540 DR JAMES W. DAWSON ON 



both brain and spinal cord, and in each the peri- ventricular and peri-aqueductal 

 localisation was marked. 



The microscopic examination, which was very thorough, revealed areas of three 

 types — hard, soft, and intermediate : frequently one area showed all three stages. 

 The hard islets, most numerous in the cord, consisted of dense neuroglia fibrils with 

 few glia cells and only an occasional axis cylinder : typical areas of softening were 

 confined to the brain, and consisted of a loose reticulum, containing a semi-fluid 

 material but no proliferated neuroglia, nor products of degeneration ; the inter- 

 mediate islets contained nerve fibres in all stages of degeneration and the pro- 

 ducts of degeneration, but no proliferated neuroglia fibrils. Tredgold thinks 

 that the essential process is one of myelin degeneration independent of vascular 

 disease, and that the initial changes are strongly suggestive of the presence of a 

 circulating toxin. 



Bramwell (1904) has studied disseminated sclerosis with special reference to the 

 frequency and etiology and prognosis of the disease, and has discussed its pathology. 

 The author inclines to the view that the disease is due to some developmental or 

 congenital defect of the neuroglial or nervous tissue (perhaps similar to or analogous 

 to the gliomatosis in cases of syringomyelia), which renders it more liable to be 

 affected by irritation than the glial or nervous tissue of the normal individual. He 

 thinks that the diversity of conditions which were thought to be the cause in 

 individual cases makes it difficult to suppose that the alleged cause was in reality 

 the starting-point or sole cause. With regard to the nature of the hypothetical 

 toxin carried to, and distributed through, the nervous tissues by the blood-vessels, 

 he writes : " The recurrence from time to time of the symptoms after periods of 

 improvement and remission is very suggestive of repeated intoxications. If dis- 

 seminated sclerosis is due to a toxin, the toxin, whatever it is, is probably produced 

 within the body. It seems much more difficult to suppose that fresh doses of the 

 toxin are introduced again and again into the body from without during a long 

 period of years." Bramwell's views as to the nature of this toxin are further 

 referred to on p. 660. 



Uinkler (1904) gives a description of the clinical and microscopical appearances 

 in a case of disseminated sclerosis in which there had been spastic paraplegia of a 

 slightly progressive character for eighteen years, but with no nystagmus, intention 

 tremor, scanning speech nor sensory disturbances. 



The distribution of the patches was peculiar in that the majority lay in the brain 

 cortex. The myelin sheaths in these areas had undergone fatty degeneration, and 

 the axis cylinders showed a distinct participation in the diseased process. Changes 

 in the ganglion cells of the cortex accompanied the changes in the nerve fibres, not 

 only in the actual areas but in the adjoining tissue. Nests of small cells, probably 

 glious in origin, surrounded each ganglion cell, causing deformity and atrophy : their 

 injurious action on the ganglion cell is compared by the author to that of osteolcasts. 



