Can atypical (second‑generation) antipsychotics cause bradykinesia?

Can Atypical Antipsychotics Cause Bradykinesia?

Yes, atypical antipsychotics definitively cause bradykinesia as part of drug-induced Parkinsonism syndrome, though at lower rates than typical antipsychotics. 1, 2

Mechanism and Clinical Presentation

Bradykinesia from atypical antipsychotics occurs through dopamine D2 receptor blockade in the nigrostriatal pathways, producing the characteristic parkinsonian triad of bradykinesia, rigidity, and tremor. 1 This drug-induced Parkinsonism represents one of three acute extrapyramidal syndromes caused by antipsychotics, alongside acute dystonia and akathisia. 1

The clinical challenge is that bradykinesia in psychosis patients can be difficult to distinguish from:

• Psychomotor slowing from negative symptoms 3
• Depression-related motor slowing 3
• Cognitive disturbances 3

Risk Stratification Among Atypical Antipsychotics

Risperidone carries the highest risk of extrapyramidal symptoms (including bradykinesia) among all atypical antipsychotics, with risk increasing significantly at doses above 6 mg/24 hours. 2, 4, 5

The hierarchy of risk from lowest to highest is:

• Clozapine: lowest risk 5, 6
• Quetiapine and olanzapine: intermediate-low risk 1
• Risperidone: highest risk among atypicals 2, 4, 5

Despite being "atypical," these agents have not eliminated extrapyramidal symptoms as initially expected—they simply occur at lower rates than with typical antipsychotics. 5

Management Algorithm

Early diagnosis and rapid withdrawal or dose reduction of the antipsychotic improves the possibility of complete recovery. 1 Follow this approach:

1. Confirm the diagnosis: Use objective measures when possible, as observer-based rating scales may underestimate bradykinesia (detecting only 46% of cases versus 64% with objective testing). 3

2. Immediate intervention based on clinical status:

   • If patient is in full remission: Continue current dose only if dose changes risk precipitating relapse 1
   • If patient is not in full remission: Proceed to step 3 1

3. Medication adjustment (choose one):

   • Lower the current antipsychotic dose 1
   • Switch to an atypical antipsychotic with lower EPS risk (preferably clozapine or quetiapine) 1
   • Add an anticholinergic agent (though this should be temporary and reevaluated after the acute phase) 1
   • Add amantadine (dopaminergic agonist) 1

4. Avoid chronic anticholinergic use: Anticholinergic agents like benztropine or trihexyphenidyl should be avoided in elderly patients and reevaluated in all patients after the acute phase, as many no longer need them during long-term therapy. 1

Critical Monitoring Considerations

Establish baseline abnormal movement assessments before starting antipsychotics, then reassess every 3-6 months using standardized scales like the Abnormal Involuntary Movement Scale. 1 This allows early detection not just of bradykinesia but also tardive dyskinesia, which occurs in 5% of young patients per year. 1, 2

The proportion of nonballistic handwriting movements in bradykinetic patients appears unrelated to current antipsychotic dose, negative symptoms, or depression severity, suggesting the bradykinesia is truly drug-induced rather than illness-related. 3

Common Pitfall

Do not dismiss bradykinesia as simply "negative symptoms" or depression without considering drug-induced Parkinsonism, as this delays intervention and reduces the likelihood of complete recovery. 1 The overlapping presentation requires active consideration of medication effects in any patient on antipsychotics presenting with motor slowing. 3