爱荷华博弈任务(IGT)与决策的认知神经机制

爱荷华博弈任务(IGT)是一项检查情感性决策机制的常用实验范式。据此, Damasio等人提出了躯体标记假设(SMH)解释情绪影响决策的神经生理机制。近期, 大量研究在IGT究竟是模糊决策还是风险决策、与情绪和认知的关系、与工作记忆和陈述性记忆的关系以及IGT的神经网络与分子遗传机制等方面积累了丰富资料。结果显示, IGT加工的早期由模糊决策主导, 情绪性躯体信号对引导决策选项的偏好可能起关键作用, 后期则倾向是一种风险决策, 认知评价和预期对选项偏向逐渐占优势; IGT与工作记忆的加工成分有相互重叠, 也需陈述性记忆的参与; IGT的加工不仅依赖于杏仁核、腹内侧前额皮层、眶额皮层等组成的情绪脑网络的活动, 还与背外侧前额皮层、海马、腹侧纹状体、岛叶皮层、辅助运动前区、扣带回皮层等许多脑区的活动有关; COMT和5-HTT的基因多态性会调节IGT相关的决策加工。总之, IGT是一项需要多重神经系统协同活动的决策加工任务, 且模糊与风险决策可能具有不同的遗传基础。     

高低行为激活系统个体在赌博任务下的决策模式

为考察不同行为激活系统/行为抑制系统下的个体在Iowa赌博任务反应模式下的决策行为,本研究采用人格问卷与行为实验相结合的方式,探讨了人格、冲动和行为决策间的关系。结果发现:(1)行为激活系统三个维度与行为决策存在显著负相关,行为激活系统低分组的IGT得分较高,行为激活系统高分组的IGT得分较低,而冲动特征与IGT得分相关不显著;(2)行为激活系统高、低分者在IGT任务上差异显著,且行为激活系统高分组者在收益-风险并存情境中表现出"即时收益优先"的决策模式。结果提示,在收益-风险并存情境中,高行为激活的人格特征者倾向风险决策模式。     

不公平感及相关决策的认知神经机制

公平是人类社会生活的基本规范之一,不公平感及其相关决策则是研究者们关注的重要课题。长期以来,该领域的研究一般采用最后通牒博弈或其变式展开。大量脑成像研究探查了关于不公平感及相关决策的认知神经机制,尤其集中探讨了最后通牒博弈的回应者对不公平提议进行反应的脑区及其对应功能。经常得到关注的脑区包括了前脑岛、前扣带皮层、背外侧前额叶、内侧前额叶、杏仁核和颞顶交界等。对特殊人群的不公平感及相关决策进行研究可以帮助检验或澄清上述重要脑区及脑网络在不公平感及相关决策中扮演的角色,同时也阐释特殊人群的社会认知功能的特点。近年来,相当数量的研究关注了不同情境因素(包括分配方案相关因素和社会情境相关因素)调制不公平感及相关决策的过程,并讨论其背后的认知神经机制。未来的研究更应利用多模态数据分析方法,同时结合基因和激素层面的研究,以期深入对不公平感及相关决策的心理和生理机制的理解。     

Relationships between executive function,working memory,and decision-making on the Iowa Gambling Task: Evidence from ventromedial patients,dorsolateral patients,and normal subjects

The results of previous studies are inconsistent in regard to the relationship between the Iowa Gambling Task (IGT), working-memory (WM), and executive tasks, and whether these cognitive processes could be considered as mechanisms underlying a decision-making deficit. Moreover, the relationship between the IGT and executive measures is examined based on a limited number of executive tasks, within different populations showing diffuse damage. In addition, there are fewer studies carried out within control participants, with those studies also being inconclusive. It is also suggested that the association of the IGT performance with executive tasks depends on whether the IGT was running under ambiguity or under risk. In this work, all of these issues are studied. Results showed that both patients with ventromedial (VMPFC, N = 10) and dorsolateral (DLPFC, N = 10) prefrontal cortex lesions are significantly impaired on almost all executive tasks, WM tasks, and the IGT. Furthermore, when the IGT is run under risk, there are significant correlations between executive measures and the IGT for the DLPFC patients and the control participants (N = 34) but not the VMPFC patients. No correlation was found between WM tasks and the IGT for both frontal subgroups and control participants. These findings suggested that the mechanisms underlying the IGT deficit differ according to the lesion locations.     

Cortical neuroanatomical correlates of behavioral deficits produced by lesion of the basal forebrain in rats

Morphological changes in the frontoparietal cortex were assessed in rats that exhibited deficits in a go/no go alternation task due to electrolytic lesion of the basal forebrain. Cortical area, laminar thickness, neuronal density, and soma area were examined in frontal, hindlimb, forelimb, and parietal areas of the cortex. Quantitative morphological analysis of the frontoparietal cortex in lesioned rats revealed a decrease in laminar thickness due to reduced soma size in particular cortical laminae. Neuronal density was not affected. These effects were present in all cortical areas examined and most pronounced in laminae II-III. Similar morphological changes were observed in the same cortical areas following lesions of the basal forebrain made with ibotenic acid, allowing a discrimination of lesion effects from those induced by damage to fibers of passage or differential behavioral testing. Lesions of the basal forebrain have previously been shown to produce both behavioral deficits and changes in cortical cholinergic activity. The cortical morphological changes observed in the present study following basal forebrain lesion provide further evidence for the importance of ascending cholinergic inputs to the cortex and their role in learning and memory.     

大脑视知觉调控的神经机制

大脑的知觉加工并非单纯由外部刺激驱动,而是存在自上而下的知觉调控。尽管这一现象被大量实验研究证实,但其神经机制仍然是认知神经科学研究的重要问题。本研究系统介绍了知觉调控的神经基础、实现形式、研究范式,及其理论模型,分析指出了当前研究面临的主要问题,并对未来的研究进行了展望,以期促进该问题研究的进一步开展。     

Predictors of decision-making on the Iowa Gambling Task: independent effects of lifetime history of substance use disorders and performance on the Trail Making Test

Poor decision-making and executive function deficits are frequently observed in individuals with substance use disorders (SUDs), and executive deficits may contribute to poor decision-making in this population. This study examined the influence of lifetime history of an alcohol, cocaine, heroin, or polysubstance use disorder on decision-making as measured by the Iowa Gambling Task (IGT) after controlling for executive ability, demographic characteristics, and current substance use. Participants (131 with lifetime history of SUD and 37 controls) completed the IGT and two neuropsychological tests: the Trail Making Test and the Controlled Oral Word Association Test. Control participants performed significantly better than those with a lifetime SUD history on the IGT, but performance on the neuropsychological tests was comparable for the two groups. A lifetime SUD diagnosis was associated with performance on the IGT after controlling for covariates, and Trail Making Test performance was associated with IGT performance in both SUD and control participants.     

Hemispheric visual atentional imbalance in patients with traumatic brain injury

We find a spatially asymmetric allocation of attention in patients with traumatic brain injury (TBI) despite the lack of obvious asymmetry in neurological indicators. Identification performance was measured for simple spatial patterns presented briefly to a locus 5 degrees into the left or right hemifield, after precuing attention to the same (ipsilateral) or opposite (cross-hemifield) side. Though the cue was non-predictive of target location overall, performance was significantly slower for cross than for ipsilateral trials in both patients and controls. We tested 21 TBI patients without overt focal brain damage and nine control subjects. Only patients demonstrated significantly worse performance for left side presentation in the ipsilateral condition. Furthermore, in the cross-hemifield condition, the left-right difference seen in TBI patients was significantly larger-reflecting a failure in producing a leftward attention shift. Again no significant difference was found in controls. These hemifield effects suggest an asymmetry in the ability of TBI patients in shifting attention to the left hemifield, whether from central fixation or from a cue in the contra-lateral hemifield. The results support basic hypotheses regarding visual attention: Attentional control may be asymmetric and attention may be a distributed, rather than localized cortical function.     

An attempt towards differentiating attentional deficits in traumatic brain injury

Attentional deficits in patients suffering traumatic brain injury (TBI) can occur with minor to severe impact to the brain. Based on reviews of both the cognitive and neurobehavioral literature, the following three concepts of attention are addressed: (a) arousal/alertness, (b) selective attention, and (c) energetic aspects of attention, which include such components as effort, resource allocation, and speed of processing. Within each concept, definitions are proposed, the underlying brain mechanisms are identified, and the specific deficits associated with TBI are explored. This review combines theoretical perspectives and clinical findings with the objective of leading toward a diagnostic differentiation that in turn will benefit treatment planning.     

Mental time travel,somatic markers and “myopia for the future”

Patients with damage to the ventromedial prefrontal cortex (VMPFC) are often described as having impaired ability for planning and decision making despite retaining intact capacities for explicit reasoning. The somatic marker hypothesis is that the VMPFC associates implicitly represented affective information with explicit representations of actions or outcomes. Consequently, when the VMPFC is damaged explicit reasoning is no longer scaffolded by affective information, leading to characteristic deficits. These deficits are exemplified in performance on the Iowa Gambling Task (IGT) in which subjects with VMPFC perform significantly worse than neurotypicals in a task which requires them learn from rewarding and punishing experience to make decisions. The somatic marker theory adopts a canonical theory of emotion, in which emotions function as part of a valencing system, to explain the role of affective processes. The first part of the paper argues against this canonical account. The second part provides a different account of the role of the role of the VMPFC in decision-making which does not depend on the canonical account of emotion. Together the first and second parts of the paper provide the basis for a different interpretation of results on the Iowa Gambling Task (IGT). In fact the IGT may be probing a deficit in what has been called mental time travel: the ability to access and use information from previous experience and imaginatively rehearse future experiences as part of the process of deliberation.     

Cortical electrophysiological network dynamics of feedback learning

Understanding the neurophysiological mechanisms of learning is important for both fundamental and clinical neuroscience. We present a neurophysiologically inspired framework for understanding cortical mechanisms of feedback-guided learning. This framework is based on dynamic changes in systems-level oscillatory synchronization, reflecting changes in synaptic plasticity between stimulus-processing and motor areas that are modulated in a top-down fashion by different areas of the prefrontal cortex. We make new and testable predictions for how large-scale cortical networks support learning from feedback. Testing these predictions may provide new insights into the basic mechanisms underlying learning and how these mechanisms may be impaired in clinical disorders in which feedback learning is compromised.     

精神病态暴力犯执行功能的缺陷*

为了解精神病态罪犯可能存在的执行功能缺陷及其是否受冲动性影响,研究采用精神病态检核表（PCL-R）筛选出30名精神病态组被试和30名非精神病态组被试,通过爱荷华赌博任务（IGT）和河内塔任务（TOH）对两组被试执行功能的特点进行分析,并结合冲动性量表（BIS-11）对其冲动性进行测量。研究发现精神病态组的冲动性显著高于控制组;精神病态组选择高风险的不利牌显著多于对照组,即对惩罚不敏感;精神病态组在河内塔任务中的错误次数及所消耗时间都显著高于控制组;冲动性水平与两任务得分均无显著相关。结果表明,精神病态暴力犯在与前额叶相关的执行功能上存在缺陷,并与个体的高冲动性无关。     

Central executive system impairment in traumatic brain injury

The aim of the present study was to identify cognitive functions affected by traumatic brain injury (TBI) and to verify the mechanism underlying cognitive impairment. More precisely, cognitive deficits following TBI can be considered as a consequence of (a) a speed processing deficit, that is a general slowing of perceptual, motor and cognitive subroutines; (b) an impairment of the Central Executive System of working memory (CES).Thirty-seven patients were submitted to a neuropsychological battery, aimed to evaluate different cognitive functions.Results showed severe deficits in speed processing, divided attention,working memory, executive functions and long term memory.Regression analyses, performed to test the two hypotheses, showed that the working memory deficit hypothesis is able to explain divided attention, executive functions and long term memory deficits more than speed processing hypothesis.     

品牌消费旅程中消费者的认知心理过程——神经营销学视角

品牌消费旅程通常指的是对于品牌消费服务的多维度(包括认知, 情绪, 感觉, 行为和品牌关系)响应。揭示品牌消费旅程的认知心理过程是目前营销学领域之中研究的重点与热点。在梳理当前神经营销领域内有关功能性核磁共振(fMRI)、事件相关电位(ERP)、事件相关震荡(ERO)的相关研究成果后, 将消费者在品牌消费旅程之中的认知心理进程划分为注意吸引、决策形成、消费体验和品牌忠诚四个阶段, 并系统阐述了每个阶段之中消费者心理进程的神经机制与脑区活动, 进而全面立体地揭示消费心理的全貌。未来研究可以进一步探索不同神经指标在具体营销情境下的表征意义, 并结合超扫描技术进一步解析多个被试间的神经耦合情况。     

Recovery in Memory Function,and its Relationship to Academic Success,at 24 Months Following Pediatric TBI*

While a number of research papers have reported findings on memory deficits following traumatic brain injury (TBI), only limited studies have monitored the recovery of these skills over time. The present study examined memory ability and its effect on academic success in a group of children who had sustained a mild, moderate, or severe traumatic brain injury (TBI). Results showed that the severe TBI group exhibited greater deficits on memory tasks, irrespective of modality, in the acute, 6-, 12-, and 24-month postinjury stages, in comparison to mild and moderate TBI groups. Performance on academic measures was dependent on both injury severity and task demands. Preinjury academic ability and verbal memory indices best predicted academic success.     

Recovery in memory function, and its relationship to academic success, at 24 months following pediatric TBI.

While a number of research papers have reported findings on memory deficits following traumatic brain injury (TBI), only limited studies have monitored the recovery of these skills over time. The present study examined memory ability and its effect on academic success in a group of children who had sustained a mild, moderate, or severe traumatic brain injury (TBI). Results showed that the severe TBI group exhibited greater deficits on memory tasks, irrespective of modality, in the acute, 6-, 12-, and 24-month postinjury stages, in comparison to mild and moderate TBI groups. Performance on academic measures was dependent on both injury severity and task demands. Preinjury academic ability and verbal memory indices best predicted academic success.     

Constitutive activation of the G-protein subunit Galphas within forebrain neurons causes PKA-dependent alterations in fear conditioning and cortical Arc mRNA expression

Memory formation requires cAMP signaling; thus, this cascade has been of great interest in the search for cognitive enhancers. Given that medications are administered long-term, we determined the effects of chronically increasing cAMP synthesis in the brain by expressing a constitutively active isoform of the G-protein subunit Galphas (Galphas*) in postnatal forebrain neurons of mice. Previously, we showed that Galphas* mice exhibit increased adenylyl cyclase activity but decreased cAMP levels in cortex and hippocampus due to a PKA-dependent increase in total cAMP phosphodiesterase (PDE) activity. Here, we extend previous findings by determining if Galphas* mice show increased activity of specific PDE families that are regulated by PKA, if Galphas* mice show PKA-dependent deficits in fear memory, and if these memory deficits are associated with PKA-dependent alterations in neuronal activity as mapped by Arc mRNA expression. Consistent with previous findings, we show here that Galphas* mice exhibit a significant compensatory increase in cAMP PDE1 activity and a trend toward increased cAMP PDE4 activity. Further, inhibiting the presumably elevated PKA activity in Galphas* mice fully rescues short- and long-term memory deficits in a fear-conditioning task, while extending the training session from one to four CS-US pairings partially rescues these deficits. Mapping of Arc mRNA levels suggests these PKA-dependent memory deficits may be related to decreased neuronal activity specifically within the cortex. Galphas* mice show decreased Arc mRNA expression in CA1, orbital cortex, and cortical regions surrounding the hippocampus; however, only the deficits in cortical regions surrounding the hippocampus are PKA dependent. Our results imply that chronically stimulating targets upstream of cAMP may detrimentally affect cognition.     

The effect of age-at-testing on verbal memory among children following severe traumatic brain injury

Memory deficits are a common sequelae following childhood traumatic brain injury (TBI), which often have serious implications on age-related academic skills. The current study examined verbal memory performance using the Rey Auditory Verbal Learning Test (RAVLT) in a pediatric TBI sample. Verbal memory abilities as well as the effect of age at-testing on performance were examined. A sample of 67 children following severe TBI (age average = 12.3 ± 2.74) and 67 matched controls were evaluated using the RAVLT. Age effect at assessment was examined using two age groups: above and below 12 years of age during evaluation. Differences between groups were examined via the 9 RAVLT learning trials and the 7 composite scores conducted out of them. Children following TBI recalled significantly less words than controls on all RAVLT trials and had significantly lower scores on all composite scores. However, all of these scores fell within the low average range. Further analysis revealed significantly lower than average performance among the older children (above 12 years), while scores of the younger children following TBI fell within average limits. To conclude, verbal memory deficits among children following severe TBI demonstrate an age-at-testing effect with more prominent problems occurring above 12 years at the time of evaluation. Yet, age-appropriate performance among children below 12 years of age may not accurately describe memory abilities at younger ages following TBI. It is therefore recommended that clinicians address child’s age at testing and avoid using a single test as an indicator of verbal memory functioning post TBI.     

Neurocognitive outcomes following pediatric brain injury: A developmental approach

Developmental neuropsychologists postulate that “immaturity” of the cerebral cortex should no longer be perceived as a protective factor. They argue that injury to the young brain may affect new learning by disrupting the skills in the midst of being acquired and skills that are yet to be developed. Cognitive deficits or weaknesses that are not detectable in the acute phase following a traumatic brain injury (TBI) may emerge over development as more complex skills are needed, thereby creating a developmental lag between children who sustained a pediatric TBI and typical age peers. This literature review was conducted to evaluate the developmental perspective on neurocognitive recovery/development following a TBI. Overall, the described findings support a developmental view and suggest that predictions of prognosis should be based on the child's remaining ability to learn.