Tardive Dyskinesia in an Autistic Patient Treated With Risperidone
To the Editor: Several open-label trials and case reports have suggested the usefulness of risperidone in treating maladaptive behaviors associated with autism (1–3). More recently, a double-blind, placebo-controlled study (4) has shown that risperidone reduces symptoms such as irritability, stereotypy, hyperactivity, aggression, and self-injurious behavior in children with autism. However, these reports also acknowledged that the relatively brief periods of treatment have precluded conclusions about the safety of risperidone with respect to tardive dyskinesia in children with autism. The following is a case report of an adolescent boy with autism who developed tardive dyskinesia while being treated with risperidone.
Alex was a 14-year-old boy who was brought to the Stanford University Pervasive Developmental Disorders Clinic for increasingly aggressive and disruptive behavior. He had been diagnosed with autism at an early age. The diagnosis was confirmed with DSM-IV criteria. Although the aggression began earlier in childhood, he was becoming progressively more dangerous in his community because of his increasing size and the increasingly frequent and indiscriminate nature of his assaultive behavior. Previously, numerous medications were prescribed for Alex, including stimulants, selective serotonin reuptake inhibitors, tricyclic antidepressants, buspirone, and secretin. Of note, Alex had never received any antipsychotic medications.
Risperidone was begun at 0.5 mg/day in our clinic and was increased gradually because of ongoing episodes of aggression and impulsivity. Alex’s dose eventually reached 3 mg/day after 16 months of treatment. Shortly thereafter, Alex’s behavior improved dramatically, with decreased aggression, less hyperactivity, improved language functioning, and increased sociability.
By the 23rd month of treatment, Alex began to develop a “jerking” of his trunk and abdomen. He and his mother reported that he was moving and writhing his shoulders and trunk throughout the day. Upon examination, Alex had periodic choreic movements of his shoulders and trunk. No oral, lingual, or buccal movements were seen or reported. A neurological examination revealed no other abnormalities. Trials of anticholinergic agents and vitamin E proved to be of little to no benefit. When risperidone was reduced to 2 mg/day, Alex’s behavior deteriorated dramatically, so his dose was returned to 3 mg/day. Subsequently, Alex also experienced dyskinetic movements in the oculomotor muscles.
After numerous discussions with Alex and his parents about the risks and benefits of risperidone, Alex continues to take risperidone at 3 mg/day, along with benztropine, 2 mg b.i.d., and a vitamin E supplement. He continues to benefit behaviorally from the drug regimen.
This report presents the emergence of tardive dyskinesia secondary to risperidone in an individual with autism who had previously been naive to antipsychotics. This case demonstrates the effectiveness of risperidone in treating the disruptive behaviors of autism. The use of atypical antipsychotics to ameliorate the maladaptive behaviors associated with autism is likely to increase, given the absence of treatments that robustly address its core symptoms. The case points to the need for a careful discussion of the potential risks and benefits of risperidone, the identification of specific target symptoms, and education regarding the time course of treatment. The risk of tardive dyskinesia should be discussed explicitly. There should also be thorough discussions about pharmacological and nonpharmacological interventions that may need to be exhausted before considering the use of antipsychotic medications.
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