Abstract
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) usually manifests in early life. Clinical hallmarks of the disease are mitochondrial myopathies, encephalopathy with stroke-like episodes, seizures, and lactic acidosis. It rarely manifests in late adulthood. Here we present the case of a 63-year-old female patient who developed recurrent stroke-like symptoms with typical resolving and remitting pattern of findings on imaging. Later on, it was confirmed as a case of MELAS upon genetic analysis.
Highlights
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is a maternally inherited multi-systemic disorder caused by mutations of mitochondrial DNA, which leads to a respiratory chain deficiency
We present the case of a female patient who developed late-onset MELAS at 63 years of age
She had left upper extremity ataxia, moderate expressive and receptive aphasia with paraphasic errors, and anomia. Her National Institutes of Health Stroke Scale (NIHSS) score was 3. She had a medical history of diabetes mellitus, hyperlipidemia, chronic obstructive pulmonary disease (COPD), and transient ischemic strokes
Summary
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is a maternally inherited multi-systemic disorder caused by mutations of mitochondrial DNA, which leads to a respiratory chain deficiency. MRI of the brain without contrast (nine months later from the baseline MRI; Figure 1) showed cortical swelling and increased T2/FLAIR signal involving the left temporal lobe. DWI delineated increased signal (T2 shine-through) without any significant change on ADC, which was thought to represent vasogenic rather than cytotoxic edema It was likely suggestive of sub-acute infarct similar to the previously seen lesion in the right temporal lobe. The patient denied any sudden change in vision and speech, lateralized weakness, numbness, or incoordination during that one-month interval upon her follow-up visit.
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