Javad Hekmatpanah1. 1. Section of Neurosurgery, Department of Surgery, The University of Chicago Medical Center, Chicago, IL 60637, USA. hekmat@surgery.bsd.uchicago.edu <hekmat@surgery.bsd.uchicago.edu>
Abstract
BACKGROUND: In cerebral compression, deterioration of consciousness and coma are traditionally thought to be caused by compression, shift, hemorrhage, or herniation of the brain stem. The objective of this study was to evaluate vascular perfusion and pathologic alteration in the entire brain during drowsiness and coma. METHODS: Brain tumors were developed in 3 newborn rat litters by inoculation of KSV (a murine erythroblastosis virus) into their brain. Within several weeks, brain tumors developed. When the animals became drowsy or comatose, their brains were perfused with microbarium, India ink, or paraformaldehyde solution. In 2 animals, the brain vasculature was casted with plastic materials. The brains were either fixed for magnification radiography or prepared for histologic examination. RESULTS: The brains of control animals showed an abundance of microvessels and penetrating capillaries located perpendicular to the cortex and deep within the brain. The latter entities cannot be detected even in the best routine cerebral angiography in human beings. Microvessels were obstructed, in a patchy and dispersed fashion, during drowsiness, especially in the ipsilateral hemisphere. Obstruction of microvessels was present not only in the brain stem but also in the rest of the brain and in the cerebellum of comatose animals; larger vessels appeared to be markedly narrowed. The study also revealed evidence of diffuse infarcts, cellular ischemia, swelling, and periventricular damage throughout the brain. CONCLUSIONS: During drowsiness and coma caused by cerebral compression, cerebral capillaries progressively obstruct not only in the brain stem but also throughout the brain, considerably in a more severe pattern during coma than during drowsiness. These likely cause the diffuse neurologic disabilities and behavioral changes often seen after recovery from coma caused by cerebral compression.
BACKGROUND: In cerebral compression, deterioration of consciousness and coma are traditionally thought to be caused by compression, shift, hemorrhage, or herniation of the brain stem. The objective of this study was to evaluate vascular perfusion and pathologic alteration in the entire brain during drowsiness and coma. METHODS:Brain tumors were developed in 3 newborn rat litters by inoculation of KSV (a murineerythroblastosis virus) into their brain. Within several weeks, brain tumors developed. When the animals became drowsy or comatose, their brains were perfused with microbarium, India ink, or paraformaldehyde solution. In 2 animals, the brain vasculature was casted with plastic materials. The brains were either fixed for magnification radiography or prepared for histologic examination. RESULTS: The brains of control animals showed an abundance of microvessels and penetrating capillaries located perpendicular to the cortex and deep within the brain. The latter entities cannot be detected even in the best routine cerebral angiography in human beings. Microvessels were obstructed, in a patchy and dispersed fashion, during drowsiness, especially in the ipsilateral hemisphere. Obstruction of microvessels was present not only in the brain stem but also in the rest of the brain and in the cerebellum of comatose animals; larger vessels appeared to be markedly narrowed. The study also revealed evidence of diffuse infarcts, cellular ischemia, swelling, and periventricular damage throughout the brain. CONCLUSIONS: During drowsiness and coma caused by cerebral compression, cerebral capillaries progressively obstruct not only in the brain stem but also throughout the brain, considerably in a more severe pattern during coma than during drowsiness. These likely cause the diffuse neurologic disabilities and behavioral changes often seen after recovery from coma caused by cerebral compression.