透過您的圖書館登入
IP:3.149.254.35
  • 期刊

Dyskinesia from Manganism in a Hepatic Dysfunction Patient

錳中毒引致運動障礙:一病例報告

摘要


錳中毒主要見於錳礦工人或錳鐵熔煉工作場所通風不良引致的職業疾病,常引發類似巴鎦金森症的運動障礙性肝病、肝功能障礙病人有報告類似錳中毒的腦影像表現一以蒼白球爲主,下視丘,腦下垂體於T1-weighted磁振造影有高密度信號的變化,T2-weighted磁振造影變化不顯,一般甚少臨床症狀。我們報告一例十四歲男孩罹患先天低免疫球蛋白症併有肝功能障礙,發生手足徐動等運動不良症狀。磁振造影有以上的影像變化,血及組織的錳含量過高,證明爲肝功能障礙所引致的錳中毒。

關鍵字

錳中毒 運動不良 磁振造影

並列摘要


A 14-year-old boy came to the neurological chinic because of involuntary movement. He represented a case of common variable hypogammaglobulinemia, with hepatosplenomegaly noted for 5 years and jaundice for 1 month. Neurological and laboratory examinations revealed choreoathetosis and hyperbilirubinemia, hypoalbuminemia, increased hepatic aminotransferase, and decreased indocyanine green clearance; as well as increased signal change over the globus pallidus, subthalamic area, internal capsule, tegmentum, brain stem and pituitary gland revealed by a brain magnetic resonance(T1-weighted) imaging study. A manganese study confirmed high body manganese loading. Trihexyphenidyl administration ameliorated the dyskinesia; however, the patien died from hepatic failure later. Though rare in incidence, manganese intoxication should be considered in cases with dyskinesia and the characteristic brain MRI findings. Even if no environmental exposure is involeved, total parenteral nutrition, porto-systemic shunt and chronic hepatic dysfunction could lead to a heavy manganese load resulting in symptomatic manifestation.

延伸閱讀