[Cognitive deterioration in multiple sclerosis].

Abstract

Amongst the varied symptomology of multiple sclerosis is to be found the alteration of higher functions (cognitive deficit), which has considerable repercussions on the quality of life of patients. The old descriptions of the disease rarely differentiate cognitive affectation from the more general category of "mental symptoms", which also includes a broad range of affective disorders. Towards 1960 neuropsychological tests began to be employed, and it was from the 1970s onwards that a clear distinction was drawn between deterioration of the higher functions and psycho-affective aspects in the disease. The pattern of cognitive deterioration in patients with multiple sclerosis is not uniform. During the initial phases of the disease it is, in general, light and it has an insidious start, although inter-individual variability is wide, depending on the predominant pathological alterations in the lesions and on their number and localisation. In more severe cases, it is possible to include within the debatable term of subcortical dementia, intellectual slowness, problems of attention, alterations in abstract reasoning, shortcomings in the resolution of problems and memory dysfunction. It is an almost invariable complication of the advanced stages of the disease, since the lesions characterised by axonal loss affect broad areas of white matter, which determines the deafferentation of several areas of cortical association. There does not appear to be any correlation between cognitive deterioration and the variables of the disease considered in an independent way, such as demographic data, clinical course, alterations of mood, consumption of medicines or fatigue. Although, evidently, the disease's progressive secondary forms of greater duration and the accumulation of lesions are what present the greatest deterioration. With present-day techniques of neuroimaging it has been possible to show a correlation between cognitive deterioration and the existence of an increase in ventricular size, periventricular lesions and atrophy of the callous body.