Marco Falletti, Federica Di Flumeri, Alessandro Zampogna, Martina Patera, Giovanni Fabbrini, Antonio Suppa
{"title":"Acute and reversible dyskinesias secondary to lithium toxicity: case report and literature review.","authors":"Marco Falletti, Federica Di Flumeri, Alessandro Zampogna, Martina Patera, Giovanni Fabbrini, Antonio Suppa","doi":"10.1186/s12883-025-04419-7","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Lithium can cause several neurological side effects, including altered consciousness, delirium, cerebellar symptoms, parkinsonism, and seizures. Also, dyskinesias can be a possible manifestation of lithium intoxication. The clinical picture of dyskinesias secondary to lithium intoxication is still unclear.</p><p><strong>Case presentation: </strong>We here describe the case of a 75-year-old woman who developed acute and reversible dyskinesia manifesting as generalised chorea because of lithium intoxication. The patient had a medical history of bipolar disorder type 2 and at least 20 years of continuous lithium monotherapy (150 mg, 1 tablet 3 times/day). Dyskinesias were associated with a high serum lithium level of 2.15 mEq/L. Imaging and EEG showed no relevant abnormalities. On the sixth day after admission, dyskinesias faded away when the lithium serum level decreased to 0.4 mmol/L. When critically reviewing the existing literature, we found a total of 33 cases, with an average age of 59.7 years, predominantly female. In these cases, the average lithium peak at the onset of dyskinesia was 2.25 mEq/L, with symptoms typically appearing 4.2 days after reaching peak lithium levels.</p><p><strong>Discussion: </strong>Lithium toxicity, even at therapeutic serum concentrations, may induce abrupt-onset dyskinesia in susceptible individuals, likely mediated by reversible functional disturbances within the basal ganglia.</p>","PeriodicalId":9170,"journal":{"name":"BMC Neurology","volume":"25 1","pages":"393"},"PeriodicalIF":2.2000,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481728/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Neurology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12883-025-04419-7","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
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Abstract
Background: Lithium can cause several neurological side effects, including altered consciousness, delirium, cerebellar symptoms, parkinsonism, and seizures. Also, dyskinesias can be a possible manifestation of lithium intoxication. The clinical picture of dyskinesias secondary to lithium intoxication is still unclear.
Case presentation: We here describe the case of a 75-year-old woman who developed acute and reversible dyskinesia manifesting as generalised chorea because of lithium intoxication. The patient had a medical history of bipolar disorder type 2 and at least 20 years of continuous lithium monotherapy (150 mg, 1 tablet 3 times/day). Dyskinesias were associated with a high serum lithium level of 2.15 mEq/L. Imaging and EEG showed no relevant abnormalities. On the sixth day after admission, dyskinesias faded away when the lithium serum level decreased to 0.4 mmol/L. When critically reviewing the existing literature, we found a total of 33 cases, with an average age of 59.7 years, predominantly female. In these cases, the average lithium peak at the onset of dyskinesia was 2.25 mEq/L, with symptoms typically appearing 4.2 days after reaching peak lithium levels.
Discussion: Lithium toxicity, even at therapeutic serum concentrations, may induce abrupt-onset dyskinesia in susceptible individuals, likely mediated by reversible functional disturbances within the basal ganglia.
期刊介绍:
BMC Neurology is an open access, peer-reviewed journal that considers articles on all aspects of the prevention, diagnosis and management of neurological disorders, as well as related molecular genetics, pathophysiology, and epidemiology.