## Diagnosis: Tardive Dyskinesia (TD) **Key Point:** Tardive dyskinesia is a late-onset, potentially irreversible movement disorder caused by chronic dopamine D2 receptor blockade with first-generation antipsychotics (FGAs). It typically emerges after months to years of exposure. ### Clinical Features of TD - **Orofacial dyskinesia:** lip smacking, tongue protrusion, jaw deviation, grimacing - **Limb dyskinesia:** choreiform movements of extremities - **Trunk dyskinesia:** rocking, swaying movements - Symptoms may persist or worsen even after drug discontinuation (irreversibility paradox) ### Management Hierarchy | Step | Intervention | Rationale | |------|--------------|----------| | **First-line** | Switch to second-generation antipsychotic (SGA) | SGAs have lower D2 occupancy and lower TD risk; may improve or stabilize existing TD | | **Alternative** | Reduce FGA dose if possible | Lowers dopamine blockade burden | | **Adjunctive** | Valbenazine or deutetrabenazine | VMAT2 inhibitors; FDA-approved for TD; reduce involuntary movements | | **Avoid** | Anticholinergics (benztropine) | May worsen TD; only use if concurrent parkinsonism | **High-Yield:** Switching from haloperidol to an SGA (olanzapine, aripiprazole, quetiapine, risperidone at lower doses) is the gold standard because: 1. SGAs have lower affinity and faster dissociation from D2 receptors 2. Aripiprazole (partial D2 agonist) has the lowest TD risk 3. Existing TD may stabilize or improve over months **Clinical Pearl:** Anticholinergics like benztropine WORSEN tardive dyskinesia and should be avoided. They were historically used for acute dystonia/parkinsonism (early-onset), not late-onset TD. **Warning:** Continuing haloperidol or reducing dose alone without switching class is suboptimal—the underlying mechanism (chronic D2 blockade) persists. ### Mnemonic: "SGA FIRST for TD" - **S**witch to **G**eneration **A**ntipsychotic - **F**irst-line for **I**rreversible **R**ate-limiting **S**ide effect - **T**ardive **D**yskinesia [cite:Harrison 21e Ch 387]
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