Movement Disorders in Toxoplasmosis: A Systematic Review

Background: Movement disorders are an uncommon but important manifestation of central nervous system toxoplasmosis. Their phenotypes, lesion patterns, and outcomes have not been systematically characterized. Methods: A PRISMA-based systematic review identified all published patient-level reports of central nervous system toxoplasmosis with movement disorders. Eligible case reports and case series confirmed infection via serology, neuroimaging, polymerase chain reaction, or histopathology. Extracted data included demographics, immune status, clinical and neuroimaging features, lesion location, movement disorder type, treatment, outcomes, and proposed mechanisms. Cases were classified as hyperkinetic, hypokinetic, or cerebellar/ataxia syndromes and summarized descriptively. Results: Sixty patients were included: hyperkinetic (n = 42), hypokinetic (n = 9), and ataxia/cerebellar (n = 9). HIV-related immunosuppression was the predominant risk factor. Reactivation of latent toxoplasmosis was most frequent (40.5%, 55.6%, 88.9%). Hemichorea/hemiballismus was the leading hyperkinetic phenotype (47.6%), parkinsonism the main hypokinetic form (77.8%), while all ataxia patients exhibited cerebellar signs. Neuroimaging showed basal ganglia involvement in hyperkinetic (47.4%) and hypokinetic (88.9%) cases, whereas ataxia cases consistently demonstrated cerebellar lesions, often with brainstem or hemispheric extension. Standard pyrimethamine–sulfadiazine therapy was used in 59.5%, 33.3%, and 44.4%, respectively. Symptomatic therapy was phenotype-specific: neuroleptics and benzodiazepines for hyperkinetic, levodopa for hypokinetic, and none specified for ataxia. Outcomes varied, with recovery or marked improvement in 57.1%, 33.3%, and 66.7%, and mortality in 33.3%, 33.3%, and 22.2%, respectively. Mechanisms implicated basal ganglia disruption, nigrostriatal degeneration, and cerebellar invasion. Conclusions: Central nervous system toxoplasmosis-associated movement disorders show distinct phenotype–lesion correlations, with hyperkinetic syndromes most common. Outcomes vary by type, and early recognition with targeted therapy may improve prognosis.