SEQUENCE OF X-RAY DAMAGE IN MOUSE CEREBELLUM 



199 



parts of the irradiated cerebellar tissue (Fig. 7). Within the necrotic area 

 there were sca\enger cells and gitter cells as well as proliferating and 

 naked glial cells. The nuclei of most altered granule cells were disintegrated 

 and lysed. Only segregated groups of pyknotic nuclei together with nuclear 

 debris were observed within the irradiated field. In contrast to the animals 

 of shorter survival, edema was seen within the Bergmann layer and in 

 adjacent parts of the molecular and granular layers. Frequently, the 

 edematous process extended a short distance into the nonirradiated part 

 of the Bergmann layer and was associated with hydropic swelling of adjacent 

 Purkinje cells. Homogenization of Pinkinje cells was no longer found, as 

 cells which had suffered this change seemed to have been removed. 



When the survival period was extended by reducing the x-ray doses to 

 20,000 to 10,000 r, resorption and repair occurred in the irradiated cere- 

 bellar tissue in the same manner as in necrosis of brain tissue resulting from 

 other causes. The final stage consisted of cystic licjuefaction of the necrotic 

 brain tissue. By 20 days after irradiation with 16.000 r much of the necrotic 

 cerebellar tissue had been removed. The resulting cyst-like areas contained 

 remnants of necrotic debris and were traversed by partly preserved blood 

 vessels. The processes of resorption and repair were e\ident at the margin 



^ri; 





Fig. 7. Total tissue necrosis 90 hours after irradiation with 70.000 r (0.5 X 2 mm 

 field). X 35. Hematoxylin-eosin. 



