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[This study estimated that among US adults, 5 million have FM.
They also mentioned 59 million with low back pain and 30.1
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J Musculoskeletal Pain 13(3). This editorial
pinpoints some problems in the development of the field of
chronic pain management. One is the use of pain
clinics as dumping grounds for complex cases. Much of
chronic pain is preventable, but it is not being prevented.
“Chronic illness will become the major health care issue in
the 21st century, as the population ages and
infectious diseases are better treated.” “...we will
need pain managements who have a broad overview of the
diagnostic and therapeutic strategies that will provide the
best possible outcomes.” “Payers and providers will
need to recognize that chronic pain is like diabetes: cure
is not the goal. Instead, management with the goal of
minimizing morbidity, improving function, and containing
costs is the optimal outcome.”
Loeser,
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the problem? Rheum Dis Clin North Am
29(4):653-673. These
authors realize that OA is not an inevitable part of getting
old, and that the progression of structural deterioration in
OA may be prevented by improving neuromuscular function.
Structural damage does not always correspond to joint
deterioration, and proprioception is often involved, as is
muscle weakness and lack of balance. What is missing in
this article is often at the heart of these things: myofascial
trigger points.
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result of cardiovascular complications. Insulin
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and should be appropriately addressed to ensure the best
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immune function by signaling target cells of the immune system
through autonomic and neuroendocrine pathways.
Neurotransmitters and hormones produced and released by these
pathways interact with immune cells to alter immune functions,
including cytokine production. Cytokines produced by cells
of the immune and nervous systems regulate sleep.
Cytokines released by immune cells, particularly
interleukin-1beta and tumor necrosis factor-alpha, signal
neuroendocrine, autonomic, limbic and cortical areas of the CNS
to affect neural activity and modify behaviors (including
sleep), hormone release and autonomic function. In this
manner, immune cells function as a sense organ, informing the
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than normal speakers, which could interfere with
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[This study did not evaluate patients for myofascial
TrPs, which can often cause proprioceptive dysfunction,
although it does mention that movement dysfunction is
often associated with stuttering. Some cases of
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depend strongly on what the patient feels. The caveat
that FMS patients are prone to be hyperreactive to ultrasound
therapy and need to be treated less vigorously is consistent
with their strong reaction to other treatments and life
experiences. It takes much more skill and gentleness to
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suggesting that they should be treated. Mechanisms that
might mediate the effects observed are proposed.” [Latent
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IRS, and therefore diabetes and cardiovascular disease, can
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to understand that myofascial TrPs cause pain at the end of the
range of motion, and it is logical for the patient to avoid
range of motion when there is pain at the end of that range of
motion. The TrPs must be treated and the range of motion
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nicotinic acetylcholine receptors in the neurons. This
medication blocks the main pain transmitter receptors (acute
and chronic pain) and also affects local pain signaling that
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the regional muscle pain disorder (myofascial) is similar or
different from the more generalized disorder
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treatment of chronic pain. These drugs modulate
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can quickly find and treat TrPs. [There was no
significant change in range of motion, which may
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the pain levels were reduced significantly. This
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with subjects who did not practice T'ai Chi. More T'ai-Chi
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fatigue and a loss of stamina; poor balance; and a change in
personality. Injury victims experience a loss of
motivation, emotional lability, and a decrease in libido.
It is hypothesized that the collision impact produces an
inertial strain injury to the anterior regions of the brain
which depresses the functions of the frontotemporal lobes,
at the same time, sensitizing somatosensory neural afferent
systems. Damage to the orbital surfaces of the
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The outcomes appear to be related to the program design and
the characteristics of the populations studied. As the
patients with fibromyalgia form a heterogeneous population,
more research is required to identify the characteristics of
patients who benefit from specific modes of exercise.
Moreover, long-term planning is needed to motivate the
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This study found that “Interactions between the
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A good, positive support group may provide the same
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energy to muscle confirms that muscle function is globally
impaired in FMS patients. The results suggest that the
impairment predominated on aerobic processes."
Marchettini, P., F.
Formaglio and M. Lacerenza. 1999. Clinical interpretations of
intraneural muscle nociceptors recordings in humans. J
Musculoskel Pain 7(1-2):55-59.
Marchioni D, Ghidini A, Daari S et al.
2005. The normal-weight snorer: polysomnographic study
and correlation with upper airway morphological alterations.
Ann Otol Rhinol Laryngol. 114(2):144-146. “The
major risk factor for developing OSAS in normal-weight
snorers appears to be anatomic abnormalities. The
normal-weight snorer needs to be thoroughly investigated
because of the significant risk of developing OSAS and for
the detection of multiple concomitant sites of obstruction.”
[This paper does not discuss muscle contracture due to TrPs,
but it could be a variable factor as well, and the presence
of TrPs in some muscle may indicate the need for
automatically adjusting CPAP set to maximum high equal to
that of the sleep study need of the patient.]
Marcus DA. 2006. A review of
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adult chronic pain. J Headache Pain 7(1):3-8.
“Over the last decade, studies have suggested that exposure
to repeated painful procedures during the early perinatal
period results in profound changes in sensitivity of
nociceptive pathways. Both animal and human studies
show that early pain experiences increase pain responses
beyond the period of infancy. These data suggest a
need to increase implementation of guidelines for minimizing
pain exposures during infancy.”
Marcus, D. A. 2000.
Treatment of nonmalignant chronic pain. Am Fam Physician
61(5):1331-8, 1345-6.
Margoles M. 1983.
Stress neuromyelopathic pain syndrome (SNPS): Report of 333 patients.
J Neuro Ortho Surg 4(4):317-322. This is an older but very important study using the term “stress neuromyelopathic pain syndrome” for what Travell and Simons describe in their later texts as “post-traumatic hyperirritability syndrome.”
The authors agree that these are the same conditions. This condition can be caused by severe or repeated trauma especially to the head, neck and back, but can also be caused by biochemical trauma. This author found that patients with this condition often have low levels of B vitamins but may not respond to oral supplements, and 30-50% of these patients have abnormally high vitamin A.
Eating foods high in vitamin A could lead to a flaring of symptoms.
This condition often starts locally but can spread to overlapping pain patterns.
Clinical findings are clearly specified, and the fact that this can often be mistakenly diagnosed as neuropathy caused by disc problem when the disc is not the cause at all, but the metabolic changes that this syndrome has brought about.
[After extensive discussion with Drs. Michael S. Margoles and David G. Simons, I am convinced that these are early descriptions of what can happen when early myofascial trigger points and fibromyalgia are not treated promptly and aggressively.
This paper clearly describes in detail a scenario of the unfolding of this condition.
I advise any clinician to get a copy of this important paper. DJS]
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been increasingly used in the interventional treatment of
several other disorders characterized by excessive or
inappropriate muscle contractions. BoNT is being
investigated for the control of the pain, and for the
management of tension or migraine headaches and myofascial
pain syndrome. This paper presents current data on the
use of BoNT to treat pelvic floor disorders.”
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found that acupuncture significantly improved symptoms
of fibromyalgia. Symptomatic improvement was not
restricted to pain relief and was most significant for
fatigue and anxiety.” [The subset of FMs patients
who have anxiety and fatigue may benefit from specific
acupuncture therapy. DJS]
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sympathetically maintained pain syndrome. Curr Pain
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display signs of relentless sympathetic hyperalgesia...”
Martinez-Lavin,
M. 2002. The autonomic nervous system, and fibromyalgia. J
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Fibromyalgia is a multisystem illness. Many researchers
have found indications that fibromyalgia is a form of
autonomic nervous system dysfunction.
Martinez-Lavin,
M. 2002. Management of dysautonomia in fibromyalgia. Rheum
Dis Clin North Am 28(2):379-87. "The realization of
dysautonomia in FM has opened the possibility for new and
different therapeutic interventions. Much more research
is needed to better define the role of ANS in the pathogenesis
of FM. If this research supports current hypotheses,
therapeutic trials with disciplines and substances intended to
correct autonomic dysfunction will be indicated."
Martinez-Lavin, M., A.
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found that a masseter trigger point was the source of tooth
pain in this patient. The patient had immediate relief
after trigger point injection, with no recurrence of the pain.
Dental practitioners need myofascial medicine as part of their
training and their differential diagnosis.
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promising therapeutic target against different GI
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results of a pilot clinical trial. Altern Ther
Health Med. 13(3):32-34. “IVNT appears to be safe to
reduce FM symptoms.” The patients in this study had FM for
at least 8 years and had no significant, lasting relief with
conventional therapies.
Mathias
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Serotonin regulates mammary gland development via an autocrine-paracrine loop.
Dev Cell 6(2):193-203. Dysfunctional serotonin signaling may be part of the reason some women with FMS experience problems nursing.
Nursing may begin normally, but the milk [production] hesitates or stops.
Matsumoto, Y. 1999.
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genetic and epigenetic factors could contribute to decreased
serotonin-selective reuptake transporter in irritable bowel
syndrome. A serotonin-selective reuptake transporter
gene promoter polymorphism may cause a genetic
predisposition, and inflammatory mediators can induce
serotonin-selective transporter downregulation. While
a psychiatric co-morbidity exists with IBS, changes in
mucosal serotonin handling support the concept that there is
a gastrointestinal component to the aetiology of irritable
bowel syndrome.” [There are many patients with IBS and
without a “psychiatric component” except for the general
depression that one gets when one is given that “It’s All In
Your Head” diagnoses. Current research indicates that
chronic illness often has intestinal permeability as a
contributor. When patients have invisible illnesses
causing chronic pain and are given or take aspirin and NSAID
that can contribute to intestinal permeability (see Galland,
L. and
www.functionalmedicine.org), IBS is a logical
consequence. It is nice to know that some researchers
are finally discovering the GI component, but they are still
stuck in the mindset that IBS is a basically psychological
dysfunction. DJS]
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to demonstrate that those with established, and those
psychologically at risk of, chronic widespread pain
demonstrate abnormalities of HPA axis function, which are
more marked in the former group.” “We conclude that
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“New perceptions included disorientation, pain, perceived
changes in temperature, limb weight or body image.
Conclusions: Our findings support the hypothesis that
motor-sensory conflict can exacerbate pain and sensory
perceptions in those with FMS to a greater extent than in Hvs.
[healthy volunteers]”
McCain, G. A. 1999.
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Fibromyalgia. J Rheumatol 30(4):809-14.
If the body mass index is taken into consideration,
there is no significant association between premenopausal FMS
patients and healthy controls with regard to average peak
growth hormone. The
authors indicate that increase in age and obesity are both
strongly linked to the GH-IGF-1 axis, and are factors that
must be considered in research concerning FMS and the GH-IGF-1
axis.
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impairment in an attentional set shifting that is comparable
to the executive function and cognitive deficits observed in
humans with sleep apnea or after a night of experimental
sleep fragmentation.”
McCracken, L. M. 1998.
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adjustment in persons with chronic pain. Pain
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McDaniel
WW. 2003. Electroconvulsive therapy in complex regional
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one of the cases, concomitant fibromyalgia was not relieved
during 2 separate series of ETC.”
McDermott BE, Feldman MD. 2007.
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North Am. 30(4):645-662. “…the physician should
generally suspect malingering when there are tangible
incentives and when reported symptoms do not match the
physical examination or no organic basis for the physical
complaints is found.” [The authors take for granted
that their readers, psychiatrists, can diagnose ALL diseases
with standard tests and examinations. Shame on them.
Whatever happened to the oath to “Do no harm?” This
paper is food for lawyers to deny patients care.
Intelligent and trained lawyers can make mincemeat out of it
once they understand that many physicians are untrained in
diagnosis of MTPs, and there are documented changes in FM
patients that are not practical for the physician to
perform. [see: Harris RE, Clauw DJ, Scott DJ et al.
2007 and countless other references in this section. DJS]
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2005. NO-mediated alterations in skeletal muscle nutritive
blood flow and lactate metabolism in fibromyalgia. Pain
[Dec 20 Epub Ahead of Print] “FM may be more sensitive than HC
(healthy women) to the suppressive effect of nitric oxide on
oxidative phosphorylation.”
McKee, D. D. and J. N.
Chappel. 1992. Spirituality and medical practice. J Fam
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et al. 2005. The association of acetaminophen,
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aspirin or ibuprofen] is associated with an
increased risk of asthma and COPD [chronic
obstructive pulmonary disease], and with decreased
lung function.”
McLean SA, Williams DA,
Harris RE et al. 2005. Momentary
relationship between cortisol secretion and
symptoms in patients with fibromyalgia.
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“Among women with FM, pain symptoms early in
the day are associated with variations in
function of the
hypothalamic-pituitary-adrenal axis.”
McLean SA, Clauw DJ. 2005.
Biomedical models of fibromyalgia.
Disabil Rehabil. 27(12):659-665. “The
tender point criteria for FM have resulted in
the common misconception among health care
professionals that this spectrum of disorders is
limited to women with high degrees of
psychological distress. A hallmark of FM
is the presence of non-nociceptive, central
pain. There is evidence of centrally
augmented pain processing, which can be detected
both with sensory testing and by more objective
measures (e.g., evoked potentials, functional
neuroimaging). An appreciation of the
neurobiological basis for these disorders, and
an understanding of some of the abnormalities of
pain processing present in patients with FM,
will hopefully provide greater understanding of
these patients. It may also serve to
decrease the level of frustration and improve
the care experience of both chronic pain
patients and physicians.”
McLean SA, Williams DA,
Clauw DJ. 2005. Fibromyalgia after motor
vehicle collision: evidence and implications.
Traffic Inj Prev. 6(2):97-104. “The
evidence that MVC trauma may trigger FM meets
established criteria for determining causality,
and has a number of important implications, both
for patient care, and for research into the
pathophysiology and treatment of these
disorders.”
McNicholas WT, Bonsignore
MR. 2007. Sleep Apnoea as an independent
risk factor for cardiovascular disease: current
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29(1):156-178. “Considerable evidence is
available in support of an independent
association between obstructive sleep apnoea
syndrome (OSAS) and cardiovascular disease,
which is particularly strong for systemic
arterial hypertension and growing for ischaemic
heart disease, stroke, heart failure, atrial
fibrillation and cardiac sudden death. The
pathogenesis of cardiovascular disease in OSAS
is not completely understood but likely to be
multifactorial, involving a diverse range of
mechanisms including sympathetic nervous system
overactivity, selective activation of
inflammatory molecular pathways, endothelial
dysfunction, abnormal coagulation and metabolic
dysregulation, the latter particularly involving
insulin resistance and disordered lipid
metabolism.”
McPartland JM, Giuffrida A,
King J et al. 2005. Cannabimimetic effects of
osteopathic manipulative treatment. J Am
Osteopath Assoc. 105(6):283-291. “Healing
modalities popularly associated with changes in the
endorphin system, such as OMT [osteopathic
manipulative treatment], may actually be mediated by
the endocannabinoid system.”
McPartland JM. 2004.
Travell trigger points – molecular and osteopathic
perspectives. JAOA |
NOTE:
New Nomenclature