阿尔茨海默病患者脑皮质神经原脱失和淀粉样脑血管病改变(英文)  

Cortical neuron loss and amyloid cerebroangiopathy in patients with Alzheimer disease

作　　者：张利平[1] 徐惠琴[1] 王耀山[1] 

机构地区：[1]解放军沈阳军区总医院药剂科,辽宁省沈阳市110015

出　　处：《中国临床康复》2005年第29期205-207,共3页Chinese Journal of Clinical Rehabilitation

摘　　要：背景:阿尔茨海默病是老年期或老年前期发病的大脑变性疾病。老年性痴呆患者和患有阿尔茨海默类型的老年性痴呆患者常常在认知力方面、神经病学、电生理、影像学以及神经组化改变等方面混淆在一起,使得对阿尔茨海默病更难作出诊断。目的:测定阿尔茨海默病患者脑皮质神经原脱失和淀粉样脑血管病改变情况。设计:抽样调查。单位:解放军沈阳军区总医院神经内科。材料:在1984/1991解放军沈阳军区总医院神经内科连续尸检的300例脑标本中,筛选出60岁以上18例阿尔茨海默病的标本。另选择18例阿尔茨海默病与脑血管病并存的脑标本作为对照组。方法:详细观察脑皮质神经元脱失和淀粉样脑血管病改变。取自额上回切片在1.45mm×1.45mm组织(×100)下进行神经元计数,观察阿尔茨海默组和对照组的神经元脱失情况。主要观察指标:①各组标本的神经元计数,对海马、杏仁核、Meynert核、中脑、桥脑、延髓、基底核、丘脑、小脑等区域的神经细胞脱失、胶质增生、脂褐素沉积、淀粉样小体等改变。②观察阿尔茨海默病例组织学缺血改变的容积、大小及数目。结果:①18例阿尔茨海默病标本病理检查可见重度脑萎缩4例,中度8例,轻度6例,镜下于脑叶皮质和海马区见大量老年斑及神经原纤维缠结,8例海马区有颗粒空泡变性。18例脑皮质神经元均明显减少,11例阿尔茨海默病并存有淀粉样脑血管病。②全部阿尔茨海默标本均在额叶皮质见有不同数量的老年斑改变,3例海马区未见老年斑改变,而严重的在海马区也可见到大量老年斑。皮质神经原纤维缠结计数范围3～30个/mm2,多数标本在海马区可见弥漫皮质神经原纤维缠结改变,严重痴呆标本中老年斑和皮质神经原纤维缠结还可见于杏仁核、Meynert核、中脑、桥脑、基底核、丘脑。除特征性的老年斑和皮质神经原纤维缠BACKGROUND： Alzheimer disease （AD） is a progressive and irreversible brain disorder that occurs in geratic period or even before that. Patients with senile dementia and dementia due to AD cannot be distinguished in the respects of the changes in cognition, neuropathy, electrophysiology, imaging and neurohistochemistry, which makes the diagnosis of AD more difficult. OBJECTIVE： To probe into the changes of cortical neuron loss and amyloid cerebroangiopathy in patients with AD. DESIGN： Sampling investigation. SETTING： Neurological Department of the General Hospital of Shenyang Military Area Command of Chinese PLA. MATERIALS： Brain samples were collected from 300 corpuses receiving consecutive autopsy between 1984 and 1991 in the Neurological Department of the General Hospital of Shenyang Military Area Command of Chinese PLA. Of them 18 hrain samples from AD corpuses aged above 60 years old were enrolled in this study; meanwhile, another 18 cases of AD accompanied with cerebroangiopathy were used as controls. METHODS： The changes in cortical neuron loss and amyloid cerebroangiopathy were observed. Neurons per 1.45 mm×1.45 mm area in superior frontal gyrus slices were counted （×100） so as to investigate neuron loss in AD group and control group. MAIN OUTCOME MEASURES： ①The count of neurons; neuron loss, collagen hyperplasia, lipofuscin deposition and amyloid corpuscle in the hippocampus, amygdala, Meyncrt nucleus, midbrain, pons, macromyelon, basal ganglia, thalamus, and cerebellum; ② the volume, size and number of ischemic regions in AD group. RESULTS： ① Of the 18 AD cases, cortical atrophy was severe in 4 cases, moderate in 8 cases, and mild in 6 cases. A large number of senile plaques and neurofibrillary tangles could he observed in the cerebral cortex and hippocampus under microscope, with granular vacuole changes observed in hippocampus region in 8 cases. Cortical neurons were found to be obviously decreased in 18 cases, and AD was found to coexist with amyloid angiopathy in 11 ca

关 键 词：阿尔茨海默病/病理学 淀粉样变 脑血管意外 

分 类 号：R743[医药卫生—神经病学与精神病学]