中重度颅脑损伤患者应用颅内压监测对判断病情预后和指导治疗的价值

目的探讨颅内压监测对中重度颅脑损伤患者判断病情预后和指导治疗的临床价值。方法选择中重度颅脑损伤患者108例,随机分为研究组和对照组各54例。研究组患者入院后行有创颅内压监护,对照组根据传统方法评估颅内压。比较2组患者GCS评分和GOS评分和并发症发生率,比较不同预后患者的颅内压水平。结果 2组治疗前GCS评分无显著差异(P0.05),治疗后研究组GCS评分显著优于对照组(P0.01)。研究组GOS评分显著优于对照组(P0.05)。研究组并发症发生率显著低于对照组(P0.05)。不同预后组间颅内压力差异有统计学意义(P0.01)。结论中重度颅脑损伤患者行颅内压检测可有效判断患者病情并指导治疗,改善患者预后,具有临床应用价值。     

颅内压及中心静脉压监测在脑水肿治疗中的应用

目的探讨联合监测颅内压(ICP)及中心静脉压(CVP)在重型颅脑损伤患者伤后脑水肿治疗中的临床应用价值。方法 45例重型颅脑颅脑损伤患者随机分为对照组(21例)及治疗组(24例)。对照组以常规治疗方法控制ICP;治疗组在常规治疗基础上,联合监测ICP及CVP,并根据监测结果调整治疗方案。治疗终结后随访半年,采用格拉斯哥预后评分(GOS)对患者恢复情况进行评分。结果治疗组1周内日均甘露醇用量较对照组显著减少(P0.01);治疗组GOS评分较对照组显著提高(P0.05)。结论 ICP及CVP联合监测既能保证ICP的精准调控,又能保证血容量的平衡,可改善重型颅脑损伤患者的预后。     

血管内降温治疗重型颅脑损伤的临床研究

目的研究血管内降温治疗重型颅脑损伤的临床效果。方法将51例重型颅脑损伤病人随机分为对照组(n=20),传统亚低温组(n=20)和血管内降温组(n=11)。两个治疗组31病人均于伤后20 h内使直肠温度降至33~34℃,治疗持续4~7 d,当颅内压降至正常后24 h,停止亚低温治疗。同时床旁监测生命体征、颅内压等。根据GOS评估法判定疗效。结果三组病人的年龄及GCS评分等临床特征无明显统计学差异(P0.05);伤后第7天,两组亚低温治疗的病人颅内压明显低于对照组(P0.05),且基本降至正常。经6个月随访,两组亚低温治疗病人的病死率明显低于对照组,恢复良好率显著高于对照组(P0.05)。结论血管内降温治疗重型颅脑损伤与传统亚低温治疗效果相似,其可减少肌松药和镇静药的使用及机械通气所带来的并发症。该方法治疗重型颅脑损伤安全、有效。     

颅内压监测在重型颅脑损伤病人甘露醇应用中的意义

目的探讨动态颅内压监测在指导重型颅脑损伤病人甘露醇应用中的作用。方法 2013年5月至2015年3月收治重型颅脑损伤136例,其中65例在颅内压监测下规范应用甘露醇治疗(监测组),71例进行常规脱水治疗(常规组)。监测组根据颅内压的变化适时调整甘露醇的应用,常规治疗组则根据临床经验常规应用甘露醇。结果监测组甘露醇应用次数、剂量均明显低于常规组(P0.05)。监测组肾功能损害发生率、电解质紊乱发生率和预后不良率均明显低于常规组(P0.05)。结论重型颅脑损伤病人行持续颅内压监测能够明显减少甘露醇的应用时间和剂量,降低并发症发生率,改善预后。     

闪光视觉诱发电位颅内压无创检测仪在颅脑损伤脱水剂应用中的意义

目的评价在重型颅脑损伤治疗过程中,根据无创颅内压检测仪所测得颅内压情况来确定脱水剂的剂量及疗效。方法选择重型颅脑损伤患者192例,按随机数字表法分为两组:观察组(98例)根据无创颅内压检测情况使用脱水剂(20%甘露醇),对照组(94例)根据病人症状、体征及头颅CT片经验性使用脱水剂(20%甘露醇)。结果观察组治疗过程中人均使用甘露醇(548.47±71.39)g,对照组人均使用(802.66±78.6)g,两组比较差异显著(P<0.05)。观察组恢复良好95例(96.94%),中重残3例,无死亡病例;对照组恢复良好85例(90.43%),中重残7例,死亡2例。两组恢复良好率比较差异不显著(P>0.05)。结论无创颅内压检测仪在重型颅脑损伤治疗过程中,指导脱水剂的应用,可大大减少了患者使用脱水剂的剂量,这对减少术后并发症和提高患者的生存质量是有帮助的。     

颅内压监测联合置管引流术在中重度颅脑损伤的应用研究

目的探讨颅内压监测联合置管引流术在中重度颅脑损伤的临床疗效。方法回顾性分析123例中重度颅脑损伤病人的临床资料,其中采用颅内压监测联合置管引流术(治疗组)39例,仅采用颅内压监测(对照组)84例。比较两组颅内压值、甘露醇使用率、再出血率、感染率、二次开颅率及预后。结果与对照组相比,治疗组术后颅内压值逐渐降低,说明该方法能明显减少甘露醇使用率和二次开颅率,且差异均有统计学意义(P0.05)。术后6个月治疗组病人预后良好率明显提高,两组GOS评分差异有统计学意义(P0.05)。结论颅内压监测联合置管引流术通过颅内压监测、血肿或脑脊液外引流,降低颅内高压,减少二次开颅率,减少病人创伤,节省医疗资源,预后良好,是治疗中重度颅脑损伤的有效方法之一。     

有创颅内压监测在中重型颅脑创伤中的应用价值

目的探讨有创颅内压监测在中重型颅脑创伤治疗过程中的指导作用和预后判断价值。方法溧水区人民医院神经外科于2016年11月至2017年10月收治并行手术治疗的55例中重型颅脑外伤患者,其中入院格拉斯哥昏迷量表(GCS)评分在3~5分者22例,GCS评分6~8分者10例,GCS评分9分者23例;行脑室型ICP传感器置入8例,脑实质型ICP传感器置入47例。根据患者的预后分为预后良好组[格拉斯哥预后量表(GOS)评分4~5分]和预后不佳组(GOS评分1~3分),分析并比较两组患者有创颅内压监测值的波动情况及其对手术操作和预后的影响。结果本组患者中预后良好者(GOS评分5分)6例(11%),中残(GOS评分4分)15例(28%),重残(GOS评分3分)9例(17%),植物状态(GOS评分2分)7例(13%),死亡(GOS评分1分)18例(31%)。两组的颅内压数值在置入时初始、术后变化的均值,以及两组各步骤间颅内压波动变化的差异有统计学意义(均P0.01)。结论颅内压实时监测能够在重型颅脑外伤患者治疗过程中及时反映大脑顺应性变化及血流供应状况,有效指导阶梯治疗操作;同时也是患者预后评估的重要参考依据。     

不同去骨瓣减压术式治疗重型颅脑损伤对比研究

目的分析不同去骨瓣减压术式治疗重型颅脑损伤的临床效果及对预后的影响。方法选取2011-01—2016-01张家港市第一人民医院治疗的重型颅脑损伤患者72例。根据手术方法分为观察组(n=37)与对照组(n=35)。2组均给予常规的术前治疗,观察组采取标准大骨瓣减压术,对照组采取常规去骨瓣减压术。观察2组治疗效果,术后颅内压、并发症发生情况及术后6个月GOS评分。结果观察组良好率64.86%,对照组为40.00%。观察组良好率明显高于对照组,差异有统计学意义(P0.05)。观察组术后颅内压明显低于对照组,差异有统计学意义(P0.05)。2组并发症发生率差异无统计学意义(P0.05)。观察组术后6个月GOS评分(4.34±0.44)分,对照组为(3.89±0.43)分。观察组GOS评分明显高于对照组(t=6.18,P0.05)。结论标准大骨瓣减压术治疗重型颅脑损伤的临床效果显著,术后颅内压下降快,值得推广。     

颅内压监测下亚低温治疗重型颅脑损伤的临床研究

目的研究颅内压监测下亚低温治疗重型颅脑损伤患者的临床效果。方法将100例重型颅脑损伤(sTBI)患者按随机数字表法分为对照组与亚低温组,每组各50例。两组患者入院后均予以常规对症治疗;亚低温组患者加用亚低温治疗,控制直肠温度(RT)为32℃~34℃;对照组患者控制RT在36℃~37℃;均监测患者的脑组织氧分压(PbtO_2)和颅内压(ICP)。比较两组患者入院时、入院24 h、48 h、72 h、96 h的ICP、脑组织PbtO_2及血乳酸、脑源性神经细胞营养因子(BDNF)水平的变化;治疗前、后给患者进行美国国立卫生研究院卒中量表(NIHSS)、格拉斯哥预后量表(GOS)评分;统计两组并发症发生率。结果 (1)入院时,两组ICP、PbtO_2比较,差异无统计学意义(均P0.05);入院24 h、48 h、72 h、96 h,两组ICP均降低、PbtO_2均升高,亚低温组入院不同时间点ICP均低于、PbtO_2均高于对照组(均P0.05)。(2)入院时,两组血乳酸、BDNF水平比较,差异无统计学意义(均P0.05);入院24 h、48 h、72 h、96 h,两组的血乳酸水平降低,BDNF水平上升;亚低温组入院后各时间点血乳酸水平低于、BDNF水平高于对照组(均P0.05)。(3)治疗前,两组NIHSS、GOS评分的差异无统计学意义(均P0.05);治疗后3个月时,两组的NIHSS评分均降低,GOS评分均上升,但亚低温组的NIHSS评分低于、GOS评分高于对照组,差异有统计学意义(均P0.05)。(4)亚低温组的并发症发生率略低于对照组,但差异无统计学意义(P0.05)。结论 ICP监测下亚低温治疗重型颅脑损伤可快速降低患者的ICP,改善其神经功能及预后。     

脑疝复位天幕切开治疗重型颅脑损伤

目的探讨脑疝复位天幕切开对重型颅脑损伤后脑水肿、颅内血肿脑疝病人的治疗效果。方法回顾性分析58例重型颅脑损伤脑水肿、颅内血肿脑疝病人的临床资料,其中观察组30例病人采取标准大骨瓣减压术+脑疝复位天幕切开手术治疗;对照组28例仅采取标准大骨瓣减压术,对比两组病人手术效果。结果术后1周复查,观察组病人GCS显著高于对照组(P0.05),颅内压显著低于对照组(P0.05)。术后并发症发生情况:观察组病人的脑积水、应激性溃疡发生率均显著低于对照组(P0.05)。术后随访,观察组病人术后6个月GOS优于对照组(P0.05)。结论脑疝复位天幕切开能够尽快降低重型颅脑损伤后脑水肿、颅内血肿脑疝病人颅内压,有利于病人远期预后。     

Tau-induced neurodegeneration: mechanisms and targets

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau’s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau’s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.     

The effect of risperidone on reward‐related brain activity is robust to drug‐induced vascular changes

Dopamine (DA) mediated brain activity is intimately linked to reward‐driven cerebral responses, while aberrant reward processing has been implicated in several psychiatric disorders. fMRI has been a valuable tool in understanding the mechanism by which DA modulators alter reward‐driven responses and how they may exert their therapeutic effect. However, the potential effects of a pharmacological compound on aspects of neurovascular coupling may cloud the interpretability of the BOLD contrast. Here, we assess the effects of risperidone on reward driven BOLD signals produced by reward anticipation and outcome, while attempting to control for potential drug effects on regional cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). Healthy male volunteers (n = 21) each received a single oral dose of either 0.5 mg, 2 mg of risperidone or placebo in a double‐blind, placebo‐controlled, randomised, three‐period cross‐over study design. Participants underwent fMRI scanning while performing the widely used Monetary Incentive Delay (MID) task to assess drug impact on reward function. Measures of CBF (Arterial Spin Labelling) and breath‐hold challenge induced BOLD signal changes (as a proxy for CVR) were also acquired and included as covariates. Risperidone produced divergent, dose‐dependent effects on separate phases of reward processing, even after controlling for potential nonneuronal influences on the BOLD signal. These data suggest the D2 antagonist risperidone has a wide‐ranging influence on DA‐mediated reward function independent of nonneuronal factors. We also illustrate that assessment of potential vascular confounds on the BOLD signal may be advantageous when investigating CNS drug action and advocate for the inclusion of these additional measures into future study designs.     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra

Summary. The β-carboline norharman is present in cooked food and tobacco smoke and show structural resemblance to the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. C57BL/6 mice were injected subcutaneously with norharman (3 and 10 mg/kg) twice per day for five consecutive days. Eighteen hours after the last dose an increased expression of glial fibrillary acidic protein and fluoro-jade staining were demonstrated whereas the number of tyrosine hydroxylase positive cells were unchanged in the substantia nigra. Two weeks after the last treatment a decreased motor activity was observed whereas cognitive functions remained intact. In cultured PC12 cells norharman treatment induced mitochondrial dysfunction and increased the number of caspase-3 and TUNEL-positive cells. The results demonstrate that norharman induced apoptosis in cultured cells as well as early neurodegeneration, glial activation and sustained motor deficits in mice and suggest that exposure to norharman may contribute to idiopathic Parkinson’s disease.     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

The ENIGMA‐Epilepsy working group: Mapping disease from large data sets

Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.     

缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布特点的超声造影研究

目的 应用超声造影观察缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布情况,明确其 斑块内新生血管分布特征。 方法 病例组选取因急性缺血性卒中住院的糖尿病患者40例（入组前未服用降糖药）,卒中同侧颈 动脉斑块形成;对照组为同期门诊就诊的颈动脉斑块形成患者,无卒中病史,性别及年龄匹配的非 糖尿病患者32例。两组患者行弓上计算机断层扫描血管造影（computed tomography angiography,CTA） 检查排除主动脉弓斑块及颅内动脉病变,排除卵圆孔未闭及心房颤动等。对所有患者均行常规超声 及超声造影检查。常规超声观察斑块厚度及内部回声,超声造影观察斑块增强情况,横切面多角度 观察,将超声造影结果分为近内膜处有增强（代表新生血管）及近内膜处无增强两种。 结果 两组患者颈动脉斑块厚度及回声情况差异无统计学意义。超声造影结果显示病例组颈动脉 斑块近内膜处增强者34例（85%）,对照组近内膜处增强12例（37.5%）,差异有统计学意义（χ 2=17.38, P＜0.01）。 结论 未服用降糖药的2型糖尿病并发急性缺血性卒中的患者颈动脉粥样硬化斑块内近内膜处新生 血管增生多于无糖尿病患者,提示血糖升高与颈动脉斑块内血管新生有关。     

Yohimbine increases the binding potential for [11C]flumazenil in the monkey brain

Summary. We evaluated the impact of yohimbine administration on benzodiazepine (BDZ) receptor binding in the central nervous system of non-human primates (rhesus monkeys). Estimates of the binding potential (B_max/K_d) of BDZ receptors were made following intravenous administration of yohimbine, an α₂-adrenoceptor antagonist. Positron emission tomography was used in conjunction with [¹¹C]flumazenil (Ro 15-1788), a tracer for central BDZ receptor binding activity. The effects of yohimbine were compared with a control condition in which saline was administered. Yohimbine significantly increased the binding potential in the hippocampus, as assessed using a Student's t-test with Bonferroni correction. The result that the administration of yohimbine readily induces an increase in the binding potential for BDZ receptors in the primate brain suggests that the presence of an anxiety state potentiates the effect of anxiolytics. Accepted August 10, 2001