X-IRRADIATION AND DELAYED MYELOMALACIA 245 



x-irradiation of the spinal cord in experimental rats is different from the 

 ravaging necrobiosis wreaked on all areas of the spinal cord (gray and white 

 matter) when the animals are exposed to extremely high doses, with survival 

 from a few days to a week. From the few neuropathologic studies on human 

 cases (Itabashi ct ai, 1957), delayed irradiation myelopathy in rats appears 

 to be a similar process, with the exception of the absence in rats of unmistak- 

 able changes in the wall of vessels. In the spinal cord, white matter seems 

 more sensitive than gray. Irradiations could possibly ha\e some direct effect 

 on myelin sheaths and axis cylinders, aside from any changes caused in the 

 endothelium or walls of vessels. This might be suggested by the work of 

 Leboucq (1934). on the inhibitory effect of irradiation on the developing 

 myelin of baby rats. 



There might be some concern about the definition of the process, whether 

 it should be designated a demyelinating or malacic one. It is demyelinating 

 in the sense of predilection for attack on the white matter, and no doubt 

 it could start as such. However, it seems that once the lesion starts it is a 

 rapidly progressive one and then it cannot be regarded as anything but a 

 \ery severe liquefacti\e process. A large variety of histochemical methods 

 on sections through such a lesion failed to identify with precision any specific 

 degradation products of myelin breakdown. The almost negligible glial reac- 

 tion is of importance, and in the white matter the oligodendroglia seem to 

 disappear as fast as the myelin sheaths. 



Regarding the changes in the walls of vessels, which ha\e been depicted 

 as hyaline, amyloid, or para-amyloid degeneration in human postirradiation 

 myelopathy (Zeman. 1955: Scholz ft ai, 1959: Pennybacker and Russell, 

 1948) but which were not found by O'Connell and Brunschwig, (1937) 

 it is important to note there was no evidence in the rat lesions of the depo- 

 sition of any imusual degenerati\e substance in or around vessels. Whether 

 dynamic alterations in capillary permeability are responsible for an irre\o- 

 cable destruction of white matter is another problem. 



A spontaneous demyelinating disease of the spinal cord ! and not the 

 brain) in two rats was reported by Pappenheimer i 1952). From his descrip- 

 tions and illustrations, the condition cannot be distinguished clinically or 

 pathologically from experimental postirradiation myelopathy. We know that 

 comparable types of disease processes can be produced in the ner\ous system 

 by divergent types of causal agents; but that spontaneous demyelinating 

 myelopathy can also occur in rats, should be recognized. Pappenheimer was 

 unable to transmit the disease to other rats or mice: the cause was never 

 ascertained, nor has any similar disorder been reported by others. Despite 

 this, we cannot relegate into the limbo of forgotten things the remote feasa- 

 bility that Pappenheimer's murine disease was caused by a virus and that 

 irradiation might not light up some latent neurotropic infection. 



There remains to be considered the degeneration and necrosis of the 



