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Valproate-induced Parkinsonism in Epilepsy Patient
Conference Paper/Poster - Oct 30, 2014
Scherrer Michael, Zieglgänsberger Dominik, Tettenborn Barbara
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Brief description/objective
Medical History:
A 75-year-old Patient is affected by structural epilepsy caused by an ischemic stroke of the right posterior circulation in May 2012. After a convulsive status epilepticus in November 2012, antiepileptic therapy with valproate (1500 mg/day) was initiated. Due to a focal onset evolving to a bilateral convulsive seizure in February 2013, the dose was increased to 2000 mg/day. After six month of therapy, a rapidly progressive bradykinesia, rigidity, tremor and gait disorder appeared as signs of parkinsonism (VPA level 115 mg/l). In August 2013, the Unified Parkinson’s Disease Rating Scale (UPDRS) III already showed 41 / 108 points. Stepwise dose reduction of valproate (replaced by Levetiracetam 1000 mg/day) gradually improved the parkinsonism until the UPDRS III showed 0 / 108 points in March 2014.
Diagnostics:
Dopamine transporter scintigraphy (DaT scan) investigation showed no signs of presynaptic dopaminergic deficits (as in idiopathic parkinsonism) supporting the diagnosis of a valproate-induced secondary parkinsonism.
Background:
Valproate is used in the treatment of focal as well as generalized seizures. Besides the well-known side effects of nausea, dizziness, headache or tremor, it has been described to occasionally cause a reversible form of secondary parkinsonism. Mitochondrial respiratory chain dysfunction induced by valproate may be the underlying mechanism for reversible valproate-induced parkinsonism and cognitive impairment. After discontinuation of valproate, the course of improvement can take days to months.
Conclusion:
Increased clinical awareness is required to diagnose valproate-induced parkinsonism. Due to the delayed and insidious onset, the association with valproate use may be overlooked. Moreover, drug-induced parkinsonism can appear identical to idiopathic parkinsonism. A DaT scan is able to assess presynaptic dopaminergic function and can support the diagnosis of secondary parkinsonism with normal nigrostriatal system.