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A longitudinal study of callosal atrophy and interhemispheric dysfunction in relapsing-remitting multiple sclerosis

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ARCHIVES OF NEUROLOGY
卷 58, 期 1, 页码 105-111

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AMER MEDICAL ASSOC
DOI: 10.1001/archneur.58.1.105

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Objectives: To determine if callosal atrophy and interhemispheric dysfunction can be detected in the early stages of relapsing-remitting, multiple sclerosis (MS) and to evaluate their progression in relation to the disability and evolution of lesions seen on magnetic resonance imaging during a 5-year period. Methods: We compared 30 patients who had clinically definite early-onset replasing-remitting MS and mild disability with control subjects. Regional and segmental callosal size and extent of white matter abnormalities on magnetic resonance imaging, as well as performance on tasks exploring interhemispheric transfer of motor, auditory, and sensory information were assessed. Patients with MS were evaluated at baseline and after 5 years. Physical disability was determined at both rimes using the Expanded Disability Status Scale score. Results: Patients with MS were seen with significant callosal atrophy and functional impairment of interhemispheric transfer at baseline that worsened during the 5-year study. A significant correlation was found between the mag nitude of disability and the severity of morphological and functional callosal involvement at baseline. This association persisted at rear 5. Baseline clinical characteristics such as age and prestudy relapse rate were unrelated to callosal size or interhemispheric performance. However, the number of baseline T2-weighted lesions was correlated with callosal involvement and this relation persisted at year 5. Conclusion: Patients who had relapsing-remitting MS in the early stages of the disease and mild disability had significant callosal involvement that progressed over time. The relationship between disability, T2-weighted lesions load, and degree of morphological and functional callosal impairment confirm the potential value of using callosal dysfunction as a surrogate marker of disease progression in MS.

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