Brain atrophy with mental and neurologic deterioration developing a few months after radiation therapy in patients without residual or recurrent brain tumors has been recognized. Two illustrative case reports of this pathologic entity are presented. Six autopsy cases with this entity including the two cases were reviewed neurologically, radiographically, and histopathologically. All patients presented progressive disturbances of mental status and consciousness, akinesia, and tremor-like involuntary movement. Computerized tomography (CT) demonstrated marked enlargement of the ventricles, moderate widening of the cortical sulci, and a moderately attenuated CT number for the white matter in all six patients. Four of the six patients had CSF drainage (ventriculoperitoneal shunt or continuous lumbar drainage), however, none of them improved. Histologic examination demonstrated swelling and loss of the myelin sheath in the white matter in all patients, and reactive astrocytosis in three of the six patients. Neither prominent neuronal loss in the cerebral cortex or basal ganglia, nor axonal loss in the white matter was generally identified. The blood vessels of the cerebral cortex and white matter were normal. Ependymal layer and the surrounding brain tissue were normal in all patients. These findings suggested that this pathologic condition results from demyelination secondary to direct neurotoxic effect of irradiation. The authors' previous report was reviewed and the differential diagnoses, the risk factors for this pathologic entity, and the indication for radiation therapy in aged patients with a malignant brain tumor are discussed.
We investigated the temperature changes and their distribution in agar phantoms and dog normal brains induced by 8 MHz radiofrequency interstitial hyperthermia and observed the histological changes, with respect to the neurons and myelinated nerve fibres, induced by the same heat source in dog normal brains. We also examined the change of blood-brain barrier permeability using Evans blue solution. The heating limits of dog normal brain were 42 degrees C for 45 min or 43 degrees C for 15 min and the breakdown of the BBB was observed at 43 degrees C for 60 min.
We investigated the temperature distribution, early histological changes, blood brain barrier (BBB) disruption and sequential changes in cerebral blood flow (CBF) following hyperthermia ranging from 37 to 45 degrees C in a new rat model of radiofrequency-induced localized cerebral hyperthermia. Significant histological changes and BBB disruption were observed in brain regions heated to 43 degrees C and above. In the cortex heated to 41 degrees C, the CBF doubled 20 min after hyperthermia induction, and then returned gradually to the pre-hyperthermic level. In the cortex heated to 43 degrees C, the CBF increased to 134% of the baseline level 10 min after hyperthermia induction, and then fell gradually to reach its minimum level (31% of the baseline level). In the cortex heated to 45 degrees C, the CBF decreased immediately after hyperthermia induction to reach 10% of the baseline level. The results indicate that hyperthermia-induced cellular injury in the central nervous system is associated with cerebral ischaemia and the threshold temperature for such injury is 43 degrees C. This model is useful for investigating the effects of hyperthermia on various cerebral functions and the CBF changes demonstrated in the present study may provide key information for the analysis of other cerebral functions.
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