Facco
E, Ceccherelli F. 2005. Myofascial pain mimicking radicular
syndromes. Acta Neurochir 92:147-150. “Myofascial
pain is very often underscored and misunderstood in clinical practice.
In many cases the localization of myofascial pain may resemble other
diseases, such as radicular syndromes and even diseases of internal
organs. When vertebral abnormalities are present on CT or MRI, it
should be checked whether the cause of pain is radicular, myofascial, or
both. On the other hand, the conventional approach to painful
disorders may lead to errors and wrong diagnosis, depending on several
factors: a) pain is often considered a symptom of an organic disease; b)
the diagnosis is usually directed towards the structural cause of pain
only; c) the functional components of the suffering patient are
underscored; d) the site of pain may introduce some bias.”
Faerber L, Drechsler S, Ladenburger S et al. 2007.
The neuronal 5-HT(3) receptor network after 20 years of research –
evolving concepts in management of pain and inflammation. Eur J
Pharmacol. 560(1):1-8.
Falla D, Bilenkij G, Jull G. 2004.
Patients with chronic neck pain demonstrate altered patterns of muscle
activation during performance of a functional upper limb task.
Spine 29(13):1436-1440. “Patients with neck pain demonstrated
greater activation of accessory neck muscles during a repetitive upper
limb task compared to asymptomatic controls.”
Falla D, Jull G, Edwards S et al. 2004.
Neuromuscular efficiency of the sternocleidomastoid and anterior scalene
muscles in patients with chronic neck pain. Disabil Rehabil.
26(12):712-717. “Reduced NME in the superficial cervical flexor muscles in
patients with neck pain may be a measurable altered muscle strategy for
dysfunction in other muscles. This aberrant pattern of muscle
activation appears to be most evident under conditions of low load.
NME, when measured at 25% MVC, may be a useful objective measure for future
investigation of muscle dysfunction in patients with neck pain.”
Fang L., Wu J., Lin Q. et
al. 2002. Calcium-calmodulin-dependent protein kinase II contributes to
spinal cord central sensitization. J Neurosci 22(10):4196-4204.
Fannelli Jr., G. M. and I. M. Weiner. 1975. Species variations
among primates in responses to drugs which alter the renal excretion of uric acid. J
Pharmacol Exp Ther 193(2):363-375.
Farella M., Michelotti A.,
Gargano A et al. 2002. Myofascial pain syndrome misdiagnosed as odontogenic
pain: a case report. Cranio 20(4):307-11. When the cause
of dental pain cannot be clearly identified, consider all possible causes of
dental pain, including the nonodontogenic ones such as myofascial pain,
before any irreversible dental procedures are considered.
Farajidavar A, Gharibzadeh S, Towhidkhah F et al. 2006. A
cybernetic view on wind-up. Med Hypotheses [Mar 21 Epub
ahead of print] “Wind-up may aggravate the pain in clinical
hyperalgesic situations such as post-surgical states, some neuropathic
pains, fibromyalgia syndrome, and post-herpetic neuralgia. [This
work was based on wind-up in Abeta fibers, and other wind-up studies
have been based on afferent C-fibers. DJS]
Farina S, Casarotto M, Benelle M et al. 2004.
A randomized controlled study on the effect of two different treatments (FREMS
AND TENS) in myofascial pain syndrome. N Eura Medicophys.
40(4):293-301. Both methods appeared effective for myofascial pain,
although FREMS seemed better.
Farrell, J and G. O. Littlejohn. 1999. Pain, nature of task, and
body part used in fibromyalgia syndrome. J Musculoskel Pain 7(1-2):279-284.
Fasmer, B. 1990. [Do antidepressive agents have analgesic effects?] Tidsskr
Nor Laegeforen 110(18:2370-2. [Norwegian]
Fass R, Naliboff
BD, Fass SS et al. 2007. The effect of auditory stress on perception
of intraesophageal acid in patients with gastroesophageal reflux disease.
Gastroenterology [Dec 7 Epub ahead of print]. “Acute auditory
stress can exacerbate heartburn symptoms in GERD patients by enhancing
perceptual response to intraesophageal acid exposure. This greater
perceptual response is associated with greater emotional responses to the
stressor.” [For those of us with FM amplification and GERD, auditory
stress may be an even greater peril. DJS]
Fass, R, Quan SF, O’Connor GT et al. 2005.
Predictors of heartburn during sleep in a large prospective cohort
study. Chest 127:1658-1666. “Heartburn during sleep
is very common in the general population. Reports of this type of
symptom of GERD are strongly associated with increased BMI, carbonated
soft drink consumption, snoring and daytime sleepiness, insomnia,
hypertension, asthma, and usage of benzodiazepines. Overall,
heartburn during sleep may be associated with sleep complaints and
excessive daytime sleepiness.”
Faucett, J. A. 1994. Depression in painful chronic disorders:
the role of pain and conflict about pain. J Pain Symptom Manage 9(8):520-526.
Faucett, J. A. and J. D. Levine. 1991. The contributions
of interpersonal conflict to chronic pain in the presence of absence of organic
pathology. Pain 44(1):35-43.
Feder KP, Majnemer A. 2007. Handwriting
development, competency and intervention. Dev Med Child Neurol.
49(4):312-317. “Poor handwriting may be related to intrinsic factors, which
refer to the child’s actual handwriting capabilities, or extrinsic factors
which are related to environmental or biomechanical components, or both.”
“There is evidence to indicate that handwriting difficulties do not resolve
without intervention and affect between 10 and 30% of school-aged children.”
[Students with these problems should be evaluated for myofascial TrPs. DJS]
Feinberg, B. I. and R. A. Feinberg. 1998. Persistent pain after
total knee arthroplasty: treatment with manual therapy and trigger point
injections. J Musculoskel Pain 6(4):85-95.
Feldman, D. and A. Krishnan. 1995. Estrogens in
unexpected places: possible implications for researchers and consumers. Environ
Health Perspect 103 Suppl 7: 129-33.
Feldman, R. D. and N. D. Schmidt. 1999. Moderate dietary
salt restriction increases vascular and systemic insulin resistance. Am J
Hypertens 12(6):643-7.
Ferencik, M., M. Novak and J.
Rovensky. 1998. [Relation
and interactions between the immune and neuroendocrine systems]. Bratisl Lek
Listy 99(8-9):454-64 [Slovak].
Ferguson AR, Crown ED, Grau JW. 2006.
Nociceptive plasticity inhibits adaptive learning in the spinal
cord. Neuroscience [May 5 Epub ahead of print] “Recent
data suggest links between the learning deficit and the
sensitization of pain circuits associated with inflammation or
injury (central sensitization).” “Central sensitization enhances
reactivity to mechanical stimulation (allodynia) and depends on the
N-methyl-d-aspartate receptor (NMDAR).”
Fernandez-Carnero J, Fernandez-de-Las-Penas
C, de la Liave-Rincon AI et al. 2007. Prevalence of and
referred pain from myofascial trigger points in the forearm muscles
in patients with lateral epicondylalgia. Clin J Pain.
23(4):353-360. “Lower PPT (pressure pain threshold) and larger
referred pain patterns suggest that peripheral and central
sensitization exists in LE (lateral epicondamgia).”
Fernandez-de-las-Penas C, Alonso-Blanco C, Del Amo-Perez
A et al. 2007. Trigger points in the masticatory muscles in
subjects presenting with ankylosing spondylitis. J Musculoskel
Pain. 15(3):39-47. “Trigger points in the masticatory muscles
were more conspicuous in AS subjects than in HNCs. Patients showed
a reduced active mouth opening and cervical flexion-extension motion
than matched HNCs. The AS subjects with lesser mouth opening
showed a greater occiput-to-wall distance and a greater number of TrPs
in the masticatory muscles.”
Fernandez-de-las-Penas C,
Cuadrado ML, Arendt-Nielsen L et al. 2007. A pain model for
tension type headache based on muscle trigger points. J
Musculoskel Pain 15 (Supp 13):20 item 30. [Myopain 2007
Poster] “Our studies suggest that TTH (tension-type headache) can be
explained by referred pain from active TrPs in neck-shoulder muscles.
Since chemical mediators most likely are released by active TrPs,
nociceptive inputs from these TrPs may lead to increased afferent
barrage into the trigeminal nucleus caudalis. This updated pain
model proposes that TrPs may be primary hyperalgesic zones, while
referred pain areas in the head could be viewed as secondary
hyperalgesic zones.”
Fernandez-de-las-Penas C,
Cuadrado M, Pareja J. 2007. Referred pain from
extra-ocular muscle trigger points in chronic headache. J
Musculoskel Pain 15 (Supp 13):19 item 27. [Myopain 2007
Poster] “Nociceptive inputs from the extra-ocular muscles may
provoke a continuous afferent bombardment to the trigeminal nerve
nucleus caudalis in CTTH (chronic tension-type headache). The
prolonged nociceptive activation by such muscle inputs might
contribute to central sensitization.” [This exciting research
indicates that even constant pain from facial muscles around the eye
could be enough to contribute to body-wide central nervous system
sensitization. DJS]
Fernandez-de-las-Penas
C, Cuadrado ML, Pareja JA. 2007. Muscle atrophy of
the suboccipital muscles associated with active trigger points
in chronic tension type headache. J Musculoskel Pain
15 (Supp 13):19 item 28. [Myopain 2007 Poster] “Muscle
atrophy in the RCPmin, but not in the RCPmaj, was associated to
active TrPs in the suboccipital muscles in CTTH.
Nociceptive inputs originated in active TrPs might contribute to
a greater muscle atrophy of the involved muscles.” [This
study is interesting in that it suggests that pain from MTPs
could contribute to muscle atrophy. As MTPs can cause
nerve entrapment and blood vessel entrapment, this would be
logical. DJS]
Fernandez-de-las-Penas C, De-la-Llave-Rincon
A, Miangolarra J. 2007. Uncommon referred pain from
scalene muscle trigger points in chronic tension type headache.
J Musculoskel Pain 15 (Supp 13):21 item 31.
[Myopain 2007 Poster] “Nine CTTH (chronic tension type
headache) patients had an uncommon referred pain pattern from
scalene muscle TrPs, so these headache patients may need
examination for scalene TrPs. It is known that CTH show
sensitization of central pathways, which may provoke larger
referred pain areas of active muscle TrPs. Further, there
are examples of neurologically related exceptional pain patterns
in other muscles [e.g. the soleus].” [I believe that this
is not so uncommon, and I have seen it several times before, but
it may be more common in patients with CMP and central
sensitization. DJS]
Fernandez-de-las-Penas C, Fernandez-Carnero
J, Miangolarra J. 2007. Multifidus muscle trigger point
management and stabilizing exercises in low back pain.
J Musculoskel Pain 15 (Supp 13):21 item 32. [Myopain
2007 Poster] “In some CLBP (chronic low back pain) patients, it
would be necessary to treat lumbar multifidus TrPs before
starting a stability exercise program because it includes
voluntary contraction of this muscle. Nociceptive barrage
originated in active TrPs could act as a contributing factor for
muscle inhibition.” [Multifidi, especially with nerve
entrapment, is exceedingly common in patients with CMP and
central sensitization. Treatment of the nerve pain is
before the TPM will increase the efficacy of the TPM treatment.
DJS]
Fernandez-de-las-Penas C,
Perez-de-Heredia-Torres M, Miangolarra J. 2007. Trigger
point management in lateral epicondylalgia. J
Musculoskel Pain 15 (Supp 13):20 item 29. [Myopain
2007 Poster] “Referred pain from TrPs in these patients was
causing the usual pain reported by patients with lateral
epicondylalgia. Muscle tension provoked by TrP taut band
may play an important role in the genesis and relief of the pain
commonly seen in lateral epicondylalgia.”
Fernandez-de-Las-Penas C, Cuadrado M,
Arendt-Nielsen L et al. 2007. Myofascial trigger points and
sensitization: an updated pain model for tension-type headache.
Cephalalgia [Mar 14 Epub ahead of print] “Based on available
data, an updated pain model for CTTH is proposed in which headache can
at least partly be explained by referred pain from TrPs in the posterior
cervical, head and shoulder muscles. In this updated pain model,
TrPs would be the primary hyperalgesic zones responsible for the
development of central sensitization in CTTH.”
Fernandez-de-las-Penas C, Carratala-Tejada M, Luna-Oliva
L et al. 2006. The immediate effect of hamstring muscle stretching
in subjects’ trigger points in the masseter muscle. J
Musculoskel Pain 14(3):27-35. “The present study demonstrated an
increase in active mouth opening and a decrease in TrP sensitivity in
the masseter muscle in response to the stretch of the hamstring
muscles.” Treatment, and constriction, in the myofascia of one area can
significantly alter the myofascia in another area, even long distance.
Fernandez-de-Las-Penas
C, Alonso-Blanco C, Luz Cuadrado M et al. 2006. Myofascial trigger
points in the suboccipital muscles in episodic tension-type headache.
Man Ther. 11(3):225-230.
Fernandez-de-Las-Penas
C, Alonso-Blanco C, Miangolarra JC. 2006. Myofascial trigger
points in subjects presenting with mechanical neck pain: a blinded,
controlled study. Man Ther. [Jun 10 Epub ahead of print]
“Active TrPs were more frequent in patients presenting with mechanical
neck pain than in healthy subjects.”
Fernandez-de-Las-Penas
C, Cuadrado M, Pareja J. 2006. Myofascial trigger points, neck
mobility and forward head posture in unilateral migraine.
Cephalalgia. 26(9):1061-1070. “Active TrPs located ipsilateral
to migraine headaches might be a contributing factor in the initiation
or perpetuation of migraine.”
Fernandez-de-Las-Penas
C, Ge HY, Arendt-Nielsen L et al. 2006. Referred pain from
trapezius muscle trigger points shares similar characteristics with
chronic tension type headache. Eur J Pain. [Aug 17 Epub
ahead of print] Patients with chronic tension type headache may
have spatial summation of perceived pain and mechanical pain, with
referral pain characteristics of myofascial TrPs.
Fernandez de las Penas CF, Carnero JF, Page JCM.
2005. Musculoskeletal disorders in mechanical neck pain: myofascial
trigger points versus cervical joint dysfunction – a clinical study.
J Musculoskeletal Pain 13(1). “There is a possible relationship
between the presence of TrPs in the upper trapezius muscle and the presence
of cervical dysfunctions at C3 and C4 vertebrae in patients suffering from
mechanical neck pain. However, it cannot be established as a
cause-effect relationship. Moreover, there is clinical evidence
showing that joint dysfunctions can induce TrP activity, and that TrP
activity can aggravate corresponding joint dysfunction.”
Fernstrom, J. D. 1994. Dietary amino acids and brain
function. J Am Diet Assoc 94(1):71-77.
Ferranninni, E. A. Q. Galvan, A.
Gastaldelli, S. Camastra, A. M. Sironi, E. Toschi, S. Baldi, S. Frascerra, F.
Monzani, A. Antonelli, M. Nannipieri, A.
Mari, G. Seghieri, and A. Natali. 1999. Insulin: New roles for an ancient hormone. Eur
J Clin Invest 29(10):842-52.
Ferrari R., H. Schrader and D.
Obelieniene. 1999. Prevalence
of temporomandibular disorders associated with whiplash injury in Lithuania. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 87(6):653-7.
Fetler L, Amigorena S. 2005.
Neuroscience. Brain under surveillance: the microglia patrol.
Science 309(5733):392-393. Opioids can activate pain
inhibitory and facilitatory systems, but opioid-induced hyperalgesia
may be prevented by strategies such as concomitant administration of
NSAIDS or NMDA antagonists, use of combinations of opioids with
different receptor selectivity, and other methods.
Field T, Diego M, Cullen C et al. 2002.
Fibromyalgia pain and substance P decrease and sleep improves after
massage therapy. J Clin Rheumatol. 8(2):72-76.
Field T, Hernandez-Reif M, Diego M et al. 2007.
Lower back pain and sleep disturbance are reduced following massage
therapy. J Bodywork Move Ther. 11, 141-145. “…the
massage therapy group, as compared to the relaxation group, reported
experiencing less pain, depression, anxiety and sleep disturbance.
They also showed improved trunk and pain flexion performance.”
Field T, Diego M, Cullen C et al. 2002.
Fibromyalgia pain and substance P decrease and sleep improves after
massage therapy. J Clin Rheumatol. 8(2):72-76. “Both
groups showed a decrease in anxiety and depressed mood immediately
after the first and last therapy sessions. However, across the
course of the study, only the massage therapy group reported an
increase in the number of sleep hours and a decrease in their sleep
movements. In addition, substance P levels decreased, and the
patients’ physicians assigned lower disease and pain ratings and
rated fewer tender points in the massage therapy group.”
Figueroa J. 2007. Multidrug therapy including gamma
hydroxybuterate as used in the treatment of fibromyalgia and associated
anxiety, depression and post traumatic stress disorder. J
Musculoskel Pain 15 (Supp 13):46 item 80. [Myopain 2007
Poster] “GHB, when used in a CMTM, can benefit FMS but also anxiety,
depression and PTSD.”
Figueroa J, Kobus B. 2007. Tizanidine and tender point pain. J
Musculoskel Pain 15 (Supp 13):46 item 79. [Myopain 2007
Poster] “Of the 22 patients, 21 observed a decrease in sleep duration,
latency and fragmentation. Fatigue also decreased. All 22
patients had a significant decrease in TeP pain [i.e. a mean decrease of
2.09] which was continuous and sustained [mean of 11.9 months].” “These
data suggest combination therapy of tizanidine with
analgesic/anti-inflammatory agents benefit sleep and additionally result
in reduced TeP pain.”
Filipovic V, Viskic-stalec N. 2006. The
mobility capabilities of persons with adolescent idiopathic
scoliosis. Spine. 31(19):2237-2242. When there is a
lack of normal mobility functions, especially with weak postural
control mechanisms and proprioception, the body compensates and
scoliosis can result.
Fillingim RB, Gear RW. 2004. Sex differences in opioid analgesia:
clinical and experimental findings. Eur J Pain 8(5):413-425.
Filos, K.S. and C.E.Vagianos. 1999. Pre-emptive analgesia: how
important is it in clinical reality? Eur Surg Res 31(2): 122-32.
Finckh A, Berner IC, Aubry-Rozier B et al. 2005.
A randomized controlled trial of dehydroepiandrosterone in postmenopausal
women with fibromyalgia. J Rheumatol 32(7):1336-1340.
This study did not find that taking DHEA brought about any useful changes.
Fine, PG. 1987. Myofascial trigger point pain in children.
J Pediatr.111(4):547-548. This article is noteworthy in that it
misidentified myofascial pain syndrome as part of fibromyalgia. This is
too common a mistake. It does encourage early diagnosis and
treatment, but to do that doctors will have to know which condition – or
both – are involved.
Fink, G., B. Sumner, R. Rosie, H. Wilson and J. McQueen.
1999. Androgen actions on central serotonin neurotransmission: relevance for mood,
mental state and memory. Behav Brain Res 105(1):53-68.
Fishbain DA, Cutler RB, Rosomoff HL et
al. 2000. Clonazepam open clinical treatment trial for myofascial
syndrome associated chronic pain. Pain Med. 1(4):332-339.
Clonazepam may help some myofascial pain.
Fishbain, D. A., H. L. Rosomoff and R. S. Rosomoff. 1992. Drug
abuse, dependence, and addiction in chronic pain patients. Clin J Pain
8(2):77-85.
Fishbain, D. A., M. Goldberg, R. S. Rosomoff and H.
Rosomoff.
1991. Completed suicide in chronic pain. Clin J Pain 7(1):29-36.
Fischer, A. A. 1999. Treatment of myofascial pain. J Musculoskel
Pain 7(1-2):131-142.
Fischer, A. A. 1999. Algometry in diagnoses of musculoskeletal
pain and evaluation of treatment outcome: an update. J Musculoskel Pain 6(1): 5-32.
Fischer, H. P., W. Eich and I. J. Russell. 1998. A
possible role for saliva as a diagnostic fluid in patients with chronic pain. Semin
Arthritis Rheum 27(6):348-59.
Fischer, A. A. 1988. Documentation of myofascial trigger
points. Arch Phys Med Rehabil 69(4):286-91.
Fishman SM. 2006. The role of the pain
psychologist, trigger point injections, reflex sympathetic dystrophy.
J Pain Palliat Care Pharmacother. 20(4):93-97. “This feature
presents information for patients in a question and answer format. It
is written to simulate actual questions that many pain patients ask and to
provide answers in a context and language that most pain patients will
comprehend. Issues addressed in this issue are the role of the pain
psychologist, trigger point injections, and reflex sympathetic dystrophy.”
Fishman SM, Mahajan G, Jung SW et al. 2002. The trilateral opioid
contract. Bridging the pain clinic and the primary care physician
through the opioid contract. J Pain Symptom Manage.
24(3):335-344. “We have extended the traditional use of opioid contracts
to involve the primary care physician (PCP). The PCP was asked to
collaborate with the pain specialist’s decision to use opioids by
cosigning an opioid contract. Explicit in the agreement was the
understanding that the primary care physician would assume prescribing
the refills for these medications once the opioid regimen had become
stabilized. In all cases in which a contract was completed, the
patient successfully stabilized on an appropriate opioid regimen and
then discharged to the care of the PCP for long-term opioid treatment.
The opioid contract made an effective tool for networking specialty and
primary care services in…chronic opioid therapy.” [Too often the
physician is neglected as part of the contract, and very often the pain
is vastly undertreated.]
Fitzcharles M.A., Boulos P.
2003. Inaccuracy in the diagnosis of fibromyalgia syndrome: analysis
of referrals. Rheumatology (Oxford) 42(2):263-7. “At
the final evaluation the accuracy of the diagnosis regarding FM by either
the referring physician or by the rheumatologist at the time of the initial
visit was correct in 34% of patients.” This finding may help explain
the current high rates of FM and caution physicians to consider other
diagnostic possibilities when addressing diffuse musculoskeletal pain.
Fitzcharles, M. A. and J. M. Esdaile. 1997. The overdiagnosis of
fibromyalgia syndrome. Am J Med 103(1):44-50.
Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. I: Background and patient
evaluation. Int Urogynecol J Pelvic Floor Dysfunct.
14(4):261-268. (See next entry)
Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. II: Treatment of the patient
with the short pelvic floor. Int Urogynecol J Pelvic Floor
Dysfunct. 14(4):269-275. These articles provide options for patient
care and help for the diagnoses and treatment of many common but often
misdiagnosed pelvic and lower abdominal pain cases. Care providers
are reminded that myofascial TrPs can cause dysfunction such as muscle
weakness as well as pain, and many cases of bladder and bowel
dysfunction, vulvodynia, and similar ailments may be greatly relieved by
TrP treatment.
Flanagan, D. E. , J. C. Vaile, G. W.
Petley, V. M. Moore, I. F. Godsland, R. A. Cockington, J. S. Robinson and D. I. Phillips. 1999. The autonomic control
of heart rate and insulin resistance in young adults. J Clin Endocrinol Metab
84(4):1263-7.
Flanagan, D., P. Wood, R. Sherwin, K. Debrah and D. Kerr.
1998. Gin and tonic and reactive hypoglycemia: what is important–the gin, the
tonic, or both? J Clin Endocrinol Metab 83(3): 796-800.
Flato, B., A. Aasland, I. H. Vandvik and O.
Forre. 1997.
Outcome and predictive factors in children with chronic idiopathic musculoskeletal
pain. Clin Exp Rheumatol 15(5):567-577.
Flax, B. J. 1995. Myofascial pain syndomes–the
great mimicker. Bol Assoc Med P R 87(10-12):167-170.
Fleischmann R. 2007. Primer: establishing
a clinical trial unit – regulations and infrastructure. Nat
Clin Pract Rheumatol. 3(4):234-239. [This comprehensive
review would be very helpful for physicians interested in doing a
clinical trial. DJS]
Fleury B. 2000. [Pharyngeal musculature and
obstructive sleep apnea syndromes] Rev Mal Respir. 17 Suppl
3:S15-20. [French] “The caliber of the pharynx at the soft palate
depends on the action of the tensor veli, the palatoglossus, the
palatopharyngeus and the uvula muscles. At the lingual level, the
action of the genioglossus and the geniohyoideus predominate.
These different muscle groups contract in coordination before the
diaphragm contracts. Their activity is diminished and disorganized
during sleep. These muscles appear to have a histological
composition adapted to short duration intense contractions making them
vulnerable to fatigue. In apneic patients, these muscles are
solicited constantly. Muscular lesions related to overwork have
been suggested.” [Muscle tension can affect sleep apnea.
Myofascial TrPs can affect muscle tension. Therefore, myofascial
TrPs can affect sleep apnea. DJS]
Florian H, Young Jr. J, Haig G et al. 2007. Pregabalin is
effective for the long-term treatment of pain associated with
fibromyalgia syndrome: a 1-year, open-label study. J
Musculoskel Pain 15 (Supp 13):47 item 81. [Myopain 2007
Poster] “Pregabalin administered for up to 1 year was associated with
improvements in FMS-related pain. Pregabalin was generally well
tolerated.”
Floyd, J. A. 1999. Sleep promotion in adults. Annu Rev Nurs Res
17:27-56.
Fogel RB, Triner J,
White DP 2005. The effect of sleep onset on upper airway muscle
activity in patients with sleep apnoea versus controls. J Physiol
564(Pt 2):549-562. “Although CPAP eliminated differences in UAR (Upper
Airway Resistance) during wakefulness and sleep, GGEMG genioglossus
(activity) remained greater in the OSA patients.” [TrPs in the pharyngeal
dilator muscles can significantly affect OSA. Their previous work
indicated tensor palatini muscle activity is high in OSA patients as well.
DJS]
Ford, ES,
Giles WH, Dietz WH. 2002. Prevalence of the metabolic syndrome
among US adults: findings from the third National Health and
Nutrition Examination Survey. JAMA Jan16;287(3):356-9. About 47
million US residents have the metabolic syndrome, according to
2000 census data.
Forrest JB, Schmidt S. 2004. Interstitial
cystitis, chronic nonbacterial prostatitis and chronic pelvic pain syndrome
in men: a common and frequently identical clinical entity. J Urol.
172(6 Pt 2):2561-2562. “Interstitial cystitis in males appears to be
more common than historically reported. Interstitial cystitis in males
and patients with chronic pelvic pain syndrome and chronic nonbacterial
prostatitis share many clinical findings. A higher incidence of
interstitial cystitis had been found in American Indian males of Cherokee
descent and deserves further investigation.”
Forseth KO, Mengshoel AM. 2007.
Multidimensional therapy in warm climate for patients with fibromyalgia
syndrome – a pilot study. J Musculoskel Pain 15 (Supp 13):47
item 82. [Myopain 2007 Poster] “The multiple improvements indicate
that multidimensional treatment in warm climate may have short and long
lasting effect in patients with FMS. Further controlled studies are
needed to confirm these findings.” [FM patients are heterogenous.
Some patients do better in warm dry climates and some do better in cold dry
climates. Some patients are both cold and heat sensitive, some are
helped by humidity and others feel worse with humidity. There are so
many environmental variables that can affect a climate reactor that studies
such as this may be very difficult to interpret. DJS]
Forseth, K. O. , O. Forre and J. T.
Gran. 1999. A 5.5 year
prospective study of self-reported musculoskeletal pain and of fibromyalgia in a female
population: significance and natural history. Clin Rheumatol 18(2):114-21.
Forseth, K. O. and J. T. Gran. 1992. The prevalence of
fibromyalgia among women aged 20-49 years in Arendal, Norway. Scand J Rheumatol
21(2):74-78.
Forst R, Ingenhorst A. 2005. [Myofascial pain syndrome]
Internist [Oct 15 Epub ahead of print] [German] “Untreated, the
myofascial pain syndrome leads to a reduced extensibility of the
involved muscle with consecutive decrease of the range of motion and
development of a muscular imbalance resulting in a disturbance of
complex movement and evolution of a chronic pain disease. An early
started and aimed therapy can prevent effectively the chronification.”
Fox, A. W. and R. L. Davis. 1998. Migraine
chronobiology. Headache 38(6):436-41.
Fraenkel, L., Y. Zhang, C. E.
Chaisson, S. R. Evans, P. W. Wilson
and D. T. Felson. 1998. The association of estrogen replacement therapy and the
Raynaud phenomenon in postmenopausal women. Ann Intern Med 129(3):208-11.
Fraenkel, L., Y. Zhang, C. E.
Chaisson, H. R. Maricq, S. R. Evans,
F. Brand, P. W. Wilson and D. T. Felson. 1999. Different factors influencing
the expression of Raynaud’s phenomenon in men and women. Arthritis Rheum 42(2):306-10.
Frampton
M, Harvey RJ, Kirchner V. 2003. Propentofylline for dementia. Cochrane
Database Syst Rev (2):CD002853. This
study is included on this website because this medication is being studied
as a spinal glial cell modulator for central sensitization. It crosses
the blood-brain barrier.
Franco C, Bengtsson BA, Johannsson G. 2001.
Visceral obesity and the role of the somatotropic axis in the
development of metabolic complications. Growth Horm IGF Res
11:S97-S102. “Several studies have described a range of metabolic
disturbances associated with abdominal obesity, including glucose
intolerance, hyperinsulinaemia, insulin resistance, hypertension and
dyslipoproteinaemia, now widely known as the metabolic syndrome.
Several abnormalities in the hypothalamic-pituitary axis have been
described associated with visceral obesity, suggesting a central
neuroendocrine dysregulation including increased cortisol concentration
and impaired gonadotropin and growth hormone (GH) secretion.”
Franco C, Bengtsson BA, Johannsson G. 2001.
Visceral obesity and the role of the somatotropic axis in the development of
metabolic complications. Growth Horm IGF 11:S97-S102.
“Several studies have described a range of metabolic disturbances associated
with abdominal obesity, including glucose intolerance, hyperinsulinaemia,
insulin resistance, hypertension and dyslipoproteinaemia, now widely known
as the metabolic syndrome. Several abnormalities in the
hypothalamic-pituitary axis have been described associated with visceral
obesity, suggesting a central neuroendocrine dysregulation including
increased cortisol concentration and impaired gonadotropin and growth
hormone (GH) secretion.”
Francois, P. P., K. T. Preissner, M. Herrmann, R. P.
Haugland, P. Vaudaux, D. P. Lew and K. H. Krause. 1999.
Frank, E. M. 1999. Myofascial trigger point diagnostic criteria in
the dog. J Musculoskel Pain 7(1-2):231-237.
Franssen JLM, Beersma B, Bron C. 2007.
Shoulder pain during swallowing: the use of surface electromyography as a
valuable diagnostic and therapeutic tool in myofascial pain syndrome.
J Musculoskel Pain 15 (Supp 13):22 item 33. [Myopain 2007
Poster] “MPS should be considered as a possible cause of musculoskeletal
complaints in neck or shoulder disorders. Surface electromyography can
be of great benefit in the process of differential diagnosis and may be
illuminate non-physiological motor behavior, which is one of the
perpetuating factors in MPS. The knowledge of referred pain patterns
may be helpful in identifying the muscle to be treated.” [This is a
very interesting study, as the MTPs were initiated due to use of
endotracheal tube during surgery, and the referral pain pattern occurred
during swallowing. Having experienced TPM cascade from endotracheal
intubation myself, I know how difficult this can be and how unaware most
anesthesiologists and other medical team members are that this can occur.
DJS]
Franken P, Chollet D, Tafti M. 2001. The
homeostatic regulation of sleep need is under genetic control.
Jour of Neuroscience 21(8):2610-2621.
Fredheim OM, Kaasa S, Fayers P et al. 2007.
Chronic non-malignant pain patients report as poor health-related
quality of life as palliative cancer patients. Acta
Anaesthesiol Scand. [Nov 13 Epub ahead of print]. “CNMP patients
admitted to multidisciplinary pain centres report significantly reduced
HRQoL, in addition to severe pain. They consider their HRQoL to be
as poor as HRQoL reported from dying cancer patients and substantially
poorer than national norms.” [This leaves one to wonder about the
ethics of having a substantial group of patients, those with chronic
non-cancer pain, with a quality of life lower than terminal cancer
patients. How can any system allow this situation, and what will it
take to improve it? DJS]
Fredheim OM, Borchgrevink PC, Klepstad P et al. 2006. Long
term methadone for chronic pain: a pilot study of pharmacokinetic
aspects. [Nov 16 Epub ahead of print] Eur J Pain
“...a 3-day opioid switch from morphine to methadone followed by a
one week titration seems pharmacologically sound.” These patients
had chronic non-malignant pain. Methadone serum concentrations
did not change significantly from dose titration through 9 months
therapy.
Fredheim OM, Kaasa S, Dale O et al. 2006. Opioid switching
from oral slow release morphine to oral methadone may improve pain control
in chronic non-malignant pain: a nine-month follow-up study.
Palliat Med. 20(1):35-41.
Freedenfeld RN, Murray M, Fuchs PN et al. 2006.
Decreased pain and improved quality of life in fibromyalgia patients treated
with olanzapine, an atypical neuroleptic. Pain Pract.
6(2):112-118. “In general, the data provide strong support that olanzapine
can, in certain patients, improve symptoms associated with fibromyalgia in
patients who have had limited success with other treatment modalities.”
There were significant side-effects that caused discontinuance of treatment
in a number of patients.
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.
Friederich HC, Schellberg D,
Mueller K et al. 2004. [Stress and autonomic dysregulation in patients
with fibromyalgia syndrome.] Schmerz [Epub May 12 ahead of
print] [German] This study indicates that the stress system in FMS
patients is hyporeactive.
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.”
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 FMS.
Gatchel RJ, Okifuji A. 2006. Evidence-based
scientific data documenting the treatment and cost effectiveness of
comprehensive pain programs for chronic nonmalignant pain. J Pain
7(11):779-793. “This review clearly revealed that CPPs offer the most
efficacious and cost effective treatment for persons with chronic pain,
relative to a host of widely used conventional medical treatment.” [Chronic
pain programs for patients with FMS and CMP must include care providers with
the skills to diagnose and treat these conditions. DJS]
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. [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.”
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.
2007. Firing rate and conduction velocity of single motor units in the
trapezius muscle in fibromyalgia patients and healthy controls. J
Electromyogr Kinesiol. [Apr 23 Epub ahead of print]. “CV (conduction
velocity) was significantly higher in FM than in healthy controls; this
might be due to alterations in histopathology and microcirculation.”
[It is unfortunate that patients were not screened for co-existing
myofascial trigger points. DJS]
Germanowicz D, Lumertz MS, Martinez D et al. 2006.
Sleep disordered breathing concomitant with fibromyalgia syndrome.
J Bras Pneumol. 32(4):333-338. “…the more than ten-fold higher
proportion of fibromyalgia cases seen in this sample supports the hypothesis
that there is an association between sleep disordered breathing and
fibromyalgia syndrome.
Gerster, J. C. and A.
Hadj-Djilani. 1984. Hearing and
vestibular abnormalities in primary fibromyalgia syndrome. J Rheumatol
11(5):678-680.
Gervais Tougas G. 1999. The autonomic nervous system in
functional bowel disorders. Can J Gastroenterol 13 Suppl A:15A-7A. [ED, THIS
NOTATION IS CORRECT]
Gerwin R. 2007. Trigger points: a
comprehensive hypothesis of trigger point formation. J Musculoskel
Pain 15 (Supp 13):12 item 14. [Myopain 2007 Poster] Dr.
Gerwin’s hypothesis may fill in the missing elements in the formation of
myofascial trigger points (MTPs). We did not have an explanation for
the excess release of acetylcholine, the excess release of calcium, and the
excessive motor endplate noise, nor did we understand why the taut band
forms. These phenomenon could be explained by a dysfunctional
ryanodine receptor calcium channel. This dysfunctional ion channel
could promote the excessive calcium release from the sarcoplasmic reticulum,
resulting in persistent muscle fiber contraction. Gates in the cell wall,
like tiny airlocks in a space station, allow charged particles such as
calcium, potassium and other minerals to flow in and out of the cell
membrane and affect the interior metabolism of the cell. The pathways
are called ion channels. An illness caused by dysfunction of the gate
mechanism is called a channellopathy. This important piece of the puzzle
indicates that myofascial pain due to trigger points could be a
channellopathy. Dysfunctional mitochondria and/or second messenger
dysfunction metabolically upstream could also be responsible or be
associated with the ryanodine dysfunction. [I found this to be one of the
most exciting revelations at the Myopain ‘07 Congress, offering great hope
to those of us with myofascial pain. This offers a whole new way of
looking at myofascial pain, and perhaps a whole new way of treating it. I
hope researchers will take note and mobilize forces to investigate this.
DJS]
Gerwin R. 2004. Differential diagnosis of
trigger points. J Musculoskeletal Pain 12(3/4):23-28.
“Trigger points pain can have many different causes that must be identified
and treated specifically.”
Gerwin 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.
Ghione
S, Del Seppia C, Mezzasalma L et al. 2004. Human head exposure to a 37
Hz electromagnetic field: Effects on blood pressure, somatosensory
perception, and related parameters. Bioelectromagnetics
25(3):167-175. Specific
electromagnetic field exposure can alter pain sensitivity in human beings.
Giamberardino MA, Vecchiet J, Affaitati G et al.
2007. Antioxidative treatment for muscle symptoms in chronic fatigue
syndrome. J Musculoskel Pain 15 (Supp 13):64 item 113.
[Myopain 2007 Poster] “In CFS, prolonged treatment with Vitamin E produces
parallel improvement of oxidative stress and muscle fatigue/hyperalgesia.
The results suggest an important pathophysiologic role for OS in the genesis
of muscle symptoms in CFS.”
Giamberardino, M. A., G.
Affaitati, S. Iezzi and L. Vecchiet. 1999. Referred muscle pain and hyperalgesia from viscera. J Musculoskel Pain 7(1-2):61-69.
Giamberardino, M. A., K. J. Berkley, S.
Iezzi, P. de Bigontina, and L. Vecchiet. 1997. Pain threshold variations in somatic wall tissues
as a function of menstrual cycle, segmental site and tissue depth in non-dysmenorrhic
women, dysmenorrhic women and men. Pain 71(2):187-97.
Giesecke T,
Gracely RH, Williams DA et al. 2005. The relationship
between depression, clinical pain, and experimental pain in a
chronic pain cohort. Arthritis Rheum.
52(5):1577-1584. This study suggests a parallel but different
sensory matrix for pain and for depression. In a patient with
both pain and depression, treating the depression alone is not
adequate. The pain must also be treated.
Giesecke T, Williams DA, Harris RE et al.
2003. Subgrouping of fibromyalgia patients on the basis of pressure-pain
thresholds and psychological factors. Arthritis Rheum 48
(10):2916-2922. The authors separate FMS subsets based on several
factors.
Gil, I. A., C. M. Barbosa, V. M. Pedro, K. C.
Silverio, D.
P. Goldfarb, V. Fusco and C. M. Navarro. 1998. Multidisciplinary approach to
chronic pain from myofascial pain dysfunction syndrome: a four-year experience at a
Brazilian center. Cranio 16(1):17-25.
Gill K. A., Woodroofe, M.
N. 2002. Effect of extracellular matrix components on the presentation
of chemokines and migration of microglia and astrocytes cell lines. Glia
(Suppl 1):S43 [Abstract]. These researchers “conclude that the effect of
chemokines is significantly influenced by the extracellular environment, and
the composition of the ECM may be important in the design of therapeutic
strategies for inflammatory conditions.”
Gilula MF. 2007. Cranial electrotherapy
stimulation and fibromyalgia. Expert Rev Med Devices.
4(4):489-495. “Future medicine for FM and related conditions may
increasingly involve multimodality treatment that features CES as one
significant part of the therapeutic regimen. Future medicine may also
include CES as an invaluable, cost-effective add-on to many facets of
clinical pharmacology and medical therapeutics.”
Giovengo, S. L. , I. J. Russell and A. A. Larson.
1999. Increased concentrations of nerve growth factor (NGF) in cerebrospinal fluid of
patients with fibromyalgia. J Rheumatol 26(7):1564-9.
Giske L, 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. 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 FMS patients is
conspicuously greater than that experienced by other patients with
typical neuropathic complaints. Furthermore, this pain is
associated with more severe co-morbidities such as depression/anxiety
and sleep disturbance.”
Godfrey, R. G. 1996. A guide to the
understanding and use of tricyclic antidepressants in the overall management of
fibromyalgia and other chronic pain syndromes. Arch Intern Med156(10):1047-1052.
Gogas KR. 2005. Glutamate-based therapeutic
approaches: NR2B receptor antagonists. Curr Opin Pharmacol Dec
20; [Epub ahead of print] “...phosphorylation of the NR2B subunit
(-containing NMDA receptor) could be responsible for the initiation and
maintenance of the central sensitization seen in neuropathic pain states.”
Gold AR, Dipalo F, Gold MS et al. 2004.
Inspiratory airflow dynamics during sleep in women with fibromyalgia.
Sleep 27(3):459-466. “Inspiratory airflow limitation is a
common inspiratory airflow pattern during sleep in women with fibromyalgia.
Our findings are compatible with the hypothesis that inspiratory flow
limitation during sleep plays a role in the development of the functional
somatic syndromes.”
Gold, D. R., S. Rogacz, N. Bock, T. D.
Tosteson, T. M.
Baum, F. E. Speizer and C. A. Czeisler. 1992. Rotating shift work, sleep, and accidents
related to sleepiness in hospital nurses. Am JPublic Health 82(7):1011-4.
Goldenberg DL,
Burckhardt C, Crofford L. 2004. Management of fibromyalgia syndrome.
JAMA 292(19):2388-2395. “A number of commonly used FMS therapies,
such as trigger point injections, have not been adequately evaluated.”
[This is a noteworthy quote, in so much as there are no such things as
fibromyalgia trigger points and thus no FMS trigger point injections to be
evaluated. Myofascial trigger point injections, however, have been
adequately evaluated. It is fundamental that clinicians and researchers
need to understand that there are no fibromyalgia trigger points, and that
myofascial pain is not the same as fibromyalgia. Until this happens,
the research will be skewed and the conclusions reached not viable.
DJS]
Goldenberg DL, Burchkardt C, Crofford L. 2004. JAMA 292(19):2388-2395.
“Despite the chronicity and complexity of FMS, there are pharmacological and
nonpharmacological interventions available that have clinical benefit.”
[FMS is treatable,]
Goldenberg, DL. 1999. Fibromyalgia syndrome a
decade later: what have we learned? Arch Intern Med 159(8):777-85.
Goldberg, G. M., R. D. Kerns and R. Rosenberg. 1993.
Pain-relevant support as a buffer from depression among chronic pain patients low in
instrumental activity. Clin J Pain 9(1):34-40.
Goldberg, R. T., W. N. Pachas and D. Keith.
1999. Relationship between traumatic events in childhood and chronic pain. Disabil
Rehabil 21(1):23-30.
Goldberg, R. L. , J. P. Huff, M. E. Lenz, P.
Glickman, R.
Katz and E. J. Thonar. 1991. Elevated plasma levels of hyaluronate in patients with
osteoarthritis and rheumatoid arthritis. Arthritis Rheum 34(7):799-807.
Goldstein, L. B., F. C. Last and V. M. Salerno.
1997. Prevalence of hyperactive digastric muscles during swallowing as measured by
electromyography in patients with myofascial pain dysfunction syndrome. Funct Orthod 14(3):18-22.
Golinski, M. A. and D. M. Fill. 1995.
Preemptive analgesia. CNRA 6(1):16-20.
Gonzalez-Viejo MA,
Avellanet M, Hernandez-Morcuende MI. 2005. [A comparative
study of fibromyalgia treatment: ultrasonography and physiotherapy
versus sertraline treatment.] Ann Readapt Med Phys.
[Epub ahead of print June 22] [French] “Patients treated with
sertraline had a better outcome in terms of pain, morning stiffness
and sleep disorders, than the group treated with ultrasonography and
physical therapy.”
Gordon, D. A. 1999. Chronic widespread pain as
a medico-legal issue. Baillieres Best Pract Res Clin Rheumatol
13(3):531-43.
Gordon, N. P., P. D. Cleary, C. E. Parker and C. A.
Czeisler. 1986. The prevalence and health impact of shiftwork. Am J
Public Health 76(10):1225-8.
Gotlin, R. S., S.
Hershkowitz, P. M. Juris, E. G. Gonzalez,
W. N. Scott and J. N. Insall. 1994. Electrical stimulation effect on extensor lag and length of
hospital stay after total knee arthroplasty. Arch Phys Med Rehabil
75(9):957-959.
Gottrup H, Juhl G, Kristensen AD et al.
2004. Chronic oral gabapentin reduces elements of central
sensitization in human functional hyperalgesia. Anesthesiology
101(6):1400-1408.
Goucke CR. 2001. Australian management
strategies for oral opioid use in non-malignant pain. Eur J Pain 5
Suppl A:99-101.
Govender C, Cassimjee N, Schoeman J et al. 2007.
Psychological characteristics of FMS patients. J Musculoskel Pain
15 (Supp 13):55 item 98. [Myopain 2007 Poster] “The majority of
subjects exhibited secure attachment and the results questions the existence
of a single FMS-prone psychological profile.”
Gowans SE, Dehueck A. 2007. Pool exercise for
individuals with fibromyalgia. Curr Opin Rheumatol.
19(2):168-173. “Pool exercise can be an effective intervention for
individuals with fibromyalgia.” [One must be careful of the
temperature of the pool and the type of exercise, especially if patients
have co-existing myofascial TrPs. DJS]
Gowans SE, DeHueck A. 2004.
Effectiveness of exercise in management of fibromyalgia. Curr Opin Rheumatol 16(2):138-42.
“Individuals with fibromyalgia also need to be able to access community exercise programs that are appropriate for them.
This may require community instructors to receive instruction on exercise prescription and progression for individuals with fibromyalgia.”
[ It is also vitally important that these individuals receive instruction on the dangers of repetitive exercise for individuals with co-existing CMP. DJS]
Gowing LR, Ali RL, Christie P et al. 1998.
Therapeutic use of cannabis: clarifying the debate. Drug
Alcohol Rev. 17(4):445-452. “The debate regarding therapeutic
use of cannabis is being confused by a lack of distinction between
therapeutic and social use of cannabis.” “At present the evidence
is limited, it mostly relates to the use of synthetic cannabinoids, and
much of it fails to compare cannabis with the best therapies available
for the conditions of interest.” “There is sufficient evidence of
potential therapeutic benefit to justify the facilitation of further
research.”
Gowri V, Krolikowski A. 2001. Chronic pelvic
pain. Laparoscopic and cystoscopic findings. Saudi Med J.
22(9):769-770. [Another study that failed to include myofascial
TrPs in the differential diagnosis. DJS]
Gracely RH, Geisser ME, Giesecke T et al. 2004. Pain
catastrophizing and neural responses to pain among persons with
fibromyalgia. Brain 127(Pt 4):835-843. [Epub ahead of print Feb
11] “Catastrophizing influences pain perception through altering attention
and anticipation, and heightening emotional responses to pain.
Activation associated with catastrophizing in motor areas of the brain may
reflect expressive responses to pain that are associated with greater pain
catastrophizing.”
Gracely R.H., Petzke F.,
Wolf J.M. et al. 2002. Functional magnetic resonance imaging evidence
of augmented pain processing in fibromyalgia. Arthritis Rheum
46(5):1333-43.
Gracely RH, Petzke F,
Wolf JM, Clauw DJ.2002. Functional magnetic resonance imaging
evidence of augmented pain processing in fibromyalgia.
Arthritis Rheum 46(5):1333-43.
"Supports the hypothesis that FM is
characterized by cortical or subcortical augmentation of pain
processing."
Graff-Radford SB. 2004. Myofascial pain:
diagnosis and management. Curr Pain Headache Rep.
8(6):463-467. “Clinical understanding and management of
myofascial pain is overlooked frequently when dealing with pain.”
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.
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
tiss | 
NOTE:
New Nomenclature