Evaluation and Management of Involuntary Orofacial Dyskinesia
Autoimmune Encephalitis
NMDA‑receptor antibody encephalitis typically presents in young adults (median age 25 years) with a 2:1 female predominance. The disease evolves in two phases: an initial stage of seizures, confusion, amnesia and psychosis, followed by a second stage characterized by choreo‑athetosis and orofacial dyskinesia, fluctuating consciousness, dysautonomia and central hypoventilation. Ovarian teratomas are identified in 20‑50 % of affected women, while tumor rates are lower in men and children. Cerebrospinal fluid frequently shows lymphocytosis and detectable NMDA antibodies, whereas brain MRI is normal in ≈ 77 % of cases. Treatment requires combined immunosuppression with high‑dose corticosteroids plus either plasma exchange or intravenous immunoglobulin; refractory disease may need rituximab or cyclophosphamide. 1
VGKC‑complex antibody encephalitis commonly presents with a sub‑acute course, hyponatraemia, and brief dystonic seizures affecting the arms and face. Brain MRI shows hippocampal high‑signal swelling in about 60 % of patients (bilateral in most, unilateral in ≈ 15 %). The condition responds well to high‑dose oral steroids (≈ 0.5 mg/kg/day), with antibody titres normalising within 3–6 months; it is usually monophasic and relapses are rare once antibodies become undetectable. 1
Diagnostic screening for autoimmune encephalitis:
Management of confirmed autoimmune encephalitis:
Common pitfall: NMDA‑receptor encephalitis is frequently misdiagnosed as a primary psychiatric disorder because behavioural symptoms dominate early presentation. 1
Medication‑Related Dyskinesia
Tardive dyskinesia can persist indefinitely after discontinuation of dopamine‑blocking agents, including antipsychotics (e.g., haloperidol, droperidol) and anti‑emetics such as metoclopramide. 2
Metoclopramide may cause irreversible tardive dyskinesia, especially in elderly patients, even after short‑term use. 4
Trazodone has been reported to induce tardive dyskinesia in patients treated for insomnia. 3
Withdrawal dyskinesia may appear after either gradual or abrupt cessation of neuroleptic agents and typically resolves over time, helping to distinguish it from persistent tardive dyskinesia. 2
Up to 50 % of youths receiving neuroleptics may develop some form of tardive or withdrawal dyskinesia. 2
Diagnostic step – comprehensive medication history: document all current and past medications, including over‑the‑counter anti‑emetics, antipsychotics (even single emergency‑department doses), and antidepressants such as trazodone. [2][3]
Management of medication‑induced dyskinesia:
Diagnostic Algorithm Overview
Step 1 – Medication review: obtain a detailed list of all past and present drugs, focusing on dopamine‑blocking agents and anti‑emetics. 2
Step 2 – Autoimmune work‑up: screen serum/CSF antibodies (NMDA, VGKC), perform brain MRI for characteristic findings, and conduct tumour surveillance as outlined above. 1
Step 3 – Structural/metabolic assessment: use brain MRI to exclude stroke, tumour, or basal‑ganglia lesions; assess ceruloplasmin and 24‑hour urine copper when Wilson’s disease is a consideration; evaluate thyroid function, glucose and electrolytes. 1