HYPERTENSIVE ENCEPHALOPATHY WITH CORTICAL DISORDERS OF VISION.
HYPERTENSIVE ENCEPHALOPATHY WITH CORTICAL DISORDERS OF VISION.
复制标题
高血压脑病伴皮质性视力障碍。
DOI：
10.1093/oxfordjournals.qjmed.a067018
复制
发表时间：
1964
期刊：
影响因子：
--
通讯作者：
R. R. Russell
中科院分区：
文献类型：
--
作者：
E. Jellinek;M. Painter;J. Prineas;R. R. Russell
Bright病的早期观察者倾向于将其脑表现归因于尿毒症，但眼压测量法的引入很快使人们认识到血管因素。1905年，他在关于血管危象的论文《Gefaesskrisen》中，将肾炎患者的失明与收缩压的短暂升高联系起来。Volhard（1923）和Blackfan（1926）都强调在某些“尿毒症性黑蒙”病例中没有尿毒症，并将血压升高归咎于此。术语高血压脑病是由奥本海默和Fischberg于1928年创造的，用于治疗患有Bright病的年轻人的复发性局灶性发作。目前，高血压病被用于一种有限的、可描述在无脑血栓形成或出血证据的情况下，与血脑屏障升高相关的大部分可逆性脑疾病的治疗。这是一种罕见的疾病，文献记载丰富的CSB 8 S很少：除了Blackfan（T926）和Oppenheimer和Fischberg（1928）的病例报告外，Evans（1933）的一篇论文中描述了6例。随着急性肾炎发病率的降低，它变得更加罕见。在上一次大战前几年里，伦敦医院收治的225例肾炎病人中，有11例发生高血压性脑病，发病率为6%~ 4%。其中4例患者有视力障碍，但眼底无改变（Wilson，1963）。在我们自己的病例中，皮质盲是两名急性肾炎患者和一名肾动脉血栓形成患者的主要症状。第四例患者在非典型复发性肾炎过程中出现色盲和睡眠障碍。
THE earlier observers of Bright's disease were inclined to ascribe its cerebral manifestations to uraemia, but the introduction of tonometry soon led to recognition of vascular factors. Pal (1905) in his treatise on vascular crises ('Gefaesskrisen'), associated an episode of blindness in a case of nephritis with a transient rise in systolic pressure. Pal (1905), Volhard (1923), and Blackfan (1926) all stressed the absence of uraemia in some cases of'uraemic amaurosia'and incriminated the raised blood-pressure. The term hypertensive encephalopathy was coined in 1928 by Oppenheimer and Fischberg for the recurrent focal fits of a young man with Bright's disease. At present, hypsrJbensixe encaphalapathy is used in a restricted, senae to jde^ cribe largely reversible cerebral disorders associated with raised blood-pretganrfl in the absence of evidence of cereBral thrombosis or haemorrhage. It is an uncommon condition, and well-documented CSB8S are lew: apart Tfomlihe case reports ofBlackfan (T926) and Oppenheimer and Fischberg (1928), six were described in a paper by Evans (1933). With the lessening incidence of acute nephritis it is becoming even more of a rarity. In a series of 225 patients with nephritis admitted to the London Hospital in the years before the last war hypertensive encephalopathy ocourred in 11, an incidence of 6-4 per cent, in this disease. Four of these patients had disturbances of vision without changes in the optic fundi (Wilson, 1963). In our own cases, cortioal blindness was the presenting symptom in two patients with acute nephritis and in one patient with renal artery thrombosis. The fourth patient became colour-blind and dyslexic in the course of an atypical relapsing nephritis.