关于国外渗透性脱髓鞘综合征部分文献之重新分析_反思_英文摘要与说明_张海鹏

2001年创刊 第15卷　第64期 2015年8月11日　周二刊277·医学教学·《关于国外渗透性脱髓鞘综合征部分文献之重新分析：反思》英文摘要与说明张海鹏1，8，9，张 力2，杜长生3，陈宗羡4，曾伏虎4，5，翟所鑫4，李玉清1，刘庆梅1，朱玉忠1，王荣明8，杨子军1，闫四梅3，陈 萌6，崔松7（1.涿鹿县医院/河北北方学院第七教学医院神经外科，8普外科，9放射医学与应用物理研究所，涿鹿；2.河北北方学院神经药理学系，张家口；3.中国人民武警部队总医院脑系科，北京；4.河北北方学院第二附属医院脑系科，张家口；5.佛山市南海区第二人民医院，广东；6.东营市鸿港医院神经内科，山东；7.华北石油总医院神经内科，河北）关键词：脑桥中央髓鞘溶解症；渗透性脱髓鞘综合征；肝移植术；胎肝移植；脾脏部分切除，脾-腔/肾静脉分流术；脑桥外髓鞘溶解症；Wernicke脑病；肝硬化；低钾性肌麻痹，乏力，非，周期性；环孢素，FK506；癫痫；脑桥下部旁正中（血管）综合征，双侧型；低钠性脑病；碱中毒性脑病；脚气性心脏病，维生素B1缺乏症；Fukui中图分类号：R-013 文献标识码：B DOI：10.3969/j.issn.1671-3141.2015.64.221Something Related to the Beriberi Secondary to Hepatic Transplantation，the Hypokalemic Non-periodic Paralysis or the Encephalopathy of Alkalosis：A Primary Reretro-consideration on Some International Documentations Concerning the “Osmotic Demyelination Syndrome”Seeming to Include Central Pontine Myelinolysis Zhang Hai-peng 1, 8, 9, Zhang Li2, Du Chang-sheng 3, Chen Zong-xian4, Zeng Fu-hu4, 5, Zhai Suo-xin4, Li Yu-qing1, Liu Qing-mei1, Zhu Yu-zhong1, Wang Rong-ming8, Yang Zi-jun 1, Yan Si-mei3, Chen Meng6, Cui Song7(1.Department of Neurosurgery, 8Department of General Surgery or 9Institute of Radiation Medicine and Applied Physics, Zhuolu-county Hospital & The 7thTeach-learning Hospital of Hebei North University, Sanggan-river, Zhuolu, Zhangjiakou 075600, Hebei, China;2.Department of Neuropharmacology, Hebei North University, Zhangjiakou075000, Hebei, China;3.Department of Neurology, General Hospital of the People's Armed Police Forces of China, Beijing100039, China;4.Department of Neurology, The 2nd Hospital Attached to Hebei North Uni versity, Zhangjiakou075100, Hebei, China;5.The people’s 2nd Hospital of the Nanhai District of Foshan City, Guangdong528251, China;6.Department of Neurology, Hong-gang Hospital of Dongying City, Shandong257061, China;7.Department of Neurology, General Hospital of Oilfield in Northern China, Hebei062500, China)ABSTRACT Objectives: To explore the main etiological factors of central pontine myelinolysis (CPM) and of the “osmotic demyelination syndrome(ODS)”that occurs after hepatic transplantation, to explore the differential diagnosing the manifestation consisting of dysarthria, dysphagia and quadriplegia presented after vomiting for a number of times, and to explore which fraction to be mainly involved by the “ODS”, what to be the pathological mechanism of the “ODS”, and how to prevent the “ODS”. Methods: Physiopathological principles are applied on the base of the clinical certificates, the diagnostic results differring from those in the case reports (that have been analyzed again by us). Results and Conclusions: It could be suggested that (1) CPM based mainly on alcoholism should result mainly from beriberi, as was mentioned by HUANG Ke-wei, the well-known Chinese neurologist, before or in 1960; (2) The coma secondary to hepatic transplantation could be often caused by Wernicke encephalopathy(WE, one of beriberi), which could be asscociated with the postoperative elevated corticosteroid or/and high-starch food for liver cirrhosis, which complicated by hepatic encephalopathy; (3)The case that was in 1995 reported by Kabeer et al, of possiblity of the earliest reported CPM due to cyclosporine, appeared to be the bilateral type of pontine lower paracentral hematal syndrome, a bilateral uncomplete Foville syndrome.It should be considerable whether an epileptic attack related to both cyclosporine and corticosteroid could result from reverible posterior leukoencephalopath syndrome with negative MRI owing to the effect of corticosteroid; (4) It is cerebral cortex that could be mainly involved by the “ODS” following a number of times of vomiting, of which one of evidences has been the 2 cases reported by Tomlinson et al in 1976.The kind of “ODS” following the encephalopathy of alkalosis yet without hypoxemic hypoxia, is possibly preventable not only if the correction of hypokalemia is firstly comsidered and also if corticosteroid(for 3 days or shorter) is preventivly applied before correction of hyponatremia(0.9%NaCl, via digestive tract).Dose -filled vitamin B1 (i.m.), however, ought to be given so as not to induce beriberi including CPM before corticosteroid is used; (5) The hypokalemia caused by vomiting and alkalosis thereof, can maybe account for dysarthria, dysphagia and quadriplegia, when there is not obvious difference between the severity of bulbar paralysis and that of quadriplegia ; and quadriceps reflex often plays down in patient with hypokalemic non-periodic paralysis(HNP).Thereby, each of some reported cases with (clinical)CPM, including several of 22 ones reported by Heng, et al(2007), the one by Shintani, et al(2005) and the one by Bähr, et al(1990), has shown itself rather as sub-clinical CPM (with HNP) than clinical CPM (without HNP) suggested only by MRI.(6)It is supposed that why for CPM to involve the pyramidal tract inside pone, could be based on that the pontine paracentral branch of basilar artery had tended to “degeneration”in a limited degree since the cerebellar branches and posterior cerebral branch precedently developed following the evolution of the zoogenetic cerebellum and occipital lobe towards human brain, therefore, the pathologic mechanism of a beriberi CPM could be similar to the compensatory process of the bilateral type of the “chronic作者简介：张海鹏（1970-），大专学历（毕业于河北北方学院），神经外科专业主治医师。