HISTOPATHOLOGY OF CNS RADIATION 171 



nervous system is no exception. There is general agreement that aherations 

 in vessel walls are found in all phases of radiation reaction in the brain and 

 spinal cord. The sequences in\olved and the importance of these changes in 

 the total picture of radiation injury are still not entirely established. 



Clemente ct al. (1960) consider the earliest and most constant vascular 

 reaction to be a swelling- of the cytoplasm of endothelial cells and an increase 

 in the intensity of basic staining in the nucleus. They feel that this process 

 may be reversible or arrested or may progress to capillary rupture and in- 

 flammatoiy cell infiltration. Polymorphonuclear leucocytes appear soon after 

 radiation, as early as 6 hours (Clemente and Hoist, 1954), and tend to dis- 

 appear after about fi\e days (Clemente and Hoist, 1954; Haymaker ct al.. 

 1958). Rachmanow 1926) has demonstrated accumulation of trypan blue 

 in the endothelial cells at this stage. These early reactions are most con- 

 spicuous in capillaries, where they may be associated with detectable necrosis 

 of the wall. Such lesions of capillaries would accoimt for the frequent occur- 

 rence of minute hemorrhages in the acute phase of radiation reaction 

 (Alquier and Faure-Beaulieu. 1909; Clemente and Hoist. 1954; Haymaker 

 rt al., 1958 1 . In animals surviving longer after radiation, hemosiderin deposits 

 mark the location of pre\ious small hemorrhages i Fig. 1 ) . Larger hemor- 

 rhages rarely ha\e been described (Rachmanow, 1926: Scholz, 1935) and 

 usually in animals surviving 3 or 4 weeks after radiation. C'apillary changes 

 may be related to the increased permeability of the blood-brain barrier 

 (Clemente and Hoist. 1954; Mogilnitzki and Podljaschuk, 1930) and per- 

 haps less directly to brain swelling noted by sexeral authors ( Gerstner rt al., 

 1954; Ross <■? a/., 1953). 



Damage to larger \essels becomes more obvious at longer inter\als after 

 radiation. Severe necrosis with disruption of vessel walls occurs in the brain, 

 spinal cord and meninges. This is accompanied by cellular infiltration which 

 presumably is at first polymorphonuclear, but at the stage usually seen is 

 predominantly lymphocytic with a component of macrophages. In well 

 marked examples, few vestiges of the structure of the \asculai wall remain 

 (Fig. 2). The line of the endothelium and its basement membrane are sepa- 

 rated from an adventitia which is hea\ily infiltrated with inflammatory cells, 

 but is not necrotic i McLaurin ct al.. 1955). With time, there is repair and 

 reshaping of the vascular wall, the media retaining its form, but being com- 

 posed mostly or entirely of fibrous tissue i Fig. 3 i. Vascular occlusion is often 

 completed by an organi"ed thrombus filling the lumen. This process as a 

 general phenomenon of \ascular repair has certain analogies with the repair 

 of vessels in hypersensiti\ity reactions i Hawn and Janeway. 1947, especially 

 their Fig. 12). Such similarities should not be interpreted as indicating a 

 related pathogenesis, but as reparatixe phenomena in ncciosis of similar 

 distribution. 



