Risperidone and Dysphagia in a Developmentally Disable Woman

Abstract

Sir: Dysphagia represents an infrequently reported adverse effect secondary to use of neuroleptic agents.1 The presentation of dysphagia is often associated with parkinsonian symptoms.2 Autonomic dysfunction is due to changes in the hypothalamus, locus ceruleus, dorsal vagal nucleus, and sympathetic ganglia.3 Neuroleptic medications may induce swallowing difficulties by similar mechanisms.1 Atypical antipsychotic agents are believed to have a more advantageous side effect profile with fewer extrapyramidal effects.1 This medication-mediated reversible effect may be underdiagnosed in populations with additional neurologic impairments. Case report. Ms. A, a 60-kg, 46-year-old white woman diagnosed with dementia due to lithium toxicity and profound mental retardation (IQ = 20), resides in a state-run facility. Her verbal ability is limited to single words. The patient has a long-standing history of aggression and aberrant behaviors addressed with behavioral interventions and medication use. She presented to the psychiatric clinic in September 2006 with a significant increase in drooling, difficulty swallowing, and gurgling sounds. The total daily doses for the psychoactive medication regimen at the time dysphagia was diagnosed included risperidone 2 mg daily for psychosis and mood lability, clozapine 500 mg for mood lability, clonidine 0.3 mg for aggression and dyskinesia, and benztropine 1 mg for drooling and extrapyramidal symptoms. The most recent medication change, which occurred the previous month, was an increase in risperidone from 1.5 mg to 2 mg that followed increases in behavioral dyscontrol without an identifiable antecedent. In clinic, Ms. A was not appreciably calmer. The dose was subsequently decreased to the previous dose of 1.5 mg. On follow-up 3 days later, drooling and swallowing difficulties were resolving. Case reports related to dysphagia secondary to atypical antipsychotic use have been reported previously. Two reports involved risperidone use; one followed an increase to a total daily dose of 1.5 mg and resolved with risperidone discontinuation and substitution of olanzapine 2.5 mg.1 The other occurred following a single 4-mg risperidone dose and resolved after administration of benztropine.4 Dysphagia was also reported 5 days after initiation of olanzapine 20 mg.5 Olanzapine-associated dysphagia resolved with medication discontinuation. Concurrent use of clozapine and risperidone may have predisposed our patient to adverse effects. Clozapine atypicality is thought to be associated with its greater affinity for serotonin 5-HT2A receptors than dopamine D2 receptors and rapid dissociation from the basal ganglia D2 receptors. In addition, its anticholinergic effects may act to moderate the risk of extrapyramidal effects.6 Risperidone has pharmacologic properties resembling those of clozapine, with antagonistic activity primarily at serotonin 5-HT2A and dopamine D2 receptors.7 Concurrent therapy may negatively impact the rapid D2 dissociation times that have been reported8 and increase the potential for adverse effects. We believe this is the first report of dysphagia identified secondary to atypical antipsychotic use in a person with developmental disabilities. The presence of mental retardation is an indication of neurologic impairment, and dysphagia may be overlooked.9 Limited verbal abilities may impede self-reporting. Clinicians should be aware of the potential for this infrequently reported adverse effect in both the general population and those with developmental disabilities, particularly with concurrent therapy regimens.