Genetic factors influence the development of mechanical hypersensitivity, motor deficits and morphological damage after transient spinal cord ischemia in the rat.

Genetic influence on the sensory, motor and histopathological outcome of transient spinal cord ischemia was studied in Sprague-Dawley (SD), spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats. Ischemia caused minor motor deficits and no identifiable morphological damage in the spinal cord of the majority of SD rats after 1 min laser irradiation. However, severe mechanical hypersensitivity, characterized by an allodynia-like reaction to non-noxious tactile and pressure stimuli, was observed for several days in SD rats after spinal cord ischemia. SH rats exhibited less allodynia than SD rats, but developed profound motor deficits. WKY rats, the normotensive progenitor of SH rats, developed both severe mechanical allodynia and motor impairment after spinal cord ischemia. Histological examination revealed that there was significantly more extensive morphological damage in the epicenter of the irradiated segments of the spinal cord in SH and WKY rats than in SD rats after transient spinal cord ischemia. The results indicated that SH rats are more resistant to the development of central pain after central nervous system ischemia, but SH and WKY rats are more susceptible to neuronal damage than SD rats. Thus, genetic variability can lead to variable predisposition for the development of pain and spinal cord damage after ischemia. Such factors may underlie the wide variability in the occurrence of pain after central nervous system injury in humans.