Authors: Charles J Vierck Christopher D King Sara A Berens Robert P Yezierski
Publish Date: 2013/08/08
Volume: 231, Issue: 1, Pages: 19-26
Abstract
Studies of humans monkeys and rodents have implicated combined gray and white matter damage as important for development of chronic pain following spinal cord injury SCI Belowlevel chronic pain and hyperalgesia following injury to the spinal white matter including the spinothalamic tract STT can be enhanced by excitotoxic influences within the gray matter at the site of SCI Also excitotoxic injury of thoracic gray matter without interruption of the STT results in belowlevel heat hyperalgesia The present study evaluates the possibility that thoracolumbar gray matter injury increases sensitivity to nociceptive heat stimulation by altering spinal sympathetic outflow Thermal preferences of rats for heat 45 °C versus cold 15 °C were evaluated before and after thoracolumbar injections of quisqualic acid QUIS A preinjury preference for heat changed to a postinjury preference for cold Systemic activation of the sympathetic nervous system by restraint stress decreased the heat preference preinjury and increased the cold preference postinjury The heat aversive effect of stress was magnified and prolonged postinjury compared to preinjury Also peripheral sympathetic activation by nociceptive stimulation was evaluated pre and postinjury by measuring thermal transfer through a hindpaw during stimulation with 445 °C Skin temperature recordings revealed enhanced sympathetic activation by nociceptive heat stimulation following spinal QUIS injury However increased sympathetic activation with peripheral vasoconstriction should enhance cold aversion in contrast to the observed increase in heat aversion Thus peripheral sympathetic vasoconstriction can be ruled out as a mechanism for heat hyperalgesia following excitotoxic gray matter injury
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