Journal of neurotrauma
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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.
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Journal of neurotrauma · Jun 1994
The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma.
The purpose of this study was to evaluate the role of barbiturate therapy as an adjunctive treatment for control of intracranial hypertension when conventional methods failed. To this end, a retrospective chart review was conducted on 21 neurosurgical trauma patients with uncontrolled intracranial pressure (ICP) admitted to a trauma/intensive care unit. ⋯ The survival of patients experiencing ICP control with barbiturate coma was better than those patients who failed therapy (71% vs 14%, p = 0.021). Thus, in a subgroup of neurosurgical trauma patients who are refractory to conventional management of elevated ICP, barbiturates appear to improve survival, suggesting that this therapy has an important role in the management of neurotrauma patients.
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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.