Abstract
INTRODUCTION: Survivors of nontraumatic intraventricular hemorrhage are often left with memory impairment, however, underlying mechanisms of this dysfunction remain to be elucidated. METHODS: The experimental design included two groups of Sprague Dawley rats (n=30): intraventricular hemorrhage (control) and intraventricular hemorrhage with sustained high intracranial pressures (experimental). The autologous intraventricular blood injection model was used. In the experimental group the intracranial pressure was artificially elevated. Ten days following surgery, each rat underwent Morris water maze. T test was used with a p value of < 0.05 considered statistically significant. RESULTS: The average maximum intracranial pressure in the experimental group was 75.6 ± 17.5 mmHg compared to 66.5 ± 17.3 mmHg in the control group (p = 0.260). The experimental group experienced elevated intracranial pressure for two hours following induction of intraventricular hemorrhage, whereas the intracranial pressure normalized within minutes in the control group. The mean cerebral perfusion pressure tended to be lower in the experimental group (20 ± 25.6 mmHg) compared to the control group (30 ± 19.4 mmHg) (p = 0.302). In Morris water maze, the experimental group needed more time to reach the platform (37.3 ± 21.8 seconds) compared to the control group (19.7 ± 14.3 seconds) (p = 0.041). The experimental group also spent less time in 5% and 10% target quadrants, 2.4 ± 1.8 and 5.7 ± 3.9 seconds, respectively (p = 0.004) compared to the control group, 5.3 ± 2.2 and 10 ± 3 seconds, respectively (p < 0.001). CONCLUSIONS: Animals who have prolonged elevated intracranial pressures following intraventricular hemorrhage perform poorly in spatial memory and learning. The authors suggest that a rise in intracranial pressure might be the driver for activating pathways responsible for subsequent memory dysfunction.
Published Version
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