Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head 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). All rats were assessed on all tasks for 5 days following their respective treatments. Results revealed that both the mild and moderate injury levels produced significant deficits in the ability of the animals to perform the rotarod task. Performance on the beam-balance and beam-walking tasks were not significantly impaired at the mild injury level. It was only at the moderate injury level that the beam-balance and beam-walking tasks detected deficits in motor performance. This result demonstrated that the rotarod task was a sensitive index of injury-induced motor dysfunction following even mild fluid percussion injury. A power analysis of the three tasks indicated that statistically significant group differences could be obtained with the rotarod task with much smaller sample sizes than with the beam-balance and beam-walking tasks. 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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Traumatic brain injury produces significant cognitive deficits in humans. This experiment used a controlled cortical impact model of experimental brain injury to examine the effects of brain injury on spatial learning and memory using the Morris water maze task. Rats (n = 8) were injured at a moderate level of cortical impact injury (6 m/sec, 1.5-2.0 mm deformation). Eight additional rats served as a sham-injured control group. Morris water maze performance was assessed on days 11-15 and 30-34 following injury. Results revealed that brain-injured rats exhibited significant deficits (p less than 0.05) in maze performance at both testing intervals. Since the Morris water maze task is particularly sensitive to hippocampal dysfunction, the results of the present experiment support the hypothesis that the hippocampus is preferentially vulnerable to damage following traumatic brain injury. These results demonstrate that controlled cortical impact brain injury produces enduring cognitive deficits analogous to those observed after human brain injury.

Summary: These experiments examined the effects of moderate hypothermia on mortality and neurological def icits observed after experimental traumatic brain injury (TBI) in the rat. Brain temperature was measured contin uously in all experiments by intraparenchymal probes, Brain cooling was induced by partial immersion (skin pro tected by a plastic barrier) in a water bath (OOe) under general anesthesia (1.5% halothane170% nitrous oxide/ 30% oxygen). In experiment I, we examined the effects of moderate hypothermia induced prior to injury on mortal ity following fluid percussion TBI. Rats were cooled to 36°e (n = 16), 33°e (n = 17), or 300e (n = II) prior to injury and maintained at their target temperature for I h after injury. There was a significant (p < 0.04) reduction in mortality by a brain temperature of 30oe. The mortality rate at 36°e was 37.5%, at 33°e was 41 %, and at 300e wasThe cerebral protective effects of profound hypo thermia «18°C) have been known for many years. As early as 1950, reports of cerebral protection from global ischemia by profound hypothermia in animals stimulated clinical interest (Mohri and Me rendino, 1969). By 1955, 100 cardiac surgical cases had been performed under deep hypothermia with cardiac arrest (Mohri and Merendino, 1969). As pump oxygenators became more efficient, deep hy pothermia and cardiac arrest were only occasion ally used in adult cardiac surgery (Crawford and Saleh, 1981). In pediatric cardiac surgery, however, conditions were encountered routinely where total cessation of circulation at temperatures of 17-20°C Abbreviations used: ANOYA, analysis of variance; TB1, trau matic brain injury, 114 9.1 %. In experiment II, we examined the effects of mod erate hypothermia or hyperthermia initiated after TBI 01 long-term behavioral deficits. Rats were cooled to 36°e (I = 10), 33°e (n = 10), or 300e (n = 10) or warmed to 38°( (n = 10) or 400e (n = 12) starting at 5 min after injury an( maintained at their target temperatures for I h. Hypother mia-treated rats had significantly less beam-walking beam-balance, and body weight loss deficits compared t( normothermic (38°C) rats. The greatest protection wa: observed in the 300e hypothermia group, Since a temper ature of 300e can be induced in humans by surface cool ing without coagulopathy or ventricular fibrillation, hy pothermia to 300e may have potential clinical value fOJ treatment of human brain injury.