Gabapentin for spasticity and autonomic dysreflexia after severe spinal cord injury.
METHODS
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.


OBJECTIVE
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.


METHODS
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.


CONCLUSIONS
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.
Rabchevsky
A G
AG
Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536-0509, USA. agrab@uky.edu
Patel
S P
SP
Duale
H
H
Lyttle
T S
TS
O'Dell
C R
CR
Kitzman
P H
PH
D000588:Amines / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D020211:Autonomic Dysreflexia / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D003509:Cyclohexanecarboxylic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D005260:Female; D000077206:Gabapentin; D009128:Muscle Spasticity / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013119:Spinal Cord Injuries / Q000150:complications* / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology* / Q000627:therapeutic use
D000588:Amines; D003509:Cyclohexanecarboxylic Acids; D005680:gamma-Aminobutyric Acid; D000077206:Gabapentin