230 W. SCHOLZ, VV. SCHLOTE AND W. HIRSCHBERGER 



primarily caused by irradiation. Krogh and Bergedcr (1957), who produced 

 cerebellar lesions by a high x-ray dosage, did not decide whether the break- 

 down of the granular layer is secondary to edema or is a primary lesion. In 

 experiments with Co''", Vogel et al. (1958) produced a reversible pyknosis 

 of the same gramdar cells. Since we know that the granular layer of the 

 cerebellar cortex is rather sensitive to edema, we must consider the possibility 

 that it is the radiation-induced edema that produces the granular cell 

 changes. However, this does not mean that all tissue changes shoidd be con- 

 sidered secondary to the edema-like loosening of the tissue. In the cerebral 

 cortex, nerve cells remain resistant to a simple edema for a long time. More- 

 over, we failed to find in acute radionecroses the dangerous plasmatic infil- 

 tration of tissue that can inhibit oxygen difTusion. As all cellular elements 

 demonstrate an early and rapid structural breakdown, the assumption may 

 be justified that x-irradiation of high dosage and intensity may cause a co- 

 ordinated breakdown of the hcmatoencephalic barrier and a primary destruc- 

 tion of all other tissue constituents as well. It seems that in delayed lesions, 

 the latent period becomes progressively shorter with an increase of x-ray 

 dose and intensity, and the hcmatoencephalic barrier, in common with other 

 tissue constituents, is at last simultaneously affected by the increased ionizing 

 radiation. 



Conclusions 



X-irradiation of the spinal cords of 36 rabbits produced results similar to 

 the previously reported delayed x-ray lesions in the brains of dogs. The 

 fractionated application of doses up to 1 1 ,000 r within 40 days and single 

 doses of 2,000 r were followed by focal zones of disintegration, mainly situ- 

 ated in the white matter, but also affecting the gray substance. These changes 

 occurred after latent periods of from 4 to 33 weeks. The fibrinoid disor- 

 ganization of the vessel walls, erythrodiapedesis, and infiltration of plasmatic 

 material into the central nervous tissue seem to be the primary lesions and 

 demonstrate a breakdown of the hcmatoencephalic barrier. All other changes 

 of the tissue, including demyelination and breakdown of cellular constituents, 

 were preceded by permeability distiubance and may be considered secondary. 

 In the brains of approximately 100 Syrian hamsters, acute radionecroses 

 were produced by single applications of large x-ray doses of high intensity. 

 In animals receiving 5,000 r, necroses were fully developed within 8 days; 

 within 6 days after 10,000 r, and within 3 days after 45,000 r. Several animals 

 receiving 20,000 r showed distinct disintegration of tissue in the field of 

 irradiation after 24 hours, and initial stages in these cases could be detected 

 after only 7 hours. The sharply limited semicircularly shaped lesions covered 

 exactly the field of irradiation and decreased in depth with the diminution 



