Rabbit syndrome in a neuroleptic naive patient with associated basal ganglia perfusion alterations treated with madopar fade‒out of perioral tremor after administration of L‒DOPA: role of thalamus in pathophysiology of post‒stroke rabbit syndrome

Abstract

Rabbit syndrome, termed for the resemblance to a rabbit chewing, is characterized by regular movements of the oral and masticatory musculature at a frequency of 4 to 6Hz without involvement of the tongue.1 Most commonly, rabbit syndrome is associated with prolonged exposure to antipsychotics and has a prevalence of 2‒5% among these patients.2 Because the symptoms are associated with drug treatment, rabbit syndrome is described as an extrapyramidal side effect of antipsychotics that is seen most often in middle‒ aged to elderly patients. In addition, rabbit syndrome has been described in a limited number of cases to arise in antipsychotic patients without administration of antipsychoticsnaive patients, although in all of these cases, rabbit syndrome was secondary to a brain structural abnormality or mood disorder.3‒5 Rabbit syndrome can be distinguished from tardive dyskinesia by the latter involving motion of the tongue while the former sparing the tongue, and this distinction is important because tardive dyskinesia worsens whereas rabbit syndrome improves with antiparkinsonian medication.1,2,5‒7 The mechanism responsible for antipsychotic‒induced rabbit syndrome is thought to involve dopamine receptor blockade in the basal ganglia.7 Furthermore, one study showed decreased basal ganglia perfusion by single photon emission computed tomography (SPECT) in a patient displaying rabbit syndrome.8 Here, we report a case of rabbit syndrome in an antipsychotic naïve naive patient with increased basal ganglia/thalamus perfusion during symptoms. Case report