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
Fais A, Cacace E, Corda M et al. 2012. Purine metabolites in fibromyalgia syndrome. Clin Biochem. [Sep 18 Epub ahead of print]. "Study results suggest that purines, in particular adenosine and inosine, may be involved in pain transmission in fibromyalgia."
Falla D, Andersen H,
Danneskiold-Samsoe B et al. 2009. Adaptations of upper
trapezius muscle activity during sustained contractions in women
with fibromyalgia. J Electromyogr Kinesiol. [Aug 12
Epub ahead of print]. “The results indicate that muscle pain
prevents the adaptation of upper trapezius activity during sustained
contractions as observed in non-painful conditions, which may induce
overuse of similar muscle compartments with fatigue.” [This
study may actually have been done on co-existing myofascial TrPs in
the trapezius muscle. It may also be showcasing the increasing
interaction of these 2 conditions. DJS]
Falla D, Bilenkij G, Jull G. 2004.
Patients with chronic neck pain demonstrate altered patterns of muscle
activation during performance of a functional upper limb task.
Spine 29(13):1436-1440. “Patients with neck pain demonstrated
greater activation of accessory neck muscles during a repetitive upper
limb task compared to asymptomatic controls.”
Falla D, Jull G, Edwards S et al. 2004.
Neuromuscular efficiency of the sternocleidomastoid and anterior scalene
muscles in patients with chronic neck pain. Disabil Rehabil.
26(12):712-717. “Reduced NME in the superficial cervical flexor muscles in
patients with neck pain may be a measurable altered muscle strategy for
dysfunction in other muscles. This aberrant pattern of muscle
activation appears to be most evident under conditions of low load.
NME, when measured at 25% MVC, may be a useful objective measure for future
investigation of muscle dysfunction in patients with neck pain.”
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.
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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
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Feng B, La JH, Schwartz ES et al. 2012. Neural and neuro-immune mechanisms of visceral hypersensitivity in irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol. [Mar 8 Epub ahead of print]. "Irritable bowel syndrome (IBS) is characterized as 'functional' because a pathobiological cause is not readily apparent. Considerable evidence, however, documents that sensitizing pro-inflammatory and lipotoxic lipids, mast cells and their products, tryptases, enteroendocrine cells and mononuclear phagocytes and their receptors are increased in tissues of IBS patients with colorectal hypersensitivity. It is also clear from recordings in animals of the colorectal afferent innervation that afferents exhibit long-term changes in models of persistent colorectal hypersensitivity. Such changes in afferent excitability and responses to mechanical stimuli are consistent with relief of discomfort and pain in IBS patients, including relief of referred abdominal hypersensitivity, upon intra-rectal instillation of local anesthetic. In the aggregate, these experimental outcomes establish the importance of afferent drive in IBS, consistent with a larger literature with respect to other chronic conditions in which pain is a principal complaint (e.g., neuropathic pain, painful bladder syndrome, fibromyalgia). Accordingly, colorectal afferents and the environment in which these receptive endings reside constitute the focus of this review."
Feng J, Zhang Z, Li W et al. 2009.
Missense mutations in the MEFV gene are associated with fibromyalgia
syndrome and correlate with elevated IL-1beta plasma levels. PLoS
One. 4(12):e8480. “Since misregulation of IL-1beta expression has
been predicted for patients with mutations in the MEFV gene, we conclude
that patients heterozygous for rare missense variants of this gene may be
predisposed to FMS, possibly triggered by environmental factors.”
Fenton BW, Palmieri P, Diantonio G et al. 2011. Application of patient-reported outcomes measurement information system to chronic pelvic pain. J Minim Invasive Gynecol. 18(2):189-193. "A total of 149 consecutive patients with chronic pelvic pain provided evaluable results....Pain-related and global PROMIS (Patient-Reported Outcomes Measurement Information System) scores were significantly worse than in the reference population..... The presence of myofascial pain was also associated with worse PROMIS scores.....Chronic pelvic pain is associated with impaired quality of life regardless of the diagnosis, including myofascial pain."
Fenton BW, Palmieri PA, Durner C et al.
2009. Quantification of abdominal wall pain using pain pressure
threshold algometry in patients with chronic pelvic pain. Clin J
Pain. 25(6):500-505. Pressure algometry is a very useful tool for
those who cannot palpate TrPs. There was a 75% improvement in pressure
point testing after treating abdominal wall TrPs. The authors seem unaware
of the explicit specifications of myofascial TrPs. They also seem unaware
that most chronic pelvic pain comes from TrPs in the pelvic floor and other
related areas, although they are to be commended for their work confirming
the ubiquity of abdominal wall TrPs.
Feraco P, Bacci A, Pedrabissi F et al. 2011. Metabolic Abnormalities in Pain-Processing Regions of Patients with Fibromyalgia: A 3T MR Spectroscopy Study. AJNR Am J Neuroradiol. [Jul 28 Epub ahead of print]. "The presence of elevated Glu/Cr levels in VLPFC strengthens the opinion that a complex neurophysiologic imbalance of different brain areas involved in pain processing underlies FM. These data may be useful in the diagnosis and development of more effective pharmacologic treatments."
Ferencik, M., M. Novak and J.
Rovensky. 1998. [Relation
and interactions between the immune and neuroendocrine systems]. Bratisl Lek
Listy 99(8-9):454-64 [Slovak].
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)."
La Touche R,
R et al. 2010.
effects of dry needling of active myofascial trigger points in the
masseter muscle in patients with temporomandibular disorders.
J Orofac Pain. 24(1):106-112. “The application of dry
needling into active TrPs in the masseter muscle induced significant
increases in PPT (pressure pain threshold) levels and maximal jaw
opening when compared to the sham dry needling in patients with
myofascial TMD.” [Treatment of related TrPs can significantly ease
symptoms of TMJ, including pain and jaw restriction. It is essential
that treatment be as prompt as possible to avoid unequal tension on
the discs of the jaw. DJS]
J, Ge HY, Kimura Y. 2010. Increased spontaneous electrical
activity at a latent myofascial trigger point after nociceptive
stimulation of another latent trigger point. Clin J. Pain
26(2):138-143. This groundbreaking paper shows how activity at
a latent TrP in the infraspinus muscle may increase sensitivity
and activity of a TrP in the forearm. This study demonstrates
both the formation of satellite TrPs and TrP cascades, showing a
sensory connection between distant TrPs. It also shows a
decrease in sensitivity of the forearm TrP after the shoulder
TrP was successfully treated. [This is a critical paper. I hope
it quiets critics who disbelieve in the formation of satellite
TrPs and TrP cascades. Thank you, authors. DJS]
Fernandez-Carnero J, Fernandez-de-Las-Penas
C, de la Liave-Rincon AI et al. 2007. Prevalence of and
referred pain from myofascial trigger points in the forearm muscles
in patients with lateral epicondylalgia. Clin J Pain.
23(4):353-360. “Lower PPT (pressure pain threshold) and larger
referred pain patterns suggest that peripheral and central
sensitization exists in LE (lateral epicondamgia).”
Fernandez-de-las-Penas C. 2010. New evidence for trigger point involvement in tension-type headaches. J Musculoskel Pain. 18(4):354-360. "Tension-type headache (TTH) is the most common form of headache and its chronic form (chronic tension-type headache (CTTH)) is one of the most neglected and difficult headaches to treat. TTH is an overarching syndrome of 'featureless' headaches characterized by nothing but pain in the head….The term 'tension-type' has been chosen by the International Headache Society (ICHD-II) to offer a new heading underlining the uncertain pathogenesis, but indicating that some form of muscle tension may play a role….Hyperalgesic and allodynic responses support the role of both peripheral and central mechanisms in the development of the clinical picture of CTTH. In fact, it is suggested that central sensitization, a reduction in inhibitory pain mechanisms, and peripheral sensitization of muscle nociceptors are mechanisms involved in perceived pain in CTTH….Subjects who develop TTH have showed normal tenderness scores and pressure pain threshold levels before the beginning of the symptoms, which suggests that the mechanical hypersensitivity is rather a consequence than a risk factor for the development of TTH." "Previous studies have found that TTH patients described their head pain as pressing, tightening, or soreness. Dull and tight heaviness are also pain quality features of TTH attacks. These pain features resemble the descriptions of clinically referred pain elicited by TrPs as described by Simons et al." "Recent clinical studies have clearly demonstrated the relevance of active TrPs in CTTH. In fact, recent studies have described the referred pain elicited from two extra-ocular muscles, i.e., superior oblique and lateral rectus in patients with CTTH."
Fernández-de-Las-Peñas C, Ambite-Quesada S, Gil-Crujera A et al. 2012. Catechol-O-Methyltransferase Val158Met Polymorphism Influences Anxiety, Depression, and Disability, but not Pressure Pain Sensitivity, in Women with Fibromyalgia Syndrome. J Pain. [Sep 28 Epub ahead of print]. "Our aim was to assess the relationship of the Val158 Met polymorphism to pain, anxiety, depression, functional ability, and pressure pain sensitivity in women with fibromyalgia (FMS).... This study suggests that the Val158Met COMT polymorphism modulated some psychological variables but not pressure pain sensitivity in FMS because women with FMS carrying the Met/Met genotype exhibit higher disability, depression, and anxiety than but similar PPTs to those with Val/Met and Val/Val genotypes. This study provides further evidence of potential genetic factors that predispose women with FMS to exhibit the disease more severely."
Galan-Del-Rio F, Alonso-Blanco C et al. 2010. Referred pain from
muscle trigger points in the masticatory and neck-shoulder
musculature in women with temporomandibular disorders. J
Pain. [May 20 Epub ahead of print]. “The current study
showed the existence of multiple active muscle TrPs in the
masticatory and neck-shoulder muscles in women with myofascial
TMD pain. The local and referred pain elicited from active TrPs
reproduced pain complaints in these patients. Further, referred
pain areas were larger in TMD pain patients than in healthy
controls. The results are also in accordance with the notion of
peripheral and central sensitization mechanisms in patients with
myofascial TMD.” [Another paper showing the association of TrPs
and the central sensitization of FM. DJS]
Fernandez-de-las-Penas C, Grobli C, Ortega-Santiago R et al. 2012. Referred pain from myofascial trigger points in head, neck, shoulder, and arm muscles reproduces pain symptoms in blue-collar (manual) and white-collar (office) workers. Clin J Pain. 28(6):511-518. "Blue-collar and white-collar workers exhibited a similar number of TrPs in the upper quadrant musculature. The referred pain elicited by active TrPs reproduced the overall pain pattern. The distribution of TrPs was not significantly different between groups. Clinicians should examine for the presence of muscle TrPs in blue-collar and white-collar workers." [TrPs are common in people no matter what type of work they do. DJS]
pain sensitivity topographical maps reveal bilateral
hyperalgesia of the hands in patients with unilateral carpal
tunnel syndrome. Arthritis
Care Res (Hoboken). [Mar
16 Epub ahead of print]. “Our findings revealed bilateral
generalized pressure pain hyperalgesia in unilateral CTS (carpal
tunnel syndrome) since lower PPT (pressure pain threshold)
levels were found in all the points. The pressure pain
hyperalgesia was not uniformly distributed since PPTs were lower
in points over the proximal phalanx of the fingers and the
thenar eminency as compared to those points located over the
distal phalanx of the fingers. The decrease in PPT levels was
associated with the intensity and the duration of the pain
symptoms supporting a role of both peripheral and central
sensitization mechanisms in this pain condition.” [TrPs are
frequently the cause of symptoms described as “carpal tunnel.”
It is essential to find the cause of the pain and treat that as
soon as possible, so that surgery can be avoided. DJS]
Fernandez-de-las-Penas C, Cleland
JA, Cuadrado ML et al. 2008. Predictor variables for
identifying patients with chronic tension-type headache who are
likely to achieve short-term success with muscle trigger point
therapy. Cephalalgia. 28(3):264-275. “The
present CPR (clinical prediction rule) provides the potential to
identify CTTH (chronic tension-type headache) patients who are
likely to experience short-term and 1-month follow-up
success...” with manual TrP therapy.
Fernandez de las Penas C, Cuadrado
ML, Gerwin RD et al. 2005. Referred pain from the
trochlear region in tension-type headache: a myofascial trigger
point from the superior oblique muscle. Headache.
45(6):731-737. “This pain was perceived as a deep ache
located at the retro-orbital region, sometimes extending to the
supra-orbital region or the homo-lateral forehead. Pain
intensity was greater in CTTH (chronic tension-type headache)
patients than in ETTH (episodic tension-type headache) patients
or control subjects (P<.001)... MTrPs in the SOM (superior
oblique muscle) may evoke a typical referred pain pattern in
patients with TTH (tension-type headache). The presence of
a myofascial disorder in the trochlear region might contribute
to the pathogenesis of TTH.” [It is with gratitude that I
post this confirmation of the extrinsic eye TrPs mentioned in my
books, and I hope to see much more work from this excellent
Fernandez-Carnero J, Fernandez-de-Las-Penas
C, de la Liave-Rincon AI et al. 2007. Prevalence of and
referred pain from myofascial trigger points in the forearm muscles
in patients with lateral epicondylalgia. Clin J Pain.
23(4):353-360. “Lower PPT (pressure pain threshold) and larger
referred pain patterns suggest that peripheral and central
sensitization exists in LE (lateral epicondamgia).”
Fernandez-de-las-Penas C. 2009. Interaction between trigger points and joint hypomobility: a clinical perspective. J Man Manip Ther. 17(2):74-77. "Reduction of joint mobility appears related to local muscles innervated from the segment, which suggests that muscle and joint impairments may be indivisible and related disorders in pain patients. …There is scientific evidence showing change in muscle sensitivity in muscle TrP after spinal manipulation, which suggests that clinicians should include treatment of joint hypomobility in the management of TrPs. Nevertheless, the order in which these muscle and joint impairments should be treated is not known and requires further investigation." [The intriguing hypotheses mentioned here did not include the possibility that muscle contracture caused by TrPs can torque the joint, provoking hypermobility in the opposite direction. It is to be hoped that more investigations on this interrelationship will be forthcoming. DJS]
Fernandez-de-las-Penas C, 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.”
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.
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, Carratala-Tejada M, Luna-Oliva
L et al. 2006. The immediate effect of hamstring muscle stretching
in subjects’ trigger points in the masseter muscle. J
Musculoskel Pain 14(3):27-35. “The present study demonstrated an
increase in active mouth opening and a decrease in TrP sensitivity in
the masseter muscle in response to the stretch of the hamstring
muscles.” Treatment, and constriction, in the myofascia of one area can
significantly alter the myofascia in another area, even long distance.
Fernandez-de-Las-Penas C, Cleland JA, Palomeque-Del-Cerro L et al. 2010. Development of a clinical prediction rule for identifying women with tension-type headache who are likely to achieve short-term success with joint mobilization and muscle trigger point therapy. Headache Nov 4 [Epub ahead of print] The current clinical prediction rule may allow clinicians to make an a priori identification of women with TTH who are likely to experience short-term self-report improvement with a multimodal session including joint mobilization and TrP therapies."
Fernandez-de-Las-Penas C, Cleland JA, Ortega-Santiago R et al. 2010. Central sensitization does not identify patients with carpal tunnel syndrome who are likely to achieve short-term success with physical therapy. Exp Brain Res. 207(1-2):85-94. "The aim of the current study was to identify whether hyperexcitability of the central nervous system is a prognostic factor for individuals with carpal tunnel syndrome (CTS) likely to experience rapid and clinical self-reported improvement following a physical therapy program including soft tissue mobilization and nerve slider neurodynamic interventions.... The physical therapy sessions included both soft tissue mobilization directed at the anatomical sites of potential median nerve entrapment and a passive nerve slider neurodynamic technique targeted to the median nerve.... Our results support that widespread central sensitization may not be present in women with CTS who are likely to achieve a successful outcome with physical therapy."
Fernandez-de-Las-Penas C, 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.”
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
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.”
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
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
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
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.
Fernandez-de-las-Penas C, Fernandez-Mayoralas DM, Ortega-Santiago R et al. 2011. Referred pain from myofascial trigger points in head, neck and shoulder muscles reproduces head pain features in children with chronic tension type headache. J Headache Pain. 12(1):35-43. TrPs are a common cause of chronic tension type headaches in children. [Pediatricians must become aware of this fact, and be trained in diagnosis and treatment of TrPs. DJS]
C, Ge HY, Arendt-Nielsen L et al. 2006. Referred pain from
trapezius muscle trigger points shares similar characteristics with
chronic tension type headache. Eur J Pain. [Aug 17 Epub
ahead of print] Patients with chronic tension type headache may
have spatial summation of perceived pain and mechanical pain, with
referral pain characteristics of myofascial TrPs.
Fernandez-de-Las-Penas C, Ortega-Santiago R, Cuandrado ML et al. 2010. Bilateral widespread mechanical pain hypersensitivity as a sign of central sensitization in patients with cluster headaches. Headache Nov 4 [Epub ahead of print] Pain hypersensitivity was global, including tibialis (calf muscle), in chronic headache patients. "Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with CH confirming the presence of central sensitization mechanisms in this headache condition." [Chronic headache, even from TrPs, can lead to a central sensitization state such as fibromyalgia. DJS]
Perez-de-Heredia-Torres M, Miangolarra J. 2007. Trigger
point management in lateral epicondylalgia. J
Musculoskel Pain 15 (Supp 13):20 item 29. [Myopain
2007 Poster] “Referred pain from TrPs in these patients was
causing the usual pain reported by patients with lateral
epicondylalgia. Muscle tension provoked by TrP taut band
may play an important role in the genesis and relief of the pain
commonly seen in lateral epicondylalgia.”
Fernandez de las Penas CF, Carnero JF, Page JCM.
2005. Musculoskeletal disorders in mechanical neck pain: myofascial
trigger points versus cervical joint dysfunction – a clinical study.
J Musculoskeletal Pain 13(1). “There is a possible relationship
between the presence of TrPs in the upper trapezius muscle and the presence
of cervical dysfunctions at C3 and C4 vertebrae in patients suffering from
mechanical neck pain. However, it cannot be established as a
cause-effect relationship. Moreover, there is clinical evidence
showing that joint dysfunctions can induce TrP activity, and that TrP
activity can aggravate corresponding joint dysfunction.”
Fernandez-Lao C, Cantarero-Villanueva I, Fernanndez-de-Las-Penas C et al. 2010. Widespread Mechanical Pain Hypersensitivity as a Sign of Central Sensitization after Breast Cancer Surgery: Comparison between Mastectomy and Lumpectomy. Pain Med. [Dec 10 Epub ahead of print]. "The current study found widespread pressure pain hyperalgesia in women who received breast cancer surgery suggesting central spreading sensitization. The degree of central sensitization was similar between lumpectomy and mastectomy surgery."
Fernandez-Lao C, Cantarero-Villanueva I, Fernandez-de-Las-Penas C et al. 2010. Myofascial Trigger Points in Neck and Shoulder Muscles and Widespread Pressure Pain Hypersensitivity in Patients with Postmastectomy Pain: Evidence of Peripheral and Central Sensitization. Clin J Pain. [Sep 8 Epub ahead of print]. "Our findings revealed bilateral widespread pressure pain hypersensitivity in patients with postmastectomy pain. In addition, the local and referred pain elicited by active TrPs reproduced neck and shoulder/axillary complaints in these patients. These results suggest peripheral and central sensitization in patients with postmastectomy pain." [Other research has found evidence of TrPs causing post-surgical pain. This also indicates that the TrPs are at least contributing, and possibly causing, the development of hypersensitivity in other areas. This is one way central sensitization can develop. DJS]
Fernández-Pérez AM, Villaverde-Gutiérrez C, Mora-Sánchez A et al. 2012. Muscle trigger points, pressure pain threshold, and cervical range of motion in patients with high level of disability related to acute whiplash injury. J Orthop Sports Phys Ther. 42(7):634-641. This study was created to..."analyze the differences in the prevalence of trigger points (TrPs) between patients with acute whiplash-associated disorders (WADs) and healthy controls, and to determine if widespread pressure hypersensitivity and reduced cervical range of motion are related to the presence of TrPs in patients with acute WADs....Patients had significantly lower PPTs (pressure pain threshold) in all tested locations and less active cervical range of motion than controls.... In the patient group, there were significant negative correlations between the number of active TrPs and PPT over the C5-C6 joints and cervical range of motion in flexion, extension, and rotation in both directions: the greater the number of active TrPs, the lower the bilateral PPT over the neck and the greater the cervical range of motion limitation....The local and referred pain elicited from active TrPs reproduced neck and shoulder pain patterns in individuals with acute WADs with higher levels of disability. Patients with acute WADs exhibited widespread pressure hypersensitivity and reduced cervical mobility. The number of active TrPs was related to higher neck pain intensity, the number of days since the accident, higher pressure pain hypersensitivity over the cervical spine, and reduced active cervical range of motion."
Fernstrom, J. D. 1994. Dietary amino acids and brain
function. J Am Diet Assoc 94(1):71-77.
Ferranninni, E. A. Q. Galvan, A.
Gastaldelli, S. Camastra, A. M. Sironi, E. Toschi, S. Baldi, S. Frascerra, F.
Monzani, A. Antonelli, M. Nannipieri, A.
Mari, G. Seghieri, and A. Natali. 1999. Insulin: New roles for an ancient hormone. Eur
J Clin Invest 29(10):842-52.
Ferrari R. 2012. Quantitative assessment of the "inexplicability" of fibromyalgia patients: a pilot study of the fibromyalgia narrative of "medically unexplained" pain. Clin Rheumatol. [Jul 22 Epub ahead of print]. "Compared to other patients with chronic, widespread pain, fibromyalgia patients report a much greater degree of difficulty in understanding the cause of their pain and explaining the cause of their pain to others. This phenomenon may reflect the narrative of 'inexplicability' in fibromyalgia patients that distinguishes them from other widespread pain populations."
Ferrari R., H. Schrader and D.
Obelieniene. 1999. Prevalence
of temporomandibular disorders associated with whiplash injury in Lithuania. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 87(6):653-7.
Fetler L, Amigorena S. 2005.
Neuroscience. Brain under surveillance: the microglia patrol.
Science 309(5733):392-393. Opioids can activate pain
inhibitory and facilitatory systems, but opioid-induced hyperalgesia
may be prevented by strategies such as concomitant administration of
NSAIDS or NMDA antagonists, use of combinations of opioids with
different receptor selectivity, and other methods.
Field T, 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.
Finan PH, Zautra AJ, Davis MC et al. 2010. COMT moderates the relation of daily maladaptive coping and pain in fibromyalgia. Pain. [Dec 2 Epub ahead of print]. "Forty-five women with fibromyalgia (FM) engaged in a 30-day electronic diary assessment, recording daily ratings of pain and 2 forms of maladaptive coping: pain catastrophizing and pain attention. Participants were genotyped for the val(158)met single nucleotide polymorphism (rs4680) in the catechol-O-methyltransferase (COMT) gene. COMT genotype moderated the daily relations of both maladaptive coping processes and pain. FM women with the homozygous met/met genotype evidenced more pain on days when pain catastrophizing was elevated relative to heterozygous and homozygous val(158) carriers. FM women with the homozygous met/met genotype evidenced more pain on days when pain attention was elevated relative to those with the homozygous val/val genotype. Evidence is presented to suggest that these are independent effects. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process, which has been previously characterized in a sample of postoperative shoulder pain patients. Further, the findings advance our understanding of the role of COMT in FM, suggesting that genetic variation in the val(158)met polymorphism may affect FM pain through pathways of pain-related cognition. This study examined 2 forms of maladaptive coping: pain catastrophizing and pain attention. The findings provide multimeasure and multimethod support for genetic moderation of a maladaptive coping and pain process and suggest that genetic variation in the val(158)met polymorphism may affect fibromyalgia pain through pathways of pain-related cognition."
et al. 2010.
on the dynamics of pain and affect in fibromyalgia.
Health Psychol. 29(2):134-142. “This finding supports a role for
catecholamines in positive affective reactivity to FM pain. A gene x
experience interaction for OPRM1 also emerged, indicating that
individuals with at least one asp allele maintained greater positive
affect despite elevations in daily pain than those homozygous for the
asn allele. This finding may be explained by the asp allele's role in
reward processing. …Together, the findings offer researchers ample
reason to further investigate the contribution of the catecholamine and
opioid systems, and their associated genomic variants, to the still
poorly understood experience of FM.” [We are honing in on some of the
genetic combinations that may be involved in subsets of FM central
Finckh A, Berner IC, Aubry-Rozier B et al. 2005.
A randomized controlled trial of dehydroepiandrosterone in postmenopausal
women with fibromyalgia. J Rheumatol 32(7):1336-1340.
This study did not find that taking DHEA brought about any useful changes.
Fine PG. 1987. Myofascial trigger
point pain in children. J Pediatr. 111(4):547-548.
Fine PG, Milano R, Hare BD. 1988.
The effects of myofascial trigger point injections are naloxone
reversible. Pain. 32(1):15-20. “These results
demonstrate a naloxone-reversible mechanism in TPI (trigger point
injection) therapy. This suggests an endogenous opioids system
as a mediator for the decreased pain and improved physical findings
following injection...” of TrPs with local anesthetic.
Fine, PG. 1987. Myofascial trigger point pain in children.
J Pediatr.111(4):547-548. This article is noteworthy in that it
misidentified myofascial pain syndrome as part of fibromyalgia. This is
too common a mistake. It does encourage early diagnosis and
treatment, but to do that doctors will have to know which condition – or
both – are involved.
Fink, G., B. Sumner, R. Rosie, H. Wilson and J. McQueen.
1999. Androgen actions on central serotonin neurotransmission: relevance for mood,
mental state and memory. Behav Brain Res 105(1):53-68.
Fischer AA. 1987. Reliability of the
pressure algometer as a measure of myofascial trigger point sensitivity.
Fishbain DA, Lewis JE, Cole B et al. 2006.
Lidocaine 5% patch: an open-label naturalistic chronic pain treatment
trial and prediction of response. Pain Med. 7(2):135-142.
This article shows some parameters in predicting the use of lidocaine
patch response. [There is also the necessity to locate the main
pain generators. If someone has a spinal abnormality instigating the
TrPs or central sensitization, an articular area that is causing a TrP
cascade or central sensitization, or one or two primary TrPs that are
setting off others, then the lidocaine patch(es) could be very
helpful. If there are TrPs all over, or diffuse pain with no specific
instigator that has been found, the patch may not be a good choice. One
to three patches may be used, and only for 12 hours at a time, with a 12
hour break. The patient may have to make the choice of being able to
sleep, if pain is causing unrestorative sleep or wakefulness, or being
able to function during the day. DJS]
Fishbain DA, Cutler RB, Rosomoff HL et
al. 2000. Clonazepam open clinical treatment trial for myofascial
syndrome associated chronic pain. Pain Med. 1(4):332-339.
Clonazepam may help some myofascial pain.
Fishbain, D. A., H. L. Rosomoff and R. S. Rosomoff. 1992. Drug
abuse, dependence, and addiction in chronic pain patients. Clin J Pain
Fishbain, D. A., M. Goldberg, R. S. Rosomoff and H.
1991. Completed suicide in chronic pain. Clin J Pain 7(1):29-36.
Fischer, A. A. 1999. Treatment of myofascial pain. J Musculoskel
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
Fiz J, Duran M, Capella D et al. 2011. Cannabis use in patients with fibromyalgia: effect on symptoms relief and health-related quality of life. PLoS One. 6(4):e18440. "The use of cannabis was associated with beneficial effects on some FM symptoms. Further studies on the usefulness of cannabinoids in FM patients as well as cannabinoid system involvement in the pathophysiology of this condition are warranted."
Flanagan, D. E. , J. C. Vaile, G. W.
Petley, V. M. Moore, I. F. Godsland, R. A. Cockington, J. S. Robinson and D. I. Phillips. 1999. The autonomic control
of heart rate and insulin resistance in young adults. J Clin Endocrinol Metab
Flanagan, D., P. Wood, R. Sherwin, K. Debrah and D. Kerr.
1998. Gin and tonic and reactive hypoglycemia: what is importantthe gin, the
tonic, or both? J Clin Endocrinol Metab 83(3): 796-800.
Flato, B., A. Aasland, I. H. Vandvik and O.
Outcome and predictive factors in children with chronic idiopathic musculoskeletal
pain. Clin Exp Rheumatol 15(5):567-577.
Flax, B. J. 1995. Myofascial pain syndomesthe
great mimicker. Bol Assoc Med P R 87(10-12):167-170.
Fleckenstein J, Zaps D, Ruger LJ et
al. 2010. Discrepancy between prevalence and perceived effectiveness of
treatment methods in myofascial pain syndrome: Results of a
cross-sectional, nationwide survey. BMC Musculoskel Disord.
11(1):32. “Myofascial pain is a common dysfunction with a lifetime
prevalence affecting up to 85% of the general population. Current
guidelines for the management of myofascial pain are not available. In
this study we investigated how physicians on the basis of prescription
behavior evaluate the effectiveness of treatment options in their
management of myofascial pain…..Effectiveness ratings of the various
treatment options between specialties were widely variant. 54.3% of all
physicians characterized the available treatment options as
insufficient.” “Myofascial pain was estimated a prevalent condition.
Despite a variety of commonly prescribed treatments, the moderate
effectiveness ratings and the frequent characterizations of the
available treatments as insufficient suggest an urgent need for clinical
research to establish evidence-based guidelines for the treatment of
myofascial pain syndrome.” [We are approaching a stage where the medical
community is beginning to recognize that myofascial pain is terribly
important across a wide range of medical fields, knowledge of individual
TrPs is vital before one can hope to manage complex CMP, it takes a long
time to learn TrPs, and the number of care providers trained in
myofascial medicine is woefully low. DJs]
Fleischmann R. 2007. Primer: establishing
a clinical trial unit – regulations and infrastructure. Nat
Clin Pract Rheumatol. 3(4):234-239. [This comprehensive
review would be very helpful for physicians interested in doing a
clinical trial. DJS]
Fleury B. 2000. [Pharyngeal musculature and
obstructive sleep apnea syndromes] Rev Mal Respir. 17 Suppl
3:S15-20. [French] “The caliber of the pharynx at the soft palate
depends on the action of the tensor veli, the palatoglossus, the
palatopharyngeus and the uvula muscles. At the lingual level, the
action of the genioglossus and the geniohyoideus predominate.
These different muscle groups contract in coordination before the
diaphragm contracts. Their activity is diminished and disorganized
during sleep. These muscles appear to have a histological
composition adapted to short duration intense contractions making them
vulnerable to fatigue. In apneic patients, these muscles are
solicited constantly. Muscular lesions related to overwork have
been suggested.” [Muscle tension can affect sleep apnea.
Myofascial TrPs can affect muscle tension. Therefore, myofascial
TrPs can affect sleep apnea. DJS]
Florian H, Young Jr. J, Haig G et al. 2007. Pregabalin is
effective for the long-term treatment of pain associated with
fibromyalgia syndrome: a 1-year, open-label study. J
Musculoskel Pain 15 (Supp 13):47 item 81. [Myopain 2007
Poster] “Pregabalin administered for up to 1 year was associated with
improvements in FMS-related pain. Pregabalin was generally well
Floyd, J. A. 1999. Sleep promotion in adults. Annu Rev Nurs Res
Foerster BR, Petrou M, Edden RA et al. 2011. Reduced insular gamma-aminobutyric acid in fibromyalgia. Arthritis Rheum. [Sep 13 Epub ahead of print]. "Diminished inhibitory neurotransmission resulting from lower concentrations of GABA within the right anterior insula may play a role in the pathophysiology of FM and other central pain syndromes."
Fogel RB, Triner J,
White DP 2005. The effect of sleep onset on upper airway muscle
activity in patients with sleep apnoea versus controls. J Physiol
564(Pt 2):549-562. “Although CPAP eliminated differences in UAR (Upper
Airway Resistance) during wakefulness and sleep, GGEMG genioglossus
(activity) remained greater in the OSA patients.” [TrPs in the pharyngeal
dilator muscles can significantly affect OSA. Their previous work
indicated tensor palatini muscle activity is high in OSA patients as well.
Effects of lifestyle
physical activity on perceived symptoms and physical function in adults
with fibromyalgia: results of a randomized trial. Arthritis Res Ther.
12(2):R55. “Although exercise is therapeutic for adults with
fibromyalgia (FM), its symptoms often create obstacles that discourage
exercise…. Accumulating 30 minutes of [exercise] throughout the day
produces clinically relevant changes in perceived physical function and
pain in previously minimally active adults with FM.” [Exercise must be
carefully tailored to the patient’s tolerance, with care given to
co-existing conditions such as chronic myofascial pain. Exercise is a
treatment that is free, independent of care-providers, dosage can be
personally titrated, and, if done carefully, has limited side-effects.
Patients may have to start at a low dosage and proceed slowly, but one
must start and one must proceed. Exercise benefits are
not gained by watching exercise tapes. DJS]
Giles WH, Dietz WH. 2002. Prevalence of the metabolic syndrome
among US adults: findings from the third National Health and
Nutrition Examination Survey. JAMA Jan16;287(3):356-9. About 47
million US residents have the metabolic syndrome, according to
2000 census data.
Forman MB, Sutej PG, Jackson EK. 2011. Hypertension, tachycardia, and reversible cardiomyopathy temporally associated with milnacipran use. Tex Heart Inst J. 38(6):714-718.
"Milnacipran is a dual and equipotent inhibitor of norepinephrine and serotonin uptake. It is frequently prescribed as therapy for fibromyalgia, and the drug has a good safety profile. Herein, we report the case of a 42-year-old woman with undefined connective-tissue disease and fibromyalgia who developed a severe and reversible cardiomyopathy while taking recommended doses of milnacipran. The cardiomyopathy was associated with a hyperadrenergic state manifested by tachycardia, hypertension, and elevated plasma catecholamine levels. The discontinuation of milnacipran and the initiation of anti-failure therapy resulted in complete resolution of the cardiomyopathy in 6 months. To our knowledge, this is the first report of milnacipran as a possible cause of catecholamine-induced cardiomyopathy."
Fornasari D. 2012. Pain mechanisms in patients with chronic pain. Clin Drug Investig. 32 Suppl 1:45-52. "The mechanisms involved in the development of chronic pain are varied and complex. Pain processes are plastic and unrelieved pain may lead to changes in the neural structure involved in pain generation. Nociceptive pain announces the presence of a potentially damaging stimulus that occurs when noxious stimuli activate primary afferent neurons. Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system resulting from trauma, infection, ischemia, cancer or other causes such as chemotherapy. The exact mechanisms involved in the pathophysiology of chronic pain are not well understood, but rapid and long-term changes are thought to occur in parts of the central nervous system that are involved in the transmission and modulation of pain following injury. Peripheral and central sensitization of sensory nerve fibres are the primary reasons for hypersensitivity to pain after injury, and mainly occur in inflammatory and neuropathic pain. During these processes the sensation of pain is enhanced as a result of changes in the environment, the nerve fibres and modifications of the functional properties and the genetic program of primary and secondary afferent neurons. Non-steroidal anti-inflammatory drugs and opioid analgesics are two of the most common classes of drugs used for the treatment of pain. Response to drug treatment shows significant inter-individual variability and can lead to side effects. The neurobiological mechanisms that cause pain may account for the different types of pain observed. Identification of these mechanisms may allow us to move from an empirical therapeutic approach to one that it is specifically targeted at the particular mechanisms of the type of pain experienced by an individual patient."
Forrest JB, Schmidt S. 2004. Interstitial
cystitis, chronic nonbacterial prostatitis and chronic pelvic pain syndrome
in men: a common and frequently identical clinical entity. J Urol.
172(6 Pt 2):2561-2562. “Interstitial cystitis in males appears to be
more common than historically reported. Interstitial cystitis in males
and patients with chronic pelvic pain syndrome and chronic nonbacterial
prostatitis share many clinical findings. A higher incidence of
interstitial cystitis had been found in American Indian males of Cherokee
descent and deserves further investigation.”
Fors EA, Landmark T, Bakke O. 2012. Contextual and time dependent pain in fibromyalgia: An explorative study. BMC Res Notes. 5(1):644. "Little is known about contextual effects on chronic pain, and how vulnerability factors influence pain in different contexts. We wanted to examine if fibromyalgia (FM) pain varied between two social contexts, i.e. at home versus in a doctor office, when it was measured the same day, and if pain was stable for 14 years when measured in similar contexts (doctor office). Our secondary aim was to explore if pain vulnerability factors varied in the two different contexts.....Pain and pain predictors seem to vary by contexts and time, with less pain at home than to a doctor the same day, but with unchanged pain in the same context after 14 years. Thus, contextual pain cues should be accounted for when pain is measured and treated, e.g. by focusing more on home-measured pain and by optimizing the doctor office context. This explorative study should be followed up by a larger full-scale study."
Forseth KO, Hafstrom I, Husby G et al. 2010. Comprehensive rehabilitation of patients with rheumatic diseases in a warm climate: a literature review. J Rehabil Med. 42(10):897-902. "In groups with mixed rheumatic diagnoses, low evidence was found for reduction of pain, activity limitation, global disease impact and improved health-related quality of life. No studies on psoriatic arthritis, osteoarthritis, fibromyalgia or osteoporosis were found.....Well-designed studies to validate and improve the low-to-moderate evidence found for the efficacy of comprehensive rehabilitation in a warm climate among patients with inflammatory rheumatic disease are greatly needed."
Forseth KO, Mengshoel AM. 2007.
Multidimensional therapy in warm climate for patients with fibromyalgia
syndrome – a pilot study. J Musculoskel Pain 15 (Supp 13):47
item 82. [Myopain 2007 Poster] “The multiple improvements indicate
that multidimensional treatment in warm climate may have short and long
lasting effect in patients with FMS. Further controlled studies are
needed to confirm these findings.” [FM patients are heterogenous.
Some patients do better in warm dry climates and some do better in cold dry
climates. Some patients are both cold and heat sensitive, some are
helped by humidity and others feel worse with humidity. There are so
many environmental variables that can affect a climate reactor that studies
such as this may be very difficult to interpret. DJS]
Forseth, K. O. , O. Forre and J. T.
Gran. 1999. A 5.5 year
prospective study of self-reported musculoskeletal pain and of fibromyalgia in a female
population: significance and natural history. Clin Rheumatol 18(2):114-21.
Forseth, K. O. and J. T. Gran. 1992. The prevalence of
fibromyalgia among women aged 20-49 years in Arendal, Norway. Scand J Rheumatol
Forst R, Ingenhorst A. 2005. [Myofascial pain syndrome]
Internist [Oct 15 Epub ahead of print] [German] “Untreated, the
myofascial pain syndrome leads to a reduced extensibility of the
involved muscle with consecutive decrease of the range of motion and
development of a muscular imbalance resulting in a disturbance of
complex movement and evolution of a chronic pain disease. An early
started and aimed therapy can prevent effectively the chronification.”
Fox AD, Kunins HV, Starrels JL. 2012. Which skills are associated with residents' sense of preparedness to manage chronic pain? J Opioid Manag. 8(5):328-336. "Few internal medicine residents felt prepared to manage CNMP. Our findings suggest that educational interventions to improve residents' preparedness to manage CNMP should target complex pain syndromes (e.g., fibromyalgia and neuropathic pain), safer opioid prescribing practices, and alternatives to opioid analgesics." [I strongly urge them to add myofascial trigger points and chronic myofascial pain to this list of pain sources. DJS]
Fox, A. W. and R. L. Davis. 1998. Migraine
chronobiology. Headache 38(6):436-41.
Fraenkel, L., Y. Zhang, C. E.
Chaisson, S. R. Evans, P. W. Wilson
and D. T. Felson. 1998. The association of estrogen replacement therapy and the
Raynaud phenomenon in postmenopausal women. Ann Intern Med 129(3):208-11.
Fraenkel, L., Y. Zhang, C. E.
Chaisson, H. R. Maricq, S. R. Evans,
F. Brand, P. W. Wilson and D. T. Felson. 1999. Different factors influencing
the expression of Raynauds phenomenon in men and women. Arthritis Rheum 42(2):306-10.
Fraga BP, Santos EB, Farias Neto JP et al. 2012. Signs and symptoms of temporomandibular dysfunction in fibromyalgic patients. J Craniofac Surg. 23(2):615-618. "The most common signs (A) and symptoms (B) reported by FM patients were (A) pain in the masticatory muscles (masseter, 80%; posterior digastric, 76.7%), pain in the temporomandibular joint (83.3%), and 33.3% and 28.3%, respectively, presented joint sounds when opening and closing the mouth; (B) headache (97%) and facial pain (81.7%). In regard to the classic triad for the diagnosis of the TMD, it was found that 35% of the FM patients presented, at the same time, pain, joint sounds, and alteration of the mandibular movements. It was verified that myofascial pain without limitation of mouth opening was the most prevalent diagnosis (47%) for the RDC subgroup I. For the subgroup II, the disk displacement with reduction was the most prevalent diagnosis (21.6%). For the subgroup III, 36.7% of the subjects presented osteoarthritis.....Thus, there is a high prevalence of signs and symptoms of TMD in FM patients, indicating the need for an integrated diagnosis and treatment of these patients, which suggest that the FM could be a medium- or long-term risk factor for the development of TMD." [It is of critical importance that research papers specify the criteria used for the identification of for myofascial trigger points. All of these symptoms can be caused by TrPs, including disc displacement and restricted mouth opening. Most patients with osteoarthritis also have TrPs. We need to shift the focus from FM (the central sensitization) to the cause of the central sensitization (TrPs) DJS].
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.
Franken P, Chollet D, Tafti M. 2001. The
homeostatic regulation of sleep need is under genetic control.
Jour of Neuroscience 21(8):2610-2621.
Fredheim OM, Borchgrevink PC, Klepstad
P et al. 2007. Long term methadone for chronic pain: a pilot
study of pharmacokinetic aspects. Eur J Pain. 11(6):599-604.
This study showed that a 3-day switch from morphine to methadone,
followed by a week-long titration period, is a pharmaceutically
sound way of moving chronic non-malignant pain patients from
morphine to methadone.
Fredheim OM, Kaasa S, Fayers P et al.
2008. Chronic non-malignant pain patients report as poor
health-related quality of life as palliative cancer patients.
Acta Anaesthesiol Scand. 52(1):143-148.
Fredheim OM, Kaasa S, Fayers P et al. 2007.
Chronic non-malignant pain patients report as poor health-related
quality of life as palliative cancer patients. Acta
Anaesthesiol Scand. [Nov 13 Epub ahead of print]. “CNMP patients
admitted to multidisciplinary pain centres report significantly reduced
HRQoL, in addition to severe pain. They consider their HRQoL to be
as poor as HRQoL reported from dying cancer patients and substantially
poorer than national norms.” [This leaves one to wonder about the
ethics of having a substantial group of patients, those with chronic
non-cancer pain, with a quality of life lower than terminal cancer
patients. How can any system allow this situation, and what will it
take to improve it? DJS]
Fredheim OM, 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
Fredheim OM, Kaasa S, Dale O et al. 2006. Opioid switching
from oral slow release morphine to oral methadone may improve pain control
in chronic non-malignant pain: a nine-month follow-up study.
Palliat Med. 20(1):35-41.
Freedenfeld RN, Murray M, Fuchs PN et al. 2006.
Decreased pain and improved quality of life in fibromyalgia patients treated
with olanzapine, an atypical neuroleptic. Pain Pract.
6(2):112-118. “In general, the data provide strong support that olanzapine
can, in certain patients, improve symptoms associated with fibromyalgia in
patients who have had limited success with other treatment modalities.”
There were significant side-effects that caused discontinuance of treatment
in a number of patients.
Freeman MD, Nystrom A, Centeno C. 2009.
Chronic whiplash and central sensitization; an evaluation of the role of
a myofascial trigger point in pain modulation. J Brachial Plex
Peripher Nerve Inj. 4:2. “Conclusion: the present data suggest
that myofascial trigger points serve to perpetuate lowered pain
thresholds in uninjured tissues.” [This study indicates that TrPs
perpetuate central sensitization (FM). The effects of TrP treatment on
lowered pain thresholds were temporary, perhaps because the perpetuating
factors and follow-up treatment did not occur. The authors contemplated
surgical removal or ablation of TrPs, which is not logical considering
the physiology of TrP formation, and it is hoped that the authors will
study the Travell and Simons texts and current research before
continuing to treat myofascial pain. Trauma, including surgery, can be
an initiator and perpetuator of TrPs and could promote further chronic
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
Freitas, J. P. , P. Filipe, I.
Emerit, P. Meunier, C. F. Manso and
F. Guerra Rodrigo. 1996. Hyaluronic acid in progressive systemic sclerosis. Dermatology.
Fricton, J. R. 2002. "Masticatory
myofascial pain" an explanatory model of regional muscle pain
syndromes. J Musculoskel Pain 10(1/2)131-150. The presence of myofascial
trigger points should be explored in cases of masticatory pain.
Fricton, J. R. 1996. Myofascial pain of the head and
neck: diagnosis and management. J Back & Musculoskeletal Rehab 6:177-194.
Fricton JR, Kroening R, Haley D et al.
1985. Myofascial pain syndrome of the head and neck: a review of
clinical characteristics of 164 patients. Oral Surg Oral Med Oral
Pathol. 60(6):615-623. “Misdiagnosis or inadequate management
of this disorder after onset may lead to development of a complex
chronic pain syndrome.” [This is a study of 164 patients, as true
today as it was when it was written. Far too many dentists have no
knowledge of myofascial pain, and this lack of knowledge on their part
results in far too many chronic pain patients. DJS]
Fricton JR, Steenks MH. 1996.
[Diagnosis and treatment of myofascial pain] Ned Tijdschr Tandheelkd.
103(7):249-253. [Dutch] “MFP is frequently overlooked as a
diagnosis because it is often accompanied by signs and symptoms in
addition to pain….” “The difficulty in managing MFP lies in the
critical need to match the level of complexity of the management program
with the complexity of the patient. Failure to address the entire
problem may lead to failure to resolve the pain and perpetuation of a
chronic pain syndrome.”
Friedberg F, Williams DA, Collinge W. 2012. Lifestyle-oriented non-pharmacological treatments for fibromyalgia: a clinical overview and applications with home-based technologies. J Pain Res. 5:42535. Many of these treatments help and are cost-effective. [It is unfortunate that co-existing conditions such as myofascial trigger points, insulin resistance and other illnesses were not considered, although the study was basically aimed at controlling some common perpetuating factors. DJS]
Friederich HC, Schellberg D,
Mueller K et al. 2004. [Stress and autonomic dysregulation in patients
with fibromyalgia syndrome.] Schmerz [Epub May 12 ahead of
print] [German] This study indicates that the stress system in FMS
patients is hyporeactive.
Friedman, D. P. 1990. Perspectives on the medical use of drugs
of abuse. J Pain Symptom Manage 5(1 Suppl):S2-S5.
Friedman M, Gurpinar B, Lin HC et al. 2007.
Impact of treatment of gastroesophageal reflux on obstructive sleep apnea-hypopnea
syndrome. Ann Otol Rhinol Laryngol. 116(11):805-811.
“Treatment of GERD had a significant impact on the reduction of the apnea-hypopnea
index, snoring, and daytime sleepiness. Elimination of GERD should be
part of a comprehensive treatment plan for patients with OSAHS.”
Friedrich M, Hahne J, Wepner F. 2009.
A controlled examination of medical and psychosocial factors associated
with low back pain in combination with widespread musculoskeletal pain.
Phys Ther. [Jun 18 Epub ahead of print].
Frieri M. 2003. Identification of masqueraders of autoimmune disease in the office.
Allergy Asthma Proc 24(6):421-9. Fibromyalgia is included as one of the diseases that often masquerades as and may be misdiagnosed as an autoimmune disease.
[This may result in inappropriate medications and therapies. DJS]
Fries E, Hesse J, Hellhammer J et al. 2005. A new view on
hypocortisolism. Psychoneuroendocrinology [Epub ahead
of print June 8]. “Low cortisol levels have been observed in
patients with different stress-related disorders such as chronic
fatigue syndrome, fibromyalgia, and post-traumatic stress disorder.
We propose that the phenomenon of hypocortisolism may occur after a
prolonged period of hyperactivity of the
hypothalamic-pituitary-adrenal axis due to chronic stress as
illustrated in an animal model. Despite symptoms such as pain,
fatigue and high stress sensitivity, hypocortisolism may also have
beneficial effects on the organism.”
Frokjaer JB, Andersen SD,
Gale J et al. 2005. An experimental study of viscero-visceral
hyperalgesia using an ultrasound-based multimodal sensory testing approach.
Pain [Nov 15 Epub ahead of print]. “Central mechanisms can explain
the remote hyperalgesia to mechanical visceral stimulation and the increase
in referred pain areas.”
Frost J, Okun S, Vaughan T et al. 2011. Patient-reported Outcomes as a Source of Evidence in Off-Label Prescribing: Analysis of Data from PatientsLikeMe. J Med Internet Res. 13(1):e6. "Evaluating a new use for an existing drug can be expensive and time consuming. Providers and patients must all too often rely upon their own individual-level experience to inform clinical practice, which generates only anecdotal and unstructured data....In this work, we explored how a patient-centered online research platform could supplement traditional trials to create a richer understanding of medical products postmarket by efficiently aggregating structured patient-reported data. PatientsLikeMe is a tool for patients, researchers, and caregivers (currently 82,000 members across 11 condition-based communities) that helps users make treatment decisions, manage symptoms, and improve outcomes. Members enter demographic information, longitudinal treatment, symptoms, outcome data, and treatment evaluations. These are reflected back as longitudinal health profiles and aggregated reports. Over the last 3 years, patients have entered treatment histories and evaluations on thousands of medical products. These data may aid in evaluating the effectiveness and safety of some treatments more efficiently and over a longer period of time course than is feasible through traditional trials.....Patient-reported outcomes, like those entered within PatientsLikeMe, offer a unique real-time approach to understand utilization and performance of treatments across many conditions. These patient-reported data can provide a new source of evidence about secondary uses and potentially identify targets for treatments to be studied systematically in traditional efficacy trials."
Fruchwald-Schultes B, Kern W, Born J, et al.. 2001.
Hyperinsulinemia causes activation of the
hypothalamus-pituitary-adrenal axis in humans. Int J Obes
Relat Metab Disord 25 Suppl 1:S38-40. Hyperinsulinemia acutely
increases HPA secretory activity in healthy men.
Fruth SJ. 2006. Differential diagnosis and treatment in a patient
with posterior upper thoracic pain. Phys Ther. 86(2):254-268.
“This case suggests that CV/CT mobilizations and active TrP release may
have been beneficial in reducing pain and restoring function in this
patient.” This case is interesting in that myofascial dysfunction
occurred after a 35-year old man had been on the bleachers at a hockey
game for 3 hours. Two days later he had pain in the right scapular area
and spine that increased during the next 6 weeks. He had considerable
pain, lost some function and range of motion and had difficulty sleeping
due to movement-triggered pain. He was subjected to weeks of physical
therapy including spine mobilization, and given many expensive
radiological tests. After months of this, trigger points were found in
multiple area muscles. After 4 weeks of specific treatment the patient
had full return to function. [How much pain is needless, and how much
time and other resources are wasted, because we do not have care
providers who are adequately trained in the diagnosis and treatment of
myofascial TrPs? DJS]
Frye, J. 1997. Homeopathy in office practice. Prim
Fuentes CT, Bastian AJ. 2009. Where is your
arm? Variations in proprioception across space and tasks. J
Neurophysiol. [Oct 28 Epub ahead of print] “The sense of limb position
is crucial for movement control and environmental interactions.” “In sum,
we have uncovered fundamental aspects of proprioceptive processing,
demonstrating both predictable biases that are dependent on joint
configuration and independent of task as well as improved precision when
integrating information across joints.” [Patients with proprioceptive
dysfunction, which can be associated with myofascial TrPs, vestibular
dysfunction, eye inequalities, or brain injury, or a combination of all of
them (which many FM and CMP patients have), may feel clumsy, but in
actuality, it is a magnificent thing that some of us can walk across a
room. The endless compensation that goes on is often unnoticed and
unremarked until a compensation mechanism fails, and we feel “clumsy.” DJS]
Fugh-Berman, A. and J. M.
Cott. 1999. Dietary
supplements and natural products as psychotherapeutic agents. Psychosom Med
Fujioka, M., K. Okuchi, K. I.
Hiramatsu, T. Sakaki, S.
Sakaguchi and Y. Ishii. 1997. Specific changes in human brain after hypoglycemic injury.
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
Furnes B, Dysvik E. 2010. Dealing with grief related to loss by death and chronic pain: An integrated theoretical frame work. Part 1. Patient Prefer Adherence. 4:135-140.
"Two main themes were formulated, 'relearning the world' and 'adaptation'. Between these themes a continuous movement emerged involving experience such as: 'despair and hope', 'lack of understanding and insight', 'meaning disruption and increased meaning', and 'bodily discomfort and reintegrated body'." "Grief as a distinctive experience means that health care must be aimed at each individual experience and situation." [This article explains why care providers and supporters of patients dealing with chronic pain situations need to understand the enormity of life disruption that a chronic pain state can bring.]
Furuta A, Suzuki Y, Honda M et al. 2011. Time-dependent changes in bladder function and plantar sensitivity in a rat model of fibromyalgia syndrome induced by hydrochloric acid injection into the gluteus. BJU Int. [Aug 2 Epub ahead of print]. "HCl injection (pH 4.0) into the gluteus can induce plantar hypersensitivity and urinary frequency (in the rat) for up to 2 weeks after the injection, suggesting that somatic (gluteus)-to-visceral (bladder) cross-sensitization might underlie bladder hypersensitivity in patients with FMS. Moreover, intervention at specific tender points outside the bladder could be effective in treating urinary frequency because lidocaine injection into the gluteus normalized bladder function in FMS rats for up to 2 weeks."
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
Gagliardi GS, Shah AP, Goldstein M et al.
2009. The effect of zolpidem on the sleep arousal response to
nocturnal esophageal acid exposure. Clin Gastroenterol Hepatol.
[May 5 Epub ahead of print]. “Zolpidem reduced the arousal response to
nocturnal acid exposure and increased the duration of each esophageal acid
reflux event in healthy individuals and patients with GERD. Since
nocturnal acid exposure was prolonged, hypnotic use by GERD patients could
lead to increased risk for complicated disease.”
Gagliese, L. and R.
Melzack. 1997. Chronic pain
in elderly people. Pain 70(1):3-14.
I, Swaine B, Friedman D et al. 2004. Children show decreased dynamic
balance after mild traumatic brain injury.
Arch Phys Med Rehabil 85(3):444-452.
Even mild traumatic brain injury can cause postural balance
dysfunction in children 10 weeks after the injury.
Galic MA, Persinger MA. 2007. Lagged
association between geomagnetic activity and diminished nocturnal pain
thresholds in mice. Bioelectromagnetics [Jul 26 Epub ahead of
print]. “If the geomagnetic activity was greater 3 days before a given
hotplate trial, subjects tended to exhibit shorter response latencies,
suggesting lower pain thresholds or less analgesia. These results are
supported by related experimental findings and suggest that natural
variations in geomagnetic intensity may influence nociceptive behaviors in
mice.” [This study, although done in mice, may have implications for
electromagnetic sensitivity observed in some FM patients. DJS]
Galinier, M., J. Fourcade, N.
Ley, S. Boveda, S. Solera, M.
L. Solera, P. Massabuau, S. Elhabaj, J. M. Fauvel, P. Valdiguie and J. P.
Bounhoure. 1999. [No
title available] Arch Mal Coeur Vaiss 92(8):1105-9. [French]
Gallagher L, McAuley J, Moseley GL. 2013. A randomized-controlled trial of using a book of metaphors to reconceptualize pain and decrease catastrophizing in people with chronic pain. Clin J Pain 29(1):20-25. In this randomized single-blind crossover controlled trial, a group of chronic pain patients were taught by giving them a booklet of metaphors and stories and a control group was given advice on how to manage pain according to cognitive behavior principles. Pain biology knowledge and catastrophizing were measured at intervals. The educational material provided by the metaphors and stories helped patients to reconceptualize pain and reduce catastrophizing, and gains were maintained for at least 3 months. Changes were replicated in the advice booklet group when they were crossed over to the booklet with metaphors and stories. There was no change in self-reported disability. Metaphor and story appears to be a preferred precursor to functional capacity interventions.
Gallagher, R. M. 1999. Primary care and pain
medicine. A community solution to the public health problem of chronic pain. Med
Clin North Am 83(3):555-83,v.
Gallagher, R. M. and S.
Verma. 1999. Managing
pain and comorbid depression: A public health challenge. Semin Clin
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
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
Galski, T., J. B. Williams and H. T.
2000. Effects of opioids on driving ability. J Pain Symptom Manage
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
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
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.
2010. Chemokines, neuronal-glial interactions, and central processing of
neuropathic pain. Pharmacol Ther. [Jan 28 Epub ahead of print] “It
has been increasingly recognized that spinal cord glial cells such as
microglia and astrocytes play a critical role in the induction and
maintenance of neuropathic pain by releasing powerful neuromodulators such
as proinflammatory cytokines and chemokines. Recent evidence reveals
chemokines as new players in pain control. In this article, we review
evidence for chemokine modulation of pain via neuronal-glial interactions by
focusing on the central role of two chemokines, CX3CL1 (fractalkine) and
CCL2 (MCP-1), because they differentially regulate neuronal-glial
interactions. Release of CX3CL1 from neurons is ideal to mediate
neuronal-to-microglial signaling, since the sole receptor of this chemokine,
CX3CR1, is expressed in spinal microglia and activation of the receptor
leads to phosphorylation of p38 MAP kinase in microglia. Although CCL2 was
implicated in neuronal-to-microglial signaling, a recent study shows a novel
role of CCL2 in astroglial-to-neuronal signaling after nerve injury. In
particular, CCL2 rapidly induces central sensitization by increasing the
activity of NMDA receptors in dorsal horn neurons. Insights into the role of
chemokines in neuronal-glial interactions after nerve injury will identify
new targets for therapeutic intervention of neuropathic pain.”
Gao YJ, Xu ZZ, Liu YC et al. 2009.
The c-Jun N-terminal kinase 1 (JNK1) in spinal astrocytes is required for
the maintenance of bilateral mechanical allodynia under a persistent
inflammatory pain condition. Pain. [Dec 16 Epub ahead of
print] “Peripheral inflammation induces persistent central sensitization
characterized by mechanical allodynia and heat hyperalgesia that are
mediated by distinct mechanisms.” “…we investigated the distinct role
of spinal JNK in heat hyperalgesia, mechanical allodynia, and contralateral
pain in an inflammatory pain model.” “…our data suggest that spinal
JNK, in particular HNK1, plays an important role in the maintenance of
persistent inflammatory pain. Our findings also reveal a unique role
of JNK1 and astrocyte network in regulating tactile allodynia and
contralateral pain.” [This article is relevant as astrocytes (glial cells)
are implicated in the development of the central sensitization of FM, and
opposite side, contralateral) pain occurs in TrPs when the pain fields are
expanding and central sensitization is developing. Since we have
recently found that FM patients have myofascial TrPs, TrPs are responsible
for generating some FM pain and can of themselves maintain central
sensitization, this is an important piece of the puzzle. DJS]
Gao YJ, Zhang L, Ji RR. 2010. Spinal injection of TNF-alpha-activated astrocytes produces persistent pain symptom mechanical allodynia by releasing monocyte chemoattractant protein-1. Glia. [Aug 24 Epub ahead of print]. "Accumulating evidence suggests that spinal astrocytes play an important role in the genesis of persistent pain, by increasing the activity of spinal cord nociceptive neurons, i.e., central sensitization.....We investigated whether and how spinal injection of activated astrocytes could produce mechanical allodynia, a cardinal feature of chronic pain, in....mice.....our results suggest that activated astrocytes are sufficient to produce persistent pain symptom in our mice...." [We can look forward to the development of astrocyte modulators to minimize central sensitization. DJS]
Garbuzenko E, Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis and
lattice contraction: a direct role for mast cells in skin fibrosis.
Clin Exp Allergy. 32(2):237-246. This study indicates that co-existing
allergies and the presence of more numerous mast cells may have a
significant affect on scarring, formation of adhesions and fibrosis.
One of the two main mast cell mediators involved is histamine, one of the
biochemicals produced during MTrP local twitch response. Allergies may thus
be interactive with other conditions in yet one more way.
Garbuzenko E., Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis
and lattice contraction: a direct role for mast cells in skin fibrosis.
“...mast cells have a direct and potentiating role in skin remodeling
and fibrosis.” [Excess histamine in the system, from allergy,
fibromyalgia imbalance, myofascial TrP twitch response, and/or other
reasons may directly affect the formation of adhesion and scar tissue.
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.
Garcia-Martinez AM, De Paz JA, Marquez S. 2011. Effects of an exercise program on self-esteem, self-concept and quality of life in women with fibromyalgia: a randomized controlled trial. Rheumatol Int. [Mar 27 Epub ahead of print]. "Compared to the control group, statistically significant improvements in self-esteem, self-concept, FIQ (Fibromyalgia Impact Questionnaire), physical functioning, role physical, bodily pain, vitality, role emotional, social functioning, mental health, isometric strength, muscular endurance and flexibility were evident in the exercise group at the end of treatment. Self-esteem and self-concept scores were correlated positively with role emotional, mental health and the mental component summary of SF-36 and were negatively correlated to FIQ scores. No significant correlation existed between self-esteem or self-concept and isometric strength, muscular endurance or flexibility. Our results highlight the need for a broader array of physical and mental outcomes and the importance of examining patient's perceptions in future research therapies." [Co-existing trigger points must be taken into consideration when constructing an exercising program. When TrPs are causing weakness in a muscle, you cannot strengthen it though exercise. DJS]
Gardner, J. R. and G.
Sandhu. 1997. The stigma
and enigma of chronic non-malignant back pain (CNMBP) treated with long-term opioids
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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
Garrett CG, Cohen SM. 2008.
Otolaryngological perspective on patients with throat symptoms and laryngeal
irritation. Curr Gastroenterol Rep. 10(3):195-199. Laryngeal
reflux is an increasingly common condition. Symptoms include an urge
to clear the throat, sore throat, hoarseness, cough, and sensation of a
foreign body in the throat. It is usually treated with anti-reflux
medication. The article indicates that failure to consider other
diagnoses may result in unnecessary treatment and diagnostic delay. [TrPs
in the laryngeal muscles are frequently irritated by reflux, and must be
considered as part of treatment regimen. They can also mimic other
laryngeal conditions. Symptoms including vocal dysfunctions may be
considerably helped by TrP treatment, but the perpetuating factors must be
removed as well. DJS]
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Thyroid resistance may be a key perpetuating factor of FMS.
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prospective, randomized, double-blind evaluation of trigger point injection
therapy for low back pain. Spine 14(9):962-964. “Trigger
point therapy seems to be a useful adjunct in treatment of low back strain.
The injected substance apparently is not the critical factor, since direct
mechanical stimulus to the trigger point seems to give symptomatic relief
equal to that of treatment with various types of injected medication.”
[Chronic low back pain is often due to TrPs. This has long been known
but has not filtered down to the clinician level. DJS]
Gatchel RJ, Okifuji A. 2006. Evidence-based
scientific data documenting the treatment and cost effectiveness of
comprehensive pain programs for chronic nonmalignant pain. J Pain
7(11):779-793. “This review clearly revealed that CPPs offer the most
efficacious and cost effective treatment for persons with chronic pain,
relative to a host of widely used conventional medical treatment.” [Chronic
pain programs for patients with FMS and CMP must include care providers with
the skills to diagnose and treat these conditions. DJS]
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mechanisms underlying balance improvement with short term Tai Chi training.
Aging Clin Exp Res. 18(1):7-19. “TC (t’ai chi) enhanced
neuromuscular responses controlling the ankle joint of the perturbed leg.
Fast, accurate neuromuscular activation is crucial for efficacious response
to slips or trips.”
Gavish A., Winocur E., Ventura Y.S.
et al. 2002. Effects of stabilization splint therapy on pain during
chewing in patients suffering from myofascial pain. Patients with
masticatory myofascial pain who used flat occlusal splints experienced less
intense pain than the control patients. [Part of the reduction in pain may
be due to TrPs becoming latent because of using the splint. DJS]
Ge HY. 2010. Prevalence of myofascial trigger points in fibromyalgia: the overlap of two common problems. Curr Pain Headache Rep. 14(5):339-345. Now that we have objective evidence of the reality of myofascial trigger points, it is becoming more apparent that they contribute to many chronic regional and widespread pain conditions. "Active MTrPs as tonic peripheral nociceptive input contribute tremendously to the initiation and maintenance of central sensitization, to the impairment of descending inhibition, to the increased excitability of motor units, and to the induction of sympathetic hyperactivity observed in FM. The considerable overlap of MTrPs and FM in pain characteristics and pathophysiology suggests that FM pain is largely due to MTrPs."
Ge HY, Arendt-Nielsen L. 2011. Latent myofascial trigger points. Curr Pain Headache Rep May 11 [Epub ahead of print] The treatment of latent TrPs may improve function, decrease sensitivity to pain, prevent the activation of those TrPs, and, if caught in time, may prevent the development of myofascial pain syndrome.
Ge HY, Fernandez-de-Las-Penas C, Yue SW. 2011. Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med. 6(1):13.
"Referred pain is dependent on the sensitivity of myofascial trigger points. Active myofascial trigger points may play an important role in the transition from localized pain to generalized pain conditions via the enhanced central sensitization, decreased descending inhibition and dysfunctional motor control strategy."
Ge HY, Wang Y, Danneskiold-Samsoe B et al.
2009. The predetermined sites of examination for tender points in
fibromyalgia syndrome are frequently associated with myofascial trigger
points. J Pain. [Nov 13 Epub ahead of print] “The
current study provides first evidence that pain from active MTrPs at TP
sites mimics fibromyalgia pain. MTrPs may relate to generalized
increased sensitivity in FMS due to central sensitization.” “…This
article underlies the importance of active MTrPs in FMS patients.
Most of the TP sites in FMS are MTrPs. Active MTrPs may serve as a
peripheral generator of fibromyalgia pain and inactivation of active
MTrPs may thus be an alternative for the treatment of FMS.” [It is very
good to have such fine research confirm that TrPs themselves can be the
cause or maintainer of much FM pain, and that one cannot adequately
treat FM without being able to diagnose and treat co-existing TrPs. DJS]
Ge HY, Nie H, Madeleine P et al. 2009.
Contribution of the local and referred pain from active myofascial trigger
points in fibromyalgia syndrome. Pain. [Oct 8 Epub ahead of
print]. “The generalized hypersensitivity associated with fibromyalgia
syndrome (FMS) may in part be driven by peripheral nociceptive sources.”
“Active MTrPs bilaterally in the upper trapezius muscle contribute to the
neck and shoulder pain in FMS. Active MTrPs may serve as one of the
sources of noxious input leading to the sensitization of spinal and
supraspinal pain pathways in FMS.” [We are getting more confirmation
that myofascial TrPs can be in some if not many instances at least one way
that the central sensitization we know of as fibromyalgia is maintained.
To treat fibromyalgia adequately, co-existing myofascial TrPs MUST be
treated. Any doctor who treats fibromyalgia patients MUST know how to
diagnose and treat patients with myofascial TrPs or they cannot justifiably
take money to treat patients for these conditions. DJS]
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.
Ge HY, Wang Y, Fernandez-de-Las-Penas C et al. 2011. Reproduction of overall spontaneous pain pattern by manual stimulation of active myofascial trigger points in fibromyalgia patients.
Arthritis Res Ther. 13(2):R48. "The overall spontaneous FM pain pattern can be reproduced by mechanical stimulation of active MTPs located in different muscles, suggesting that fibromyalgia pain is largely composed of pain arising from muscle pain and spasm. Targeting active MTPs and related perpetuating factors may be an important strategy in FM pain control." [More research is showing that one cannot treat FM without treating the pain generators, including myofascial TrPs. DJS]
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syndrome. J Musculoskel Pain. 17(2):178-188. “Essential
aims in the tailored management of FMS are enhancement of functional
capacity and quality of life, and symptomatic treatment of individual
symptoms such as pain, distress, and sleep disturbances. Patient
education, pharmacological interventions with analgesics and
antidepressants, cognitive-behavioral therapy, sleep hygiene training, and
low-intensity physical exercise training are commonly employed in tailored
management of FMS. Our review suggests that favorable neuroendocrine
changes are to be expected as part of a successful outcome of these
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
Geiss A, Rohleder N, Anton F. 2011. Evidence for an association between an enhanced reactivity of interleukin-6 levels and reduced glucocorticoid sensitivity in patients with fibromyalgia. Psychoneuroendocrinology. [Oct 13 Epub ahead of print]. "Whereas FMS patients were found not to differ from controls in cortisol awakening response, daytime profile of cortisol secretion and cortisol suppression after overnight DST, they did exhibit a reduced GC sensitivity of inflammatory cytokine production. PPT measurement did induce three times higher cortisol and four times higher IL-6 levels in FMS patients, but no change in their ACTH levels. The enhanced IL-6 reactivity after PPT measurement was accompanied by an increase in the severity of FMS patients' pain and fatigue ratings. The findings of the present study provide evidence for the pathophysiologic relevance of a disturbed glucocorticoid receptor (GR) function, rather than reduced cortisol levels for the maintenance of FMS core symptoms." [It would be interesting to have a companion study to see how many of these patients also had insulin resistance and thyroid resistance, as these are common coexisting conditions with FM. DJS]
Geletka BJ, O'Hearn MA, Courtney CA. 2012. Quantitative sensory testing changes in the successful management of chronic low back pain. J Man Manip Ther. 20(1):16-22.
"Individuals with chronic low back pain (LBP) represent a significant percentage of patients in physical therapy practice. The clinical pattern often includes diffuse pain and a variety of sensory complaints, making categorization difficult and leading to diagnoses such as non-specific LBP. Objective measures of sensory changes through quantitative sensory testing may help identify central sensitization of nociceptive pathways in this population. Identification of these somatosensory changes may contribute to clinical decision making and patient management. The purpose of this case report is to present objective evaluation findings, including altered somatosensation, in a patient with a 2-year history of LBP, and to describe changes in function and quantitative sensory testing with successful management."
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after TBI, with rigorous outcome measurement needed to examine long-term
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issues. Best Pract Res Clin Rheumatol 17(4):575-592.
“Patients pain reports can be systematically biased by a number of
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Gerbershagen HJ. 2013. [Transition from acute to chronic postsurgical pain: Physiology, risk factors and prevention.] Schmerz. [Feb 2 Epub ahead of print]. [Article in German]
"Chronic postsurgical pain (CPSP) is defined as pain persisting for longer than 3 months postoperatively. The frequency of occurrence ranges from 5 % to 60 % in all types of surgery and 1-3 % of patients with CPSP will suffer from severe pain and pain-related interference with daily activities. The pathological mechanisms which lead to the development of CPSP are complex and have not yet been analyzed. Neuropathic pain after surgical nerve lesions has been reported. Many patients with CPSP, however, do not present with any neuropathic pain characteristics. Peripheral and central sensitization are the essential mechanisms of the development of pain chronicity in the postoperative period. As treatment of CPSP is demanding it is attempted to prevent central sensitization before CPSP develops." [It would be wise to assess each post-surgical patient for developing TrPs in a follow-up exam at least a month after surgery. DJS]
Gerdle B, Forsgren MF, Bengtsson A et al. 2013. Decreased muscle concentrations of ATP and PCR in the quadriceps muscle of fibromyalgia patients – A (31) P-MRS study. Eur J Pain. [Jan 30 Epub ahead of print]. "Alterations in intramuscular ATP, PCr and fat content in FMS probably reflect a combination of inactivity related to pain and dysfunction of muscle mitochondria." [OR, they may reflect the presence of co-existing TrPs. DJS]
Gerdle B, Grönlund C, Karlsson SJ et al. 2010.
control mechanisms of the trapezius muscle in fibromyalgia.
BMC Musculoskelet Disord. 11:42. “For decades, the association
between motor control strategies and chronic pain has been a topic for
debate. One long held functional neuromuscular control mechanism is
differential activation between regions within a single muscle. The aim of
this study was to investigate differences in neuromuscular control, i.e.
differential activation, between myalgic trapezius in fibromyalgia patients
and healthy controls. METHODS: 27 fibromyalgia patients and 30 healthy
controls performed 3 minutes bilateral shoulder elevations with different
loads (0-4 Kg) with a high-density surface electromyographical (EMG) grid
placed above the upper trapezius. Differential activation was quantified by
the power spectral median frequency of the difference in EMG amplitude
between the cranial and caudal parts of the upper trapezius. The average
duration of the differential activation was described by the inverse of the
median frequency of the differential activations. RESULTS: the median
frequency of the differential activations was significantly lower, and the
average duration of the differential activations significantly longer in
fibromyalgia compared with controls at the two lowest load levels (0-1 Kg)
(p < 0.04), but not at the two highest load levels (2 and 4 Kg). CONCLUSION:
these findings illustrate a different neuromuscular control between
fibromyalgia patients and healthy controls during a low load functional
task, either sustaining or resulting from the chronic painful condition. The
findings may have clinical relevance for rehabilitation strategies for
fibromyalgia.” [I believe that this article, although claiming to be about
FM, actually deals with co-existing myofascial trigger points, known to
cause the different EMG effects described. Fibromyalgia is central nervous
system sensitivity. Until we get the researchers clear on these frequently
co-existing but very different conditions, we will have misleading research
with misleading conclusions. DJS]
Gerdle B, Ostlund N, Gronlund C et al.
2007. Firing rate and conduction velocity of single motor units in the
trapezius muscle in fibromyalgia patients and healthy controls. J
Electromyogr Kinesiol. [Apr 23 Epub ahead of print]. “CV (conduction
velocity) was significantly higher in FM than in healthy controls; this
might be due to alterations in histopathology and microcirculation.”
[It is unfortunate that patients were not screened for co-existing
myofascial trigger points. DJS]
Germanowicz D, Lumertz MS, Martinez D et al. 2006.
Sleep disordered breathing concomitant with fibromyalgia syndrome.
J Bras Pneumol. 32(4):333-338. “…the more than ten-fold higher
proportion of fibromyalgia cases seen in this sample supports the hypothesis
that there is an association between sleep disordered breathing and
Gerster, J. C. and A.
Hadj-Djilani. 1984. Hearing and
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Gervais Tougas G. 1999. The autonomic nervous system in
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NOTATION IS CORRECT]
Gerwin R. 2012. Botulinum Toxin Treatment of Myofascial Pain: A Critical Review of the Literature. Curr Pain Headache Rep. [Jul 10 Epub ahead of print]. "This is a review of literature relevant to the treatment of myofascial pain syndrome by botulinum injections. The objective is to critically review the studies to see if they are appropriately designed, conducted, and interpreted to provide guidance in the management of myofascial pain. The intent is to better understand the mixed results that these studies have provided. A search was made utilizing PubMed for literature relevant to the use of botulinum toxin in the treatment of myofascial pain. All identifiable series were reviewed, including open label, single-blinded and double-blinded studies, randomized and controlled, or not. In general, small case series of only a few patients were not included unless they made a relevant point and there were no available randomized studies or larger studies.... Problems that were common to the studies were robust placebo responders, incomplete treatment of a regional myofascial pain syndrome, inappropriate or confounding control populations or treatments, and inappropriate time periods for assessment of outcomes, or misinterpretation of the time-frame of action of botulinum toxin. The studies of the effect of botulinum toxin treatment of myofascial trigger points have had mixed results. However, few studies have been designed to avoid many of the pitfalls associated with a trial of botulinum toxin treatment of trigger points. Better-designed studies may give results that can be used to guide practice based on reliable evidence. At the present time, one must conclude that the available evidence is insufficient to guide clinical practice."
Gerwin R. 2010. Myofascial pain syndrome: here we are; where must we go? J Musculoskel Pain. 18(4):329-347.
"MPS was first defined clinically by Janet Travell, MD, and later by David Simons, MD. Pain neurophysiology has only recently provided the basis for understanding the sensorimotor manifestations of MPS. This article reviews the current state of knowledge concerning MPS. MPS is a form of myalgia characterized by local regions of muscle hardness and tenderness that cause referred pain. The signature feature is the trigger point, a tender, taut band of muscle that can be painful spontaneously or when stimulated. The active trigger point has identifiable pathophysiologic changes. Levels of substance P, calcitonin gene related peptide, bradykinin, and assorted cytokines, are elevated, indicating a chemical inflammation. Trigger point milieu pH is low, about pH 5, consistent with hypoxia and ischemia. Persistent, low-amplitude, high-frequency electrical discharges that look like endplate potentials characteristic. The taut band can be visualized using high definition ultrasonograpy and magnetic resonance sonography. Central scanning. The role of MPS in headache and pelvic pain has been extensively studied in the last few years. Although great progress has been made, studies are still needed to substantiate the energy crisis hypothesis of trigger point formation, to understand the nature of sustained muscle contraction that forms the taut band and of referred pain in humans, and to develop a more rationale and effective treatment."
"Nociceptive activity from TrPs activates spinal cord dorsal horn neurons and sensitizes the central nervous system, causing central sensitization, hyperalgesia, and referred pain. Muscle weakness without atrophy occurs due to TrP-induced motor inhibition. Restricted range of motion occurs because of the shortening of the contracted taut band, and perhaps because of pain. The range of motion in hypermobile individuals must be interpreted cautiously, because it can appear to be normal, but can still be restricted. Impaired reciprocal inhibition results in co-contraction of agonists and antagonists, thus interfering with fine motor control and coordination. Autonomic disturbances can accompany TrP activation leading to changes in skin temperature and color, piloerection (goosebumps), and lacrimation (tearing)….The clinically evident progression from a non-tender taut band to a tender taut band suggests that the first change in muscle is the development of the contracted, taut group of muscle fibers that can become painful when sufficiently stressed."
"Myofascial pain syndrome presents as acute and chronic muscle pain….It may be regional or widespread. It may be accompanied by a sensory component of parasthesias or dysesthesias. MPS may persist long after the initiating cause of pain has resolved. Thus, myofascial pain can be complex." "Muscles harboring a TrP are often weak. Weakness in affected muscles occurs without atrophy, and is not neuropathic or myopathic. It is rapidly reversible immediately on inactivation of the TrP, suggesting that it is caused by the inhibition of muscle action….a TrP in one muscle can inhibit effort or contractile force in another muscle." "The TrP causes a disordered recruitment of muscles that work together to produce an action." "Reciprocal inhibition, whereby contraction of one muscle is inhibited by the contraction of its antagonist muscle, is reduced or absent when the activated muscle contains a TrP. The lack of reciprocal inhibition causes co-contraction that reduces the quality of movement and leads to clumsiness and an incoordination of fine movement." "The range of motion around a joint moved by muscles with TrPs is often limited. The end range may be painful, but limitation of the range may be painless unless the patient is pushed to move beyond comfort. Limitation of range of motion is not a reliable indicator of the presence of a TrP in persons who are hypermobile….
Changes in spatial distribution also occur with muscle contraction, the changes correlating with the duration of contraction. This suggests that a more long-lasting nociceptive irritant like a TrP would also cause a functional spatial reorganization of muscle activity….The TrP is a tender focus in muscle, the region of tenderness always located on the taut band. The region of greatest hardness is usually also the region of greatest tenderness. A tender TrP always means that there is hyperalgesia or allodynia."
"Miniature endplate potentials are thought to be the result of spontaneous release of acetylcholine from motor nerve potentials….It is now clear that motor endplates are more widely distributed throughout the muscle than just the endplate zone….A greater endplate activity and consequently greater focal muscle sarcomere compression can be thought of as being associated with greater local muscle injury and local release of nociceptive substances." "It is likely that TrPs are first formed as latent TrPs and then become tender as muscle is activated. Latent TrPs exist without spontaneous pain. Furthermore, TrP tenderness does not occur except in regions of muscle hardness, but regions of muscle hardness occur without local or referred pain. Hence, muscle hardness or the taut band that occurs in the absence of pain may be the first abnormality, and the active TrP is a more activated TrP." "Current thinking in keeping with the expanded integrated hypothesis of the TrP is that localized ischemia is associated with the acute development and maintenance of the TrP. Localized ischemia results from capillary compression within the taut band. In turn, the release of vasodilating substances such as calcitonin gene-related peptide (CGRP) and substance P leads to localized non-inflammatory edema that further compresses capillaries. The initial change in the muscle associated with the TrP seems to be a motor abnormality, the development of the taut band."
"Sympathetic modulation of the SEA is the most important concept because of the important role the sympathetic nervous system plays in maintaining the abnormal electrical activity at the TrP. A post-synaptic muscle dysfunction that increases intracellular calcium concentration through a leaky ryanidine receptor calcium channel on the sarcoplasmic reticulum membrane or through adrenergic-mediated second-messenger systems involving protein kinase C and cyclic adenosine monophosphate (cAMP), initiating actin-myosin interaction, may also result in muscle fibril contraction….Calcium channel activity is important in the generation of TrP endplate noise…." "The association of endplate noise and the trigger zone has led to the suggestion that the trigger zone is where the endplate zone is located and that is in mid-belly of the muscle. However, the muscle mid-belly is not always obvious and depends on the specific anatomy of the muscle." "The myofascial trigger zone or region is hypoxic, a region of severe oxygen desaturation at the core surrounded by a region of increased oxygenation, consistent with capillary compression and ischemia. The core is ischemic and the surrounding zone hyperemic. Temperature studies of the trigger zone showed an increase in temperature in the TrP region, consistent with a hyperemic outer area but inconsistent with a hypoxic trigger zone core." "TrP tenderness is associated with central sensitization and hypersensitivity, as is the case with other tissues….Central sensitization is the mechanism through which referred pain occurs….One of the consequences of central sensitization is the activation of otherwise ineffective (sometimes called 'sleeping') synaptic connections from one afferent nerve fiber to many recipient nociceptive neurons. A single dorsal horn neuron will thus respond to a larger pool of afferent fiber connections, thereby greatly expanding its receptive field." "The most common referred pain patterns are within the same or adjacent spinal segments as that of the primary sensory nerve. Thus, TrPs in muscles innervated predominantly by the C5 nerve root refer pain largely to the C5 dermatome and myotome, overlapping into the C4 and C6 innervated areas. Because muscle innervation is relatively constant, segmental referred pain patterns tend to be relatively constant from one person to another….The activation of latent TrPs in one muscle results in increased motor activity in a distant muscle latent TrP in the same segmental level." "The segmental spread of referred pain can also be bilateral." "In summary, central sensitization and widespread pain referral is clinically important because individuals who have had seemingly local injury producing persistent pain can develop extraordinarily widespread pain with hyperalgesia or allodynia that appears to involve most of the body." "The proposal discussed herein is that muscle overuse, or bio-mechanical stress, is the cause of the TrP….Supramaximal muscle contraction or overloaded eccentric contraction can damage muscle and lead to pain, including delayed onset muscle soreness. Repetitive strain is a variant of muscle overload and is thought to have the same effect….The maintenance of fixed positions for long periods of time and sustained contraction of muscle as a result of emotional stress (anxiety, fear, and depression) are also thought to produce muscle overuse….There has long been a concern about the overlap of FMS and MPS, a concern now resolved with the understanding that FMS is a central pain disorder and MPS has a major central hypersensitization component. Therefore, it is not surprising that there are TrPs at many if not all of the sites selected for tender point assessment in FMS and that TrPs present as a comorbid finding in FMS can contribute to pain in FMS. Thus, the concurrence of the two conditions in individual patients with clinical pain syndromes is to be expected. Nearly one-quarter of patients with chronic cervical myofascial pain met the criteria for FMS. An earlier study found that 75 percent of subjects with FMS had clinically significant MPS. TrPs may be a peripheral pain generator initiating or sustaining FMS, or may occur secondarily to the development of central sensitization in FMS. No study has looked at the effect of treating TrPs on comorbid FMS."
"….the hyperirritable "nodule" does not have to be a palpable nodule at all. However, the taut band is a constant finding in active and latent TrPs, and is the only consistent objective finding on physical examination." "Dommerholt and Gerwin (unpublished data) found that identification of a taut band, tenderness of the taut band, and reproduction of the patient's pain were sufficient to guide effective treatment and presented this concept at the International Myopain Congress in Italy in 1998." [This is the International Myopain President's Address from the Myopain Congress 2010, and it is dedicated to David G. Simons MD. I believe Dr. Simons is very proud of it. It is strongly suggested that interested readers obtain the whole article from Journal of Musculoskeletal Pain. In my opinion, this is the best summary of myofascial medicine available. DJS]
Gerwin RD. 2010. Fibromyalgia Tender Points at Examination Sites Specified by the American College of Rheumatology Criteria Are Almost Universally Myofascial Trigger Points. Curr Pain Headache Rep. [Oct 27 Epub ahead of print]. [Until FM researchers realize that most of the symptoms they are describing as fibromyalgia-related are actually caused by myofascial trigger points, their conclusions are suspect and resources are being wasted. DJS]
Gerwin RD. 1997. Myofascial pain
syndromes in the upper extremity. J Hand Ther.
10(2):130-136. “Myofascial pain syndromes of the upper extremity
are common causes of pain that may follow trauma and are associated with
acute or chronic musculoskeletal stress. The syndromes are
characterized by the presence of the myofascial trigger point, a
physical finding that is reliably identified by palpation. Local
and referred pain are hallmarks of the syndrome, and the referred pain
patterns may mimic such conditions as radiculopathy and nerve entrapment
syndromes. Treatment is directed toward inactivating the
myofascial trigger point, correcting underlying perpetuating factors,
and restoring the normal relationships between the muscles of the
affected functional motor units.”
Gerwin RD. 1994. Neurobiology of the
myofascial trigger point. Baillieres Clin Rheumatol.
8(4):747-762. “The clinical phenomenon of the MTrP is accessible
to any clinician who takes the time to learn to palpate skeletal muscle
gently and carefully, and who is willing to learn the functional anatomy
necessary to understand the regional spread of MTrPs through functional
muscle units (Travell and Simons, 1992).” “…researchers in the
field of pain have given us an understanding of the basis for the
hyperalgesia, allodynia and the previously difficult-to-understand
finding of referred pain zones that we see daily in our patients.”
Gerwin R. 2007. Trigger points: a
comprehensive hypothesis of trigger point formation. J Musculoskel
Pain 15 (Supp 13):12 item 14. [Myopain 2007 Poster] Dr.
Gerwin’s hypothesis may fill in the missing elements in the formation of
myofascial trigger points (MTPs). We did not have an explanation for
the excess release of acetylcholine, the excess release of calcium, and the
excessive motor endplate noise, nor did we understand why the taut band
forms. These phenomenon could be explained by a dysfunctional
ryanodine receptor calcium channel. This dysfunctional ion channel
could promote the excessive calcium release from the sarcoplasmic reticulum,
resulting in persistent muscle fiber contraction. Gates in the cell wall,
like tiny airlocks in a space station, allow charged particles such as
calcium, potassium and other minerals to flow in and out of the cell
membrane and affect the interior metabolism of the cell. The pathways
are called ion channels. An illness caused by dysfunction of the gate
mechanism is called a channellopathy. This important piece of the puzzle
indicates that myofascial pain due to trigger points could be a
channellopathy. Dysfunctional mitochondria and/or second messenger
dysfunction metabolically upstream could also be responsible or be
associated with the ryanodine dysfunction. [I found this to be one of the
most exciting revelations at the Myopain ‘07 Congress, offering great hope
to those of us with myofascial pain. This offers a whole new way of
looking at myofascial pain, and perhaps a whole new way of treating it. I
hope researchers will take note and mobilize forces to investigate this.
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.
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
Gerwin, R. D. 1991. Myofascial aspects of low
back pain. Neurosurgery Clin North Am2(4):761-782.
Ghanbari A, Rahimijaberi A, Mohamadi M et al. 2012. The effect of trigger point management by positional release therapy on tension type headache. NeuroRehabilitation. 30(4):333-339. Both positional release therapy for trigger points and routine medical therapy were equally effective in treatment of tension type headache. [This could vary tremendously in regards to control of perpetuating factors, the skill of the practitioner, and the type of routine medical therapy, as we live in a world where even the recognition of trigger points is not routine. DJS]
Gharaibeh TM, Jadallah K, Jadayel FA.
2009. Prevalence of temporomandibular disorders in patients with
gastroesophageal reflux disease: a case controlled study. J
Oral Maxillofac Surg. [Dec 1 Epub ahead of print] [Temporomandibular
disorders often coexist with GERD. It is unfortunate that patients were
not checked for co-existing TrPs, as both of these conditions can be
associated with TrPs and may be interactive. It is to be hoped that
future research will consider the affect of TrP-riddled chewing muscles
on GERD, and the affect of acid fumes on throat and jaw muscle TrPs.
In the world of chronic pain, differential diagnosis must give way to
interactive diagnoses, and doctors working in chronic pain must be so
Ghazan-Shahi S, Towheed T, Hopman W. 2012. Should rheumatologists retain ownership of fibromyalgia? A survey of Ontario rheumatologists. Clin Rheumatol. [May 2 Epub ahead of print]. "Key findings were: (1) 71 % believe that rheumatologists should not retain ownership of fibromyalgia, (2) 55 % believe that fibromyalgia is primarily a psychosomatic illness as opposed to a physical illness, (3) 89 % believe that the family physician should be the main care provider for these patients, and (4) rheumatologists who consider fibromyalgia to be a physical illness were also significantly more likely to believe that rheumatologists should retain ownership of this disease…and were more likely to continue managing these patients in their practice …. The majority of Ontario rheumatologists do not wish to retain ownership of fibromyalgia. However, most of them continue to manage these patients, even though they believe that the family physician should be the main care provider for patients with fibromyalgia. Rheumatologists may be providing care to these patients primarily because this care is not available to them from their primary care physicians."
Gheita TA, Ezzat Y, Sayed S et al. 2009.
Musculoskeletal manifestations in patients with malignant disease.
Clin Rheumatol. [Nov 8 Epub ahead of print]. “Musculoskeletal
manifestations occurring during malignancies and following the treatment
represent a significant percentage of symptoms and signs which may raise a
clue to differential diagnosis.”
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
electromagnetic field exposure can alter pain sensitivity in human beings.
Giamberardino MA, Affaitati G, Costantini R. 2010. Visceral referred pain. J Musculoskel Pain. 18(4):403-410. "Visceral referred pain occurs in somatic areas neuromerically connected with the affected organs where secondary hyperalgesia takes place mostly in deep body wall tissues, extending to superficial layers in repeated/prolonged visceral processes. When two internal organs sharing part of their central sensory projection are affected, visceral pain and referred hyperalgesia from each organ are significantly enhanced ('viscero-visceral hyperalgesia'). In this case, treatment of one visceral condition significantly improves symptoms from the other. Referred phenomena are mainly sustained by central sensitization processes, involving viscero-somatic or viscero-visceral-somatic convergent neurons, as shown by electrophysiological studies in animal models. A contribution by viscero-somatic reflexes is also present, which would account for the trophic changes of deep body wall tissues that often accompany the hyperalgesia. The expression of visceral referred pain is reduced with the aging process, which renders diagnosis more difficult in the elderly, increasing the risks in life-threatening conditions. Some of the contributing mechanisms may include age-related impaired A-Delta fiber function and a reduction in the content and turnover of neurotransmitter systems involved in nociception..... Visceral referred pain and accompanying phenomena are being increasingly understood as regards their pathophysiology. This opens new avenues for treatment strategies that are more mechanism-based and not purely symptomatic."[As it is important to understand the concepts of viscero-somatic and somato-visceral referred pain, it is also important to understand how visceral pain can lead to central sensitization. As this article demonstrates, even advanced age can lead to referred visceral pain. DJS]
Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 25(2):185-198. "This article reviews the available published knowledge about the diagnosis, pathophysiology and treatment of myofascial pain syndromes from trigger points. Furthermore, epidemiologic data and clinical characteristics of these syndromes are described, including a detailed account of sensory changes that occur at both painful and nonpainful sites and their utility for diagnosis and differential diagnosis; the identification/diagnostic criteria available so far are critically reviewed. The key role played by myofascial trigger points as activating factors of pain symptoms in other algogenic conditions - headache, fibromyalgia and visceral disease - is also addressed. Current hypotheses on the pathophysiology of myofascial pain syndromes are presented, including mechanisms of formation and persistence of primary and secondary trigger points as well as mechanisms beyond referred pain and hyperalgesia from trigger points. Conventional and most recent therapeutic options for these syndromes are described, and their validity is discussed on the basis of results from clinical controlled studies."
Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Effects of Treatment of Myofascial Trigger Points on the Pain of Fibromyalgia. Curr Pain Headache Rep. [May 5 Epub ahead of print]. "FMS is mainly rooted in the central nervous system, while TrPs have a peripheral origin. However, the nociceptive impulses from TrPs may have significant impact on symptoms of FMS, probably by enhancing the level of central sensitization typical of this condition. Several attempts have been made to assess the effects of treatment of co-occurring TrPs in FMS. We report the outcomes of these studies showing that local extinction of TrPs in patients with fibromyalgia produces significant relief of FMS pain. Though further studies are needed, these findings suggest that assessment and treatment of concurrent TrPs in FMS should be systematically performed before any specific fibromyalgia therapy is undertaken."
Giamberardino, M. A., G.
Affaitati, S. Iezzi and L. Vecchiet. 1999. Referred muscle pain and hyperalgesia from viscera. J Musculoskel Pain 7(1-2):61-69.
Giamberardino, M. A., K. J. Berkley, S.
Iezzi, P. de Bigontina, and L. Vecchiet. 1997. Pain threshold variations in somatic wall tissues
as a function of menstrual cycle, segmental site and tissue depth in non-dysmenorrhic
women, dysmenorrhic women and men. Pain 71(2):187-97.
Giamberardino MA, Vecchiet J, Affaitati G et al.
2007. Antioxidative treatment for muscle symptoms in chronic fatigue
syndrome. J Musculoskel Pain 15 (Supp 13):64 item 113.
[Myopain 2007 Poster] “In CFS, prolonged treatment with Vitamin E produces
parallel improvement of oxidative stress and muscle fatigue/hyperalgesia.
The results suggest an important pathophysiologic role for OS in the genesis
of muscle symptoms in CFS.”
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
Gil, I. A., C. M. Barbosa, V. M. Pedro, K. C.
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.
Girschick HJ, Morbach H,
Tappe D. 2009. Treatment of Lyme borreliosis. Arthritis Res Ther.
11(6):258. “Borrelia burgdorferi sensu lato is the causative agent of
Lyme borreliosis in humans. This inflammatory disease can affect the
skin, the peripheral and central nervous system, the musculoskeletal and
cardiovascular system and rarely the eyes. Early stages are directly
associated with viable bacteria at the site of inflammation. The
pathogen-host interaction is complex and has been elucidated only in
part. B. burgdorferi is highly susceptible to antibiotic treatment and
the majority of patients profit from this treatment. Some patients
develop chronic persistent disease despite repeated antibiotics. Whether
this is a sequel of pathogen persistence or a status of chronic
auto-inflammation, auto-immunity or a form of fibromyalgia is highly
debated. Since vaccination is not available, prevention of a tick bite
or chemoprophylaxis is important. If the infection is manifest, then
treatment strategies should target not only the pathogen by using
antibiotics but also the chronic inflammation by using anti-inflammatory
Giske L, Bautz-Holter E, Sandvik L et al.
2009. Relationship between pain and neuropathic symptoms in chronic
musculoskeletal pain. Pain Med. [Apr 22 Epub ahead of print].
“Our study demonstrates that neuropathic symptoms are prominent features of
chronic musculoskeletal pain and are stable over time. These symptoms
were closely related to emotional distress and to the diagnosis of
fibromyalgia. The results lend support to the theory that neuropathic
symptoms represent an underlying sensitization.”
Giske L, Vollestad NK, Mengshoel AM et al. 2007.
Attenuated adrenergic responses to exercise in women with fibromyalgia – a
controlled study. Eur J Pain. [Sep 7 Epub ahead of print]
“...the exercise was perceived as being more painful and strenuous in the FM
group. Muscle performance was altered with increased muscle activity
during the exercise. Women with FM showed an attenuated Adr (plasma
adrenalin) response to repetitive isometric exercise.”
Gjesdal S, Bratberg E, Maeland JG. 2011. Gender differences in disability after sickness absence with musculoskeletal disorders: five-year prospective study of 37,942 women and 26,307 men. BMC Musculoskel Disord. 12:37. "Having children and working full time decreased the DP risk for both genders, whereas low socioeconomic status increased the risk similarly. There was a different age effect as more women obtained a DP (disability pension) below the age of 50. Increased female risk of chronicity remained for myalgia/fibromyalgia, back disorders and 'other/unspecified' after relevant adjustments, whereas men with neck disorders were at higher risk of chronicity." "When all sociodemographic and diagnostic variables were adjusted for, no gender difference remained, except for some diagnostic subgroups."
Glass JM. 2010. Cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain. 18(4):367-372. "Fibromyalgia syndrome (FMS) is characterized by chronic, widespread, musculoskeletal pain, but symptoms other than pain are common. Dyscognition is a term used to refer to subjective feelings and objective performance measures of cognitive dysfunction. In this paper, the evidence for dyscognition in FMS is reviewed. Dyscognition is a prevalent symptom among patients with FMS that can be very disruptive. Studies using self-report measures support patient reports of dyscognition, demonstrating perceived problems across a number of cognitive domains. Tests using performance-based measures of cognitive function also support patient reports of dyscognition. Furthermore, these tests have thus far revealed a pattern of impairment in working memory and attention/executive control as well as memory impairment. Dyscognition is a real and troubling symptom for many patients with fibromyalgia. However, the body of research on dyscognition in FMS is still quite small. More research is needed to understand the factors that contribute to dyscognition and treatment approaches that help with dyscognition and to understand the cognitive symptoms that are affected, including neuroimaging studies." "Although pain is the defining symptom, it is well known that other symptoms often accompany FMS, including fatigue, somatic complaints, mood disorders, and cognitive dysfunction. Researchers have used the term 'dyscognition' to refer to both self- reported cognitive problems and objective dysfunction seen on performance-based measures of cognition. Patients refer to the subjective experience of cognitive dysfunction as 'fibrofog,' and several studies point to the salience of this particular symptom. Memory and concentration problems are reported by many patients, following pain, stiffness, fatigue, and nonrestorative sleep as the most prevalent symptoms. When dyscognition problems are present, patients report that they are very disruptive." "Glass et al. found that FMS patients reported lower memory capacity, more negative change in memory, and more anxiety about memory performance than healthy age- and education-matched controls. Of interest was the fact that patients also reported more use of strategies to support memory while at the same time reporting lower self-efficacy over memory performance….Specifically, tests that focus on working memory and on executive control of attention, as well as tests of long-term verbal episodic and semantic memory, appear to be most likely to reveal dysfunction. Working memory is the ability to briefly store a small amount of information in mind while performing other mental operations….The evidence to date suggests that the aspect of working memory that is most affected in FMS is the ability to maintain attention or to manage the items in working memory, rather than with the simple storage of items for a brief period. Consistent with this view, FMS patients perform poorly on tests that involve attentional control and the ability to ignore distraction….suggest that FMS patients have a particular difficulty dealing with distraction or managing attention. This ability to manage distraction is part of a domain of cognitive abilities called executive function….In addition to working memory and attention control tests, several studies point to problems with memory function in FMS patients." "Dick et al. found that when pain was included as a covariate in their analyses, differences between FMS patients and controls became nonsignificant. These results suggest that the most important contributor to cognitive dysfunction in FMS is pain, but this is still very much a preliminary conclusion." [This article is a masterful presentation of what we know now about FM cognitive dysfunction. DJS]
Glass JM. 2009. Review of cognitive
dysfunction in fibromyalgia: a convergence on working memory and attentional
control impairments. Rheum Dis Clin North Am. 35(2):299-311.
“Clinical and laboratory evidence confirm that dyscognition is a real and
troubling symptom in fibromyalgia (FM), and that the cognitive mechanisms
most affected in FM are working memory, episodic memory, and semantic
memory. Recent evidence provides further convergence on specific
difficulty with attentional control. Dyscognition in FM…does seem to
be related to the level of pain.” [Cognitive dysfunction is real in
FM, and the need for adequate pain control is great. DJS]
Glass JM. 2006. Cognitive dysfunction in
fibromyalgia and chronic fatigue syndrome: new trends and future directions.
Curr Rheumatol Rep. 8(6):425-429. “Fibromyalgia (FM) and chronic
fatigue syndrome (CFS) patients often have memory and cognitive complaints.
Objective cognitive testing demonstrates long-term and working memory
impairments. In addition, CFS patients have slow information
processing, and FM patients have impaired control of attention, perhaps due
to chronic pain. Neuroimaging studies demonstrate cerebral
abnormalities and a pattern of increased neural recruitment during cognitive
tasks. Future work should focus on the specific neurocognitive systems
involved in cognitive dysfunction in each syndrome.”
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
Glass JM, Lyden AK, Petzke F et al. 2004. The effect of brief
exercise cessation on pain, fatigue, and mood symptom development in
healthy, fit individuals. J Psychosom Res 57(4):391-398.
“A subset of subjects developed symptoms of pain, fatigue, mood changes
after exercise deprivation. This cohort was different from the
individuals who did not develop symptoms in baseline measures of HPA
axis, immune, and autonomic function. We speculate that a subset
of healthy individuals who have hypoactive function of the biological
stress response systems unknowingly exercise regularly to augment the
function of these systems and suppress symptoms. These individuals
may be at risk for developing chronic multisymptom illnesses when a
'stress' leads to lifestyle changes that disrupt regular exercise.”
Glass JM, Williams DA, Fernandez-Sanchez ML et al. 2011. Executive Function in Chronic Pain Patients and Healthy Controls: Different Cortical Activation During Response Inhibition in Fibromyalgia. J Pain. [Sep 24 Epub ahead of print]. "Neural activation (fMRI) during response inhibition was measured in fibromyalgia patients and controls. FM patients show lower activation in the inhibition and attention networks and increased activation in other areas. Inhibition and pain perception may use overlapping networks: resources taken up by pain processing may be unavailable for other processes." The brain can be so occupied dealing with pain input that it can't handle other tasks. Multitasking can only go so far, especially if the brain is handling pain from multiple sources.
Gleberzon B, Stuber K. 2013. Frequency of use of diagnostic and manual therapeutic procedures of the spine taught at the Canadian Memorial Chiropractic Collage: preliminary survey of Ontario chiropractors. Part 1—practice characteristics and demographic profiles. J Can Chiropr Assoc 57(1):32-41. This study got a low response rate, but those responding reported highest use for "diversified technique" with specific trigger point therapy in second.
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Gleitz M, Hornig K. 2012. [Trigger points - Diagnosis and treatment concepts with special reference to extracorporeal shockwaves]. Orthopade. 41(2):113-125. [German] "The 70-year-old trigger point theory has experienced a growing scientific confirmation and clinical significance as a consequence of recent muscle pain research....The most effective conventional forms of treatment are aimed at a direct mechanical manipulation of the trigger point as are new forms of therapy with focused and radial shockwaves. By using high pressures the focused shockwaves in particular are suitable to provoke local and referred pain and thus simplify the trigger point diagnosis....Overall, the shockwave therapy on muscles represents a confirmation and extension of the existing trigger point therapy. It seems to be suitable for treating functional muscular disorders and myofascial pain syndromes within the locomotor system."
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[This article may provide clues as to some of the mechanisms of some of
the autonomic concomitants of specific TrPs. DJS]
Gockel U, Tolle T. 2007. Fibromyalgic vs. neuropathic pain.
J Musculoskel Pain 15 (Supp 13):48 item 83. [Myopain 2007
Poster] “The pain experienced subjectively by FMS patients is
conspicuously greater than that experienced by other patients with
typical neuropathic complaints. Furthermore, this pain is
associated with more severe co-morbidities such as depression/anxiety
and sleep disturbance.”
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last 15 years, clinical and experimental data have emerged that suggest that
peripheral and central, glial-mediated neuroimmune activation is both
necessary and sufficient to sustain chronic pain. Immune modulation appears
to be, therefore, a possible new therapeutic option..... IVIG therapy may
emerge as a novel treatment modality for refractory cases. However, before
this drug can be confidently used by clinicians, important questions need to
be answered concerning optimal treatment doses, duration of treatment, and
its effect on function and quality of life.” [Other less invasive glial cell
modulators such as topical pentoxifylline may be potential sources of
calming down glial cells. DJS]
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Our findings are compatible with the hypothesis that inspiratory flow
limitation during sleep plays a role in the development of the functional
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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.
Goldenberg DL, Burchkardt C, Crofford L. 2004. JAMA 292(19):2388-2395.
“Despite the chronicity and complexity of FMS, there are pharmacological and
nonpharmacological interventions available that have clinical benefit.”
[FMS is treatable,]
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"This study aimed to evaluate the relation of disability and physical and mental health status with potentially traumatic life events (PTLE) before the onset of fibromyalgia in women diagnosed with this syndrome. We also investigated causal attribution of fibromyalgia to a triggering event, physical or psychological in nature, and its relation with the health measures and the adverse life events….There were no statistically significant relations between the health measures (disability, physical and mental health, and pain) and the PTLE. The predominant attribution was to a physical event. There were no significant differences neither in the health measures across causal attribution status….nor in the PTLE not in childhood….There were significant differences across causal attribution status in the PTLE in childhood…., specifically between the group that made a psychological attribution and the group that made no attribution….with the former having a higher score of PTLE in childhood. The results raise questions about the importance of psychological aspects in the appraisal of the adverse events and its possible relation to the psychological functioning in women with fibromyalgia." [Many symptoms now attributed to FM may be due to co-existing conditions. FM is heterogeneous. DJS]
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Sleep studies must include evaluation for UARS, and patients
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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 FMS and
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.
Gur, A., M. Karakoe, K. Nas et al.
2002. Effects of low power laser and low dose amitriptyline therapy on
clinical symptoms and quality of life in fibromyalgia: a single-blind,
placebo-controlled trial. Rheumatol Int 22(5):188-93. Active low-power
gallium-arsenide laser therapy and/or amitriptyline therapy may be effective
for fibromyalgia patients.
Gurer G, Sendur OF, Ay C. 2005. Serum lipid
profile in fibromyalgia women. Clin Rheumatol. [Oct 1 Epub
ahead of print] “In the FM group, we could not find a significant
correlation between the serum lipid profile values and the FM parameters
(p>0.05).” [This research confirms the research of Dr. Salih Ozgocmen
and his team. They found that in patients with both fibromyalgia and
chronic myofascial pain who had high lipid profiles, the high lipid profile
was related to the myofascial pain component and not the fibromyalgia. DJS]
Gursoy S, Erdal E, Sezgin M et al. 2007. Which
genotype of MAO gene that the patients have are likely to be most
susceptible to the symptoms of fibromyalgia? Rheumatol Int.
[Sep 20 Epub ahead of print] “It seems plausible to say that MAOA-dependent
metabolism of the biological amines may be partly related to high-activated
MAO-A, allele 3, in the occurrence of FS among Turkish population.”
Gursoy, S., Erdal, E., Herken, H., et
al. Significance of catechol-O-methyltransferase gene polymorphism in
fibromyalgia syndrome. Rheumatol Int 23(3):104-7. [This
research may have implications in the treatment of FMS, as well as genetic
tendency to develop FMS. It indicates that the metabolism of catechol
drugs in FMS patients may be different. DJS]
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.
Gustaw K. 2000. Myofascial pain syndrome in farmers – a
comprehensive approach to treatment. Ann Agric Environ Med
7(2):95-99. “The MPS syndrome was found to be relatively common in
Polish farmers and formed 12.7% of all chronic pain syndromes diagnosed
in the Institute of Agricultural Medicine during 18 months.”
Gutierrez-Reyes G, Lopez-Ortal P, Sixtos S
et al. 2006. Effect of pentoxifylline on levels of
pro-inflammatory cytokines during chronic hepatitis C.
Scand J Immunol 63(6):461-467. Pentoxifylline may be
helpful in controlling cytokine storms such as may occur in
hepatitis C. [And FMS, and avian influenza. DJS]
Guttu RL, Page DG, Laskin DM. 1990. Delayed healing of muscle
after injection of bupivicaine and steroid. Ann Dent
49(1):5-8. “Bupivicaine produces more tissue reaction than
procaine and that the addition of steroid to bupivicaine increases the
initial tissue damage and prolongs the healing phase.” [Some
physicians still use bupivicaine (Marcaine) for TrP injections, although
research shows that procaine or lidocaine are much less toxic and more
useful for these injections. DJS]
Guven H, Cilliler AE, Comoglu SS. 2012. Cutaneous allodynia in patients with episodic migraine. Neurol Sci. [Nov 23 Epub ahead of print]. "The results of present study revealed that cutaneous allodynia was rather frequent in episodic migraine, particularly in patients having longer disease duration. Higher frequency of allodynia in women and its association with menstrually related migraine may be related to the effects of hormonal factors on cutaneous pain thresholds and central sensitization. Association of nausea and phonophobia with allodynia may be interpreted as the common pathways are shared in the development of these symptoms."
Guymer EK, Clauw
DJ.2002 Treatment of fatigue in fibromyalgia. Rheum Dis Clin
North Am 2002 28(2):367-78. "Clearly,
fatigue is a large and challenging problem for those suffering
from fibromyalgia. It adds greatly to the morbidity and
disability associated with the disease. In the management of this
specific symptom in fibromyalgia, attention should first be
focused on identifying comorbidities that may be present and
contribute to fatigue. As with other symptoms of fibromyalgia,
education is a critical component of management. Easier access to
well designed nonpharmacologic therapies is essential, because
these treatments are underutilized in clinical practice at
Haak T, Scott
B. 2007. The effect of Qigong on fibromyalgia (FMS): a controlled
randomized study. Disabil Rehabil. [Jun 15 Epub ahead of
print] “…Qigong has positive and reliable effects regarding FMS.”
“…Qigong intervention could be a useful complement to medical treatment for
subjects with FMS.”
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Hainaut, K. and J. Duchateau. 1992. Neuromuscular
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Hadjistavropoulos, H. D., F. K. MacLeod and G. J.
Asmundson. 1999. Validation of the Chronic Pain Coping Inventory. Pain
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
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A, Birtane M, Gurcan S et al. 2003. Efficacy of low level laser
therapy in myofascial pain syndrome: An Algometric and thermographic
evaluation. Lasers Surg Med 33(5):339-343.
“LLLT seemed to be beneficial for pain in MPS...” documented by
algometry and thermography.
Hakonarson H, Thornorsson A. 2001. [Common
causes of sleep disturbances in Icelandic children who undergo sleep
studies.] Laeknabladid 87(10):799-804. [Icelandic] “…both OSA and
GER are common problems in children with sleep disturbances. We
conclude that sleep studies are important in the overall workup of children
with sleep disturbances….”
Hall AM, Maher CG, Lam P et al. 2011. Tai chi exercise for treatment of pain and disability in people with persistent low back pain: A randomized controlled trial. Arthritis Care Res (Hoboken). 63(11):1576-1583. "Tai chi exercise reduced bothersomeness of back symptoms by 1.7 points on a 0-10 scale, reduced pain intensity by 1.3 points on a 0-10 scale, and improved self-report disability by 2.6 points on the 0-24 Roland-Morris Disability Questionnaire scale. The follow-up rate was >90% for all outcomes. These results were considered a worthwhile treatment effect by researchers and participants."
Hall, S. 1999. Common pain scenarios. Aust
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Hallberg, L. R. and S. G. Carlsson. 1998.
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fibromyalgia. Eur J Pain 2(4):309-319.
Hamada H, Moriwaki K,
Shiroyama K et al. 2000. Myofascial pain in patients with postthoracotomy
pain syndrome. Reg Anesth Pain Med. 25(3):302-305.
“Postthoracotomy pain may result, at least in part, from a nonneuropathic
origin (myofascial pain). It is recommended that each patient be
examined in detail to determine whether there is a trigger point in a taut
muscular band within the scapular region. If found, this point is
suggested as a good area for anesthetic injection.”
Hameed H, Hameed M, Christo PJ. 2010. The
effect of morphine on glial cells as a potential therapeutic target for
pharmacological development of analgesic drugs. Curr Pain Headache Rep.14(2):96-104.
“Opioids have played a critical role in achieving pain relief in both modern
and ancient medicine. Yet, their clinical use can be limited secondary to
unwanted side effects such as tolerance, dependence, reward, and behavioral
changes. Identification of glial-mediated mechanisms inducing opioid side
effects include cytokine receptors, kappa-opioid receptors, N-methyl-D-aspartate
receptors, and the recently elucidated Toll-like receptors. Newer agents
targeting these receptors such as AV411, MK-801, AV333, and SLC022, and
older agents used outside the United States or for other disease conditions,
such as minocycline, pentoxifylline, and UV50488H, all show varied but
promising profiles for providing significant relief from opioid side
effects, while simultaneously potentiating opioid analgesia.”
Hameroff SR, Crago BR,
Blitt CD et al. 1981. Comparison of bupivacaine, etidocaine, and
saline for trigger-point therapy. Anesth Analg. 60(10):752-755.
“Injections of local anesthetics, saline, ‘dry needling’, or other stimuli
at specific, tender loci (trigger or acupuncture points) are reportedly
efficacious in treatment of chronic pain syndromes.” “Trigger-point
injections with bupivacaine and etidocaine were generally preferred over
saline in several pain-tested categories.” [There are other options.
It would be interesting to study the use of procaine or lidocaine, which
have been shown to be as effective as bupivicaine without being as toxic.
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.
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Hamnes B, Hauge MI, Kjeken I et al. 2011. 'I have come here to learn how to cope with my illness, not to be cured': A Qualitative Study of Patient Expectations Prior to a One-Week Self-Management Program. Musculoskeletal Care. [Jul 20 Epub ahead of print]. "Self-management programs (SMPs) have been developed to help patients with chronic rheumatic diseases to manage their health problems. Patients' expectations prior to treatment are important determinants of outcomes, and should therefore be identified, to ensure that interventions meet the participants' needs. The aim of the present study was to determine participant expectations with respect to a one-week inpatient SMP for those with fibromyalgia (FM) and rheumatoid arthritis (RA).....The findings show that the participants expected the SMP to be a turning point towards a better future and to empower them to assume more responsibility for their own health and self-care. They also expected the SMP to facilitate acceptance, help them to gain new knowledge and be a forum in which to share their experience. Participants who were employed assumed that participation in the SMP would help to ensure that they would continue in their jobs.....This qualitative study indicated that identifying expectations prior to an SMP provides important information which has implications for the program's implementation. Additional themes, such as acceptance of the illness and management of work, should also be included in the programs and they should focus more on sharing experience."
Han L, Ma C, Liu Q et al. 2013. A subpopulation of nociceptors specifically linked to itch. Nat Neurosci 16(2):174-182. This team has found a new itch-specific type of neuron in mice. This is a big first step in developing itch-specific therapies that will stop itching that anti-histamines don't help.
Han HS, Suk K. 2005. The function and
integrity of the neurovascular unit rests upon the integration of the
vascular and inflammatory cell systems. Curr Neurovasc Res.
2(5):409-423. “In an effort to understand the pathogenesis and find
rational treatments against inflammatory disorders in brain, studies have
been separately carried out using either endothelial cells or microglia.
Increased evidence, however, indicates that a crosstalk between these two
cell types is important for the brain inflammation.”
Han SC, Harrison P. 1997. Myofascial pain syndrome and
trigger-point management. Reg Anesth 22(1):89-101. “A
multidisciplinary approach to treatment appears to be most beneficial
and may include such modalities as trigger-point injections, dry
needling, stretch and spray, and transcutaneous electrical nerve
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.
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
Handwerker, H. O. , C. Forster and C. Kirchhoff. 1991.
Discharge patterns of human C-fibers into used by itching and burning stimuli. J
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Hannonen, P., K. Malminiemi, U. Yli-Kerttula, R. Isomeri
and P. Roponen. 1998. A randomized, double-blind, placebo-controlled study of
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Hansson E, Svensson H, Brorson H. 2012. Review of Dercum's disease and proposal of diagnostic criteria, diagnostic methods, classification and management. Orphanet J Rare Dis. 7(1):23. "We propose the minimal definition of Dercum's disease to be generalized overweight or obesity in combination with painful adipose tissue. The associated symptoms in Dercum's disease include obesity, fatty deposits, easy bruisability, sleep disturbances, impaired memory, depression, difficulty concentrating, anxiety, rapid heartbeat, shortness of breath, diabetes, bloating, constipation, fatigue, weakness and joint and muscle aches….The prevalence of Dercum's disease has not yet been exactly established. Aetiology: Proposed, but unconfirmed aetiologies include: nervous system dysfunction, mechanical pressure on nerves, adipose tissue dysfunction and trauma. Diagnosis and diagnostic methods: Diagnosis is based on clinical criteria and should be made by systematic physical examination and thorough exclusion of differential diagnoses. Advisably, the diagnosis should be made by a physician with a broad experience of patients with painful conditions and knowledge of family medicine, internal medicine or pain management. The diagnosis should only be made when the differential diagnoses have been excluded ….Differential diagnoses include: fibromyalgia, lipoedema, panniculitis, endocrine disorders, primary psychiatric disorders, multiple symmetric lipomatosis, familial multiple lipomatosis, and adipose tissue tumors….The following treatments have lead to some pain reduction in patients with Dercum's disease: Liposuction, analgesics, lidocaine, methotrexate and infliximab, interferon -2b, corticosteroids, calcium-channel modulators and rapid cycling hypobaric pressure. As none of the treatments have led to long lasting complete pain reduction and revolutionary results, we propose that Dercum's disease should be treated in multidisciplinary teams specialized in chronic pain. Prognosis: The pain in Dercum's disease seems to be relatively constant over time." [Dercum's may be mistaken for either FM or CMP, coexisting with insulin resistance. DJS]
Hanten WP, Olson SL,
Butts NL et al. 2000. Effectiveness of a home program of ischemic
pressure followed by sustained stretch for treatment of myofascial
trigger points. Phys Ther. 80(10):997-1003.
“Myofascial trigger points (TPs) are found among patients who have neck
and upper back pain.” “A home program, consisting of ischemic
pressure and sustained stretching, was shown to be effective in reducing
TP sensitivity and pain intensity in individuals with neck and upper
back pain. The results of this study indicate that clinicians can
treat myofascial TPs through monitoring of a home program of ischemic
pressure and stretching.” [This may provide some temporary relief,
but no treatment of TrPs will be complete without identification and
control of perpetuating factors. DJS]
Hao J, Ruel J, Coste B et al. 2013. Piezo-electrically driven mechanical stimulation of sensory neurons. Methods Mol Biol. 998:159-170. "Mechanotransduction, the conversion of a mechanical stimulus into a biological response, constitutes the basis of a variety of physiological functions such as the senses of touch, balance, proprioception, blood pressure, and hearing. In vertebrates, mechanosensation is mediated by mechanosensory neurons, whose cell bodies are located in trigeminal and dorsal root ganglia. Here, we describe an in vitro model of mechanotransduction that provides an opportunity to explore the properties of mechanosensitive channels in mammalian sensory neurons. The mechano-clamp method allows applying local force on plasma membrane of whole-cell patch-clamped sensory neurons. This technique uses a mechanical probe driven by a computer-assisted piezoelectric microstage to repeatedly stimulate sensory neurons with accurate control of stimulus strength, duration, and speed." [Considering the piezoelectrical properties of myofascia, this might prove interesting. DJS]
Hapidou, E. G. and G. B. Rollman. 1998. Menstrual
cycle modulation of tender points. Pain 77(2):151-61
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.
Hargrove JB, Bennett RM, Clauw DJ. 2012. Long-Term Outcomes in Fibromyalgia Patients Treated with Noninvasive Cortical Electrostimulation. Arch Phys Med Rehabil. [Apr 20 Epub ahead of print]. "Sixty-nine originally studied subjects were eligible, 39 of which were mailed surveys. There was a 64% survey return rate. The total FIQ score was 52.6 at baseline, 35.7 at end-of-study and 31.8 at follow-up….Subjects reported symptom improvements lasting at least two-years, with a reduction or elimination of medicine use and need to see physicians for FM….A high percentage of FM patients treated with RINCE (Reduced Impedance Noninvasive Cortical Electrostimulation) continued to experience worthwhile improvement at follow-up."
Hargrove JB, Bennett RM, Simons DG et al. 2012. A randomized placebo-controlled study of noninvasive cortical electrostimulation in the treatment of fibromyalgia patients. Pain Med. 13(1):115-124. " Noninvasive cortical electrostimulation in FM patients provided modest improvements in pain, TeP (tender points) measures, fatigue, and sleep; and the treatment was well tolerated. This form of therapy could potentially provide worthwhile adjunctive symptom relief for FM patients."
Hargrove JB, Bennett RM, Simons DG et al. 2010. Quantitative electroencephalographic abnormalities in fibromyalgia patients. Clin EEG Neurosci. 41(3):132-139. "There is increasing acceptance that pain in fibromyalgia (FM) is a result of dysfunctional sensory processing in the spinal cord and brain, and a number of recent imaging studies have demonstrated abnormal central mechanisms. The objective of this report is to statistically compare quantitative electroencephalogram (qEEG) measures in 85 FM patients with age and gender matched controls in a normative database....A consistent and significant negative correlation was found between pain severity and the magnitude of the EEG abnormalities. No relationship between EEG findings and medicine use was found. It is concluded that qEEG analysis reveals significant differences between FM patients compared to age and gender matched healthy controls in a normative database, and has the potential to be a clinically useful tool for assessing brain function in FM patients."
Harlow, B. L., L. B. Signorello, J. E. Hall, C. Dailey and
A. L. Komaroff. 1998. Reproductive correlates of chronic fatigue syndrome. Am
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Harrell JS, Chiou-Tan
FY, Zhang H et al. 2009. Procedure-oriented sectional anatomy of
the shoulder. J Comput Assist Tomogr. 33(5):814-817.
“This paper provides anatomically accurate schematics of the shoulder
anatomy relevant to needle procedures.” “The schematics allow for
safer and more accurate non-image-guided needle procedures in the
Harrington MG, Chekmenev EY, Schepkin V et al. 2011. Sodium MRI in a rat migraine model and a NEURON simulation study support a role for sodium in migraine. Cephalalgia. [Aug 4 Epub ahead of print]. During a migraine-like state in rats, "...sodium rises to levels that increase neuronal excitability. We propose that rising sodium in CSF (cerebrospinal fluid) surrounding trigeminal nociceptors increases their excitability and causes pain and that rising sodium in vitreous humor increases retinal neuronal excitability and causes photosensitivity."
Harris, A. J. 1999. Cortical origin of
pathological pain. Lancet 354(9188):1464-6.
Harris RE. 2010. Elevated excitatory neurotransmitter levels in the fibromyalgia brain. Arthritis Res Ther. 12(5):141. "Consistent brain imaging findings demonstrate that neurobiological factors may contribute to the pathology of 'central' pain states such as fibromyalgia (FM). Studies using proton magnetic resonance spectroscopy suggest that glutamate (Glu), a key excitatory neurotransmitter, may be present in higher concentrations within the brains of FM patients. This neurotransmitter imbalance is present in multiple brain regions that have been implicated in processing pain information. However, it is unknown if elevated Glu is acting at the synapse. New investigations are needed to investigate the molecular action of Glu in FM and to investigate these findings during treatment that modulates glutamatergic neurotransmission."
Harris RE, Sundgren PC, Craig AD
et al. 2009. Elevated insular glutamate in fibromyalgia is
associated with experimental pain. Arthritis Rheum.
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
There is now “overwhelming data” that indicate FMS is real, with genetic
predisposition. Functional magnetic resonance imaging (fMRI) and
single photon emission computed tomography (SPECT) show significant
difference between FMS patients and others. It is not a
psychological, functional or “somatic” disorder. A variation in
the gene that encodes the enzyme catechol-O-methyl transferase,
significantly affects pain sensitivity and pain-related emotions and
feelings. This enzyme also is related to development of TMJD. The
pain is real, and it can be shown by radiological studies.
Harrison, D. E., R. Cailliet, D. D. Harrison, S. J.
Troyanovich and S. O. Harrison. 1999. A review of biomechanics of the central nervous
systemPart I: spinal canal deformations resulting from changes in posture. J
Manipulative Physiol Ther 22(4):227-34.
Hart FX. 2009. Cytoskeletal forces
produced by extremely low-frequency electric fields acting on
extracellular glycoproteins. [Jul 10 Epub ahead of print]. This
article may explain one of the mechanisms by which microcurrent and
other electroceutical devices
can create changes in the cellular matrix.
Hart, P., S. Townley, M.
Grimbaldston et al. 2002. Mast cells, neuropeptides, histamine, and
prostagladins in UV-induced systemic immunosuppression. Methods 28(1):79.
This article points out the direct correlation between dermal mast
cell prevalence and susceptibility to UVB-induced systemic immunosuppression
in mice. [Above normal counts of mast cells have been found in fibromyalgia
patients.] The authors propose histamine and prostaglandin E2 are important
in downstream immunosuppression.
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.
Harvey, A. G. and R. A. Bryant. 1999.
Predictors of acute stress following motor vehicle accidents. J Trauma Stress
Hashkes PJ, Friedland O, Jaber
L et al. 2004. Decreased pain threshold in children with growing pains.
J Rheumatol 31(3):610-613. Growing pain may be indicative of developing fibromyalgia tender points, according to this research, but they did not check for co-existing myofascial TrPs.
Growing pains are often due to TrPs. Research that takes them into account would be more valuable, because we
can't know if the link between the tender points and the growing pains is coincidental.
Hassett AL, Epel E, Clauw DJ et al. 2012. Pain is associated with short leukocyte telomere length in women with fibromyalgia. J Pain. 13(10):959-969. "Telomere length, considered a measure of biological aging, is linked to morbidity and mortality. Psychosocial factors associated with shortened telomeres are also common in chronic pain; yet, little is known about telomere length in pain populations. Leukocyte telomere length was evaluated in 66 women with fibromyalgia and 22 healthy female controls....Our findings support a link between premature cellular aging and chronic pain. These preliminary data imply that chronic pain is a more serious condition than has typically been recognized in terms of bodily aging."
Hassett AL, Radvanski DC, Vaschillo EG et al. 2007.
A pilot study of the efficacy of heart rate variability (HRV) biofeedback in
patients with fibromyalgia. Appl Psychophysiol Biofeedback.
[Jan 12 Epub ahead of print] “These data suggest that HRV biofeedback may
be a useful treatment for FM, perhaps mediated by autonomic changes.
While HRV effects were immediate, blood pressure, baroreflex, and
therapeutic effects were delayed. This is consistent with data on the
relationship among stress, HPA axis activity, and brain function.”
Hauser W. 2005. [Fibromyalgia in the legal
procedures of the German Sozialgericht – psychosocial risk factors and
predictors of health care utilization] Psychother Psychosom Med
Psychol. 55(2):72-78 [German] “Former and current psychiatric
disorders, biographic adverse experiences, duration of generalized pain,
sex and social class had no substantial predictive value on the
extensive health care utilization (number of doctors, pain-related
hospital and rehabilitation stays and pain-related operations).”
[This is important, as other studies have indicated that some chronic
conditions, such as fibromyalgia, can impact health care utilization.
Hauser W, Bohn D, Kuhn-Becker H et al. 2012. Is the association of self-reported childhood maltreatments and adult fibromyalgia syndrome attributable to depression? A case control study. Clin Exp Rheumatol. [Nov 6 Epub ahead of print]. Systematic reviews of case-control studies demonstrated an association between self-reported childhood sexual and physical abuse and fibromyalgia syndrome (FMS). We tested in a case-control study if the association of self-reported childhood maltreatments in childhood and in adult FMS-patients is attributable to depression....Reports of FMS-patients some on childhood maltreatments were biased by depressed mood. However, the difference in self-reported childhood sexual abuse between adult FMS-patients and population controls was not attributable to depression.
Hauser W, Kuhn-Becker H, von Wilmoswky H et al. 2011. Demographic and clinical features of patients with fibromyalgia syndrome of different settings: a gender comparison. Gend Med. 8(2):116-125. "A total of 1023 patients (885 female, 138 male) were included in the analysis..... We found no relevant gender differences in the clinical picture of FMS. The assumption of well-established gender differences in the clinical picture of FMS could not be supported."
Hauser W, Petzke F, Sommer C. 2010.
Systematic review with met analysis: comparative efficacy and harms of
duloxetine, milnacipran, and pregabalin in fibromyalgia syndrome. J Pain.
[Apr 23 Epub ahead of print]. “Duloxetine (DLX), milnacipran (MLN), and
pregabalin (PGB) are the only drugs licensed by the US Food and Drug
Administration (FDA) for fibromyalgia syndrome (FMS). Evidence on the
comparative benefits and harms is still accruing. .... Outcomes of interest
were symptom reduction (pain, fatigue, sleep disturbance, depressed mood,
reduced health-related quality of life), and adverse events. 17 studies with
7,739 patients met the inclusion criteria. The 3 drugs were superior to
placebo except DLX for fatigue, MLN for sleep disturbance, and PGB for
depressed mood. Adjusted indirect comparisons indicated no significant
differences for 30% pain relief and dropout rates due to adverse events
between the 3 drugs. Significant differences in average symptom reduction
were found: DLX and PGB were superior to MLN in reduction of pain and sleep
disturbances. DLX was superior to MLN and PGB in reducing depressed mood.
MLN and PGB were superior to DLX in reducing fatigue. The risk of headache
and nausea with DLX and MLN was higher compared with PGB. The risk of
diarrhea was higher with DLX compared to MLN and PGB. There is evidence for
the short-term (up to 6 months) efficacy of DLX, MLN, and PGB. Differences
with regard to the occurrence of the key symptoms of FMS and to
drug-specific adverse events may be relevant for the choice of medication.
PERSPECTIVE: This article presents comparative data on the efficacy and
harms of duloxetine, milnacipran, and pregabalin in fibromyalgia syndrome.
The results can help clinicians in choosing medication since the 3 drugs
have different effects on the key symptoms of fibromyalgia syndrome and
differences in side effects, contraindications, and warnings.”
Hauser W, Petzke F, Uceyler N et al. 2010. Comparative efficacy and acceptability of amitriptyline, duloxetine and milnacipran in fibromyalgia syndrome: a systematic review with meta-analysis. Rheumatology (Oxford). [Nov 14 Epub ahead of print]. In adjusted indirect comparisons, AMT was superior to DLX and MLN in reduction of pain, sleep disturbances, fatigue and limitations of HRQOL. DLX was superior to MLN in reducing pain, sleep disturbances and limitations of HRQOL. MLN was superior to DLX in reducing fatigue. There were no significant differences in acceptability of the three drugs.....AMT cannot be regarded as the gold standard of FMS therapy with antidepressants because of the (major) methodological limitations of its trials."
Hauser W, Urrutia G, Tort S et al. 2013. Serotonin and noradrenaline reuptake inhibitors (SNRIs) for fibromyalgia syndrome. Cochrane Database Syst Rev. 1:CD010292. "The SNRIs duloxetine and milnacipran provided a small incremental benefit over placebo in reducing pain. The superiority of duloxetine and milnacipran over placebo in reducing fatigue and limitations of QOL (quality of life) was not substantial. Duloxetine and milnacipran were not superior to placebo in reducing sleep problems. The dropout rates due to adverse events were higher for duloxetine and milnacipran than for placebo. The most frequently reported symptoms leading to stopping medication were nausea, dry mouth, constipation, headache, somnolence/dizziness and insomnia. Rare complications of both drugs may include suicidality, liver damage, abnormal bleeding, elevated blood pressure and urinary hesitation."
Hautanen, A., K. Raikkonen and H. Adlercreutz. 1997.
Associations between pituitary-adrenocortical function and abdominal obesity,
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Havas M. 2006. Electromagnetic
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diabetes and multiple sclerosis. Electromagn Biol Med.
25(4):259-268. “Several disorders, including asthma, ADD/ADHD, diabetes,
multiple sclerosis, chronic fatigue, and fibromyalgia, are increasing at an
alarming rate, as is electromagnetic pollution in the form of dirty
electricity, ground current, and radio frequency radiation from wireless
devices. The connection between electromagnetic pollution and these
disorders needs to be investigated and the percentage of people sensitive to
this form of energy needs to be determined.” [One might want to add
CMP to this list, especially if FMS amplification is part of the picture.
Hawk C, Long CR,
Rowell RM et al. 2005. A randomized trial investigating a
chiropractic manual placebo: a novel design using standardized forces in
the delivery of active and control treatments. J Altern
Complement Med. 11(1):109-117. “Patients in the control group
were not successfully blinded; however, patients’ perceptions of
treatment group assignment did not significantly affect outcomes.
The clinically significant improvement in both groups, independent of
patient or clinician expectations, suggests the presence of therapeutic
factors common to both groups, other than biomechanical force.
Further studies examining other aspects of the clinical encounter,
considered separately from biomechanical force, are warranted before
arbitrarily designating any intervention as a ‘placebo’.”
Hawk, C., C. Long and A. Azad. 1997. Chiropractic care for
women with chronic pelvic pain: a prospective single-group intervention study. J
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Hayashi K, Ozaki N, Kawakita K et al. 2011. Involvement of NGF in the rat model of persistent muscle pain associated with taut band. J Pain. 12(10):1059-1068. In rats, the taut band associated with myofascial TrPs can be affected by the administration of nerve growth factor (NGF). Mice that received the NGF receptor (TrkA) inhibitor K252a had significantly decreased hyperalgesia related to taut bands. "...NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS."
Hayden RJ, Louis DS, Doro C. 2005.
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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
Hayes, J. A. 1998. TAC-TIC therapy: a
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“Adequate acupuncture treatment may reduce chronic pain in the neck and
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common objective abnormality in FM that is independent of measurements
of disease activity.” [ It would be helpful if co-existing TrPs
were evaluated, as muscle weakness occurs with TrPs even before pain.
Muscle weakness noted in this study could be due to co-existing TrPs.
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type of work tasks, the ability to influence the work situation, and
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More knowledge is needed about how to adjust work conditions for
people with partial work ability to the benefit of society and the
Henriksson CM. 1995. Living with continuous
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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.”
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syndrome: translating science into clinical practice. J Musculoskel
Pain. 17(2):189-194. “The biological part of FMS reflects a
long-standing or permanent change in the function of the nociceptive nervous
system that can be equated with a disease. It is hoped that upgrading
FMS from illness to disease will increase the awareness of FMS among health
personnel. This will in turn help patients with FMS to get correct
diagnosis and treatment.”
Henriksson, K. G. 2001. Is fibromyalgia
a central pain state? J Musculoskel Pain 10(1/2):45:57. "There is
strong support for the notion that pain and allodynia/hyperalgesia in FMS
have an organic cause. The hyperexcitability in the nociceptive nervous
system is mainly due to changes in the CNS." " The permanent
changes constitute a disease. There are methods for objectively diagnosing
this disease." "Many causes could initiate and maintain the
disease: e.g., long-standing local or regional musculoskeletal pain, changes
in stress-regulating systems, hormonal changes, changes in serotonin
metabolisms, and genetic factors."
[This includes chronic myofascial pain as a perpetuating factor of
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
myologists view. Baillieres Best Pract Res Clin Rheumatol 13(3):455-61.
Henriksson KG, Sorensen J. 2002. The promise
of N-methyl-D-aspartate receptor antagonists in fibromyalgia.
Rheum Dis Clin North Am. 28(2):343-351. “The combination of a
weak opioid and an NMDA-receptor antagonist with few side effects is
presently a promise for treatment of pain in a subgroup of patients with
Henriksson K. G., Sorensen
J. 2002. The promise of N-methyl-D-aspartate receptor antagonists
in fibromyalgia. Rheum Dis Clin North Am 28(2):343-51.
"The combination of a weak opioid and
an NMDA-receptor antagonist with few side effects is presently a
promise for treatment of pain in a subgroup of patients with FM."
Henriksson M, Henriksson J, Bergenius J. 2011. Gait initiation characteristics in elderly patients with unilateral vestibular impairment. Gait Posture. [Mar 28 Epub ahead of print]. "....chronically impaired vestibular function leads to a different strategy to create forward momentum to the body. In addition, there is evidence that vestibular patients have diminished postural stability, or alternatively a more cautious behavior, when initiating the second step."
Henriques DY, Cressman EK. 2012. Visuomotor adaptation and proprioceptive recalibration. J Mot Behav. 44(6):435-444. "Motor learning, in particular motor adaptation, is driven by information from multiple senses. For example, when arm control is faulty, vision, touch, and proprioception can all report on the arm's movements and help guide the adjustments necessary for correcting motor error. In recent years we have learned a lot about how the brain integrates information from multiple senses for the purpose of perception. However, less is known about how multisensory data guide motor learning. Most models of, and studies on, motor learning focus almost exclusively on the ensuing changes in motor performance without exploring the implications on sensory plasticity. Nor do they consider how discrepancies in sensory information (e.g., vision and proprioception) related to hand position may affect motor learning. Here, we discuss research from our lab and others that shows how motor learning paradigms affect proprioceptive estimates of hand position, and how even the mere discrepancy between visual and proprioceptive feedback can affect learning and plasticity. Our results suggest that sensorimotor learning mechanisms do not exclusively rely on motor plasticity and motor memory, and that sensory plasticity, in particular proprioceptive recalibration, plays a unique and important role in motor learning." [This is of importance, since most trigger points, and probably fibromyalgia, have proprioceptive components. DJS]
Henry R, Cahill CM, Wood g et al. 2012. Myofascial pain in patients waitlisted for total knee arthroplasty. Pain Res Manag 17(5):321-327. "Knee pain is one of the major sources of pain and disability in developed countries, particularly in aging populations, and is the primary indication for total knee arthroplasty (TKA) in patients with osteoarthritis (OA)....Following ethics approval, 25 participants were recruited from the wait list for elective unilateral primary TKA at the study centre. After providing informed consent, all participants were examined for the presence of active trigger points in the muscles surrounding the knee and received trigger point injections of bupivacaine. Assessments and trigger point injections were implemented on the first visit and at subsequent visits on weeks 1, 2, 4 and 8 ...Myofascial trigger points were identified in all participants. Trigger point injections significantly reduced pain intensity and pain interference, and improved mobility...All patients had trigger points in the vastus and gastrocnemius muscles, and 92% of patients experienced significant pain relief with trigger point injections at the first visit, indicating that a significant proportion of the OA knee pain was myofascial in origin. Further investigation is warranted to determine the prevalence of myofascial pain and whether treatment delays or prevents TKA."
Herald, J. and M.Pecenka. 1991. Pain doctors: the
real world of a pain practice. An interview with Lawrence A. Funt. Dental
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Heredia-Jimenez JM, Soto-Hermoso VM. 2013. Kinematics gait disorder in men with fibromyalgia. Rheumatol Int. [Jan 5 Epub ahead of print]. "We studied 12 male with fibromyalgia and 14 healthy men. Each participant of the study walked five trials along a 18.6-m walkway. Fibromyalgia patients completed a Spanish version of Fibromyalgia Impact Questionnaire. Significant differences between fibromyalgia and control groups were found in velocity, stride length, and cadence. Gait parameters of men affected by fibromyalgia were impaired when compared to those of healthy group due to bradykinesia. According to previous studies to assess gait variables in female patients, the male with fibromyalgia also showed lower values of velocity, cadence, and stride length than healthy group but not reported significant differences in swing, stance, single, or double support phase." [It would be interesting to check these men for co-existing TrPs, as TrPs usually co-exist with FM and some TrPs influence gait profoundly. DJS]
Hetrick DC, Ciol MA, Rothman I et al. 2003. Musculoskeletal
dysfunction in men with chronic pelvic pain syndrome type III: a
case-control study. J Urol. 170(3):828-831. “Men with
CPPS have more abnormal pelvic floor muscular findings compared with a
group of men without pain. Abnormalities of the pelvic muscles may
contribute to this pain syndrome.”
Heyes, M. P., K. Saito and S. P. Markey. 1992. Human
macrophages convert L-tryptophan into the neurotoxin quinolinic acid. Biochem J 283(Pt.
Hickey C, Thomas B. 2011. Delirium secondary to pregabalin. Gen Hosp Psychiatry. [Dec 14 Epub ahead of print]. "Fibromyalgia is a common and disabling disease, and treatment can be challenging. More recently, pregabalin has been approved to treat pain associated with fibromyalgia. ...Several case reports have documented delirium secondary to pregabalin, usually in older patients with multiple medical comorbidities and concurrent medications. We describe a case of delirium in a young patient without significant medical problems and in the absence of other potentially causal medications. In this case, pregabalin appears to be the single causal etiology for delirium. We recommend clinicians to consider the causal role it may play in any patient who presents with delirium."
Hicks GE, Morone N, Weiner DK. 2009. Degenerative lumbar disc and facet disease in older adults: prevalence and clinical correlates. Spine. 34(12):1301-1306. "Results demonstrated that the presence of degenerative disc and facet pathology in older adults is ubiquitous, regardless of clinical status, with greater than 90% demonstrating some level of degeneration. Higher radiographic severity scores were associated with the presence of CLBP. In fact, presence of severe disc pathology was associated with 2-fold greater odds of having CLBP. But, radiographic severity of disc and facet disease was not associated with pain severity among those with CLBP." "From a research perspective, radiographic evaluation of spinal pathology provides additional information about older adults with CLBP compared to pain-free individuals, but its clinical utility for diagnostic purposes is still in question." [Spine generated pain no longer means surgery. It has been noted in many other research articles that pain in the elderly is undertreated. If facet or interlaminary injection can provide relief to some of these patients, more of their brain would be freed from pain processing. Aside from the humanitarian reasons, which are considerable, the economic considerations are huge. Some patients might regain a significant increase of mental and physical function. Some might be able to stay in their own homes longer, and some might be considerably less disabled. Insurance companies and lawyers, as well as doctors, take note. DJS]
Hicks. R. A., D. DeHaro, G. Inman and G. J. Hicks. 1999.
Consistency of hand use and sleep problems. Percept Mot Skills 89(1):49-56.
Hill Jr., C. S. 1996. Government regulatory
influences on opioid prescribing and their impact on the treatment of pain of nonmalignant
origin. J Pain Symptom Manage 11(5):287-298.
Hill Jr., C. S. 1995. When will adequate pain
treatment be the norm? JAMA 274 (23):1881-2.
Hill, C. S. Jr. 1992 The intractable pain treatment act of
Texas. Tex Med 88(2):70-72.
Hitchcock, L. S., B. R. Ferrell and M. McCaffery. 1994 The
experience of chronic non-malignant pain J Pain Sympt Manage 9(5):312-318.
Hiyama S, Ono T, Ishiwata Y et al. 2003.
Effects of experimental nasal obstruction on human masseter and
suprahyoid muscle activities during sleep. Angle Orthod.
73(2):151-157. “Nasal obstruction could modulate the
activities of the masseter and suprahyoid muscles during
sleep.” Activity of the suprahyoid muscles tended to increase
significantly and the masseter tended to decrease significantly
with nasal obstruction during sleep. [This could affect TrPs,
and also CPAP therapy for co-existing sleep apnea. For the
latter, it may indicate need for automatically adjusting CPAP
set to maximum high equal to that of the sleep study need of the
patient, rather than standard CPAP in some patients. DJS]
Holman AJ, Neiman RA, Ettlinger RE. 2004.
Preliminary efficacy of the dopamine agonist, pramipexole for
fibromyalgia: the first, open label, multicenter experience. J
Musculoskel Pain 12(1):69-74. Dopamine agonists may be promising
pharmaceutical agents for the treatment of FMS.
Hiyama S, Ono T, Ishiwata Y et al. 2003.
Effects of experimental nasal obstruction on human masseter and
suprahyoid muscle activities during sleep. Angle Orthod.
73(2):151-157. “Nasal obstruction could modulate the
activities of the masseter and suprahyoid muscles during sleep.”
[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 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. Raynauds
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
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
Hodges PW, Mellor R, Crossley K et al.
2009. Pain induced by injection of hypertonic saline into the
infrapatellar fat pad and effect on coordination of the quadriceps
muscles. Arthritis Rheum. 61(1):70-77. “…alterations
in coordination of knee muscle activity can be caused by pain, even when
it is of nonmuscle origin. Treatment of pain is therefore
important to facilitate performance of the quadriceps muscles, which are
essential for locomotor and functional tasks as well as for knee
stability.” [Although this article does not specifically site TrPs
as part of this connection, they are involved. DJS]
Hodges PW, Sapsford R, Pengel LH. 2007.
Postural and respiratory functions of the pelvic floor muscles.
Neurourol Urodyn. 26(3):362-371. “This study provides evidence
that the PFM (pelvic floor muscles) contribute to both postural and
respiratory functions.” [Although this article does not
specifically site TrPs as part of this connection, they are involved.
Releasing the pelvic floor tightness, which is often caused by TrPs, may
indirectly aid posture and respiration. DJS]
Hodgson, M. J. and H. M. Kipen. 1999. Gulf War
illnesses: causation and treatment. J Occup Environ Med 41(6):443-52.
Hoffman D. 2011. Understanding Multisymptom Presentations in Chronic Pelvic Pain: The Inter-relationships between the Viscera and Myofascial Pelvic Floor Dysfunction. Curr Pain Headache Rep. [Jul 8 Epub ahead of print]. "Patients presenting with chronic pelvic pain frequently complain of multiple symptoms that appear to involve more than one organ system, creating diagnostic confusion. The multisymptom presentation of chronic pelvic pain has been frequently described. This article describes four proposed explanations for the clinical observation of multisymptom presentations of patients with chronic pelvic pain. These include the concepts of viscerovisceral convergence; viscerosomatic convergence; hypertonicity of pelvic floor muscles creating visceral symptoms along with somatovisceral convergence; and central sensitization with expansion of receptive fields."
Hoffman DL, Dukes EM. 2007. The health status
burden of people with fibromyalgia: a review of studies that assessed health
status with the SF-36 or the SF-12. Int J Clin Pract. [Nov 24
Epub ahead of print]. “FM groups had similar or significantly lower
(poorer) physical and mental health status scores compared to those with
rheumatoid arthritis, osteoarthritis, osteoporosis, systemic lupus
erythematosus, myofascial pain syndrome, primary Sjogren’s syndrome and
others. FM groups scored significantly lower than the pain condition
groups mentioned above on domains of bodily pain and vitality.” “People
with FM had an overall health status burden that was greater in magnitude
compared to people with other specific pain conditions that are widely
accepted as impairing.” [What does this indicate about those patients
with FM AND CMP (and perhaps multiple other conditions)? DJS]
Hoffmann RG, Kotchen JM, Kotchen TA et al. 2010. Temporomandibular Disorders and Associated Clinical Comorbidities. Clin J Pain. [Dec 20 Epub ahead of print]. "The TMJD (temporomandibular joint and muscle disorders) -affected individuals were on average 41 years of age and predominantly female (90%). Nearly 60% of both men and women reported recent pain of moderate-to-severe intensity with a quarter of them indicating interference or termination of work-related activities. In the case-control comparison, a higher frequency of headaches, allergies, depression, fatigue, degenerative arthritis, fibromyalgia, autoimmune disorders, sleep apnea, and gastrointestinal complaints were prevalent among those affected with TMJD. Many of the associated comorbid conditions were over 6 times more likely to occur after TMJD was diagnosed. Among a wide array of treatments used (46 listed), the most effective relief for most affected individuals (91%) was the use of thermal therapies-hot/cold packs to the jaw area or hot baths. Nearly 40% of individuals affected with TMJD patients reported one or more surgical procedures and nearly all were treated with one or many different medications. Results of these treatments were generally equivocal. Although potentially limited to the most severe TMJD affected individuals, the survey results provide a comprehensive dataset describing the clinical manifestations of TMJD….The data provide evidence that TMJD represent a spectrum of disorders with varying pathophysiologies, clinical manifestations, and associated comorbid conditions. The findings underscore the complex nature of TMJD, the need for more extensive interdisciplinary basic and clinical research, and the development of outcome-based strategies to more effectively diagnose, prevent, and treat these chronic, debilitating conditions." [It is unfortunate that these patients were not assessed for co-existing myofascial trigger points, which can cause TMJD, are treatable, and are often components of other co-morbidities as well. DJS]
Hojsted, J., A. Alban, K. Hagild and J. Erikson.
1999. Utilization of health care system by chronic pain patients who applied for
disability pensions. Pain 82(3):275-82.
Holick MF. 2004. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.
Am J Clin Nutr 79(3):362-371. "Vitamin D deficiency is often misdiagnosed as
Holla JF, van der Leeden M, Peter WF et al. 2012. Proprioception, laxity, muscle strength and activity limitations in early symptomatic knee osteoarthritis: Results from the CHECK cohort. J Rehabil Med. [Aug 29 Epub ahead of print]. "The results of the present study support the theory that in the absence of adequate proprioceptive input, lower muscle strength affects a patient's level of activities to a greater degree than in the presence of adequate proprioceptive input."
Hollister, L. E. 2000. An approach to the
medical marijuana controversy. Drug Alcohol Depend 58(1-2):3-7.
Holman AJ, Neradilek MB, Dryland DD et al. 2010. Patient-derived determinants for participation in placebo-controlled clinical trials for fibromyalgia. Curr Pain Headache Rep. 14(6):470-476. "Perspectives of patients with fibromyalgia influence their likelihood of participating in randomized placebo-controlled trials and potentially clash with current, well-established methodology of randomized controlled trial design. Mandates to use only acetaminophen for breakthrough pain and that require discontinuation of concomitant medications, especially in studies lacking an active comparator arm, could bias a trial cohort to thereby reduce the generalizability of study findings and conclusions. This study evaluates factors affecting willingness to participate in such clinical trials, including the impact of altruism, payment, study duration, forced discontinuation of specific medications, and subject demographics for patients seen by rheumatologists proficient and avidly interested in treating fibromyalgia." [This casts yet another shadow on current fibromyalgia research. DJS]
Holst H, Arendt-Nielsen L, Mosbech H et al. 2011. Increased capsaicin-induced secondary hyperalgesia in patients with multiple chemical sensitivity. Clin J Pain. 27(2):156-162. "Temporal summation was increased in MCS patients compared with controls.... Further, in patients with comorbidity of fibromyalgia, pain and chronic fatigue, pain continued after end stimulation, and the stimulus response function was enhanced compared with patients without comorbidity, and significant to controls....This is the first study to show facilitated pain processing in MCS and EC (eczema patients with airway symptoms from odorous chemicals) patients with the most abnormal responses in MCS."
Holsten, F. and B. Bjorvatn. 1997.
[Phototherapy. An alternative for seasonal affective disordersor sleep
disorders. Tidsskr Nor Laegeforen 117(17):2484-2488 [Norwegian].
Holman AJ, Myers RR. 2005. A randomized, double-blind,
placebo-controlled trial of pramipexole, a dopamine agonist, in patients
with fibromyalgia receiving concomitant medications. Arthritis
Rheum. 52(8):2495-2505. “In a subset of patients with
fibromyalgia, approximately 50% of whom required narcotic analgesia
and/or were disabled, treatment with pramipexole improved scores on
assessments of pain, fatigue, function, and global status, and was safe
Holland, N. W. and E. B. Gonzalez. 1998. Soft
tissue problems in older adults. Clin Geriatr Med 14(3):601-11.
Holtedahl R. 2010. [Pregabalin for
fibromyalgia – can we rely on the pharmaceutical industry?] Tidsskr Nor
Laegeforen 130(10):1032-1036. [Norwegian] “Negative results were seldom
mentioned in the abstracts, and secondary endpoints were reported
incompletely. All 19 reviews referred to one or more of the clinical trials,
and were generally limited to describing main results. Interpretation.
Recommendations for pregabalin in treatment of patients with fibromyalgia
are based on rather weak evidence. Until trials independent of
industry-funding are published, the role of pregabalin in treatment of
fibromyalgia remains unclear.”
Holton KF, Taren DL, Bennett RM et al. 2010. The excitotoxin elimination diet: a novel dietary intervention for fibromyalgia patients. International Myopain Society Eighth Clinical Meeting Oct 3-7, 2010. Toledo, Spain. Abstract No. 47. "Results suggest that the excitotoxin elimination diet, with wider food choices than a living foods diet, can significantly improve symptoms in patients with FM. Future large scale testing of the dietary intervention is warranted." [This is exciting research on a preventable perpetuating factor for both fibromyalgia and myofascial pain. Do you have aspartame, MSG and other excitotoxins in your pantry? DJS]
Holton KF, Taren DL, Thomson CA et al. 2012. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol [July 4 Epub ahead of print]. "To examine the effects of a challenge with monosodium glutamate (MSG) as compared to placebo on the symptoms of fibromyalgia (FM), in participants who initially experienced >30% remission of symptoms on an excitotoxin elimination diet....The MSG challenge, as compared to placebo, resulted in a significant return of symptoms (total symptom score.... These findings suggest that dietary glutamate may be contributing to FM symptoms in some patients. Future research on the role of dietary excitotoxins in FM is warranted." [Patients who routinely ingest aspartame, MSG and other excitotoxins take note. Diet is a perpetuating factor you can control. DJS]
Holzberg, A. D., M. E. Robinson, M. E. Geisser and H. A.
Gremillion. 1996. The effects of depression and chronic pain on psychosocial
and physical functioning. Clin J Pain 12(2):118-125.
Homann D, Louzada FM, Goes SM. 2013. Acylated ghrelin: A potential marker for fibromyalgia? Eur J Pain. [Mar 8 Epub ahead of print]. "Fibromyalgia is characterized by chronic widespread pain and sleep disturbances. Overweight and obesity, which lead to metabolic changes, are additional comorbidities that are rarely explored, although they are highly prevalent in patients with fibromyalgia....These findings indicate that the decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity."
Homko, C. J. , E. Sivan, E. A. Reece and G. Boden. 1999.
Fuel metabolism during pregnancy. Semin Reprod Endocrinol 17(2):119-25.
Hong CZ. 1996.
Pathophysiology of myofascial trigger point. J Formos Med
Assoc. 95(2):93-104. “Myofascial trigger point is a sensitive
spot in a palpable taut band of skeletal muscle fibers. Two
important clinical characteristics of trigger points, referred pain and
local twitch response, can be elicited by mechanical stimulation
(palpation or needling). The trigger point is usually activated by
acute or chronic injury to a muscle, tendon, ligament, joint, disc or
nerve. Recent human and animal studies have suggested that the
pathogenesis of either referred pain or local twitch response is related
to integration in the spinal cord. It has been proposed that there
are multiple sensitive loci in a trigger point region. A sensitive
locus may contain one or more sensitized nociceptive nerve endings.
Mechanical stimulation of a sensitive locus can elicit a local twitch
response which is frequently associated with characteristic referred
pain. Theoretically, sensitive loci can be found in any site of a
skeletal muscle, but is usually distributed with highest concentration
near the endplate region where a trigger point is frequently found.
The trigger point is a common pathogenic pathway of muscle pain from
Hong CZ. 1994.
Lidocaine injection versus dry needling to myofascial trigger point.
The importance of the local twitch response. Am J Phys Med
Rehabil. 73(4):256-263. “This study was designed to
investigate the effects of injection with a local anesthetic agent or
dry needling into a myofascial trigger point (TrP) of the upper
trapezius muscle in 58 patients. Trigger point injections with
0.5% lidocaine were given to 26 patients (Group I), and dry needling was
performed on TrPs in 15 patients (Group II). Local twitch
responses (LTRs) were elicited during multiple needle insertions in both
Groups I and II. In another 17 patients, no LTR was elicited
during TrP injection with lidocaine (9 patients, group Ia) or dry
needling (8 patients, group IIa). Improvement was assessed by
measuring the subjective pain intensity, the pain threshold of the TrP
and the range of motion of the cervical spine. Significant
improvement occurred immediately after injection into the patients in
both group I and group II. In Groups Ia and Ib, there was little
change in pain, tenderness or tightness after injection. Within
2-8 h after injection or dry needling, soreness (different from
patients’ original myofascial pain) developed in 42% of the patients in
group I and in 100% of the patients in group II. Patients treated
with dry needling had postinjection soreness of significantly greater
intensity and longer duration than those treated with lidocaine
injection. The author concludes that it is essential to elicit
LTRs during injection to obtain an immediately desirable effect.
TrP injection with 0.5% lidocaine is recommended, because it reduces the
intensity and duration of postinjection soreness compared with that
produced by dry needling.”
Hong CZ. 1994.
Persistence of local twitch response with loss of conduction to and from
the spinal cord. Arch Phys Med Rehabil. 75(1):12-16.
“These findings indicate that the transmission of LTR (local twitch
response) depends mainly on the central nervous system with a possible
minor degree of local transmission.”
Hong CZ. 1996.
Difference in pain relief after trigger point injections in myofascial
pain patients with and without fibromyalgia. Arch Phys Med Rehabil.
77(11):1161-1166. “Two weeks after injection, the degree of
improvement in PT (pain threshold) or ROM (range of motion) (but not PI
(pain intensity)) was not significantly different between two groups.
Post-injection soreness (different from myofascial pain) was more
severe, developed sooner, and lasted longer in Group 1 than in Group 2.
Conclusion: Trigger point injection is a valuable procedure for pain
relief for patients in both groups. Patients with FMS are likely
to experience significant but delayed and attenuated pain relief
following injection of their active TrPs compared to myofascial pain
patients with similar TrPs but without FMS. aAlso, FMS patients
are likely to experience significantly more post-injection soreness for
a longer period of time.”
Hong C. 2004. Myofascial pain therapy.
J Musculoskeletal Pain 12(3/4):37-43. “Myofascial pain should be
appropriately treated to inactivate TrPs completely and to avoid recurrence
permanently.” This is a good overview of common options in the
treatment of TrPs.
Hong CZ. 2000. Specific sequential myofascial
trigger point therapy in the treatment of a patient with myofascial pain
syndrome associated with reflex sympathetic dystrophy: commentary.
Australas Chiropr Osteopathy 9(1):7-11.
Hong CZ. 2002. New trends in myofascial pain
syndrome. Zhonghua Yi Xue Za Zhi 65(11):501-512. This is a
good overview of current findings in myofascial medicine.
Hong CZ. 2006. Treatment of myofascial pain
syndrome. Curr Pain Headache Rep. 10(5):345-349. “Effective
MTrP therapies include manual therapies, physical therapy modalities, dry
needling, or MTrP injection. It is also important to eliminate any
perpetuating factors and provide adequate education and home programs to
patients so that recurrent or chronic pain can be avoided.”
Hong CZ. 1994. Lidocaine injection versus
dry needling to myofascial trigger point. The importance of
the local twitch response. Am J Phys Med Rehabil
73(4):256-263. “Lidocaine reduces the intensity and duration
of postinjection soreness compared with that produced by dry
needling.” [This is important to remember for patients who
also have the central sensitization of FMS. The pain of dry
needling may needlessly further sensitize the central nervous system
in some patients with both FMS and TrPs. DJS]
Hong CZ. 2002. New trends in myofascial pain syndrome.
Zhonghua Yi Xue Za Zhi 65(11):501-512. Myofascial TrP
therapies include “...stretch, massage, thermotherapy, electrotherapy,
laser therapy, MTrP injection, dry needling, and acupuncture.”
[Dry needling is not recommended if the patient also has central
sensitization such as fibromyalgia. DJS]
Hong CZ. 1994. Lidocaine injection versus dry needling to
myofascial trigger point. The importance of the local twitch
response. Am J Phys Med Rehabil 73(4):256-263.
“Patients treated with dry needling had post-injection soreness of
significantly greater intensity and longer duration than those treated
with lidocaine injection. It is essential to elicit LTRs during
injection to obtain an immediately desirable effect. TrP injection
with 0.5% lidocaine is recommended, because it reduces the intensity and
duration of post-injection soreness compared with that produced by dry
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
Hong, C-Z. 1999. Current research on myofascial trigger
points-pathophysiological studies. J Musculoskel Pain 7(1-2):121-129.
Hong C-Z and T-C Hsueh. 1996. The difference in pain
relief after trigger point injections in myofascial pain in patients with and without
fibromyalgia. Arch Phys Med Rehabil 77:1161-1166.
Hong, C-Z, and J. Yu. 1998. Spontaneous electrical
activity of rabbit trigger after transection of spinal cord and peripheral nerve. J
Musculoskel Pain 6(4):45-58.
Hong, C. Z. and D. G. Simons. 1998.
Pathophysiologic and electrophysiologic mechanisms of myofascial trigger points. Arch
Phys Med Rehabil 79(7):863-72.
Hong, C. Z., T. S. Kuan, J. T. Chen and S. M. Chen.
1997. Referred pain elicited by palpitation and by needling of myofascial trigger
points: a comparison. Arch Phys Med Rehabil 78(9):957-960.
Hong, C. Z. 1996. Pathophysiology of myofascial
trigger point. J Formos Med Assoc 92(2):93-104.
Hoog SL, Cheng Y, Elpers J et al. 2013. Duloxetine and pregnancy outcomes: safety surveillance findings. Int J Med Sci. 10(4):413-419. "While limitations of these data are recognized, the information available to date from these two data sources suggest that the frequency of abnormal outcomes reported in duloxetine pregnancy cases is generally consistent with the historic control rates in the general population." [This study was financed by Eli Lilly and Company, manufacturers of duloxetine]
Hooper MM, Stellato TA, Hallowell PT et al.
2006. Musculoskeletal findings in obese subjects before and
after weight loss following bariatric surgery. Int J Obes
(Lond) [Apr 25 Epub ahead of print] “There was a higher frequency
of multiple MSK (musculoskeletal) complaints, including
non-weight-bearing sites compared to historical controls, before
surgery, which decreased significantly at most sites following
weight loss and physical activity. These benefits may improve
further, as weight loss may continue for up to 24 months. The
benefits seen with weight loss indicate that prevention and
treatment of obesity can improve MSK health and function.”
[Obesity can be a major perpetuating factor. DJS]
Hopman-Rock, M., F. W. Kraaimaat, E. Odding and J. W.
Bijlsma. 1998. Coping with pain in the hip or knee in relation to physical
disability in community-living elderly people. Arthritis Care Res
Hopwood, M. B. and S. E. Abram. 1994. Factors
associated with failure of trigger point injections. Clin J Pain
Horne,. J. and L. Reyner. 1999. Vehicle accidents related
to sleep: a review. Occup Environ Med 56(5):289-94.
Horning, M. R. 1997. Chronic opioids: a
reassessment. Alaska Med 39(4):103-110.
Horowits, R. 1999. The physiological role of titin in
striated muscle. Rev Physiol Biochem Pharmacol 138:57-96.
Horowitz L, Sarkin JM.
1992. Video display terminal operation: a potential risk in the
etiology and maintenance of temporomandibular disorders. Cranio.
10(1):43-50. “TMD (temporomandibular disorder) is associated with
numerous risk factors that commonly initiate sympathetic nervous system and
stress hormone response mechanisms resulting in muscle spasms, trigger point
formation, and pain in the head and neck.”
Horven, S., T. C. Stiles, A. Holst and T. Moen. 1992. HLA
antigens in primary fibromyalgia syndrome. J. Rheumatol 19(8):1269-70.
Hoseini SS, Hoseini M, Gharibzadeh S. 2005.
Sprouting phenomenon, a new model for the role of A-beta fibers in wind up.
Med Hypotheses [Dec 12 Epub ahead of print] “In this study, we have
proposed a new model for the role of Abeta fibers in wind up, through
sprouting of nerve fibers in the dorsal horn of spinal cord. We named
it “sprouting phenomenon”. It has been reported that in some clinical
hyperalgesic states induced by peripheral injury or inflammation, wind up
may aggravate the pain. Studies have indicated the presence of
…fibromyalgia syndrome…. According to sprouting phenomenon, it seems
that some clinical interventions can be assessed to alleviate
post-inflammatory pains: (1) immediate and complete relief of inflammation
by anti-inflammatory agents to prevent repetitive excitation of C-fibers and
subsequent morphological changes of dorsal horn laminae; (2) using local
anesthetics in order to prevent pain signal transmission; (3) prevention of
sprouting by intrathecal injection of some anti-proliferation agents; (4)
using NMDA or NK1 receptor antagonists to prevent central mechanism of wind
up.” “Future clinical studies are needed…”
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
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
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
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
Houle S, Descarreaux M. 2009. Conservative
care of temporomandibular joint disorder in a 35-year-old patient with
spinal muscular atrophy type III: a case study. J Chiropr Med.
8(4):187-192. “Chiropractic care was provided and included TMJ
mobilization, myofascial therapy, trigger point therapy, and light
spinal mobilizations of the upper cervical vertebrae. Final
evaluation of TMJ range of motion showed active opening of 12 mm with
absence of pain and muscle tenderness of the jaw. Conclusion: This
case suggests that a patient with musculoskeletal disorders related to
underlying neurodegenerative pathologies may benefit from chiropractic
management adapted to their condition. In the present case,
chiropractic treatment of the TMJ represented a viable, low-cost
approach with limited adverse effects compared with surgery.”
[Noninvasive successful therapy is always to be preferred. Treatment
included trigger point therapy and myofascial therapy. Much surgery
could be avoided by the prompt and successful treatment of TrPs. DJS]
Houtmeyers, E., R. Gosselink, G. Gayan-Ramirez and M.
Decramer. 1999. Effects of drugs on mucus clearance. Eur Respir J
Howard KJ, Mayer TG, Neblett R et al. 2010. Fibromyalgia Syndrome in Chronic Disabling Occupational Musculoskeletal Disorders: Prevalence, Risk Factors, and Post treatment Outcomes. J Occup Environ Med. [Nov 30 Epub ahead of print]. "OBJECTIVE: To identify the prevalence, risk factors, and treatment outcomes of patients with chronic disabling occupational musculoskeletal disorders (CDOMD) who met criteria for fibromyalgia....The CDOMD patients with fibromyalgia reported higher-level psychosocial distress. Women with fibromyalgia were 9.6 times less likely to return to work 1-year post treatment and, of those who did, were 4.3 times less likely to retain work....Of this cohort, 23.2% patients met criteria for fibromyalgia. Patients with fibromyalgia were found to show greater psychosocial distress and significantly poorer rates of work return and work retention 1-year post rehabilitation."
Howell ER. 2012. Conservative management of a 31 year old male with left sided low back and leg pain: a case report. J Can Chiropr Assoc. 56(3):225-232. "This case study reported the conservative management of a patient presenting with left sided low back and leg pain diagnosed as a left sided L5-S1 disc prolapse/herniation....A 31-year-old male recreational worker presented with left sided low back and leg pain for the previous 3-4 months that was exacerbated by prolonged sitting....The plan of management included interferential current, soft tissue trigger point and myofascial therapy, lateral recumbent manual low velocity, low amplitude traction mobilizations and pelvic blocking as necessary. Home care included heat, icing, neural mobilizations, repeated extension exercises, stretching, core muscle strengthening, as well as the avoidance of prolonged sitting and using a low back support in his work chair. The patient responded well after the first visit and his leg and back pain were almost completely resolved by the third visit....Conservative chiropractic care appears to reduce pain and improve mobility in this case of a L5-S1 disc herniation. Active rehabilitative treatment strategies are recommended before surgical referral."
Hoyle JA, Marras WS, Sheedy JE et al. 2010. Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. J Electromyogr Kinesiol. [Jun 25 Epub ahead of print]. "Musculoskeletal complaint rates are high among those performing low-level static exertions (LLSEs), such as computer users." "It was hypothesized that myofascial trigger point (MTrP) development might be one causal mechanism to help explain these complaints and that static postural and visual demands may be contributing factors." "…MTrPs developed after one hour of continuous typing, despite the stress condition." "Findings suggest that MTrPs may be one causal pathway for pain during LLSEs and both postural and visual demands may play a role in muscle activation patterns, perhaps attributing to MTrP development and resultant discomfort."
J, Janout V, Malincilova J, Horakova D, Cizek L. Detection of
insulin resistance by simple quantitative insulin sensitivity
check index QUICKI for epidemiological assessment and prevention.
J Clin Endocrinol Metab Jan;87(1):144-7.
Hrycaj P, Stratz T, Mennet P et al. 1996.
Pathogenetic aspects of responsiveness to ondansetron
(5-hydroxytryptamine type 3 receptor antagonist) in patients with
primary fibromyalgia syndrome — a preliminary study. J
Rheumatol 23(8):1418-1423. “Ondansetron appears to be an
effective drug in about 50% of patients with FM. There may be two
subsets of patients with FM that differ clinically and pathogenetically
with regard to the disturbance in the 5-HT-3R system."
Hsieh C.Y., Hong C. Z., Adams A. H., Platt K. J. ,
Danielson C. D. , Hoehler F. K., and Tobis JS 2000. Interexaminer reliability of the
palpation of trigger points in the trunk and lower limb muscles. Arch Phys Med Rehabil
Hsieh LF, Hong CZ,
Chern SH et al. 2009. Efficacy and side effects of diclofenac patch in
treatment of patients with myofascial pain syndrome of the upper trapezius.
J Pain Symptom Manage. [Oct 10 Epub ahead of print]. “This
study demonstrates that the diclofenac sodium patch was superior to the
control patch in terms of reducing pain and improving functional outcomes,
and did not result in significant adverse effects.” [This may be a
helpful option for patients with one or a small cluster of TrPs DJS]
Hsieh YL, Kao MJ, Kuan TS et al. 2007.
Dry needling to a key myofascial trigger point may reduce the irritability
of satellite MTrPs. Am J Phys Med Rehabil. 86(5):397-403.
“This study supports the concept that activity in a primary MTrP leads to
the development of activity in satellite MTrPs and the suggested spinal cord
mechanism responsible for this phenomenon.”
Hsieh YL, Yang SA, Yang CC et al. 2012. Dry needling at myofascial trigger spots of rabbit skeletal muscles modulates the biochemicals associated with pain, inflammation, and hypoxia. Evid Based Complement Alternat Med. 2012:342165. "Dry needling at the MTrSs modulates various biochemicals associated with pain, inflammation, and hypoxia in a dose-dependent manner."
Hsin ST, Yin YC, Juan
CH et al. 2002. Myofascial pain syndrome induced by malpositioning
during surgery – a case report. Acta Anaesthesiol Sin.
40(1):37-41. “It is a real challenge to the anesthesiologists to
differentiate brachial plexus injury (BPI) from myofascial pain syndrome
(MPS). The possibility of MPS should be suspected in a patient with
complaints of pain and dysfunction of the upper arm immediately after
surgery. Here we report a case of gallstone with cervical ankylosing
spondylitis who sustained myofascial pain syndrome immediately after open
cholecystectomy. We utilized dry needle stimulation to deactivate the
trigger point of the pectoris minor muscle and stretching the muscle to
relieve the muscle pain after the diagnosis was made. The patient
completely recovered 2 weeks later.”
Hsu J.C., Lee Y.S.., Chang
C.N. et al. 2002. Sleep deprivation affects nitric oxide synthesis and
glial reactions in the rat hippocampus. Glia (Suppl 1):S51
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
Hu, F. B., M. J. Stampfer, J. E. Manson, E. Rimm, G. A.
Colditz, F. E. Speizer, C. H. Hennekens and W. C. Willett. 1999. Dietary
protein and risk of ischemic heart disease in women. Am J Clin Nutr 70(2):221-7.
Huang TT, Yang LH, Liu CY. 2011. Reducing the fear of falling among community-dwelling elderly adults through cognitive-behavioral strategies and intense Tai Chi exercise: a randomized controlled trial. J Adv Nurs. Jan 7 [Epub ahead of print]. "The results of this trial suggest that the cognitive-behavioral intervention with Tai Chi exercise helped community-dwelling elderly adults to enhance their mobility, to manage their fear of falling and to increase their quality of life." [It has been my personal experience that t'ai chi chuan, at least the Yang long form I practice, helps even younger patients with mobility and balance. DJS]
Huang YT, Lin SY, Neoh CA et al. 2011. Dry needling for myofascial pain: prognostic factors. J Altern Complement Med. 17(8):755-762. "Dry needling is an effective treatment for reducing pain and pain interference. However, long pain duration, high pain intensity, poor quality of sleep, and repetitive stress are associated with poor outcomes. Treatment outcome depends not only on the dry needling protocol, but also on disease characteristics and patient demographic profile." [Outcome would also depend on the proper identification of the myofascial trigger points involved, as well as the training and skill of the practitioner. DJS]
Hubbard, D. R. and G. M. Berkoff. 1993.
Myofascial trigger points show spontaneous needle EMG activity. Spine
18(13):1803-7. Sustained spontaneous EMG activity was found in the 1-2 mm nidus of
all TrPs, and was absent in non-TrPs.
Hubbell, S. L. and M. Thomas. 1985. Postpartum
cervical myofascial pain syndrome: review of four patients. Obstet Gynecol
Huber R, Ghilardi MF, Massimini M
et al. 2004. Local sleep and learning. Nature 430(6995):78-81.
The amount of slow-wave activity in right brain areas can help
consolidate new learning. It is important for medical teams to
help FMS patients regain deep level sleep.
Hudson JI, Arnold
LM, Bradley LA et al. 2009. What makes patients with
fibromyalgia feel better? Correlations between patient global
impression of improvement and changes in clinical symptoms and
function: a pooled analysis of four randomized placebo-controlled
trials of duloxetine. J Rheumatol. 36(11):2517-2522.
“In addition to pain reduction, what makes patients with FM feel
better may include improvement in fatigue, physical functioning,
mood, and impact on daily living. An assessment of these
domains may be important in clinical trials of FM and in the
management of patients with FM.”
Hudson JL, Arnold LM, Keck PE et al. 2004.
Family study of fibromyalgia and affective spectrum disorder.
Biol Psychiatry 56(11):884-891. This study found that FMS was
associated with the other medical and psychiatric disorders that are
proposed to be grouped as affective spectrum disorder. [Since FMS
does not cover a homogenous group, lumping it as such with a group of
medical and psychiatric disorders could add to the confusion. DJS]
Hudson J.I., Mangweth B.,
Pope H.G. et al. Family study of affective spectrum disorder. Arch
Gen Psychiatry. This study suggests that some disorders such as
ADHD, IBS, migraine, OC, PTSD, fibromyalgia and other conditions may share a
genetic predisposition, as these conditions are often found clustered in
Hudson, N., M. A. Fitzcharles, M. Cohen, M. R. Starr and J.
M. Esdaile. 1998. The association of soft-tissue rheumatism and
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Arthritis Rheum. 54(1):177-183. “Being diagnosed as having FM
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“…a Muscle Pain Detection Device (MPDD) has been developed. A
muscle is stimulated and painful muscles are precisely detected,
allowing distinctions between primary and referred muscle pain as well
as distinguishing other functional muscle pain thought to cause MPS.”
“Using the MPDD appears to be more valid and potentially more reliable
than palpation to identify muscles causing regional pain that could
benefit from injections.” [It might be useful and effective to
teach palpation skills in medical, dental and other health care schools.
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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
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This paper describes two main pain patterns of pronator quadratus
myofascial trigger points.