肥大性下橄榄核变性的MRI表现

目的 总结肥大性下橄榄核变性(hypertrophic olivary degeneration，HOD)的MRI特征.方法 搜集继发于脑干和小脑病变的HOD病例15例，原发病变位于脑干9例，其中血管畸形出血4例，高血压脑干出血2例，梗死2例，脑干挫伤1例；原发病变位于小脑6例，其中小脑半球出血4例，小脑第4脑室肿瘤术后1例，小脑转移瘤1例。15例均做了MR平扫，2例做了增强扫描。结果 HOD表现为延髓腹外侧局部体积稍增大(共6例)，T1WI表现为等或稍低信号(15例)，在T2WI为高信号(15例)。原发性病变导致中脑红核或桥脑被盖束受损者，发生同侧HOD(8例)；原发病变导致小脑齿状核受损者并引起对侧HOD(4例)，双侧中央被盖束受损(1例)或双侧小脑齿状核受累及者(2例)，发生双侧HOD。结论 MRI能非常清晰地显示下橄榄核的继发性变性病变，可以提高对该变性的认识，避免误诊的发生.     

肥大性下橄榄核变性的MRI诊断

目的 分析肥大性下橄榄核变性（hypertrophic olivary degeneration,HOD）的MRI特征,提高对该病的认识.方法 回顾性分析6例HOD的MRI表现以及导致该病产生的病因,这些病例多继发于脑干或小脑病变.结果 影像学表现为延髓腹外侧局部肿胀,T1WI呈等或稍低信号,T2WI及T2-Flair均表现为高信号.结论 MRI能够显示出下橄榄核的这一特异性的退变,是诊断HOD的最佳方法.     

桥脑出血或梗死继发双侧小脑中脚Wallerian变性及肥大性下橄榄核变性的MR浅析(附5例报告)

目的探讨继发于桥脑出血或梗死并同时继发双侧小脑中脚Wallerian变性(WD)及肥大性下橄榄核变性(HOD)的发病机制、MRI特征及其与原发病灶关系,以期提高对该病的认识。方法回顾性分析5例继发于桥脑出血或梗死同时继发双侧小脑中脚WD及HOD的MRI表现,同时根据MRI表现和解剖结合文献对其进行分析。5例均行MRI常规序列和DWI、SWI或T2*WI序列扫描。结果 5例中3例桥脑基底部背侧出血,均继发双侧HOD及双侧小脑中脚WD。1例桥脑右背侧出血继发右侧HOD及双侧小脑中脚WD,1例桥脑左背侧梗死继发左侧HOD及双侧小脑中脚WD。HOD表现为单侧或双侧下橄榄核体积增大,T1WI呈等或稍低信号,T2WI呈稍高或高信号,FLAIR呈等或稍高信号,DWI呈等或稍高信号,ADC图呈等或稍高信号,SWI或T2*WI呈等或稍高信号,其对原发出血病灶显示最好。双侧小脑中脚WD早期表现为对称性DWI图高信号,ADC图低信号,T2WI稍高信号,T1等信号;中后期表现为DWI图等或稍低信号,ADC图稍高信号,T1WI稍低信号,T2WI稍高信号。结论肥大性下橄榄核变性多继发于桥脑背盖部病变,并且有特定的发病部位和较为特征的MRI表现;双侧小脑中脚对称性异常信号不难发现,但当同时存在桥脑出血或梗死、HOD及双侧小脑中脚对称性异常信号时要考虑到是桥脑出血或梗死同时继发HOD及双侧小脑中脚的WD,而不要盲目的把它们误认定为是三个原发孤立病变。     

12例继发于桥脑出血的肥大性下橄榄核变性的MRI表现

目的 探讨桥脑出血继发肥大性下橄榄核变性(HOD)的MRI表现.方法 回顾性分析12例桥脑出血后继发HOD的MRI表现,12例均行MRI常规序列和扩散加权成像(DWI)、磁敏感加权成像(SWI)或梯度回波(T2*WI)序列扫描,2例行扩散张量成像(DTI)扫描.结果 MRI表现为同侧或双侧下橄榄核体积增大或无明显变化,T1WI呈等或稍低信号,T2WI呈稍高或高信号,液体衰减反转恢复序列(FLAIR)呈等或稍高信号,DWI呈等或稍高信号,ADC图呈等或稍高信号,SWI或T2*WI呈等或稍高信号,其对原发出血病灶显示最好,DTI示病变侧纤维束稀少,3例并发双侧桥臂变性.结论 HOD多继发于桥脑背盖部出血,有特定的发病部位和较为特征的MRI表现,结合其原发病变可对HOD作出正确诊断.     

肥大性下橄榄核变性的MRI表现

目的:探讨肥大性下橄榄核变性(HOD)的MRI表现特征.方法:回顾性分析14例HOD患者的临床及影像学资料.14例均行常规磁共振平扫(T1WI、T2WI、T2FLAIR),8例行DWI检查,2例行扩散张量纤维束成像(DTT)检查.结果:14例HOD中6例为单侧(左侧5例,右侧1侧)发病,8例为双侧发病.12例原发病变为桥脑出血,1例为单侧小脑梗死,1例为双侧小脑萎缩.MRI表现为下橄榄核T2WI呈高或稍高信号,T1WI呈等或稍低信号,DWI呈等信号.7例下橄榄核存在不同程度的肿胀、肥大.1例DTT示患侧神经纤维束减少.结论:HOD多继发于齿状核-红核-下橄榄核环路病变,有特定的发病部位和较为特征性的MRI表现,结合其原发病变可对HOD作出正确诊断.     

肥大性下橄榄核变性的MRI浅析

目的 探讨肥大性下橄榄核变性(HOD)的MRI特征与临床表现,以期提高对该病的认识.方法 回顾性分析16例HOD患者的MRI表现,原发病变为脑干出血6例,脑干梗死3例,脑干挫裂伤1例,脑干脑炎1例,小脑出血4例,小脑肿瘤1例.16例均行T1WI、T2WI、FLAIR序列扫描,其中10例加做扩散加权成像和磁敏感加权成像序列.结果 MRI表现为单侧或双侧下橄榄核体积增大或无明显变化,T1WI呈等或稍低信号,T2WI呈稍高或高信号,FLAIR呈等或稍高信号,扩散加权成像上呈等信号,表观扩散系数图上呈稍高信号,磁敏感加权成像上无异常信号,对出血病灶显示最好.与原发性病变发生同侧HOD 6例,发生对侧HOD 4例,发生双侧HOD 6例.结论 MRI能非常清楚地显示下橄榄核的变性改变,但需结合临床病史、症状与体征才能对HOD做出明确诊断.     

双侧肥大性下橄榄核变性MRI表现及其发生机制(附3例报告并文献复习)

目的 探讨双侧肥大性下橄榄核变性(HOD)的MRI表现及其发生机制.方法 搜集3例双侧HOD患者的MRI与临床资料结合文献进行回顾性分析.结果 3例HOD患者中2例表现为下橄榄核T2WI呈高信号,体积未见异常(发病时间＜6个月).1例下橄榄核体积增大且T2WI呈高信号(发病时间为12个月);临床均出现腭肌阵挛、共济失调等症状;原发病变部分为双侧小脑齿状核、中脑中线处及脑桥被盖部.结论 双侧下橄榄核肥大有特定的原发病变部位,MRI表现因发病时间不同而异.     

肥大性下橄榄核变性的MRI特点分析

目的探讨肥大性下橄榄核变性(hypertrophic of olivary degeneration,HOD)的MRI特点,提高对本病的认识,减少误诊。方法回顾性分析42例HOD的MRI影像特点。结果 42例HOD患者表现为单侧或双侧下橄榄体积增大、正常或萎缩,T2WI及FLAIR序列呈稍高信号,T1WI呈等或稍低信号,DWI及ADC呈等或稍高信号,同时合并有中脑、脑桥被盖部及小脑齿状核的原发病变。结论肥大性下橄榄核变性具有特定的原发病变部位,结合其较为特征性的MRI表现可做出较为准确的诊断。     

继发于小脑病变的肥大性下橄榄核变性的MRI表现

目的　总结继发于小脑病变的肥大性下橄榄核变性 (hypertrophicolivarydegeneration ,HOD)的MR表现 ,提高对该病变的认识。方法　回顾总结 6例继发于小脑病变的肥大性下橄榄核变性的MR表现。结果　 6例病人中 ,原发病变为小脑半球出血 4例 ,小脑肿瘤手术后 1例 ,转移瘤 1例。年龄 40～ 71岁 ,平均 5 3岁 ,男 5例 ,女 1例。原发性病变位于右侧小脑半球 4例 ,累及双侧小脑半球 2例。自原发病变出现到进行MR检查时间为 4周～ 45个月。HOD在MR图像表现为T2 WI高信号 ,T1WI呈等或稍低信号。结论　MR可以清晰显示HOD ,提高对该病变的认识可以避免误诊。     

肥大性下橄榄核变性的 MRI诊断

目的：探讨肥大性下橄榄核变性（ hypertrophic olivary degeneration , HOD）的MRI信号及大小改变特征,以提高对该病的认识和诊断。方法收集继发于脑桥、小脑病变的HOD病例27例,原发病变位于脑桥25例,其中海绵状血管瘤1例,挫裂伤8例,高血压性出血14例,梗死2例;原发病变位于小脑2例,其中小脑挫裂伤1例,小脑出血1例。所有病例均行T1 WI、T2 WI、FLAIR、DWI,8例行SWI检查,分析HOD的信号特点,测量下橄榄核径线。结果 MRI表现为下橄榄核体积增大,T2 WI均呈高信号,14例DWI序列呈等信号,13例DWI序列呈稍高信号,所有病例FLAIR呈稍高信号,10例T1 WI呈等信号,17例T1WI呈稍低信号。病变下橄榄核平均横径为（6．94±0．67）mm,平均前后径为（6．69±0．83）mm,平均纵径为（16．95±1．20）mm,下橄榄核前缘与延髓前缘平均间距为（1．37±0．56）mm。结论 MRI能清晰显示下橄榄核肥大变性,正确认识该病,可避免漏诊及误诊。     

Hypertrophic olivary degeneration following surgical excision of brainstem cavernous hemangioma: a case report

Hypertrophic olivary degeneration (HOD) is a rare type of neuronal degeneration involving the dento-rubo-olivary pathway. It is distinguished from other types of neuronal degeneration in that hypertrophy, rather than atrophy, takes place in the neurons in the inferior olivary nucleus. Prior to the invention of Magnetic Resonance Imaging (MRI), HOD was difficult to be detected, and a firm diagnosis could only be made at autopsy. We present a case of bilateral HOD following surgical excision of a cavernous hemangioma in the brainstem. The literature and imaging findings of this uncommon condition are reviewed.     

Cerebellar MR changes in patients with olivary hypertrophic degeneration.

PURPOSETo describe MR changes in the cerebellar cortex and the dentate nucleus in patients with inferior olivary nucleus hypertrophy.METHODSMR scans of 11 patients with palatal myoclonus were reviewed. Among them, we selected 5 cases that showed lesions in the central tegmental tract and the ipsilateral inferior olivary nucleus. We evaluated MR changes of the cerebellar cortices and dentate nuclei contralateral to the affected inferior olivary nuclei. Evaluation was performed by side-to-side comparison in each case. Six cases were excluded, because comparison of the cerebellar hemispheres or dentate nuclei with those of the opposite sides was not possible.RESULTSThe dentate nuclei opposite affected inferior olivary nuclei showed mild to moderate shrinkage of the normal low-signal areas and increases in signal intensity on T2-weighted images in 4 of 5 patients. The cerebellar cortices on the same sides as the involved dentate nuclei showed atrophic changes in 4 of 5 patients.CONCLUSIONOur MR findings suggest that there is a degenerative process involving the dentate nucleus and the cerebellar cortex associated with the hypertrophic degeneration of the inferior olivary nucleus.     

Brainstem and cerebellar changes after cerebrovascular accidents: magnetic resonance imaging

We illustrate the various types of secondary degeneration in the brainstem and/or cerebellum detected on magnetic resonance (MR) images obtained after cerebrovascular accidents. The changes include: (a) ipsilateral nigral degeneration after striatal infarction; (b) Wallerian degeneration of the pyramidal tract in the brainstem after supratentorial pyramidal tract or motor cortex injury; (c) Wallerian degeneration of the corticopontine tract in the brainstem after frontal lobe infarction; (d) ipsilateral brainstem atrophy and crossed cerebellar atrophy due to an extensive supratentorial lesion; (e) ipsilateral superior cerebellar peduncle atrophy, contralateral rubral degeneration, contralateral inferior olivary degeneration and ipsilateral cerebellar atrophy after dentate nucleus hemorrhage; (f) ipsilateral inferior olivary degeneration after pontine tegmentum hemorrhage; (g) bilateral wallerian degeneration of the pontocerebellar tracts after ventromedial pontine infarction or basis pontis hemorrhage; and (h) ipsilateral cerebellar atrophy after middle cerebellar peduncle hemorrhage.     

MR tomographic aspects of olivary pseudohypertrophy]

MRI aspects of olivary pseudohypertrophy (OH) following pontocerebellar lesions of different etiology and localization are reviewed. OH is characterized by unilateral or bilateral enlargement of the inferior olivary nucleus and increased signal intensity in T2- and, especially, in proton-density (PD)-weighted images. Correlations between the extent and the uni- or bilateral presence of olivary hypertrophy and the localization of the primary pontocerebellar lesions are discussed.     

MR imaging of metronidazole-induced encephalopathy: lesion distribution and diffusion-weighted imaging findings

BACKGROUND AND PURPOSE: MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established. This study was undertaken to determine the topographic distributions and diffusion-weighted imaging (DWI) findings of MIE. MATERIALS AND METHODS: We retrospectively evaluated the initial MR images (n = 7), including DWI (n = 5), and follow-up MR images (n = 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. The topographic distributions of lesions were evaluated on MR images, and DWI signal intensities and apparent diffusion coefficient (ADC) values of the lesions were assessed. RESULTS: MR images demonstrated bilateral symmetric T2 hyperintense lesions in the cerebellar dentate nucleus (n = 7), midbrain (n = 7), dorsal pons (n = 6), medulla (n = 4), corpus callosum (n = 4), and cerebral white matter (n = 1). Brain stem lesions involved the following: tectum (n = 5), tegmentum (n = 4), red nucleus (n = 3) of the midbrain, vestibular nucleus (n = 6), and a focal tegmental lesion involving the superior olivary nucleus (n = 6) and abducens nucleus (n = 4) of the pons and vestibular nucleus (n = 4) and inferior olivary nucleus (n = 1) of the medulla. DWI (n = 5) showed isointensity or hyperintensity of lesions, and the decreased ADC value was found only in the corpus callosum lesions (n = 2). All detected lesions were completely reversible at follow-up except for the single corpus callosum lesion with an initial low ADC value. CONCLUSION: Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum. According to DWI, most of the lesions in MIE probably corresponded to areas of vasogenic edema, whereas only some of them, located in the corpus callosum, corresponded to cytotoxic edema.     

鼻道、鼻咽恶性黑色素瘤的MRI诊断

目的 分析鼻道、鼻咽恶性黑色素瘤的MRI表现,探讨其诊断要点.方法 回顾性分析经病理证实的8例鼻道、鼻咽恶性黑色素瘤的MRI特征及临床资料,所有患者均行MR平扫、增强及动态增强检查.结果 肿瘤位于中鼻道1例,鼻咽部2例,鼻腔、上颌窦及同侧筛窦5例.5例可见明显骨质破坏并侵犯邻近结构,累及翼腭窝3例、颞下窝2例、眼眶4例、前颅底2例、咽旁间隙1例.MRI表现:3例直径＜2 cm,呈类圆形肿块,T1WI为高信号,T2 WI为低信号,呈明显均匀强化.5例直径＞3 cm,不规则肿块,MRI表现为混杂信号,T1WI以等、低信号为主,其内有斑片状高信号;在T2WI,1例以等低、信号为主,4例以稍高信号为主,增强扫描呈轻度不均匀强化.动态增强扫描时间-信号强度曲线平台型、流出型各4例.结论 鼻道、鼻咽恶性黑色素瘤MRI信号特征与肿瘤大小相关.肿瘤较小时T1WI呈高信号,T2WI呈低信号;肿瘤较大时MRI信号混杂,轻度不均匀强化为其特征.