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Cellular changes are not restricted to neurons in the dorsal horn,
however, and there is growing evidence for involvement of glia, and
of glia-neuronal signaling, in initiating the sustaining enhancement
of nociceptive transmission. This expanded understanding of
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their recognition of myofascial trigger points as one of the most common
sources of chronic pelvic pain. Clinicians need to be aware that
terms such as levator ani syndrome, pelvic floor tension myalgia,
pudendal neuralgia and cramps are descriptions, not diagnoses, and they
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IBS, musculoskeletal aches, respiratory tract symptoms, vaginal and/or
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DJS]
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up-to-date and complete information about this entity, focused on
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to trigger points. These conditions are multifactorial and require
time and specificity for each patient. [Each patient is different,
and cookbook medicine is unlikely to be useful in dealing with these
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is the illness(es) that are difficult to manage unless adequate
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themes: (a) managing the symptoms, (b) becoming a self-advocate, (c)
medications camouflage the pain, (d) coming to grips with the
illness means making changes, (e) being accused of ‘taking a free
ride’ angers them, (f) support comes from self and spiritual
connections, and (g) a certain amount of secrecy makes it easier to
live with the illness. Recommendations focus on using a
holistic approach to help African American women achieve or maintain
their integrity.”
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simultaneously dealing with the fatigue, pain and muscle stiffness of
FMS and the lack of safe medication can be frustrating. Education for
prospective mothers and their health care providers is important.
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Spontaneous pain and mechanical hypersensitivity can develop as a
consequence of sensitization of primary afferents directly involved
in the inflammatory process, but also following sensitization of
neuronal processing in the spinal cord (central sensitization) or
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proteins at the nociceptive nerve endings such as the activating
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channels that set membrane potential and modulate discharge
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It is not to be taken lightly and can cause serious side effects, including
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DJS]
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contribute to itch. ….there is increasing evidence that also
central processing of itch can be sensitized in pruritus patients.
Interestingly, this pattern of peripheral and central sensitization in
pruritus has striking similarities to the one observed in chronic pain
patients. The presumed similarities in underlying sensitizing
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successful therapies for chronic pain might be used also in chronic
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in space during a walking task. The neck represents a complex
source of inputs capable of modifying our orientation in space during a
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disorder. They might reflect either a consequence of chronic
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fibromyalgia.”
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patients and suggest a dissociation of muscular and central processes during
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insomnia with other disturbances within and outside the range of sleep
medicine is frequent. Special problems arise in chronic
non-organic pain. It is clear from all these aspects that PSG [polysomnography–sleep
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Lack of restorative sleep plays an important role in many cases of
fibromyalgia, and not enough is done to track down the causes of
non-restorative sleep. Too often it is just dismissed as part of
FMS, when there often may be components that are treatable. DJS]
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picture. “It is suggested that insomnia in chronic pain patients should
be taken seriously and treated by its specific methods.”
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[These patients were not screened for co-existing myofascial TrPs.]
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social level, low alcohol intake, rare pregnancy and late start of first
menstruation were more common among FMS patients than other chronic pain
patients or people without chronic pain.
Schochat T, Beckmann C
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[German] “The associations with a low social level, low alcohol
intake, late menarche and rare pregnancies are specific for subjects with
fibromyalgia. These factors distinguish subjects with fibromyalgia from
subjects with other chronic pain conditions as well as from subjects with no
chronic pain. The same hormonal factors responsible for a delayed
menarche and a reduced fertility may be relevant in the development of
fibromyalgia.”
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This may be very important in treating FMS patients who often have
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unprecedented ability to safely explore and measure the local
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twitch response.” “...the local biochemical milieu does
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released. In the active TrP patient group, bradykinins,
calcitonin gene-related peptide, IL-$,
serotonin, tumor necrosis factor-",
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significantly than in the control group or the group with latent
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explains that it is a ...“serious mistake to consider the TrP in
isolation.” Patients often have clusters or chains of TrPs, and
clinicians need to be on the alert that when one TrP is present
in a patient with chronic symptoms (not always pain–TrPs can
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J Musculoskeletal Pain 3(1):7-14. This paper is of vital importance.
It explains how some researchers have been using the term “myofascial pain
syndrome (MPS)” as synonymous with temporomandibular dysfunction (TMJD),
without explaining the definition. [This practice is common in papers
written by dentists. This dangerous practice can lead to misleading or
erroneous conclusions. Others build on these conclusions, not
realizing that authors are using the term MPS to mean TMJD, and may assume
that they refer to myofascial pain due to trigger points that may occur in
all four quadrants of the body. Authors must be careful to define
their terms. DJS]
Simons
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of sarcomere groupings in individual muscle fibers, suggesting the mechanism
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misunderstood phenomenon and needs to be more carefully assessed in regards
to association with myofascial trigger points.
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about opioids and the associated risk of dependence stemmed from older
research that was fundamentally flawed. Opioid treatment must
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understanding of drug absorption, metabolism, toxic and binding
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This article is vitally important for physicians who have patients with
myofascial TrPs. Simvastatin, and, by biochemical inference, statin
medications, triggers flood of intra-cellular calcium. Increased
release of Ca2+ is an essential part of the formation of myofascial TrPs,
according to Simons’ integrated hypothesis. The addition of statins
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Staud R. 2007. The role of peripheral input
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15 (Supp 13):7 item 8. [Myopain 2007 Poster] Indications are
that the diffuse, bodywide pain of FM is maintained by peripheral pain
stimuli. “Most FMS patients present with focal tissue abnormalities
including myofascial trigger points [TrPs], ligamentous trigger points, or
osteoarthritis of the joints and spine. While not predictive for the
development of FMS, these changes nevertheless represent important pain
generators that may initiate or perpetuate chronic pain. Thus
spatially limited forms of musculoskeletal pain, including MPS, may develop
in some patients into widespread chronic pain syndromes like FMS.”
Staud R, Robinson ME, Price DD. 2007. Temporal
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widespread central sensitization of fibromyalgia patients. J Pain.
[Aug 1 Epub ahead of print]. “Perspective: The pain of FM seems to be
accompanied by generalized central sensitization, involving the length of
the spinal neuroaxis. Thus, widespread central sensitization appears
to be a hallmark of FM and may be useful for the clinical case definition of
this prevalent pain syndrome. In addition, measures of widespread
central sensitization, like TSSP-M (temporal summation of second pain and
maintenance), could also be used to assess treatment responses of FM
patients.”
Staud R, Koo E, Robinson ME et al. 2007.
Spatial summation of mechanically evoked muscle pain and painful
aftersensations in normal subjects and fibromyalgia patients. Pain.
[Apr 23 Epub ahead of print]. “…decreasing pain in some muscle areas by
local anesthetics or other means may improve overall clinical pain of FM
patients.” [This is another indication that control of peripheral pain
stimuli such as caused by myofascial trigger points and arthritis can be a
significant part of chronic pain treatment in FM. DJS]
Staud R. 2006. Biology and therapy of
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central nervous system pain processing abnormalities in FM,
including central sensitization and inadequate pain inhibition.
However, increasing evidence points towards peripheral tissues as
relevant contributors of painful impulse input that might either
initiate or maintain central sensitization, or both. It is
well known that persistent or intense nociception can lead to
neuroplastic changes in the spinal cord and brain, resulting in
central sensitization and pain. “Importantly, after central
sensitization has been established only minimal nociceptive input is
required for the maintenance of the chronic pain state.”
Staud R, Vierck CJ, Robinson ME et al. 2006.
Overall fibromyalgia pain is predicted by ratings of local pain and
pain-related negative affect – possible role of peripheral tissues.
Rheumatology (Oxford) [Apr 18 Epub ahead of print] “We
hypothesized that the overall clinical pain is largely determined by
the pain intensity of local body areas. Thus, we assessed the
role of local body pains as predictors of overall clinical pain in
FM patients.” “Peripheral factors (maximal/average local pain and
number of painful body areas) predicted most of the variance of
overall clinical FM pain, suggesting that the input of pain by the
peripheral tissues is clinically relevant. About 19% of the
pain variance was predicted by PRNA. Thus, peripheral pain and
negative affect appear to be particularly relevant for overall FM
pain and may represent important targets for future therapies.”
Staud R, Vierck CJ,
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Staud R, Cannon RC, Mauderli AP et al.
2003. Temporal summation of pain from mechanical
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102(1-2):87-95. “Temporal summation for FMS subjects
occurred at substantially lower forces and at a lower
frequency of stimulation. Furthermore, painful
after-sensations were greater in amplitude and more
prolonged for FMS subjects.” “Abnormal input from muscle
nociceptors appears to underlie production of central
sensitization in FMS that generalizes to input from
cutaneous nociceptors,”
Staud R, Price DD, Robinson ME et al. 2004.
Body pain area and pain-related negative affect predict clinical
pain intensity in patients with fibromyalgia. J Pain
5(6):338-343. “The number of painful body areas obtained by
body pain diagrams is a better predictor of clinical pain
intensity than TPS in FM patients.” [It would be helpful
if these patients were checked for co-existing myofascial TrPs.
It could be that the presence of co-existing myofascial TrPs is
the better predictor of clinical pain intensity. DJS]
Staud R, Price DD, Robinson ME et al. 2004. Body pain area and
pain-related negative affect predict clinical pain intensity in
patients with fibromyalgia. J Pain 5(6):338-343. The
combination of charts showing painful body areas, tender point
counts, and pain-related negative emotions gave a much more accurate
representation of pain intensity in FMS patients than did simple
counting of tender points.
Staud R. 2004. Predictors of
clinical pain intensity in patients with fibromyalgia syndrome. Curr
Rheumatol Rep. 6(4):281-286. “The magnitude of wind-up
after-sensations appeared to be one of the best predictors for clinical
pain intensity of fibromyalgia syndrome patients (27%).”
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