupational and social functioning, and those with more than one of these diagnoses also report greater severity of physical and mental fatigue.”

Jaspers, J. P.  1998.  Whiplash and post-traumatic stress disorder.  Disabil Rehabil 20(11):397-404.

Jaspersen D, Leodolter A. 2005.  [Sleep disorders associated with gastroesophageal reflux.]  Dtsch Med Wochenschr. 130(48):2779-2782. [German]  “Individuals with clinical sleep disorders have a greatly impaired quality of life.  The causes for sleeping disorders are complex, but evidence has recently come from different trials supporting a causal relationship between gastroesophageal reflux disease (GERD) and sleep disorders in some patients.  The majority of patients with GERD report reflux symptoms during the night.  It is well known that especially at night reflux is characterized by prolonged esophageal acid exposure.  Sleep disorders significantly improve while on efficacious antisecretory treatment.  In patients with sleep disorders but no previously known GERD, the search for it is recommended and should be followed by adequate antisecretory treatment.  In other severe diseases associated with sleep, like the obstructive sleep apnoea syndrome (OSAS), an association with esophageal acid exposure has been proven.  The sleep apnea-associated reflux has probably a multifactorial etiology: in cases with other predisposing conditions for gastro-esophageal reflux, OSAS promotes the development of reflux."

Jeal, W. and P. Benfield. 1997.  Transdermal fentanyl.  A review of its pharmacological properties and therapeutic efficacy in pain control.  Drugs 53(1):109-138.

Jennings, JR, Muldoon MF, Hall M et al. 2007.  Self-reported sleep quality is associated with the metabolic syndrome.  Sleep. 30(2):219-223.

Jennum, P., A. M. Drewes, A. Andreasen and K. D. Nielsen. 1993. Sleep and other symptoms in primary fibromyalgia and in healthy controls.  J. Rheumatol 20(10):1756-1759.

Jensen B, Wittrup IH, Wiik A et al. 2004.  Antipolymer antibodies in Danish fibromyalgia patients.  Clin Exp Rheumatol 22(2):227-229.  Although FM patients in this study had slightly higher APA levels than healthy people, the levels declined with age.

Jensen B, Wittrup IH, Bliddal H et al. 2003.  Bone mineral density in fibromyalgia patients – correlation to disease activity. 32(3):146-150.  “...the severity of FM might have a negative impact on bone mass.”

Jensen, K. A., S. K. Christensen, E. M. Nielsen, L. K. Bunemann, K. Therkelsen and F. Knudsen.1997. [Cerebral blood flow and indomethacin.  The effect of different doses administered as continuous intravenous infusions or as suppositories in healthy adults]. Ugeskr Laeger 159(27):4257-4260 [Danish].  

Jensen MP, Nielson WR, Turner JA et al. 2004.  Changes in readiness to self-manage pain are associated with improvement in multidisciplinary pain treatment and pain coping.  Pain 111(1-2):84-95.

 

Jespersen A, Dreyer L, Kendall S et al. 2007.  Computerized cuff pressure algometry: a new method to assess deep-tissue hypersensitivity in fibromyalgia.  Pain. [Jan 24 Epub ahead of print]  This is yet another study confirming Dr. J. B. Eisinger’s development of FM diagnostic testing using tensiometry, or blood pressure cuff tension.  I believe that this article would have benefitted by inclusion of Dr. Eisinger’s work. DJS]

Jevning, R., I. Wells, A. F. Wilson and S. Guich.  1987.  Plasma thyroid hormones, thyroid stimulating hormone, and insulin during acute hypometabolic states in man.  Physiol Behav 40(5):603-6.

Jevning, R., A. F. Wilson and J. M. Davidson.  1978.  Adrenocortical activity during meditation. Horm Behav 10(1):54-60.  

Jevning, R., A. F. Wilson and W. R. Smith.  1978.  The transcendental meditation technique, adrenocortical activity, and implications for stress.  Experientia 34(5):618-9.  

Jevning, R., A. F. Wilson, H. Pirkle, J. P. O’Halloran and R. N. Walsh.  1983.  Metabolic control in a state of decreased activation: modulation of red cell metabolism.  Am J Physiol 245(5 Pt 1):C457-61.

Jezova, D., Jurankova E., Mosnarova A., M. Kriska and I Skultetyova. 1996.  Neuroendocrine response during stress with relation to gender differences. Acta Neurobiol Exp (Warsz) 56(3):779-985.

Johannesson U, de Boussard CN, Brodda Jansen G et al. 2006.  Evidence of diffuse noxious inhibitory controls (DNIC) elicited by cold noxious stimulation in patients with provoked vestibulodynia.  Pain [Dec 12 Epub ahead of print]

Johansson, G., J. Risberg, U. Rosenhall, G. Orndahl, L. Svennerholm and S. Nystrom. 1995. Cerebral dysfunction in fibromyalgia; evidence from regional cerebral blood flow measurements, otoneurological tests and cerebrospinal fluid analysis. Acta Psychiatr Scand 91(2):86-94.

Johansson O, Gangi S, Liang Y, Yoshimura K, Jing C, Liu PY. 2001. Cutaneous mast cells are altered in normal healthy volunteers sitting in from of ordinary TVs/PCsBresults from open-field provocation experiments. J Cutan Pathol Nov;28(10):513-9. Normal cutaneous mast cells can be altered by exposure to television or personal computer screens.  The number of skin mast cells increase in exposed skin in many patients after such an exposure.  After 24 hours, the number of mast cells returns to normal. [This may be significant to FM patients with skin allergy symptoms. DJS]

Johnson EO, Babis GC, Soultanis KC et al. 2008.  Functional neuroanatomy of proprioception.  J Surg Orthop Adv. 17(3):159-164.  “Proprioception is the sense of body position that is perceived both at the conscious and unconscious levels.  Typically, it refers to two kinds of sensations: that of static limb position and of kinesthesia.  Static position reflects the recognition of the orientation of the different body parts, whereas kinesthesia is the recognition of rates of movement.”  This is a very relevant and important review.  When care providers who know myofascial medicine think of TrPs, they often think only of pain.  Associated proprioceptive and autonomic dysfunctions are important as well, as are muscle dysfunctions such as weakness caused by TrPs, but this often goes unrecognized. DJS]

 

Johnson EO, Kostandi M, Moutsopoulos HM. 2006.  Hypothalamic-pituitary-adrenal axis function in Sjogren’s syndrome: mechanisms of neuroendocrine and immune system homeostasis.  Ann N Y Acad Sci. 1088:41-51.  “These findings suggest not only adrenal axis hypoactivity in SS and FM patients, but also that varying patterns of adrenal and thyroid axes dysfunction may exist in patients with different rheumatic diseases.”

 

Johnson JD, O’Connor KA, Deak T et al. 2002.  Prior stressor exposure primes the HPA axis.  Psychoneuroendocrinology 27(3):353-365. 

 

Johnson JD, O’Connor KA, Deak T et al.  Psychoneuroendocrinology. 27(3):353-365.  The stress response in rats is changed after an initial HPA activation.  Neural plasticity is affected by stress, at least in rats.

 

Johnson KM, Bradley KA, Bush K et al. 2006.  Frequency of mastalgia among women veterans. 

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]

 

Jones AY, Dean E, Scudds RJ. 2005.  Effectiveness of a community-based Tai Chi program and implications for public health initiatives.  Arch Phys Med Rehabil. 86(4):619-625.  “A community-based Tai Chi program produces beneficial effects comparable to those reported from experimental laboratory trials of Tai Chi; therefore, it should be considered as a public health strategy.”  The regular practice of t’ai chi improves handgrip strength, resting heart rate, and flexibility.

 

Jones GT, Silman AJ, Macfarlane GJ. 2003.  Predicting the onset of widespread body pain among children.  Arthritis Rheum. 48(9):2402-2405.  This English study indicates that children who have behavioral problems or “common childhood somatic symptoms” are at risk for developing widespread pain.  [I would love to see these children examined for developing FM, sleep disturbances, and myofascial TrPs. DJS]

 

Jones KD, Horak FB, Winters-Stone K et al. 2009.  Fibromyalgia is associated with impaired balance and falls.  J Clin Rheumatol. 15(1):16-21.  “FM is associated with balance problems and increased fall frequency.  Patients were aware of their balance problems.  These results suggest that FM may affect peripheral and/or central mechanisms of postural control.  Further objective study is needed to identify the relative contributions of various neural and musculoskeletal and other impairments to postural stability in FM to provide clinicians with methods to maximize postural stability and help fall prevention.”  [Since most FM patients have considerable myofascial TrP involvement and specific TrPs can have a profound affect on balance, it is unfortunate that these patients were not assessed for co-existing TrPs.  DJS]

 

Jones KD, Deodhar P, Lorentzen A et al. 2007.  Growth hormone perturbations in fibromyalgia: a review.  Semin Arthritis Rheum. [Jan 12 Epub ahead of print]  This study indicates normal pituitary function in FM patients, and that dysfunction of the HP-GH-IGF-1 axis is most likely hypothalamic in origin, but notes that more research is required.

 

Joranson DE, Gilson AM. 2001.  Pharmacists’ knowledge of and attitudes toward opioid pain medications in relation to federal and state policies.  J Am Pharm Assoc 41(2):213-220.  “Pharmacists play a pivotal role in ensuring patient access to medications.  Our findings suggest that the incorrect knowledge and inappropriate attitudes of some pharmacists could contribute to a failure to dispense valid prescriptions for opioid analgesics to patients in pain.”  [This is a very sad yet accurate commentary on one more hurdle that some chronic pain patients must overcome to gain access to adequate pain control.]

 

Joranson DE, Ryan KM, Gilson AM et al. 2000.  Trends in medical use and abuse of opioid analgesics.  JAMA 283(13):1710-1714.  “The trend of increasing medical use of opioid analgesics to treat pain does not appear to contribute to increases in the health consequences of opioid analgesic abuse.”

Joranson, D. E. and A. M. Gilson.  1998.  Regulatory barriers to pain management.  Semin Oncol Nurs 14(2):158-63.

Joranson, D. E.  1994.  Are health-care reimbursement policies a barrier to acute and cancer pain management?  J Pain Symptom Manage 9(4):244-53.  

Joranson, D. E.  1990.  Federal and state regulation of opioids.  J Pain Symptom Manage5(1 Suppl):S12-S23.

Joyce, E., S. Blumentahl and S. Wessely. 1996.  Memory, attention and executive function in chronic fatigue syndrome.  J Neurol Neurosurg Psychiatry 60(5):459-503.

Joyce, P. and C. Clark.  1996.  The use of CranioSacral Therapy to treat gastroesophageal reflux in infants.  Inf Young Children 9(2):51-58. 

Juhl GI, Jensen TS, Norholt SE et al. 2007.  Central sensitization phenomena after third molar surgery: a quantitative sensory testing study.  Eur J Pain. [Jun 4 Epub ahead of print]  “Even a minor orofacial surgical procedure may be sufficient to evoke signs of both central and peripheral sensitization, which may play a role in the transition from acute to chronic pain in susceptible individuals.” 

Julien N, Goffaux P, Arsenault P et al. 2005.  Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition.  Pain 114(1-2):295-302.  “These data support a deficit of endogenous pain inhibitory systems in fibromyalgia but not in chronic low back pain.  The treatments proposed to fibromyalgia patients should aim at stimulating the activity of those endogenous systems.”  [This indicates that treatment of FM should focus on central nervous system modulation. DJS]

Jung, A. C., T. Staiger and M. Sullivan.  1997.  The efficacy of selective serotonin reuptake inhibitors for the management of chronic pain.  J Gen Intern Med 12(6):384-389. 

Just MA, Keller TA, Cynkar J. 2008.  A decrease in brain activation associated with driving when listening to someone speak.  Brain Res 1205.:70-80.  This study used functional MRI to show that, even in healthy individuals, listening carefully to anyone speaking can be dangerous.  In this study, drivers had to listen carefully as they needed to tell if statements were true or false.  This produced spatial processing associated parietal lobe activation, and resulted in significant deterioration in driving ability, even though the drivers did not have to hold or dial a phone.  [This study has profound ramifications for those of us with FM cognitive dysfunction.  There may be days that you don’t want to drive with that language tape going, days when the talking book may be out of the question or days when even music is too much to handle when driving.  If FM flares or aggravating factors are severe, driving may have to be suspended for a time until perpetuating and aggravating factors are under control.  This must be individualized, and it is important that our traveling companions understand this.  DJS]

Juul-Kristensen B, Lund H, Hanses K et al. 2007.  Poorer elbow proprioception in patients with lateral epicondylitis than in healthy controls: a cross-sectional study.  J Shoulder Elbow Surg. [Nov 22 Epub ahead of print].  “Proprioception seems...to be poorer in elbows with lateral epicondylitis elbows than in the controls’ elbows.  This needs to be taken into consideration in the management of lateral epicondylitis.”  [This could be due to co-existing MTPs. DJS]

Kabongo, M. L. and A. W. Bedell.  1987.  Nail signs of systemic conditions.  AFP 36(4):109-116.

Kahan M, Srivastava A, Wilson L et al. 2006.  Opioids for managing chronic non-malignant pain: safe and effective prescribing.  Can Fam Physician. 52(9):1091-1096.  When pain control with other medications have failed, titration to find the lowest dose opioids that might be effective is the next logical step.  “Most patients with chronic non-malignant pain can be managed with <300 mg/d of morphine (or equivalent).  Opioids are safe and effective for managing chronic pain.”  [Non-medicinal pain relief methods should be part of any pain control program. DJS]   

Kakojic, D., V. Demarin, M. Kadojic, I. Mihaljevic and B. Barac.  1999.  Influence of prolonged stress on risk factors for cerebrovascular disease.  Coll Antropol 23(1):213-9.

Kalichman L. 2009.  Association between fibromyalgia and sexual dysfunction in women.  Clin Rheumatol. [Jan 23 Epub ahead of print].  It would have been valuable to assess these patients for co-existing TrPs, as their role in sexual dysfunction in both women and men has been carefully documented.  DJS]

Kallenberg LA, Hermens HJ. 2004.  Motor unit action potential rate and motor unit action potential shape properties in subjects with work-related chronic pain.  Eur J Appl Physiol. [Epub ahead of print.]  “...more high-threshold Mus contribute to low-level computer work-related tasks in chronic pain cases. Additionally, the results suggest that the input of the central nervous system to the muscle is higher in the cases with chronic pain.”

Kalmer, J. M. and E. Cafarelli1999. Effects of caffeine on neuromuscular function. A Appl Physiol 87(2):801-808.

Kamanli A, Kaya A, Ardicoglu O et al. 2004.  Comparison of lidocaine injection, botulinum toxin injection, and dry needling to trigger points in myofascial pain syndrome.  Rheumatol Int. [Epub ahead of print.]  Lidocaine injection appears to offer the best results of the three according to this study, as it causes less problems than the dry needling and is less expensive than BTX-A.  BTX-A may be the treatment of choice in patients with resistant TrPs.  [Perpetuating factors must always be identified and brought under control.  DJS.]

 

Kandt RS, Daniel FL. 1986.  Glossopharyngeal neuralgia in a child.  A diagnostic and therapeutic dilemma.  Arch Neurol 43(3):301-302.  Symptoms were caused by TrPs in the right tonsil area.

Kang Y, Yi Y, Kim J. 2007.  Pain drawings of the phantom pain of the patients with amputation.  J Musculoskel Pain 15 (Supp 13):27 item 43.  [Myopain 2007 Poster]  “The patterns of phantom pain were very similar to the referred pain patterns of the MPS.  A new assumption would be possible: that ‘phantom pain in MPS’s clothing’ like ‘sheep in wolf’s clothing’.” [This finding agrees with other research and observation that indicates phantom limb (and breast, uterine and ovarian) pain may be due to MTPs or other tissue TrPs. DJS]

Kankaanpaa, M. S. Taimela, D. Laaksonen, O. Hanninen and O. Airaksinen.  1998.  Back and hip extensor fatigability in chronic low back pain patients and controls.  Arch Phys Med Rehabil 79(4):412-7.

Kao MJ, Hsieh YL, Kuo FJ et al. 2006. Electrophysiological assessment of acupuncture points.  Am J Phys Med Rehabil. 85(5):443-448.   “Similar to the distribution of EPN loci in an MTrP region, significantly more EPN (end plate noise) loci can be identified in an AcP (acupuncture point) region of Stomach-36 than in a nearby non-AcP site.  This study provides additional support to the hypothesis that some AcPs are also myofascial trigger points.”

Kaplan, R. M., S. M. Schmidt and T. A. Cronan.  2000.  Quality of well being in patients with fibromyalgia.  J Rheumatol 27(3):785-9. 

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.”

Kar, A., B. K. Choudhary and N. G. Bandyopadhyay. 1999. Preliminary studies on the inorganic constituents of some indigenous hypoglycaemic herbs on oral glucose tolerance test. J Ethnopharmacol 64(2):179-84.

Karalis, K. P., E. Kontopoulos, L. J. Muglia and J. A. Majzoub.  1999.  Corticotropin-releasing hormone deficiency unmask the proinflammatory effect of epinephrine.  Proc Natl Acad Sci U S A 96(12):7093-7.   

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]

 

Karmakar MK, Ho AM. 2004.  Postthoracotomy pain syndrome.  Thorac Surg. Clin. 14(3):345-352.  About 30% of posthoracotomy patients experience chronic pain as a result.  The authors advocate aggressive pain control before incision, but neglect to mention the possibility of TrPs.

 

Kashikar-Zuck S, Lynch AM, Slater S et al. 2008.  Family factors, emotional functioning, and functional impairment in juvenile fibromyalgia syndrome.  Arthritis Rheum. 59(10):1392-1398.  “Mothers of adolescents with JPFS (juvenile primary fibromyalgia syndrome) reported twice as many pain conditions and significantly greater depressive symptoms than mothers of comparison peers.  The JPFS group also had poorer overall family functioning and more conflicted family relationships.  In adolescents with JPFS, maternal pain history was associated with significantly higher functional impairment.  Conclusion: Increased distress and chronic pain are evident in families of adolescents with JPFS, and family relationships are also impacted.  Implications for child functional impairment and the need for inclusion of caregivers in treatment are discussed.”

 

Kashikar-Zuck S, Parkins IS, Graham TB et al. 2008.  Anxiety, mood, and behavioral disorders among pediatric patients with juvenile fibromyalgia syndrome.  Clin J Pain 24(7):620-626.  “There seems to be a high prevalence of anxiety disorders in patients with JPFS, and presence of anxiety disorder is associated with poorer physician-rated functioning.”  [This is written by psychology specialists, with an acknowledgment of potential co-existing myofascial TrPs that might create symptoms that could be mistaken as psychological. DJS]

 

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.”

Kashima, K., O. I. Rahman, S. Sakoda and R. Shiba.  1999.  Increased pain sensitivity of the upper extremities of TMD patients with myalgia to experimentally-evoked noxious stimulation: possibility of worsened endogenous opioid systems.  Cranio 17(4):241-6.

Kasikcioglu E, Dinler M, Berker E. 2006.  Reduced tolerance of exercise in fibromyalgia may be a consequence of impaired microcirculation initiated by deficient action of nitric oxide.  Med. Hypotheses [Jan 9 Epub ahead of print].

Kassirer,  J. P. 1997. Federal foolishness and marijuana.  N Engl J Med 366(5):336-7.

Kasteleijn-Nolst Trenite, D. G., A. M. da Silva, S. Ricci, C. D. Binnie, G. Rubboli, C. A. Tassinari and J. P. Segers.  1999.  Video-game epilepsy: a European study.  Epilepsia 40 (Suppl 4):70-4.

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]

 

Kato T, Montplaisir JY, Guitard F et al. 2003.  Evidence that experimentally induced sleep bruxism is a consequence of transient arousal.  J Dent Res. 82(4):284-288.

Katz J, McCartney CJ. 2002.  Current status of pre-emptive analgesia.  Curr Opin Anaesthesiol. 15(4):435-441.  “The application of preventive perioperative analgesia (not necessarily preincisional) is associated with a significant reduction in pain beyond the clinical duration of action of the analgesic agent, in particular for the N-methyl-D-aspartate antagonists.”

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 FM (50.9-8.8%).  Patients with FM 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 FM with memory problems alone.  Patients with rheumatic disease substantially differ in cognitive vulnerability, with patients with FM 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 FM.  That this linkage has the possibility of having a great deal to do with an important clinical variant of FM underscores the need for greater clinical recognition of this underrecognized pattern and for further research.” 

Kaufmann, H. 1997. Neurally mediated syncope and syncope due to autonomic failure: differences and similarities.  J Clin Neurophysiol 14(3):183-196.

Kaufmann I, Schelling G, Eisner C et al. 2008.  Decrease in adhesion molecules on polymorphonuclear leukocytes of patients with fibromyalgia.  Rheumatol Int.  [Dec. 4 Epub ahead of print].  This is a study indicating yet another physiological difference in FM patients.  “These changes might lower the rate of polymorphonuclear leukocyte migration to sites of inflammation and thereby compromise defense against infection and pain control.”

 

Kaufmann I, Schelling G, Eisner C et al. 2008.  Anandamide and neutrophil function in patients with fibromyalgia.  Psychoneuroendocrinology [Apr 4 Epub ahead of print].  The endocannabinoid system is a critical pathway in pain perception in mammals.  It is activated during stressful situations, and can be part of the immune system activation that, in turn, is associated with the development of chronic pain.  This study indicates that “...patients with FM might benefit from pharmacologic manipulation of the endocannabinoid signaling...”  Controlled research is needed.  [This research may help us get over the prejudice concerning cannabinoid use for chronic pain. DJS]

Kauppila, T., X. J. Xu, W. Yu and Z Wiesenfeld-Hallin.  1998.  Dextromethorphan potentiates the effect of morphine in rats with peripheral neuropathy.  Neuroreport 9(6):1071-1074.

Kavlock, R. J.  1999.  Overview of endocrine disruptor research activity in the United States. Chemosphere 39(8):1227-36.

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.

Kawamata, T., K. Omote, M. Kawamata and A. Namiki.  1998.  Premedication with oral dextromethorphan reduces postoperative pain after tonsillectomy.  Anesth Analg 86(3):594-597.

Kay, G.G. and A. G. Harris.  1999.  Loratadine [Note: Claritin]: a non-sedating antihistamine. Review of its effects on cognition, psychomotor performance, mood and sedation.  Clin Exp Allergy 29(S3):147-150.

Kayyali HA, Weimer S, Frederick C et al. 2008.  Remotely attended home monitoring of sleep disorders.  Telemed J E Health 14(4):371-374.  “A new enabling home telehealth technology for real-time sleep disorders monitoring was developed and tested with encouraging preliminary results.  The sample size is too small to derive any clinical conclusions about the sleep quality of FM patients.  However, this study validates the underlying technology and demonstrates the role of new wireless technologies in the future of sleep disorders diagnosis.”  [This is a potentially important development that may allow polysomnography to be available to those who otherwise would not be able to receive it. 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.]

Keel, P.  1999.  Pain management strategies and team approach.  Baillieres Best Pract Res Clin Rheumatol 13(3):493-506.

Keel, P.J., C. Bodoky, U. Gerhard and W. Muller. 1998. Comparison of integrated group therapy and group relaxation training for fibromyalgia. Clin J Pain 14(3):232-8.

Keitel, W. 1999. [Occupational therapy in the diseases of the locomotor system]. Z Arztl Fortbild Qualitatssich 93(5):335-40 [German].

Keitel, W. 1999. [ No title available] Fortschr Med 117(5):32-6. [German]

Kelly A, Khan K. 2008.  Prevalence of allergies in children with complex medical problems.  Clin Pediatr. 47(8):809-816.  “The authors report a higher than expected prevalence of allergic and immune abnormalities in children with complex medical problems.”  [We must be attentive to the possibility of co-existing conditions in children with FM or CMP. DJS]

Kelly G.S. 2000. Insulin resistance: lifestyle and nutritional interventions. Altern Med Rev 5(2):109-32. Insulin resistance seems to be common and contributes to several frequent health problems including sleep apnea, obesity, and type 2 diabetes.  Possible perpetuating factors include diet, exercise, smoking and stress.

Kelly M, Gagne R, Newman JD et al. 2008.  Assessment of fibromyalgia and chronic fatigue syndrome: a new protocol designed to determine work capability – chronic pain abilities determination (CPAD).  Ir Med J. 101(9):277-278.  [There are some very good aspects of this new protocol, but no protocol will be complete until it takes into account assessment of specific musculoskeletal weakness, dysfunction, proprioception and autonomic concomitants from myofascial TrPs.  When patients have multiple interactive diagnoses including chronic myofascial pain, they must all be taken into account.  DJS]

Kemeny, M. E. and T. L. Gruenewald.  1999.  Psychoneuroimmunology update.  Semin Gastrointest Dis 10(1):20-9.

Kemoun G, Carette P, Watelain E et al. 2008.  Thymocognitive input and postural regulation: a study on obsessive-compulsive disorder patients.  Neurophysiol Clin. 38(2):99-104.  This review covers the recent research on nerve networks that are common to both postural balance and psychological states.  “When interpreting symptoms, these interactions should be taken into account.”  [They should also be taken into account when designing therapies. DJS]

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]

Kendall, SA, Henriksson, KG, Hurtig, I et al. 2003.  Differences in sensory thresholds in the skin of women with fibromyalgia syndrome: a comparison between ketamine responders and ketamine non-responders.  J Muscoloskel Pain 11(2):3-9.  This is another study indicating that subsets of patients with FM have different pain processing dysfunctions. 

Kern, W., E. F. Stange, H. L. Fehm and H. H. Klein.  1999. [No title available].  Z Gastroenterol Suppl 1 (13):36-42 [German]. 

Kerns RD, Rosenberg R. 2000.  Predicting responses to self-management treatments for chronic pain: application of the pain stages of change model.  Pain 84(1):49-55.  “These findings suggest that increased commitment to a self-management approach to chronic pain may serve as a mediator or moderator of successful treatment.”

Kerr CE, Shaw JR, Wasserman RH et al. 2008.  Tactile acuity in experienced Tai Chi practitioners: evidence for use dependent plasticity as an effect of sensory-attentional training.  Exp Brain Res. 188(2):317-322.  [Practitioners of t’ai chi had greater spatial acuity than controls.  T’ai chi may be valuable in patients with proprioceptive dysfunction due to myofascial trigger points or FM. DJS]

Kerr, S. J. , P. J. Armati and B. J. Brew.  1995. Neurocytotoxity of quinolinic acid in human brain cultures. J Neurovirol 1(5-6):375-380.

Ketroser DB 2000.  Whiplash, chronic neck pain, and zygapophyseal joint disorders. A selective review. Minn Med  83(2):51-4

Keverne, E. B.  1999.  The Vomeronasal Organ.  Science 286(5440):716-720.

Khaki AM. 2006.  Pain clinic experience in a teaching hospital in Western, Saudi Arabia.  Relationship of patient’s age and gender to various types of pain.  Saudi Med J. 27(12):1882-1886.  “Various types of chronic pain managed in the pain clinic (required) full understanding of pain neurophysiology as well as familiarity with contributing factors to the prevalence of pain.”

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]

Khan MA, Lichtensteiger CA, Faroon O, Mumtaz M, Schaeffer DJ, Hansen LG. The hypothalamo-pituitary-thyroid (HPT) axis: a target of nonpersistent ortho-substituted PCB congeners.2002. Toxicol Sci Jan;65(1):52-61.

Khasar SG, Burkham J, Dina OA et al. 2008.  Stress induces a switch of intracellular signaling in sensory neurons in a model of generalized pain.  J Neurosci. 28(22):5721:5730.  “Thus, an important mechanism in generalized pain syndromes may be stress-induced coactivation of the hypothalamo-pituitary-adrenal and sympathoadrenal axes, causing a long-lasting alteration in intracellular signaling pathways, enabling normally innocuous levels of immune mediators to produce chronic hyperalgesia.”  Stress can be an important contributor to the change from acute to chronic illness, and then can maintain that chronicity.

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.”

Kharkevich, D. A. and V. V. Churukanov.  1999.  Pharmacological regulation of descending cortical control of the nociceptive processing.  Eur J Pharmacol 375(1-3):121-31.

Kidd, P. M.  1999.  A review of nutrients and botanicals in the integrative management of cognitive dysfunction.  Altern Med Rev 4(3);144-61.

Kiecolt-Glaser JK, McGuire L, Robles TF, Glaser R. Emotions, Morbidity, and Mortality: New Perspectives from Psychoneuroimmunology. 2002. Annu Rev Psychol 53:83-107.

Kim, J. Y. L. A. Nolte, P. A. Hansen, D. H. Hanm, K. Kawanaka and J. O. Holloszy. 1999. Insulin resistance of muscle glucose transport in male and female rats fed a high-sucrose diet. Am J Physiol 276(3 Pt 2): R665-R672.

Kim PS. 2002. Role of injection therapy: review of indications for trigger point injections, regional blocks, facet joint injections, and intra-articular injections. Curr Opin Rheumatol Jan;14(1):52-7. Multidiciplinary therapies for many chronic pain patients may often include injection therapies as part of effective pain management.

Kim SH, Kim DH, Oh DH et al. 2008.  Characteristic electron microscopic findings in the skin of patients with fibromyalgia-preliminary study.  Clin Rheumatol. 27(3):407-411.  “The EM findings seen in the skin of FM patients show unusual patterns of unmyelinated nerve fibers as well as associated Schwann cells.”  [This study may implicate a mechanism of hypersensitivity in a variety of tissues in the FM patient.  Larger studies are needed. DJS]

Kim SH. 2007.  Skin biopsy findings: implications for the pathophysiology of fibromyalgia.  Med Hypotheses [Jan 8 Epub ahead of print]  Skin abnormalities in FM patients may be significant.

Kim SH, Jang TJ, Moon IS. 2006.  Increased expression of N-Methyl-D-Aspartate Receptor Subunit 2D in the skin of patients with fibromyalgia.  J Rheumatol. 33(4):785-788.  “The increased expression of NMDAR found in FM skin could be indicative of a more generalized increase in other peripheral nerves.  This suggests that NR2D-selective antagonists may have implications in the treatment of allodynia in patients with FM.” 

Kim SH, Won SJ, Mao XO et al. 2005.  Molecular mechanisms of cannabinoid protection from neuronal excitotoxicity.  Mol Pharmacol. [Nov 18 Epub ahead of print].  “Cannabinoids appear to protect neurons against NMDA toxicity at least partly by activation of CB1R and downstream inhibition of PKA signaling and NO generation.”

Kimmelberg H.K., Zhou M. 2002.  Hippocampal astrocytes show heterogeneity of swelling activated anion currents.  Glia (Suppl 1):S55 [Abstract]. 

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Kinsley, C. H.., L. Madonia, G. W. Gifford, K. Tureski, G. R. Griffin, C. Lowry, J. Williams, J. Collins, H. McLearie and K. G. Lambert. 1999. Motherhood improves learning and memory. Nature 402(6758):137-8. 

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Kirchheiner J, Brockmoller J. 2005.  Clinical consequences of cytochrome P450 2C9 polymorphisms.  Clin Pharmacol Ther. 77(1):1-16.   This is a good review of the current knowledge of the effects of genetic variations on drug metabolism.   Phenotyping has potential use indicating both potential drug effectiveness and potential toxicity, but the knowledge needs to be developed.

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Kiser RS, Cohen HM, Freedenfeld RN et al. 2001.  Olanzapine for the treatment of fibromyalgia symptoms.  J Pain Symptom Manage 22(2):704-708.  This is a potential medication for FM with few serious side effects found thus far.

 

Kivimaki M, Leino-Arjas P, Kaila-Kangas L et al. 2006.  Increased sickness absence among employees with fibromyalgia.  Ann Rheum Dis June 22 [Epub ahead of print].  “FM is associated with a substantially increased risk of medically certified sickness absence...”

 

Klauenberg S, Maier C, Assion HJ et al. 2008.  Depression and changed pain perception: Hints for a central disinhibition mechanism.  Pain. [Oct 14 Epub ahead of print].  “The results contradict the former assumption of a general insensitivity to experimental pain in depressive disorder.  In the mostly pain-free patients signs of an enhanced central hyperexcitability are even more pronounced than usually found in chronic pain patients (e.g. FM), indicating common mechanisms in depressive disorder and chronic pain in accordance with the assumption of non-pain associated mechanisms in depressive disorder for central hyperexcitability, e.g. by inhibited serotonergic function.  Furthermore, this trial demonstrates the feasibility of QST (quantitative sensory testing) in depressive patients.”

Klein, R., and P. A. Berg. 1995. High incidence of antibodies 5-hydroxytryptamine, gangliosides, and phospholipids in patients with chronic fatigue and fibromyalgia syndrome and their relatives: evidence for a clinical entity of both disorders. Eur J Med Res 1(1):21-6.

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Klekner A, Felszeghy S, Tammi R et al. 2005.  Quantitative determination of hyaluronan content in cerebral aneurysms by digital densitometry.  Zentralbl Neurochir. 66(4):207-212.  “Results suggest that an elevated hyaluronan level in the extracellular matrix may affect the cerebral arterial wall architecture.  It is reasonable to suppose that the increased hyaluronan content creates a viscoelastic ECM which might improve the biomechanical resistance of the thinned vessel wall.”  [This seemingly unrelated piece of research may provide clues to the higher viscosity of the extracellular matrix of a subset of patients with both FM and CMP, especially in relation to the geloid mass.  DJS]

Klingmann PO, Kugler I, Steffke TS et al. 2008.  Sex-specific prenatal programming: a risk for fibromyalgia?  Ann N Y Acad Sci. 1148:446-455.

Knardahl, S., M. Elam, B. Olausson and B. G. Wallin.  1998.  Sympathetic nerve activity after acupuncture in humans.   Pain 75(1):19-25.

Knobler, H. A. Schattner, T. Zhornicki, S. D. Malnick, D. Keter, N. Sokolovskaya, Y. Lurie and D. D. Bass. 1999. Fatty liver-and additional and treatable feature of the insulin resistance syndrome. QMJ 9(2):73-9.

Knoll, R, Hoshijima, M, Chien, K. 2003.  Cardiac mechanotransduction and implications for heart disease.  Oct 9 [Epub ahead of print.]  This article concerns mechanotransduction, which includes the translation of mechanoreception to proprioception.  The authors ask some interesting questions concerning conversion of stimuli to electrochemical signaling and cover recent research in cardiac cytoskeleton structure.  Fascia is everywhere, and my heart tells me that the authors should be aware of myofascial medicine and the possible permutations that may be involved.  

Koch, K. L.  1999.  Illusory self-motion and motion sickness: a model for brain-gut interactions and nausea.  Dig Dis Sci 44(8 Suppl):53S-57S.

Koelback Johnson, M., T. Graven Nielsen, A. Schou Olesen and L. Arendt-Nielsen. 1999. Generalized muscular hyperalgesia in chronic whiplash syndrome. Pain 83(2):229-234.

Koenig, H. G., J. C. Hays, D. B. Larson, L. K. George, H. J. Cohen, M. E. McCullough, K. G. Meador and D. G. Blazer.  1999.  Does religious attendance prolong survival?  A six-year follow-up study of 3,968 older adults.  J Gerontol A Biol Sci Med Sci 54(7):M370-6.  

Koenig, H. G., L. K. George and B. L. Peterson.  1998.  Religiosity and remission of depression in medically ill older patients.  Am J Psychiatry 155(4):536-542.  

Koenig, H. G., H. J. Cohen, L. K. George, J. C. Hays, D. B. Larson and D. G. Blazer.  1997. Attendance at religious services, interleukin-6, and other biological parameters of immune function in older adults.  Int J Psychiatry Med 27(3):233-50.

Koenig M, Cathebras P, Guy C et al. 2005.  [Pentoxiphylline: a cheap substitute for anti-TNFalpha agents?]  Rev Med Interne. [Nov 8 Epub ahead of print] [French]   [This medication may be a useful agent for use in chronic pain states. DJS ]

Kohnen R, Farber L, Spath M. 2004.  The assessment of vegetative and functional symptoms in fibromyalgia patients: the tropisetron experience.  Scand J Rheumatol Suppl. (119):67-71.  Tropisetron, in general, helped sleep dysfunction but worsened gastrointestinal function in these FM patients.

Kohlmann T. 2003.  [Musculoskeletal pain in the population] [German]  Schmerz. 17(6):405-411.  This review indicates that about 16% of the German population has severe musculoskeletal pain.

Kolbinson, D. A. , J. B. Epstein, A. Senthilselvan and J. A. Burgess. 1998. Effect of impact and injury characteristics on post-motor vehicle accident temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod  85(6):665-73.  

Komaroff, A. L. and D. S. Buchwald.  1998.  Chronic fatigue syndrome: an update.  Annu Rev Med 49:1-13.  

Komiyama, O., M. Kawara, M. Arai, T. Asano and K. Kobayashi.  1999.  Posture correction as part of behavioral therapy in treatment of myofascial pain with limited opening.  J Oral Rehabil26(5):428-35.

Koolstra JH, van Eijden TM. 2005.  Combined finite-element and rigid-body analysis of human jaw joint dynamics.  J Biomech 38(12):2431-2439.  The (jaw) joint is subjected to loading which causes tensions and deformations in its cartilaginous structures.  These are assumed to be a major determinant for development, maintenance, and also degeneration of the joint...It was demonstrated that joint loads increase with muscle activation, irrespective of the external loads..”

Kop WJ, Lyden A, Berlin AA et al. 2005.  Ambulatory monitoring of physical activity and symptoms in fibromyalgia and chronic fatigue syndrome.  Arthritis Rheum. 52(1):296-303.  “Patients with FM and/or CFS engaged in less high-intensity physical activities than that recorded for sedentary control subjects.  This reduced peak activity was correlated with measures of poor physical function.  Activity levels appear to be contingent on, rather than predictive of, symptoms.”

 

Kopf A, Janson W, Stein C. 2003.  [Opioid therapy in chronic non-malignant pain] [German]  Anaesthesist. 52(2):103-114.  Therapeutic recommendations from the DGSS consensus conference include a validated indication for the use of opioids for chronic nonmalignant pain.

 

Koppert W. 2005.  [Opioid-induced analgesia and hyperalgesia]  Schmerz [Aug 12 Epub ahead of print] [German]  “Successful strategies that may decrease or prevent opioid-induced hyperalgesia include the concomitant administration of drugs such as NMDA antagonists, alpha(2)-agonists, or nonsteroidal anti-inflammatory drugs (NSAID), opioid rotation, or combinations of opioids with different receptor selectivity.”

Koppert W, Weigand M, Neumann F et al. 2004.  Perioperative intravenous lidocaine has preventive effects on postoperative pain and morphine consumption after major abdominal surgery.  Anesth Analg 98(4):1050-1055.

Koppert, W., S. Zeck, R. Sittl, R. Likar, R. Knoll and M. Schmelz. 1998. Low-dose lidocaine suppresses experimentally induced hyperalgesia in humans. Anesthesiology 89(6):1345-53. 

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Kornick CA, Santiago-Palma J, Moryl N et al. 2003.  Benefit-risk assessment of transdermal fentanyl for the treatment of chronic pain.  Drug Saf 26(13):951-973.  “Transdermal fentanyl is effective and well tolerated for the treatment of chronic pain caused by malignancy and non-malignant conditions when administered according to the manufacturer’s recommendations.  Compared with oral opioids, advantages of transdermal fentanyl include a lower incidence and impact of adverse effects (constipation, nausea and vomiting, and daytime drowsiness), higher degree of patient satisfaction, improved quality of life, improved convenience and compliance resulting from administration every 72 hours, and decreased use of rescue medication.”

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Korszun, A., L. Sackett-Lundeen, E. Papadopoulos, C. Brucksch, L. Masterson, N. C. Engelberg, E. Haus, M. A. Demitrack and L. Crofford.  1999.  Melatonin levels in women with fibromyalgia and chronic fatigue syndrome.  J Rheumatol 26(12):2675-80.

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Kostopoulos D. 2008.  Reduction of spontaneous electrical activity and pain perception of trigger points in the upper trapezius muscle through trigger point compression and passive stretching.  J Musculoskel Pain 16(4):266-278.  “Although each technique significantly reduced pain perception and SEA (spontaneous electrical activity) the combination of Ic (ischemic compression) and PS (passive stretching) was superior, apparently because of the complementary nature of the therapeutic interventions.”

Kotarinos RK. 2003.  Pelvic floor physical therapy in urogynecologic disorders.  Curr Womens Health Rep. 3(4):334-339.

Kotter I, Neuscheler D, Gunaydin I et al. 2007.  Is there a predisposition for the development of autoimmune diseases in patients with fibromyalgia?  Retrospective analysis with long term follow-up.  Rheumatol Int. [Jul 20 Epub ahead of print].  “The risk of CTD (connective tissue disease) is not increased in FM.  The detection of ANA (antinuclear antibodies) does not predict the development of CTD.”

Kovacevic-Ristanovic, R., R. D. Cartwright and S. Lloyd.  1991.  Nonpharmacologic treatment of period leg movements in sleep.  Arch Phys Med Rehabil 72(6):385-9.

Kovacs, F. M., V. Abraira, F. Pozo, D. G. Kleinbaum, J. Beltran, I. Mateo, C. Perez de Ayala, A. Pena, A. Zea, M. Gonzalez-Lanza and L. Morillas.  1997.  Local and remote sustained trigger point therapy for exacerbations of chronic low back pain.  A randomized, double-blind, controlled, multicenter trial.  Spine 22(7):786-797.

Kraegen EW, Cooney GJ, Ye J, et al. 2001. Triglycerides, fatty acids and insulin resistance B hyperinsulinemia.  Exp Clin Enocrinol Diabetes 109(4):S516-26. "A key issue for development of insulin resistance is skeletal muscle.  At least some of the lipid accumulation is inside the muscle cell (myocyte).  Unless there is significant weight loss, short or medium term dietary manipulation does not alter insulin sensitivity.  Evidence is growing that excess muscle and liver lipid accumulation causes or exacerbates insulin resistance."

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Kratz AL, Davis MC, Zautra AJ. 2007.  Pain acceptance moderates the relation between pain and negative affect in female osteoarthritis and fibromyalgia patients.  Ann Behav Med. 33(3):291-301.  “These findings suggest that pain patients with greater capacity to accept pain may be emotionally resilient in managing their condition.”

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Krause, K-H, J. Krause, I. Magyarosy, E. Ernst and D. Pongratz. 1998. Fibromyalgia syndrome and attention deficit hyperactivity disorder: is there a co morbidity and are their consequences for the therapy of fibromyalgia syndrome. J Musculoskel Pain 6(4): 111-116.

Kravitz HM, Esty ML, Karz RS et al. 2006.  Treatment of fibromyalgia syndrome using low-intensity neurofeedback with the Flexyx Neurotherapy System: A randomized controlled clinical trial.  J Neurother 10(2/3):41-46.

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Krishman SK, Benzon HT, Siddiqui T et al. 2000.  Pain on intramuscular injection of bupivacaine, ropivacaine, with and without dexamethasone.  Reg Anesth Pain Med 25(6):615-619.  “The pain on intramuscular injection of bupivacaine is significantly more intense than with ropivacaine.”  Yet another study documenting that Marcaine is not acceptable for TrP injections.

 

Krishnaswamy G, Ajitawi O, Chi DS. 2005.  The human mast cell: an overview.  Methods Mol Biol. 315:13-34.  “Mast cells may be capable of regulating inflammation, host defense, and innate immunity.  After activation, mast cells express histamine, leukotrienes, and prostanoids, as well as proteases, and many cytokines and chemokines.  These mediators may be pivotal to the genesis of an inflammatory response.  By virtue of their location and mediator expression, mast cells may play an active role in many diseases.  Recent data also suggest that mast cells play a vital role in host defense against pathogens by elaboration of tumor necrosis factor alpha.  Mast cells also express the Toll-like receptor, which may further accentuate their role in the immune-inflammatory response.”

Kroboth, P. D., F. S. Salek, A. L. Pittenger, T. J. Fabian and R. F. Frye.  1999.  DHEA and DHEA-S: a review.  J Clin Pharmacol 39(4):327-48.

Kroese MD, Schulpen GJ, Bessems MC et al. 2008.  Substitution of specialized rheumatology nurses for rheumatologists in the diagnostic process of fibromyalgia: a randomized controlled trial.  Arthritis Rheum. 59(9):1299-1305.  “Substituting specialized nurses for rheumatologists in the diagnostic process of FM is a trustworthy and successful approach that saves waiting time, provides greater patients satisfaction, and is cost-effective.”

Kruger, L. R., W. J. Van Der Linden and P. E. Cleaton-Jones.  1998.  Transcutaneous electrical nerve stimulation in the treatment or myofascial pain dysfunction.  S Afr J Surg 36(1):35-38.  

Kuan LC, Li YT, Chen FM et al. 2006.  Efficacy of treating abdominal wall pain by local injection.  Taiwan J Obstet Gynecol. 45(3):239-243.  “Local injection for selective abdominal wall pain patients produces significant pain relief.  The diagnosis of abdominal wall pain is an important component in avoiding unnecessary operations in patients with abdominal pain.”

Kuan TS, Hsieh YL, Chen SM et al. 2007.  The myofascial trigger point region: correlation between the degree of irritability and the prevalence of endplate noise.  Am J Phys Med Rehabil. 86(3):183-189.  “The irritability of an MTrP is highly correlated with the prevalence of EPN in the MTrP region of the upper trapezius muscle.  The assessment of EPN prevalence in an MTrP region may be applied to evaluate the irritability of that MTrP.”

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.

Kuch, K., B. J. Cox and R. J. Evans. 1996. Posttraumatic stress disorder and motor vehicle accidents: a multidisciplinary overview. Can J Psychiatry 41(7):429-434.

Kuch, K., B. Cox, R. J. Evans,  P. C. Watson and C. Bubela. 1993. To what extent do anxiety and depression interact with chronic pain? Can J Psychiatry 38(1):38(1):36-38.

Kuchinad A, Schweinhardt P, Seminowicz DA et al. 2007.  Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain?  J Neurosci. 27(15):4004-4007.  “…fibromyalgia patients had significantly less total gray matter volume and showed a 3.3 times greater age-associated decrease in gray matter than healthy controls.  The longer the individuals had had fibromyalgia, the greater the gray matter loss, with each year of fibromyalgia being equivalent to 9.5 times the loss in normal aging.  In addition, fibromyalgia patients demonstrated significantly less gray matter density than healthy controls in several brain regions, including the cingulate, insular and medical frontal cortices, and parahippocampal gyri.”   “...fibromyalgia appears to be associated with an acceleration of age-related changes in the very substance of the brain.  Moreover, the regions in which we demonstrate objective changes may be functionally linked to core features of the disorder including affective disturbances and chronic widespread pain.”

Kudo, Y. 1997. [Ca2+dynamics in glial cells]. Nippon Yakurigaku Zasshi 109(3):111-7. 

Kuhajda, M. C., B. E. Thorn and M. R. Klinger.  1998.  The effect of pain on memory for affective words.  Ann Behav Med 20(1):31-5.

Kuiper, G. G., J. G. Lemmen, B. Carlsson, J. C. Corton, S. H. Safe, P. T. van der Saag and B. van der Burg.  1998.  Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta.  Endocrinology 139(10):4252-63.

Kujala, U. M., S. Taimela and T. Viljanen.  1999.  Leisure physical activity and various pain symptoms among adolescents.  Br J Sports Med 33(5):325-8.

Kumar S, Ferrari R, Narayan Y. 2004.  Cervical muscle response to posterolateral impacts — effect of head rotation.  Clin Biomech 19(9):899-905.  “Head rotation in a right posterolateral impact modifies the cervical response mainly by generating an asymmetry in the paired sternocleidomastoid electromyograms.  This may asymmetrically affect the risk of injury to the sternocleidomastoids “  

 

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.”

 

Kundermann B, Krieg JC, Schreiber W et al. 2004.  The effect of sleep deprivation on pain.  Pain Res Manag. 9(1):25-32.  “Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture.  One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain.  Sleep deprivation produces hyperalgesic changes.  Sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action.”

 

Kuo LE, Kitlinska JB, Tilan JU et al. 2007.  Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome.  Nat Med. 13(7):803-811.

 

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.”

 

Kupers RC, Svensson P, Jensen TS. 2004.  Central representation of muscle pain and mechanical hyperesthesia in the orofacial region: a positron emission tomography study.  Pain 108(3):284-293. s “Cerebral processing of jaw-muscle pain may differ from the processing of cutaneous pain and that mechanical hyperesthesia, which often is encountered in clinical cases, has a unique representation in the brain.”

 

Kuramoto AM. 2006.  Therapeutic benefits of Tai Chi exercise: research review.  WMJ 105(7):42-46.

 

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.”

Kurosinski P, Gotz J. 2002.  Glial cells under physiologic and pathologic conditions.  Arch Nerol 59(10):1524-8. Glial cell loss may contribute to cognitive deficits such as memory impairment.

Kurtze, N., K. T. Gundersen and S. Svebak.  1999.  Quality of life, functional disability and lifestyle among subgroups of fibromyalgia patients: the significance of anxiety and depression. Br J Med Psychol 72 (Pt 4):471-84.   

Kurtze, N., K. T. Gundersen and S. Svebak.  1998.  The role of anxiety and depression in fatigue and patterns of pain among subgroups of fibromyalgia patients.  Br J Med Psychol 71(Pt 2):185-194.

Kusano M, Kouzu T, Kawano T et al. 2008.  Nationwide epidemiological study on gastroesophageal reflux disease and sleep disorders in the Japanese population.  J Gastroenterol. 43(11):833-841.  “In Japanese people, patients with heartburn had a significantly higher prevalence of sleep disorders than those without heartburn.”  [Another good study verifying this link.  Sleep studies, which should be part of all FM workups, should include testing for GERD.  GERD may often be “silent,” lacking usual symptoms.  DJS]

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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