Antipsychotic‑Induced Tardive Dyskinesia and Drug‑Induced Parkinsonism

Causative Antipsychotic Agents

Conventional (typical) antipsychotics are the primary cause of both tardive dyskinesia (TD) and drug‑induced parkinsonism (DIP), with a higher risk than atypical agents. [1][2]
High‑potency typical antipsychotics (e.g., haloperidol, fluphenazine, thiothixene) are strongly linked to extrapyramidal symptoms, including parkinsonism, and carry a significant risk for TD. [1][3]4
Low‑potency typical antipsychotics (e.g., thioridazine, chlorpromazine) have a somewhat lower TD risk but still provoke movement disorders. [1][3]
In older adults, the incidence of TD can reach ≈ 50 % after 2 years of continuous typical antipsychotic use. 4
Risperidone may cause extrapyramidal symptoms, including parkinsonism, at doses ≥ 2 mg/day. [5][4]
Olanzapine and quetiapine are generally better tolerated but still retain a measurable risk for TD and DIP. [5][4]
All atypical antipsychotics are theoretically less likely to induce TD than conventional neuroleptics, although this protection is not absolute. [5][6]

Younger individuals and males have an increased risk for acute dystonia when exposed to neuroleptics. [1][3]

DIP usually emerges early in treatment or after dose escalations. [1][2]
TD is associated with long‑term neuroleptic exposure. [1][5]
In pediatric/young populations, up to 50 % may develop some form of tardive or withdrawal dyskinesia during neuroleptic therapy. [1][5]
Withdrawal dyskinesias tend to resolve over time, whereas TD often persists despite drug discontinuation. [1][5]

Document baseline abnormal movements before initiating any antidopaminergic medication. [1][5]
Conduct dyskinesia monitoring every 3–6 months after starting neuroleptic therapy. [1][5]
Employ standardized rating tools such as the Abnormal Involuntary Movement Scale (AIMS) for systematic assessment. [1][5]

Anticholinergic agents are effective for managing DIP but should not be used for TD. 7