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A severe carnitine deficiency is thought to contribute to VHE.[5] Although the precise mechanism leading to hypocarnitinemia in patients treated with valproate is not known, a previous clinical study showed a significant decrease in carnitine concentration and changes in the ratio of acylcarnitine to free carnitine for both neurological and psychiatric indications.[6] Recently, we reported that VPA treatment induces hyperammonemia and causes concentration-dependent carnitine deficiency regardless of the use of additional mood stabilizers, while serum levels of NH3 do not correlate with VPA concentrations in psychiatric patients.[7] In the field of pediatric neurology, reports suggests carnitine supplementation tends to normalize elevated NH3 concentration by binding to VPA and relieving the inhibition of urea synthesis with favorable clinical response.[8,9] In contrast, despite the widespread use of VPA in psychiatry, carnitine supplementation for the treatment of hyperammonemia and hypocarnitinemia has not been prospectively studied in a psychiatric setting