Gabapentin for spasticity and autonomic dysreflexia after severe spinal cord injury

A. G. Rabchevsky, S. P. Patel, H. Duale, T. S. Lyttle, C. R. O'Dell, P. H. Kitzman

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


Study design: Using 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 that it acts to decrease presynaptic glutamate release. As 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 used 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 1, i.p.) significantly attenuated both autonomic dysreflexia and tail spasticity induced by noxious stimuli compared with saline-treated cohorts.Conclusion: These results show, 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.

Original languageEnglish
Pages (from-to)99-105
Number of pages7
JournalSpinal Cord
Issue number1
StatePublished - Jan 2011

Bibliographical note

Funding Information:
This study was supported by NIH/NINDS R01 NS049901 and Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) 3–11 (AGR), KSCHIRT 4–8 (PHK) and NIH/NINDS P30 NS051220.


  • Neurontin
  • blood pressure
  • hyper-reflexia
  • hypertension
  • pain
  • spasms

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology
  • Rehabilitation


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