Aphasic status epilepticus preceding tumefactive left hemisphere lesion in anti-MOG antibody associated disease

Kazuto Katsuse1, Masanori Kurihara1, Yusuke Sugiyama1

  • 1Department of Neurology, The University of Tokyo, Tokyo, Japan.

Abstract

Insights

Autoimmune epilepsy can occur in anti-myelin oligodendrocyte glycoprotein (MOG) antibody disease, even without visible brain lesions on MRI. Later development of lesions near seizure foci suggests a link between demyelination and epilepsy.

Area of Science:

  • Neuroimmunology
  • Epileptology
  • Neuroradiology

Background:

  • Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies are linked to epilepsy with MRI-visible lesions.
  • The relationship between anti-MOG antibodies and epilepsy without detectable MRI lesions remains unclear.

Observation:

  • A patient with anti-MOG antibody disease presented with global aphasia and no new MRI lesions.
  • EEG, MEG, and SPECT indicated epileptic foci in the left temporal and parietal lobes.
  • The patient responded to steroids, and later developed a tumefactive white matter lesion in the same region.

Findings:

  • Autoimmune epilepsy can manifest in anti-MOG antibody disease without initial MRI-detectable lesions.
  • The emergence of a tumefactive lesion near epileptic foci suggests a connection.

Implications:

  • This case highlights autoimmune epilepsy as a potential manifestation of anti-MOG antibody disease.
  • Further research is needed to understand the link between demyelinating lesions and epilepsy in MOGAD.

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