Bimanual coordination in chronic schizophrenia

Anomalies of movement are observed both clinically and experimentally in schizophrenia. While the basal ganglia have been implicated in its pathogenesis, the nature of such involvement is equivocal. The basal ganglia may be involved in bimanual coordination through their input to the supplementary motor area (SMA). While a neglected area of study in schizophrenia, a bimanual movement task may provide a means of assessing the functional integrity of the motor circuit. Twelve patients with chronic schizophrenia and 12 matched control participants performed a bimanual movement task on a set of vertically mounted cranks at different speeds (1 and 2 Hz) and phase relationships. Participants performed in-phase movements (hands separated by 0 degrees ) and out-of-phase movements (hands separated by 180 degrees ) at both speeds with an external cue on or off. All participants performed the in-phase movements well, irrespective of speed or cueing conditions. Patients with schizophrenia were unable to perform the out-of-phase movements, particularly at the faster speed, reverting instead to the in-phase movement. There was no effect of external cueing on any of the movement conditions. These results suggest a specific problem of bimanual coordination indicative of SMA dysfunction per se and/or faulty callosal integration. A disturbance in the ability to switch attention during the out-of-phase task may also be involved.     

Neuropsychological outcome of GPi pallidotomy and GPi or STN deep brain stimulation in Parkinson's disease

This paper highlights the neuropsychological sequelae of posteroventral pallidotomy (PVP) and deep brain stimulation (DBS) of the subthalamic nucleus (STN) and the internal segment of the globus pallidus (GPi) at 3/6 months postoperatively. Results are based on our extensive experience with PVP and our preliminary observations with DBS. Patients with borderline cognitive or psychiatric functioning risk postoperative decompensation. Nonlateralizing attentional and hemisphere-specific impairments of frontostriatal cognitive functions followed unilateral PVP. "Frontal" behavioral dyscontrol was observed in approximately 25% of patients. Three cases of staged bilateral PVP suggest that premorbid factors may predict outcome, although lesion size and location are also critical. Older patients are at risk for significant cognitive and behavioral decline after bilateral STN DBS, while GPi DBS may be safer.     

Beyond family‐level adversities: Exploring the developmental timing of neighborhood disadvantage effects on the brain

A growing literature suggests that adversity is associated with later altered brain function, particularly within the corticolimbic system that supports emotion processing and salience detection (e.g., amygdala, prefrontal cortex [PFC]). Although neighborhood socioeconomic disadvantage has been shown to predict maladaptive behavioral outcomes, particularly for boys, most of the research linking adversity to corticolimbic function has focused on family‐level adversities. Moreover, although animal models and studies of normative brain development suggest that there may be sensitive periods during which adversity exerts stronger effects on corticolimbic development, little prospective evidence exists in humans. Using two low‐income samples of boys (n = 167; n = 77), Census‐derived neighborhood disadvantage during early childhood, but not adolescence, was uniquely associated with greater amygdala, but not PFC, reactivity to ambiguous neutral faces in adolescence and young adulthood. These associations remained after accounting for several family‐level adversities (e.g., low family income, harsh parenting), highlighting the independent and developmentally specific neural effects of the neighborhood context. Furthermore, in both samples, indicators measuring income and poverty status of neighbors were predictive of amygdala function, suggesting that neighborhood economic resources may be critical to brain development.     

时间认知神经科学研究进展

当前对时间认知的脑机制探讨有三个模型：特异化计时模型、分布网络模型和定域计时模型。在这些模型的框架下,时间认知的神经心理学研究集中探讨了小脑、基底神经节、前额叶在时间信息加工中的作用和大脑两半球在时间认知中的不对称性。小脑作为内部计时系统对时间控制具有重要作用,在周期性动作任务中,小脑对不连续动作计时具有特异性。基底神经节在时间加工任务中与小脑存在明显的作用分离,其具体机制还有待深入研究。前额叶的计时功能可能与注意和工作记忆对时间信息的获得、维持和组织有关。此外,还发现大脑右半球与时问信息的加工关系密切。     

情感风格及其神经基础

情感风格是个体在情绪反应与情绪调节等方面表现出的稳定的、一致性差异。情感风格的两个主要成分是情绪反应与情绪调节差异。情感风格与情绪恢复性、趋近——退缩系统、精神疾病的易感性等密切相关。前额皮层、前扣带皮层、杏仁核等及其构成的神经回路的结构与机能差异是情感风格的神经基础。     

Violence and Latin‐American preadolescents: A study of social brain function and cortisol levels

The present study investigated exposure to violence and its association with brain function and hair cortisol concentrations in Latin‐American preadolescents. Self‐reported victimization scores (JVQ‐R2), brain imaging (fMRI) indices for a social cognition task (the ‘eyes test’), and hair cortisol concentrations were investigated, for the first time, in this population. The eyes test is based on two conditions: attributing mental state or sex to pictures of pairs of eyes (Baron‐Cohen, Wheelwright, Hill, Raste, & Plumb, 2001). The results showed an association among higher victimization scores and (a) less activation of posterior temporoparietal right‐hemisphere areas, in the mental state condition only (including right temporal sulcus and fusiform gyrus); (b) higher functional connectivity indices for the Amygdala and Right Fusiform Gyrus (RFFG) pair of brain regions, also in the mental state condition only; (c) higher hair cortisol concentrations. The results suggest more exposure to violence is associated with significant differences in brain function and connectivity. A putative mechanism of less activation in posterior right‐hemisphere regions and of synchronized Amygdala: RFFG time series was identified in the mental state condition only. The results also suggest measurable effects of exposure to violence in hair cortisol concentrations, which contribute to the reliability of self‐reported scores by young adolescents. The findings are discussed in light of the effects of exposure to violence on brain function and on social‐cognitive development in the adolescent brain. A video abstract of this article can be viewed at https://www.youtube.com/watch?v=qHcXq7Y9PBk     

情绪大脑机制研究的进展

文章综述情绪大脑机制研究的最新进展。情绪的脑机制——大脑回路,包括前额皮层、杏仁核、海马、前部扣带回、腹侧纹状体等。前额皮层中的不对称性与趋近和退缩系统有关,左前额皮层与趋近系统和积极感情有关,右前额皮层与消极感情和退缩有关。杏仁核易被消极的感情刺激所激活,尤其是恐惧。海马在情绪的背景调节中起着重要作用。前额皮层和杏仁核激活不对称性的个体差异是情绪个体差异的生理基础。情绪的中枢回路有可塑性。     

Neurochemical mechanisms underlying amygdaloid modulation of aggressive behavior in the cat

Studies designed to determine the respective roles of substance P, excitatory amino acids, and enkephalins in amygdaloid modulation of defensive rage behavior in the cat are presented. The basic design of these studies involved three stages. In stage I, cannula electrodes for stimulation and drug infusion were implanted into medial hypothalamic or midbrain periaqueductal gray (PAG) sites from which defensive rage behavior could be elicited. Then, a stimulating electrode was implanted into a site within the medial, basal, or central nuclear complex from which modulation of the defensive rage response could be obtained. Amygdaloid modulation of defensive rage was determined in the following manner: it employed the paradigm of dual stimulation in which comparisons were made of response latencies between alternate trials of dual (i. e., amygdala = medial hypothalamus [or PAG]) and single stimulation of the hypothalamus or PAG alone. Thus, stage I established the baseline level ofmodulation (i. e., facilitation or suppression of defensive rage) in the predrug stimulation period. In stage II, a selective or nonselective receptor antagonist for a given transmitter system was administered either peripherally or intracerebrally at the defensive rage site, after which time the same dual stimulation paradigm was then repeated over the ensuing 180 min postinjection period in order to determine the effects of drug delivery upon amygdaloid modulation of defensive rage. Stage III of the study took place at the completion of the pharmacological testing phase. The retrograde axonal tracer, Fluoro-Gold, was microinjected into the defensive rage site within the medial hypothalamus or PAG, and following a 6-14 day survival period, animals were sacrificed and brains were processed for histological and immunocytochemical analyses for the neurotransmitters noted above. This procedure thus permitted identification of cells within the amygdala which were labeled retrogradely and which were also immunostained positively for substance P, excitatory amino acids, or enkephalin. For studies involving substance P, defensive rage was elicited from the medial hypothalamus and for studies examining the roles of excitatory amino acids and enkephalin, defensive rage was elicited from the PAG. In the first study, facilitation of hypothalamically elicited defensive rage was obtained with dual stimulation of the medial nucleus of the amygdala. In separate experiments, the selective NK₁ non-peptide antagonist, CP 96,345, was administered both peripherally as well as intracerebrally into the hypothalamic defensive rage sites in doses of 0.5-4.0 mg/kg (i. p.) and 0.5-2.5 nmol (i. c.). Following drug delivery, the facilitatory effects of medial amygdaloid stimulation were blocked in a dose- and time-dependent manner in which the effects were noted as early as 5 min postinjection. The maximum drug dose (4.0 mg/kg) employed for peripheral administration resulted in a 42% reduction in the facilitatory effects of the medical amygdala (P < 0.002). This drug, when microinjected directly into medial hypothalamic defensive rage sites at the maximum dose level of 2.5 nmol, resulted in an 84% reduction of the suppressive effects of amygdaloid stimulation (P < 0.5) at 5 min postinjection. In the next study, an N-methyl-D-aspartate (NMDA) antagonist, DL-α-amino-7-phosphonoheptanoic acid (AP-7), was administered either peripherally (0.1-1.0 mg/kg) or intracerebrally (0.2 and 2.0 nmol) into PAG defensive rage sites. Facilitation of defensive rage behavior, which was observed following dual stimulation of the basal amygdala and PAG, was significantly reduced by either route of drug administration in a dose- and time-dependent manner. At the maximum dose level of peripheral administration, AP-7 reduced amygdaloid facilitation of defensive rage by 63% (P < 0.001) for 60 min, postinjection. A smaller (i. e., 19%) but still significant (P < 0.05) reduction in facilitation was obtained following intracerebral administration of the drug. In a third study, the non-selective opioid receptor antagonist, naloxone (27.5 nmol), infused directly into PAG defensive rage sites, totally blocked the suppressive effects of central amygdaloid stimulation for a period of 30 min (P < 0.05) in a dose- and time-dependent manner. The anatomical phase of this study revealed the following relationships: 1) that large numbers of neurons projecting to the medial hypothalamus from the medial amygdala immunoreact positively for substance P; 2) that neurons projecting to the PAG from the basal complex of amygdala immunoreact positively for glutamate and aspartate; and 3) that neurons located within the central nucleus of the amygdala which project to the PAG immunoreact positively for met-enkephalin. Collectively, these observations provide new evidence which characterizes the likely neurotransmitters linked with specific amygdaloid pathways subserving the modulation of defensive rage behavior in the cat.     

基底神经节损伤对知觉性启动效应影响的进一步研究

基底神经节的认知和记忆功能是近年认知神经科学研究的热点。该研究采用两项语义性启动效应（自由联想、偏好）和一项知觉性启动效应（字辨认）任务,发现基底神经节损伤、分别伴两侧海马或右侧丘脑损伤的两例患者的语义性启动效应正常,知觉性启动效应障碍。由于先前研究已经证实海马或丘脑结构与启动效应无关,因此该两例患者表现的知觉性启动效应障碍可归因于基底神经节损伤,进一步证实了王常生等人认为基底神经节可能具有或参与知觉性启动效应调节作用,与语义性启动效应无关的观点。     

The Neuropsychological Bases of Category Learning

There is a long history of research into how people learn new categories of objects or events. Recent advances have led to new insights about the neuropsychological basis of this critically important cognitive process. In particular, there is now good evidence that the frontal cortex and basal ganglia contribute to category learning, that medial temporal lobe structures make a more minor contribution, and that categorization rules are not represented in visual cortex. There is also strong evidence that normal category learning is mediated by at least two separate systems. A recent neuropsychological theory of category learning that is consistent with these data is described.