A case report of persistent cerebellar dysfunction following acute lithium toxicity

Acute lithium toxicity can cause cerebellar impairment, but long-term follow-up data are limited. We describe a case of acute lithium intoxication followed by progressive cerebellar atrophy and permanent cerebellar dysfunction. Five years ago, a previously healthy 38-year-old man developed a clinical syndrome consistent with neuroleptic malignant syndrome (NMS)-like syndrome in the setting of acute lithium and quetiapine toxicity. On admission, the serum lithium concentration was 4.07 mmol/L and the cerebrospinal fluid lithium concentration was 2.45 mmol/L. Continuous renal replacement therapy (CRRT) was initiated, and cerebrospinal fluid lavage was also performed as documented in the outside hospital records. Serum lithium levels subsequently decreased to below 0.2 mmol/L. After treatment, consciousness improved. However, he developed a persistent cerebellar syndrome, characterized by ataxia, gait instability, and dysarthria. Brain magnetic resonance imaging one year later revealed cerebellar atrophy. Over five years of follow-up, severe ataxia persisted, and serial MRI showed progressive isolated cerebellar atrophy without supratentorial structural abnormalities. This case suggests that severe acute lithium toxicity may be associated with progressive cerebellar degeneration, even after normalization of serum lithium levels. Clinicians should consider long-term follow-up for neurological sequelae in individuals suffering from acute lithium intoxication.