Journal of neurotrauma
-
The following general conclusions were reached at the workshop: 1. Laboratory studies suggest a potential benefit of cellular transplant therapy for SCI. 2. ⋯ Assessment criteria and methodology are available, including imaging approaches, validated neurologic scoring systems, detailed electrophysiologic studies of conduction and spinal cord reflexes, and functional scoring approaches. 4. More controlled animal studies are needed (a) to demonstrate efficacy and to evaluate the necessity for immunosuppressive therapy and the overall safety of intraspinal transplantation, (b) to obtain more supporting evidence (e.g., electrophysiologic, histopathologic, MRI, molecular) that would provide insights into ways that transplanted tissue could mediate function, (c) to provide guidance for the procurement, harvesting, preparation, storage, and other logistics related to the use of human cells for transplantation into the spinal cord, (d) to define more thoroughly the cell type(s) that would be most likely to have benefit and the conditions that affect their viability, migration, gene expressions, and proliferation after transplantation, (e) to determine the most optimal time after injury for transplantation, and (f) to clarify patient selection characteristics that might optimize success (i.e., complete vs incomplete injuries, spinal level involved, age of recipient).
-
Journal of neurotrauma · Aug 1994
Regional levels of free fatty acids and Evans blue extravasation after experimental brain injury.
The recently developed controlled cortical-impact (CCI) model of brain injury in rats serves as an excellent tool to understand some of the neurochemical mechanisms mediating the pathophysiology of traumatic brain injury. In this study, rats were subjected to lateral CCI brain injury of low-grade severity. Their brains were frozen in situ at various times after injury to measure regional levels of free fatty acids. ⋯ Extravasation of Evans blue was found to be significantly increased in the ipsilateral cortex of injured animals at 30 min and 10 h after brain injury. These results indicate the degradation of membrane phospholipids and blood-brain barrier breakdown in the ipsilateral cortex after lateral CCI brain injury. These results also suggest that arachidonic acid and its metabolites may play a role as a mediator in the blood-brain barrier breakdown associated with cortical impact brain injury in rats.
-
Journal of neurotrauma · Aug 1994
Direct measurement of hydroxyl radicals, lipid peroxidation, and blood-brain barrier disruption following unilateral cortical impact head injury in the rat.
We present data correlating the time courses of hydroxyl radical (. OH) production, lipid peroxidation, and blood-brain barrier (BBB) damage following unilateral head injury in the rat. Using a controlled cortical impact device to inflict head injury, we have directly measured brain. ⋯ The results suggest that there is an immediate, posttraumatic burst in. OH formation, followed by a progressive increase in lipid peroxidation and a similar, although slightly delayed, time-related opening of the BBB. The attenuation of BBB damage by U-74006F suggests that this chain of events can be interrupted by administration of an antioxidant/lipid peroxidation inhibitor.
-
Journal of neurotrauma · Jun 1994
Early microvascular and neuronal consequences of traumatic brain injury: a light and electron microscopic study in rats.
The purpose of this study was to document the early morphologic consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats. Normothermic rats (37 degrees C) were injured with a fluid percussion pulse (1.7-2.1 atm) administered by an injury cannula positioned parasagittally over the right cerebral cortex (n = 7). At 45 min following TBI, rats were injected with the protein tracer horseradish peroxidase (HRP) and perfusion fixed or immersion fixed 15 min later for light and electron microscopic analysis. ⋯ In nonperfused traumatized rats, luminal platelet aggregates were also detected at sites of hemorrhage. In this model of TBI, a consistent pattern of microvascular and neuronal abnormalities can be documented in the early posttraumatic period. Pathomechanisms underlying these early changes are discussed in terms of primary and secondary injury processes.
-
Journal of neurotrauma · Jun 1994
Increased anticholinergic sensitivity following closed skull impact and controlled cortical impact traumatic brain injury in the rat.
Evidence suggests that prolonged memory deficits in several neurodegenerative diseases are attributable to deficits in central cholinergic neurotransmission. In traumatic brain injury (TBI), such cholinergic deficits also may contribute to prolonged memory disturbances. This study determined whether moderate magnitudes of TBI produced by controlled cortical impact and mild magnitudes of experimental TBI produced by a new closed head impact technique in rats would produce an enhanced vulnerability to the memory disruptive effects of scopolamine, a muscarinic cholinergic receptor antagonist. ⋯ These data demonstrate that covert deficits can persist after the recovery of normal function. These deficits may be attributable to a decrease in the ability of cholinergic neurons to function properly. These data also provide important insights into features of receptor-coupled disturbances that could contribute to the maintenance of enduring cognitive deficits following TBI.