MELAS — Stroke-like Lesions


A patient with a known family history of MELAS (Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) presented with new neurological symptoms. On initial CT brain, there was a low-attenuation lesion in the right frontoparietal centrum semiovale that resembled a lacunar infarct.


However, a follow-up MRI revealed:

The lesion was hyperintense on DWI, but without corresponding ADC restriction — this indicates vasogenic edema rather than cytotoxic edema, which is not typical for an acute infarction.



There was also evidence of old cortical volume loss in the same hemisphere, in the temporal lobe suggesting previous stroke-like episodes.



Importantly, these lesions do not follow a specific vascular territory.

This pattern — recurrent, stroke-like lesions that spare strict vascular distributions and lack classic infarct diffusion restriction — is characteristic of MELAS. The underlying cause is mitochondrial dysfunction leading to metabolic failure and lactic acidosis, not thromboembolic vascular occlusion.

Key teaching point:

When you see cortical or subcortical lesions that look infarct-like but:

Don’t respect vascular territories

Have DWI hyperintensity without ADC restriction (vasogenic edema)

Accompanied by cortical atrophy or other sequelae of prior episodes


…then consider MELAS, especially if there’s a supportive family history or clinical background.

Summary for students:

Not all DWI-bright lesions in the brain are infarctions. In MELAS, stroke-like episodes mimic strokes radiologically, but their mechanism is metabolic, so they don’t behave like true infarcts.





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