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Updated: Feb 11, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Effects of pregabalin on brain edema, neurologic and histologic outcomes in experimental traumatic brain injury
Manzumeh Shamsi Meymandi1, Zahra Soltani2, Gholamreza Sepehri3
1Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran; Stem Cell Research Center, Kerman School of Medical, Kerman University of Medical Sciences, Kerman, Iran.
Insights
Pregabalin shows neuroprotective effects in experimental traumatic brain injury (TBI) by reducing brain edema and intracranial pressure (ICP). This treatment improved neurological outcomes in rats after TBI.
Area of Science:
- Neuroscience
- Pharmacology
- Trauma Research
Background:
- Traumatic brain injury (TBI) frequently causes brain edema and increased intracranial pressure (ICP), leading to neurological deficits and mortality.
- Pregabalin has demonstrated potential neuroprotective properties in various neurological conditions.
Purpose of the Study:
- To investigate the neuroprotective effects of pregabalin in an experimental model of traumatic brain injury (TBI) in male rats.
- To assess the impact of pregabalin on brain edema, intracranial pressure (ICP), and neurological outcomes following TBI.
Main Methods:
- Adult male Wistar rats were subjected to TBI using the Marmarou method and treated with pregabalin (30 or 60 mg/kg) or vehicle 30 minutes post-injury.
- Measurements included brain water content, Evans blue content, histopathological analysis, ICP monitoring, and the Veterinary Coma Scale (VCS) at various time points post-TBI.
Main Results:
- The 60 mg/kg pregabalin group exhibited significantly reduced brain water content, decreased ICP, and improved VCS scores compared to the vehicle group (P < 0.05).
- Pregabalin administration also led to a reduction in brain edema and apoptosis.
- Delayed but significant improvements in ICP and neurological outcomes were observed following post-TBI pregabalin administration.
Conclusions:
- Post-injury administration of pregabalin demonstrates significant neuroprotective effects in experimental TBI, mitigating brain edema and improving neurological function.
- Pregabalin offers a potential therapeutic strategy for managing TBI, although the precise mechanisms require further investigation.
Abstract:
Brain edema and increased intracranial pressure (ICP) are among the main causes of neurological disturbance and mortality following traumatic brain injury (TBI). Since pregabalin neuroprotective effects have been shown, this study was performed to evaluate the possible neuroprotective effects of pregabalin in experimental TBI of male rats. Adult male Wistar rats were divided into 4 groups: sham, vehicle, pregabalin 30 mg/kg and pregabalin 60 mg/kg. TBI was induced in vehicle and pregabalin groups by Marmarou method. Pregabalin was administered 30 min after TBI. Sham and vehicle groups received saline. Brain water and Evans blue content and histopathological changes were evaluated 24, 5 and 24 h after TBI, respectively. The ICP and neurological outcomes (veterinary coma scale, VCS) were recorded before, 1 h and 24 h post TBI. The results showed a significant reduction in brain water content and ICP, and a significant increase in VCS of pregabalin group (60 mg/kg) as compared to vehicle group (P < 0.05). Also, pregabalin reduced brain edema and apoptosis score as compared to vehicle group. Post TBI pregabalin administration revealed a delayed but significant improvement in ICP and neurological outcomes in experimental TBI. The underlying mechanism(s) was not determined and needs further investigation.
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