Reversible Dysphagia Associated With Neuroleptic Treatment

To the Editor: It is well established that patients with Parkinson's disease commonly develop dysphagia.1,2 Neuroleptic drugs may occasionally induce dysphagia by similar mechanisms,3–5 but this highly reversible problem is unfortunately not well appreciated. The following case is illustrative. Case Report: A 71-year-old man with a lifelong history of paranoid schizophrenia and medication noncompliance was admitted to the geropsychiatry unit because of increasing delusions, hallucinations, and combative behavior at a community nursing home. He had been refusing his trifluoperazine (5 mg tid) for about 3 weeks. Past medical history was negative for dysphagia and otherwise noncontributory; he suffered from mild buccofacial tardive dyskinesia. Because of his recurrent noncompliance, he was started on oral fluphenazine on admission and soon thereafter given a first injection of fluphenazine decanoate 25 mg IM. However, his combativeness improved very slowly, and he continued to receive up to 20 mg per day of additional oral fluphenazine. After 2 weeks, he was given fluphenazine decanoate 37.5 mg IM. Throughout this period, there was no evidence of dystonia or pseudoparkinsonism; as expected, the tardive dyskinesia was completely suppressed. Four days after the second fluphenazine decanoate injection, the patient choked on a large bolus of roast beef, responding to a Heimlich maneuver. Although it was felt that this was primarily related to the inappropriately large bolus of food, a modified barium swallow (MBS) was performed to exclude aspiration. The MBS showed a normal oral phase, but aspiration of thin and thick liquids and the presence of residual solids in the piriform sinuses with subsequent spillover into the airway. The patient's diet was modified accordingly. The patient's behavior continued to improve gradually, allowing medication reduction. He was weaned off oral fluphenazine over the next 2 weeks, and fluphenazine decanoate was reduced to 25mg IM every 2 weeks. A repeat MBS 1 week after the last oral fluphenazine showed aspiration of thin liquids only. He was ultimately discharged on the fluphenazine decanoate, and a third MBS 6 weeks later was entirely within normal limits. In Parkinson's disease, changes in both the oral (lingual bradykinesia and tremor, slowed oral transit time) and the pharyngeal phases (delayed initiation, slowed epiglottic and pharyngeal movement) of swallowing have been noted.5 In contrast, there have been very few radiographically confirmed reports of dysphagia associated with neuroleptics,3–5 and little is known about its characteristics. Our patient exhibited a normal oral phase on MBS; conversely, Leopold4 reported a patient with disproportionate oral phase deficits. In a general psychiatric population, episodes of choking are not rare. Fioritti et al.6 have noted that most cases can be attributed to either fast eating or bradykinetic dysphagia. In our patient, the inappropriately large bolus of roast beef probably represented fast eating, whereas the changes noted on the MBS represented reversible, neuroleptic-induced bradykinetic dysphagia. It is especially noteworthy that no other evidence of drug-induced pseudoparkinsonism or dystonia accompanied the dysphagia. Physicians should be aware of this potentially hidden, potentially dangerous, but eminently reversible side effect of neuroleptic treatment.