阿尔茨海默病~(18)F-FDG PET显像诊断的研究

目的 探讨阿尔茨海默病（AD）脑葡萄糖代谢及其18F-脱氧葡萄糖正电子发射计算机断层扫描（18F-FDG PET）显像的影像学特征和PET诊断标准。方法 静脉注射18F-FDG后行脑断层显像,检查13例 AD、13例非AD痴呆及13例正常人。获得纹状体、丘脑、黑质、顶叶、颞叶、额叶、枕叶、海马单位面积放射性计数与小脑计数的比值（Rcl/cb）,进行半定量分析,并与MR进行对照。结果AD患者PET异常率为100％,MR异常者占10/13。PET显像特征:①对称性双侧颞顶叶及海马伴额叶或枕叶代谢减低占9例（9/13）;②双侧颞叶对称性代谢减低伴海马或额叶代谢下降占3例（3/13）;③双顶叶对称性代谢降低1例（1/13）。12例（12/13）非AD痴呆表现为不对称、多发性代谢降低,降低区位于黑质、纹状体、丘脑及脑皮质区,MR异常率为11/13。结论 在除外脑内结构特异性损害基础上,PET发现对称性双颞顶叶、海马或颞叶、顶叶,伴或不伴枕叶、额叶代谢下降,可诊断AD。PET对AD早期诊断及鉴别诊断具有临床意义。     

不同类型痴呆脑代谢改变图型:~(18)F-FDG PET显像

目的探讨不同类型痴呆患者基于像素水平的脑代谢图型特点。方法对最终临床诊断为阿尔茨海默病(20例)、额颞叶痴呆(20例)、路易体痴呆(10例)、进行性核上性麻痹(7例)、原发性进行性失语(3例)、皮质基底节变性(1例)和多系统萎缩(1例)等认知功能障碍患者的18F-FDG PET显像资料进行回顾分析,描述各种神经变性疾病脑代谢降低区域和程度。结果 SPM分析表明,各种神经变性疾病引起的痴呆18F-FDG PET显像均表现为皮质代谢降低,但其代谢图型变化明显不同:阿尔茨海默病组以双侧颞顶叶和额叶皮质代谢降低为主,基本感觉运动皮质、枕叶、基底节和丘脑活性保留;额颞叶痴呆组额叶和颞叶皮质不对称性代谢降低,伴部分顶叶皮质和基底节、丘脑等皮质下核团不同程度代谢降低;路易体痴呆组枕叶、视皮质和双侧颞上回前部代谢降低;进行性核上性麻痹组双侧前额叶背外侧、颞叶前外侧、中脑和双侧尾状核代谢降低;原发性进行性失语组左侧额叶Broca区、左侧颞叶皮质(除左侧颞上回后部)和右侧颞叶内侧皮质代谢降低;皮质基底节变性组双侧中央沟周围额顶叶皮质(右侧显著)、右侧基底节代谢降低;多系统萎缩组双侧小脑背外侧皮质和左侧壳核代谢降低。结论神经变性疾病所致痴呆在18F-FDG PET显像中表现出各自特征性脑代谢降低图型,18F-FDG PET显像有可能成为痴呆鉴别诊断的一种辅助手段。     

~(18)F-FDG PET显像鉴别阿尔茨海默病与额颞叶痴呆临床价值

目的探讨18F-FDG PET显像在阿尔茨海默病与额颞叶痴呆鉴别诊断中的应用价值。方法对临床明确诊断的阿尔茨海默病(20例)和行为异常型额颞叶痴呆(20例)患者的18F-FDG PET显像资料进行回顾,分析两组患者皮质代谢降低脑区间的差异。结果视觉分析显示,两组患者均表现为皮质代谢降低,阿尔茨海默病患者以双侧颞顶叶和后扣带回代谢降低明显,以及部分额叶皮质代谢降低,而基底节和丘脑不受累,18/20患者双侧大脑半球皮质代谢降低范围和程度基本对称;额颞叶痴呆患者额叶和前颞叶皮质代谢均降低,其中11例同时伴部分顶叶皮质和基底节、丘脑等皮质下核团不同程度降低,16/20患者双侧大脑半球代谢降低程度和范围明显不对称,4例以右侧为主、12例以左侧为主。结论由于18F-FDG PET显像所显示的阿尔茨海默病和额颞叶痴呆患者之皮质代谢降低图型不同,故具有较好的鉴别诊断价值。     

P型多系统萎缩与帕金森病的18F-脱氧葡萄糖脑代谢比较

目的 研究P型多系统萎缩(multiple system atrophy,MSA-P)与帕金森病(Parkinson's disease,PD)的脑部葡萄糖代谢差异.方法 MSA-P患者15例,PD患者32例,无神经系统疾病的健康对照8名,进行18F-脱氧葡萄糖(FDG)PET检查.分别取尾状核、豆状核、丘脑、小脑、双侧额叶、双侧顶叶、双侧颞叶和双侧枕叶为感兴趣区(ROI).应用PET专用软件计算各ROI的FDG放射性同位素值,以颅内各部位ROI的18F-FDG代谢比值为指标.结果 MSA-P的额叶、颞叶、顶叶、纹状体、丘脑的18F-FDG脑代谢与健康对照和帕金森病相比呈现对称性下降;丘脑18F-FDG代谢高于纹状体以及额、顶叶皮质;18F-FDG代谢比值同侧豆状核与丘脑为0.493±0.085,同侧尾状核头与丘脑为0.453±0.079.PD的额、顶、颞叶皮质18F-FDG代谢分别高于纹状体、丘脑;纹状体高于丘脑,首发症状肢体对侧豆状核与丘脑18F-FDG代谢比值为1.131±0.113;基底节代谢不对称.MSA-P的豆状核与丘脑18F-FDG代谢比值,同PD的豆状核与丘脑18F-FDG代谢比值相比差异有统计学意义(P＜0.01).结论 MSA-P与帕金森病的葡萄糖代谢差异显著,可以应用18F-FDG PET检查作为鉴别诊断的重要方法之一.     

脑网络模块化分析用于阿尔茨海默病、路易体痴呆和帕金森病性痴呆脑葡萄糖代谢特点研究

目的本研究探究脑功能成像的脑网络模块化分析在阿尔茨海默病(AD),路易体痴呆(DLB),帕金森病性痴呆(PDD)脑网络模块参数特点和异同点,寻找疾病相关特异性脑葡萄糖代谢网络模块参数。方法回顾性分析复旦大学附属华山医院AD、DLB、PDD组和正常对照组的静息状态18F-FDG PET显像,采用网络模块化分析分别获得4组受试者的脑葡萄糖代谢网络模块化参数,并应用种子点相关分析得到葡萄糖代谢网络连接改变的脑区,比较4组受试者脑代谢网络连接的异同点。结果在稀疏阈值15%时,正常对照组和AD组的网络由4个模块组成,PDD组由6个模块组成,DLB组由10个模块组成。以右侧丘脑为种子点,AD组的颞叶和皮质下脑区连接增强,枕叶和左侧额叶连接减弱。PDD组的额叶、皮质下脑区连接增强,枕叶、颞叶、左侧顶叶的连接减弱。DLB组的左侧额叶和皮质下脑区连接增强,右侧枕叶和顶叶连接减弱。结论 3种不同类型痴呆患者的脑葡萄糖代谢网络具有不同的模块化特性,提示发病机制的差异,为进一步探究其神经机制提供新思路。     

老年性痴呆与血管性痴呆的^18F—FDG PET显像分析

目的 比较老年性痴呆（AD）和血管性痴呆（VD）^18F-FDG PET显像特征,为诊断和治疗提供帮助。方法 将受者分为3组：其中AD组14例,VD组6例,正常对照组6例。静脉注射^18F-FDG 185－370MBq,40min后采用PET扫描仪行脑显像。结果 正常对照组双侧各脑叶和小脑的葡萄糖代谢分布对称。VD组6例,病灶呈非对称性分布于脑叶皮层,其中4例病灶波及多叶及丘脑和基底节,并出现交叉性小脑失联络。AD组的双侧顶叶、颞叶的代谢明显减少（P＜0．001,P＜0．05）。结论 AD和VD的PET显像各有其特点,PET能敏感地区分他们。     

阿尔茨海默病的脑血流灌注研究

目的探讨AD患者脑血流灌注的特征性变化。方法选择20例确诊AD患者和10例认知正常者,对所有入组对象行SPECT脑血流灌注显像检查,对所得图像进行视觉分析和半定量分析,比较两组对象各脑区血流灌注情况的差异,并比较AD患者左、右脑叶脑血流灌注的差异。结果 (1)视觉分析结果显示,AD组以颞叶或顶叶脑血流灌注减低为主,各占55%,其中双侧颞顶叶血流灌注减低者占15%,单侧颞顶叶血流灌注减低占20%。正常认知组SPECT影像学表现各异,额叶、颞叶、顶叶、枕叶、丘脑、基底节血流灌注减少情况均存在,各占10%。但无双侧颞顶叶血流灌注减少者,40%表现完全正常。(2)半定量分析结果显示,AD组在右额叶、双侧颞顶叶、右枕叶血流灌注显著低于正常认知组(P<0.05),以右侧颞叶血流灌注降低最明显,左右颞顶叶血流低灌注程度对比无显著性差异。结论 AD患者的SPECT特征性表现为双侧对称性颞顶叶血流低灌注,其中右侧颞叶血流灌注下降最严重。     

18F-FDG SPECT显像区别阿尔茨海默病和血管性痴呆的临床研究

目的 探讨阿尔茨海默病（AD）与血管性痴呆（VD）^18 F-脱氧葡萄糖（18F-FDG）单光子发射计算机断层（SPECT）的影像特点。方法静脉注射18F-FDG 45min后行脑断层显像，获得脑显像特征，并加以分析、比较。结果22例AD患者可见双侧颞、顶、额叶对称或单侧优势半球的颞、顶、额叶异常代谢灶。20例VD患者除皮质各叶显示异常代谢灶外，合并基底节、丘脑、枕叶异常代谢灶，与基础病变（头颅CT或MRI定位）一致。结论18F-FDGSPECT可作为鉴别诊断AD、VD的有效手段。     

11C-匹兹堡复合物B正电子发射断层摄影术脑显像在阿尔茨海默病早期诊断中的临床应用

目的 探讨N-甲基[11C]2-(4'-甲基氨基苯基-6-羟基苯并噻唑){N-methyl[11C]2-(4'-methylaminophenyl-6-Hydroxybenzathiazole),11C-PIB}PET脑显像在阿尔茨海默病(AD)早期诊断中的价值.方法 分别对6例AD患者、7例轻度认知功能障碍(MCI)患者及6名智能正常的老年对照者(NC)进行临床诊断、资料收集及11C-PIB PET脑显像,并对5、25和45 min PET图像进行分析.结果 视觉分析:AD患者3个时段放射性清除情况与NC组有明显不同,药物注射45 min后脑内放射性清除较NC组明显减低;MCI组图像呈不均一改变,与AD、NC组均有重叠.统计分析:3组受试者各脑区与小脑45 min标准吸收值(SUV)比值示:AD组顶叶、额叶、颞叶、枕叶及海马比值分别为1.91±0.21、2.09±0.41、1.92±0.35、1.66±0.41、1.55±0.28,高于NC组的1.48±0.53、1.57±0.64、1.36±0.53、1.27±0.40、1.17±0.33,差异具有统计学意义(t值分别为8.114、5.620、5.705、3.650、2.866,P值分别为0.0001、0.0002、0.0002、0.0045和0.0170),MCI组顶叶、额叶、颞叶、枕叶及海马的比值分别为1.48±0.53、1.57±0.64、l_36±0.53、1.27±0.40、1.17±0.33,均高于相应NC组,但差异无统计学意义.结论 11C-PIB PET脑显像能够鉴别早期AD患者与Nc,并对MCI患者有一定预测价值.     

18F-FDG PET/CT脑显像评价认知障碍患者中的脑小血管病变对皮层功能的影响

目的 探讨18氟代脱氧葡萄糖（18F-fluorodeoxyglucose,18F-FDG）正电子发射断层成像/计算机断层扫
描（positron emission tomography/computed tomography,PET/CT）脑显像评价认知障碍患者中的脑小血
管病变对皮层功能的影响。
方法 本研究为回顾性研究,纳入2009年1月～2010年12月北京协和医院PET中心行18F-FDG PET/CT
脑显像且颅脑磁共振成像（magnetic resonance imaging,MRI）提示存在小血管病变的认知障碍患者21例,
其中临床诊断血管性痴呆（vascular dementia,VaD）10例,阿尔茨海默病（Alzheimer’s disease,AD）或混
合型痴呆（mixed dementia,MD）11例。首先目测两组患者的18F-FDG PET/CT脑显像皮层及皮层下核团代
谢减低特点,并结合颅脑MRI判断病变血管对脑代谢的影响。使用NeuroQ软件和Scenium软件对18F-FDG
PET/CT脑图像在像素基础上进行定量分析比较两组患者的皮层代谢情况。
结果 通过目测和NeuroQ软件分析发现VaD组患者18F-FDG PET/CT脑显像图像特点为无规律,不对
称皮层或皮层下核团代谢减低,其中额叶皮层代谢减低范围最广,程度最重。结合颅脑MRI改变,考
虑皮层和皮层下核团代谢减低主要为小血管病变引起。AD或MD组患者脑代谢均呈现双侧颞顶叶代谢
减低,其中8例出现皮层代谢减低不对称表现,6例出现基底节丘脑不对称代谢减低表现,与典型AD
的表现不符,结合颅脑MRI表现,考虑为病变血管所致,小血管病变可能导致相应皮层代谢减低。通
过定量分析发现两组患者的SUV比值在左右顶叶、内外颞叶和枕叶差异具有显著性。
结论 18F-FDG PET/CT脑显像作为功能影像可以推断小血管病变与皮层及皮层下核团代谢的关系。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.