SEQUENCE OF X-RAY DAMAGE IN MOUSE CEREBELLUM 201 





Fig. 8. Radiation damage ID days after irradiation witli 5.01)0 r. Dissolution of 

 central parts of the granular layer and destruction of Purkinje cells within the upper- 

 most layer followed by glial proliferation extending into the shrimken molecular layer. 

 X 215. Gallocvanin-chronialiun. 



were irreoiilaily dilated, and their walls showed remarkable hyalinosis. 

 Circumscribed aneurysmal distention of smaller blood vessels, previously 

 described by Scholz ( 1934a, b. 1937) in brain tisstie damaged by irradiation, 

 was noted at the 20-day sta^e. 



At 40 days after irradiation, the ylial reaction in the irradiated cerebellar 

 tisstie had progressed further. The entire damaged area was shrimken. Some 

 sjranule cells were preserved, but it was difficidt at times to distinguish 

 them from proliferated glial cells. As at shorter time intervals, hemosiderin- 

 containing sca\enger cells were often seen. Hemosiderin indicated previous 

 hemorrhage. 



In contrast to higher x-ray doses, 5,000 to 4,000 r produced only partial 

 necrosis of the cerebellar tissue. The molecular layer and the white matter 

 of the cerebellar folia were little affected. All the well known processes of 

 resorption and repair took place in the irradiated cerebellar tissue in the 

 same manner as in partial cerebellar necrosis due to other cause. Glial 

 scarring was the final outcome. 



