544 DR JAMES W. DAWSON ON 



segments there was a total transverse sclerosis. The vessels in most of the areas 

 showed few changes, thus differing from the usual findings in cases of acute multiple 

 sclerosis, and the extension of the areas in no way corresponded to the vessel- 

 distribution. Ganglion cells and axis cylinders in the areas were not essentially 

 changed ; there was intense glia proliferation, and an absence of any considerable 

 secondary degeneration. 



In the clinical history there was nothing to indicate infectious disease, and during 

 the course of the illness there was no rise of temperature till the onset of the 

 broncho-pneumonia from which the patient died. The author claims that this case 

 could not be regarded as a myelitis, and looks upon it as proving the existence of 

 true acute disseminated sclerosis. He considers that Muller's grouping of all such 

 cases as "secondary disseminated sclerosis" is arbitrary, as no distinction can be 

 drawn between the acute and chronic cases. 



Stadelmann and Lewandows^y (1907) also describe a case, whose acute course 

 (eight weeks) justifies the assumption of an acute multiple sclerosis or acute 

 disseminated myelitis. Areas of sclerosis, composed almost entirely of neuroglial 

 tissue, were found very widely distributed through brain and spinal cord. In the 

 areas there was a distinct vessel proliferation with increase of adventitial cell 

 elements, but no sign of small-celled infiltration. The writers look upon their 

 case as one of acute multiple sclerosis, " in virtue of the absence of any marked 

 signs of actual inflammation." 



Schob (1907), in a careful histological analysis of the sclerotic areas in a typical 

 case of disseminated sclerosis, lays special emphasis on the pathological changes 

 found in the nerve roots. From these changes he claims that the process in the 

 peripheral nervous system is analogous to that in the central nervous system — in 

 both a myelin sheath degeneration, relative integrity of the true nervous elements, 

 proliferation of the supporting tissue, and the essentially localised extension of the 

 affected tissue. He states that the case belongs to the rare observations where 

 ' with certainty," in addition to areas in the central nervous system, circumscribed 

 and analogous areas are found in the non-glial containing tissue, and relates it to 

 a combination of a neuro-fibromatosis in the nerves and a gliomatosis in the central 

 nervous system. The glia proliferation, therefore, cannot have the significance 

 of an essential and primary process, as is claimed by Strumpell and Muller 

 and others, who look upon disseminated sclerosis as an endogenous primary 

 glia sclerosis. 



The changes described are a connective-tissue proliferation which has arisen 

 almost exclusively from the Schwann sheath or the finest endoneural septa, while 

 the larger endoneural septa and the perineurium take no share in the proliferative 

 process. In some cases the process is so advanced as to form fibroma-like tumours, 

 in which the Schwann sheath has formed several concentric lamellae, the central 

 zone of which has become hyaline. In the midst of this lamellated tissue it is 



