NEUROLOGICAL RECOVERY IN DIABETIC RATS FOLLOWING SPINAL-CORD INJURY

This study was designed to assess the effect of spinal cord injury on neurobehavioral, electrophysiological, structural, and biochemical cha nges in normal and diabetic rats, Experimental diabetes was induced in Sprague-Dawley male rats (weighing 250-280 g) with streptozotocin (50 mg/kg IP). Eight weeks after the treatment with streptozotocin the an imals were anaesthetized with chloral hydrate and laminectomy was perf ormed at T 7-8 level leaving the dura intact. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was placed on the exposed spin al cord for 5 min, Postoperative neurological function was assessed us ing inclined plane test, modified Tarlov score, and vocal and sensory score daily for 10 days, Electrophysiological changes were assessed us ing somatosensory and corticomotor evoked-potentials, The animals were sacrificed at different time intervals and injured site of the spinal cord was analyzed for changes in vitamin E and glutathione levels (as markers of oxidative stress), Pathological changes in spinal cord wer e also studied using light microscopy, The data on neurobehavioral stu dy clearly indicated that the compression of spinal cord produced high ly significant neurological deficit and poor recovery in diabetic rats as compared to nondiabetic rats, Our histopathological and electrophy siological results also confirmed that diabetic animals are more susce ptible to compressive spinal cord injury as compared to nondiabetic an imals, A higher depletion of antioxidant defense markers (vitamin E an d glutathione) was observed in diabetic rats as compared to nondiabeti c rats, These results point toward the role of free radicals in poor r ecovery in diabetic rats following neurotrauma, Further studies are wa rranted to assess the neuroprotective potential of antioxidants to ret ard the secondary pathophysiological events following neurotrauma and to enhance the recovery.