海洛因海绵状白质脑病的影像学特征

目的　探讨海洛因海绵状白质脑病 (HSL E)的 CT、MRI和 PET特点。方法　对 2 9例患者的CT、MRI以及 4例患者的 PET资料进行分析。结果　 (1) CT和 MRI显示病变位于双侧小脑、内囊后肢、枕顶叶深部等部位白质 ,病灶广泛且对称 ;(2 ) CT示界限清楚的低密度病灶 ,MRI呈长 T1 WI、长 T2 WI异常信号 ,无水肿 ,快速反转恢复序列 (FL AIR)和增强扫描提示血脑屏障无破坏 ,PET显示为低代谢或无代谢病灶 ;(3)未治疗患者内囊后肢、枕叶和小脑白质无代谢 ,康复期患者代谢明显减低 ;(4 )临床症状改善者和未治疗者小脑皮质代谢降低 ,临床症状明显改善者代谢正常。结论　 HSL E患者的 CT和 MRI改变多局限于白质 ,极为相似。 PET显示病变部位低代谢或无代谢 ,小脑皮质和白质代谢的恢复对 HSL E患者的临床转归非常重要 ,故判断 HSL E患者的转归 ,PET较之 MRI更有价值     

海洛因海绵状白质脑病(附2例报道)

目的了解海洛因海绵状白质脑病的临床特征、治疗及预后.方法观察2例海洛因海绵状白质脑病患者的临床、影像学表现及治疗转归,并结合文献进行分析.结果 2例均为中年男性,有烫吸海洛因病史,其中1例尚有静脉注射史.1例以反应迟钝、行为异常为首发症状;1例以小脑症状为突出表现.头颅MRI均表现为脑白质广泛病变,其中1例影像学显示小脑中线两旁、边界清楚的对称性类圆形或蝴蝶样病灶及内囊后肢对称性受损等特征性改变.经促进脑细胞代谢药物等治疗后,随访2年均恢复良好.结论海洛因海绵状白质脑病是一种少见的与海洛因相关的特征性脑部病变,及时诊治,预后较好.     

海洛因中毒性脑病的临床与影像学观察

目的：研究海洛因中毒性脑病的临床特点及影像学（CT和MRI）特征，方法：对13例海洛因中毒性脑病患者的临床和影像学资料进行观察和分析。结果：13例为男性，均以烫吸海洛因为吸毒方式，9例是在毒品戒断过程中发病，主要临床表现为亚急性起病的弥漫性脑扣害，尤为精神症状和小脑性共济失计为突出表现。13例CT表现为脑内多发，广泛且明显对称性的低密度灶，累及双额，顶、颞、枕叶白质区及小脑半球齿状核和脑干，一般无占位征象，6例周期MRI检查显示病灶的部位，范围与CT所见大致相同。结论：本病的诊断依靠明确烫吸海洛因史及具有特征性的临床表现和影像学征象。CT与MRI一样，对本病的诊断具有重要价值。激素对本病治疗效果差。     

海洛因中毒性脑病的临床与磁共振成像

目的 研究海洛因中毒性脑病的临床表现及磁共振成像（ＭＲＩ）特征。方法 对４例海洛因中毒性脑病患者进行临床及ＭＲＩ观察。结果 ４例均为男性,均有明确的吸毒史（吸毒时间４个月至７年）,除具有反应迟钝、智力障碍等常见的中毒性脑病特征外,尚有特殊的语言及肌张力障碍;头颅ＭＲＩ显示双侧对称性大脑半球、内囊后肢、胼胝体、内侧丘系、小脑半球齿状核的广泛脱髓鞘改变。经皮质激素等治疗后１例在病后１１个月时临床症状几乎消失,２例在治疗３个月后病情减轻,１例吸毒长达７年者,病情迅速恶化,于病后第５５天死亡。结论 认识海洛因中毒性脑病的临床表现及ＭＲＩ特征,使本病患者得到及时的诊治。     

海洛因白质脑病

重点综述了海洛因白质脑病的成因 ,临床表现及病理与影像学特征 ,并突出其诊断标准     

海洛因海绵状白质脑病

海洛因海绵状白质脑病是近年才引起医学界关注的少见疾病，其临床与病理改变颇具特点，但国外报告的文献很少，国内仅见数例报告。本文主要查阅近几年的文献，对该病的病因、病理机制、临床表现、影像学特点、诊断与鉴别诊断、治疗及预后各方面进行了总结。     

低血糖脑病的影像学特征

目的探讨低血糖脑病的影像学特征。方法回顾性分析7例低血糖脑病患者的核磁共振资料。结果低血糖脑损害有高度的区域选择性,可不对称。主要累及大脑皮层、海马、基底节和胼胝体压部,甚至皮层下白质;MRI表现为等或稍长T1、长T2信号,DWI呈高信号,伴ADC值降低,部分病变可逆;MRS示病变区乳酸峰无明显变化。结论低血糖脑损害有很强的区域选择性、可不对称;DWI对病变更敏感;大脑皮层和基底节区受累者预后不佳,侵犯胼胝体压部者预后好。     

海洛因海绵状白质脑病2例报告

海洛因中毒所致的海绵状白质脑病近年来陆续有报道。现将我们遇到的2例报告如下。     

脱髓鞘脑病及多发性硬化的临床表现与影像学

本文对照分析了２３例脱髓鞘性脑病和３８例多发性硬化的临床表现，ＭＲＩ表现及预后，发现两组病例虽在起病形式，发病性别和年龄之间无明显差异，但在受累部位，ＭＲＩ表现及预后方面有不同的特点，急性多发性硬化有时与脱髓鞘脑病难以鉴别。     

慢性海洛因中毒性脑病

目的 :报道 3例 (男 2例 ,女 1例 )慢性海洛因中毒性脑病的临床和 MRI特征 ,并结合文献进行分析。 3例均有明确吸毒史 (吸毒时间 3～ 5年 ) ,表现为进行性智能障碍、言语障碍、肌张力障碍及共济失调等慢性脑损害的特点 ,1例 (女性 )发展为意识障碍。头颅 MRI显示双侧镜像般对称性大脑白质、内囊后肢、内侧丘系、胼胝体、中脑及小脑半球内白质广泛性长 T1 、长 T2 信号 ,无强化 ,似脱髓鞘改变。经皮质激素治疗后 ,2例 (男性 )好转 ,1例无改善。因此 ,认识慢性海洛因中毒性脑病的临床及影像学特征是十分重要的 ,及时诊治可望使病情得到缓解     

Wernicke脑病综合征10例临床分析

目的:探讨Wernicke脑病(WE)的病因、临床表现特点、MRI表现及预后。方法:对10例WE患者的病因、临床表现、头颅MRI特点和预后进行了回顾性分析。结果:WE病因多与维生素B1缺乏有关,主要临床表现为眼肌麻痹,共济失调、精神异常三联症,但也可以表现为周围神经病、言语障碍等。头颅MRI有特异性部位的异常信号改变。及时予以维生素B1治疗者预后多良好。结论:提高临床对WE的认识,有利于早诊断、早干预,有助于改善WE的预后。     

海络因白质脑病的临床特征及影像学观察

目的　分析和探讨海络因白质脑病 (heroin leukoencephalopathy,HLE)的临床特点、诊断规律、发病机制及防治经验。方法　对 2例男性 HLE患者的临床症候进行观察 ,均行头颅 CT及磁共振 (MRI)检查 ,其中 1例行弥散加权成像 (DWI)。结果　 2病例均为急性起病 ,以言语含糊、行走不稳等小脑共济运动障碍表现为主 ,反应迟钝 ,锥体束征阳性。头颅 CT及 MRI可见双侧小脑、内囊后肢、枕顶叶深部白质、胼胝体、脑干等白质区域异常信号 ,CT示低信号 ,MRI呈长 T1、长 T2信号影 ,DWI为高信号影。结论　 HLE可根据有吸毒史 ,并结合临床及影像学特点进行诊断 ,对于戒毒者戒毒时应在神经保护的前提下进行 ,或许能减少或避免 HLE的发生。     

2例肥厚性硬脑膜炎的临床和磁共振影像学特征

目的:报道2例肥厚性硬脑膜炎(HCP),探讨其临床和磁共振(MRI)成像特征。方法:分析2例患者临床和MRI特点,结合文献讨论HCP的病因、临床表现和影像学特点等。结果:HCP病因多样。临床以头痛和多组脑神经损害为主。1例低颅压性头痛为HCP罕见症状。MRI增强扫描以颅内硬脑膜弥漫性异常增厚为特点。结论:HCP是以头痛和硬脑膜弥漫性增厚为特点。根据临床缓慢局灶和全脑功能障碍症状,结合增强MRI特点,有利于早期作出较明确的诊断。     

低血糖脑病的临床及脑部磁共振特征

目的探讨低血糖脑病的临床及脑部磁共振特征。方法回顾分析69例低血糖昏迷患者的临床、脑磁共振（MRI）成像资料。结果低血糖昏迷诱因较为复杂,常见的为进食减少、腹泻、上呼吸道感染、降糖药物应用不当等。临床表现复杂多样,除意识障碍外,还可表现为偏瘫、四肢瘫、凝视麻痹等,多数伴有Babinski征。69例患者中有18例出现脑MRIDWI异常高信号病灶,病灶主要累及海马、基底节、大脑皮质以及皮质下白质,多为对称性损害。3个月后随访,不伴有脑部MRI损害的患者预后良好率明显高于伴有脑部MRI损害的患者（94．12％对22．22％;P=0．0011）。伴有脑部MRI损害者有10例患者预后不良,其中9例（90％）发生于皮质受累患者。结论低血糖脑病临床表现不具有特异性,对于昏迷患者,应当考虑到低血糖的可能。降糖药物应用不当为低血糖脑病的主要诱发因素。脑部MRI要优于脑部CT检查,其中DWI序列对于检测低血糖所致的脑部损害有着非常重要的意义。皮质受累者预后不良。     

低血糖脑病的临床和神经影像学特点

目的 探讨低血糖脑病(HE)的临床和神经影像学特点.方法 回顾性分析49例HE患者的临床和神经影像学资料.结果 本组HE患者临床表现为意识障碍26例,精神行为异常19例,癫癎发作6例,言语不清、反应迟钝10例,偏瘫和单肢瘫5例,去脑强直发作3例.23例行头颅CT检查,除10例见有脑梗死和脑萎缩外余无异常改变.13例行MRI检查,7例异常,其中显示弥漫性皮质和海马受累者3例(2例同时波及基底节区,1例仅累及右侧大脑皮质,MRS示病变区乳酸峰无明显异常),胼胝体压部受损2例(1例患者10 d后病变恢复,1例伴内囊后肢受累),壳核和放射冠区白质受累各1例,表现为等或稍长T1、长T2异常信号,DWI呈高信号伴表观扩散系数(ADC)降低.结论 HE的临床表现多不典型;MRI有高度特异性,DWI序列对病变更敏感.     

Wernicke脑病

Wernicke脑病（WE）是一种急性或亚急性起病的维生素B1缺乏症。表现为眼部体征、躯干性共济失调、意识障碍和情感淡漠及多发性周围神经病。M砌的表现有助于提示本病。WE是由于胃肠道手术、酗酒和胰腺炎等病因引起,补充维生素B1有助于恢复。     

Magnetic Resonance Reflects the Pathological Evolution of Wernicke Encephalopathy

BACKGROUND AND PURPOSE: Wernicke encephalopathy (WE) is an acute phase of Wernicke-Korsakoff syndrome. Pathologic findings change between acute and chronic phases. Only a few magnetic resonance imaging (MRI) studies have been done to date. METHODS: To correlate the MRI findings in acute and chronic stages of WE with the known pathologic information, 15 consecutive patients with WE were examined with MRI: 3 before thiamine treatment, 7 within 24 hours of thiamine treatment, 4 between the second and sixth day after thiamine treatment, and 1 fifty-five days after thiamine treatment. Nine of the patients had follow-up MRI between 2 days and 33 months. T1-weighted, proton, and T2-weighted axial images were obtained with additional 5-mm-thick T1-weighted sagittal and coronal images to better visualize the mammillary bodies. RESULTS: In the acute WE, MRI showed high signal intensityon T2-weighted images in periaqueduct and medial thalamic regions. In a few patients with alcoholism, vermian and mammillary body atrophies and third ventricular enlargements were noted. In the chronic phase of WE, T2 hyperintensity disappeared but mammillary bodies and cerebellar vermis became atrophic and third ventricular enlargements were evident. High signal intensity on T2-weighted images disappeared as early as 2 days, and atrophic changes appeared as early as 1 week. CONCLUSION: MRI is useful for in vivo monitoring and reflects the pathological evolution in acute and chronic phases of WE.     

MR Atypical Wernicke Encephalopathy Showing Extensive Brain Stem and Diencephalic Involvement

Wernicke encephalopathy (WE) is a serious neurological disorder caused by thiamine (vitamin B1) deficiency. We report a case of atypical and extensive location of abnormal signal lesions on magnetic resonance imaging (MRI) in a man with alcohol abuse with WE. MRI performed on the first hospital day showed signal intensity alterations extending in the whole brain stem and diencephalon; the mismatch between diffusion‐weighted images and apparent diffusion coefficient map was highly suggestive of vasogenic edema. This report further supports the view that WE may represent a spectrum of radiological entities and can have a wide spectrum of manifestations on MRI; thus, clinical features are essential to diagnose it.     

Wernicke encephalopathy☆ Clinical presentation and MR images in two nonalcoholic patients

The aim of the present study was to investigate the importance of and correlation between clinical presentations and magnetic resonance imaging （MRI） of two different cases of nonalcoholic Wernicke encephalopathy. Case l ： A 63-year-old man with a diagnosis of incomplete mechanical intestinal obstruction. His abdominal symptoms were improved by gastrointestinal decompression, but blurred vision, hypoacusis, dizziness, and unsteady gait were noted. His illness deteriorated to confusion on day seven. MRI showed hyperintense lesions in the medial thalami, tectum of the midbrain, and the periaqueduct region on T2- and diffusion-weighted images. Thiamine therapy was commenced immediately with good results. Case 2： A 22-year-old woman was admitted for sudden-onset confabulation and unsteady gait after hyperemesis gravidarum. She had no history of alcohol or any medication. Brain MRI was normal. The patient experienced relief after Vitamin B1 treatment. These results suggest that brain MRI can define characteristic abnormalities in Wernicke encephalopathy, and that diffusion-weighted imaging may improve the diagnosis sensitivity. In addition, the MRI images may be correlated to the clinical stage and severity of the disease. Nevertheless, the clinical features are essential for correct diagnosis.