Gabapentin for Spasticity and Autonomic Dysreflexia after Severe Spinal Cord Injury

Abstract

Study Design

Utilizing a complete transection spinal cord injury (SCI) model at the fourth thoracic vertebral level in adult rats, we evaluated whether blocking noxious stimuli below the injury diminishes abnormal somatic and autonomic motor reflexes, manifested in muscular spasticity and hypertensive autonomic dysreflexia, respectively. Gabapentin (GBP) is well-tolerated and currently used to manage neuropathic pain in the SCI population; evidence suggests it acts to decrease presynaptic glutamate release. Since clinical evidence indicates that GBP may suppress muscular spasticity in the chronic SCI population, we hypothesized that preventing neurotransmission of noxious stimuli with GBP eliminates a critical physiological link to these distinct, debilitating SCI-induced secondary impairments.

Objectives

Behavioural assessments of tail muscle spasticity and mean arterial blood pressure responses to noxious somatic and/or visceral stimulation were used to test the effects of GBP on these abnormal reflexes.

Setting

Lexington, Kentucky

Methods

We employed femoral artery catheterization and radio-telemetric approaches to monitor blood pressure alterations in response to noxious colorectal distension (CRD) weeks after complete SCI.

Results

At 2-3 weeks post-SCI, acute GBP administration (50 mg/kg, i.p.) significantly attenuated both autonomic dysreflexia and tail spasticity induced by noxious stimuli compared to saline-treated cohorts.

Conclusion

These results demonstrate, for the first time, that a single pharmacological intervention, GBP, can effectively attenuate the manifestation of both muscular spasticity and autonomic dysreflexia in response to noxious stimuli.