Articles: brain-pathology.
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Zh Nevropatol Psikhiatr Im S S Korsakova · Jan 1990
Comparative Study Historical Article[Structural and functional comparisons in neurology and psychiatry (historical aspect)].
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Arch Neurol Chicago · Mar 1989
Case ReportsOsmotic demyelination syndrome. Lack of pathologic and radiologic imaging correlation.
An otherwise healthy diabetic woman developed severe hyponatremia, her serum sodium ion levels were rapidly corrected to normal, and she had a course of improvement then neurologic deterioration, with seizures and coma developing in the subsequent two days. Imaging studies, including computed tomography and magnetic resonance images of the brain as late as 19 days after the osmotic insult, failed to show pathologically demonstrated demyelinating lesions. Osmotic brain injury induces demyelination in areas of gray-white apposition and, clinically, results in a delayed neurologic deterioration one to three days following the osmotic challenge. Even with magnetic resonance imaging, review of the literature and this experience suggest that osmotic demyelination cannot reliably be imaged during the first month after the insult.
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Trimethyltin is a neurotoxicant which produces a distinct pattern of neuronal cell death following peripheral administration of a single dose (8 mg/kg, i.p.) in rats. The cupric-silver degeneration stain was used to produce an atlas documenting the distribution and time course of trimethyltin-induced neuronal damage in adult, male Long-Evans rats. Animals were examined at survival times of 1, 2, 3, 4, 5, 7, 10 and 18 days after intoxication. ⋯ Protein-O-carboxyl methyltransferase immunoreactivity was altered in neuronal populations damaged by trimethyltin, but did not appear to be either as sensitive or selective an assay of neuronal damage as the silver stain, especially at short survival times. Glial fibrillary acidic proteins were dramatically elevated 21 days after trimethyltin intoxication, particularly in areas of extensive damage. These studies revealed advantages and problems encountered in the use of each technique in assessing neurotoxic effects, forming a basis for discussion of the relative merits of using a battery of specific molecular probes for neurotoxicity evaluations.
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J. Cereb. Blood Flow Metab. · Jun 1987
Comparative StudyHistopathological and hemodynamic consequences of complete versus incomplete ischemia in the rat.
The primary objective of this study was to compare the histopathological consequences of complete versus incomplete ischemia under experimental conditions that limit lactate accumulation. Fasted rats underwent 1 h of either complete or incomplete ischemia by a procedure combining bilateral common carotid artery occlusion, halothane-induced systemic hypotension, and CSF pressure elevation. Histopathological outcome was evaluated 4 h later and was graded on a 4-point scale. ⋯ When recirculation was instituted for 1 h following 1 h of complete ischemia, regions of nonperfusion were detected autoradiographically. Thus, when the degree of lactic acidosis is controlled, prolonged periods of complete ischemia result in a more severe pathological outcome compared to incomplete ischemia. Focally impaired postischemic cerebral perfusion appears to be an important factor in infarct formation under the present experimental conditions.