Department of Neurology and Psychiatry, Assiut University Hospital, Assiut, Egypt.
Department of Internal Medicine, Assiut University Hospital, Assiut, Egypt.
Can J Neurol Sci. 2020 May;47(3):350-365. doi: 10.1017/cjn.2020.29.
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.
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.
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.
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.
基底节(BG)病变在尿毒症患者中很少见,可能表现为运动障碍。然而,其确切的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患者 BG 病变的频率、类型、风险变量(临床、实验室和影像学)以及表现,以及患者的神经学结局。
这项观察性研究纳入了 70 名成年人(平均年龄:45.87 ± 3.36 岁;尿毒症病程:5.5 ± 1.5 年)。他们接受了广泛的评估(临床、实验室和神经影像学),并在 2 年内每 3 个月进行前瞻性临床评估。对有运动障碍的患者进行重复磁共振成像(MRI)脑部检查,并与他们的神经学结局相关联。
15 名患者(21.4%)发现 BG 病变,其中 6 名(8.6%)在尿毒症发病后出现运动障碍[帕金森病(n = 4)、舞蹈-肌张力障碍(n = 1)和肌张力障碍(n = 1)](平均发病时间为 10 个月)。没有特征性的风险变量可以区分有运动障碍和无运动障碍的患者。5 名患者在研究期间之前出现运动障碍,1 名患者为新发病例。大多数患者为女性,有糖尿病,肾功能异常、代谢紊乱和 MRI 上的白质高信号的频率更高。尽管有 3 名患者的神经影像学得到了缓解,但所有患者的运动障碍仍持续存在。
由于 BG 病变导致的肾功能衰竭导致运动障碍没有明确的阈值。临床结局因每位患者的合并症和并发症而异。持续性神经元损伤(由于尿毒症毒素/代谢/营养和缺血/微血管因素)被认为是导致不良神经学结局的原因。