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Modeling Mitochondrial Disease Using Brain Organoids: A Focus on Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like Episodes
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Slowly progressive spread of the stroke-like lesions in MELAS

Takahiro Iizuka1, Fumihiko Sakai, Shinichi Kan

  • 1Department of Medicine (Neurology), School of Medicine, Kitasato University, Sagamihara, Kanagawa, Japan. takahiro@med.kitasato-u.ac.jp

Neurology
|November 12, 2003
PubMed
Abstract

Insights

Stroke-like lesions in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) slowly spread over weeks. This progression may involve neuronal metabolic issues and brain swelling, often linked to seizures.

Area of Science:

  • Neurology
  • Neuroimaging
  • Mitochondrial Diseases

Background:

  • Limited understanding of acute stroke-like lesion progression in MELAS.
  • MELAS involves mitochondrial dysfunction, leading to neurological episodes.

Purpose of the Study:

  • To investigate the temporal and spatial progression of stroke-like lesions in MELAS during the acute phase.
  • To correlate imaging findings with clinical symptoms and electrophysiological data.

Main Methods:

  • Serial MRI, EEG, and SPECT were performed within one month of onset in four stroke-like episodes across three MELAS patients.
  • Analysis focused on lesion evolution, diffusion characteristics (ADC maps), epileptiform discharges, and cerebral blood flow (SPECT).

Main Results:

  • Stroke-like lesions slowly spread over weeks, evolving from temporal to surrounding cortical areas.
  • Decreased ADC values indicated active lesion evolution; focal hyperemia and periodic epileptiform discharges were observed.
  • Cortical laminar necrosis was evident in the subacute stage.

Conclusions:

  • Slowly spreading stroke-like lesions in MELAS suggest ongoing metabolic derangement.
  • Vasogenic edema, potentially triggered by prolonged seizures, may contribute to lesion progression.

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