一氧化碳中毒迟发性脑病的MRI表现

目的:研究一氧化碳(CO)中毒迟发性脑病的MRI特征.方法:回顾性分析32例CO中毒迟发性脑病患者的MRI和临床资料.结果:CO中毒迟发性脑病MRI表现可分为三型:①神经核团受累型;②脑白质受累型;③皮层受累型.MRI特征:苍白球为对称性的卵圆形长T1、长T2信号,皮层下白质为对称性的弥漫、模糊云雾状长T1、长T2信号,侧脑室周围、半卵圆中心白质亦为对称云絮状长T1、长T2信号,胼胝体常受累.MRI显示苍白球合并脑白质受累者及皮层受累者,临床表现较重.结论:CO中毒迟发性脑病MRI表现有一定特征性,且能反应其病理过程,并对CO中毒迟发性脑病的诊断和评价临床表现、预后均有意义.     

急性CO中毒迟发性脑病的MRI表现

目的：探讨急性CO中毒迟发性脑病（DEACMP）的MRI特征。方法：回顾性分析21例急性CO中毒迟发性脑病患者的MRI和临床资料。结果：急性CO中毒迟发性脑病MRI表现可分为3种：①神经核团受累：21例,典型表现为双侧苍白球对称性的长T1、长T2信号;②脑白质受累：11例,表现为双侧大脑半球白质对称云絮状长T1、长T2信号,胼胝体常受累;③皮层受累：6例,表现为双侧大脑半球皮层对称性弥漫长T1、长T2信号。结论：急性CO中毒迟发性脑病MRI表现有一定特征性,MRI对急性CO中毒迟发性脑病的诊断、鉴别诊断、判断预后具有重要价值。     

有机磷中毒性脑病恢复期MRI表现(附4例报告)

目的:探讨有机磷中毒性脑病恢复期的MRI特征.方法:回顾性分析4例重度有机磷中毒慢性期脑结构变化.结果:双侧巴宾斯基征阳性4例,脑电图轻度异常4例.1例右侧小脑半球和中脑长T1长T2信号.1例双侧尾状核和壳核对称性长T2信号,T1WI高信号.1例双侧尾状核、壳核和苍白球对称性长T1长T2信号,侧脑室扩大,小脑萎缩.1例双侧尾状核、壳核和苍白球对称性异常信号,T1WI部分萎缩的小脑回呈高信号;脑室扩大,双侧枕叶内侧回、脑干和小脑萎缩.结论:有机磷中毒性脑病恢复期MRI表现主要累及尾状核、苍白球、丘脑、中脑和小脑;严重者皮质出现软化灶,伴有脑萎缩.     

放射性脑损伤的MRI分析

目的：分析放射性脑损伤的MRI表现及MRI诊断的意义。方法：回顾性分析25例放射性脑损伤患者的MRI资料,观察并比较病变的部位、范围及增强表现。结果：急性放射性脑损伤1例,深部脑白质及胼胝体压部对称性长T2信号,脑白质和胼胝体压部肿胀,增强扫描无强化;早期迟发性放射性脑损伤18例,深部脑白质对称性长T2信号,增强扫描无强化;晚期迟发性放射性脑损伤6例,双侧颞叶不均匀长T1长T2信号,增强扫描呈明显花环样强化。结论：放射性脑损伤具有特征性MRI表现,MRI对诊断放射性脑损伤具有重要价值。     

新生儿急性胆红素脑病的低场磁共振表现

目的 探讨急性胆红素脑病在低场磁共振的MRI表现.方法回顾分析15例急性胆红素脑病患儿的头颅MRI图像,同期的8例正常新生儿头颅MRI作对照.结果 15例急性胆红素脑病中,10例双侧苍白球T1WI呈对称性高信号,T2WI呈正常的稍高信号,其余5例未见明显异常.结论 低场MRI可较好地显示高胆红素血症对基底节苍白球的损伤,双侧苍白球T1WI对称性高信号是新生儿急性胆红素脑病的重要特征.     

低场强MRI对急性CO中毒脑损伤的诊断价值

目的探讨低场强MRI在急性CO中毒脑损伤诊断中的价值。方法回顾性分析29例经临床确诊的急性CO中毒脑损伤患者的颅脑MRI和临床资料。结果CO中毒脑损伤的MRI表现主要为双侧大脑半球白质及苍白球出现长T1、长T2信号灶,两侧对称。MRI表现可分3型,即脑白质型、苍白球型及脑混合型。结论MRI检查可确定急性CO中毒脑损伤的程度及范围,对急性CO中毒脑损伤的治疗和判断预后有重要的临床指导价值。     

磁共振弥散加权成像对急性一氧化碳中毒的诊断价值

目的 :评价磁共振弥散加权成像对急性一氧化碳中毒的诊断价值。方法 :回顾性分析 6例急性一氧化碳中毒的MRI表现 ,分别采用SE序列T1WI、T2 WI、FLAIR和DWI。结果 :急性一氧化碳中毒MRI表现为两侧大脑皮层、皮层下区及苍白球T1WI等信号、T2 WI高信号 ,所有异常信号均呈两侧对称性改变。结论 :磁共振弥散加权成像对急性一氧化碳中毒具有重要诊断价值。     

急性一氧化碳中毒脑损伤的磁共振扩散张量成像

目的：利用磁共振扩散张量成像(DTI )评估急性一氧化碳(CO)中毒患者的脑结构损伤情况。方法25例急性(5.0 d±1.44 d) CO 中毒患者和37例性别、年龄、利手、受教育程度匹配的健康志愿者进行 DTI 扫描,获得扩散张量纤维束成像(DTT)图像,并分别测量双侧小脑半球(齿状核)、黑质、海马、额叶白质(侧脑室前角前下方、侧脑室体部上方)、尾状核头、苍白球、丘脑、内囊前肢、内囊后肢、枕叶白质(视中枢)、顶叶白质(侧脑室体部上方)及胼胝体膝部、压部共26个感兴趣(ROI)的各向异性分数(FA)值和表观扩散系数(ADC)值,进行组间配对 t 检验。结果病患组双侧苍白球、双侧内囊前肢、双侧黑质、右侧小脑、左侧额叶下部白质、右额叶上下部白质、胼胝体膝部的 FA 值显著低于对照组(P <0.05)。病患组右侧黑质、左侧苍白球的 ADC 值显著降低(P <0.05),病患组右额叶上下部白质及双侧枕叶白质 ADC 值显著升高(P <0.05)。结论急性 CO 中毒患者广泛脑微结构受损,提示脑微结构的原发损伤可能是 CO 中毒迟发性脑病潜在的病理生理基础。     

非酒精性Wernicke脑病的MRI表现

目的探讨非酒精性Wernicke脑病的MRI特点,以提高对该种脑病的认识。方法回顾性分析5例非酒精性Wernicke脑病的MRI表现。结果 5例非酒精性Wernicke脑病中,3例显示为导水管周围、四叠体、第三脑室旁、双侧丘脑对称性稍长T1长T2信号,FLAIR、DWI呈高信号;1例显示为双侧丘脑、侧脑室旁、脑桥被盖对称性稍长T1长T2信号,脑沟旁大脑皮质等T1长T2信号,FLAIR、DWI呈均为高信号,1个半月后头颅MRI复查,两侧丘脑略增大,FLAIR序列见少许对称性稍高信号改变;1例T1WI、T2WI、FLAIR未发现异常,DWI序列显示四叠体边缘少许高信号。结论非酒精性Wernicke脑病具有典型的MRI表现,对临床诊断及治疗有重要意义。     

颅内真菌感染合并室管膜炎1例

患者 男,44岁.因头痛、呕吐于2006-04-08行MRI检查未见异常.21 d后因头痛加重,伴持续低热再次行MRI检查见左侧侧脑室前、后角旁白质内有斑片样长T1长T2信号影,右侧侧脑室内于体中部出现细条样等T1长T2信号病变;FLAIR像上病灶均呈高信号;DWI左侧侧脑室后角旁病灶信号不增高,另两处病灶信号增高.     

表观扩散系数值对急性一氧化碳中毒后迟发性脑病的诊断价值

目的 探讨ADC值对急性CO中毒后迟发性脑病(DEACMP)的诊断价值.方法 回顾件分析经临床确诊的32例DEACMP患者的临床和MR资料,同时选取头颅MRI表现正常的健康志愿者40名作为正常对照组.所有受试者均进行常规MR扫描及DWI,分别对称性测量苍白球、白质(侧脑室周围白质、半卵圆中心)、皮层(额叶、顶叶)的平均ADC值(ADCav).32例DEACMP患者根据常规MRI上有无异常信号分为有异常信号DEACMP组(20例)、无异常信号DEACMP组(12例),所有患者跟踪随访1年以上,13例患者无明显症状,3例偶有轻微头痛、头晕(预后较好组);15例有智能障碍、精神异常,1例反应迟钝、生活不能自理、大小便失禁(预后不良组).DEACMP组与正常对照组、异常信号与无异常信号DEACMP组、无异常信号DEACMP组与正常对照组、预后较好组与预后不良组间各个部位ADC值的比较采用独立样本t检验.结果 32例DEACMP患者20例有异常影像表现.MRI表现可分为3个类型:(1)脑白质受累型;(2)神经核团受累型;(3)皮层受累型.12例常规MRI上无肉眼所见异常信号.32例DEACMP患者ADCav值均下降,ADCav值[侧脑室周围白质(0.62±0.06)×10~(-3) mm~2/s、苍白球(0.67±0.05)×10~(-3)mm~2/s、半卵圆中心(0.57±0.07)×10~(-3)mm~2/s]较正常对照组[(0.74±0.03)×10~(-3)、(0.74±0.04)×10~(-3)、(0.73±0.05)×10~(-3)mm~2/s]降低(t值分别为2.82、2.89、2.98,P值均＜0.01);有异常信号DEACMP组的ADCav值[侧脑室周围白质(0.58±0.08)×10~(-3)mm~2/s、半卵圆中心(0.52±0.09)×10~(-3)mm~2/s]与无异常信号DEACMP组[(0.66±0.05)×10(-3)、(0.62±0.06)×10(-3)mm~2/s]比较,差异有统计学意义(t值分别为4.45、3.98,P值均＜0.01);无异常信号DEACMP组ADCav值[侧脑室周围白质(0.66±0.05)×10~(-3) mm~2/s,半卵圆中心(0.62±0.06)×10(-3) mm~2/s]与正常对照组[(0.74±0.03)×10(-3)、(0.73±0.05)×10~(-3)mm~2/s]比较,差异有统计学意义(t值分别为2.45、3.72,P值均＜0.05).预后不良组ADCav值[侧脑室周围白质(0.56±0.02)×10~(-3)mm~2/s、半卵圆中心(0.50±0.06)×10~(-3)mm~2/s]与预后较好组[(0.63±0.04)×10~(-3)、(0.58±0.05)×10~(-3) mm~2/s]比较,差异有统计学意义(t值分别为6.19、4.12,P值均＜0.01).结论 白质区(尤其是半卵圆中心)ADC值降低对DEACMP诊断具有重要价值,对常规MRI有异常信号的DEACMP患者,定量ADCav值可以量化中毒程度,作为DEACMP的发生、发展及预后评估的参考;对有临床症状而常规MRI上无异常信号患者,ADC值是诊断DEACMP较敏感指标.     

Delayed encephalopathy after acute carbon monoxide intoxication: MR imaging features and distribution of cerebral white matter lesions.

Magnetic resonance (MR) images obtained in 15 patients with delayed encephalopathy after acute carbon monoxide (CO) intoxication were reviewed. Images had been obtained 4-9 weeks after exposure to CO, during the relapse of neuropsychiatric symptoms after initial recovery. Bilateral symmetric confluent high signal intensity in the periventricular white matter and centrum semiovale was seen on long-repetition-time images (n = 15). The high intensity extended into the corpus callosum (n = 11), subcortical U fibers (n = 12), and external (n = 9) and internal (n = 7) capsules. Bilateral diffuse low-intensity signal in the thalamus and putamen on T2-weighted images, suggesting iron deposition, was demonstrated in 10 patients. Bilateral ischemia or necrosis of the globus pallidus was seen in nine patients. In three of four patients with follow-up MR imaging studies, a decrease in extent and signal intensity of white matter lesions accompanied lessening of clinical symptoms. These results suggest that the main pathologic feature of delayed encephalopathy associated with CO intoxication is a reversible demyelinating process of the cerebral white matter.     

Marchiafava—Bignami病的影像学诊断（附4例报告及文献复习）

目的探讨Marchiafava—Bignami病（MBD）的CT和MRI表现特征。方法回顾性分析4例MBD的CT和MRI表现,总结其影像学特征。结果急性型2例,CT表现为苍白球密度降低,MR表现为胼胝体呈长T1、较长T2信号改变,DWI弥散受限;亚急性2例,胼胝体中层呈夹层状表现,MR呈长T1、长T2信号改变,1例增强后有边缘性轻度强化。4例均有双侧对称性侧脑室周围白质和半卯圆中心变性表现,局部有坏死。结论根据胼胝体及其伴随的双侧大脑半球白质和苍白球等部位的变性、坏死等影像表现,MBD可以得到明确诊断。     

急性一氧化碳中毒的颅脑CT观察(附100例分析)

分析了100例急性一氧化碳中毒及迟发脑病患者的颅脑CT改变。在未出现迟发脑病68例(A组)及出现迟发脑病的32例(B组)中,各有28例发现颅脑CT异常,异常率分别为41.2％、87.5％。两组CT异常主要表现为双侧大脑皮层下白质及苍白球或内囊大致对称的密度减低区,后期出现脑室扩大或脑沟增宽。对CT改变与病理特点、昏迷时间、检查时间,以及与神经系统症状体征间的关系进行了分析与讨论,指出颅脑CT对重度急性CO中毒及迟发脑病具有辅助定位诊断与鉴别诊断、判断病情及预后的作用。     

亚急性1,2-二氯乙烷中毒性脑病的CT、MR表现

目的:探讨1,2-二氯乙烷中毒性脑病的CT、MR表现.方法:回顾性分析5例经临床证实的1,2-二氯乙烷中毒性脑病的CT和MR资料,CT检查5例,MR检查3例.结果:CT检查病灶表现为低密度,两侧对称.5例均广泛累及两侧大脑半球白质(累及皮层下弓形纤维为主).累及两侧齿状核4例,丘脑、苍白球受累各3例.3例MRI均表现为上述部位广泛性T1WI低信号,T2WI高信号.CT、MRI都显示脑回肿胀,脑室系统受压变小.结论:1,2-二氯乙烷中毒性脑病具有较典型的CT、MRI特征,结合毒物接触史可明确诊断.     

Brain MR imaging in patients with hepatic cirrhosis: relationship between high intensity signal in basal ganglia on T1-weighted images and elemental concentrations in brain

In patients with hepatic cirrhosis, the globus pallidus and putamen show high intensity on T1-weighted MRI. While the causes of this high signal have been thought to include paramagnetic substances, especially manganese, no evidence for this has been presented. Autopsy in four cases of hepatic cirrhosis permitted measurement of metal concentrations in brain and histopathological examination. In three cases the globus pallidus showed high intensity on T1-weighted images. Mean manganese concentrations in globus pallidus, putamen and frontal white matter were 3.03 ± 0.38, 2.12 ± 0.37, and 1.38 ± 0.24 (μg/g wet weight), respectively, being approximately four- to almost ten-fold the normal values. Copper concentrations in globus pallidus and putamen were also high, 50 % more than normal. Calcium, iron, zinc and magnesium concentrations were all normal. The fourth case showed no abnormal intensity in the basal ganglia and brain metal concentrations were all normal. Histopathologically, cases with showing high signal remarkable atrophy, necrosis, and deciduation of nerve cells and proliferation of glial cells and microglia in globus pallidus. These findings were similar to those in chronic manganese poisoning. On T1-weighted images, copper deposition shows no abnormal intensity. It is therefore inferred that deposition of highly concentrations of manganese may caused high signal on T1-weighted images and nerve cell death in the globus pallidus. Received: 12 August 1996 Accepted: 17 December 1996     

Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions

BACKGROUND AND PURPOSE: Carbon monoxide intoxication has delayed effects on the cerebral white matter characterized by bilateral, confluent lesions that reflect diffuse demyelination. To increase our understanding of this process, we assessed the diffusion characteristics of these lesions. METHODS: Five consecutive patients with delayed encephalopathy of CO intoxication were examined with diffusion MR imaging. Diffusion-weighted images (DWIs) were obtained 25-95 days after their exposure to CO and during a relapse of neuropsychiatric symptoms, which occurred after an initial recovery. Imaging was performed at 1.5 T by using a spin-echo echo-planar sequence with diffusion gradients of 0, 500, and 1000 s/mm(2). DWIs and apparent diffusion coefficient (ADC) maps were visually evaluated, and mean ADCs were calculated from the periventricular white matter and the centrum semiovale, where confluent hyperintensity was seen on T2-weighted images. Findings were compared with those of normal-looking white matter. RESULTS: In all five patients, both T2-weighted images and DWIs showed the white matter lesions as bilateral, diffuse, confluent areas of hyperintensity in the periventricular white matter and centrum semiovale. On ADC maps, these lesions were isointense, with focal areas of hypointensity (n = 4) or diffuse hypointensity (n = 1). Mean ADC values of the white matter lesions were significantly lower than those of normal-looking white matter, regardless of their isointensity or hypointensity on ADC maps (P <.05). CONCLUSION: Bilateral, confluent, white matter lesions in patients with delayed encephalopathy of CO intoxication show decreased diffusivity.