63例小脑肿瘤的MRI分析

目的回顾性分析经临床、手术及病理证实的63例小脑肿瘤的MRI表现.方法63例病人,男39例,女24例,年龄6～78岁,平均年龄49.27岁.均采用横轴位、矢状位、冠状位及增强扫描.结果63例病人中,髓母细胞瘤10例,血管母细胞瘤7例,胶质瘤6例,动静脉畸形2例,囊虫病2例,转移瘤36例.结论发病年龄及发病部位对于小脑肿瘤的鉴别诊断具有重要价值,在诊断小脑肿瘤中,MRI优于CT.     

颅内幕下转移瘤CT诊断(54例分析)

该文通过对54例幕下转移瘤病灶的分析，认为：小脑半球的转移思CT表现为囊性低密区环和高密度强化带；小脑中线部位转移瘤以等高可均匀强化结节表现；小脑转移瘤单发病灶的鉴别诊断中不能忽视了转移瘤的可能性。     

16例小脑毛细胞型星形细胞瘤MRI及病理分析

目的 探讨小脑毛细胞型星形细胞瘤的磁共振成像(MRI)影像特点和病理学特征.方法 回顾性分析16例小脑毛细胞型星形细胞瘤的术后病理、术前MRI资料.结果 16例小脑毛细胞型星形细胞瘤中,发生于小脑蚓部11例,小脑半球5例.小脑毛细胞型星形细胞瘤可呈单纯囊肿型、囊肿附壁结节型或瘤囊型.MRI平扫肿瘤境界清楚,无明显瘤周水肿;增强扫描囊壁瘤结节或瘤体部分明显强化,囊壁光滑、强化或不明显强化.显微镜下瘤组织内致密、疏松区双相交替,瘤细胞呈细长梭形,致密区见数量不等Rosenthal纤维,疏松区有微囊样结构、嗜酸性小体形成;肿瘤免疫组化GFAP强阳性.结论 小脑毛细胞型星形细胞瘤MRI影像表现和病理组织学具有特征性,把握其病理特点有助于术前影像诊断.     

颅内表皮样囊肿的影像学诊断

目的:分析颅内表皮样囊肿的CT和MRI表现。方法:对30例经手术及病理确诊的颅内表皮样囊肿的CT和MRI表现作回顾性分析,其中30例作MRI平扫与增强扫描;20例作CT平扫检查。结果:肿瘤位于桥前池及桥小脑角池18例,4例位于鞍上,2例位于鞍旁,5例位于第四脑室,1例位于小脑延髓池。肿瘤大小不等,形态不规则,轮廓光整或呈分叶状。CT平扫17例呈均匀低密度,2例呈稍不均匀低密度,CT值为-15～10Hu,1例呈高密度。MRI平扫28例T1加权像上肿瘤呈不均的低信号,T2加权像上呈不均匀高信号,部分病例在FLAIR图象上表现为不均匀高信号,与周围低信号的脑脊液分界清晰;2例表现为T1加权像上为高信号,T2加权像上为低信号。增强后,2例肿瘤边缘有轻微强化,其余肿瘤均无明显强化。结论:典型的颅内表皮样囊肿,通过CT和MRI检查可做出准确诊断,并可以与颅内其他疾病相鉴别;在鉴别诊断中,MRI优于CT。非典型的颅内高密度囊肿,必须CT和MRI相结合诊断,为准确的术前诊断提供更多的信息。     

CT在甲状腺癌诊断中的价值

目的 探讨CT在甲状腺癌的诊断及鉴别诊断中的价值.方法 回顾性分析25例甲状腺癌的CT资料.所有病例均行CT平扫,19例行增强扫描.结果 CT平扫显示,23例(92%)表现为低密度;20例(80%)密度不均匀;23例(92%)边缘模糊不规则;16例(64%)出现钙化,其中细颗粒钙化10例,混合性钙化6例.19例增强扫描显示,10例表现为不同程度的均匀强化,4例肿瘤边缘呈"半岛状"瘤结节强化,5例可见"强化残圈"征.14例(56%)肿瘤侵犯周围器官组织,11例(44%)颈部淋巴结转移.结论 CT在甲状腺癌的诊断及鉴别诊断中有较高的价值.     

肝脏肿瘤的CT诊断与鉴别

目的　探讨肝脏肿瘤的CT表现及鉴别诊断。方法　收集病理或临床证实的 10 0例肝脏肿瘤的螺旋CT平扫及增强资料。结果　 10 0例肝脏肿瘤中 ,3 9例肝细胞肝癌 ,3 1例肝血管瘤 ,2 0例肝转移瘤 ,10例肝胆管细胞癌。定性总准确率 94%。结论　肝细胞肝癌、肝血管瘤、肝转移瘤、肝胆管细胞癌各自具有特征性CT表现 ,CT检查具有诊断和鉴别诊断价值。     

颅内幕下转移瘤CT诊断（54例分析）

该文通过了对５４例幕下转移瘤病灶的分析，认为：小脑半球的转移瘤ＣＴ为囊性低密区环和高密度强化带；小脑中线部位转移瘤以等高可均匀强化结节表现；小脑转移瘤单病灶的鉴别诊断中不能忽视了转换瘤的可能性。     

颅内血管外皮瘤的影像学诊断：9例回顾性总结

背景与目的：颅内血管外皮瘤的影像学表现与脑膜瘤相似，鉴别诊断困难。本文通过分析颅内血管外皮瘤的CT、MRI和血管造影表现．探讨其影像学特征。材料和方法：回顾性分析9例经手术和病理学证实的颅内血管外皮瘤患者的影像学资料。9例均行CT平扫．4例行CT增强．7例行MRI平扫和增强检查．2例行全脑血管造影。结果：肿瘤位于前颅窝2例、中颅窝3例、后颅窝3例、顶叶大脑镰旁1例；肿块直径5．8cm，呈分叶状．并与脑膜广基相连，肿瘤周围有水肿伴占位效应．肿块内可见囊变和坏死区。CT平扫肿瘤均为高密度为主的混杂密度影。2例有骨侵蚀，9例均无骨质增生和钙化。CT增强扫描，病灶明显强化。MRI平扫为等或长T1稍长T2信号为主的混杂信号影。注人对比剂后病灶明显强化。5例可见“脑膜尾征”。血管造影示肿瘤血供丰富，血供来自脑内、外血管。结论：当影像学上表现为以下3个特点时，应考虑颅内血管外皮瘤：(1)起自脑膜较大的分叶状、无钙化肿块，肿瘤有囊变及瘤周明显水肿；(2)CT及MRI增强检查时肿块明显强化；(3)血管造影检查为富血供的肿瘤。     

小脑原发性淋巴浆细胞性淋巴瘤一例

1病例报告患者男,35岁。因头晕10余天,加重伴走路不稳7d,于2005年2月7日入院。体格检查:血压110/70mmHg,神志清,左侧鼻唇沟变浅。全身浅表淋巴结未触及肿大。共济运动检查:闭目难立征阳性,步态不稳。无浅感觉障碍。神经系统病理反射未引出,生理反射存在。脑CT示小脑高密度灶,颅脑MR强化示小脑肿瘤并积水。于2005年2月14日在全麻下行小脑肿瘤切除术,术中见肿瘤位于小脑蚓部及左侧小脑半球,无包膜,将肿瘤完整切除。病理巨检:肿物及部分小脑组织,总体积8cm×6cm×4cm,其内见肿物2个,分别为3cm×3cm×2cm和4cm×3cm×3cm,切面均灰红色,鱼肉状,…     

脂肪肝背景下肝转移瘤的CT诊断研究

 目的　探讨脂肪肝背景下肝脏转移性肿瘤的CT表现 ,对产生误诊、漏诊的原因进行分析。方法　分析 31例脂肪肝合并转移瘤病人的CT征象 ,全部病例均行CT平扫和增强扫描。结果　发现转移灶共 91个 ,其中单发 13个 ;误诊、漏诊 11个病灶。转移灶表现为高密度结节 4 0个 ,高密度环 12个 ,随脂肪肝程度加重 ,高密度结节或环的比率增高。增强扫描多检出病灶 2 6个。结论　脂肪肝合并肝内转移瘤平扫常表现为高密度结节或环 ,易误诊为肝岛。分析观察高密度结节或环的形态、增强扫描后的密度变化 ,楔形高密度灶的形态、位置、边缘 ,肝缘的轮廓、血管走行、门脉细小分支瘤栓有助于鉴别诊断。增强扫描可以提高脂肪肝内转移瘤的检出率。     

Capecitabine-induced cerebellar toxicity

Capecitabine is an oral prodrug of 5-fluorouracil used in the treatment of adenocarcinoma of the colon. Neurotoxicity is an infrequently reported toxicity of capecitabine. We report a case of cerebellar ataxia secondary to capecitabine therapy.     

Paraneoplastic cerebellar degeneration

Summary Six patients developed a pancerebellar syndrome with symptoms preceding the diagnosis of neoplasia in five (median - 4 months) and following in one (2 years). In all patients, the initial cranial computed tomographic (CT) scans were normal. Five patients had repeat CTs and of these three were abnormal; cerebellar atrophy appearing 7 to 25 months following the initial CT. Median follow-up was 31 months (range 12–84 months) without evidence of CNS metastatic disease. In five of six patients the neurologic impairment did not progress. One patient's neurologic signs improved markedly with mantle radiation therapy of her Hodgkin's disease. An initially negative CT does not preclude the diagnosis of remote effect cerebellar atrophy. Paraneoplastic cerebellar degeneration is a self-limited nonprogressive process in the majority of patients.Presented in part at the 35th Annual Meeting of the American Academy of Neurology, San Diego, CA, April 28–30, 1983.     

Primary cerebellar glioblastoma multiforme

Summary Glioblastoma multiforme in adults arising in the cerebellum is a rare tumor, well documented in only 13 cases in the literature. We report a fourteenth case, an 80-year-old female, and reassess the clinical and CT aspects of this tumor based on a review of the world's literature. The median age of patients is 53 years with a median survival of three months, which is less than adult cerebral hemisphere malignant gliomas.     

Antibodies to cerebellar nerve fibres in two patients with paraneoplastic cerebellar ataxia

The aim of this study was to characterize two new atypical anti-neuronal antibodies using an immunohistochemical method on rat cerebellum and Western blot techniques with primate cerebellar tissue and with recombinant neuronal proteins. Atypical sera from two patients with paraneoplastic neurological syndromes associated with different tumours were detected. Case number 1 presented cerebellar degeneration and Merkel cell carcinoma and case number 2 paraneoplastic brainstem encephalitis and malignant fibrous histiocytoma. By immunohistochemistry, the two new atypical antibodies showed a similar fibrillar positivity in the molecular and granular layers and around the Purkinje cells. The dot blot with recombinant neuronal proteins (HuD, NOVA-1, CDR62/Yo, Amphiphysin) was negative, whereas the Western blot with neuronal antigens of primate cerebellum identified two different proteins with molecular weights (64 kD in case number 1, and 70 kD in case number 2). In conclusion, the two new antibody reactivities against nerve fibres should be integrated into the diagnostic paraneoplastic neurological syndromes guidelines.     

Primary cerebellar myxopapillary ependymoma

Journal of Neuro-Oncology -     

Ultrastructure of cerebellar hemangioblastoma.

Light and ultrastructural features of a cerebellar hemangioblastoma in a 56-year-old man are described in detail. The neoplasm was composed of three major cell types: endothelial cells, pericytes, and stromal cells. The endothelial cells lined the fenestrated vascular channels. The pericytes were ensheathed by their own basal lamina which separated them from the basal lamina covering the endothelium. The stromal cells contained, in addition to the conventional organelles, numerous membrane-bound lipid inclusions, annulate lamellae, and nuclear bodies. There were also present transitional cells which shared the fine structure of all the three major cell types. Histogenetically, the tumor was considered to be of vascular origin. The stromal cells represented the stem cells which, under the neoplastic influence, continued to proliferate and differentiate into "vasoformative" elements (pericytes and endothelium) which formed new blood vessels. The transitional forms between the stromal cells and the "vasoformative" elements suggested that the cellular components of a hemangioblastoma shared a common ancestry, most likely of an angioblastic lineage.     

Malignant transformation of benign cerebellar astrocytoma

A patient who had a well-differentiated cerebellar astrocytoma resected at 4 years of age, had glioblastoma multiforme of the cerebellum after a symptom-free interval of 28 years. Late malignant transformation of a cerebellar astrocytoma of childhood is rare and previous cases are reviewed. Cerebellar astrocytomas are typically among the most benign of primary brain malignancies with excellent long-term survival rates, sometimes with incomplete resection. This patient indicates that follow-up needs to be long-term because biologic behavior cannot be predicted fully in all cases.     

Breast cancer and paraneoplastic cerebellar degeneration

Of the remote effects of cancer on the neurologic system, paraneoplastic cerebellar degeneration (PCD), characterized by global cerebellar dysfunction, is second only to paraneoplastic neuropathies in frequency. Recent evidence, including the finding of anti-Purkinje cell (now termed anti-Yo) antibodies directed against specific protein antigens shared by Purkinje's and tumor cells, supports an autoimmune etiology for this disorder. Increasingly, a link between breast cancer and PCD is being recognized. The authors report a case, as well as a comprehensive overview, of 62 women with breast cancer and PCD, identified through a Medline (National Library of Medicine, Washington, DC) computer search (1966 to 1991) and comprehensive reference follow-up of the medical literature. The current understanding of the pathophysiology of PCD, with particular emphasis upon those features both salient and unique to breast cancer, is discussed. Whereas PCD will affect only a small number of patients with breast cancer, recognition of this syndrome is important. Anti-Purkinje cell (anti-Yo) antibody titers are now commercially available through several reference laboratories, and a serum anti-Purkinje cell antibody titer will assist in establishing the diagnosis. Presence of consistent symptoms and elevated titers of anti-Yo antibodies should prompt a search for an otherwise occult, and potentially treatable, malignancy. Only therapy initiated early in the patient's course appears to be of benefit. Finally, investigations into the pathogenesis of this syndrome may shed further light upon other diseases presumed secondary to autoimmune dysfunction.