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Chronic Pain: Myofascial Pain and Fibromyalgia

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ISSN: 2329-9096
International Journal of Physical Medicine & Rehabilitation
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International Journal of Physical Medicine & Rehabilitation
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University at Buffalo, USA
Joe Edward Springer
University of Kentucky, USA
Masayoshi Yamaguchi
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Carmen M. Terzic
Mayo Clinic, Minnesota, USA
Jin J Luo
Temple University School of Medicine, USA
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International Journal of
Physical Medicine & Rehabilitation
Luo and Dun, Int J Phys Med Rehabil 2013, 1:6
http://dx.doi.org/10.4172/2329-9096.1000e102
Editorial Open Access
Volume 1 • Issue 6 • 1000e102
Int J Phys Med Rehabil
ISSN: 2329-9096 JPMR, an open access journal
Chronic Pain: Myofascial Pain and Fibromyalgia
Jin Jun Luo1,2* and Nae J Dun2
1Department of Neurology, Temple University School of Medicine Philadelphia, PA19140, USA
2Department of Pharmacology, Temple University School of Medicine Philadelphia, PA19140, USA
*Corresponding author: Dr. JJ Luo, Departments of Neurology and Pharmacology,
Temple University School of Medicine, 3401 North Broad Street, Suite C525,
Philadelphia, PA 19140, USA, Tel: 1-215-707-3040; Fax: 1-215-707-8235; E-mail:
jluo@temple.edu
Received July 30, 2013; Accepted August 03, 2013; Published August 05, 2013
Citation: Luo JJ, Dun NJ (2013) Chronic Pain: Myofascial Pain and Fibromyalgia.
Int J Phys Med Rehabil 1: e102. doi:10.4172/2329-9096.1000e102
Copyright: © 2013 Luo JJ, et al. This is an open-access article distributed under
the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Chronic pain is a common dilemma encountered in daily practice.
However, optimal treatment of chronic pain is a clinical challenge,
especially for patients with chronic myofascial pain (CMP) and
bromyalgia, known as bromyalgia syndrome(FMS). CMP has also
been termed myofascial pain syndrome, the usage of which is not
recommended, because CMP is now recognized as a disease (see below).
CMP is characterized bychronic pain caused by fascial constrictions
and multiple regional trigger points. A fascia is a connective
tissuesurrounding muscles. A trigger point is a highly sensitive area
within the muscle resulting from noxious stimuli and is painful to touch.
Myofascial pain is extremely common, and everyone may develop a
trigger point at some time in life. In the United States, an estimated
14.4% of the general population suer from chronic musculoskeletal
pain and 21-93% of patients with regional pain complaints of having
CMP [1]. FMS is another medical condition characterized by chronic,
widespread musculoskeletal pain accompanied by fatigue, sleep,
memory and mood disturbances [2,3].e term “bromyalgia” derives
from Latin,bro-, meaning “brous tissues”, Greekmyo-, “muscle”, and
Greekalgos-, “pain”, which means “muscleandconnective tissue pain”.
FMS is estimated to aect 2–4% of the population [4,5], with a female to
male incidence ratio of approximately 9:1 [6]. In contrast, CMP aects
men and women equally. Both CMP and FMS most oen aect 30-60
years-old individuals. e cost in care for chronic musculoskeletal pain
is high in developed countries [7]. e annual cost of chronic pain in
the United States, including healthcare expenses, lost income, and lost
productivity, is estimated more than $100 billion [8].
CMP causes distinct, isolated or regional muscle pain, such as
pain in the neck, shoulders, upper and lower back, usually unilateral
or worse on one side of the body. e muscular pain is persistent,
aching, and deep, ranging from mild discomfort to excruciating and
“lightning-like” pain.It usually does not resolve on its own, even aer
typical, rst-aid self-care such as ice, heat, and rest. A hallmark of
CMP is the presence of trigger points. A trigger point is a small, hard
knot that may be visible and felt under the skin. e knot itself can be
painful, especially when poked. Trigger points typically form as a result
of trauma to the tissue. Trigger points might be “active” or “latent”. An
active trigger point is a sensitive area of extreme tenderness that usually
lies within the skeletal muscle and is associated with local or regional
pain. Alatent trigger point is a dormant area that has the potential to
act like a trigger point. A latent trigger point does not cause pain during
normal activities, but is tender when touched and can be activated when
the muscle is strained, fatigued, or injured. Studies have demonstrated
that 25-54% of asymptomatic individuals have latent trigger points [1].
e cardinal symptoms of FMS are chronic widespread pain,
fatigue, and allodynia, a condition of non-painful stimuli causing
painful sensation. Other symptoms may include tingling, muscle
spasm and weakness,morning stiness, fatigue, anxiety, panic attacks,
cognitive or memory impairment (“brofog”) [4,9], depression [2,10],
functional bowel disturbances [11],feeling overwhelmed due to high
levels of sensory input and chronicsleep disturbances [12]. Although
FMS is generally accompanied with chronic widespread pain, the latter
may be localized [13]. For the diagnosis of FMS, the American College
of Rheumatology published ocial criteria in 1990, known as “the
ACR 1990”, including 1) widespread pain for at least three months in
three quadrants of the body, and 2) abnormal sensitivity to palpation
in at least 11 of 18 specic tender points. Notably, a tender point is
dierent from a trigger point [14,15]. Guidelines for the diagnosis and
management of bromyalgia have been published in various countries
[16-18].
CMP and FMS may coexist and share some common symptoms,
including musculoskeletal pain, headaches and/or migraines,
sleep disturbances, imbalance and/or dizziness, memory decline,
unexplained sweating, worsening symptoms due to stress, changes
or extremes in weather, and physical activity. However, the two
conditions are distinct. FMS is pervasive with chronic generalized pain
and hyperirritability. In contrast, CMP may aect many parts of the
body but is limited to trigger points.
More recently, CMP is recognized as a disease rather than
a syndrome because muscle trauma leads to malformations of
neuromuscular junction, where the nerve cells connect to muscle cells.
is suggests CMP is a neuromuscular disease. FMS is a syndrome due
to central sensitization to the underlying nociceptive or neuropathic
pain, or a combination of the two.
Distinction between CMP and FMS is crucial because their
response to treatment and prognosis are dierent. Trigger points can
be eectively manipulated. A growing body of evidence shows that
chronic pain can inuence the central nervous system (CNS) and
cause central sensitization [13]. CMP, if untreated, may incite and
exacerbate FMS. Early treatment of CMP may help prevent FMS. e
term central sensitivity syndrome has emerged for FMS, CMP, and
other conditions involving central sensitization.
e precise etiologies of CMP and FMS are not fully understood.
It is commonly accepted that CMP may be caused by prior muscle
injury [19]. CMP may subsequently develop into FMS manifesting
widespread chronic pain and allodynia. e pathogenesis of FMS
is likely due to a central sensitivity mechanism resulting from
neuro-chemical inbalances. Activation of inammatory pathway
in the brain may cause aberrant pain processing [3,13]. Central
sensitization occurs due to the presence of a lower threshold for
pain and hyperactivity of pain-sensitive nerve cells in the spinal cord
or brain. Importantly, neuroendocrine disruption such as growth
hormone, insulin-like growth factor-1, cortisol, prolactin, androgens,
leptin, and neuropeptide Y may also play a role [20-26], although
disagreement exists [27-30] and administration of growth hormone
in patients failed to show signicant improvement [31]. ese chronic
neuroendocrine disruptive changes may activate hypothalamic
corticotrophin-releasing hormone neurons, disrupt normal function
Citation: Luo JJ, Dun NJ (2013) Chronic Pain: Myofascial Pain and Fibromyalgia. Int J Phys Med Rehabil 1: e102. doi:10.4172/2329-9096.1000e102
Page 2 of 3
Volume 1 • Issue 6 • 1000e102
Int J Phys Med Rehabil
ISSN: 2329-9096 JPMR, an open access journal
of the pituitary-adrenal axis, and cause an increased stimulation of
hypothalamic somatostatin secretion, which in turn could inhibit the
secretion of other hormones [32]. Alterations in neuroendocrine and
neurotransmitters may alter exercise-induced analgesic response [33]
and potentiate nociceptive system causing allodynia [34,35]. Genetic
predisposition also plays a role in the development of CMP and FMS
[36]. For example, apolipoprotein E4 (Apo E4) genotype and selected
environmental exposures (e.g. motor vehicle accidents) increases the
risk of FMS [37]. Indeed, genetic polymorphisms of serotoninergic
[38], dopaminergic [39] and catecholaminergic[40] systems have
been shown in FMS, though not specic as they are also seen in
other disorders, including chronic fatigue syndrome [41], irritable
bowel syndrome [42], and depression [43], which all are common
comorbidities of FMS.Individuals with the 5-HT2A receptor 102T/C
polymorphism have been shown at increased risk of developing FMS
[44]. A high aggregation of bromyalgia in families was demonstrated
[45]. Using self-reporting of chronic widespread pain (CWP) as a
surrogate marker for bromyalgia, theSwedish Twin Registryreports
monozygotic twinswith CWP have a 15%, and Dizygotic 7%, increased
chance of having CWP [46,47]. However, the mode of inheritance is
most probablypolygenic [36].
Although no specic lab tests conrm a diagnosis of CMP and FMS,
tests do help identify predisposing risk factors. Current treatment for
CMP includes pharmacological and non-pharmacological approaches.
Pharmacological treatment includes non-steroidalanti-inammatory
drugs, tricyclic antidepressants, muscle relaxants, and anticonvulsants.
Non-pharmacological treatment includes physical therapy, massage,
stretching, heat, and ultrasound. Acupuncture and needle injection
with or without medications into a trigger point can help relieve pain.
In this issue of JPMR, there are two articles related to the chronic
pain. Dhadwal et al. present their clinical retrospective study on the
ecacy of lidocaine trigger point injection (LTPI) in alleviating
CMP. Of the 24 patients in the study who answered questionnaires
aer having received LTPI, 22 reported a signicant pain relief (92%,
P<0.0001). e pain level on a scale of 1-10 was 8.9 ± 0.4 (± SE) prior
to treatment and 2.7 ± 0.5 aer treatment, showing a signicant
pain reduction (70%, P<0.0001); which lasted for 26 ± 5 days post
injection. Dhadwal et al. conclude that LTPI appears to be an eective
and tolerable adjunct treatment modality for CMP. Although several
limitations in their study such as the small number of subjects, lack
of a control group, and no discussion of the mechanism of LTPI in
alleviating CMP, Dhadwal et al. provided additional evidence that
peripheral manipulation by LTPI relieves CMP, which warrants further
evaluation. In another article, Malemud reviewed recent literature
regarding the mechanism accounting for the chronic pain in FMS. Low
levels of serotonin and norepinephrine in the peripheral circulation
appear to correlate with chronic pain. Increasing and/or maintaining
higher levels of these neurotransmitters through inhibition of selective-
serotonin or serotonin/norepinephrine (SSRI/SNRI) reuptake may
form the pharmacological basis of treating chronic pain in FMS.
However, previous studies showed that circulating levels of epinephrine
and norepinephrine may be low, normal or high in FMS [48,49] and
clinically not all FMS patients respond well to SSRI or SNRI therapy.
Nevertheless, more studies are needed to explore the pathogenesis and
the central sensitization mechanism of CMP and FMS to establish
eective treatment for these entities.
References
1. Finley JE (2013) Physical medicine and rehabilitation for myofascial pain.
eMedicine.
2. Maletic V, Raison CL (2009) Neurobiology of depression, bromyalgia and
neuropathic pain. Front Biosci (Landmark Ed) 14: 5291-5338.
3. Clauw DJ, Arnold LM, McCarberg BH; FibroCollaborative (2011) The science
of bromyalgia. Mayo Clin Proc 86: 907-911.
4. Buskila D, Cohen H (2007) Comorbidity of bromyalgia and psychiatric
disorders. Curr Pain Headache Rep 11: 333-338.
5. Chakrabarty S, Zoorob R (2007) Fibromyalgia. Am Fam Physician 76: 247-254.
6. Bartels EM, Dreyer L, Jacobsen S, Jespersen A, Bliddal H, et al. (2009)
[Fibromyalgia, diagnosis and prevalence. Are gender differences explainable?].
Ugeskr Laeger 171: 3588-3592.
7. Gore M, Sadosky A, Stacey BR, Tai KS, Leslie D (2012) The burden of chronic
low back pain: clinical comorbidities, treatment patterns, and health care costs
in usual care settings. Spine (Phila Pa 1976) 37: E668-677.
8. National institutes of health (1998) nih guide: New directions in pain research:
1. Bethesda, MD, USA.
9. Glass JM (2006) Cognitive dysfunction in bromyalgia and chronic fatigue
syndrome: new trends and future directions. Curr Rheumatol Rep 8: 425-429.
10. Leavitt F, Katz RS, Mills M, Heard AR (2002) Cognitive and dissociative
manifestations in bromyalgia. J Clin Rheumatol 8: 77-84.
11. Wallace DJ, Hallegua DS (2004) Fibromyalgia: the gastrointestinal link. Curr
Pain Headache Rep 8: 364-368.
12. Moldofsky H, Scarisbrick P, England R, Smythe H (1975) Musculosketal
symptoms and non-REM sleep disturbance in patients with “brositis syndrome”
and healthy subjects. Psychosom Med 37: 341-351.
13. Yunus MB (2007) Role of central sensitization in symptoms beyond muscle
pain, and the evaluation of a patient with widespread pain. Best Pract Res Clin
Rheumatol 21: 481-497.
14. Schneider MJ (1995) Tender points/bromyalgia vs. Trigger points/myofascial
pain syndrome: A need for clarity in terminology and differential diagnosis. J
Manipulative PhysiolTher 18: 398-406.
15. Vázquez-Delgado E, Cascos-Romero J, Gay-Escoda C (2010) Myofascial pain
associated to trigger points: a literature review. Part 2: differential diagnosis
and treatment. Med Oral Patol Oral Cir Bucal 15: e639-643.
16. Sommer C, Häuser W, Alten R, Petzke F, Späth M, et al. (2012) [Drug therapy
of bromyalgia syndrome. Systematic review, meta-analysis and guideline].
Schmerz 26: 297-310.
17. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, Pereira JX, Abbey S, et
al. (2013) 2012 Canadian Guidelines for the diagnosis and management of
bromyalgia syndrome: executive summary. Pain Res Manag 18: 119-126.
18. Carville SF, Arendt-Nielsen S, Bliddal H, Blotman F, Branco JC, et al. (2008)
Eular evidence-based recommendations for the management of bromyalgia
syndrome. Ann Rheum Dis 67: 536-541.
19. Fricton JR, Kroening R, Haley D, Siegert R (1985) Myofascial pain syndrome of
the head and neck: a review of clinical characteristics of 164 patients. Oral Surg
Oral Med Oral Pathol 60: 615-623.
20. Anderberg UM, Liu Z, Berglund L, Nyberg F (1999) Elevated plasma levels of
neuropeptide Y in female bromyalgia patients. Eur J Pain 3: 19-30.
21. Gur A, Cevik R, Sarac AJ, Colpan L, Em S (2004) Hypothalamic-pituitary-
gonadal axis and cortisol in young women with primary bromyalgia: the
potential roles of depression, fatigue, and sleep disturbance in the occurrence
of hypocortisolism. Ann Rheum Dis 63: 1504-1506.
22. Griep EN, Boersma JW, Lentjes EG, Prins AP, van der Korst JK, et al. (1998)
Function of the hypothalamic-pituitary-adrenal axis in patients with bromyalgia
and low back pain. J Rheumatol 25: 1374-1381.
23. Bennett RM (2002) Adult growth hormone deciency in patients with
bromyalgia. Curr Rheumatol Rep 4: 306-312.
24. Neeck G, Riedel W (1992) Thyroid function in patients with bromyalgia
syndrome. J Rheumatol 19: 1120-1122.
25. Riedel W, Layka H, Neeck G 91998) Secretory pattern of gh, tsh, thyroid
hormones, acth, cortisol, fsh, and lh in patients with bromyalgia syndrome
following systemic injection of the relevant hypothalamic-releasing hormones.
Z Rheumatol 57: 81-87.
Citation: Luo JJ, Dun NJ (2013) Chronic Pain: Myofascial Pain and Fibromyalgia. Int J Phys Med Rehabil 1: e102. doi:10.4172/2329-9096.1000e102
Page 3 of 3
Volume 1 • Issue 6 • 1000e102
Int J Phys Med Rehabil
ISSN: 2329-9096 JPMR, an open access journal
26. Dessein PH, Shipton EA, Joffe BI, Hadebe DP, Stanwix AE, et al. (1999)
Hyposecretion of adrenal androgens and the relation of serum adrenal steroids,
serotonin and insulin-like growth factor-1 to clinical features in women with
bromyalgia. Pain 83: 313-319.
27. Shuer ML (2003) Fibromyalgia: symptom constellation and potential therapeutic
options. Endocrine 22: 67-76.
28. Yuen KC, Bennett RM, Hryciw CA, Cook MB, Rhoads SA, et al. (2007) Is further
evaluation for growth hormone (GH) deciency necessary in bromyalgia
patients with low serum insulin-like growth factor (IGF)-I levels? Growth Horm
IGF Res 17: 82-88.
29. Bennett RM, Cook DM, Clark SR, Burckhardt CS, Campbell SM (1997)
Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients
with bromyalgia. J Rheumatol 24: 1384-1389.
30. McCall-Hosenfeld JS, Goldenberg DL, Hurwitz S, Adler GK (2003) Growth
hormone and insulin-like growth factor-1 concentrations in women with
bromyalgia. J Rheumatol 30: 809-814.
31. Jones KD, Deodhar P, Lorentzen A, Bennett RM, Deodhar AA (2007) Growth
hormone perturbations in bromyalgia: a review. Semin Arthritis Rheum 36:
357-379.
32. Neeck G, Crofford LJ (2000) Neuroendocrine perturbations in bromyalgia and
chronic fatigue syndrome. Rheum Dis Clin North Am 26: 989-1002.
33. Staud R, Robinson ME, Price DD (2005) Isometric exercise has opposite
effects on central pain mechanisms in bromyalgia patients compared to
normal controls. Pain 118: 176-184.
34. Desmeules JA, Cedraschi C, Rapiti E, Baumgartner E, Finckh A, et al.
(2003) Neurophysiologic evidence for a central sensitization in patients with
bromyalgia. Arthritis Rheum 48: 1420-1429.
35. Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD (2001) Abnormal
sensitization and temporal summation of second pain (wind-up) in patients with
bromyalgia syndrome. Pain 91: 165-175.
36. Buskila D, Sarzi-Puttini P (2006) Biology and therapy of bromyalgia. Genetic
aspects of bromyalgia syndrome. Arthritis Res Ther 8: 218.
37. Reeser JC, Payne E, Kitchner T, McCarty CA (2011) Apolipoprotein e4
genotype increases the risk of being diagnosed with posttraumatic bromyalgia.
PM R 3: 193-197.
38. Cohen H, Buskila D, Neumann L, Ebstein RP (2002) Conrmation of an
association between bromyalgia and serotonin transporter promoter region
(5- httlpr) polymorphism, and relationship to anxiety-related personality traits.
Arthritis Rheum 46: 845-847.
39. Buskila D, Cohen H, Neumann L, Ebstein RP (2004) An association between
bromyalgia and the dopamine D4 receptor exon III repeat polymorphism and
relationship to novelty seeking personality traits. Mol Psychiatry 9: 730-731.
40. Zubieta JK, Heitzeg MM, Smith YR, Bueller JA, Xu K, et al. (2003) COMT
val158met genotype affects mu-opioid neurotransmitter responses to a pain
stressor. Science 299: 1240-1243.
41. Narita M, Nishigami N, Narita N, Yamaguti K, Okado N, et al. (2003)
Association between serotonin transporter gene polymorphism and chronic
fatigue syndrome. Biochem Biophys Res Commun 311: 264-266.
42. Camilleri M, Atanasova E, Carlson PJ, Ahmad U, Kim HJ, et al. (2002) Serotonin-
transporter polymorphism pharmacogenetics in diarrhea-predominant irritable
bowel syndrome. Gastroenterology 123: 425-432.
43. Hudson JI, Arnold LM, Keck PE Jr, Auchenbach MB, Pope HG Jr (2004) Family
study of bromyalgia and affective spectrum disorder. Biol Psychiatry 56: 884-
891.
44. Lee YH, Choi SJ, Ji JD, Song GG (2012) Candidate gene studies of bromyalgia:
a systematic review and meta-analysis. Rheumatol Int 32: 417-426.
45. Arnold LM, Hudson JI, Hess EV, Ware AE, Fritz DA, et al. (2004) Family study
of bromyalgia. Arthritis Rheum 50: 944-952.
46. Kato K, Sullivan PF, Evengård B, Pedersen NL (2006) Importance of genetic
inuences on chronic widespread pain. Arthritis Rheum 54: 1682-1686.
47. Foell J (2013) Conventional and complementary approaches to chronic
widespread pain and its comorbidities. Acupunct Med .
48. van Denderen JC, Boersma JW, Zeinstra P, Hollander AP, van Neerbos
BR (1992) Physiological effects of exhaustive physical exercise in primary
bromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity?
Scand J Rheumatol 21: 35-37.
49. Adler GK, Kinsley BT, Hurwitz S, Mossey CJ, Goldenberg DL (1999) Reduced
hypothalamic-pituitary and sympathoadrenal responses to hypoglycemia in
women with bromyalgia syndrome. Am J Med 106: 534-543.
Citation: Luo JJ, Dun NJ (2013) Chronic Pain: Myofascial Pain and Fibromyalgia.
Int J Phys Med Rehabil 1: e102. doi:10.4172/2329-9096.1000e102
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The scheduled update to the German S3 guidelines on fibromyalgia syndrome (FMS) by the Association of the Scientific Medical Societies ("Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften", AWMF; registration number 041/004) was planned starting in March 2011. The development of the guidelines was coordinated by the German Interdisciplinary Association for Pain Therapy ("Deutsche Interdisziplinären Vereinigung für Schmerztherapie", DIVS), 9 scientific medical societies and 2 patient self-help organizations. Eight working groups with a total of 50 members were evenly balanced in terms of gender, medical field, potential conflicts of interest and hierarchical position in the medical and scientific fields. Literature searches were performed using the Medline, PsycInfo, Scopus and Cochrane Library databases (until December 2010). The grading of the strength of the evidence followed the scheme of the Oxford Centre for Evidence-Based Medicine. The recommendations were based on level of evidence, efficacy (meta-analysis of the outcomes pain, sleep, fatigue and health-related quality of life), acceptability (total dropout rate), risks (adverse events) and applicability of treatment modalities in the German health care system. The formulation and grading of recommendations was accomplished using a multi-step, formal consensus process. The guidelines were reviewed by the boards of the participating scientific medical societies. Amitriptyline and-in case of comorbid depressive disorder or generalized anxiety disorder-duloxetine are recommended. Off-label use of duloxetine and pregabalin can be considered in case of no comorbid mental disorder. Strong opioids are not recommended. The English full-text version of this article is available at SpringerLink (under "Supplemental").
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To study the hormonal perturbations in FMS patients we injected sixteen FMS patients and seventeen controls a cocktail of the hypothalamic releasing hormones: Corticotropin-releasing hormone (CRH), Thyrotropin-releasing hormone (TRH), Growth hormone-releasing hormone (GHRH), and Luteinizing hormone-releasing hormone (LHRH) and observed the hormonal secretion pattern of the pituitary together with the hormones of the peripheral endocrine glands. We found in FMS patients elevated basal values of ACTH and cortisol, lowered basal values of insulin-like growth factor I (IGF-I) and of triiodothyronine (T-3), elevated basal values of follicle-stimulating hormone (FSH) and lowered basal values of estrogen. Following injection of the four releasing-hormones, we found in FMS patients an augmented response of ACTH, a blunted response of TSH, while the prolactin response was exaggerated. The effects of LHRH stimulation were investigated in six FMS patients and six controls and disclosed a significantly blunted response of LH in FMS. We explain the deviations of hormonal secretion in FMS patients as being caused by chronic stress, which, after being perceived and processed by the central nervous system (CNS), activates hypothalamic CRH neurons. CRH, on the one hand, activates the pituitary-adrenal axis, but also stimulates at the hypothalamic level somatostatin secretion which, in turn, causes inhibition of GH and TSH at the pituitary level. The suppression of gonadal function may also be attributed to elevated CRH by its ability to inhibit hypothalamic LHRH release, although it could act also directly on the ovary by inhibiting FSH-stimulated estrogen production. We conclude that the observed pattern of hormonal deviations in FMS patients is a CNS adjustment to chronic pain and stress, constitutes a specific entity of FMS, and is primarily evoked by activated CRH neurons.
Myofascial pain syndrome (MPS) is a common but misunderstood muscular pain disorder involving pain referred from small, tender trigger points within myofascial structures in or distant from the area of pain. Misdiagnosis or inadequate management of this disorder after onset may lead to development of a complex chronic pain syndrome. A review of the clinical characteristics of 164 patients whose chief complaints led to the diagnosis of MPS revealed that these patients had (1) tenderness at points in firm bands of skeletal muscle that were consistent with past reports, (2) specific patterns of pain referral associated with each trigger point, (3) frequent emotional, postural, and behavioral contributing factors, and (4) frequent associated symptoms and concomitant diagnoses.
Article
Retrospective analysis of an insurance claims database. To examine the comorbidities, treatment patterns, health care resource utilization, and direct medical costs of patients with chronic low back pain (CLBP) in clinical practice. Although the socioeconomic impact of CLBP is substantial, characterization of comorbidities, pain-related pharmacotherapy, and health care resource use/costs of patients with CLBP relative to non-CLBP controls have been infrequently documented. Using the LifeLink Health Plan Claims Database (IMS Health Inc., Watertown, MA), patients with CLBP, defined using the International Classification of Diseases, Ninth Revision, Clinical Modification, were identified and matched (age, sex, and region) with non-CLBP individuals. Comorbidities, pain-related pharmacotherapy, and health care service use/costs (pharmacy, outpatient, inpatient, total) were compared for the 2 groups during 2008. A total of 101,294 patients with CLBP and controls were identified (55% women; mean age was 47.2 ± 11.6 years). Relative to controls, patients with CLBP had a greater comorbidity burden including a significantly higher (P < 0.0001) frequency of musculoskeletal and neuropathic pain conditions and common sequelae of pain such as depression (13.0% vs. 6.1%), anxiety (8.0% vs. 3.4%), and sleep disorders (10.0% vs. 3.4%). Pain-related pharmacotherapy was significantly greater (P < 0.0001) among patients with CLBP including opioids (37.0% vs. 14.8%; P < 0.0001), nonsteroidal anti-inflammatory drugs (26.2% vs. 9.6%; P < 0.0001), and tramadol (8.2% vs. 1.2%; P < 0.0001). Prescribing of "adjunctive" medications for treating conditions associated with pain (i.e., depression, anxiety, and insomnia) was also significantly greater (P < 0.0001) among patients with CLBP; 36.3% of patients received combination therapy. Health care costs were significantly higher in the CLBP cohort (P < 0.0001), reflecting greater resource utilization. Total direct medical costs were estimated at $8386 ± $17,507 in the CLBP group and $3607 ± $10,845 in the control group; P < 0.0001). Patients with CLBP are characterized by greater comorbidity and economic burdens compared with those without CLBP. This economic burden can be attributed to greater prescribing of pain-related medications and increased health resource utilization.
Article
Fibromyalgia (FM) is a common chronic widespread pain disorder. Our understanding of FM has increased substantially in recent years with extensive research suggesting a neurogenic origin for the most prominent symptom of FM, chronic widespread pain. Neurochemical imbalances in the central nervous system are associated with central amplification of pain perception characterized by allodynia (a heightened sensitivity to stimuli that are not normally painful) and hyperalgesia (an increased response to painful stimuli). Despite this increased awareness and understanding, FM remains undiagnosed in an estimated 75% of people with the disorder. Clinicians could more effectively diagnose and manage FM if they better understood its underlying mechanisms. Fibromyalgia is a disorder of pain processing. Evidence suggests that both the ascending and descending pain pathways operate abnormally, resulting in central amplification of pain signals, analogous to the "volume control setting" being turned up too high. Patients with FM also exhibit changes in the levels of neurotransmitters that cause augmented central nervous system pain processing; levels of several neurotransmitters that facilitate pain transmission are elevated in the cerebrospinal fluid and brain, and levels of several neurotransmitters known to inhibit pain transmission are decreased. Pharmacological agents that act centrally in ascending and/or descending pain processing pathways, such as medications with approved indications for FM, are effective in many patients with FM as well as other conditions involving central pain amplification. Research is ongoing to determine the role of analogous central nervous system factors in the other cardinal symptoms of FM, such as fatigue, nonrestorative sleep, and cognitive dysfunction.
Article
To determine whether the apolipoprotein E4 (Apo E4) allele may be a genetic risk factor for fibromyalgia syndrome (FMS). A retrospective assessment of associations between Apo E4 genotype and selected environmental exposures among a cohort diagnosed with FMS compared with control subjects. Marshfield Clinic Research Foundation's Personalized Medicine Research Project (PMRP) biobank. One hundred fifty-one case subjects with fibromyalgia and 300 age- and gender-matched control subjects. Fibromyalgia case subjects were identified according to a strict phenotypic definition from among the nearly 20,000 subjects enrolled in the PMRP. Age- and gender-matched control subjects also were identified from the PMRP in a 2:1 control/case ratio. Apo E4 genotype was determined by single nucleotide polymorphism analysis for both case subjects with fibromyalgia and control subjects. Case subjects with fibromyalgia and control subjects were asked to assess their level of function and stress by completing the Short Form-36 and the Perceived Stress Scale. Statistical associations between the Apo E4 genotype and phenotypic criteria (diagnosis of FMS) as well as historical environmental exposures as documented in the electronic medical record were assessed. Approximately one quarter of both case subjects with fibromyalgia and control subjects were found to carry at least one Apo E4 allele. The odds ratio (OR) for case subjects with fibromyalgia who had ever been in a motor vehicle accident and subsequently had been diagnosed with FMS was increased among those with at least one copy of the Apo E4 allele (OR 7.04) compared with those without an Apo E4 allele (OR 1.90). The presence of an Apo E4 allele did not influence the degree of pain or level of function among those with FMS. These data suggest that specific interactions between genetically susceptible individuals (eg, those with at least one copy of the Apo E4 allele) and the environment (eg, involvement in a motor vehicle accident) may contribute to the risk of being diagnosed with FMS, although Apo E4 allele status does not appear to modulate perceived FMS severity.