纹状体梗死后继发性黑质损害

由于纹状体与黑质间存在纤维联系,纹状体梗死可导致黑质继发性损害.近年来,已出现了一系列有关黑质继发性损害的临床特征、病理生理学机制以及如何在纹状体梗死患者活体内进行检测的研究.文章就该领域的研究进展做了综述.     

脊髓亚急性联合变性周围神经损害临床及神经电生理表现特点

脊髓亚急性联合变性(SCD)主要累及脊髓侧索和后索,临床表现以侧索受累的锥体束征和后索受累的深感觉障碍为主;此外,周围神经、视神经、大脑白质亦可受累,且周围神经受损较常见.本文分析42例SCD周围神经损害患者的临床表现及神经电生理改变特点,希望对SCD周围神经损害的早期诊断提供有意义的依据.     

脑出血继发脑水肿的15例临床分析

脑出血是一种发病率、死亡率和致残率均很高的急性脑血管病,至今仍无特别有效的治疗方法.近年来,人们注意到有一部分脑出血患者在发病后一段时间内仍出现进行性神经功能恶化,提示除血肿引起的急性神经组织损害外,还存在有血肿周边的继发性损害--脑水肿持续性加重.现将我院2000年6月至2003年3月住院的124例脑出血患者,其中脑出血继发脑水肿15例的临床资料分析报告如下.     

老年人脑白质结构的扩散张量成像研究

目的应用扩散张量成像（diffusion tensor imaging，DTI）阐明老年人脑白质结构平均弥散系数（ADCavg）和部分各向异性（FA）的变化。方法老年组及非老年组各30例。所有受检者均进行神经科查体和简易智能精神状态量表（MMSE）测试，无影响神经系统的疾病。所有受检者均行DTI检查，选择额叶白质、顶叶白质、半卵圆中心、胼胝体膝部、胼胝体压部为兴趣区，定量测量ADCavg与FA值。结果ADCavg、FA值男、女性别差异无统计学意义（P〉0．05），左右半球无明显改变。随着年龄增长，ADCavg值与年龄呈正相关，FA值与年龄呈负相关。在额叶白质（ADCavg：r=0．449，P〈0．05；FA：r=0．350，P〈0．05）、半卵圆中心（ADCavg：r=0．347，P〈0．05；FA：r=0．409，P〈0．05）、胼胝体膝部（ADCavg：r=0．452，P〈0．01；FA：r=0．556，P〈0．01）、压部（ADCavg：r=0．296，P〉0．05；FA：r=0．289，P〉0．05）、顶叶白质（ADCavg：r=0．367，P〈0．05；FA：r=0．287，P〉0．05）。老年组额叶白质、胼胝体膝部、半卵圆中心的ADCavg、FA值与简易智能精神状态量表（MMSE）相关，尤其是额叶白质的FA值相关更显著（r=0．466，P〈0．01）。结论与年龄相关的定量DTI分析，可有助于评价与年龄相关的变化。并且可建立一个与神经变性疾病比较对照的标准。DTI功能与结构的结合，表明老年人认知功能的衰退与白质微结构密切相关。     

脑出血后继发性水肿和神经损害的机制

脑出血后血肿周围继发性水肿和神经损伤是脑出血患者预后不良的重要因素。近年来，对针对脑出血后继发性神经损害机制的干预措施进行了一些研究，并取得了一些进展。     

血管性脑白质损害及其对认知功能的影响

神经影像学显示的腩白质损害常见于正常老年人和多种认知障碍患者,其病理学特征包括脱髓鞘、轴突丢失和腔隙性梗死,病理生理学机制可能是低灌注和脑血流紊乱引起的慢性脑缺血.血管性脑白质损害可引起不同程度的认知障碍,但与白质损害相关的确切痴呆病理学哑型尚无定论.     

脑梗死后远隔部位继发性损害的影像学诊断及其临床意义

局灶性脑梗死会引起顺行性和逆行性远隔部位的继发性损害,远隔部位继发性损害在一定时间内会逐渐进展,并对患者的神经功能恢复造成不良影响.     

脑梗死远隔区继发性损害的弥散张量成像

尸检和动物实验已证实脑梗死远隔区的继发性损害。由于受到研究方法和手段的限制,临床研究一直滞后。近年来,弥散张量成像技术在这一领域的临床应用取得了一些新的进展。     

大脑中动脉供血区梗死的远隔损害

大脑中动脉供血区梗死后远隔部位损害的研究近年来取得了显著的进展,更多的动物实验从细胞、生化以及分子水平上对远隔部位损害进行了深入细致的研究,氧化损伤、B淀粉样蛋白沉积等新的损伤机制被发现.新的影像学检测手段,如磁共振弥散张量成像也逐渐被应用于远隔部位损害的诊断.     

脑梗死远隔区继发性损害的弥散张量成像

尸检和动物实验已证实脑梗死远隔区的继发性损害。由于受到研究方法和手段的限制，临床研究一直滞后。近年来，弥散张量成像技术在这一领域的临床应用取得了一些新的进展。     

大脑中动脉供血区梗死后远隔部位继发性损害的研究进展

临床和动物实验研究均已证明，脑梗死造成的神经功能缺损不仅与梗死灶局部损伤有关，而且也与远离梗死灶的相关部位的继发性损害有关。大鼠一侧大脑中动脉永久闭塞不仅造成同侧大脑皮质、尾壳核和豆状核梗死，而且引起远离梗死灶与大脑皮质有大量纤维联系的丘脑、黑质、海马、脑干和脊髓继发性退行性改变。脑梗死后远隔部位继发性损害的机制可能与轴突的退行性改变、神经营养障碍、存在神经生长抑制因子、局部脑血流减少、神经递质调节失衡和蛋白合成抑制等因素有关。这些研究有助于指导卒中后的康复治疗。     

大脑中动脉供血区梗死后远隔部位继发性损害的研究进展

临床和动物实验研究均已证明,脑梗死造成的神经功能缺损不仅与梗死灶局部损伤有关,而且也与远离梗死灶的相关部位的继发性损害有关。大鼠一侧大脑中动脉永久闭塞不仅造成同侧大脑皮质、尾壳核和豆状核梗死,而且引起远离梗死灶与大脑皮质有大量纤维联系的丘脑、黑质、海马、脑干和脊髓继发性退行性改变。脑梗死后远隔部位继发性损害的机制可能与轴突的退行性改变、神经营养障碍、存在神经生长抑制因子、局部脑血流减少、神经递质调节失衡和蛋白合成抑制等因素有关。这些研究有助于指导卒中后的康复治疗。     

Functional Imaging of Cognitive Control During Acute Alcohol Intoxication

Background: The anterior cingulate and several other prefrontal and parietal brain regions are implicated in error processing and cognitive control. The effects of different doses of alcohol on activity within these brain regions during a functional magnetic resonance imaging (fMRI) task where errors are frequently committed have not been fully explored. Methods: This study examined the impact of a placebo [breath alcohol concentration (BrAC) = 0.00%], moderate (BrAC = 0.05%), and high (BrAC = 0.10%) doses of alcohol on brain hemodynamic activity during a functional MRI (fMRI) Go/No‐Go task in 38 healthy volunteers. Results: Alcohol increased reaction time and false alarm errors in a dose‐dependent manner. fMRI analyses showed alcohol decreased activity in anterior cingulate, lateral prefrontal cortex, insula, and parietal lobe regions during false alarm responses to No‐Go stimuli. Conclusions: These findings indicate that brain regions implicated in error processing are affected by alcohol and might provide a neural basis for alcohol’s effects on behavioral performance.     

Multiple Previous Alcohol Detoxifications Are Associated With Decreased Medial Temporal and Paralimbic Function in the Postwithdrawal Period

BACKGROUND: Functional neuroimaging studies after alcohol cessation have demonstrated that chronic alcohol use globally reduces neuronal activity for several weeks. Less is known about the effects of previous alcohol use patterns on regional brain activity. Multiple previous alcohol detoxifications are associated with a worse clinical course and increased risk of seizures, perhaps due to sensitization of key brain structures. We performed the following imaging study in alcoholics in the postwithdrawal period to determine if blood flow in medial temporal structures would differ as a function of previous alcohol use (i.e., whether regions were kindled or sensitized due to multiple detoxifications). METHODS: Fourteen adults meeting DSM-IV criteria for alcohol dependence (mean age 35, 8 SD; 10 men) and participating in a double-blind detoxification medication study underwent a brain perfusion Tc99 m-ECD (Neurolite) single photon emission computed tomography scan on days 7 through 9 (mean 7.6, .5 SD) after their last drink and 2 to 3 days since their last detoxification medication. Seven nonpsychiatrically ill, nonalcohol-dependent healthy adults were scanned as control subjects. RESULTS: Alcoholics compared with controls had widely reduced relative activity in cortical secondary association areas and relatively increased activity in the medial temporal lobes (p < 0.01). Five alcoholic patients with > or = 2 previous detoxifications were compared with five patients in their first detoxification (age and detoxification medication matched). Multiple detoxification patients had significantly lower relative activity in bilateral anterior temporal poles and medial temporal lobes and in visual cortex (p < 0.01) compared with first episode patients. CONCLUSIONS: These studies are consistent with other studies comparing alcoholics and controls. They also suggest that on day 7 of detoxification, alcoholic subjects with multiple previous detoxifications have decreased visual cortex, medial temporal lobes, and anterior paralimbic blood flow, compared with those in their first detoxification. Further studies seem warranted to confirm these initial exploratory results.     

Reduced cortical thickness in abstinent alcoholics and association with alcoholic behavior

Background: Chronic misuse of alcohol results in widespread damage to the brain. Prior morphometric studies have examined cortical atrophy in individuals with alcoholism; however, no previous studies have examined alcohol‐associated atrophy using cortical thickness measurements to obtain regional mapping of tissue loss across the full cortical surface. Methods: We compared cortical thickness measures from 31 abstinent individuals with a history of prior alcohol abuse to 34 healthy nonalcoholic control participants (total sample size = 65). Cortical surface models were created from high‐resolution T1‐weighted images, and cortical thickness was then estimated as the distance between the gray matter/white matter boundary and the outer cortical surface. Results: Abstinent alcoholics showed reduced whole‐brain thickness as compared to nonalcoholic participants. Decreases in thickness were found bilaterally in (i) superior frontal, (ii) precentral, (iii) postcentral, (iv) middle frontal, (v) middle/superior temporal, (vi) middle temporal, and (vii) lateral occipital cortical regions. Decreased cortical thickness in the alcoholic group was associated with severity of alcohol abuse. Conclusions: These findings demonstrate widespread reduction in cortical thickness as a consequence of chronic alcoholism, with most severe reductions in frontal and temporal brain regions.     

缺血性卒中后非流利型失语患者局部一致性变化：静息态功能性磁共振成像研究

目的 探讨缺血性卒中后非流利性失语患者静息态功能磁共振成像（functionalmagnetic resonance imaging fMRI）的脑功能特点.方法 对17例缺血性卒中后非流利性失语患者以及19名年龄、性别和受教育程度均匹配的健康对照者进行静息态fMRI检查,采用局部区域一致性（regional homogeneity,ReHo）分析方法计算静息态下脑区的ReHo情况.结果 与对照组比较,患者组左侧额上回、右侧额下回、右侧脑岛以及右侧缘上回ReHo值增高,右侧小脑半球、左侧颞上回、颞中回以及右侧颞下回脑区ReHo值降低.结论 在静息状态下,缺血性卒中后非流利性失语患者存在多个脑区ReHo异常,这种异常改变可能与其功能损伤后修复的代偿作用有关.     

脑缺血的全脑保护概念

就卒中后功能恢复而言,所有脑区、细胞类型和细胞成分均应受到保护,而不仅仅是保护某一脑区或某一细胞类型。神经保护治疗的临床试验至今依然令人失望,未来脑缺血的治疗可能有赖于全脑保护,而不是选择性地保护灰质或神经元核周质。在脑缺血的全脑保护概念中,脑白质和神经胶质细胞的保护以及远离缺血核心的脑保护尤为重要。     

Effects of Alcohol on Performance on a Distraction Task During Simulated Driving

Background:  Prior studies report that accidents involving intoxicated drivers are more likely to occur during performance of secondary tasks. We studied this phenomenon, using a dual-task paradigm, involving performance of a visual oddball (VO) task while driving in an alcohol challenge paradigm. Previous functional MRI (fMRI) studies of the VO task have shown activation in the anterior cingulate, hippocampus, and prefrontal cortex. Thus, we predicted dose-dependent decreases in activation of these areas during VO performance.
Methods:  Forty healthy social drinkers were administered 3 different doses of alcohol, individually tailored to their gender and weight. Participants performed a VO task while operating a virtual reality driving simulator in a 3T fMRI scanner.
Results:  Analysis showed a dose-dependent linear decrease in Blood Oxygen Level Dependent activation during task performance, primarily in hippocampus, anterior cingulate, and dorsolateral prefrontal areas, with the least activation occurring during the high dose. Behavioral analysis showed a dose-dependent linear increase in reaction time, with no effects associated with either correct hits or false alarms. In all dose conditions, driving speed decreased significantly after a VO stimulus. However, at the high dose this decrease was significantly less. Passenger-side line crossings significantly increased at the high dose.
Conclusions:  These results suggest that driving impairment during secondary task performance may be associated with alcohol-related effects on the above brain regions, which are involved with attentional processing/decision-making. Drivers with high blood alcohol concentrations may be less able to orient or detect novel or sudden stimuli during driving.     

老龄大鼠慢性脑灌注不足与认知功能障碍的研究

目的　探讨老龄大鼠慢性脑灌注脑损害和认知功能障碍及其机制。方法　 5 0只老龄大鼠用于实验 ,其中 2 0只接受环孢菌素A(CsA)胃灌治疗。用光镜和电镜观察组织学改变 ,免疫组织化学法检测免疫细胞的活动 ,采用微机控制穿梭箱双向主动回避反应实验系统检测大鼠认知功能。结果　大鼠持久性双侧颈总动脉结扎 (2VO)诱导的慢性脑灌注不足造成了脑组织广泛免疫细胞活动和进行性脑损害 ,导致了大鼠进行性学习和记忆能力下降。CsA治疗组大鼠脑内免疫细胞的活动明显减少 ,脑损害明显减轻 ,学习和记忆能力显著提高。结论　脑组织免疫细胞的活动贯穿于大鼠慢性脑灌注不足脑损害的病理过程 ,在脑损害和认知功能障碍的发生和发展中起重要作用 ;CsA可明显减轻脑内免疫细胞的活动 ,防治了大鼠的脑损害和认知功能障碍。     

Sex-dependent association of common variants of microcephaly genes with brain structure

Loss-of-function mutations in the genes associated with primary microcephaly (MCPH) reduce human brain size by about two-thirds, without producing gross abnormalities in brain organization or physiology and leaving other organs largely unaffected [Woods CG, et al. (2005) Am J Hum Genet 76:717–728]. There is also evidence suggesting that MCPH genes have evolved rapidly in primates and humans and have been subjected to selection in recent human evolution [Vallender EJ, et al. (2008) Trends Neurosci 31:637–644]. Here, we show that common variants of MCPH genes account for some of the common variation in brain structure in humans, independently of disease status. We investigated the correlations of SNPs from four MCPH genes with brain morphometry phenotypes obtained with MRI. We found significant, sex-specific associations between common, nonexonic, SNPs of the genes CDK5RAP2, MCPH1, and ASPM, with brain volume or cortical surface area in an ethnically homogenous Norwegian discovery sample (n = 287), including patients with mental illness. The most strongly associated SNP findings were replicated in an independent North American sample (n = 656), which included patients with dementia. These results are consistent with the view that common variation in brain structure is associated with genetic variants located in nonexonic, presumably regulatory, regions.