HISTOPATHOLOGY OF CNS RADIATION 179 



There is evidence ( Bailey <"/ «/., 1958: Gerstner c/ ai, 1955; McLaurin ct ai, 

 1955; Yamazaki ft ai, 1960) that in this latent period there may be func- 

 tional changes related to the radiation injury before histologic change is 

 established. The demonstration and definition of this latent interval is the 

 role of the light microscopist ; the electron microscopist and chemist must 

 elucidate the processes durino- that time. Such enzyme studies as that of 

 Clammermeyer and Haymaker ( 1958) are promisino;. 



Effects of Radiation on Glia 



Arnold and P. liailey (1954) have pointed out that the response to 

 \-radiation involves damage to all types of adult glial cells, depending on the 

 total dose of radiation, the intensity of dose administration, the uniformitv 

 of dose distribution, and the time inter\als between radiation and sacrifice of 

 the animals. 



The oligodendroglia are early and se\erely affected, with swelling of the 

 cytoplasm (Arnold and Bailey, 1954) followed by pyknosis and disintegra- 

 tion of the cells (Hicks and Montgomery, 1952; Hicks ft ai, 1956). In \iew 

 of the generally accepted role of oligodendroglia in the maintenance of the 

 myelin sheath, this finding is of considerable interest because of the relatively 

 early disintegration of myelin in radiated areas (Hicks ft <?/., 1956) and the 

 severity of radiation damage at the period of acti\e myelination (C'lemente 

 ft a!., 1960). 



There is little, if any, lormation of compound granular corpuscles in areas 

 of necrosis (Arnold and Bailey, 1954), indicating inhibition or destruction of 

 microglia. 



A similar but more striking eflect is exerted on the astrocytes, lliey at first 

 swell, then fragment, and by 4 to 6 weeks after radiation the area is de\oid 

 of astrocytes ( Arnold and Bailey, 1 954 l . Only after many months is there 

 resumption of the expected astrocytic proliferation in repair of necrotic 

 areas. 



Fig. 7. Patchy loss of myelin in dorsal spinocerebellar fasciculus, suggesting direct 

 injury not mediated through blood vessel changes. Weil's method X30. Monkey re- 

 ceived 12,048 r Ta^"" in 67 hours. X-ra\- 10.000 r in 3 days given 5 months after 

 completion of Ta'"" radiation. Complete paraplegia 48 hours after Ta""" radiation: 

 partial recovery in 2 months; paraplegia again complete after x-radiation. Sacrifice 6 

 weeks after completion of x-radiation. See also Fig. 1 1. 



Fig. 8. Degeneration and fragmentation of nerve fibers in posterior columns of 

 spinal cord. Hortega's silver carbonate X350. Dosage 10,000 r x-radiation in 2 days. 

 Clomplete paraplegia 36 hours after completion of radiation. Sacrifice 5 days after 

 radiation. 



