Abstract

Introduction: Patients with multiple sclerosis (MS), disease history of 11.5 years, an expanded disability status scale (EDSS) up to 6.0 and an involvement of verbal and/or spatial and long-term memory showed a bilateral reduction of glucose metabolism in the cingulate gyrus, thalamus, associative occipital cortex and cerebellum. To our knowledge no similar studies in early stages of MS are reported. Therefore we stressed the question of possible correlation of quality of life, objective cognitive impairment and FDG-PET findings in newly diagnosed definite MS according to McDonald criteria. Methods: In 11 patients (f=4, m=7, mean age: 35 years (CI 25–42), IQ 112 (CI 97–118)) with newly diagnosed definite MS and minor disability (mean EDSS=1.0) neuropsychological testing (VLMT, d2, Benton, TMT) and quality of life measurement (MSQOL-54) were done and correlated with age and education matched healthy group (mean age 33 years (CI 25–38), IQ 112 (100–124)). Additionally all patients were investigated by a FDG-PET. Results: Cognitive impairment reported by patients (MSQOL-54) was correlated with impairment of alertness, processing speed and concentration measured by neuropsychological testing (p<0.05). The FDG-PET analysis showed an increased metabolism of glucose at Brodmann-area 7, 18, 19, 21, and a decrease of glucose metabolism at the thalamus and cerebellum in these patients compared to a age-related healthy group. Discussion: In patients with newly diagnosed MS a increased glucose metabolism in cortical areas associated with secondary visual alertness processing could be demonstrate in contrast to prior findings in long-term MS. We suppose unconscious reactions of the MS patients lead to hyperactivity within the visual cortical regions to equalize the impairment of verbal memory and alertness. In correlation to patients with long-term history of MS reduction of glucose metabolism was found at the thalamus und cerebellum. According to previous studies the significant relationship between reduction of glucose metabolism at the cerebellum and memory scanning speed suggests that functional damage in the posterior fossa may contribute to slowed cognitive processing.

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