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[Multiple sclerosis with higher cerebral dysfunction: a case report].

K Hatakeyama1, M Aihara, A Shimizu

  • 1Department of Pediatrics, Yamanashi Medical College.

No to Hattatsu = Brain and Development
|January 1, 1991
PubMed
Summary
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Higher cerebral dysfunctions are rarely seen in multiple sclerosis (MS). This case highlights parietal white matter lesions causing these higher cognitive deficits in a young patient with MS.

Area of Science:

  • Neuroscience
  • Neurology
  • Immunology

Background:

  • Higher cerebral dysfunctions like aphasia, apraxia, and agnosia are infrequently reported in Multiple Sclerosis (MS).
  • Understanding the neuroanatomical basis of these cognitive deficits in MS is crucial for diagnosis and management.

Observation:

  • A 12-year-old boy presented with initial symptoms of unsteadiness and headache, followed by visual disturbances, facial and extremity weakness, and sensory deficits.
  • The patient exhibited significant higher cerebral dysfunctions, including amnestic aphasia, acalculia, ideomotor apraxia, finger agnosia, and right-left disorientation.

Findings:

  • Cerebrospinal fluid analysis revealed elevated IgG, myelin basic protein, and neuron-specific enolase.
  • Neuroimaging (CT and MRI) identified sclerotic lesions in the left parietal white matter and right mid-brain, consistent with MS.

Related Experiment Videos

  • Post-treatment, MRI showed persistent high signal intensity in the left parietal white matter, suggesting ongoing demyelination or axonal damage.

    • Implications:

    • The study suggests that lesions in the left parietal white matter may lead to higher cerebral dysfunctions in MS by causing disconnection between cortical areas.
    • This case underscores the importance of considering subtle neuroanatomical lesions in the white matter for explaining complex cognitive deficits in pediatric MS.
    • Early recognition and targeted treatment of MS-related white matter lesions are essential for mitigating long-term neurological sequelae.