Journal of neurotrauma
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Journal of neurotrauma · Apr 1994
The rotarod test: an evaluation of its effectiveness in assessing motor deficits following traumatic brain injury.
The purpose of the present experiment was to examine the effectiveness of a modified rotarod test in detecting motor deficits following mild and moderate central fluid percussion brain injury. In addition, this investigation compared the performance of the rotarod task with two other commonly used measures of motor function after brain injury (beam-balance and beam-walking latencies). Rats were either injured with a mild (n = 14) or moderate (n = 8) level of fluid percussion injury or were surgically prepared but not injured (n = 8). ⋯ Performance on the rotarod, beam-walk, and beam-balance tasks were compared and evaluated by a multivariate stepdown analysis (multiple analysis of variance followed by univariate analyses of covariance). This analysis indicated that the rotarod task measures aspects of motor impairment that are not assessed by either the beam-balance or beam-walking latency. These findings suggest that compared to the beam-balance and beam-walking tasks, the rotarod task is a more sensitive and efficient index for assessing motor impairment produced by brain injury.
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Journal of neurotrauma · Feb 1994
In vitro investigations of the effects of nonfreezing low temperatures on lesioned and uninjured mammalian spinal neurons.
This two-part investigation explored the parameters and mechanisms of: (1) injury to spinal cord (SC) neurons by nonfreezing low temperatures, and (2) hypothermic protection of SC neurons subjected to a defined, physical injury (dendrite transection). Conclusions from the studies of hypothermic injury were: (1) morphologic and ultrastructural signs of stress developed in SC neurons as the temperature was decreased below 17 degrees C; (2) most neurons showing stress during cooling died upon rewarming to 37 degrees C; (3) spontaneous SC network activity was not significantly changed by cooling to 17 degrees C for 2 hours and rewarming, but cooling to 10 degrees C for 1 hour caused a reduction of burst frequency after rewarming, and cooling to 10 degrees C for 2 hours resulted in electrical silence after rewarming; and (4) application of N-methyl-D-aspartate (NMDA) antagonists before cooling prevented neuronal death, ultrastructural damage, and loss of activity upon rewarming, but application after cooling (before rewarming) was not protective. Conclusions from the studies of hypothermic protection were: (1) cooling at 17 degrees C for 2 hours followed by rewarming to 37 degrees C significantly increased lesioned neuron survival, but protection was lost when the period at 17 degrees C was increased to 6 hours; (2) NMDA blockade under normothermic (37 degrees C) or hypothermic (17 degrees C or 10 degrees C for 2 hours) conditions was not more protective of lesioned neurons than cooling to 17 degrees C (no NMDA antagonist); and (3) 200 microM thiopental or 100 microM pentobarbital increased lesioned neuron survival to a degree comparable to cooling for 2 hours at 17 degrees C.
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Journal of neurotrauma · Jan 1993
Randomized Controlled Trial Clinical TrialA phase II study of moderate hypothermia in severe brain injury.
Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. ⋯ Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.
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Journal of neurotrauma · Jan 1993
Mild experimental brain injury in the rat induces cognitive deficits associated with regional neuronal loss in the hippocampus.
Memory dysfunction following mild human traumatic brain injury (TBI) is a common clinical observation, but the pathologic substrate underlying this loss of function has not been well-characterized. In the present study, we examined the effects of a mild lateral fluid percussion (FP) brain injury on memory dysfunction, neuronal cell loss in specific regions of the hippocampus, and breakdown of the blood-brain barrier (BBB). A Morris Water Maze (MWM) memory paradigm was used to assess memory retention in rats 42 h after lateral FP brain injury (n = 11) or sham injury (n = 10). ⋯ Immunoreactivity to anti-rat IgG was used to evaluate the extent of BBB disruption. A significant correlation was observed between posttraumatic memory scores and neuronal loss in the hilus of the dentate gyrus (p < 0.005). To our knowledge, these observations are the first to suggest an association between cognitive deficits following a mild experimental brain injury and neuropathological changes in the hippocampus.
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Journal of neurotrauma · Jan 1993
Behavioral protection by moderate hypothermia initiated after experimental traumatic brain injury.
The effects of postinjury hypothermia on behavioral outcome following moderate fluid percussion traumatic brain injury (TBI) were examined. In Experiment I, three groups of rats were examined. The first group was normothermic (37.5 degrees C); and hypothermia (30 degrees C) was initiated 15 min and 30 min postinjury in the second and third groups, respectively. ⋯ In Experiment II, subcortical brain temperature was compared to temporalis muscle temperature in normothermic (37.5 degrees C) and hypothermic (30 degrees C) rats subjected to TBI. In both groups brain temperature tracked within 0.4 degree C of temporalis muscle temperature. These results are similar to post-TBI excitatory receptor antagonist studies and indicate a therapeutic window for moderate hypothermia of less than 30 min after moderate fluid percussion TBI in the rat.