Classify these as extrapyramidal symptoms and prescribe benztropine, since anticholinergic agents are the standard treatment for antipsychotic-induced movement disorders.

Acute EPS (dystonia, parkinsonism) respond to anticholinergics like benztropine. Tardive dyskinesia does not respond to anticholinergics and may actually worsen with anticholinergic treatment.

Assess for tardive dyskinesia using the AIMS, since gradual-onset orofacial and choreiform movements during long-term antipsychotic use are characteristic of TD rather than acute EPS.

The clinical picture — gradual-onset involuntary orofacial and digital movements after long-term first-generation antipsychotic use — is classic tardive dyskinesia. The AIMS provides standardized severity measurement and monitoring. TD has gradual onset (vs. acute EPS), predominantly affects the orofacial region, and is not responsive to anticholinergic treatment. Treatment considerations include switching to a lower-risk antipsychotic and VMAT2 inhibitors (valbenazine or deutetrabenazine, the only FDA-approved treatments for TD).

Increase the haloperidol dose, since the involuntary movements suggest breakthrough psychotic symptoms from inadequate dopamine blockade at the current dosage.

Increasing the antipsychotic may temporarily mask TD symptoms by increasing dopamine blockade, but this does not treat the underlying condition and may worsen TD over time.

Add diphenhydramine to the current regimen to manage the involuntary movements, since first-generation antihistamines have established efficacy for movement disorders.

Anticholinergics (including diphenhydramine) are not effective for tardive dyskinesia and may worsen the condition. This is a critical distinction from acute EPS.