Journal
JOURNAL OF REHABILITATION RESEARCH AND DEVELOPMENT
Volume 46, Issue 1, Pages 95-107Publisher
JOURNAL REHAB RES & DEV
DOI: 10.1682/JRRD.2008.06.0074
Keywords
central pain; cortex; excitotoxicity; inflammation; microglia; plasticity; secondary injury; sensitization; signaling pathways; synaptic plasticity; thalamus
Categories
Funding
- NINDS NIH HHS [NS40096] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS040096] Funding Source: NIH RePORTER
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Altered sensations, including pain, are well- documented consequence, associated with spinal cord injury (SCI). Although loss of sensory and motor functions at and below the level of injury is commonly thought to affect individuals with SCI most significantly, secondary consequences that include spasticity, bladder and bowel dysfunctions, infertility, and pain rank among the most difficult conditions to deal with following injury. Understanding the mechanisms responsible for the condition of pain requires one to appreciate the pathological, physiological, neurochemical, and molecular events associated with injury of the spinal cord parenchyma. Over the past 15 years, a systematic examination related to the pathophysiology, clinical characteristics, and treatment of pain associated with SCI has provided insights into the spinal and supraspinal mechanisms associated with the development of at-and below-level pain. In this review, experimental studies focusing on the spinal and supraspinal mechanisms associated with pain at and below level will be discussed.
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