Cardiac arrest (CA) causes severe
spinal cord injury and evokes
spinal cord disorders including
paraplegia. It has been reported that
risperidone, an
antipsychotic drug, effectively protects neuronal cell death from transient
ischemia injury in gerbil brains. However, until now, studies on the effects of
risperidone on
spinal cord injury after asphyxial CA (ACA) and
cardiopulmonary resuscitation (
CPR) are not sufficient. Therefore, this study investigated the effect of
risperidone on hind limb motor deficits and neuronal damage/death in the lumbar part of the spinal cord following ACA in rats. Mortality, severe motor deficits in the hind limbs, and the damage/death (loss) of motor neurons located in the anterior horn were observed two days after ACA/
CPR. These symptoms were significantly alleviated by
risperidone (an atypical
antipsychotic) treatment after ACA. In vehicle-treated rats, the immunoreactivities of
tumor necrosis factor-alpha (TNF-α) and
interleukin 1-beta (IL-1β), as pro-inflammatory
cytokines, were increased, and the immunoreactivities of
IL-4 and
IL-13, as anti-inflammatory
cytokines, were reduced with time after ACA/
CPR. In contrast, in
risperidone-treated rats, the immunoreactivity of the pro-inflammatory
cytokines was significantly decreased, and the anti-inflammatory
cytokines were enhanced compared to vehicle-treated rats. In brief,
risperidone treatment after ACA/
CPR in rats significantly improved the survival rate and attenuated
paralysis, the damage/death (loss) of motor neurons, and
inflammation in the lumbar anterior horn. Thus,
risperidone might be a therapeutic agent for
paraplegia by attenuation of the damage/death (loss) of spinal motor neurons and
neuroinflammation after ACA/
CPR.