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سال جهانی مبارزه با
درد
هاي
عضلانی-استخوانی
October
19, 2009
27 مهرماه 1388 الی 27
مهرماه 1389
با شعار :
چه وقت، حرکت زیان آور است؟
بسنجیم ،
درک کنیم و پیشگیری نمائیم
Click on this links:
Musculoskeletal Pain,
some facts
IASP fact sheets on Musculoskeletal Pain
Musculoskeletal Pain
Introduction
Musculoskeletal pain is a known consequence of repetitive strain, overuse, and
work-related musculoskeletal
disorders. These injuries include a variety of disorders that cause pain in
bones, joints, muscles, or surrounding
structures. The pain can be acute or chronic, focal or diffuse. Low back pain is
the most common example of
chronic musculoskeletal pain. Other examples include tendonitis and tendinosis,
neuropathies, myalgia, and
stress fractures.
Epidemiology and Economics
· Musculoskeletal pain from overuse affects 33% of adults and accounts for 29%
of lost workdays due to
illness.
· Low back pain is most prevalent and most common work-related injury in Western
society, and it is the
most costly work-related musculoskeletal disorder.
· While incidence rates for overexertion injury due to lifting are 1.3 times
greater in males, rates are higher
in females for the following conditions: 3.0 times greater for carpal tunnel
syndrome, 2.3 times greater for
tendonitis, and 2.0 times greater for injuries caused by repetitive motion.
· The economic burden of musculoskeletal pain is second only to that of
cardiovascular disease.
Pathophysiology
The pathophysiology of musculoskeletal pain is not completely clear, but
inflammation, fibrosis, tissue
degradation, neurotransmitters, and neurosensory disturbances have been
implicated.
· Inflammation: Injury induces increased pro-inflammatory cytokines and
mediators in affected tissues and
systemically. This increase leads to peripheral nociceptor sensitization.
· Fibrosis: Inflammation can induce fibrotic scarring (i.e., increased collagen
within and between cells and
tissues), which reduces gliding of tissues during movement, leading to stretch
injuries and more pain.
· Tissue degradation: Increased inflammatory mediators induce increases in
matrix metalloproteinases
(enzymes that degrade extracellular matrices), lowering tissue load tolerance
and leading to further injury
and more pain.
· Neurotransmitters: Levels of substance P, calcitonin-related related peptide,
and N-methyl-D-aspartate
(NMDA) are elevated in tendons, dorsal root ganglia, and spinal cord dorsal
horns.
· Neurosensory/neuroimmune factors: Hypersensitivity, with increased levels of
neurotransmitters,
inflammatory mediators and cytokines, causes peripheral nociceptor sensitization
or central amplification
of pain. Hyposensitivity occurs with nerve compression from fibrosis.
Clinical Features
· The pain can be acute or chronic, focal or diffuse, in musculoskeletal or
associated neural tissues.
· Clinical symptoms include:
o local symptoms of pain or widespread and persistent pain
o tenderness
o peripheral nerve irritation
o weakness
o limited motion and stiffness
· Symptoms progressively increase with greater tissue injury and inflammation,
with an increase in affected
anatomical sites, i.e., increased tender points.
· Symptoms are exacerbated by work-related or personal stress, for example, poor
control over one’s work,
difficult relationships, and time pressure.
· Nerve conduction velocity decreases in an involved peripheral nerve.
· Symptoms have diurnal fluctuation. At first, symptoms subside with cessation
of work (i.e., between shifts,
over weekends, and during vacations). As exposure persists and tissue injury
progresses, symptoms may
be insufficiently alleviated by rest, and constant pain may develop.
Diagnostic Criteria
· Local and then later intermittent or persistent pain in musculoskeletal
tissues can be tested using a visual
analogue pain scale; disability (e.g., weakness), can be tested using the Roland
Morris Disability
Questionnaire (RMDQ). These tests are recommended by the Multinational
Musculoskeletal Inception
Cohort Study.
· The UBMA (upper-body musculoskeletal assessment) instrument developed by
Kramer can be used to
diagnose upper-extremity musculoskeletal pain and disorders.
· A systemic inflammatory response during the early phase can be confirmed by
increased serum Creactive
protein, interleukin-6, or tumor necrosis factor alpha. Increases are associated
with increased
UBMA scores, chronic low back pain, and pain associated with a range of
musculoskeletal disorders.
Diagnosis and Treatment
· Diagnoses include peripheral neuropathies; lateral or medial
epicondylitis/tendonitis; rotator cuff, bicipital,
or wrist tendonitis; wrist sprain or strain; Achilles tendonitis; myositis and
myalgia; osteoarthritis; cervical
strain; and lower back pain.
· Management is typically multimodal:
o Physical therapy, primarily with an exercise program (aerobic, strengthening,
stretching), together
with physical modalities, such as heat or ice
o Splinting and/or orthoses
o Use of nonsteroidal anti-inflammatory drugs (NSAIDs), e.g., ibuprofen
o Reduction in workload or increased rest
o Stress management/behavioral intervention
· Unfortunately, recovery from inflammation-induced fibrotic tissue changes is
negligible, even with
complete cessation of strain/activity for up to 12 months. Thus, the pain
resulting from fibrotic scarring is
chronic.
References
1. Barbe MF, Elliott MB, Abdelmagid SM, Amin M, Popoff SN, Safadi FF, Barr AE.
Serum and tissue cytokines and
chemokines increase with repetitive upper extremity tasks. J Orthop Res
2008;26:1320–6.
2. Bureau of Labor Statistics. Nonfatal occupational injuries and illnesses
requiring days away from work, 2007. Washington,
DC: United States Department of Labor News, USDL 08-1716, November 20, 2008.
Available at:
http://www.bls.gov/iff/home.htm. Accessed March 3, 2009.
3. Carp SJ, Barbe MF, Winter KA, Amin M, Barr AE. Inflammatory biomarkers
increase with severity of upper-extremity
overuse disorders. Clin Sci (Lond) 2007;112:305–14.
4. Elliott MB, Barr AE, Clark BD, Amin M, Amin S, Barbe MF. High force reaching
task induces widespread inflammation,
increased spinal cord neurochemicals and neuropathic pain. Neuroscience
2009;23:158:922–31.
5. Koch A, Zacharowski K, Boehm O, Stevens M, Lipfert P, von Giesen HJ, Wolf A,
Freynhagen R. Nitric oxide and proinflammatory
cytokines correlate with pain intensity in chronic pain patients. Inflamm Res
2007;56:32–7.
6. Kramer JF, Potter P, Harburn KL, Speechley M, Rollman GB. An upper body
musculoskeletal assessment instrument for
patients with work-related musculoskeletal disorders: a pilot study. J Hand Ther
2001;14:115–21.
7. Stauber WT, Smith CA, Miller GR, Stauber FD. Recovery from 6 weeks of
repeated strain injury to rat soleus muscles.
Muscle Nerve. 2000;23:1819–25.
8. Wang H, Schiltenwolf M, Buchner M. The role of TNF-alpha in patients with
chronic low back pain-a prospective comparative longitudinal study. Clin J Pain
2008;24:273–8.
© 2009 International Association for the Study of Pain®
Edited by:
M. SHARIFY, MD
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