Levodopa/benserazide
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Mania: case report A man in his early 60s [exact age at the time of reaction onset not stated] developed mania following treatment with levodopa/ benserazide for parkinsonism. The man presented at the age of 58 years with changes in personality. Following evaluation, he was suspected to have developed a behavioural variant frontotemporal dementia (bvFTD). One year later, he developed a mild akinetic-rigid parkinsonism with right sided bradykinesia and rigidity. He was initiated on treatment with oral levodopa/benserazide [Madopar] 62.5mg × 3 tablets. Thereafter, improvement was observed. After two years of treatment, levodopa/benserazide dose was gradually increased to 125 mg × 3. He received 1-2 tablets several times a day as required. However, in the following months, his behavioral symptoms worsened with increasing hyperactivity and impulsivity. His need for sleep had also reduced. He spent large amounts of money on random objects. He threatened his wife with a knife when she tried to stop him from opening one of the packages he had ordered [time to reaction onset not clearly stated]. The man’s levodopa/benserazide dose was decreased. Despite advised to reduce the intake, he continued levodopa/benserazide therapy. His agitation and hyperactivity worsened. Subsequently, levodopa/benserazide was discontinued. He was treated with quetiapine. However, he had to be admitted to a psychiatric facility. On the day of admission, he had to be restrained by police officers. He was described as manic. However, no hallucinations were reported. The mania was considered to have developed secondary to levodopa. During hospitalisation he was treated with olanzapine and lithium. Quetiapine therapy was tapered off. Over the course of admission, his manic symptoms slowly improved. After 10 weeks, he was discharged home. Two months later, all antipsychotic treatment was discontinued and he showed marked improvement in behavioral symptoms. He was later found to be heterozygous for a hexanucleotide repeat expansion (G4C2)30+) within the C9orf72 gene, supporting the diagnosis of underlying bvFTD with concomitant parkinsonism. Eventually, he developed hypomanic symptoms. Therefore lithium therapy was re-initiated six months after its discontinuation. He continued to experience mild parkinsonism in the absence of levodopa treatment. Thorlacius-Ussing G, et al. Mania triggered by levodopa treatment in a patient with frontotemporal dementia caused by A C9orf72 repeat expansion: A case report. Clinical 803500878 Neurology and Neurosurgery 198: 2020. Available from: URL: http://doi.org/10.1016/j.clineuro.2020.106147
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Reactions 12 Sep 2020 No. 1821
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