Journal of neurotrauma
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Journal of neurotrauma · Oct 1999
Cerebral hemodynamic effects of pentobarbital coma in head-injured patients.
The purpose of this study was to examine the changes in cerebral hemodynamics of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variables were measured in 67 severely head-injured patients at the following times: before the loading dose of pentobarbital; after the loading dose of pentobarbital (average pentobarbital level 28.1+/-8.3 microg/mL); and 3 days later, when the peak pentobarbital level averaged 42.5+/-17.2 microg/mL. Intracranial pressure (ICP) and mean arterial blood pressure (MAP) were decreased by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, respectively. ⋯ In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, partly because their CMR(O)2 is already markedly reduced by the injury and partly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because hypotension limits the amount of barbiturates that can be given.
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Journal of neurotrauma · Oct 1999
Cognitive function following traumatic brain injury: effects of injury severity and recovery period in a parasagittal fluid-percussive injury model.
Previous work in this laboratory has demonstrated that rats show substantial deficits on the cued and hidden versions of the Morris water maze, as well as an apparent time-dependent recovery over a period of months, following moderate parasagittal fluid-percussion (FP) injury. However, the longitudinal nature of those studies precluded definitive statements regarding recovery because of the possible confound of practice-dependent improvements in performance. The present experiments were undertaken to address this issue and to investigate more closely the relationship between impact severity and posttraumatic learning/memory deficits, which have not been examined thoroughly in this model. ⋯ Mildly injured animals exhibited no significant deficits on either task at either time point. The results indicate that deficits on the hidden platform task are more robust than those on the cued platform task, and that performance on both tasks is dependent on injury severity. They also indicate that the learning/memory deficits in this model are relatively enduring, suggesting that the model is a reasonable one for assessing potential treatment regimens.
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Journal of neurotrauma · Sep 1999
Multicenter StudyAge, outcome, and rehabilitation costs after paraplegia caused by traumatic injury of the thoracic spinal cord, conus medullaris, and cauda equina.
The object of this study was to investigate the relationships of age on neurologic and functional outcome, hospitalization length of stay (LOS), and hospital charges after spinal cord injury (SCI). At 20 medical centers, 2,169 consecutive adult patients with paraplegia SCI were assessed in acute care and inpatient rehabilitation. Outcome and treatment measures included the ASIA motor index score, functional independence measure, discharge to community ratio, LOS, and hospital charges. ⋯ Significant differences between age categories were found with regard to the following treatment measures: ASIA motor index scores at acute-care admission and at discharge, rehabilitation LOS, inpatient rehabilitation hospitalization charges, total LOS, total hospitalization charges, FIM scores at inpatient rehabilitation admission and discharge, FIM change, and FIM efficiency. In conclusion, in patients with paraplegia, age appears to adversely affect functional outcome, rehabilitation LOS, and hospital costs. However, neurologic recovery as defined by the ASIA motor scores does not appear to be related to age.
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Journal of neurotrauma · Sep 1999
Secondary neurologic injury resulting from nonhypotensive hemorrhage combined with mild traumatic brain injury.
Although the emergency physician often treats patients with multiple injuries, there are relatively few clinically relevant models that mimic these situations. To describe the changes after a hemorrhagic insult superimposed on traumatic brain injury (TBI), anesthetized and ventilated juvenile pigs were assigned to 35% hemorrhage (35H), TBI (via fluid percussion); TBI + 35H, and TBI + 40H (40% hemorrhage). Animals were resuscitated with shed blood and crystalloid. ⋯ There was no evidence of intracranial injury in the 35H group. Only in animals receiving a secondary insult of hemorrhage following the primary TBI were cerebral contusions found. These experiments demonstrate the evolution of cerebral contusions as a form of secondary neurologic injury following resuscitation from traumatic brain injury and hemorrhage, even in the absence of significant blood pressure changes.
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Journal of neurotrauma · Sep 1999
Calpain activation and cytoskeletal protein breakdown in the corpus callosum of head-injured patients.
Calpain-mediated breakdown of the cytoskeleton has been proposed to contribute to brain damage resulting from head injury. We examined the corpus callosum from patients who died after a blunt head injury in order to determine if there was evidence of these pathophysiological events in a midline myelinated commissure that is susceptible to damage after human head injury. Western blotting revealed marked reductions in the levels of neurofilament triplet proteins 200 and 68kDa in the corpus callosum of head-injured patients compared with control subjects. ⋯ However, there was a significant increase in the levels of calpain-mediated spectrin breakdown products in head-injured patients compared with the control subjects. The results demonstrate that following human blunt head injury, there is a significant degradation of neurofilament proteins and increased levels of calpain-mediated spectrin breakdown products within the corpus callosum. Therefore, our data support the hypothesis that calpain-mediated breakdown of the cytoskeleton may contribute to axonal damage after head injury.