Gabapentin suppresses spasticity in the spinal cord-injured rat

Spasticity poses a major detrimental impact on the quality of life in a significant number of people with spinal cord injury (SCI). Recent observations in our laboratory suggest that spinal transection at the sacral S(2) level induces a significant increase in glutamatergic input to sacrocaudal motoneurons during the time spasticity is present in the tail muscles. The present study examined the efficacy of gabapentin, an agent that has been shown to reduce glutamate release, in managing spasticity within the tail musculature.

In this blinded, crossover study adult Sprague-Dawley rats with S(2) spinal transections were tested behaviorally for the progression of spasticity in the tail musculature using our established system. When the animals demonstrated a significant level of spastic behavior (e.g. increased response to quick stretch, noxious and non-noxious cutaneous stimuli), they received either saline or the antiepileptic agent gabapentin (GBP; 50 mg/kg i.p.) and were assessed behaviorally and electrophysiologically at 1, 3, 6, 12 and 24 h post-injection.

Both spastic behavior and electromyography (EMG) activity were significantly decreased at 1 and 3 h post-GBP injection when compared with the activity level following administration of saline. Spastic behavior and EMG activity gradually increased over time and returned to baseline activity by 24 h post-injection.

Gabapentin diminishes both the behavioral and electrophysiological manifestation of SCI-induced spasticity, in the tail musculature, in a time dependent manner.