PHYSIOLOGY OF RADIATION INJURY 995 



Gross dysfunction of the adult nervous system is not apparent following 

 total-body irradiation in the median lethal range (Prosser, Painter, 

 Lisco, et al., 1947), and there is no histological evidence of injury resulting 

 from such exposures (Snider, 1948). Although it is true that cytological 

 damage may occur following heavy irradiation, Shields Warren (1943a) 

 has pointed out that this can be largely indirect and perhaps attributed 

 to disturbance of the vascular system rather than to a direct effect of the 

 radiation on the cellular components of nervous tissue. This limiting 

 factor in the interpretation of radiation effects on the nervous system 

 has been emphasized by others (Campbell and Novick, 1949). 



Early changes consisting of chromatolysis and vacuolization of the 

 ganglion cells have been observed following irradiation with several 

 thousand roentgens (Campbell et al., 1946; Novick, 1946). Changes in 

 the trigeminal ganglia of rabbits after local X irradiation of the head 

 with 3000 r can be separated temporally into three phases: an initially 

 severe chromatolysis immediately post-exposure, a recovery phase begin- 

 ning several hours later, and a second wave of chromatolysis beginning on 

 the third day and persisting for several weeks (Novick, 1946). The 

 clinical picture parallels the condition of the ganglion cells. Thus, 

 dyspnea, exopthalmos, somnolence, and postural abnormalities are evi- 

 dent upon termination of irradiation. These signs disappear rapidly 

 and are followed by a second phase of illness, characterized by emaciation 

 and excessive salivation during the delayed chromatolysis of the ganglion 

 cells. Delayed necrosis of brain cells, which appears several months 

 after exposure, has been described in rabbits and monkeys (Davidoff et al., 

 1938; Russell et al., 1949). Localized necrosis in the central nervous 

 system of man, notably transverse myelitis, also may follow local irradia- 

 tion by 3000 r or more and may occur after months or years (Holmes and 

 Schulz, 1950). It is thought that vascular damage may be of importance 

 as an etiologic factor. 



Local irradiation of the cerebral cortex of cats with small, high-energy 

 radon applicators results within a few hours in a sharp gradient of tissue 

 reactions. This technique has been used by Campbell and Novick 

 (1949) who have found that astrocytes are the most susceptible of the 

 various cells of the cerebral cortex; oligodendroglia and microglia are 

 highly radioresistant. Large dosages of X rays applied to one side of 

 the cerebrum of monkeys result in paralysis of the contralateral limbs 

 (Davidoff et al., 1938). Hemiplegia occurs rapidly with 4000 r and after 

 several months with 2000 to 3000 r. Massive irradiation of the mid- 

 thoracic spinal cord likewise results in a paralysis. Cerebellar lesions 

 may appear several months after irradiation of the cerebrum. 



Irradiation of the whole body of the mouse with dosages in excess of 

 6000 r results in a hyperacute reaction that is characterized by motor 

 excitability (Quastler et al., 1951). Motor symptoms become more con- 



