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Reversible Valproate-Induced Subacute Encephalopathy Associated With a
Giovanna De Michele1, Pierpaolo Sorrentino1, Claudia Nesti2
1Department of Neurosciences and Reproductive and Odontostomatological Sciences, Università degli Studi di Napoli Federico II, Napoli, Italy.
Frontiers in Neurology
|September 15, 2018
Summary
Valproic acid (VPA) can cause neurological impairment in patients with specific mitochondrial DNA variants. Early consideration of mtDNA abnormalities is crucial when VPA-treated patients develop neurological symptoms.
Area of Science:
- Neuroscience
- Genetics
- Mitochondrial Biology
Background:
- Valproic acid (VPA) is associated with neurological impairment in some patients.
- Mitochondrial dysfunction is a potential mechanism underlying VPA-induced neurotoxicity.
Observation:
- A 65-year-old woman developed subacute encephalopathy with motor and cognitive deficits after VPA treatment.
- Clinical presentation included drowsiness, gaze palsy, weakness, and ataxia.
- Neuroimaging and muscle biopsy revealed leukoencephalopathy, ragged red fibers, and mitochondrial electron transport chain deficiencies.
Findings:
- The patient harbored the MT-ATP8 gene variant mt.8393C>T in homoplasmy.
- This variant was previously linked to VPA sensitivity in a pediatric case.
- Neurological symptoms significantly improved after VPA withdrawal.
Implications:
- This case highlights the MT-ATP8 mt.8393C>T variant in homoplasmy as a cause of VPA-induced encephalopathy.
- Mitochondrial DNA (mtDNA) abnormalities should be considered in VPA-treated patients presenting with neurological symptoms, after ruling out hyperammonemia and liver failure.
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