392 



JANSSEN ET AL. 



200 400 600 800 1000 



Tissue depth .microns 



1200 



Fig. 6. Distribution of pyknotic cerebellar granule cells (illustrated in Fig. 5) as a 

 function of depth, superimposed on the physically measured Bragg curve, assuming 

 linear tissue shrinkage of 35 9f. This assumption was fairly well substantiated by 

 direct measurements of fresh cerebellum and of the stained section. 



in the cerebellum (and scattered pyknotic granule cells above the band) and 

 a significantly wider band of ner\e cell damage or loss in the cerebral cortex. 

 In the cerebellum in the region corresponding to the Bragg peak, the nuclei 

 of occasional Purkinje cells were chromatin-poor, while others had under- 

 gone the homogenizing type of necrosis; the molecular layer had a somewhat 

 disrupted appearance. 



At the 6,000 rad surface dose a distinct zone of nerve cell damage was 

 first encountered in the cerebellar cortex, namely at 6 hours in 4 of 6 

 animals exposed to alpha particles or protons, and it consisted of a fairly 

 even row of pyknotic granule cells in pale, somewhat loculated tissue (Fig. 

 7A). No alterations were seen in Purkinje or Golgi cells or in nerve cells of 

 the molecular layer. The earliest time interval at which nerve cell damage 

 was encountered in the cerebral cortex was also 6 hours, but only isolated 

 nerve cells were affected, chiefly in the region adjacent to the interhemi- 

 spheric fissure. Such changes were foimd consistently in the first 2 days, and 

 were virtually limited to the region corresponding to the Bragg peak. Some 

 of the aflFected ner\e cells exhibited the homogenizing type of necrosis (Fig. 

 7B) ; others, fading of nuclear chromatin, often advancing to complete nu- 

 clear "skeletonization" ( Fig. 7C ) . Cellular damage at these early stages 

 made it diflScult to determine whether some of the elements implicated were 

 nerve cells or glia ( Fig. 8 ) . Both cell types appeared to be affected simulta- 

 neously. The earliest time at which a distinct zone of damage was found in 

 the cerebral cortex was 42 hours, but such damage, which was in the form 

 of fairly broad interrupted segments, was found in only 1 of 4 brains studied. 

 Some areas within the zone were spongy, and ner\'e cells showed the homog- 

 enizing type of necrosis; in nonspongy areas within the zone of damage, the 



