THE EXPERIMENTAL PRODUCTION OF AN INTERNAL HYDROCEPHALUS. 443 



may be considered inflammatory, with more or less rapid deposition of fibrin and 

 possibly the arousing of the fixed tissue-cells in the neighborhood. The reaction of 

 the cells lining the subarachnoid spaces to the presence of carbon granules has 

 already been noted (Weed, 1917). It may be assumed, then, that the block to flow 

 of the cerebro-spinal fluid is dependent upon an aggregation of the granules into an 

 impervious mass, the process probably being facilitated and the block perfected 

 by the inflammatory reaction. 



Question immediately arises as to the possible explanation of the failure of 

 cinnabar and other granules, when injected in similar amounts into the cerebral 

 ventricles and into the subarachnoid space, to give rise to internal hydrocephalus. 

 This failure seems best explained by the assumption that these granules are not able 

 to form as efficient aggregations even after the inflammatory reaction, so that the 

 flow of the cerebro-spinal fluid is not impeded. This seems the more surprising for 

 such a substance as lycopodium. With the cinnabar a minimal toxicity may modify 

 the necessary inflammatory reaction. 



It is quite difficult, after such injections of foreign participate matter, to deter- 

 mine the exact point of obstruction to the flow of the cerebro-spinal fluid. The 

 fact that similar pictures may be produced by intraventricular and by subarach- 

 noid injections of lampblack indicates that in general a similar area of obstruction 

 exists. Consideration of the density and distribution of the granules at autopsy 

 inclines one to the view that the obstruction is primarily meningeal in character, 

 and is probably a somewhat diffuse process in the basilar and possibly in the cortical 

 portions of the subarachnoid space. The gross accumulation of granules occupies a 

 portion of the cisterna cerebello-medullaris and the smaller cisterns of the base of 

 the brain, but the mesh of the subarachnoid space is here of the maximum. To 

 block this widened mesh completely seems more difficult than to do so in the cor- 

 tical portion of the space, where the mesh is very fine and where a few granules and 

 a reactive inflammatory process seem to have greater facilities for effecting a block- 

 age of the channels for the cerebro-spinal fluid. It is very difficult to determine 

 with certainty the ultimate obstruction to flow in these channels, but it must be 

 considered as a diffuse intrameningeal process, whether in the basilar regions, or 

 over the cortex, or about the various dural venous sinuses. The explanation, in 

 these experimental animals as in man, for such obstruction to the flow of cerebro- 

 spinal fluid through the meninges can not yet be given. 



With the intrameningeal block of marked efficacy, the acute reduction of 

 thickness of the cerebral cortex does not seem so remarkable. With such thinning 

 to a very few millimeters, there is a possibility of two processes taking part. First, 

 the thinning may be largely due to actual compression or destruction of brain- 

 tissue. That this plays an important part in the enlargement of the ventricles in 

 adults, where the cranial volume is fixed, must be granted; also, in cases of an infec- 

 tive hydrocephalus the two factors of compression and destruction work together. 

 In the kittens, however, where the cranial capacity may be enlarged, the latter 

 factor does not play the essential role. This is demonstrated by such findings as 

 the retention (in the process of dilatation of the ventricles and thinning of the 



