Tardive dyskinesia
1
Profiles Tardive dyskinesia Orofacial dyskinesia and abnormal involuntary trunk and limb movements (choreiform) are features of tardive dyskinesia. The movement disorder is caused by dopamine antagonists, mainly anti psychotics but includes antiemetics such as metoclopramide and prochlorperazine, and was first reported within 5 years of introducing antipsychotics. The current explanation for pathogenesis is the development of postsynaptic dopamine receptors in the striatum in response to dopamine antagonist blockade. However inconsistencies with this theory have been noted. The condition only develops in a few patients suggesting other important variables and no distinct relationship between developing tardive dyskinesia and duration and type of antipsychotic therapy has been demonstrated. The condition tends to occur more commonly and more severely in the elderly with associated abnormal movements usually appearing after the age of 60 years. The trend may be caused by age-related changes in the brain, possibly degeneration in the nigrostriatal system. Remission occurs more commonly in younger patients, often without discontinuation of drug therapy. Limited evidence suggests that development of parkinsonism, acute akathisia or acute dystonia during early drug therapy indicates vulnerability to tardive dyskinesia. There is a high risk of the condition developing within 2 years of initiating antipsychotic therapy in patients with both unipolar and bipolar affective disorders. Akathisia and tardive dyskinesia often coexist in schizophrenic patients receiving long term antipsychotic therapy and evidence indicates that more signs of organic brain damage and cognitive impairment are observed in schizophrenic patients with tardive dyskinesia. Although double-blind placebo-controlled trials are required to substantiate their benefits, calcium channel blockers (verapamil, diltiazem) and a- tocopheral (vitamin E) have had some success as potential treatments. For severe dyskinetic cases, a specific antidyskinetic drug (tetrabenazine) may be administered although the therapeutic effect may decrease over time. 2 REACTIONS' 30 January 1988 Because of the association of tardive dyskinesia with antipsychotic therapy the following points should be considered. Antipsychotics should only be prescribed where clearly indicated and use in patients with affective disorders tempered with the knowledge of the high risk of early dyskinesia. Their use should only be continued where benefit is evident. Daily dosage should be maintained at the minimum effective dose and intermittent treatment avoided as interruptions may increase the risk of psychotic relapse and persistent dyskinesia. Without precipitating severe parkinsonism, concomitant administration of anticholinergic drugs should cease if possible . Barnes TRE British Medical Journal 296 t SO· 151 . 16 Jan 1988 0157-7271 / 88/ 0130-0002/ 0$01.00/ 0 © ADIS Press
Transcript of Tardive dyskinesia
Profiles Tardive dyskinesia
Orofacial dyskinesia and abnormal involuntary trunk and limb movements (choreiform) are features of tardive dyskinesia. The movement disorder is caused by dopamine antagonists , mainly anti psychotics but includes antiemetics such as metoclopramide and prochlorperazine, and was first reported within 5 years of introducing antipsychotics . The current explanation for pathogenesis is the development of postsynaptic dopamine receptors in the striatum in response to dopamine antagonist blockade. However inconsistencies with this theory have been noted. The condition only develops in a few patients suggesting other important variables and no distinct relationship between developing tardive dyskinesia and duration and type of antipsychotic therapy has been demonstrated. The condition tends to occur more commonly and more severely in the elderly with associated abnormal movements usually appearing after the age of 60 years . The trend may be caused by age-related changes in the brain, possibly degeneration in the nigrostriatal system. Remission occurs more commonly in younger patients , often without discontinuation of drug therapy . Limited evidence suggests that development of parkinsonism, acute akathisia or acute dystonia during early drug therapy indicates vulnerability to tardive dyskinesia. There is a high risk of the condition developing within 2 years of initiating antipsychotic therapy in patients with both unipolar and bipolar affective disorders. Akathisia and tardive dyskinesia often coexist in schizophrenic patients receiving long term antipsychotic therapy and evidence indicates that more signs of organic brain damage and cognitive impairment are observed in schizophrenic patients with tardive dyskinesia.
Although double-blind placebo-controlled trials are required to substantiate their benefits , calcium channel blockers (verapamil , diltiazem) and atocopheral (vitamin E) have had some success as potential treatments . For severe dyskinetic cases, a specific antidyskinetic drug (tetrabenazine) may be administered although the therapeutic effect may decrease over time.
2 REACTIONS' 30 January 1988
Because of the association of tardive dyskinesia with antipsychotic therapy the following points should be considered . Antipsychotics should only be prescribed where clearly indicated and use in patients with affective disorders tempered with the knowledge of the high risk of early dyskinesia. Their use should only be continued where benefit is evident. Daily dosage should be maintained at the minimum effective dose and intermittent treatment avoided as interruptions may increase the risk of psychotic relapse and persistent dyskinesia. Without precipitating severe parkinsonism, concomitant administration of anticholinergic drugs should cease if possible . Barnes TRE British Medical Journal 296 t SO· 151 . 16 Jan 1988
0157-7271 / 88/ 0130-0002/ 0$01.00/ 0 © ADIS Press
