There is a dearth of longitudinal studies on psychometric and psychiatric change in multiple sclerosis (MS) particularly on the evolution of these abnormalities early in the disease process. A 41 year follow up study documenting magnetic resonance imaging (MRI), psychometric, and psychiatric abnormalities was undertaken in a group of 48 patients with clinically isolated lesions-for example, optic neuritis-which are frequently the harbinger of MS. At follow up about half the subjects had developed clinically definite MS, with memory deficits becoming apparent. Deficits in attention documented at initial assessment were present but unchanged in those subjects who still had a clinically isolated lesion status. However, after MS was categorised into a relapsing-remitting or chronic progressive course, patients with a chronic progressive course were found to have significantly deteriorated with regard to auditory attention tasks. T1 relaxation times in apparently normal white matter correlated with certain indices of cognitive impairment. In developing a model to explain the pathogenesis of intellectual and emotional change in MS, the interaction of organic, psychological, and social factors needs to be emphasised. (7 Neurol Neurosurg Psychiatry 1992;55:869-876 tions were controlled for,'6 the preliminary evidence after a 1 to 2 year follow up period showed little cognitive deterioration. The only available longer follow up study also suggested that cognitive deterioration had occurred in less than a quarter of patients with multiple sclerosis four years after initial assessment and that there was considerable individual variation. 7An analogous position exists with respect to psychiatric disturbance in MS. The high prevalence of affective symptomatology is now well established.'8 Though there is firm evidence linking the presence of euphoria to cerebral involvement'9 it is unclear to what extent depressive features can be similarly explained.20 The developent and evolution of early psychiatric symptoms and the interplay of organic and social factors in their pathogenesis have yet to be studied.The study over time of patients with clinically isolated lesions (CIL-namely, optic neuritis and the brain stem and spinal cord syndromes-which are frequently the harbinger of MS,2' provides an unique opportunity to monitor cognitive and psychiatric changes early in the disease. Cognitive abnormalities are already discernible in some of these studies at presentation,22 23 and a follow up of such cases would allow the early natural history to be observed. In addition, the initial paucity of psychiatric symptomatology in subjects with CIL24 offers the opportunity to unravel the various aetiological factors that contribute to greater psychiatric morbidity in those who subsequently develop MS.In an earlier study, we reported that patients with CIL had significantly greater deficits in auditory and visual attention when compared with a physically disabled control group without brain involvement, matched for age, sex, and pr...

Three patients are described with slowly progressive loss of speech and dysarthria associated with orofacial dyspraxia, initially with intact written language, who subsequently developed more widespread cognitive abnormalities. Positron emission tomography (PET) revealed bifrontal hypometabolism in all of the patients, most marked in the inferior and lateral portions of both frontal lobes, with some extension into the parietal and temporal cortices in one case. These patients may represent a further example of focal progressive cortical degeneration.

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We examined 13 patients with neurological manifestations of systemic lupus erythematosus (SLE) based on previous and/or current neurological or psychotic episodes by magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (MRS) together with psychiatric and cognitive assessment. MRI was abnormal in 7 patients, showing high signal lesions in the white matter and/or cerebral atrophy. Proton MRS centred on white matter lesions in 5 patients showed a reduction in the N-acetyl aspartate creatine ratio compared with normal appearing white matter in the SLE group and in 10 healthy controls. This pattern of abnormality does not allow differentiation of SLE lesions from the chronic plaques occurring in multiple sclerosis. There was a very high incidence of current psychiatric morbidity in the SLE group, namely in 12 of the 13 patients. There was no correlation between the presence of current psychiatric involvement and/or cognitive dysfunction and abnormalities detected with MRI or MRS.