CLINICAL HANDBOOK OF SCHIZOPHRENIA

170 III. SOMATIC TREATMENTParkinsonism is addressed by one of two methods: (1) switching to an atypicalantipsychotic with a low propensity to induce Parkinsonism or (2) adding an anticholinergicmedication such as benztropine, trihexyphenidyl, or diphenhydramine. In general,switching to an atypical antipsychotic is preferred over adding a medication that maycause its own side effects in an attempt to treat or prevent an antipsychotic-induced sideeffect.Akathisia is experienced subjectively as an unpleasant sensation of restlessness andobserved objectively as restlessness, anxiety, and agitation. Akathisia can be very frighteningand distressful to patients, and is a known risk factor for antipsychotic nonadherence.Similar to antipsychotic-induced Parkinsonism, akathisia is most commonly associatedwith the use of high-potency conventional antipsychotics and is unlikely with low-doserisperidone, uncommon with olanzapine and quetiapine, and extremely unlikely withclozapine. Although akathisia is unlikely to be caused by ziprasidone and aripiprazole,both agents can produce anxiety and agitation as side effects that may resemble akathisia.Antipsychotic-induced akathisia can be treated by switching to an atypical antipsychoticwith a low risk of akathisia, or by adding one of several medications: (1) a low-dose betablocker(e.g., propanolol, 10–20 mg three times daily); (2) an anticholinergic (e.g.,benztropine, 1–2 mg twice daily; or (3) benzodiazepine (e.g., lorazepam, 1 mg three timesdaily).Tardive DyskinesiaTardive dyskinesia (TD) is a syndrome of chronic or permanent abnormal, involuntarymovements that presents usually with athetoid movements of the tongue, facial, and neckmuscles, extremities, or trunk usually after at least 3–6 months of antipsychotic treatmentin younger adults and 1 month of treatment in older adults. This often irreversible side effectis a well-known consequence of typical antipsychotics, with long-term studies reportingincidence rates of 5% per year in adults, and rates 5–6 times that in older adults. Althoughthe mechanism of antipsychotic-induced TD remains unclear, it is clear that theuse of conventional antipsychotics and age (i.e., patients 50 years of age and older) areassociated with an increased risk of developing TD. Other clinical correlates of TD inschizophrenia, confirmed in the results from the CATIE schizophrenia study, includeduration of antipsychotic use, presence of EPS, treatment with anticholinergics, and substanceabuse (Miller et al., 2005). Atypical antipsychotics have been shown to involve asubstantially lower risk of EPS compared to conventional antipsychotics, and researchershave hoped that this would also translate into less TD—a hope that has been confirmedin a number of studies. A scholarly review of all long-term trials (i.e., at least 1 year) involvingboth typical and atypical antipsychotics that reported newly identified cases ofTD was conducted. Eleven such studies involving over 2,700 patients were identified. Theinvestigators reported that the weighted mean annual incidence of TD related to atypicalantipsychotic use was 0.8% in adults, 6.8% in mixed adult and older adult patients, and5.3% in patients 54 years of age and older. In contrast, adults treated with haloperidolwere found to have a weighted mean annual incidence of 5.4% (Correll, Leucht, & Kane,2004). Thus, these findings support the idea that long-term use of atypical antipsychoticsis associated with a lower incidence of TD, but that important consideration must begiven to patients prescribed any antipsychotic on a long-term basis.Because there is no reliable treatment for TD, prevention is crucial. The risk of TDcan be minimized by prescribing antipsychotics only when there is a clear indication andby avoiding conventional antipsychotics. Prior to initiating any antipsychotic therapy, cliniciansshould establish baseline motor functioning with a standardized scale such as the