Histopathologic response of the immature rat to diffuse traumatic brain injury

Citation
Pd. Adelson et al., Histopathologic response of the immature rat to diffuse traumatic brain injury, J NEUROTRAU, 18(10), 2001, pp. 967-976
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROTRAUMA
ISSN journal
08977151 → ACNP
Volume
18
Issue
10
Year of publication
2001
Pages
967 - 976
Database
ISI
SICI code
0897-7151(200110)18:10<967:HROTIR>2.0.ZU;2-W
Abstract
The purpose of this study was to characterize the histopathologic response of rats at postnatal day (PND) 17 following an impact-acceleration diffuse traumatic brain injury (TBI) using a 150-g/2-meter injury as previously des cribed. This injury produces acute neurologic and physiologic derangements as well as enduring motor and Morris water maze (MWM) functional deficits. Histopathologic studies of perfusion-fixed brains were performed by gross e xamination and light microscopy using hematoxylin and eosin, Bielschowsky s ilver stain, and glial fibrillary acidic protein (GFAP) immunohistochemistr y at 1, 3, 7, 28, and 90 day after injury. Gross pathologic examination rev ealed diffuse subarachnoid hemorrhage (SAH) at 1-3 days but minimal suprate ntorial intraparenchymal hemorrhage. Petechial hemorrhages were noted in ve ntral brainstem segments and in the cerebellum. After 1-3-day survivals, li ght microscopy revealed diffuse SAH and intraventricular hemorrhage (IVH), mild edema, significant axonal injury, reactive astrogliosis, and localized midline cerebellar hemorrhage. Axonal injury most commonly occurred in the long ascending and descending fiber tracts of the brainstem and occasional ly in the forebrain, and was maximal at 3 days, but present until 7 days af ter injury. Reactive astrocytes were similarly found both in location and t iming, but were also significantly identified in the hippocampus, white mat ter tracts, and corpus callosum. Typically, TBI produced significant diffus e SAH accompanied by cerebral and brainstem astrogliosis and axonal injury without obvious neuronal loss. Since this injury produces some pathologic c hanges with sustained functional deficits similar to TBI in infants and chi ldren, it should be useful for the further study of the pathophysiology and therapy of diffuse TBI and brainstem injury in the immature brain.