Cortical deficits in multiple sclerosis on the basis of subcortical lesions

Patients suffering from multiple sclerosis have a high frequency of cognitive deficits usually attributable to demyelination and axonal loss in the subcortical white matter. Neurologic abnormalities referable to cortical function are uncommon but have been described. The present study describes thre...

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Bibliographic Details
Published in:Multiple sclerosis 2000-02, Vol.6 (1), p.50-55
Main Authors: Jeffery, Douglas R, Absher, John, Pfeiffer, Frederick E, Jackson, Hagan
Format: Article
Language:English
Subjects:
Adult
Apraxias - diagnostic imaging
Apraxias - pathology
Apraxias - therapy
Biological and medical sciences
Cerebral Cortex - metabolism
Cerebral Cortex - pathology
Cognition Disorders - diagnostic imaging
Cognition Disorders - pathology
Cognition Disorders - therapy
Energy Metabolism
Female
Humans
Immunotherapy
Magnetic Resonance Imaging
Male
Medical sciences
Middle Aged
Multiple Sclerosis - diagnostic imaging
Multiple Sclerosis - pathology
Multiple Sclerosis - therapy
Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis
Nerve Fibers - metabolism
Nerve Fibers - pathology
Neurology
Tomography, Emission-Computed
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Summary:Patients suffering from multiple sclerosis have a high frequency of cognitive deficits usually attributable to demyelination and axonal loss in the subcortical white matter. Neurologic abnormalities referable to cortical function are uncommon but have been described. The present study describes three patients with clinically definite MS with deficits in cognitive function referable to cortical location. Two of the patients underwent positron emission tomography and showed profound cortical hypometabolism adjacent to subcortical white matter lesions seen on MRI. This paper points out that neurologic deficits referable to cortical sites may be caused by subcortical white matter lesions and that cognitive dysfunction in patients with MS may progress rapidly in the absence of motoria deficits or other evidence of clinical deterioration.
ISSN:1352-4585
1477-0970
DOI:10.1177/135245850000600110