MORPHOLOGICAL EFFECT OF X-RAYS TO THE CNS 229 



the plasmatic material can be found as an amyloid-like substance, resistant 

 to absorption and behavins; like a foreign body. This substance has not been 

 demonstrated in large amounts in the central nervous system of experimental 

 animals. Whereas most investigators, including in recent years Berg and 

 Lindgren ( 1958). and Zeman (1955), acknowledge this pathogenic mecha- 

 nism of the delayed radiolesions, it is much more difficult to explain the 

 pathogenesis of the acute radionecrosis occurring within hours following the 

 single application of extremely large doses of ionizing radiation of high 

 intensity. We did not see convincing morphologic changes either with 80,000 

 r after 134 hours or with 45,000 r after 1 /a hours; however, necroses were 

 fully developed with 30,000 r after 67 hoins. They cover exactly the field 

 of irradiation, are apparently not related to regions of arterial irrigation, 

 and do not depend on vascular occlusions. As to the restriction of the lesions 

 to the field of irradiation and the morphologic appearance of the nerve cell 

 changes, our results are largely in accordance with the observations of Krogh 

 and Bergeder (1957) and of Schiimmelfeder (1957), though there was some 

 difference in the application and measurement of the x-irradiation. It is true 

 that fully developed acute radionecroses closely resemble anemic infarctions, 

 but we think that such a designation, used by Russel ct al. ( 1949), is not 

 justified, since during the development of the necrosis, the free passage 

 through the capillary bed has been made exident by India ink. In these cases, 

 we find hemorrhages not only in the region of neciosis but also at some 

 distance from the necrotic zone, invading the unaltered nervous tissue which 

 was exposed to a lower intensity of irradiation and indicating a distiubance 

 in the permeability of the blood vessels. Usually, the centers of the necroses 

 are surrounded by a broad shell of spongy tissue which raises the question 

 of whether we deal simply with a demarcation zone as seen around every 

 more or less complete necrosis. However, the initial stages of such necroses 

 produced by an irradiation of 20.000 and 45,000 r after 7 and 6 hours, 

 respectively, consist only of such spongy loosened tissue, suggesting a local 

 edema and demonstrating no distinct signs of cellular necrosis. Efforts to 

 stain these earliest lesions intravitally with trypan blue were not successful, 

 probably because the disorder of the blood-brain barrier is still incomplete in 

 this stage. But already in the next stage, when only minor changes of the 

 cellular constituents of the tissue manifest themselves and only a few vessels 

 show beginning diapedesis, we find a distinct blue coloration, pointing to 

 the important role of permeability disorders in the pathogenesis of the acute 

 radionecroses also. As soon as distinct necrosis is present, the trypan blue 

 staining spreads far beyond the necrotic center throughout the whole spongy 

 zone. It may therefore be reasonable to consider the sponginess of the tissue 

 as well as the multiple hemorrhages within and out of the necrotic center 

 as being due to a disturbance of penneability of the blood-brain barrier, 



