Schizophrenia patient on haloperidol was responding well for last 2 years. Now presented with orofacial dyskinesia, choreiform, tick like movements, and dystonia features. What can be the probable diagnosis and treatment?

Explanation

## Correct Answer: B. Tardive dyskinesia - Valbenazine Tardive dyskinesia (TD) is a late-onset involuntary movement disorder that develops after prolonged antipsychotic exposure (typically >3 months, often years). The clinical presentation—orofacial dyskinesia (lip smacking, tongue protrusion, jaw movements), choreiform movements (irregular, flowing), tics, and dystonia—is pathognomonic for TD. The 2-year haloperidol exposure and good initial response followed by emergence of these involuntary movements is the classic timeline. TD results from dopamine receptor supersensitivity in the basal ganglia following chronic D2 blockade. Valbenazine is a vesicular monoamine transporter 2 (VMAT2) inhibitor approved by FDA and increasingly used in India for TD management. It reduces monoamine packaging into synaptic vesicles, thereby decreasing dopamine release and suppressing involuntary movements. Valbenazine is preferred over older agents (tetrabenazine) due to better tolerability and once-daily dosing. It is the first-line pharmacological treatment for established TD in current guidelines. ## Why the other options are wrong **A. Oral tremor – amantadine** — Oral tremor is not a feature of TD; tremor is a sign of Parkinsonism. Amantadine is used for antipsychotic-induced Parkinsonism (rigidity, bradykinesia, resting tremor), not dyskinesia. The clinical picture here is choreiform and dystonic, not parkinsonian. This is an NBE trap pairing a wrong movement disorder with a wrong drug. **C. Akathesia - Propranolol** — Akathesia (subjective restlessness, inability to sit still) is an acute or subacute side effect appearing within days to weeks, not after 2 years. Propranolol is used for akathesia, but the clinical presentation here—orofacial dyskinesia, choreiform, dystonic movements—does not match akathesia. The timeline and phenomenology exclude this diagnosis. **D. Acute dystonia - Ropinirole** — Acute dystonia (muscle spasms, torticollis, oculogyric crisis) occurs within hours to days of antipsychotic initiation or dose increase, not after 2 years of stable treatment. Ropinirole (dopamine agonist) is contraindicated in schizophrenia and worsens psychosis. The late onset and orofacial dyskinesia pattern rule out acute dystonia. ## High-Yield Facts - **Tardive dyskinesia** develops after ≥3 months (often years) of antipsychotic exposure; characterized by orofacial dyskinesia, choreiform, tics, and dystonia. - **Valbenazine** (VMAT2 inhibitor) is first-line pharmacological treatment for TD; dosed 40–80 mg daily; superior to tetrabenazine. - **Dopamine receptor supersensitivity** in basal ganglia is the pathophysiological mechanism of TD following chronic D2 blockade. - **Risk factors for TD**: older age, female sex, mood disorder comorbidity, higher antipsychotic dose, longer duration of exposure, typical antipsychotics > atypical. - **Prevention**: use lowest effective antipsychotic dose, prefer atypical agents, regular AIMS (Abnormal Involuntary Movement Scale) monitoring every 6–12 months. ## Mnemonics **TD vs Acute Dystonia (LATE vs EARLY)** **LATE** = Tardive Dyskinesia (Late-onset, After prolonged Treatment Exposure). **EARLY** = Acute Dystonia (Emerges Rapidly, within hours/days). Use when timeline is given. **VMAT2 = Vesicular Monoamine Transport** Valbenazine blocks VMAT2 → reduces dopamine packaging → less dopamine release → suppresses TD. Remember: VMAT2 inhibitor = modern TD treatment. ## NBE Trap NBE pairs "oral tremor" with amantadine to exploit confusion between Parkinsonism (tremor, rigidity) and dyskinesia (involuntary choreiform movements). Students may incorrectly think "tremor" = Parkinsonism and select amantadine, missing the dyskinetic phenomenology and 2-year timeline that define TD. ## Clinical Pearl In Indian psychiatric practice, TD is increasingly recognized as a major cause of non-adherence and social disability in long-term schizophrenia patients on typical antipsychotics. Early switch to atypical agents and AIMS monitoring every 6 months can prevent progression; once established, valbenazine offers the best evidence-based reversal, though partial improvement is more common than complete remission. _Reference: KD Tripathi Ch. 12 (Antipsychotics & Adverse Effects); Harrison Ch. 387 (Movement Disorders); Kaplan & Sadock's Synopsis of Psychiatry (Antipsychotic-Induced Movement Disorders)_