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EV0197

Rapid-onset extrapyramidal symptoms and tardive dyskinesia following a lithium dose increase in bipolar disorder: a case report

RAPID ONSET OF EXTRAPYRAMIDAL SYMPTOMS AND TARDIVE DYSKINESIA FOLLOWING LITHIUM DOSE ESCALATION IN BIPOLAR DISORDER: A CASE REPORT

A severe hyperkinetic movement disorder that developed within two weeks of a relatively small lithium dose increase at a therapeutic blood level and persisted for six months despite drug discontinuation demonstrates that SILENT is not solely associated with toxicity.

The aim is to present a case demonstrating that the Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT), a rare and severe complication distinct from lithium's well-known adverse effects, can develop rapidly following a small dose increase. The patient was a 53-year-old woman with a 19-year history of bipolar disorder and two previous hospitalizations, who was being treated with lithium 600 mg/day and extended-release quetiapine 300 mg/day; written informed consent was obtained in accordance with the Declaration of Helsinki. Within two weeks of increasing the lithium dose to 900 mg/day, she developed dysarthria, dysphagia, dyspnea, orofacial dyskinesia, severe gait ataxia, and transient perceptual disturbances. A neurological consultation supported the impression of drug-induced extrapyramidal symptoms (EPS), lithium was tapered and discontinued, and the patient was monitored through serial clinical assessments. Despite a serum lithium level within the therapeutic range (0.77 mmol/L) and complete discontinuation of the drug, extrapyramidal and cerebellar symptoms persisted, and the clinical presentation was considered consistent with SILENT. At the six-month follow-up, involuntary jaw movements and a positive Romberg sign persisted and were considered permanent neurological sequelae. The authors highlight four atypical features of the case: rapid onset; a fulminant course; a presentation involving lower-extremity choreoathetoid movements and involuntary jaw movements, together with marked rigidity and cognitive decline, rather than an isolated fine tremor; and the emergence of these findings at a low daily dose and a therapeutic serum level. In conclusion, the assumption that severe motor complications are solely concentration-dependent should be questioned, neurological monitoring should be performed following dose increases, and the drug should be discontinued early because of the risk of progression to tardive dyskinesia.

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