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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.”
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greater activation of accessory neck muscles during a repetitive upper
limb task compared to asymptomatic controls.”
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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.”
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al. 2002. Calcium-calmodulin-dependent protein kinase II contributes to
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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.
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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]
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stressor.” [For those of us with FM amplification and GERD, auditory
stress may be an even greater peril. DJS]
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soft drink consumption, snoring and daytime sleepiness, insomnia,
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heartburn during sleep may be associated with sleep complaints and
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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]
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total knee arthroplasty: treatment with manual therapy and trigger point
injections. J Musculoskel Pain 6(4):85-95.
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data suggest links between the learning deficit and the
sensitization of pain circuits associated with inflammation or
injury (central sensitization).” “Central sensitization enhances
reactivity to mechanical stimulation (allodynia) and depends on the
N-methyl-d-aspartate receptor (NMDAR).”
Fernandez-Carnero J, Fernandez-de-Las-Penas
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referred pain from myofascial trigger points in the forearm muscles
in patients with lateral epicondylalgia. Clin J Pain.
23(4):353-360. “Lower PPT (pressure pain threshold) and larger
referred pain patterns suggest that peripheral and central
sensitization exists in LE (lateral epicondamgia).”
Fernandez-de-las-Penas C, Alonso-Blanco C, Del Amo-Perez
A et al. 2007. Trigger points in the masticatory muscles in
subjects presenting with ankylosing spondylitis. J Musculoskel
Pain. 15(3):39-47. “Trigger points in the masticatory muscles
were more conspicuous in AS subjects than in HNCs. Patients showed
a reduced active mouth opening and cervical flexion-extension motion
than matched HNCs. The AS subjects with lesser mouth opening
showed a greater occiput-to-wall distance and a greater number of TrPs
in the masticatory muscles.”
Fernandez-de-las-Penas C,
Cuadrado ML, Arendt-Nielsen L et al. 2007. A pain model for
tension type headache based on muscle trigger points. J
Musculoskel Pain 15 (Supp 13):20 item 30. [Myopain 2007
Poster] “Our studies suggest that TTH (tension-type headache) can be
explained by referred pain from active TrPs in neck-shoulder muscles.
Since chemical mediators most likely are released by active TrPs,
nociceptive inputs from these TrPs may lead to increased afferent
barrage into the trigeminal nucleus caudalis. This updated pain
model proposes that TrPs may be primary hyperalgesic zones, while
referred pain areas in the head could be viewed as secondary
hyperalgesic zones.”
Fernandez-de-las-Penas C,
Cuadrado M, Pareja J. 2007. Referred pain from
extra-ocular muscle trigger points in chronic headache. J
Musculoskel Pain 15 (Supp 13):19 item 27. [Myopain 2007
Poster] “Nociceptive inputs from the extra-ocular muscles may
provoke a continuous afferent bombardment to the trigeminal nerve
nucleus caudalis in CTTH (chronic tension-type headache). The
prolonged nociceptive activation by such muscle inputs might
contribute to central sensitization.” [This exciting research
indicates that even constant pain from facial muscles around the eye
could be enough to contribute to body-wide central nervous system
sensitization. DJS]
Fernandez-de-las-Penas
C, Cuadrado ML, Pareja JA. 2007. Muscle atrophy of
the suboccipital muscles associated with active trigger points
in chronic tension type headache. J Musculoskel Pain
15 (Supp 13):19 item 28. [Myopain 2007 Poster] “Muscle
atrophy in the RCPmin, but not in the RCPmaj, was associated to
active TrPs in the suboccipital muscles in CTTH.
Nociceptive inputs originated in active TrPs might contribute to
a greater muscle atrophy of the involved muscles.” [This
study is interesting in that it suggests that pain from MTPs
could contribute to muscle atrophy. As MTPs can cause
nerve entrapment and blood vessel entrapment, this would be
logical. DJS]
Fernandez-de-las-Penas C, De-la-Llave-Rincon
A, Miangolarra J. 2007. Uncommon referred pain from
scalene muscle trigger points in chronic tension type headache.
J Musculoskel Pain 15 (Supp 13):21 item 31.
[Myopain 2007 Poster] “Nine CTTH (chronic tension type
headache) patients had an uncommon referred pain pattern from
scalene muscle TrPs, so these headache patients may need
examination for scalene TrPs. It is known that CTH show
sensitization of central pathways, which may provoke larger
referred pain areas of active muscle TrPs. Further, there
are examples of neurologically related exceptional pain patterns
in other muscles [e.g. the soleus].” [I believe that this
is not so uncommon, and I have seen it several times before, but
it may be more common in patients with CMP and central
sensitization. DJS]
Fernandez-de-las-Penas C, Fernandez-Carnero
J, Miangolarra J. 2007. Multifidus muscle trigger point
management and stabilizing exercises in low back pain.
J Musculoskel Pain 15 (Supp 13):21 item 32. [Myopain
2007 Poster] “In some CLBP (chronic low back pain) patients, it
would be necessary to treat lumbar multifidus TrPs before
starting a stability exercise program because it includes
voluntary contraction of this muscle. Nociceptive barrage
originated in active TrPs could act as a contributing factor for
muscle inhibition.” [Multifidi, especially with nerve
entrapment, is exceedingly common in patients with CMP and
central sensitization. Treatment of the nerve pain is
before the TPM will increase the efficacy of the TPM treatment.
DJS]
Fernandez-de-las-Penas C,
Perez-de-Heredia-Torres M, Miangolarra J. 2007. Trigger
point management in lateral epicondylalgia. J
Musculoskel Pain 15 (Supp 13):20 item 29. [Myopain
2007 Poster] “Referred pain from TrPs in these patients was
causing the usual pain reported by patients with lateral
epicondylalgia. Muscle tension provoked by TrP taut band
may play an important role in the genesis and relief of the pain
commonly seen in lateral epicondylalgia.”
Fernandez-de-Las-Penas C, Cuadrado M,
Arendt-Nielsen L et al. 2007. Myofascial trigger points and
sensitization: an updated pain model for tension-type headache.
Cephalalgia [Mar 14 Epub ahead of print] “Based on available
data, an updated pain model for CTTH is proposed in which headache can
at least partly be explained by referred pain from TrPs in the posterior
cervical, head and shoulder muscles. In this updated pain model,
TrPs would be the primary hyperalgesic zones responsible for the
development of central sensitization in CTTH.”
Fernandez-de-las-Penas C, Carratala-Tejada M, Luna-Oliva
L et al. 2006. The immediate effect of hamstring muscle stretching
in subjects’ trigger points in the masseter muscle. J
Musculoskel Pain 14(3):27-35. “The present study demonstrated an
increase in active mouth opening and a decrease in TrP sensitivity in
the masseter muscle in response to the stretch of the hamstring
muscles.” Treatment, and constriction, in the myofascia of one area can
significantly alter the myofascia in another area, even long distance.
Fernandez-de-Las-Penas
C, Alonso-Blanco C, Luz Cuadrado M et al. 2006. Myofascial trigger
points in the suboccipital muscles in episodic tension-type headache.
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Fernandez-de-Las-Penas
C, Alonso-Blanco C, Miangolarra JC. 2006. Myofascial trigger
points in subjects presenting with mechanical neck pain: a blinded,
controlled study. Man Ther. [Jun 10 Epub ahead of print]
“Active TrPs were more frequent in patients presenting with mechanical
neck pain than in healthy subjects.”
Fernandez-de-Las-Penas
C, Cuadrado M, Pareja J. 2006. Myofascial trigger points, neck
mobility and forward head posture in unilateral migraine.
Cephalalgia. 26(9):1061-1070. “Active TrPs located ipsilateral
to migraine headaches might be a contributing factor in the initiation
or perpetuation of migraine.”
Fernandez-de-Las-Penas
C, Ge HY, Arendt-Nielsen L et al. 2006. Referred pain from
trapezius muscle trigger points shares similar characteristics with
chronic tension type headache. Eur J Pain. [Aug 17 Epub
ahead of print] Patients with chronic tension type headache may
have spatial summation of perceived pain and mechanical pain, with
referral pain characteristics of myofascial TrPs.
Fernandez de las Penas CF, Carnero JF, Page JCM.
2005. Musculoskeletal disorders in mechanical neck pain: myofascial
trigger points versus cervical joint dysfunction – a clinical study.
J Musculoskeletal Pain 13(1). “There is a possible relationship
between the presence of TrPs in the upper trapezius muscle and the presence
of cervical dysfunctions at C3 and C4 vertebrae in patients suffering from
mechanical neck pain. However, it cannot be established as a
cause-effect relationship. Moreover, there is clinical evidence
showing that joint dysfunctions can induce TrP activity, and that TrP
activity can aggravate corresponding joint dysfunction.”
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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
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Field T, Hernandez-Reif M, Diego M et al. 2007.
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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
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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.”
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scoliosis can result.
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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.
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Clonazepam may help some myofascial pain.
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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
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Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. I: Background and patient
evaluation. Int Urogynecol J Pelvic Floor Dysfunct.
14(4):261-268. (See next entry)
Fitzgerald MP, Kotarinos R. 2003.
Rehabilitation of the short pelvic floor. II: Treatment of the patient
with the short pelvic floor. Int Urogynecol J Pelvic Floor
Dysfunct. 14(4):269-275. These articles provide options for patient
care and help for the diagnoses and treatment of many common but often
misdiagnosed pelvic and lower abdominal pain cases. Care providers
are reminded that myofascial TrPs can cause dysfunction such as muscle
weakness as well as pain, and many cases of bladder and bowel
dysfunction, vulvodynia, and similar ailments may be greatly relieved by
TrP treatment.
Flanagan, D. E. , J. C. Vaile, G. W.
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Fleischmann R. 2007. Primer: establishing
a clinical trial unit – regulations and infrastructure. Nat
Clin Pract Rheumatol. 3(4):234-239. [This comprehensive
review would be very helpful for physicians interested in doing a
clinical trial. DJS]
Fleury B. 2000. [Pharyngeal musculature and
obstructive sleep apnea syndromes] Rev Mal Respir. 17 Suppl
3:S15-20. [French] “The caliber of the pharynx at the soft palate
depends on the action of the tensor veli, the palatoglossus, the
palatopharyngeus and the uvula muscles. At the lingual level, the
action of the genioglossus and the geniohyoideus predominate.
These different muscle groups contract in coordination before the
diaphragm contracts. Their activity is diminished and disorganized
during sleep. These muscles appear to have a histological
composition adapted to short duration intense contractions making them
vulnerable to fatigue. In apneic patients, these muscles are
solicited constantly. Muscular lesions related to overwork have
been suggested.” [Muscle tension can affect sleep apnea.
Myofascial TrPs can affect muscle tension. Therefore, myofascial
TrPs can affect sleep apnea. DJS]
Florian H, Young Jr. J, Haig G et al. 2007. Pregabalin is
effective for the long-term treatment of pain associated with
fibromyalgia syndrome: a 1-year, open-label study. J
Musculoskel Pain 15 (Supp 13):47 item 81. [Myopain 2007
Poster] “Pregabalin administered for up to 1 year was associated with
improvements in FMS-related pain. Pregabalin was generally well
tolerated.”
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Fogel RB, Triner J,
White DP 2005. The effect of sleep onset on upper airway muscle
activity in patients with sleep apnoea versus controls. J Physiol
564(Pt 2):549-562. “Although CPAP eliminated differences in UAR (Upper
Airway Resistance) during wakefulness and sleep, GGEMG genioglossus
(activity) remained greater in the OSA patients.” [TrPs in the pharyngeal
dilator muscles can significantly affect OSA. Their previous work
indicated tensor palatini muscle activity is high in OSA patients as well.
DJS]
Ford, ES,
Giles WH, Dietz WH. 2002. Prevalence of the metabolic syndrome
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Forrest JB, Schmidt S. 2004. Interstitial
cystitis, chronic nonbacterial prostatitis and chronic pelvic pain syndrome
in men: a common and frequently identical clinical entity. J Urol.
172(6 Pt 2):2561-2562. “Interstitial cystitis in males appears to be
more common than historically reported. Interstitial cystitis in males
and patients with chronic pelvic pain syndrome and chronic nonbacterial
prostatitis share many clinical findings. A higher incidence of
interstitial cystitis had been found in American Indian males of Cherokee
descent and deserves further investigation.”
Forseth KO, Mengshoel AM. 2007.
Multidimensional therapy in warm climate for patients with fibromyalgia
syndrome – a pilot study. J Musculoskel Pain 15 (Supp 13):47
item 82. [Myopain 2007 Poster] “The multiple improvements indicate
that multidimensional treatment in warm climate may have short and long
lasting effect in patients with FMS. Further controlled studies are
needed to confirm these findings.” [FM patients are heterogenous.
Some patients do better in warm dry climates and some do better in cold dry
climates. Some patients are both cold and heat sensitive, some are
helped by humidity and others feel worse with humidity. There are so
many environmental variables that can affect a climate reactor that studies
such as this may be very difficult to interpret. DJS]
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Gran. 1999. A 5.5 year
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population: significance and natural history. Clin Rheumatol 18(2):114-21.
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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.”
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disturbances associated with abdominal obesity, including glucose
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dyslipoproteinaemia, now widely known as the metabolic syndrome.
Several abnormalities in the hypothalamic-pituitary axis have been
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Franco C, Bengtsson BA, Johannsson G. 2001.
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“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.
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valuable diagnostic and therapeutic tool in myofascial pain syndrome.
J Musculoskel Pain 15 (Supp 13):22 item 33. [Myopain 2007
Poster] “MPS should be considered as a possible cause of musculoskeletal
complaints in neck or shoulder disorders. Surface electromyography can
be of great benefit in the process of differential diagnosis and may be
illuminate non-physiological motor behavior, which is one of the
perpetuating factors in MPS. The knowledge of referred pain patterns
may be helpful in identifying the muscle to be treated.” [This is a
very interesting study, as the MTPs were initiated due to use of
endotracheal tube during surgery, and the referral pain pattern occurred
during swallowing. Having experienced TPM cascade from endotracheal
intubation myself, I know how difficult this can be and how unaware most
anesthesiologists and other medical team members are that this can occur.
DJS]
Franken P, Chollet D, Tafti M. 2001. The
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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
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“...a 3-day opioid switch from morphine to methadone followed by a
one week titration seems pharmacologically sound.” These patients
had chronic non-malignant pain. Methadone serum concentrations
did not change significantly from dose titration through 9 months
therapy.
Fredheim OM, Kaasa S, Dale O et al. 2006. Opioid switching
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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.
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trials.”
Fricton, J. R. 2002. "Masticatory
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trigger points should be explored in cases of masticatory pain.
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“Treatment of GERD had a significant impact on the reduction of the apnea-hypopnea
index, snoring, and daytime sleepiness. Elimination of GERD should be
part of a comprehensive treatment plan for patients with OSAHS.”
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patients is hyporeactive.
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[This may result in inappropriate medications and therapies. DJS]
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hypocortisolism. Psychoneuroendocrinology [Epub ahead
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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,
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the remote hyperalgesia to mechanical visceral stimulation and the increase
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“This case suggests that CV/CT mobilizations and active TrP release may
have been beneficial in reducing pain and restoring function in this
patient.” This case is interesting in that myofascial dysfunction
occurred after a 35-year old man had been on the bleachers at a hockey
game for 3 hours. Two days later he had pain in the right scapular area
and spine that increased during the next 6 weeks. He had considerable
pain, lost some function and range of motion and had difficulty sleeping
due to movement-triggered pain. He was subjected to weeks of physical
therapy including spine mobilization, and given many expensive
radiological tests. After months of this, trigger points were found in
multiple area muscles. After 4 weeks of specific treatment the patient
had full return to function. [How much pain is needless, and how much
time and other resources are wasted, because we do not have care
providers who are adequately trained in the diagnosis and treatment of
myofascial TrPs? DJS]
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for pain and function in all types of CNCP. Other drugs
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relief they were outperformed only by strong opioids. Despite
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Ga
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lidocaine injection to trigger points in myofascial pain syndrome.
J Rehabil Med. 39(5):374-378. “In managing myofascial pain syndrome,
after one month intramuscular stimulation resulted in more significant
improvements in pain intensity, cervical range of motion and depression
scales than did 0.5% lidocaine injection of trigger points.
Intramuscular stimulation is therefore recommended for myofascial pain
syndrome.”
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hotplate trial, subjects tended to exhibit shorter response latencies,
suggesting lower pain thresholds or less analgesia. These results are
supported by related experimental findings and suggest that natural
variations in geomagnetic intensity may influence nociceptive behaviors in
mice.” [This study, although done in mice, may have implications for
electromagnetic sensitivity observed in some FM patients. DJS]
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12(4):62-70. “Functional medicine
is essentially patient centered, rather than disease centered. A
structure is presented for uniting a patient-centered approach to diagnosis
and treatment with the fruits of modern clinical science (which evolved
primarily to serve the prevailing model of disease-centered care).
The core scientific concepts of disease
pathogenesis are antecedents, triggers, and mediators. Antecedents are
factors, genetic or acquired, that predispose to illness; triggers are
factors that provoke the symptoms and signs of illness; and mediators are
factors, biochemical or
psychosocial, that contribute to pathological changes and
dysfunctional responses.
Understanding the antecedents, triggers, and mediators that underlie illness
or dysfunction in each patient permits therapy to be targeted to the
needs of the individual. The conventional diagnosis assigned to the
patient may be of value in identifying
plausible antecedents, triggers or mediators for each patient, but is not
adequate by itself for the designing of patient-centered care.
Applying the model of person-centered diagnosis to patients facilitates the
recognition of disturbances that are
common in people with chronic illness. Diet, nutrition, and exposure
to environmental toxins play central roles in functional medicine because
they may predispose to illness, provoke symptoms, and modulate the activity
of biochemical mediators through a complex and diverse set
of mechanisms. Explaining those
mechanisms is a key objective of the Textbook of Functional Medicine (from
which this article is excerpted). A patient's beliefs
about health and illness are critically
important for self-care and may influence
both behavioral and physiological
responses to illness. Perceived self-efficacy is an important mediator
of health and healing. Enhancement of patients' self-efficacy
through information, education, and the development of a collaborative
relationship between patient and
healer is a cardinal goal in all clinical
encounters.” [ I strongly
recommend this textbook for any doctor who has patients with chronic
illness. It will help them get to the cause of some of the metabolic
dysfunctions. DJS]
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neuromodulators that are not stored in cell vesicles, but rather
synthesized by the cell on demand. The endogenous cannabinoid
system could play a central role in several neuropsychiatric disorders
and is also involved in other conditions such as pain, spasticity and
neuroprotection.”
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can activate mast cells, a type of connective tissue cell, causing
the release of a number of informational substances including
hyaluronic acid, vasoactive intestinal polypeptide (VIP, a
substance which has been implicated in keeping our HPA-axis in the
"fight or flight" stress mode), histamine (which can add to
swelling, itching, pain, allergic manifestations and
hypersensitivity,) and cause other cells to release somatostatin
(which can enhance sensations of inflammation and light
sensitivity).
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Suarez-Almazor. 1998. Referral and diagnosis of common rheumatic diseases by
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[Feb 1 Epub ahead of print] These conditions are common, and there may be
racial differences that seem to develop early.
Garbuzenko E, Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis and
lattice contraction: a direct role for mast cells in skin fibrosis.
Clin Exp Allergy. 32(2):237-246. This study indicates that co-existing
allergies and the presence of more numerous mast cells may have a
significant affect on scarring, formation of adhesions and fibrosis.
One of the two main mast cell mediators involved is histamine, one of the
biochemicals produced during MTrP local twitch response. Allergies may thus
be interactive with other conditions in yet one more way.
Garbuzenko E., Nagler A, Pickholtz D et al. 2002.
Human mast cells stimulate fibroblast proliferation, collagen synthesis
and lattice contraction: a direct role for mast cells in skin fibrosis.
“...mast cells have a direct and potentiating role in skin remodeling
and fibrosis.” [Excess histamine in the system, from allergy,
fibromyalgia imbalance, myofascial TrP twitch response, and/or other
reasons may directly affect the formation of adhesion and scar tissue.
DJS]
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metabolic complications in patients with excess body fat (obesity) or
markedly reduced body fat (lipodystrophy). Alterations in free fatty
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complications.” Adipose tissue is more than a mechanical perpetuating
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efficacious and cost effective treatment for persons with chronic pain,
relative to a host of widely used conventional medical treatment.” [Chronic
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the skills to diagnose and treat these conditions. DJS]
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chewing in patients suffering from myofascial pain. Patients with
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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]
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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.
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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.
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facilitation, and this sensitization factor must be considered when
determining evaluation and treatment.
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in future evaluations should be to try to find the combined pharmacological
or non-pharmacological treatment of choice for specific subgroups of
patients.”
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“Patients pain reports can be systematically biased by a number of
methodological factors.”
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into account methodological differences, particularly in the hypoglycemic range.
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2007. Firing rate and conduction velocity of single motor units in the
trapezius muscle in fibromyalgia patients and healthy controls. J
Electromyogr Kinesiol. [Apr 23 Epub ahead of print]. “CV (conduction
velocity) was significantly higher in FM than in healthy controls; this
might be due to alterations in histopathology and microcirculation.”
[It is unfortunate that patients were not screened for co-existing
myofascial trigger points. DJS]
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proportion of fibromyalgia cases seen in this sample supports the hypothesis
that there is an association between sleep disordered breathing and
fibromyalgia syndrome.
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NOTATION IS CORRECT]
Gerwin R. 2007. Trigger points: a
comprehensive hypothesis of trigger point formation. J Musculoskel
Pain 15 (Supp 13):12 item 14. [Myopain 2007 Poster] Dr.
Gerwin’s hypothesis may fill in the missing elements in the formation of
myofascial trigger points (MTPs). We did not have an explanation for
the excess release of acetylcholine, the excess release of calcium, and the
excessive motor endplate noise, nor did we understand why the taut band
forms. These phenomenon could be explained by a dysfunctional
ryanodine receptor calcium channel. This dysfunctional ion channel
could promote the excessive calcium release from the sarcoplasmic reticulum,
resulting in persistent muscle fiber contraction. Gates in the cell wall,
like tiny airlocks in a space station, allow charged particles such as
calcium, potassium and other minerals to flow in and out of the cell
membrane and affect the interior metabolism of the cell. The pathways
are called ion channels. An illness caused by dysfunction of the gate
mechanism is called a channellopathy. This important piece of the puzzle
indicates that myofascial pain due to trigger points could be a
channellopathy. Dysfunctional mitochondria and/or second messenger
dysfunction metabolically upstream could also be responsible or be
associated with the ryanodine dysfunction. [I found this to be one of the
most exciting revelations at the Myopain ‘07 Congress, offering great hope
to those of us with myofascial pain. This offers a whole new way of
looking at myofascial pain, and perhaps a whole new way of treating it. I
hope researchers will take note and mobilize forces to investigate this.
DJS]
Gerwin R. 2004. Differential diagnosis of
trigger points. J Musculoskeletal Pain 12(3/4):23-28.
“Trigger points pain can have many different causes that must be identified
and treated specifically.”
Gerwin RD. 2005.
A review of myofascial pain and fibromyalgia—factors that
promote their persistence. Acupunct Med.
23(3):121-134. Fibromyalgia and myofascial pain are common
and different conditions, although they may occur in the same
patient. “Fibromyalgia is a chronic, widespread muscle
tenderness syndrome, associated with central sensitization. It
is often accompanied by chronic sleep disturbance and fatigue,
visceral pain syndromes like irritable bowel syndrome and
interstitial cystitis. Myofascial pain syndrome is an
overuse or muscle stress syndrome characterized by the presence
of trigger points in muscle.” It is important to uncover
the cause of chronic muscle pain so that treatment will be
effective. “Chronic myalgia may not improve until
underlying precipitating or perpetuating factor(s) are
themselves managed.” These causes may include structural and
metabolic conditions. If the underlying
conditions are brought under control, the
chronic myalgia may resolve.
Gerwin RD,
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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.
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the immediate cause of pain, and correcting those factors that
predispose to recurrence.”
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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.”
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5(5):412-420. Myofascial pain can be primary or secondary to another
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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
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to chronic pain. Neuroimaging studies demonstrate cerebral
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stress response systems unknowingly exercise regularly to augment the
function of these systems and suppress symptoms. These individuals
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[This is a noteworthy quote, in so much as there are no such things as
fibromyalgia trigger points and thus no FMS trigger point injections to be
evaluated. Myofascial trigger point injections, however, have been
adequately evaluated. It is fundamental that clinicians and researchers
need to understand that there are no fibromyalgia trigger points, and that
myofascial pain is not the same as fibromyalgia. Until this happens,
the research will be skewed and the conclusions reached not viable.
DJS]
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