Cetirizine is a carboxylated metabolite of hydroxyzine (a piperazine histamine H 1 receptor antagonist) (1). Piperazines have central dopamine D 2 receptor blockade (5). Cetirizine’s large size, lipophobic nature, and greater affinity for peripheral H 1 receptors are believed to reduce CNS penetration and central side effects (2). However, one positron emission tomography study of cetirizine revealed approximately 30% H 1 receptor binding in the cerebral cortex (1, 2). Cetirizine has negligible anticholinergic activity (6). We speculate that as a piperazine derivative, cetirizine blocked the striatal D 2 receptors and resulted in an acute dystonic reaction in our patient. In addition, we also speculate that our patient’s 3-month cetirizine use resulted in D 2 receptor hypersensitivity similar to that observed in long-term antipsychotic use, with subsequent involuntary movements after its discontinuation. It is also possible that her cetirizine use and the subsequent development of involuntary movements are independent events. More research is needed to clarify cetirizine’s effect on central D 2 receptors.
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