carbar
06-30-2006, 09:16 AM
Are S Carlton's findings on neuropathic pain a breakthrough in understanding how to treat it???
http://www.medscape.com/viewarticle/537117
Sensitization Secondary to Spinal Cord Injury
S. Carlton,[1] of the University of Texas Medical Branch, Galveston, Texas, presented data on sensitization secondary to spinal cord injury. Using an injury model wherein a rat's spinal cord is contused at T10, she showed that dorsal horn nuclei develop enhanced responses to peripheral stimulation not only at the thoracic level but also at the cervical level above. She recorded dorsal root reflexes in A delta and C fibers being stimulated in the dorsal horn by afferent nociceptors. Such stimulation results in antidromic volleys down sensory afferents causing neurogenic inflammation at the site of injury. This sensitization was blocked by intrathecal injection of the GABA antagonist bicuculline.
Carlton postulated that a reverberating central-peripheral nervous system loop is established following spinal cord injury. Following such injury, a "glutamate surge" is initiated, causing central sensitization of dorsal horn nuclei and the generation of dorsal root reflexes. This results in the peripheral release of neuropeptides and inflammatory mediators, which cause neurogenic inflammation and peripheral sensitization, and in turn cause central sensitization. These findings imply that mechanisms giving rise to central neuropathic pain are not exclusively central. In fact, peripheral nociceptors contribute to pain following a central injury. Peripheral targets or interventions may therefore be appropriate for treating chronic pain in that reduction of nociceptor activity reduces central and peripheral sensitization. This may help explain the conundrum of regionalization of central pain.
http://www.medscape.com/viewarticle/537117
Sensitization Secondary to Spinal Cord Injury
S. Carlton,[1] of the University of Texas Medical Branch, Galveston, Texas, presented data on sensitization secondary to spinal cord injury. Using an injury model wherein a rat's spinal cord is contused at T10, she showed that dorsal horn nuclei develop enhanced responses to peripheral stimulation not only at the thoracic level but also at the cervical level above. She recorded dorsal root reflexes in A delta and C fibers being stimulated in the dorsal horn by afferent nociceptors. Such stimulation results in antidromic volleys down sensory afferents causing neurogenic inflammation at the site of injury. This sensitization was blocked by intrathecal injection of the GABA antagonist bicuculline.
Carlton postulated that a reverberating central-peripheral nervous system loop is established following spinal cord injury. Following such injury, a "glutamate surge" is initiated, causing central sensitization of dorsal horn nuclei and the generation of dorsal root reflexes. This results in the peripheral release of neuropeptides and inflammatory mediators, which cause neurogenic inflammation and peripheral sensitization, and in turn cause central sensitization. These findings imply that mechanisms giving rise to central neuropathic pain are not exclusively central. In fact, peripheral nociceptors contribute to pain following a central injury. Peripheral targets or interventions may therefore be appropriate for treating chronic pain in that reduction of nociceptor activity reduces central and peripheral sensitization. This may help explain the conundrum of regionalization of central pain.