EFFECTS ON BLOOD-BRAIN BARRIER, CEREBRAL BLOOD VESSELS 419 



x-rays. With his:her doses, these vascular reactions were followed by petechial 

 hemorrhatres at the capillary le\el and polymorphonuclear perivasculitis. 



A pattern of cerebral vascular damage followins,- radiation could be ob- 

 served. The earliest and commonest change with the lowest radiation thresh- 

 old was a simple swelling of the endothelial cell with an increase in nuclear 

 basophilia. With a longer survival time this process either was arrested and 

 re\ersible (with lower radiation dosages) or progressed to peri\asculitis or 

 the development of petechial hemorrhages (with higher radiation dosages, 

 Clemente ct al., 1960). Russell ft al. i 1949) described similar findings in the 

 brains of rabbits. 



Radiation damage in larger sized arteries and \eins becomes manifested in 

 the pathologic changes observable in vessel walls. The inflammatory radia- 

 tion reaction in the vascular tunics of the brain seems indistinguishable from 

 arteritis or phlebitis obser\ed during inflammation in other tissues. Incom- 

 petency of the vessel walls leads to plasma leakage and cellular migration. 

 These degenerative and subsequent reparative phenomena in cerebral vessels 

 ot radiated brain contribute to narrowing of the lumen and at times to com- 

 plete occlusion of the vessel with apparent cessation of blood flow. Charac- 

 teristically obser\ed is intimal fibrosis and hyalin degeneration of fibrous 

 and muscle tissue. Ot prime importance is the fact that a radiation dose 

 capable of producing exudation and leucocytic emigration through the en- 

 dothelium of capillaries is not especially sufficient to produce a generalized 

 inflammatory reaction in the walls of larger arteries and veins i Borak, 

 1942a,b,c). A considerable increase in dose is necessary to produce the gen- 

 eralized vasculitis often described. We wish to stress the fact that low doses 

 to the brain i under 1,000 r) are capable of interfering with the competency 

 ol the cerebral capillary system and that this may eventually be manifested by 

 localized or more widespread efTects on the electrical activity of neuronal 

 pools, even though histopathologic efTects have not often been detected at 

 these dosage levels. 



The delayed white matter necrosis obser\ed (Fig. 4) by Clemente and 

 Hoist ( 1954 I in monkeys who.se heads had been radiated with 1..500 r ( 4 to 

 8 months before sacrifice ) may have been a chronic manifestation of nerve 

 fiber pathology due to small blood vessel damage. This .seems especially 

 likely since the areas of degeneration were close to small \essels whose walls 

 revealed intimal thickening. Animals in this group which were administered 

 trypan blue just before sacrifice showed a blue staining of the brain in the 

 degenerated areas only, another indication of a localized incompetent \ascu- 

 lature at the lesion sites. 



The phenomenon of delayed cerebral necrosis due to radiation is difficult, 

 if not impossible, to explain except by implication of \ascular pathology. 

 The necrotic areas are limited to the regions irradiated and the immediate 



