PET在神经系统中的应用（附精彩影像图片+影像征集）加分从优

PET在神经系统中的应用（附精彩影像图片+影像征集）加分从优

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PET在神经系统疾病中的应用越来越广，开此贴的目的是向各位战友系统介绍一下PET在神经系统中的应用，以下综述为专贴，由PDF转化而来，（中间可能有些错别字，我已尽量改正了），便于各位战友阅读。

PET在神经系统疾病中的应用
作者 赵军林 祥通
PET基木原理及主要机型
正电子发射计算机断层显像(Positron Emission Tamography，简称PET)为目前影像技术中较为有前途的功能性显像技术，能够无创性探测生理性放射性核素在机体内的分布。人体许多疾病往往很长一段时间处于一个相对静止的无症状时期，如帕金森病(PD)的临床症状直到黑质丢失70%左右的多巴胺能神经元时才表现出来。此阶段虽然不表现症状，但疾病的生化改变是存在的，能够用分子显像技术(例如受体显像)予以探测。PET实现了医学影像学从观察人体结构变化向功能、代谢变化的根本转变，可以在活体水平研究组织细胞的血流灌注、葡萄糖、氨基酸及核酸代谢、受体分布、基因变化，对神经系统疾病的早期诊断、监测疗效、发病机制的研究以及脑认知功能的研究等方面提供了客观、科学的观察手段。其基本原理是根据正电子核素衰变产生的正电子与体内的负电子结合产生一对能量相同(511ke)但方向相反的γ光子即湮没过程(annihilation)，采用符合探测技术，即可同时接收到两个γ光子信号，将两个探测器的输出信号加以符合时间窗判断，只要两个信号的输人时间差在符合时间窗间隔内，则被认为是有效计数，通过采集无数个T光子对产生的符合计数，由计算机进行图像重建处理，得到人体内标记化合物的分布图像。
闪烁晶体的选择对PET成像质量是关键。早期用Na1(T1)晶体较多，后来发现BGO(锗酸秘)密度大，探测效率高，且稳定性好，使用比较广泛，但其闪烁光通量低，为Na1(T1)晶体的15%，衰变时间长(300ns),高计数时存在高的随机符合分数。目前研究较多且最有前途的晶体材料为LSO，其具备与BGO非常相同的密度(7.4g.ml-1),原子序数为59,1,S。发射5倍的光通量，小动物PET及新一代的PET已应用LSO作为晶体材料。根据PET晶体材料不同分为;① BGO晶体PET:为目前正电子成像中最先进、最完备的仪器。它图像质量好、灵敏度及分辨率高，适用面广，适用于全身各个部位的断层显像，对肿瘤转移、复发的诊断尤为有利，另外对脑及心脏的显像质量佳。Siemens 公司及GE公司均有BGO晶体的PET，为科研/临床兼用型，其脑成像质量最佳。NaI晶体PET:ADAC公司生产的CPE 由6块曲线形的Nat晶体连接48个光电倍增管形成一个直接为90cm的全环，入口直径为56cm,横向空间分辨率为5 rmum,轴向分辨率5.5二，能量分辨率12%a，主要应用于肿瘤的全身显像，脑成像质量不及BGO晶体PET。
除PET之外，符合探测成像(MCD)与高能准直成像也可进行正电子成像。但由于空间分辨率和灵敏度都很差，图像质量欠佳，不适宜做脑显像，对较小的肿瘤( < 2cm)及深部病变探测也比较困难。

临床应用
癫痫 癫痫根据病因分为原发性和继发性两类。对药物难治性原发性癫痫，手术切除癫痫灶是有效的治疗方法，而成功的关键是术前准确定位。此类病人头皮脑电图(EEG),CY,MR检查难以发现致痫灶。FDG PEI.研究表明，癫痫发作期病灶部位葡萄糖代谢增高，而发作间期代谢减低颞叶EEG患者低代谢可波及同侧海马及额叶、顶叶，丘脑的低代谢可作为癫痫灶定侧诊断的一个有价值的指标。小脑的低代谢可发生于对侧、双侧或同侧。Newberg等报道丘脑代谢的不对称性尚可作为癫痫预后评价的一个指标，颞叶癫痫丘脑代谢不对称，特别是对侧丘脑代谢减低病人，颖叶切除手术后预后较差。对MRI结构显像阴性的颞叶癫疯,PET癫痫灶定位灵敏度在60% 一90%.病理学显示往往存在神经胶质增生、变性或神经细胞发育不良，但范围多小于PET所见异常代谢区。颞叶癫痫病人，FDG PET结果与视频EEG密切相关，能够预测颞叶切除术后病人的预后，广泛低代谢的病人手术效果差，致痫灶低代谢程度越严重，手术切除后癫痫不发作的概率越高。发作间期O15-H2O PET显像或fMRI对术前功能区定位(如语言区、运动区等)具有极重要的价值，PET检查的环境较舒适，适于有幽闭恐怖症或有医学禁忌症不适合fMRI的检查者(如金属牙、心脏起博器、或外科夹等)。癫痫发作期癫痫灶血流和葡萄糖代谢增高，但是由于正电子核素的半衰期较短，进行发作期PET显像的机会较少。另外发作期脑葡萄糖代谢的升高幅度变化较大(30%一300%)，复杂部分发作全身性强直痉挛发作持续时间短，低于FDG在脑内的摄取时间(30一40min)，因而发作期显像实际土包含了发作间期、发作期和发作后的代谢时相，这取决于癫痫发作与注射显像剂的间隔时间。目前主张发作间期FDG PET结合发作期99m Te-HMPAO或Tc-ECD脑血流灌注显像对癫痫灶的定位具有重要价值。PET在癫痫受体方面的研究主要是阿片受体和γ氨基丁酸/苯二氮罩受体。C11-carfentanil PET显示癫病灶部位μ阿片受体增高, μ阿片受体的作用可使癫痫发作停止或降低痫性活动向脑邻近区域的传播。C11Diprenorphine是一种对μ、μ、κ受体具有相同亲和力的显像剂，可用于研究脑内阿片受体总的分布情况，这两种显像剂结合起来，可以显示癫痫灶区μ受体的增加，同时伴有μ和(或)κ受体正常或减低。C11-Flumazenil显示癫疯灶苯二氮覃受体密度降低，受体密度的降低与F18-FDG的低代谢范围相比要小。在颞叶中部苯二氮罩受体密度降低，颞叶新皮质中阿片受体密度增高。受体显像已用于癫痫灶的诊断，可提高人们对癫痫病理生理学的了解，从根本上反映癫痫的神经化学改变。

正常老化和痴呆应用 FDG-PET研究一组年龄范围在5d-1年的婴儿来探讨发育中人脑葡萄糖代谢的变化情况。5 -26日龄的婴儿，脑葡萄糖代谢占优势的部位是初级感觉运动皮质、丘脑、脑干和小脑蚓部，联合皮质和基底节的代谢相对较低，提示此阶段脑功能主要用于支配完成初级固有的反射活动。至12周，基底节和颞、顶叶皮质代谢明显增高。1岁时，包括额叶在内的脑葡萄糖代谢已接近**，而额叶认知功能在9个月左右已经具备。

痴呆的早期临床诊断和各种类型痴呆的鉴别诊断以及与老年短期的记忆和认知功能的减退鉴别仍是困难的。随着进人老龄化社会，AD发病率明显上升。虽然导致AD的分子机制尚不清楚，但是胆碱酷酶抑制剂作为早期AD有效的治疗方式。据估计如果治疗将降低AD的行为缺陷，病人的生命质量将提高5年，费用也将降低一半。文献报道PET有助于AD的早期诊断与鉴别诊断。前瞻性研究发现，PET比临床诊断方法(包括血液学检查、反复性的神经心理测试,EEG和结构影像)能提前2.5年检测AD，其准确性在90%以上。PET对痴呆治疗的评价也是重要的，一方面因为PET早期准确诊断AD与其他类型痴呆及与正常老化的鉴别、病程生物学分期及治疗的生物学反应。血管性痴呆表现为多发性非对称性代谢减低。Pick病痴呆以额叶受损为特点;Wilson病痴呆主要受损部位在豆状核;而Huntington病(RD)痴呆无论早、晚期尾状核代谢始终减低。PD伴痴呆除颖顶叶代谢减低外，纹状体糖代谢异常，特别是初级视觉皮质CMRglc明显减低，侧枕叶中度减低，中颜叶相对保留。AD早期可见双侧顶叶出现对称性减低，晚期双侧颖叶出现减低，常累及额叶，最后导致全脑的代谢减低。另外药物本身可进行标记，研究药物在脑内的代谢。FDG-PET还可对检查后一定时期记忆能力的减退作出预后评价，例如相关皮质的相对低代谢能够预测是否会发生认知功能的下降，而且有关记忆的标准测试2年期间下降的幅度发现与下顶叶、上颞叶及后扣带回初期的低代谢程度明显相关(r=0.71)。Silerrnan与Phelps报道FDC PEI，用于数年内(可长达9年，平均3年)临床病理转归的预测灵敏度90%一93%，特异性74%-77%a,准确性83%一85%.痴呆病人的神经功能缺失症状往往与低代谢或低灌注区相吻合，有明显语言功能障碍或出现失语时，可见左额、颞、顶叶以及外侧裂区代谢明显减低;记忆缺失者，双侧中颖叶血流灌注减低且以右侧为著。

PET对HD与家族性AD两种疾病的研究表明，PET可探测静止期、无症状的疾病。前瞻性研究的结果提示代谢的异常可在临床症状出现之前大约7年被检测。Smal等与Reirnar,等比较了家族性AD家庭中无症状AD者的PET代谢与APOE-4危险因子，结果发现顶叶皮质的代谢缺陷与APOE-4的存在高度相关。Smal等研究结果表明PET代谢的异常在症状出现之前大约5年可被检测。

帕金森病(PD)和帕金森综合征 PD是由于黑质和锥体外系含色素的神经元的丢失引起，色素神经元的减少与多巴胺产量的减少、多巴胺贮存减少以及黑质纹状体系统功能失常有关，一般认为初期有多巴胺受体的上行调节，继而随疾病进展出现下行调节，最后PD可导致20%一30%病人出现痴呆。
MR可以发现由于神经元的变性或铁剂沉积引起的黑质大小减小，但是CT/MR主要用于排除其他一些颅内疾患。Haber等人研究发现MR不能用于PD引起的痴呆和AD的鉴别，PET，不仅能够用于研究脑部代谢，而且可用于研究多巴胺递质受体系统，后者对PD的诊断和病理过程的判定都具有重要价值。Playford等人对PD和对照组进行C15O2 PET的自由运动试验对比研究，对照组左侧原发感觉运动皮质、左侧豆状核、左侧前运动皮质、左前额叶背外侧及辅助运动皮质、前扣带回、双侧顶叶相关区域激活，而即病人左侧原发感觉和前运动皮质活性激活，豆状核、前扣带回、辅助运动皮质和前额叶背外侧皮质活性减低，这些区域功能失常往往导致PD病人初期运动困难。一些研究报道早期未治疗的PD基底节区呈现高代谢，偏侧震颤麻痹与对侧基底节的高代谢有关。另有一组报道，偏侧震颤麻痹一偏侧萎缩综合征患者在症状对侧基底节葡萄糖代谢减低。PD与正常对照组比较，有轻度弥漫性皮质低代谢，这种低代谢与运动减少的严重程度相关，而与疾病的病程无关。PD病理涉及到突触前和突触后的复杂改变，不仅存在黑质纹状体系统多巴胺合成功能的减退，而巨有突触后多巴胺受体活性的改变和突触前多巴胺转运体释放、回收多巴胺功能的改变。18F-FDOPA PET显像用于评价PD突触前多巴胺功能，结果表明黑质纹状体多巴胺投射系统异常，基底节活性减低，特别是具有“开关”现象的患者。Garnett等人研究发现偏侧震颤麻痹对侧基底节活性显著减低，同侧基底节尽管程度较轻也呈现活性减低。F18-DOPA也可用于检测MPTP和其他化合物引起的帕金森综合症患者的多巴胺旁路。F18-DOPA可用于研究PD的临床病程和治疗的效果，经过长期随访，发现每年F18-DOPA的聚集量减少1.7%，认为多巴胺活性减低与运动减少恶性程度的评分相关。在潜在发展为PD危险性的高危人群中F18-DOPA PET显示黑质纹状体投射系统示踪剂摄取不对称性减少。PD早期未经替代治疗病变侧纹状体D:受体出现明显的上调效应，而替代治疗后或随病程延长D2受体则无明显变化或出现下调。近年采用F18-FPCIT行多巴胺转运蛋白显像发现，PD早期患肢对侧壳核后部示踪剂摄取减少，中后期成为两侧受损o Frey等应用C11dihydrotetrabenazine(DTBZ)测定转运体的可利用率，结果发现可作为特发性PD进展的一项有价值的指标。Bankiewicz等应用PET评价单侧MPTP帕金森病猴模型基因治疗后多巴胺合成的恢复。

Huntington舞蹈病(HD)是基底节和大脑皮质变性的一种显性遗传性疾病，其特征为慢性进行性舞蹈样动作和痴呆。本病主要侵犯基底节和大脑皮质，尾状核和壳核受累最严重。HD早期X线CT示尾状核头部解剖结构完整，晚期则见尾状核头部明显萎缩，而FDG PET显像早期即可见尾状核头部LCMRgk明显降低，有助于早期诊断o Mazizota等研究HD病人无症状的儿童，发现在部分携带疾病基因的病人尾状核与豆状核有代谢缺陷，所有有症状的病人均显示PET的代谢异常。

脑肿瘤 PEI在脑肿瘤的评价和处理中起重要作用，包括肿瘤分级、放射性坏死与肿瘤复发的鉴别、预后判断。FDG PET显像结果表明，高度恶性肿瘤为高代谢而低度恶性肿瘤为低代谢。Di Chiro等对72例病人研究结果表明，低度恶性肿瘤CMRglc为(4.01±1.8)mg葡萄糖/100g.min-1，而高度恶性肿瘤为(7.4±3.5)mg葡萄糖/IOOg.min-1。低代谢与局部水肿、囊性变、肿瘤附近的坏死以及与肿瘤在神经元有联系的区域也有关系，另外还可见远处代谢的异常，如对侧小脑半球(CCD) 。PET比CT, MRI能精确预测胶质瘤病人的生存期，Alai等发现高代谢胶质瘤从明确诊断平均生存期为7一11个月，而低代谢胶质瘤平均生存期为33个月(1一7年以上)。值得注意的是FDG PET显像并不总是与CT显像相关，尽管绝大多数高代谢肿瘤CT为增强，仅50%的低度恶性肿瘤显示强化，强化通常为恶性程度高的一个标志。当两者矛盾时，FDG PEI，比CT或MR1更能精确地判定恶性程度。PEI能够鉴别肿瘤的复发与坏死，通常坏死区为低代谢，而肿瘤复发为高代谢。Di Chiro等人研究发现放射性坏死只与白质内低代谢有关，而化疗引起的坏死除与白质异常外还与灰质变化有关。Ogawa等人应用PET测定放疗后血液容积和肿瘤组织的葡萄糖代谢的改变，治疗后1个月，肿瘤组织葡萄搪代谢明显减少(30%一65%)，而周围脑组织无明显变化，放疗后肿瘤代谢减低者比无反应者预后良好，因而PET在评价肿瘤疗效中有一定价值。PET可测定肿瘤rCBF, rCMRO2和应用15O2、C1502测定脑皮质功能的改变。rCBF在肿瘤变化很大，从接近于零(囊肿、坏死区)到超过正常灰质。rCBF和rCMR02的减少可发生于邻近区和远离肿瘤的部位(如肿瘤外周水肿区、同侧大脑皮质)，在颅内压增高患者，对侧半球的脑血流和氧代谢与正常对照相比也减低，然而这种减低在颅内减压手术(如颅骨切除或肿瘤切除)后可恢复。11C一蛋氨酸可用于评价脑肿瘤的氨基酸代谢，与18F-FDG结合能准确评价脑肿瘤的分级与治疗后肿瘤复发和纤维化的鉴别诊断，18F -FUDR研究核酸代谢，通常FUDR在脑肿瘤研究中具有很高的对比度(正常脑组织摄取低)。对脑转移瘤而言，PET可评价转移瘤的活性、治疗效果及有否脑膜转移，同时可检测原发灶及全身其他部位的转移。

缺血与脑卒中 15O-H20和FDG PEI，对脑卒中的研究表明PET比X-CT更早地发现病灶，并且所显示病灶的范围超过X-CT所显示的范围。正常的脑组织显示rCBF与rCMRglc和(或)rCMRO:之间紧密匹配。脑梗死后即刻rOEF(局部氧摄取分数)增加而rCBF明显下降，rCMRglc轻度下降，血流和代谢的这种不一致表现为灌注减低后代谢代偿性转变，称为“misery perfusion”（贫乏灌注）。1周后梗死的脑区倾向于rCBF增加而rCMBglc仍降低，这种现象称为“luxury perfusion(过度灌注)，往往提示预后良好。1个月后，rCBF与rCMRglc在较对侧正常脑组织低的水平(可能比梗死前低)再一次匹配。
有关严重脑缺血或梗死区周围有活力的脑组织是否可以恢复仍是值得研究的课题,PET可以提供梗死区周围的脑区在足够的rCBF得以恢复后是否可以挽救的信息。当rCBF和CMRglc/rCMR02在比基础值低的水平再匹配时将到达脑卒中的晚期，通过介人方式增加TCBF神经元的功能将不能恢复。依赖于梗死区传人的远处区域代谢率与rCBF脑卒中后将降低。运动皮质的脑卒中将干扰皮质脑桥小脑束的传导引起对侧小脑半球的血流与代谢的减低，此种现象称为“交叉性小脑失联络”(CCD)。 Kuhl发现不仅脑皮质可以出现失联络，而且梗死灶对侧的纹状体、丘脑、小脑都可以出现，所有的这些结构在X-CT没有异常改变。梗死灶对侧相应部位出现代谢减低称为镜灶“mirrorfoci"，这表示双侧半球纤维联系的中断。主要动脉支梗死后形成交通循环以维持脑组织的存活，此时靠局部脑血流容积(rCB)的增加来部分补偿灌注压的降低，动脉舒张降低血流的阻力使rCBF, rCMRglc,rCMR02维持在正常水平，rCB的增加提示与之有关的脑区已经应用补偿机制来保持灌注，PE，可以灵敏的测量rCBF/rCB比率定量评价灌注贮备。低灌注贮备的脑区血管扩张，rOEF增加，可以预测梗死将来的危险性。对脑卒中PEI，尚可用于监测药物(如尼莫地平)的疗效，提供生理方面的信息帮助医生解释临床的转归，同时也有助于理解急性脑梗死的病程。

其他 PET对脑外伤的价值在于了解脑外伤后有无功能的受损，观察疗效和评估预后，了解脑功能是否恢复。AIDS、梅毒可有神经系统损害,PET可早期发现AIDS是否存在脑的代谢和血流异常，诊断是否并发脑淋巴瘤及评价放疗的疗效等。

图1Normal subject

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图2Misery Perfusion
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图3Luxury Perfusion
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图4Alzheimer's disease
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图5Pick's disease
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图6Parkinson's disease
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图7Striatonigral Degeneration
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图8 Astrocytoma
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图9 Radation Necrosis
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图10 Temporal Lobe Epilepsy
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图11 Actiation Study
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Emerging role of PET in epilepsy
International Congress Series 1264 (2004) 10–25

[color=yellow]1 FDG PET in medial temporal lobe epilepsy[/color]
Medial temporal lobe epilepsy is well known for its pathologic, diagnostic criteria of
hippocampal sclerosis and/or atrophy. These changes are easily found on the recent
generation MRI machines. Both the quantitatie and the qualitatie MRI interpretation
gie similar diagnostic effectieness for temporal lobe epilepsy with the recently
deeloped, new MRI machines. FDG PET reeals equally well identification for the
epileptogenic zones in medial temporal lobe epilepsy (Fig. 1).

Fig. 1. FDG PET of medial temporal lobe epilepsy; a typical matching case with hippocampal atrophy andhypometabolism in the left temporal lobe. SPM analysis is showing clear decreased hypometabolic area incorresponding seizure induction lesion.
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2 Diagnostic performance of FDG-PET in neocortical epilepsy
In contrast to temporal lobe epilepsy, neocortical epilepsy has seeral problems in terms
of the localization of epileptogenic zones. About one third to one half of intractable
patients are suspected to hae neocortical epilepsy in many institutions, including my
institution [10–12]. In its order of prealence, the sites of extratemporal lesion are lateral
temporal, frontal, occipital and parietal lobe.
Neocortical epilepsy has two kinds of problems in localization of seizure foci, which
can definitely be soled by nuclear medicine modalities, particularly using PET technology.
The first one is multiple, suspected foci of epileptogenic zones on MRI. On MRI, we
cannot clearly determine which lesion would be the pathologic for seizure induction. The
second one is the MR negatie case without any structural lesion, that is to say
cryptogenic. In this cryptogenic case, it is difficult to determine where to apply subdural
grids and strips during subdural EEG studies.
PET and ictal SPECT are really helpful in these situations. They may make it clear
that PET can contribute to increase confidence and to localize totally cryptogenic lesions
(Fig. 2).

Fig. 2. FDG PET of cryptogenic lateral temporal lobe epilepsy: this patient suffered from complex partial seizure,but he had normal finding on MRI. There is decreased metabolism on conentional PET scan, as well as SPM imaging, in the left lateral temporal lobe.

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According to our preious study , presented at the annual meeting of SNM seeral
years ago, positie predictie alues of PET and ictal SPECT in cryptogenic epilepsy wereoer 75% (it is 76% and 78%, respectiely). Localization rates were different between epileptogenic areas. For example, the localization rate in parieto-occipital lesions is much
lower than that in frontotemporal areas. The sensitiity of FDG PET was 36% in patients
without structural lesions on MRI and 73% in patients with structural lesions in frontal
lobe epilepsy [14]. In non-lesional cryptogenic cases, epileptogenic zones yield decreased
metabolism (Fig. 3).

Fig. 3. In this case with cryptogenic frontal lobe epilepsy, MRI was normal and ictal EEG was also nonlocalizing.FDG PET showed definitie hypometabolism in the left frontal lobe. After successful frontal lobectomy, thispatient became seizure-free.
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On the other hand, it is not easy to localize epileptogenic zones in occipital lobe
epilepsy [15]. In some cases, the increased perfusion in the occipital lobe is seen on thelesion side and this finding can be the only clue to the correct localization in this case,because MR is normal. Areas showing the most seere hypometabolism are limited to theoccipital lobes in some patients (Fig. 4); howeer, this is not true in all patients. The areasof highest perfusion were not limited to occipital lobes, either.

Fig. 4. FDG PET and ictal SPECT in occipital lobe epilepsy. (A) MRI was normal, but ( metabolism was decreased in a case of right occipital lobe epilepsy. (C) In another case, the MRI was normal, but (D) perfusion was increased in the left occipital lobe on ictal SPECT. Both of the patients became seizure-free after neocorticalresection.
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Parkinson Disease: 123I -β - CIT SPECT
人纹状体
A 正常人
B Hoen-Yahr I期
C Hoen-Yahr I期
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The areas of the most seere hypometabolism show a much wider metabolically
abnormal region than expected. The areas of the most increased perfusion are demonstrated with ery heterogeneous and nonspecified abnormal findings in different areas,maybe due to rapid propagation (Fig. 5).

Fig. 5. Regional prealence if interictal hypometabolism on F-18 FDG PET in occipital lobe epilepsy.
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18F-Dopa PET显像用于PD诊断
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神经外科疾病之PET影像1――星形细胞瘤
Figure 1. Left temporal low-grade astrocytoma (Patient 7). A, T1-weighted axial MRI slices, without (lower) and with (upper) delineation of ROIs. B,FDG study, without and with ROIs delineated from the MRI study. C, 11C-MET study, without and with ROIs delineated from the MRI study. D, histograms of the ratio alues for FDG (upper) and 11C-MET (lower). Along the abcissa, the different ratio alues of the tumoral tracer uptake are shown, and the percentages of all pixels exhibiting each ratio alue are presented in the ordinate.

翻译：左侧颞叶低级星形细胞瘤，A,MRI之T1有无感兴趣区（ROI）描记。B：FDG（荧光脱氧葡萄糖）有或无感兴趣区描记。 C：11C-MET，11碳蛋氨酸有或无感兴趣区描记。D：FDG (upper)和11C-MET分析柱状图。

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神经外科疾病之PET影像2――少枝胶质细胞瘤
Figure 2. Left temporal Grade II oligodendroglioma (Patient 3). A, T1-weighted axial MRI slices, without (lower) and with (upper) delineation of ROIs. B,FDG study, without and with ROIs delineated from the MRI study. C, 11C-MET study, without and with ROIs delineated from the MRI study. D, histograms of the ratio alues for FDG (upper) and 11C-MET (lower). Along the abcissa, the different ratio alues of the tumoral tracer uptake are shown, and the percentages of all pixels exhibiting each ratio alue are presented in the ordinate.

翻译：左颞叶少枝胶质细胞瘤。A,MRI之T1有无感兴趣区（ROI）描记。B：FDG（荧光脱氧葡萄糖）有或无感兴趣区描记。 C：11C-MET，11碳蛋氨酸有或无感兴趣区描记。D：FDG (upper)和11C-MET分析柱状图。

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胰岛素在人脑葡萄糖代谢中的作用

图中可见胰岛素浸润和未浸润区域表现出明显差异性

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AD

Brain 18F-FDG PET in the Diagnosis of Neurodegeneratie Dementias: Comparison with Perfusion SPECT and with Clinical Ealuations Lacking Nuclear Imaging

18F-FDG PET scans of a patient with false-positie findings and an AD patient. Shown are representatie axial (left) and sagittal (middle) slices through an 18F-FDG PET brain scan of a 79-y-old woman undergoing clinical ealuation for cognitie impairment. The patient had a history of depression and thyroid disease and was receiing thyroid hormone replacement therapy at time of PET. The interpreting nuclear medicine physician had read the scan as consistent with early neurodegeneratie changes in an Alzheimer-like pattern, because of the apparent relatie decreased actiity in the parietal cortex (bold white arrows), relatie to the adjacent frontal and temporal cortex (thin white arrows). Longitudinal clinical follow-up for 2.5 y after the scan showed no progressie dementia, so the scan interpretation was classified as false positie. If this scan were being read now, the false-positie interpretation might hae been aoided by comparing the thalamic actiity (red arrows) to the parietal actiity, with which it is approximately isometabolic, and to the (higher) frontal actiity—in contrast to the pattern found in AD (right), in which parietal cortex becomes hypometabolic relatie to the (presered and normally isometabolic) thalamus.

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早期诊断AD

Figure 1. [18F]Fluorodeoxyglucose Positron Emission Tomography Brain Scan of a 52-Year-Old Woman With Cognitie Complaintsa
aContiguous planes of brain tissue with slice thickness of 2.5 mm are displayed from superior to inferior leels. Images are displayed with anterior brain at top and posterior brain at the bottom of each image; the left side of the brain is on the right side of the images (often referred to as "radiological conention"). The scan shows the actiity of brain cells in different regions of the brain with use of a "rainbow scale": red, orange, and yellow areas are the most actie regions; green areas hae midrange actiity; and blue and iolet areas are the least actie. In Alzheimer’s disease, brain actiity is lower, especially in the posterior portion of the brain, in areas important for processing language and memories. Metabolism was lower in this brain in the midparietal lobes bilaterally (see green to blue cortex in posterior portion of planes 16–19) and in the left cortex inferiorly (see cortical asymmetry in planes 40–45, where right cortex is yellow to red and left cortex is green to blue).

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AD

Brain Areas With Significant Decline in Glucose Metabolism From Baseline to 1-Year Follow-Up in 14 Patients With Alzheimer’s Diseasea
aoxels with significantly reduced metabolism (p<0.005, uncorrected for multiple comparisons) are shown in the orange color scale on lateral and medial projections for the right and left hemispheres. Declines in metabolism oer time were obsered in parietal, temporal, and frontal association regions.
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AD

Brain Areas With Significantly Lower Glucose Metabolism at Baseline in 14 Patients With Alzheimer’s Disease Than in 34 Healthy Subjectsa
aoxels with significantly lower metabolism in the patients (p<0.001, uncorrected for multiple comparisons) are shown in the orange color scale on lateral and medial projections for the right and left hemispheres. Lower metabolism in the patients was obsered in the association cortex, including parietal, temporal, occipital, and frontal brain regions.
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神经外科疾病之PET影像3――脑膜瘤1
Fig. 4 PET analysis for patient 6. A, before treatment. B, decreased methionine uptake after treatment with IFN-_ for 42 months and 24 days. C,decreased methionine uptake before withdrawal of IFN-_ treatment after 54 months and 20 days. D, increased methionine uptake 11 months and 10 days after withdrawal of treatment. E, MR image in axial projection demonstrating the large skull base meningioma with tumor growth extending into the orbit.
翻译：病人6，A治疗前。B在干扰素治疗肿瘤42个月24天显示蛋氨基摄入少。C在干扰素治疗肿瘤54个月20天显示蛋氨基摄入情况。D在干扰素治疗肿瘤结束后11个月10天显示蛋氨基摄入情况。E轴位MRI显示颅底大的脑膜瘤长入眶。
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神经外科疾病之PET影像4――脑膜瘤2
Fig 1. A, Contrast-enhanced axial T1-weighted gradient-echo MR (450/9 [repetition time/echo time], flip angle, 908) shows a round, enhancing tumor in the left middle cranial fossa. The tumor is heterogeneously enhanced and the central part (arrows) is markedly enhanced. The gray matter of the insula and the temporal lobe facing the tumor are compressed medially and posteriorly. B, FDG PET scan shows that the central part of the tumor, which is markedly enhanced, has a high glucose metabolic rate, whereas the glucose metabolic rate of the left frontal and temporal cortices surrounding the tumor is low.
翻译：A对比增强MRI显示左侧中颅窝低脑膜瘤，肿瘤信号不均，箭头指示强化。岛叶和颞叶皮质受压。B：FDP荧光葡萄糖PET扫描肿瘤中心强化，说明葡萄糖代增强。位于肿瘤周边的额叶前部及颞叶代谢率降低。
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神经外科疾病之PET影像5――血管畸形
FIG. 1. Case 18. Imaging studies obtained in a 23-year-old woman with a high-flow AM. Upper Left: Lateral iew of the right ICA demonstrating an AM. Because normal arterial structures in front of the nidus are faintly opacified, this
AM is recorded as the high-flow type. Upper Right: A T2-weighted axial MR image demonstrating the nidus and the main draining ein of the lesion. Lower Left: The PET image settings of rCBF, rCMRO2, rOEF, and rCB. Lower Right: Enlargement of PET imaging. Initially, six ROIs were set on the rCB image.
翻译：23岁高血流的AM女性病人。上左：右侧颈内动脉造影侧位发现，窦前方正常的结构模糊。上右：T2见窦及引流静脉。下左：脑血流，吸氧后，含氧，脑血容量PET影像。下右：PET放大，设置6个感兴趣区。

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神经外科疾病之SPECT影像6――头部外伤
FIG. 2. Studies in a 61-year-old man who fell down a flight of concrete stairs. He was conscious on admission to the neurosurgical unit but remained in posttraumatic amnesia for 7 days. The magnetic resonance (MR) (upper left) and single-photon emission computerized tomography (SPECT) (upper right) images were obtained 2 days after injury. UpperLeft: An MR image indicating edematous tissue associated with a contusion in the left frontal region. Upper Right: ASPECT study showing corresponding flow reduction, but there is also an extensie region of abnormally high flow. This hyperemic region underlies a left frontal subdural hematoma that can be seen on MR imaging. Lower Left: A repeat SPECT scan after 16 days reealing that this hyperemia is still eident. Lower Right: A follow-up SPECT at 3 months indicating that hyperemia is no longer eident.
翻译：61老年人从水泥楼梯上跌下，在神经外科治疗后出现遗忘7天。左上：SPECT。左下：2天后情况。左上：MRI显示左额挫伤，周边见脑水肿。上右：上述部位见血流量减少，但硬膜下有正常血流部位。同时见硬膜下血肿。左下:16天复查SPECT见充血仍然明显。右下：随访3个月见血量正常。

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皮质基底节变性之PET
资料来自
PET study of cerebral glucose metabolism and fluorodopa uptake in
patients with corticobasal degeneration
Journal of the Neurological Sciences 139 ( 1996) 2 I O-2 17

关于本病更详细资料请到
http://www.dxy.cn/bbs/post/iew?bid=46&id=2926548&sty=1&tpg=1&age=0

文摘

Rebeiz et al. described the clinical and pathological
findings in three patients who presented in late middle age
with ariable combinations of an asymmetric akinetic-rigid
syndrome, apraxia, supranuclear palsy and frontal lobe
sign, and they described “corticodentatonigral degeneration
with neuronal achromasia” as a noel degeneratie
disease (Rebeiz et al., 1986). Thereafter, Gibb et al. reported
three patients and reiewed the clinical and pathological
features of corticobasal degeneration (Gibb et al.,
1989). The diagnosis of corticobasal degeneration can be
predicted during life on the basis of clinical features
referable to both cerebral cortical and basal ganglionic
dysfunctions, but a definitie diagnosis requires confirmation
by autopsy (Riley et al., 1990). Howeer, recent
studies using positron emission tomography (PET) indicated
that distinctie supportie findings for the diagnosis
could be obtained with this technique (Watts et al., 1985;
Eidelberg et al., 1989; Sawle et al., 199 1; Nagasawa et al.,
1993a). In the present study, we measured regional glucose
utilization and striatal [‘*F]dopa uptake in clinically diagnosed
cases of corticobasal degeneration and we indicated
that this unique combination of PET studies could proide
efficient information to differentiate them from other degeneratie
diseases with cognitie and moement disorders.

[colore=red]Fig. 1. Representatie images obtained by [lxF]FDG positron emission tomography and magnetic resonance at the leels of corresponding brain slices from
patients I, 3, 5 and 6. The colour scale in the present study is ranged from 0 to 10 mg/lOO g/min.[/color]

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Fig. 2. Two different images obtained by [‘*F]fluorodopa @DOPA) positron emission tomography and magnetic resonance were oerlapped at the leel of
the caudate nucleus and the putamen from a normal subject (C) and four patients (l-4) with corticobasal degeneration. FDOPA actiity was symmetrically
accumulated in the caudate nucleus and the putamen on both hemispheres of a normal control (C). In the patients, howeer, FDOPA accumulation was
decreased in an asymmetric pattern with more seere impairment in the dominantly affected caudate nucleus and putamen.

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左颈内动脉闭塞

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癫痫发作期脑血流显像（男，15岁）
来自影像医学及核医学讨论版,作者yiyisue
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癫痫间歇期脑血流显像（男，15岁）
来自影像医学及核医学讨论版,作者yiyisue
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脑多巴胺转运体显像

来自影像医学及核医学讨论版,作者yiyisue
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感谢各位战友对影像征集工作的支持！
下面就各位战友未提供的影像作一补充：
1、PET与Astrocytoma
Glioblastoma Multiforme (Grade I Astrocytoma)
MRI shows a rim-enhancing lesion in the right hemisphere. FDG-PET reeals a hypermetabolic rim (red arrow) consistent with high-grade astrocytoma. Note that such regions of hypermetabolism can be used as a guide for potential biopsy sites
MRI显示右半球一边缘强化影像，FDG-PET显示边缘区高代谢（红箭头），符合高等级的星型细胞瘤。显示高代谢区可作为活检的潜在区域。
screen.width-333)this.width=screen.width-333" width=459 height=292 title="Click to iew full pet(Astrocytoma).jpg (459 X 292)" border=0 align=absmiddle>

2、PET与Huntington's Disease
资料：63 year old male with Huntington's Disease.
Abnormal 18F FDG P.E.T. brain scan. The findings of markedly hypometabolic basal ganglia is consistent with the adanced state of this patient's Huntington's Disease
FDG PET扫描显示：基底节区明显低代谢，与患者亨延顿舞蹈病进展期相符。
screen.width-333)this.width=screen.width-333" width=360 height=344 title="Click to iew full Huntington's Disease.jpg (360 X 344)" border=0 align=absmiddle>

3、PET与Moyamoya disease

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4、PET与fMRI
In a study comparing the results from fMRI and PET on a semantic task (J. Delin et.al. (2000)), temporal lobe actiations found using PET were not replicated with fMRI.

As gradient echo echo planar imaging is used in fMRI, susceptibilty artifacts are hypothesized as causing this problem
(很用以理解，就不译了)

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5、PET对癫痫手术的指导
上图，致痫灶代谢减低
Epilepsy surgery candidate; 11 year old female. Right temporal lobe epilepsy PET 5/95, Surgery 10/96. Seizure-free, doing well in school
下图，致痫灶代谢增高
Epilepsy surgery candidate;10 year old male. MRI read as normal PET 8/97, Surgery 9/97. Seizure-free, doing well in school
screen.width-333)this.width=screen.width-333" width=496 height=340 title="Click to iew full Epilepsy-3.jpg (496 X 340)" border=0 align=absmiddle>

neurotome wrote:
神经外科疾病之PET影像5――血管畸形
Because normal arterial structures in front of the nidus are faintly opacified, this
AM is recorded as the high-flow type. Upper Right: A T2-weighted axial MR image demonstrating the nidus and the main draining ein of the lesion.
翻译：窦前方正常的结构模糊。上右：T2见窦及引流静脉。

更正一下，nidus意为“畸形血管团”，“血管巢”的意思。而不是“窦“。

PET对室管膜下灰质异位的诊断
此例与fangqu主任的星期二门诊关于此病的报道如出一辙。

fangqu版主的星期二门诊系列
http://www.dxy.cn/bbs/post/iew?bid=46&id=3086998&sty=3&keywords=%BB%D2%D6%CA%D2%EC%CE%BB

FDG PET Imaging of Subependymal Gray Matter Heterotopia
出自clinical Nuclear Medicine。 olume 30(1) January 2005


A 25-year-old woman underwent interictal F-18 FDG PET for ealuation of long-standing intractable epilepsy. She had no sign or family history of tuberous sclerosis, and she demonstrated no interictal neurologic deficit. PET showed perientricular and deep white matter FDG metabolism that was congruent anatomically to the pattern of nodular gray matter heterotopia (GMH) demonstrated on MRI. This case adds information concerning the spectrum of interictal FDG metabolism within GMH, when it is performed without actiation task. It further illustrates the importance of recognizing GMH to aoid their misinterpretation as independent, subclinical ictal foci.

FIGURE 1. Axial FDG PET sections (aboe) and corresponding axial MRI sections (below) demonstrate 2 heterotopic gray matter nodules within the left hemisphere. One lies adjacent to the lateral entricle and extends outward into the hemispheric white matter (white arrows), whereas the other courses along the occipital horn (open arrows). Metabolism within the heterotopia is slightly below that of oerall cortical metabolism. These sections and others demonstrate that the oerlying cerebral cortex is normal in thickness and metabolism. The actiity ratio between the nodules and their adjacent cerebral cortices was approximately 0.7. The basal ganglia and corpus callosum were normal. PET was acquired on a Siemens ECAT EXACT in 2D mode with attenuation correction, 45 minutes following administration of 8 mCi FDG intraenously. The MR image was obtained using a 3475/98 (TR/TE) spin echo sequence on a Siemens Somatom Symphony. The term gray matter heterotopia (GMH) actually refers to a group of cortical malformations that are belieed to result from improper migration of neuroblasts during brain deelopment.1 arious classification schemes hae been applied to their description. Traditional schemes diide heterotopia between those that are presumed to arise from an arrest in migration, and those that are presumed to arise from excessie migration. Classic pathologic subtypes of the former include nodular, laminar, and double cortical forms, whereas clinical subtypes include subependymal (perientricular), subcortical, and band forms. These classifications are eoling, and recent adances in neuroscience permit a fairly elaborate classification of cortical malformations in general.2,3 Among the heterotopias, the subependymal type frequently presents clinically. Indiiduals with subependymal heterotopia hae a high prealence of epilepsy, with onset of seizures typically in the second decade of life.1 Scattered descriptions of PET findings in GMH hae appeared in the literature.In most cases, FDG metabolism of the heterotopia has been similar to or slightly greater than normal cortical gray matter. Two actiation studies using O-15-labeled water showed increased regional blood flow within heterotopia during select motor, language, and isuospatial tasks. Identification of GMH is important during the interpretation of interictal FDG PET, because their uptake is not to be confused with subclinical ictal phenomena. Careful correlation, or image fusion, between PET and MRI will establish the proper diagnosis.

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