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本文引用的文献

1
Clinical and functional outcome and factors predicting prognosis in osmotic demyelination syndrome (central pontine and/or extrapontine myelinolysis) in 25 patients.25 例渗透性脱髓鞘综合征(脑桥中央和/或脑桥外髓鞘溶解症)的临床和功能预后及预后预测因素。
J Neurol Neurosurg Psychiatry. 2011 Mar;82(3):326-31. doi: 10.1136/jnnp.2009.201764. Epub 2010 Sep 8.
2
Centropontine myelinolysis after correction of hyponatremia: role of associated hypokalemia.低钠血症纠正后发生的脑桥中央髓鞘溶解症:伴发低钾血症的作用
Clin Nephrol. 2007 Jun;67(6):345-51. doi: 10.5414/cnp67345.
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Central pontine myelinolysis: case series and review.中央桥脑髓鞘溶解症:病例系列及综述
WMJ. 2005 Aug;104(6):56-60.
4
Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes.中央桥脑及脑桥外髓鞘溶解症:渗透性脱髓鞘综合征
J Neurol Neurosurg Psychiatry. 2004 Sep;75 Suppl 3(Suppl 3):iii22-8. doi: 10.1136/jnnp.2004.045906.
5
Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients.中央pontine髓鞘溶解症:一种迄今未被描述的疾病,发生于酗酒和营养不良的患者。
AMA Arch Neurol Psychiatry. 1959 Feb;81(2):154-72.
6
A review of the causes of central pontine myelinosis: yet another apoptotic illness?中央桥脑髓鞘溶解症病因综述:又是一种凋亡性疾病?
Eur J Neurol. 2001 Mar;8(2):103-9. doi: 10.1046/j.1468-1331.2001.00176.x.
7
Mechanisms of hyponatraemia in alcohol patients.酒精性患者低钠血症的机制。
Alcohol Alcohol. 2000 Nov-Dec;35(6):612-6. doi: 10.1093/alcalc/35.6.612.
8
Blood-brain barrier disruption and complement activation in the brain following rapid correction of chronic hyponatremia.慢性低钠血症快速纠正后血脑屏障破坏及脑内补体激活
Exp Neurol. 2000 Oct;165(2):221-30. doi: 10.1006/exnr.2000.7474.
9
Outcome of central pontine and extrapontine myelinolysis (n = 44).中央桥脑和脑桥外髓鞘溶解症的结果(n = 44)。
J Neurol. 1999 Aug;246(8):700-5. doi: 10.1007/s004150050435.
10
Myelinolysis after correction of hyponatremia.低钠血症纠正后的髓鞘溶解症。
Ann Intern Med. 1997 Jan 1;126(1):57-62. doi: 10.7326/0003-4819-126-1-199701010-00008.

中央桥脑髓鞘溶解症:电解质及其他相关因素

Central pontine myelinolysis: electrolytes and beyond.

作者信息

Mascarenhas J V, Jude E B

机构信息

Department of Diabetes and Endocrinology, Tameside NHS Foundation Trust, Manchester, UK.

出版信息

BMJ Case Rep. 2014 Mar 28;2014:bcr2013203516. doi: 10.1136/bcr-2013-203516.

DOI:10.1136/bcr-2013-203516
PMID:24682140
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3975522/
Abstract

Central pontine myelinolysis (CPM), which is a component of the osmotic demyelination syndrome (ODS), is a frequent neurological complication that follows rapid correction of hyponatraemia. However, there are other predisposing risk factors (chronic alcoholism, hypokalaemia) that perpetuate the development of ODS. We report a case of a 39-year-old woman with a history of chronic alcoholism who presented to us with progressive neurological deficits (paraparesis, paresthesias). She was initially detected to have coexisting hypokalaemia which was eventually rectified with potassium supplementation. However, she continued to experience progressive worsening of her neurological symptoms despite adequate potassium supplementation. Therefore, a neurological opinion was sought for and she was diagnosed with CPM based on a background of chronic alcoholism and malnutrition; an MRI of the brain showed a hyperintense signal in the central pontine region. Following the diagnosis of CPM, she was rehabilitated with occupational and physiotherapy.

摘要

中央脑桥髓鞘溶解症(CPM)是渗透性脱髓鞘综合征(ODS)的一个组成部分,是快速纠正低钠血症后常见的神经系统并发症。然而,还有其他诱发危险因素(慢性酒精中毒、低钾血症)会促使ODS的发展。我们报告一例有慢性酒精中毒病史的39岁女性,她出现进行性神经功能缺损(双下肢轻瘫、感觉异常)前来就诊。最初检测发现她同时存在低钾血症,最终通过补充钾得到纠正。然而,尽管补充了足够的钾,她的神经症状仍持续进行性加重。因此,寻求了神经科会诊意见,基于慢性酒精中毒和营养不良的背景,她被诊断为CPM;脑部MRI显示脑桥中央区域有高信号。诊断为CPM后,她接受了职业治疗和物理治疗进行康复。