682 DR JAMES W. DAWSON ON 



spinal, vestibular, cerebellar, and cerebral components, it is co-extensive with the 

 nervous system : some part of this extensive system is almost invariably implicated. 

 Nystagmus, tremor, - — both static and intentional — and ataxia all occur : the 

 spasticity to a certain extent masks the inco-ordination in the gait and gives 

 rise to a spastic cerebellar type of progression. In spite of the length of the 

 afferent paths of common sensation, loss of common sensibility is rare : the cause 

 of this anomaly is uncertain, but it is possible that a considerable degree of 

 involvement of the sensory columns may occur without a marked loss of sensibility, 

 and that afferent sensory stimuli survive when weaker efferent stimuli fail. 



It has been already pointed out that many of the symptoms are due to loss of 

 cerebral inhibition, and this loss of cerebral control is a source of great confusion in 

 interpreting the symptoms. Just as the interception of the volitional motor 

 impulses permits increased irritation of the reflex mechanism, so does the loss of the 

 unconscious cerebral control permit increased irritation of the automatic, the 

 sympathetic, and the reflex mechanism. 



The frequent presence of daily variations in the symptoms after the disease has 

 become established emphasises the importance of the mental factor in the 

 symptomatology. Structural lesions do not thus vary, but the external evidences 

 of them — the patient's reaction to them — may vary. This variation probably 

 depends upon environmental stress, upon nutritive factors, and probably chiefly upon 

 the intermittent evolution of endogenous toxins. 



(vii) It is suggested, therefore, that fleeting early motor paralyses and psychic 

 symptoms may be related to the presence of areas in association paths : that 

 remission of these symptoms is possibly due to the linking up of other association 

 paths, or their compensation by the opening up of new paths ; and, further, that the 

 variation of the symptoms in all stages of the disease emphasises the importance of 

 the mental factor in the symptomatology. 



We are now in a position to turn to the conclusions based on definite histological 

 data. An explanation has already been offered for the formation of certain types of 

 areas, but one or two changes related to these areas still require to be mentioned. 



(viii) The "areolar" zones, the true "areolar" areas, and the peri-vascular sieve- 

 like areas must probably be referred to an oedema of the peri-focal and peri-vascular 

 tissue, due to alterations in the blood and lymph circulation, firstly within the area, 

 and then in the general tissue — through the presence of numerous foci. This is a 

 secondary process, and is the result and not the cause of the sclerotic areas. 



Areas of "shadow" sclerosis which have a definite outline or surround, with such 

 an outline, true sclerotic areas must be ascribed to a diffusion of the toxic lymph in 

 concentration insufficient to cause a complete demyelination. Such areas are often 

 accompanied by a diffuse glia hyperplasia. 



Further, areas of diffuse and lighter staining, which connect true sclerotic areas 



