《关于国外渗透性脱髓鞘综合征部分文献之重新分析:反思》英文摘要与几点声明.doc
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1、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8,崔 松91.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,涿鹿桑干河075600;2.河北北方学院神经药理学系,张家口075000;3.中国人民武警部队总医院脑系科,北京100039;4.河北北方学院第二附属医院脑系科,张家口075100;5.佛山市南海区第二人民医院,广东528251;6.东营市鸿港医院神经内科,山东257061;7.华北石油总医院神
2、经内科,河北062500(通讯作者:张海鹏,e-mail: ;张力,e-mail:zmczl )Something 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
3、 Syndrome”Seeming to Include Central Pontine MyelinolysisZhang 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,8Depart
4、ment of General Surgery or 9Institute of Radiation Medicine and Applied Physics,Zhuolu-county Hospital & The 7th Teach-learning Hospital of Hebei North University, Sanggan-river,Zhuolu, Zhangjiakou 075600, Hebei, China;2.Department of Neuropharmacology, Hebei North University ,Zhangjiakou075000, Heb
5、ei, China;3.Department of Neurology, General Hospital of the Peoples 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 peoples 2nd Hospital of the Nanhai District of Foshan City ,G
6、uangdong528251, 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.The authors answerable for the article: Zhang Hai-peng,e-mail: ;Zhang Li,e-mail:zmczl Abstract Object
7、ives: 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
8、 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 diffe
9、rring 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 se
10、condary 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 rep
11、orted 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 corticos
12、teroid 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 T
13、omlinson 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 hypon
14、atremia(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 th
15、ere 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
16、(2007) ,the one by Shintani, et al(2005) and the one by Bhr,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 para
17、central 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 beri
18、beri CPM could be similar to the compensatory process of the bilateral type of the “chronic medipontine paracentral hematal syndrome” assumed by us. The whole essay including the aforementioned things has been published in No.1 of Vol.2012 of Academy Journal of Medical College of Henan University of
19、 China in Chinese language in March,20121.Key words Central pontine myelinolysis;osmotic demyelination syndrome; orthotopic liver transplant;fetus-liver transplant,the renal-splenic venous shunt after partial splenectomy; extropontine myelinolysis; Wernicke encephalopathy,Wernicke-Korsakoffs syndrom
20、e;hypokalemic paralysis,non-,periodic; cyclosporine;FK506;reverible posterior leukoencephalopath syndrome ;liver cirrhosis; epileptic attack; Foville syndrome, bilateral and uncomplete ; pontine(intra pontine) lower paracentral(paramedian) hematal syndrome,the bilateral type;hyponatremia,hyponatremi
21、c encephalopathy;the encephalopathy of alkalosis;cardiopathy, beriberi; alcoholism;Fukui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 笔者著述关于国外渗透性脱髓鞘综合征部分文献之重新分析:反思肝移植术后并发或严重呕吐导致的疑似VB1缺乏系
22、列症、低钾性肌麻痹与碱中毒性脑病终于于2012年见刊于河南大学(医学版)1。补充说明如下。1本文提供的上述英文摘要和关键词,是当时投稿时的原稿。英文摘要采用会议论文的大英文摘要的形式,以利于国外读者了解拙文的主要观点2. 检索万方医学网、万方知网和中国知网等网站不难发现,自笔者文献1发表以来,省级(含)以上医院神经内科的“渗透性脱髓鞘综合征”、“脑桥外髓鞘溶解症”及脑桥中央髓鞘溶解症的病例报告几乎绝迹迄今已3年有余了!而2012年以前,上述病例报告每年均有几十例3.参考文献更正:笔者著述的文献1的原参考文献5应为本文的参考文献2;原参考文献1216应为本文参考文献37;原参考文献2123应为本
23、文参考文献810;原参考文献31、32应为本文参考文献11、12;原参考文献47应为本文参考文献13;原参考文献49应为本文参考文献14;原参考文献50应为本文参考文献15;原参考文献5356应为本文参考文献1619;原参考文献60、61应为本文参考文献20、21;原参考文献7477应为本文参考文献2225;原参考文献8284应为本文参考文献2628;原参考文献86、87应为本文参考文献29、30;原参考文献89应为本文参考文献31;原参考文献91、92应为本文参考文献32、33。更正上述,恢复原投稿绝大多数参考文献的原貌,以使文献1广大读者可以找到原参考文献扩展阅读、扩展了解。注明原参考文献
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