RADIATION NECROSIS OF THE CEREBELLUM AFTER SINGLE, HIGH-DOSAGE X IRRADIATION (in German)
Histopathologic changes were examined following exposure to a single high dose of 50-kv x rays of the cerebellum of mice (10 to 60 kr at a rate of 3 kr/min to the surface of the cerebellum). Within the first hours, morphologic signs of radiation damage in the cerebellar cortex were observed; these were limited strictly to the irradiated field (3 x 3 mm). The first pathological finding observed was nuclear and cytoplasmic swelling in the nerve cells of the molecular and granular layers. In addition to these changes, at a sufficiently high x-ray doses (40 to 60 kr), vacuolation of the interstitial material was present within the molecular layer. The swelling of the nerve cells was followed by a second phase of the radiation damage which revealed interstitial edema and increasing nuclear pyknosis of the irradiated nerve cells of the molecular and granular layers. In the subsequent, third phase of the radiation damage, necrosis of irradiated cerebellar tissue occurred. Severity and appearance as well as the development of this acute radionecrosis were related to the x-ray dose. Sequence and full manifestation of this necrosis could be followed only by using lower x-ray doses (10 to 20 kr). A latent period of 1 to 20 days was noted for full manifestation of brain necrosis. The early cellular reaction, within a few hours of irradiation, is attributed to the direct effects of radiation on intracellular structures, possibly enzymes or nucleic acids, The second, or edematous, phase is attributed to radioinduced increase of vascular permeability of leaking of fluid from the blood vessels into intercellular space. The nuclear pyknosis occurring in this phase is the result of primary cell damage and not secondary to the subsequent edema, since edema beyond the irradiated area did not cause pyknosis of cell nuclei. Late brain cell injury is caused by proliferation and subsequent hyalinization of blood vessels resulting in interruption of flow of metabolites from the circulation to brain cells. It is concluded that radiation injury to the brain stems from the combined effects of primary damage to parenchymal cells followed by vascular disturbances depriving the cells of nutrient materials, both processes leading to death of neural cells and replacement by fibrous tissue. (BBB)
- Research Organization:
- Universitat, Bonn
- NSA Number:
- NSA-18-015830
- OSTI ID:
- 4073469
- Journal Information:
- Arch. Pathol. Anat. Physiol., Journal Name: Arch. Pathol. Anat. Physiol. Journal Issue: 1 Vol. Vol: 334; ISSN 0945-6317
- Country of Publication:
- Country unknown/Code not available
- Language:
- German
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