| Literature DB >> 972336 |
H G Sullivan, J Martinez, D P Becker, J D Miller, R Griffith, A O Wist.
Abstract
Mechanical brain injury was produced in 36 cats with a fluid-percussion model in which brain damage or dysfunction is produced by a single, brief, hydraulically-induced pressure transient that is conducted through the brain. Fluid-percussion injury induce elastic deformation of the brain resembling the brain deformation known to occur following head impact. Physiological responses and pahtological changes following injury were expressed as a function of peak pressure. Macroscopic central nervous system lesions concentrated at the pontomesencephalic junction, cervicomedullary junction, and in the cerebellar tonsils were consistently observed at and above 2.6 atmospheres (atm). At higher levels of injury (greater than or equal to 3.2 atm) there was extensive basal subarachnoid hemorrhage. At very high levels of injury (greater than 4.0 atm) hemorrhagic contusions were noted at the cerebral hemisphere impact site. A spectrum of neuronal alterations was identified in the damaged areas. Computer analysis showed correlation of electroencephalographic (EEG) changes with the neuropathological changes, since EEG recovery became severely impaired above 2.6 atm. No EEG changes were noted below 1.5 atm. From 1.5 to 2.2 atm there was a physiological response to injury but no significant changes were seen on neuropathological examination. This range of injury should permit further studies of the more subtle changes following mechanical brain injury without intraparenchymal hemorrhage or subarachnoid hemorrhage. The fluid-percussion model relates brain deformation following mechanical loading to a single pressure transient that is easily measured and controlled. Further quantitative investigation into the pathobiology of mechanical brain injury following graded brain deformation is thus made possible.Entities:
Mesh:
Year: 1976 PMID: 972336
Source DB: PubMed Journal: J Neurosurg ISSN: 0022-3085 Impact factor: 5.115