弓形虫病的运动障碍:系统综述。

IF 2.1 Q2 CLINICAL NEUROLOGY
Tremor and Other Hyperkinetic Movements Pub Date : 2025-09-30 eCollection Date: 2025-01-01 DOI:10.5334/tohm.1093
Ravindra Kumar Garg, Shweta Pandey, Manoj Agarwal, Sanjay Singhal
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引用次数: 0

摘要

背景:运动障碍是中枢神经系统弓形虫病不常见但重要的表现。它们的表型、病变模式和结果尚未被系统地描述。方法:基于prisma的系统评价确定了所有已发表的伴有运动障碍的中枢神经系统弓形虫病的患者报告。符合条件的病例报告和病例系列通过血清学、神经影像学、聚合酶链反应或组织病理学证实感染。提取的数据包括人口统计学、免疫状态、临床和神经影像学特征、病变部位、运动障碍类型、治疗、结果和可能的机制。病例被分类为多动、少动或小脑/共济失调综合征,并进行描述性总结。结果:纳入60例患者:运动过度(n = 42),运动不足(n = 9),共济失调/小脑性(n = 9)。hiv相关的免疫抑制是主要的危险因素。潜伏性弓形虫病再激活率最高(40.5%,55.6%,88.9%)。偏缩/偏瘫是主要的多运动型(47.6%),帕金森病是主要的低运动型(77.8%),而所有共济失调患者均表现出小脑体征。神经影像学显示运动多(47.4%)和运动少(88.9%)的患者基底神经节受累,而共济失调患者一致表现为小脑病变,通常伴有脑干或半球延伸。标准乙胺嘧啶-磺胺嘧啶治疗分别占59.5%、33.3%和44.4%。对症治疗是表现型特异性的:抗精神病药和苯二氮卓类药物用于运动亢进,左旋多巴用于运动亢进,没有指定用于共济失调。结果各不相同,恢复或显著改善的分别为57.1%、33.3%和66.7%,死亡率分别为33.3%、33.3%和22.2%。机制涉及基底节区破坏,黑质纹状体变性和小脑侵袭。结论:中枢神经系统弓形虫病相关的运动障碍表现出明显的表型-病变相关性,其中多动综合征最为常见。结果因类型而异,早期识别和靶向治疗可能改善预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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来源期刊
CiteScore
4.00
自引率
4.50%
发文量
31
审稿时长
6 weeks
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