Physiologic,Histopathologic,and Cineradiographic Characterization of a New Fluid–Percussion Model of Experimental Brain Injury in the Rat

The fluid–percussion technique produces experimental brain injury by rapid injection of a fluid volume into the closed cranial cavity. The experiments reported here characterize a new, more controlled technique for fluid–percussion brain injury in the rat and systematically examine systemic physiologic, histopathologic, and electroencephalographic responses in the rat at two levels of injury severity. The new technique was developed to permit independent variation of the fluid pressure pulse parameters and, thus, more accurately define the brain loading conditions associated with fluid–percussion injury. The new technique produced changes in mean arterial blood pressure similar to previous techniques; however, bradycardia was not observed. Significant increases in heart rate were produced by both injury levels and were more prolonged at the high level of injury severity. Both magnitudes of injury produced significant decreases in EEG amplitude immediately postinjury, but high severity injury produced a greater decrease in delta frequency band (1–4 Hz) activity than did low severity injury. Both levels produced hemorrhage at the site of injury, thalamus, corpus callosum, hippocampus, and fimbria hippocampus similar to previous techniques. Higher levels of injury produced more extensive cerebral hemorrhage and greater spinal involvement. In a separate group of animals, cineradiographic images were made at coronal, sagittal, and dorsal orientations during the fluid pressure pulse. Intracranial fluid movement was characterized by rapid radial movement within the epidural space. The data suggest that the distributed nature of fluid–percussion induces pathology, and dysfunction may reflect a diffuse mechanical loading of the brain surface. The model appears to give repeatable effects useful in the study of closed head injury.