Withdrawal-emergent Dyskinesia Research Articles

Case Presentation: Iatrogenic Psychosis

Tardive dyskinesia (TD) is a neuromuscular disorder that can precipitate following the administration of dopamine receptor antagonists such as neuroleptics. Withdrawal-emergent dyskinesia (WE-D), a less recognized subtype of TD, can manifest shortly after abrupt cessation of antipsychotic use regardless of the neuroleptic subclass used. Super sensitivity psychosis is another possible symptom of acute withdrawal from neuroleptics that can occur alone or concomitant with WE-D. Because of their ever increasing off-label indications and attenuated extrapyramidal side effect profiles, atypical antipsychotics are becoming ubiquitous in both inpatient and outpatient settings, reflecting their utility. However, it is likely that this trend will also result in a greater prevalence of WE-D and super sensitivity psychosis. Clinicians without expertise in the utilization of neuroleptics are likely to misattribute withdrawal symptoms precipitated by abrupt cessation of antipsychotics with toxicity to these agents and erroneously withhold or delay their reinitiation, thereby exacerbating symptoms and inadvertently prolonging patient distress. This case report will illustrate the unique and perplexing presentation of WE-D and super sensitivity psychosis in an acute setting, and provide an effective diagnostic and treatment approach to resolving these conditions.

Withdrawal-Emergent Dyskinesia Following Abrupt Discontinuation of Desvenlafaxine

Withdrawal-Emergent Dyskinesia Following Abrupt Discontinuation of Desvenlafaxine

Amisulpride withdrawal dyskinesia: a case report

BackgroundThe effects of antipsychotic drug withdrawal have been inadequately studied. Case reports have described dyskinesia occurring in patients with several antipsychotics withdrawn, but studies on amisulpride withdrawal dyskinesia are lacking.Case presentationA 63-year-old man, who was diagnosed with schizophrenia at age 49, received amisulpride treatment since age 62. The dosage of amisulpride was reduced from 200 to 50 mg/day because of occurrence of akathisia during one admission. Severe withdrawal dyskinesia, mixed with dystonia and akathisia, was noted immediately after the dosage reduction. The abnormal involuntary movement showed improvement 2 weeks later when the dosage was increased to 100 mg/day.ConclusionsWithdrawal dyskinesia and other abnormal involuntary movements could be noted in a patient with reduction of amisulpride dosage or sudden termination. Withdrawal dyskinesia may subsequently lead to persistent tardive dyskinesia. Therefore, withdrawal-emergent dyskinesia should be promptly identified, and appropriate medical interventions should be given early.

Tardive Dyskinesia Induced by a Switch From Haloperidol Depot to Paliperidone Palmitate

Tardive Dyskinesia Induced by a Switch From Haloperidol Depot to Paliperidone Palmitate

Withdrawal-emergent dyskinesia in a patient taking risperidone/citalopram

Withdrawal-emergent dyskinesia in a patient taking risperidone/citalopram

Withdrawal-emergent dyskinesia in patients with schizophrenia during antipsychotic discontinuation

We examined whether patients exhibiting withdrawal-emergent dyskinesia (WE-D) represent a group vulnerable to subsequent development of tardive dyskinesia (TD). WE-D was defined as moderate abnormal movements during antipsychotic withdrawal in persons without persistent TD. We assessed patients with schizophrenia-spectrum illness participating in withdrawal from antipsychotic medication. Patients with WE-D were compared to those without dyskinesia and to those with persistent TD. Clinical measures included duration of illness and antipsychotic exposure, negative symptoms, and neurologic soft signs. We hypothesized that WE-D patients would not differ from persistent-TD patients across the above variables, but would differ from non-TD patients. Patients without TD significantly differed from persistent TD in duration of illness, medication exposure and neurologic soft signs. WE-D did not differ from TD across these measures. No-TD patients also showed less duration of medication exposure and neurologic soft signs than those with WE-D.