Akathisia is a common and often disabling adverse effect of antipsychotic treatment. Although previous studies have linked akathisia to dopamine D 2 ‑receptor blockade in the basal ganglia, there is limited evidence from 18Ffluorodeoxyglucose PET (18FFDG PET) acquired during clinically manifest akathisia. We report the case of a woman in her 50s with bipolar disorder and autoimmune diseases who developed marked akathisia after augmenting lithium with aripiprazole 10 mg/day. During the symptomatic period, a whole‑body 18FFDG PET computed tomography was performed to investigate recurrent fevers and gastrointestinal symptoms. Brain images incidentally showed bilateral putaminal hypermetabolism relative to the cerebral cortex. Neurological and rheumatology consultations were negative. No other medications were modified during the same timeframe. Akathisia remitted completely after aripiprazole discontinuation and clonazepam up‑titration, and the Naranjo Adverse Drug Reaction Probability Scale score indicated a probable adverse drug reaction. Basal ganglia hypermetabolism relative to the cerebral cortex is reminiscent of PET findings in reversible hyperkinetic disorders. To our knowledge, this is the first case report showing an association between bilateral putaminal hypermetabolism on 18FFDG PET and aripiprazole-induced akathisia. This hypothesis-generating observation warrants replication in prospective studies to elucidate how dopaminergic dysfunction in the basal ganglia may contribute to the emergence of akathisia.
Meda et al. (2026) studied this question.