THIS study evaluated treatment with riluzole, a neuroprotective agent,
following thoracic spinal cord compression in the rat. Animals receiv
ed riluzole (2 mg kg(-1)) or vehicle twice daily for 10 days following
the trauma. Motor deficits, somatosensory evoked potentials (SEP) and
lesion histology were evaluated. Although paralysis was seen followin
g trauma, seven of 10 animals receiving riluzole recovered motor funct
ion and nearly normal behaviour, unlike animals receiving vehicle. Tra
uma dramatically disturbed SEPs with falls in amplitude and increases
in latency. After riluzole SEP returned towards pre-injury levels, whi
le untreated animals showed no recovery. Morphological studies reveale
d significant (53%) reduction in the degree of spinal cord infarcted a
fter riluzole treatment.