正常人安静和催眠状态下脑葡萄糖代谢的自身对照研究

目的 研究健康正常人催眠静息状态和清醒安静状态下脑内葡萄糖代谢的差异,初步探索催眠状态的神经生理基础。方法 正常人在清醒安静状态下行^18F—FDG PET扫描。隔日后,采用凝视法将受试者诱导进入催眠状态,再次行^18F—FDG PET扫描。两种状态皆应采用3D模式进行PET脑显像,应用SPM分析对催眠静息状态和清醒安静状态^18F—FDG PET图像进行组间体元统计,统计所得到的一系列数值构成了统计参数地图（SPM）。比较催眠静息状态和清醒安静状态脑局部糖代谢的变化,根据变化差异显著（P〈0．001）区域的Talariach坐标值确定其部位。结果 SPM分析显示催眠静息状态较清醒安静状态右侧枕叶（BA17,18）、左侧枕叶（BA17,18）、左侧顶叶（BA40,）、左侧颞上回（BA22）、右侧尾状核、右侧小脑后叶、右侧额叶（BA6）、左侧额中回（BA8,9）和右侧丘脑葡萄糖代谢明显降低（P〈0．001）。结论 催眠静息状态脑葡萄糖代谢不同于清醒安静状态,催眠静息状态存在神经生理基础。     

后部皮质萎缩患者脑部葡萄糖代谢特征及其与认知功能的相关性分析

目的 利用¹⁸F-脱氧葡萄糖(¹⁸F-FDG)正电子发射断层(PET)显像分析后部皮质萎缩(PCA)患者脑部葡萄糖代谢特点及其与认知评分相关性。方法 12例临床诊断为PCA的患者和20例年龄、性别匹配的健康对照者行静息状态下脑¹⁸F-FDG PET成像,运用统计参数图(SPM)两样本t 检验比较两组的PET图像在体素水平的差异,获得PCA患者脑葡萄糖代谢异常脑区并分析其与认知量表评分的相关性。结果 SPM分析显示,与健康对照组比较,PCA患者双侧顶叶(包括楔前叶、角回)、颞中回的葡萄糖代谢降低,基底节区、额叶、小脑的葡萄糖代谢相对增高。楔前叶局部葡萄糖代谢率与视空间觉、记忆、Gerstmann’s综合征相关测验评分呈正相关(R=0.3982～0.8229,P<0.05);角回局部葡萄糖代谢率与记忆、执行功能相关测试评分呈正相关(R=0.5949～0.7317,P<0.05)。结论 脑¹⁸F-FDG PET显像可应用于PCA的临床诊断及疾病严重度评估。     

老年抑郁症患者的脑正电子发射体层摄影术显像分析

目的 探讨老年抑郁症患者脑^18氟-脱氧葡萄糖（18^F-FDG）正电子发射体层摄影术（PET）显像的特点。方法 分别对6例老年抑郁症患者（GD组）及10名健康体检者（对照组）进行脑^18 F-FDGPET显像，按年龄、简易智力状态检查量表总分和性别构成配对，用统计参数图第2版软件比较两组间脑局部葡萄糖代谢的差别。结果 GD组较对照组在双侧尾状核、额下回、颞上回、额中回，右侧核外、额上回、舌回和左侧扣带回、中央前回等脑区局部葡萄糖代谢减低（均P〈0．005）。GD组无局部脑葡萄糖代谢增加的脑区。结论 老年抑郁症患者存在基底节区、前额叶、颞叶和边缘系统的局部葡萄糖代谢下降。     

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.     

~(18)F-FDG PET显像观察特发性快眼动睡眠期行为障碍患者脑葡萄糖代谢特点的研究

目的探讨~(18)F-FDG PET显像观察特发性快眼动睡眠期行为障碍(iRBD)患者脑葡萄糖代谢改变和iRBD脑葡萄糖代谢改变与病程间的相关性。方法纳入多导睡眠监测(PSG)确诊的iRBD患者20例(iRBD组)和年龄、性别匹配的健康对照者19例(对照组)。两组均行~(18)F-FDG PET脑显像。基于自动解剖标记模板将大脑划分为90个左右对称的脑区,计算各脑区葡萄糖代谢半定量值。对iRBD组和对照组各脑区葡萄糖代谢半定量值进行独立样本t检验;并对iRBD组脑葡萄糖代谢改变与病程行Pearson相关分析。结果 (1)与对照组比较,iRBD组的双侧背外侧额上回、双侧眶部额上回、双侧眶部额中回、双侧海马、双侧海马旁回、双侧杏仁核、左侧眶部额下回、左侧岛叶、左侧内侧与旁扣带脑回、左侧中央旁小叶、左侧苍白球的葡萄糖代谢半定量值均增高(P0.05);双侧距状裂周围皮质、双侧楔叶、双侧舌回、双侧枕上回、双侧枕中回、双侧枕下回、双侧角回、双侧颞上回、双侧颞中回、右侧颞横回的葡萄糖代谢半定量值均降低(P0.05)。Pearson相关分析结果,iRBD组双侧杏仁核、双侧颞上回、右侧楔叶、右侧枕上回、右侧颞横回、左侧海马、左侧颞中回的葡萄糖代谢半定量值与病程呈正相关(P0.05);而双侧眶部额上回、双侧眶部额中回、左侧中央旁小叶、左侧眶部额下回、左侧内侧和旁扣带回、右侧背外侧额上回、右侧海马旁回的葡萄糖代谢半定量值与病程呈负相关(P0.05)。结论 iRBD患者脑内存在疾病相关的葡萄糖代谢水平改变,有助于客观评估iRBD病情的变化。     

行为变异型额颞叶痴呆患者脑葡萄糖代谢特征研究

目的利用~(18)F-FDG正电子发射断层扫描(PET)成像分析行为变异型额颞叶痴呆(bvFTD)患者脑葡萄糖代谢特征以及在阿尔茨海默病(AD)鉴别诊断中的应用价值。方法纳入临床确诊的bvFTD患者(bvFTD组,14例)、健康对照者(对照组,14例)和AD患者(AD组,14例),先将bvFTD和对照组的PET图像分别进行统计参数图(SPM)及尺度子轮廓模型/主要成分分析(SSM/PCA)分析,获得bvFTD患者脑部葡萄糖代谢图谱并建立bvFTD相关脑代谢网络模式(bvFTDRP);计算bvFTD组、对照组和AD组的bvFTDRP个体表达值,并进行ROC分析。结果 SPM和SSM/PCA分析均显示bvFTD组表现出双侧前额叶和基底节区葡萄糖代谢显著减低。bvFTDRP表达值在3组间差异均有显著统计学意义(ANOVA:F[2,39]=86.663, P0.001),且可有效鉴别bvFTD和AD患者。结论 bvFTD存在与疾病特异相关的脑葡萄糖代谢特征,为~(18)F-FDG PET应用于痴呆诊断提供了客观依据。     

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。     

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。     

研究儿童癫痫的新技术--1999年23届国际癫痫大会专题扎记(1999.10.布拉格)

PET应用 18F标记的脱氧葡萄糖(FDG)注射后,在PET下测定脑部的葡萄糖代谢.并结合EEG、MR来研究癫痫.FDP-PET可早期发现局灶性葡萄糖代谢的异常,以找出病损区域.     

帕金森病脑深部刺激术后FDG—PET／CT变化及临床意义

目的研究帕金森病（PD）脑深部刺激术（DBS）后全脑葡萄糖代谢（FDG）正电子发射断层扫描（PET）／计算机断层扫描（CT）功能影像学变化，探讨其评估手术疗效的临床价值。方法2011年2月至2011年7月，18例接受丘脑底核（STN）DBS治疗的PD患者分别在术前1w和术后6个月进行脑部18-F—FDG—PET／CT。结果术前大部分PD患者FDG影像学表现符合PD相关模式（PDRP）。术后异常代谢区域代谢趋向正常改变：纹状体区、中脑、感觉运动区和运动前区皮层的异常高代谢有明显下降；双侧前额叶、扣带回和辅助运动区皮层的异常低代谢有轻度升高。结论FDG影像对PD的诊断、鉴别诊断、病情评估和手术疗效有指导意义，但目前尚不能指导临床手术。     

Reproducible network and regional topographies of abnormal glucose metabolism associated with progressive supranuclear palsy: Multivariate and univariate analyses in American and Chinese patient cohorts

Progressive supranuclear palsy (PSP) is a rare movement disorder and often difficult to distinguish clinically from Parkinson's disease (PD) and multiple system atrophy (MSA) in early phases. In this study, we report reproducible disease‐related topographies of brain network and regional glucose metabolism associated with PSP in clinically‐confirmed independent cohorts of PSP, MSA, and PD patients and healthy controls in the USA and China. Using ¹⁸F‐FDG PET images from PSP and healthy subjects, we applied spatial covariance analysis with bootstrapping to identify a PSP‐related pattern (PSPRP) and estimate its reliability, and evaluated the ability of network scores for differential diagnosis. We also detected regional metabolic differences using statistical parametric mapping analysis. We produced a highly reliable PSPRP characterized by relative metabolic decreases in the middle prefrontal cortex/cingulate, ventrolateral prefrontal cortex, striatum, thalamus and midbrain, covarying with relative metabolic increases in the hippocampus, insula and parieto‐temporal regions. PSPRP network scores correlated positively with PSP duration and accurately discriminated between healthy, PSP, MSA and PD groups in two separate cohorts of parkinsonian patients at both early and advanced stages. Moreover, PSP patients shared many overlapping areas with abnormal metabolism in the same cortical and subcortical regions as in the PSPRP. With rigorous cross‐validation, this study demonstrated highly comparable and reproducible PSP‐related metabolic topographies at network and regional levels across different patient populations and PET scanners. Metabolic brain network activity may serve as a reliable and objective marker of PSP, although cross‐validation applying recent diagnostic criteria and classification is warranted.     

不同严重程度帕金森病患者脑葡萄糖代谢变化特点的临床研究

目的:探讨早、晚期帕金森病（PD）患者不同脑区葡萄糖代谢变化的特点,寻求PD严重度的新型生物学标志物。方法:19例早期PD（H-YⅠ～Ⅱ级）组、14例中晚期PD（H-YⅢ～V级）组患者及50名年龄匹配的健康对照组接受静脉注射¹⁸F-FDG PET脑断层显像,应用参数图分析法进行数据分析,比较各组间受试者脑内葡萄糖代谢变化的差异和特点。结果:与健康对照组比较,早期PD患者的丘脑、豆状核、小脑葡萄糖代谢增高;中晚期双侧丘脑、豆状核、小脑代谢增高,双侧顶叶葡萄糖代谢减低。结论:PD患者存在双侧丘脑、豆状核、小脑葡萄糖代谢增高,双侧顶叶葡萄糖代谢减低的代谢异常模式,且随着病情严重度的不同而变化,应用于PD严重度的客观评价,值得进一步研究。     

~(11)C-PIBPET和~(18)F-FDGPET显像诊断阿尔茨海默病与遗忘型轻度认知损害的临床价值

目的应用11C-PIB PET和18F-FDG PET显像研究阿尔茨海默病和遗忘型轻度认知损害患者β-淀粉样蛋白(Aβ)沉积与葡萄糖代谢之间的关系,联合载脂蛋白E(ApoE)基因型进一步探讨遗忘型轻度认知损害与阿尔茨海默病的相关性。方法利用PET显像对阿尔茨海默病(14例)、遗忘型轻度认知损害(10例)和正常对照者(5例)脑组织Aβ沉积和葡萄糖代谢变化进行分析,采用聚合酶链反应-限制性片段长度多态性方法对ApoE基因型进行分析。结果阿尔茨海默病组患者11C-PIB标准化摄取比值在下顶叶、颞叶外侧、额叶、后扣带回皮质和楔前叶、枕叶和纹状体均高于正常对照组(P0.05);遗忘型轻度认知损害组患者脑组织11C-PIB结合水平呈双峰形。11C-PIB+aMCI亚组与阿尔茨海默病组、11C-PIB-aMCI亚组与正常对照组之间11C-PIB标准化摄取比值差异均无统计学意义(P0.05)。18F-FDG PET显像显示,3/5例11C-PIB+aMCI亚组患者双侧顶叶、颞叶和楔前叶代谢减低,其中2例ApoEε4等位基因携带者随访期间进展至阿尔茨海默病;3/5例11C-PIB-aMCI亚组患者双侧额叶和前扣带回代谢减低。结论11C-PIB PET显像是筛查具有阿尔茨海默病病理特点的遗忘型轻度认知损害患者的有效工具。具有阿尔茨海默病病理特征的遗忘型轻度认知损害患者可伴有顶叶、颞叶外侧皮质和楔前叶代谢减低,其中ApoEε4等位基因携带者更易进展至阿尔茨海默病痴呆。     

致死性家族性失眠患者脑葡萄糖代谢分析

目的 研究致死性家族性失眠(fatal familial insomnia,FFI)患者脑葡萄糖代谢变化特征.方法 对病程分别为2个月的患者1和6个月的患者2以及20名健康对照者进行18F-脱氧葡萄糖(18F-fluorodeoxyglucose,18F-FDG)PET静态显像.采用视觉分析的方法判断2例患者脑代谢改变情况,然后利用统计参数图分析方法对每例患者和与其年龄相匹配的10名健康对照者进行组间分析,判断其代谢改变特征.结果 与10名年龄相匹配的健康对照组相比,患者1表现为明显的丘脑、顶叶、尾状核、后扣带回和前额叶的代谢减低(t＞2.82,P＜0.01).患者2表现为明显的丘脑、顶叶、后扣带回和前额叶的代谢减低,其代谢减低的范围和程度明显大于患者1(t＞2.82,P＜0.01),并伴有颞叶和枕叶代谢减低(t＞2.82,P＜0.01).结论 FFI患者脑葡萄糖代谢改变主要为双侧丘脑和大脑皮质代谢减低,大脑皮质所累及的范围和程度随病程发展而增大.18F-FDG PET显像对FFI的诊断和鉴别诊断具有一定的参考价值.     

进行性核上性麻痹与多系统萎缩的头部MRI和FDG-PET比较

目的对比研究进行性核上性麻痹(PSP)与多系统萎缩(MSA)的脑干MRI表现和头部葡萄糖代谢特征。方法对11例PSP患者、37例MSA患者和43例健康对照进行头部MRI平扫检查,并计算MRI正中矢状面T1加权像上中脑截面面积,其中5例PSP和19例MSA进行了18F-FDG PET检查。结果(1)MRI:11例PSP正中矢状位T1加权像均可见中脑上缘平坦或凹陷表现,呈"蜂鸟征",而MSA患者和健康对照组未见上述表现。37例MSA患者中有34例轴位T2加权像桥脑可见"十字征"样长T2异常信号。PSP患者正中矢状位T1加权像上中脑截面面积分别低于MSA组和健康对照组(P<0.01)。(2)PET:PSP组主要表现为对称性额叶低代谢;MSA组主要表现为额、顶、颞叶普遍低代谢,纹状体对称性代谢降低,丘脑代谢高于纹状体。结论PSP中脑MRI特征和头部葡萄糖代谢特征与MSA和健康对照有明确差异,有助于PSP与MSA的鉴别诊断。     

Familial progressive supranuclear palsy: detection of subclinical cases using 18F-dopa and 18fluorodeoxyglucose positron emission tomography.

BACKGROUND: Progressive supranuclear palsy (PSP) is generally considered to be a sporadic disease; however, occasional cases of familial PSP have been described. The rarity of reports of familial PSP may be attributed in part to an inability to detect subclinical disease in affected relatives who subsequently die before symptoms clinically develop. OBJECTIVE: To study regional cerebral dopaminergic function and glucose metabolism in members of 2 large kindreds with familial PSP to identify subclinical cases. METHODS: Three clinically affected members from the 2 PSP kindreds were scanned with both (18)F-dopa and (18)fluorodeoxyglucose ((18)FDG) positron emission tomography (PET). Fifteen asymptomatic first-degree relatives were scanned with (18)F-dopa PET; 10 of them also underwent a second PET study with (18)FDG. RESULTS: All 3 clinically affected PSP patients showed a significant reduction in caudate and putamen (18)F-dopa uptake along with a significant reduction in striatal, lateral, and medial premotor area and dorsal prefrontal cortex glucose metabolism. In 4 of the 15 asymptomatic relatives, caudate and putamen (18)F-dopa uptake was 2.5 SDs lower than the normal mean. These 4 subjects and a fifth asymptomatic relative with normal (18)F-dopa uptake showed a significant reduction of cortical and striatal glucose metabolism in a pattern similar to that of their affected relatives. CONCLUSION: (18)F-dopa and (18)FDG PET allowed us to identify 5 cases with subclinical metabolic dysfunction among 15 subjects (33%) at risk for PSP, suggesting that this approach is useful for characterizing the pattern of aggregation in PSP kindreds.     

Cerebral glucose metabolism abnormalities in patients with major depressive symptoms in pre-dialytic chronic kidney disease: statistical parametric mapping analysis of F-18-FDG PET, a preliminary study

Aims: The aim of the present study was to investigate the relationship between depressive symptoms and cerebral glucose metabolism in pre‐dialytic chronic kidney disease (PDCKD) patients. Methods: Twenty‐one patients with stage 5 CKD and 21 healthy volunteers underwent depressive mood assessment and statistical parametric mapping (SPM) using F‐18‐fluorodeoxyglucose (FDG) positron emission tomography (PET). Results: Several voxel clusters of significantly decreased cerebral glucose metabolism were found in PDCKD patients. The largest cluster was left prefrontal cortex (Brodmann area [BA] 9). The second largest cluster was also left prefrontal cortex (BA 9). The third largest clusters were right prefrontal cortex (BA 10) and right basolateral prefrontal cortex (BA 46). Other brain areas also showed decreased cerebral glucose metabolism including left anterior cingulate gyrus (BA 32), left premotor cortex (BA 6), left transverse temporal gyrus (BA 41), left superior temporal gyrus (BA 42), right basolateral prefrontal cortex (BA 44), right inferior parietal lobule (BA 39), left middle temporal gyrus (BA 19), and left angular gyrus (BA 39). Hypermetabolized brain areas, however, were not found in PDCKD patients compared to normal controls. For the right orbitofrontal cortex there was a negative correlation of cerebral glucose metabolism with Hamilton Depression Rating Scale (HDRS) in PDCKD patients (BA 11). Conclusion: PDCKD patients with depressive symptoms had decreased cerebral glucose metabolism in several brain areas. For the right orbitofrontal cortex there was a negative correlation with HDRS in PDCKD patients. The present findings provide functional neuroimaging support for abnormal cerebral glucose metabolism in PDCKD patients with depressive symptoms.     

Voxel-based comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration

OBJECTIVES: Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are neurodegenerative disorders that may be accompanied by dementia and parkinsonism as clinical symptoms. The purpose of this study was to elucidate cerebral metabolic differences of these two diseases with cognitive impairments by [18F] fluorodeoxyglucose (FDG) and positron emission tomography (PET). METHODS: A total of 12 patients with PSP (age: 62.8+/-6.0 years old, m: 7, f: 5, Mini-Mental State Examination (MMSE): 23.4+/-2.6), 12 patients with CBD (age: 64.8+/-6.3 years old, m: 6, f: 6, MMSE: 22.9+/-4.5), and age-matched healthy subjects (normal control (NC)) (age: 63.8+/-7.7 years old, m: 7, f: 5) were subjected to FDG-PET to obtain glucose metabolic images. We compared regional cerebral metabolic images by a voxel-by-voxel analysis with statistical parametric mapping (SPM) among PSP, CBD, and NC subjects, and evaluated differences of hypometabolic regions. RESULTS: The patients with PSP showed reduced cerebral glucose metabolism in the medial and lateral frontal gyri, basal ganglia, and midbrain compared with NC, whereas the patients with CBD showed significant reduction in the parietal lobes (p<0.001). SPM also revealed parietal hypometabolism in CBD patients compared with PSP patients (p<0.001). CONCLUSIONS: The predominant parietal glucose metabolic reduction in CBD patients was different from previously reported findings. This finding would be the characteristic substance of patients with CBD accompanying cognitive impairments. Our findings suggest that measurement of glucose metabolism by PET and a voxel-based analysis is useful to understand the pathophysiology of these two diseases with cognitive impairments.     

Prefrontal cortex dysfunction and depression in atypical parkinsonian syndromes.

Depressive symptoms are common in patients with neurodegenerative disorders. Imaging studies suggest that a disruption of frontal-subcortical pathways may underlie depression associated with basal ganglia disease. This pilot study tested the hypothesis that frontal dysfunction contributes to depression associated with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP). Depressed patients with MSA (n = 11), PSP (n = 9), and age-matched controls (n = 25) underwent measures of cerebral glucose metabolism applying positron emission tomography with (18)F-fluorodeoxyglucose. Regional metabolism in the patient groups was compared to the normal subjects using the voxel-based statistical parametric mapping. Depressive symptom severity (Hamilton Depression Rating) and degree of locomotor disability (Hoehn & Yahr) were assessed in the patient groups. The association between prefrontal metabolism and the occurrence of depressive symptoms and the degree of locomotor disability was investigated. When compared to controls, MSA patients revealed significant metabolic decreases in bilateral frontal, parietal, and cerebellar cortex and in the left putamen. In PSP patients, significant hypometabolism was demonstrated in bilateral frontal cortex, right thalamus, and midbrain. Depression severity but not the patients' functional condition was significantly associated with dorsolateral prefrontal glucose metabolism in both patient groups. The findings of this pilot study support the hypothesis that depressive symptoms in MSA and PSP are associated with prefrontal dysfunction.