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首页> 外文期刊>The Canadian Journal of Neurological Sciences: le Journal Canadien des Sciences Neurologiques >Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia
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Movement Disorders Due to Selective Basal Ganglia Lesions with Uremia

机译：由于尿毒症的选择性基础神经节病变，运动障碍

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摘要

Background: Basal ganglia (BG) lesions are rarely reported in patients with uremia and may manifest by movement disorders. However, their exact incidence and pathogenesis have not been extensively studied. This study aimed to determine the frequency, types, risk variables (clinical, laboratory, and imaging), and manifestations of BG lesions with uremia and patients' neurologic outcomes. Methods: This observational study included 70 adults (mean age: 45.87 +/- 3.36 years; duration of uremia: 5.5 +/- 1.5 years). They underwent extensive evaluations (clinical, laboratory, and neuroimaging) and had prospectively evaluated clinically every 3 months for 2 years. Repeated magnetic resonance imaging (MRI) brains were done to patients with movement disorders and correlated with their neurologic outcomes. Results: BG lesions were found in 15 patients (21.4%) and 6 (8.6%) had movement disorders [Parkinsonism (n = 4), choreo-dystonia (n = 1) and dystonia (n = 1)] after the onset of uremia (mean = 10 months). There were no characteristic risk variables that distinguished patients with movement disorders from those without. Five developed movement disorders prior to the period of the study and one was de novo. The majority was females and had diabetes and higher frequencies of abnormal renal dysfunction, metabolic derangements, and white matter hyperintensities in MRIs. Movement disorders persisted in all patients despite the resolution of neuroimaging in three patients. Conclusions: There is no clear threshold for renal failure to result in movement disorders due to BG lesions. The clinical outcome is variables depending on each patient's comorbidities and complications. Persistent neuronal damage (due to uremic toxins/metabolic/nutritional and ischemic/microvascular factors) has been suggested as the cause of poor neurologic outcomes.
机译：背景：尿毒症患者很少报道基底神经节（BG）病变，并且可能通过运动障碍表现出来。然而，它们的确切发病率和发病机制尚未得到广泛研究。本研究旨在确定尿毒症和患者神经原因的BG病变的频率，类型，风险变量（临床，实验室和成像）和表现形式。方法：该观察项研究包括70例成人（平均年龄：45.87 +/- 3.36岁;尿毒症持续时间：5.5 +/- 1.5岁）。他们接受了广泛的评估（临床，实验室和神经影像体），并在每3个月临床上进行一次临床评估2年。对患有运动障碍的患者进行反复磁共振成像（MRI）大脑并与其神经内结果相关。结果：BG病变在15名患者（21.4％）和6名（8.6％）中发现了运动障碍[帕金森主义（n = 4），在开始后尿毒症（平均值= 10个月）。没有特征风险变量，使患者与没有的运动障碍的患者。在研究期间的五个发达的运动障碍，一个是德诺维。大多数是女性，患有糖尿病和高肾功能紊乱，代谢紊乱和MRIS的白质超收缩频率。尽管在三名患者中，所有患者持续存在的运动障碍。结论：肾功能衰竭没有明确的阈值，以导致BG病变导致运动障碍。临床结果是根据每位患者的患者的合并症和并发症的变量。持续的神经元损伤（由于尿毒症毒素/代谢/营养和缺血性和缺血性/微血管因子）被提出为神经内结果差的原因。

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