非脑膜瘤所致脑膜异常强化的MRI研究

目的分析不同脑膜病变(不包括脑膜瘤导致的脑膜改变)MRI表现,探讨MRI对不同病因所致脑膜异常强化的诊断及鉴别诊断。方法资料完整的脑膜病变28例,MRI常规扫描后均加增强扫描(Gd-DTPA0.1mmol/kg)。对显示脑膜异常强化的病例进行回顾性分析。结果有7例MRI平扫显示脑膜有异常表现,增强扫描28例均有异常表现。按脑膜主要异常强化方式可以分为:硬脑膜-蛛网膜强化10例,软脑膜-蛛网膜强化15例,全脑膜强化3例。按病因不同分为:感染性脑膜炎8例,脑膜转移瘤12例,脑梗死2例,开颅术6例。结论不同脑膜病变MRI上表现形式不同,特别是MRI增强扫描。MRI检查有助于明确脑膜病变。全面分析MRI表现并结合临床对鉴别不同病因的脑膜病变具有重要作用。     

增强FLAIR成像在诊断软脑膜转移中的价值及临床意义

目的 探讨增强FLAIR在软脑膜转移诊断中的价值.方法 收集有明确原发肿瘤病史、经临床和实验室检查证实的软脑膜转移癌23例,其中7例仅行T1WI增强,16例同时行T1WI和FLAIR增强.对2组病例的MR诊断准确率,以及两序列对病灶的显示情况进行回顾性对照分析.结果 (1)单纯T1WI增强组病例中2例漏诊,1例提示性诊断;同时行T1WI及FLAIR增强组16例诊断均与临床最终诊断相符.(2)后组病例中11例显示细线样强化及7例显示小结节样强化在增强FLAIR上更明显,但粗线样强化两序列上显示相似;4例在增强FLAIR上显示病变范围更广;在相同病变部位上,增强FLAIR强化程度高于增强T1WI.结论 增强FLAIR在软脑膜转移的诊断中具有重要价值.     

非脑膜瘤脑膜病变的MRI表现及强化模式

目的 分析不同脑膜病变的MR成像表现，探讨MRI尤其是脑膜强化模式对各种脑膜病变的诊断及鉴别诊断价值。方法 临床资料完整的脑膜病变61例，其中感染性脑膜炎27例；非感染性脑膜炎4例，包括嗜酸性肉芽肿2例，wegener肉芽肿l例，病因不明l例；脑膜转移瘤12例；脑膜淋巴瘤2例；脑梗死8例；手术后脑膜改变8例。MR常规扫描后均行钆喷替酸葡甲胺(Gd-DTPA)增强扫描。结果 (1)MR平扫：异常脑膜改变仅3例，其中脑膜增厚l例，脑膜结节2例。(2)MR增强扫描：61例呈3种脑膜强化模式，分别为I型、Ⅱ型、Ⅲ型强化模式。I型强化模式即硬脑膜-蛛网膜强化，有19例；Ⅱ型强化模式即蛛网膜-软脑膜强化，有32例；Ⅲ型强化模式即全脑膜强化(包括硬脑膜及软脑膜)，有10例。结论 不同脑膜病变MR成像表现尤其是增强模式有一定特点。各种脑膜病变增强模式对于鉴别各种脑膜病变，发现病变细节，提示临床诊疗均有明显意义。     

恶性肿瘤脑膜转移的MRI表现及强化模式

目的：分析系统性恶性肿瘤脑膜转移的MRI表现，探讨脑膜强化对脑膜转移的诊断及鉴别诊断价值。方法：根据临床恶性肿瘤病史、脑脊液及病理检查确诊的脑膜转移瘤12例，其中原发肿瘤肺癌5例，乳腺癌3例，黑色素瘤1例，淋巴瘤2例，原发肿瘤不明1例。MR常规扫描后均行钆喷替酸葡甲胺(Gd—DTPA)增强扫描。结果：①MR平扫：异常脑膜改变仅2例，表现为沿软脑膜分布的多发结节；②MR增强扫描：12例呈3种脑膜强化模式，硬脑膜强化模式(硬脑膜～蛛网膜强化)3例，软脑膜强化模式(蛛网膜下腔一软脑膜强化)6例，全脑膜强化模式(硬脑膜、蛛网膜及软脑膜均强化)3例，其中2例表现为沿软脑膜分布的多发结节，10例表现为线样弥漫性脑膜强化；③其它征象：脑内转移3例，脑积水3例。结论：恶性肿瘤脑膜转移在MR增强扫描上可以表现为3种脑膜强化模式，其中软脑膜强化模式多见，结节性脑膜强化及脑内转移具有特异性。     

不同途径脑膜转移瘤的MRI分析

目的 回顾性分析经手术及病理证实的59例不同途径脑膜转移瘤的MRI表现及诊断作用。方法 59例病人,男42例,女17例;年龄17－65岁。其中血源性脑膜转移24例,邻近肿瘤直接侵犯脑膜29例,颅内肿瘤经脑 脊液播散6例,59例脑膜转移均经平扫及注射钆喷替酸葡甲胺（Gd-DTPA）后扫描。结果 血源性脑膜转移主要表现为硬脑膜－蛛网膜或脑膜－蛛网膜的增厚或结节,肿瘤直接侵犯脑膜均表现为肿瘤向远 端延伸的由粗变细的类似“靶征”或“鼠尾征”,经脑脊液播散的脑膜转移均为沿脑蛛网膜下腔或室管膜下大小不等的结节灶。MRI平扫阳性：结节型12例,线状增厚型11例,混合型6例。增强扫描均有较明显的强化。结论 MRI是检出脑转移的重要方法,疑有脑膜转移时应行增强MRI扫描。     

不同病因致脑膜异常强化的MRI分析

目的：分析不同脑膜病变的MRI表现，探讨MRI对不同病因所致脑膜异常强化的诊断价值。资料与方法：对58例MR增强扫描显示脑膜异常强化的病例进行回顾性分析。结果：按脑膜强化方式分为：硬脑膜－蛛网膜强化21例，软脑膜－蛛网膜下腔强化37例。按病因不同分：感染性脑膜炎16例，脑梗死21例，脑膜癌病12例，硬膜下积液或血肿5例，开颅术后4例。结论：MRI增强扫描有助于显示脑膜病变，全面分析MRI表现及结合临床对鉴别不同病因的脑膜病变具有重要作用。     

脑型血吸虫病MRI表现临床分析

目的探讨脑型血吸虫病的MRI表现及特征。方法分析7例经手术病理证实的脑型血吸虫病的MRI表现。患者行T1WI、T2WI、Flair、T1WI、DWI、SWI、MRS及增强扫描。结果单发结节型1例,多发结节型4例,环状强化结节型1例,脑炎型和脑梗塞型各1例。脑炎型MRI表现为脑组织肿胀,脑沟裂池广泛变窄,增强扫描脑膜明显强化。其余4型病变增强扫描呈结节状、成蔟状、斑片状、条状及环状强化,邻近脑膜明显强化,DWI不受限。病变周围水肿明显而占位效应轻,与水肿一起形成"佛手"征或"握球"征。结论 MRI能较清晰的显示脑型血吸虫病的影像特征,MRI增强及DWI序列扫描对脑型血吸虫诊断至关重要。     

颅内结核的MRI诊断

目的:通过分析26例颅内结核的MRI表现,探讨MRI在脑结核影像学诊断中的应用价值。方法:回顾性分析26例脑结核的MRI特征并进行分类,总结不同种类颅内结核的MRI特点。全部病例均获取IR-TSE序列T1WI、TSE序列T2WI及FlAIR图像,对比剂使用Gd-DTPA。结果:14例脑膜炎、结核瘤与脑炎同时存在,2例脑膜炎与结核瘤同时存在,6例结核瘤与脑炎同时存在。结核性脑膜炎主要发生于基底池脑膜(18处)、软脑膜(42处)、室管膜(4处)。结核瘤可发生于脑实质(54处)、基底池脑膜(20处)、软脑膜(40处)、室管膜(4处),亦可呈粟粒样弥漫性分布。结核性脑炎表现为脑实质水肿(39处)。结论:MRI诊断脑结核具有特征性表现,可以为临床颅内结核的诊断及治疗提供有力参考。     

血源性脑膜转移瘤MRI诊断价值

目的　探讨MRI对血源性脑膜转移瘤的诊断价值。方法　回顾性分析 48例血源性脑膜转移瘤的平扫及注射钆喷替酸葡甲胺 (Gd DTPA)后的MRI表现。结果　 48例共发现病灶 12 5灶。结节型 2 2例 ,线状增厚型 6例 ,混合型 2 0例。增强扫描均有较明显的强化。合并脑内转移 36例。结论　MRI是诊断血源性脑膜转移瘤的首选影像检查方法 ,疑有血源性脑膜转移瘤时应行增强MRI扫描     

隐球菌性脑膜脑炎的CT和MRI表现

目的:探讨CT和MRI在隐球菌性脑膜脑炎诊断中的应用.方法:回顾性分析通过脑脊液墨汁染色或培养证实的隐球菌性脑膜脑炎21例,其中男13例,女8例,年龄8～53岁,主要症状有头痛、恶心、呕吐、发热.21例患者中6例同时行头颅CT和MRI检查,6例仅行MRI检查,9例仅行CT检查.结果:21例患者20例影像学检查为阳性,主要表现有软脑膜异常强化13例,脑内斑片样损害灶4例,基底节区、半卵圆中心多发点片状异常信号或密度灶5例,脑积水5例.结论:CT及MRI表现能够反映隐球菌性脑膜脑炎的病理学特征,软脑膜强化及伴发的深部脑组织病变是隐脑的常见表现.     

Contrast-enhanced fluid-attenuated inversion recovery imaging for leptomeningeal disease in children

BACKGROUND AND PURPOSE: To develop an MR imaging method that improves detection of leptomeningeal disease when compared with the current reference standard, contrast-enhanced T1-weighted imaging. METHODS: We investigated the cases of 10 children who were at high risk of intracranial leptomeningeal disease (Sturge-Weber syndrome and medulloblastoma). The cases of Sturge-Weber syndrome were investigated by using one MR imaging examination, and the cases of medulloblastoma were investigated by using four MR imaging examinations performed over 18 months. In all cases, contrast-enhanced fluid-attenuated inversion recovery (FLAIR) images were acquired in addition to the routine sequences. The parameters of the FLAIR sequence were chosen to maximize the T1 component of the signal intensity, to maximize detection of leptomeningeal enhancement. We made subjective and objective assessments of the presence and extent of leptomeningeal disease as shown on contrast-enhanced T1-weighted images and contrast-enhanced FLAIR images. RESULTS: In three of the four cases of Sturge-Weber syndrome, the T1 and FLAIR sequences showed comparable extent of leptomeningeal enhancement. For one child, FLAIR images showed unexpected bilateral disease and more extensive leptomeningeal enhancement on the clinically suspected side. In four of six cases of medulloblastoma, no leptomeningeal enhancement was shown on any examinations during the 18-month period. In two cases, FLAIR images showed more extensive leptomeningeal enhancement when compared with T1-weighted images. CONCLUSION: Contrast-enhanced FLAIR imaging seems to improve detection of leptomeningeal disease when compared with routine contrast-enhanced T1-weighted imaging. This seems to be partly because of suppression of signal intensity from normal vascular structures on the surface of the brain by FLAIR, which allows easier visualization of abnormal leptomeninges. We think that these findings can be extrapolated to the investigation of leptomeningeal disease of all causes and at all ages.     

Choroid plexus size in young children with Sturge-Weber syndrome.

PURPOSETo assess the size of the choroid plexus in young children with unilateral and bilateral Sturge-Weber syndrome.METHODSSubjects included 15 children 4 years old or younger with Sturge-Weber syndrome. Eleven cases were unilateral and four were bilateral. Unilateral or bilateral involvement was determined by the distribution of abnormal leptomeningeal enhancement on MR images. The diameters of the choroid plexus were measured on contrast-enhanced axial MR images. The choroid plexus of the affected and unaffected sides in these cases were compared with those of 15 age-matched children without Sturge-Weber syndrome who were being examined for seizures.RESULTSOur results show a wide variation in the size of the choroid plexus in children with Sturge-Weber syndrome; however, plexus associated with a hemisphere affected by Sturge-Weber syndrome were significantly larger than those on the unaffected side and in the age-matched control group. The size of the choroid plexus was positively correlated with the extent of leptomeningeal involvement as demonstrated by abnormal contrast enhancement.CONCLUSIONThe choroid plexus is enlarged early in the course of Sturge-Weber syndrome in both unilateral and bilateral cases. There is a positive correlation between choroid plexus size and extent of leptomeningeal involvement in children with Sturge-Weber syndrome.     

Subcortical low intensity on MR images of meningitis, viral encephalitis, and leptomeningeal metastasis

BACKGROUND AND PURPOSE: Subcortical low-intensity lesion on T2-weighted images is an uncommon manifestation of ischemia, multiple sclerosis, and Sturge-Weber disease. This study was performed to determine whether subcortical low signal intensity is an MR feature of meningitis, viral encephalitis, or leptomeningeal metastasis and to investigate a cause of subcortical low intensity. METHODS: We retrospectively reviewed MR images of 117 patients with meningitis, encephalitis (viral or unknown), or leptomeningeal metastasis for the presence of subcortical low intensity, meningeal enhancement, signal intensity change of cortex, and change in subcortical low intensity on follow-up images. Diffusion-weighted (DW) images and apparent diffusion coefficient (ADC) maps were obtained in 55 patients. Subcortical low-intensity lesions were also quantitatively analyzed on T2-weighted, fluid-attenuated inversion recovery (FLAIR), and DW images. RESULTS: Subcortical low intensity was found in nine (23.7%) of 38 patients with encephalitis (viral, 31; unknown origin, 7), five (24%) of 21 with leptomeningeal metastasis, and five (9%) of 58 with meningitis. Leptomeningeal enhancement was observed in 100% and cortical hyperintensity in 14 (74%) of 19 patients with subcortical low intensity. Leptomeningeal enhancement was seen in 46 (47%) and cortical hyperintensity in 33 (34%) of 98 patients without subcortical low intensity. Subcortical low intensity disappeared or decreased in extent on follow-up MR images in all seven patients who underwent follow-up. ADC of subcortical low-intensity lesions was lower than that of the contralateral area and decreased by 9.3 +/- 11.4%. CONCLUSION: Subcortical low intensity was uncommonly found in meningitis, viral encephalitis, and leptomeningeal metastasis. It is a nonspecific MR sign of various meningeal and cortical diseases. Although the cause of subcortical low intensity remains uncertain, free radical formation may play a role as a causative factor.     

Diagnosis of Sturge-Weber syndrome: comparison of the efficacy of CT and MR imaging in 14 cases.

Sturge-Weber syndrome is a neurocutaneous syndrome that includes facial and leptomeningeal angiomas. Imaging findings include cerebral lobar atrophy, brain calcifications, choroid plexus enlargement, cranial diplo? prominence, and venous abnormalities. We compared the efficacy of CT and MR imaging in making the diagnosis in 14 consecutive patients. CT, with and without contrast enhancement, was performed in all patients, and 11 of the 14 had MR imaging (eight before and after administration of IV gadopentetate dimeglumine). MR imaging was better than CT in showing the extent and degree of brain parenchymal atrophy, the presumed ischemic changes affecting the gray and white matter, and the cranial diploetic prominence on the affected side. MR imaging after contrast administration permitted a better evaluation of the extent and patency of the leptomeningeal angiomatous malformation and the parenchymal venous anomalies. CT was better than MR imaging in showing the presence and extent of cortical calcifications. Enhanced CT and MR imaging were equal in evaluating the prominence of the ipsilateral choroid plexus. Our experience indicates that contrast-enhanced MR imaging is the method of choice in the diagnosis of Sturge-Weber syndrome. Unenhanced CT should be used only if MR findings are normal, to exclude the presence of intracranial calcifications.     

Abnormal ocular enhancement in Sturge-Weber syndrome: correlation of ocular MR and CT findings with clinical and intracranial imaging findings.

PURPOSETo estimate the prevalence of abnormal ocular enhancement in children with Sturge-Weber syndrome as detected with MR imaging and CT and to correlate this with the clinical, fundoscopic, and intracranial imaging findings.METHODSFifteen children, 4 years old or younger, with Sturge-Weber syndrome were examined with enhanced CT and MR imaging. Eleven children had unilateral intracranial involvement and 4 had bilateral involvement, for a total of 19 abnormal hemispheres and related orbits. The presence of ocular enhancement was compared with the fundoscopic findings independently. Ocular enhancement was correlated with the extent of leptomeningeal disease, the severity of the cutaneous lesion, and the presence of glaucoma by the calculation of likelihood ratios and 95% confidence limits.RESULTSSeven of the 15 patients had abnormal ocular enhancement, which was present in 10 (53%) of the eyes associated with the 19 abnormal hemispheres. MR imaging showed choroidal hemangioma in 7 of 8 patients in whom hemangiomas were shown at fundoscopy. The likelihood of ocular enhancement was increased with the presence of bilateral disease, extensive facial nevi, and glaucoma; there was no significant correlation with the extent of hemispheric involvement.CONCLUSIONBoth enhanced MR imaging and CT can show diffuse choroidal hemangioma in patients with Sturge-Weber syndrome. However, MR imaging is more sensitive and is recommended to aid in the detection of abnormalities with preventable late complications.     

增强FLAIR T2WI诊断脑膜转移瘤的价值

目的:探讨脑膜转移瘤的MRI表现及增强后FLAIR序列T2WI的诊断价值。方法:回顾性分析20例脑膜转移瘤患者的病例资料,其中硬脑膜转移瘤5例,软脑膜转移瘤15例。所有病例行常规MRI平扫及SE T1WI和FLAIR序列T2WI增强扫描并进行对比分析。结果:MRI平扫检出6例,病灶边界均显示不清;MRI增强扫描检出所有病例,SE-T1WI上病变主要表现为脑膜的线状和/或结节状强化,FLAIR T2WI对软脑膜转移瘤病灶范围的显示更清楚,可鉴别强化的血管与病变。结论:MRI增强扫描是诊断脑膜转移瘤的重要检查方法,增强后FLAIR序列T2WI与SE T1WI同时使用,可提高对软脑膜转移瘤的检出率及诊断准确性。     

颅内原发恶性肿瘤柔脑膜转移的MRI诊断

目的：探讨颅内原发恶性肿瘤柔脑膜转移的MR影像学特征,为临床提供早期诊断和治疗依据。方法：搜集33例诊断颅内原发恶性肿瘤柔脑膜转移惠者的MR扫描资料,扫描选用常规自旋回波脉冲序列,10例加扫液体衰减反转恢复脉冲序列,全部病例均行增强扫描。结果：平扫表现为不同范围脑池、脑沟和／或脑室变形、移位,结构模糊,其中28例伴有明显脑回肿胀．合并脑室壁不均匀增厚8例;合并蛛网膜下腔肿瘤结节9例,共发现结节17个,合并脑积水10例,部分病例上述表现合并存在。其中10例另选用液体衰减反转恢复脉冲序列扫描后,转移病灶轮廓显示较常规SE序列清晰,信号略高于TSE—T2WI。瘤体边缘与周围水肿难于分辨。增强扫描后脑内瘤体均明显增强,柔脑膜转移显示呈不同强化特征,8例尾征,14例线征,6例条索征及9例环征或结节征,少部分病例合并两种征象存在。结论：加深对颅内原发恶性肿瘤柔脑膜转移的MR影像特征的认识,选择适当的MR成像技术,提高脑膜病变的早期检出率,对临床选择治疗方案具有十分重要的意义。     

硬脑膜肥厚的MRI诊断及鉴别诊断分析

目的分析硬脑膜肥厚的MRI表现,探讨不同病理情况的影像学特点,以提高定性诊断水平。方法回顾分析36例经手术病理或临床证实的硬脑膜肥厚性疾病例纳入研究,其中男20例,女16例,年龄6～68岁,平均年龄(34±3.5)岁,采用西门子1.5T超导MR成像仪,完成横断面T2WI、T1WI、FLAIR和矢状面T2WI平扫,横断面、冠状面和矢状面T1WI增强及横断面FLAIR增强,2名高级职称影像医师共同回顾性分析MRI表现。结果低颅压综合征10例(27.8%),肥厚性硬脑膜炎10例(27.8%),其中1例为特发性,9例为感染性,硬脑膜转移瘤8例(22.2%),其中合并脑实质内小结节病灶5例,单纯局限性脑膜增厚3例,白血病颅内浸润1例(2.8%),系统性黄斑狼疮1例(2.8%),脑外伤后血肿形成2例(5.6%),脑肿瘤放疗后2例(5.6%),侵袭性脑膜瘤2例(5.6%),上述病例于MRI检查上均表现为硬脑膜弥漫性或局限性增厚。结论硬脑膜增厚疾病种类繁多,但根据病灶所发生的范围和是否伴随软脑膜及脑实质内强化结节等特征,并结合临床表现,多数能做出明确诊断。     

Imaging of Sturge-Weber syndrome: cranial CT and MR findings

Sturge-Weber syndrome (SWS) is a phakomatosis characterized by vascular nevus flammeus, leptomeningeal venous angiomatosis, seizures, dementia, hemiplegia, hemianopsia, and glaucoma. Various imaging findings (gyriform calcification, atrophy of the ipsilateral hemisphere, leptomeningeal enhancement, ipsilateral choroid plexus enlargement, thickened calvarium, enlargement of paranasal sinuses and mastoid air cells, enlargement of deep veins, and white matter change adjacent to leptomeningeal enhancement) are seen in SWS. We examined the efficacy of CT and MR imaging in making the diagnosis in 14 patients. All patients underwent CT and MRI, and 11 of 14 patients underwent contrast-enhanced MRI. The most specific finding was leptomeningeal enhancement. Gyriform calcification, atrophy of the ipsilateral hemisphere, and ipsilateral chroid plexus enlargement were seen at high frequencies. Thickened calvarium was more frequent in adult patients. Enlargement of paranasal sinuses and mastoid air cells, enlargement of deep veins, and white matter change adjacent to leptomeningeal enhancement were seen in some (3-5) patients. A combination of findings of plain CT and MRI (including postcontrast MRI and MR venography) are useful for diagnosing SWS.