REVIEW OF RESEARCH IN U.S.S.R. 471 



Allowance must be made for possible tissue autolysis after spontaneous deaths 

 and for intercurrent intoxication, focal or general infection, hemorrhagic 

 diathesis, fever, and other well known concomitants of acute radiation sick- 

 ness. Thus, a clear and explicit statement must be made about when the 

 injuries were seen in respect to occurrence of an acute radiation syndrome. 

 Changes in the nutritional state of the animal and use of any drugs must be 

 considered. Development of low level viremia is entirely possible after sub- 

 stantial radiation exposures and would be expected to cause CNS reactions. 

 Interpretation of nerve injury in specific organs, such as the spleen, is com- 

 plicated by the extensive cellular changes known to take place in this struc- 

 ture after radiation. The extensive cellular restructuring seen after exposure 

 may cause reactions in nerve endings. In general, most of these papers find 

 much more significant damage during the acute radiation syndrome, with 

 only reactive or irritative changes in the latent period. Effects on receptors 

 are of great interest from the standpoint of possible abnormal afferent flow to 

 the CNS during developing radiation sickness. 



Soviet and Western workers agree that the very young CNS is much more 

 radiosensitive than the developed CNS. By way of illustration, Olenov and 

 Pushnitsyna (1952) find extensive neuronal injury in young animals after 

 only 40-120 r. Kosmarskaya and Barashnev (1958) describe reactions in 

 neonatal rats exposed to 250-500 r. Others have described radiation-induced 

 congenital anomalies in the CNS. 



In regard to histologically apparent findings, one can say that while scat- 

 tered, random injury to some nerve structures would not be too surprising 

 following several hundred r, there is a heavy burden on the experimenter to 

 prove whether this is direct or due to somatic radiation injury. He must also 

 control and eliminate all possible secondary mechanisms known to injure 

 neurons, such as fever, viremia, hemorrhage, and general cachexia. In the 

 absence of full details on control measures, reports on low level neuronal 

 injury are hard to interpret. 



Functional Damage to Nerve Structures which is Not Apparent 

 Histologically 



Important changes may take place in synapses, neuronal membranes, and 

 elsewhere, but not cause any notable alteration in histologic preparations. 

 Because of well known difficulties in the electron micoscope study of the 

 nervous system, the discovery of random minimal injury is not going to be 

 easy. One can cite a great many possible mechanisms of nonmorphological 

 radiation damage. 



Several papers have dealt with direct radiation effects on simple nerve- 

 muscle preparations. For example, Pshennikova (1958) reported both local 



