Pain following spinal cord injury: pathophysiology and central mechanisms

Publisher Summary This chapter reviews the results of experimental and clinical studies that provide insights into possible mechanism(s) underlying selected pain states following spinal injury. Emphasis is placed on studies related to central dysesthetic pain, perhaps the most disabling of all sensory complications associated with spinal cord injury (SCI). The epidemiological and clinical characteristics of different SCI pain syndromes are reviewed. The most obvious pathological characteristics associated with traumatic or ischemic injury to the spinal cord include but are by no means limited to the dramatic loss of neurons, damage to surrounding white matter, astrocytic scarring, syrinx formation, and breakdown of the spinal blood brain barrier. Common central injury cascade was proposed for the initiation of pain-related behaviors following central or peripheral injury. The different components of this central cascade are shown that include anatomical, neurochemical, excitotoxic, and inflammatory events that collectively interact to influence the functional state of spinal sensory neurons leading to the onset of different clinical pain states. Continued research directed towards specific components of the spinal injury cascade should provide a better understanding of spinal and supraspinal mechanisms responsible for this condition and the future development of novel therapeutic strategies.