吸食海洛因致海绵状白质脑病的CT及MRI诊断

目的评价海洛因中毒所致的海绵状白质脑病的CT、MRI表现及诊断价值.方法搜集6例海洛因海绵状白质脑病的CT及MRI资料,全部患者均进行MRI检查,检查序列包括T1WI、T2WI、FLAIR序列,其中2例同时行颅脑CT扫描. 结果全部患者MRI显示对称性双侧小脑半球、大脑半球后部、内囊后肢、胼胝体压部、脑干等皮质下白质为主的多发性大片状长T1、长T2信号,加强后病灶无强化;2例行头颅CT检查显示两大脑半球皮质下白质、基底节及两侧小脑呈对称性广泛低密度灶,无占位效应.结论海洛因中毒所致的海绵状白质脑病具有特征性的MRI表现,MRI对本病的诊断具有重要价值.     

海洛因海绵状白质脑病的临床及MRI(附3例报告)

目的 :研究海洛因中毒所致的海绵状白质脑病临床与磁共振成像特点。方法 :本文报告 3例并结合文献分析海洛因海绵状白质脑病临床和 MRI资料。结果 :本病的主要临床表现 ,起病前有明确的吸服海洛因病史 ,急性或亚急性起病 ,早期以构音障碍、步态不稳、小脑性共济失调等小脑损害症状和体征为突出表现。 MRI检查显示对称性双侧小脑半球、大脑半球后部、内囊后肢、胼胝体压部、脑干等皮质为主的多发性大片状长 T1、长 T2信号 ,加强后病灶无强化。脑病理特点是脑白质呈对称性海绵样脱髓鞘改变。结论 :本病的诊断主要依靠其临床特点、影像学及脑病理学检查 ,MRI对本病的诊断具有重要价值。     

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。     

慢性一氧化碳中毒的临床与MRI表现

目的研究慢性一氧化碳(CO)中毒患者的临床和。MRI表现。方法回顾性分析5例慢性CO中毒患者的临床及MRI资料。结果5例患者早期均表现为间断性头痛、头昏、疲劳等非特异性症状，中晚期3例出现视力严重下降，2例出现认知障碍。5例患者头部MRI均可见双侧基底节区类圆形长T1、长T2改变，3例大脑白质呈弥漫性长T1、长T2改变，2例视神经呈长T1、长T2改变并可见视神经萎缩。结论慢性CO中毒患者早期症状无特异性，晚期主要表现视力减退和认知功能障碍。长期低浓度CO接触史是诊断的可靠依据。MRI检查对本病的诊断有重要意义。     

临床常见脑病的临床及影像学特点分析

目的探讨临床常见的脑病,包括代谢、中毒及放射性脑病等临床常见脑病的临床及影像学表现特点。方法收集作者医院收治的临床常见脑病患者43例,其中中毒性脑病17例(包括装修苯中毒1例、鼠药氟乙酰胺中毒1例、化疗药物中毒5例、有机磷农药中毒4例、一氧化碳中毒5例、海洛因中毒1例)、放射性脑病5例及代谢性脑病21例(包括Wernick脑病2例、低血糖脑病4例、肝性脑病4例、尿毒症性脑病5例、桥本脑病3例、甲基丙二酸尿症1例、卟啉病1例、伴有囊肿及钙化的白质脑病1例),总结分析临床常见脑病的临床及影像学特点。结果 (1)临床表现:不同病因脑病患者多表现为不同程度的认知功能障碍、精神行为异常、言语含糊及计算力减退等,部分患者表现为肢体力弱或无力,少数患者表现为语音障碍、眼球固定、发作性肢体抽搐及腹痛等。(1)表现为认知功能障碍:包括不同程度的反应迟钝伴记忆力减退(脑病中苯中毒1例、有机磷农药中毒2例、化疗药物中毒5例、一氧化碳中毒2例、放射性脑病5例、尿毒症性脑病5例、桥本脑病3例),以及不同程度的意识障碍(有机磷农药中毒2例、一氧化碳中毒3例、低血糖脑病2例、肝性脑病4例);(2)精神行为异常(桥本脑病3例、甲基丙二酸尿症1例);(3)表现为言语含糊伴计算力减退(海洛因脑病1例);(4)部分患者表现为肢体力弱或无力,少数患者表现为语音障碍、眼球固定、发作性肢体抽搐及腹痛等,其中包括放射性脑病3例、低血糖脑病2例、甲基丙二酸尿症1例、卟啉病1例、伴有囊肿及钙化的白质脑病1例表现为肢体力弱,Wernick脑病2例表现为进行性声音嘶哑伴双下肢力弱及眼球固定,苯中毒及鼠药氟乙酰胺中毒各1例表现为发作性肢体抽搐,卟啉病1例表现为发作性腹痛、肢体无力伴言语不清。(2)影像学表现:影像学表现病变主要累及白质、基底节核团,少数可累及脑室旁及导水管区域,仅1例表现为广泛性脑萎缩。病变表现以白质脑病为主者包括苯中毒、鼠药氟乙酰胺中毒、化疗药物中毒、有机磷农药中毒、一氧化碳中毒、海洛因中毒、尿毒症性脑病及桥本脑病患者;伴钙化与囊变的脑白质病患者表现为双侧大脑半球脑白质区多发大小不等囊状病灶;以基底节核团病变为主者包括低血糖性脑病、肝性脑病、卟啉病、有机磷农药中毒性脑病,一氧化碳中毒迟发性脑病及海洛因中毒性脑病;Wernick脑病患者病灶多位于三脑室旁、侧脑室旁及导水管周围;甲基丙二酸尿症1例表现为广泛脑萎缩。结论临床上常见类型的脑病病因多样,均有不同程度的认知功能障碍,影像学表现包括广泛的白质脱髓鞘、皮层萎缩及基底节区病变等,诊断应结合临床、影像学特点及相应的病史进行诊断。     

烫吸海洛因致白质脑病2例报告及文献复习

目的 研究烫吸海洛因蒸汽引起海绵状白质脑病的临床表现及影像学特征，探讨吸毒方式与病理改变的关系。方法 对2例烫吸海洛因引起的海绵状白质脑病的患者进行了临床和MRI观察，复习中外文献，对该病的临床表现、影像学特征、病理组织改变、吸毒方式与病理机制之间的关系进行了总结与讨论。结果 2例患者均采用烫吸的方式摄入海洛因，时间为1．5年、8年，均在戒毒数日后发病，以小脑性共济失调、智力减退为主要临床表现。MRI显示对称性小脑齿状核、双大脑半球半卵圆中心、胼胝体压部、内囊后肢、内侧丘系、红核、黑质、脑桥长T1T2信号改变，给予地塞米松、脑多肽、胞二磷胆碱、B族维生素、高压氧、低激光血疗等治疗有近期疗效。结合文献资料显示本病可能与海洛因的烫吸方式有关，提出突然戒断与发病的可能关系。结论 烫吸海洛因引起海绵状白质脑病临床表现、影像学改变具有特征性，从而使本病能够得到早期确诊。     

酷似中毒性脑病的可逆性后部白质脑病综合征:6例临床分析

目的探讨可逆性后部白质脑病综合征(RPLS)的临床及影像学特点,为与中毒性脑病进行鉴别提供依据。方法回顾性分析6例RPLS患者的临床特点、影像学资料及治疗经过。结果 6例患者分别有大量饮酒史、海洛因吸食史、煤气中毒史、长期接触油漆涂料史、一氧化碳吸入史和有机溶剂接触史。临床主要表现为头痛、恶心、呕吐、癫痫发作以及血压升高。头部MRI主要表现为双侧颞叶、顶叶、额叶、侧脑室旁白质、小脑、脑干病灶,呈长T1、长T2信号,无强化。6例患者对症及去除病因治疗后临床表现及影像学表现均明显好转。结论 RPLS患者可以出现与中毒性脑病相似的临床及影像学特点,特别是当患者有毒物吸入史时,应根据该病相对特征性的临床、影像学及疗效尽早排除。     

国人海洛因白质脑病的临床特点分析

目的:分析和探讨国人海洛因白质脑病(HLE)的发病机制、临床特点、诊断规律及防治经验。方法:对国内11例及我院2例HLE的临床症候进行分析,对图像学特点进行总结。结果:患者11例男性,2例女性,发病年龄在24～55(平均32.7±8.3)岁。吸毒史除1例为4个月,其余均在3年以上,最长为11年。吸毒方式有12例是采取了烫吸(“追龙法”)的方法仅1例为静脉注射。均为急性起病,其中10例均以反应迟钝、言语含糊、行走不稳、乏力等为首发症状;2例以意识障碍起病;1例以胡言乱语,发音不清、幻觉及行为异常起病。查体9例发音含糊,仅1例轻微眼震,肌张力3例增高9例减低、1例正常,肌力记载的11例均轻度减低,Romberg征8例阳性,4例无法配合。Babinski征10例阳性,3例阴性。头颅CT(6例)及MRI(11例)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,在CT示低信号,在MRI上为长T1、长T2信号影,1例在弥散加权成像(DWI)上为高信号影。13例中治疗后7例有不同程度的好转,4例无记录,1例无变化,1例死亡。结论:烫吸海洛因的方式及戒断毒品是与HLE发病的主要原因之一,临床表现主要以脑功能障碍,特别是以共济运动障碍、言语含糊、反应尽钝为主,严重者可有意识障碍。HLE可以根据有烫吸海洛因史,并结合临床及影像学特点进行?     

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。     

海洛因脑病的临床表现与影像学特征

目的:探讨海洛因脑病患者临床表现和影像学特点。方法:回顾性分析经临床和实验室确诊的7例海洛因脑病患者的相关资料。结果:所有患者有吸食海洛因病史,在突然戒断期间中发病,临床以言语障碍,共济失调、锥体束征阳性为特征,MRI表现为对称性大脑、小脑白质、内囊以及脑干的长T1、长T2信号,Gd～DTPA增强后无强化,脑脊液检查一般未见异常。结论:海洛因脑病多见于青年男性,有吸食海洛因史,临床表现多变,影像学有较典型的特点。     

Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.     

缺氧性脑病16例报告

目的　探讨缺氧性脑病的临床特征。方法　回顾分析 16例缺氧性脑病的病因、主要临床表现、磁共振成像 (MRI)结果、治疗方法及疗效。结果　 16例均有明确的脑缺氧病史。临床主要表现意识障碍、锥体外系症状、锥体束征、精神症状、智能减退及去皮层综合征 ,部分病人呈迟发性脑病表现。头颅MRI检查主要见两侧基底节区对称性异常信号 ,呈长T1长T2 改变。本组多数病人经对症、神经营养、改善脑循环、高压氧仓等治疗 ,脑受损症状基本消失或好转。结论　认识缺氧性脑病有助于该病得到及时合理的治疗 ;头颅MRI检查对缺氧性脑病有重要诊断价值。     

Long-term findings on brain magnetic resonance imaging in acute encephalopathy with bilateral striatal necrosis associated with measles

The long-term findings on brain magnetic resonance imaging (MRI) in a 7 10/12-year-old boy with a history of acute encephalopathy with bilateral striatal necrosis following measles at the age of 22 months are described. At the early stage of illness, brain MRI studies revealed bilateral, symmetric basal ganglia lesions, predominant on the globi pallidi, appearing as hyperintense signals on T1- and T2-weighted images. Six years later, follow-up brain MRI studies showed that the bilateral, symmetric lesions on the globi pallidi persisted with low signal on T1- and high signal on T2 weighted images. At present, the patient has some persistent neurologic signs. These findings suggest that both clinical and neuroradiologic findings may persist in children with acute encephalopathy with bilateral striatal necrosis following measles.     

An outbreak of encephalopathy after eating autumn mushroom (Sugihiratake; Pleurocybella porrigens) in patients with renal failure: a clinical analysis of ten cases in Yamagata, Japan]

In September and October, 2004, an outbreak of encephalopathy of unknown etiology occurred in certain areas of Japan including Yamagata, Akita, and Niigata prefectures. These patients had a history of chronic renal failure, most of them had undergone hemodialysis, and also had a history of eating Sugihiratake (Pleurocybella porrigens), an autumn mushroom without known toxicity. Since clinical details of this type of encephalopathy remain unknown, we analyzed the clinical, radiological and electroencephalographic (EEG) features of ten cases of this encephalopathy in Yamagata prefecture. The summary of the present study is as follows: 1. Ten patients had chronic renal failure, and seven underwent hemodialysis. 2. Each patient had a history of eating Sugihiratake within 2-3 weeks of the onset of neurological symptoms. 3. The onset was subacute; the initial symptoms were tremor, dysarthria, and/or weakness of the extremities, which lasted an average of 4.5 days (ranging from 2 to 11 days), followed by severe consciousness disturbance and intractable seizures, resulting in status epilepticus in 5 patients. Myoclonus was also seen in 4 patients and Babinski reflex in 3. 4. Brain CT and MRI examinations were unremarkable in the early stages of the disease. Three to eight days after onset, however, conspicuous lesions appeared in the areas of the insula and basal ganglia in 6 patients. On MRI, these brain lesions were hyperintense on T2-weighted and FLAIR images, and hypointense on T1-weighted images. 5. EEG examination was performed in 6 patients, all of whom showed abnormal EEG findings. Periodic synchronous discharge (PSD) was seen in 2 patients, spike and wave complex in one patient, and non-specific slow waves in 3. 6. Prognosis was different from case to case. Three patients died at 13, 14, and 29 days after onset. Two patients still showed persistent disturbance of consciousness one month after onset. One patient showed parkinsonism after recovering from consciousness disturbance. Four patients recovered nearly completely around one month after onset In 3 of the 4 recovered patients, renal failure was not severe and they did not need to undergo hemodialysis. This suggests that the degree of renal failure is a key for the prognosis of this type of encephalopathy. The present study suggests that this endemic disease is a newly recognized clinical entity of encephalopathy.     

安钠咖相关脑损害三例临床与磁共振成像特点

目的 探讨安钠咖相关脑损害的临床表现及磁共振成像(MRI)特征.方法 对3例安钠咖相关脑损害患者进行临床及MRI观察.结果 3例均为男性,均有明确的烫吸安钠咖史(烫吸时间3～7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、双侧大脑脚、脑桥的广泛脱髓鞘改变.3例经皮质激素、神经营养等治疗,在病后40 d病情均明显好转,仅例1残留轻度情感控制障碍.结论 安钠咖相关脑损害有特殊的语言及肌张力障碍,MRI存在广泛脱髓鞘,了解这些特点可为预防和治疗安钠咖引起的并发症提供帮助.     

Clinico-radiological correlation of Wilson's disease by magnetic resonance imaging, computed and positron emission tomography

Follow-up magnetic resonance imaging (MRI) and computed tomography (CT) examinations were performed on five patients with Wilson's disease at intervals from 6 to 29 months. We studied the clinical correlation with MRI and CT, and whether the examination of MRI and CT could be useful for evaluation of the therapeutic effect. Positron emission tomography (PET) was also carried out on 4 cases except for an asymptomatic case (patient 2, sister of patient 1). Close relationship has been observed by MRI between dystonia and the lesion of the lenticular nuclei, abnormality of smooth pursuit eye movements and the brain stem lesion, and severe dysarthria/dysphagia and the lesion of the caudate and lenticular nuclei, respectively. In patient 4, repeated MRI of an interval of 18 months demonstrated decrease of the abnormal high signal in the lateral part of the putamen on T2-weighted image in accordance with marked improvement of clinical manifestations. In patient 3, who had severe dystonia of the extremities and trunk, T2-weighted image showed high signals in the lenticular nuclei. Marked decrease of the high signal in the lenticular nuclei was observed by MRI in this patient after 29 months, when her neurological manifestations were markedly improved. Patient 5 with severe cerebellar signs disclosed abnormal signals in the middle cerebellar peduncles, brain stem and dentate nuclei in addition to low signals in the caudate and lenticular nuclei, and high signals in the lateral part of the putamen on T2-sequence.(ABSTRACT TRUNCATED AT 250 WORDS)     

Wernicke's encephalopathy associated with chronic disulfiram intoxication

INTRODUCTION: We report the case of a patient with an unusual association of Wernicke encephalopathy and chronic disulfiram intoxication. CASE REPORT: A 41-year-old man presented with progressive frontal decline and akineto-rigid parkinsonism under chronic disulfiram therapy. He also developed acute confusion with ataxia, blepharospasm, and supranuclear ophthalmoplegia following a severe malnutrition due to refusal of food intake. Brain MRI revealed symmetrical and reversible hyperintense lesions on T2 and FLAIR in the posterior putaminal regions, dorso-medial thalamic and subthalamic nuclei, the periaqueducal gray matter, the cerebellar peduncles, and the pontine tegmentum. A slow partial clinical recovery with persistent frontal syndrome was observed after discontinuation of disulfiram and parenteral administration of thiamine. DISCUSSION: The symmetry and reversibility of the MRI lesions in the basal ganglia and brain stem were suggestive of a deficiency, a toxic or a metabolic neurological disease. The dorso-medial thalamo-subthalamic and brainstem localizations, as well as their occurrence in a state of malnutrition, were consistent with Wernicke encephalopathy. Moreover, chronic disulfiram intoxication might explain the frontal syndrome and the akineto-rigid parkinsonism, associated with MRI putaminal lesions. Similar MRI lesions have been described in the so-called "energy deprivation syndromes", which are toxic, genetic or nutritional disorders that disrupt enzymes involved in energy generating metabolic pathways such as glycolysis and pyruvate oxidation.     

可逆性后部白质脑病综合征的临床及影像学特点

目的 探讨可逆性后部白质脑病综合征（PRES）的临床和影像学特点。方法 回顾性分析7例PRES患者临床及影像学资料。结果 本组继发于妊娠高血压综合征3例,肾功能衰竭3例,高血压1例。临床表现：7例均有头痛及视物模糊,伴有癫痫发作6例,恶心、呕吐4例,轻偏瘫、共济失调各1例。6例行头颅CT检查,3例枕叶低密度影,其中2例广泛脑白质水肿;1例多发小血肿;2例未发现异常。7例MRI检查显示枕叶均受累,同时伴小脑受累3例,脑干2例,额顶叶皮质下白质2例,尾状核、丘脑各1例。在脑叶呈脑回样、在其他部位呈斑片样异常信号;T1WI呈略低或等信号,T2WI和Fair像呈高信号。2例增强扫描1例无强化,1例呈脑回样、斑片样和环状强化。4例DWI扫描,2例呈略高信号,1例呈低信号,1例未见异常。结论 头痛、视觉障碍和癫痫发作是PRES主要临床表现,影像学特征主要为大脑后部白质对称性长T1、长T2信号。