Parkinsonism and high-intensity midbrain lesions on T2-weighted imaging in hepatic encephalopathy: a case report.
Parkinsonism and high-intensity midbrain lesions on T2-weighted imaging in hepatic encephalopathy: a case report.
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肝性脑病的帕金森病和 T2 加权成像的高强度中脑病变：病例报告。
DOI：
10.1007/s10072-017-2976-8
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Nakazato M
中科院分区：
文献类型：
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作者：
Ishii N.;Mochizuki H.;Sakai K.;Shiomi K.;Nakazato M
由NAFIC评分系统定义[4]。由于她有明显的肝硬化，没有进行肝活检。免疫介导的肝炎形式，例如自身免疫性肝炎或原发性胆汁性肝硬化，不太可能，因为没有检测到特异性抗体。患者因年龄原因不适合肝移植，接受支链氨基酸和乳果糖治疗。在她的高氨血症解决后，她的意识水平立即改善，帕金森综合征的症状在几天内完全消失。治疗后10天，中脑被盖的T2加权病变略有改善（图1 j）。患者出院，并作为门诊患者接受药物治疗，未发生帕金森综合征复发。患者中脑被盖病变在出院后1年时尚未完全消失，但病变边界变得更模糊，异常高强度减弱，提示改善（图1 k）。HE患者表现出交替的意识水平，当HE更严重时，他们有时会出现波动性神经系统症状，如帕金森综合征和小脑功能障碍[1]。HE治疗不仅改善了精神状态的改变，还改善了神经系统症状。在肝硬化患者的T1加权MRI图像上经常观察到苍白球和黑质的高信号;这些成像结果与长期锰中毒病例中观察到的结果相同，表明脑锰浓度增加可能是帕金森综合征的原因[2，3，5]。在我们的病人中，短暂的帕金森综合征可能不仅与基底节的T1高信号有关，而且与中脑被盖的T2高信号有关。我们
defined by the NAFIC scoring system [4]. Hepatic biopsy was not performed because she had evident hepatic cirrhosis. Forms of immune-mediated hepatitis, for instance autoimmune hepatitis or primary biliary cirrhosis, were less likely because no specific antibodies were detected. The patient was ineligible for liver transplantation because of her age and was treated with branched-chain amino acids and lactulose. After her hyperammonemia resolved, her level of consciousness immediately improved, and symptoms of parkinsonism completely disappeared within a few days. Ten days after treatment, the T2-weighted lesions in the midbrain tegmentum improved slightly (Fig. 1j). She was discharged and managed medically as an outpatient, and no recurrence of parkinsonism occurred. Her midbrain tegmental lesion had not completely disappeared at 1 year after discharge, but the boundary of the lesion became vaguer and the abnormal high intensity diminished, suggesting improvement (Fig. 1 k).Patients with HE exhibit alternating levels of consciousness, and they sometimes have fluctuating neurological symptoms such as parkinsonism and cerebellar dysfunction when their HE is more severe [1]. Therapy for HE improves not only altered mental status but also neurological symptoms. Hyperintensities in the globus pallidus and substantia nigra on T1-weighted MRI images are often observed in patients with liver cirrhosis; these imaging findings are identical to those observed in cases of long-term manganese intoxication, indicating that increased brain concentrations of manganese may be a cause of parkinsonism [2, 3, 5]. In our patient, transient parkinsonism may have been related not only to the T1 hyperintensity in the basal ganglia, but also to the T2 hyperintensity in the midbrain tegmentum. We