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Central mechanisms in the maintenance of chronic widespread noninflammatory muscle pain.
- Source :
-
Current pain and headache reports [Curr Pain Headache Rep] 2008 Oct; Vol. 12 (5), pp. 338-43. - Publication Year :
- 2008
-
Abstract
- Chronic widespread pain (CWP) conditions such as fibromyalgia and myofascial syndromes are characterized by generalized pain, tenderness, morning stiffness, disturbed sleep, and pronounced fatigue. However, CWP pathophysiology is still unclear. A number of hypotheses have been proposed as the underlying pathophysiology of CWP: muscular dysfunction/ischemia, central sensitization, and a deficit in endogenous pain-modulating systems. This article reviews the current and emerging literature about the pathophysiology and neurobiology of chronic widespread -musculoskeletal pain. Widespread musculoskeletal pain results in changes in the central nervous system in human subjects and animal models. These changes likely reflect alterations in supraspinal modulation of nociception, and include increases in excitatory and decreases in inhibitory modulation pathways. These alterations in excitation and inhibition likely drive changes observed in the spinal cord to result in central sensitization, and the consequent pain and hyperalgesia.
- Subjects :
- Amides therapeutic use
Anesthetics, Local therapeutic use
Aspartic Acid metabolism
Chronic Disease
Cyclic AMP physiology
Fatigue epidemiology
Fibromyalgia metabolism
Glutamic Acid metabolism
Humans
Myofascial Pain Syndromes metabolism
Nerve Block methods
Nociceptors physiology
Ropivacaine
Signal Transduction physiology
Synaptic Transmission physiology
Fibromyalgia physiopathology
Fibromyalgia therapy
Myofascial Pain Syndromes physiopathology
Myofascial Pain Syndromes therapy
Subjects
Details
- Language :
- English
- ISSN :
- 1534-3081
- Volume :
- 12
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Current pain and headache reports
- Publication Type :
- Academic Journal
- Accession number :
- 18765138
- Full Text :
- https://doi.org/10.1007/s11916-008-0057-7