Search

Deficits in cognitive control have been considered a core dysfunction of psychopathy, responsible for disrupted self-control. We investigated cognitive control impairments, including difficulties with task switching, failure of response inhibition, and inability to adjust speed of responding. Participants included 16 subjects with psychopathic traits (Ps), and 22 healthy controls (HCs). We recorded behavioral responses during a Task Switching paradigm, a probe of flexible behavioral adaptation to changing contexts; and a Go/NoGo Task, which assesses response inhibition and indexes behavioral impulsivity. During task switching, Ps evidenced impairments shifting set when conflicting (incongruent) information was presented, but performed as well as HCs in the absence of such conflict. In addition, when they encountered these difficulties, they failed to adjust their speed of responding. Ps presented also with deficits in response inhibition, with many commission errors on the Go/NoGo Task. This study identified impairments in response inhibition and in set shifting in psychopathic individuals. When shifting set, they evidenced difficulties refocusing on a new task when it was incongruent with the previous task. These deficits interfere with regulation of ongoing behavior and disrupt self-regulation. Our findings suggest abnormal neural processing during suppression of inappropriate responses in psychopathic individuals.

Aging is associated with reduced abilities to selectively allocate attention across multiple domains. This may be particularly problematic during everyday multitasking situations when cognitively demanding tasks are performed while walking. Due to previous limitations in neuroimaging technology, much remains unknown about the cortical mechanisms underlying resource allocation during locomotion. Here, we utilized an EEG-based mobile brain/body imaging (MoBI) technique that integrates high-density event-related potential (ERP) recordings with simultaneously acquired foot-force sensor data to monitor gait patterns and brain activity concurrently. To assess effects of motor load on cognition we evaluated young (N=17; mean age=27.2) and older adults (N=16; mean age=63.9) and compared behavioral and ERP measures associated with performing a Go/No-Go response inhibition task as participants sat stationary or walked on a treadmill. Stride time and variability were also measured during task performance and compared to stride parameters obtained without task performance, thereby assessing effects of cognitive load on gait. Results showed that older, but not young adults' accuracy dropped significantly when performing the inhibitory task while walking. Young adults revealed ERP modulations at relatively early (N2 amplitude reduction) and later (earlier P3 latency) stages within the processing stream as motor load increased while walking. In contrast, older adults' ERP modulations were limited to later processing stages (increased P3 amplitude) of the inhibitory network. The relative delay and attenuation of ERP modulations accompanied by behavioral costs in older participants might indicate an age-associated loss in flexible resource allocation across multiple tasks. Better understanding of the neural underpinnings of these age-related changes may lead to improved strategies to reduce fall risk and enhance mobility in aging.

article i nfo Visual processing studies have repeatedly shown impairment in patients with schizophrenia compared to healthy controls. Electroencephalography (EEG) and, specifically, visual evoked potential (VEP) studies have identified an early marker of this impairment in the form of a decrement in the P1 component of the VEP in patients and their clinically unaffected first-degree relatives. Much behavioral and neuroimaging re- search has implicated specific dysfunction of either the subcortical magnocellular pathway or the cortical vi- sual dorsal stream in this impairment. In this study, EEG responses were obtained to the contrast modulation of checkerboard stimuli using the VESPA (Visual Evoked Spread Spectrum Analysis) method. This was done for a high contrast condition and, in order to bias the stimuli towards the magnocellular pathway, a low con- trast condition. Standard VEPs were also obtained using high contrast pattern reversing checkerboards. Re- sponses were measured using high-density electrical scalp recordings in 29 individuals meeting DSM-IV criteria for schizophrenia and in 18 control subjects. Replicating previous research, a large (Cohen's d=1.11) reduction in the P1 component of the VEP was seen in patients when compared with controls with no corresponding difference in the VESPA response to high contrast stimuli. In addition, the low- contrast VESPA displayed no difference between patients and controls. Furthermore, no differences were seen between patients and controls for the C1 components of either the VEP or the high-contrast VESPA. Based on the differing acquisition methods between VEP and VESPA, we discuss these results in terms of con- trast gain control and the possibility of dysfunction at the cortical level with initial afferent activity into V1 along the magnocellular pathway being intact when processing is biased towards that pathway using low contrast stimuli.

Evidence has emerged for age-related amplification of basic sensory processing indexed by early components of the visual evoked potential (VEP). However, since these age-related effects have been incidental to the main focus of these studies, it is unclear whether they are performance dependent or alternately, represent intrinsic sensory processing changes. High-density VEPs were acquired from 19 healthy elderly and 15 young control participants who viewed alphanumeric stimuli in the absence of any active task. The data show both enhanced and delayed neural responses within structures of the ventral visual stream, with reduced hemispheric asymmetry in the elderly that may be indicative of a decline in hemispheric specialization. Additionally, considerably enhanced early frontal cortical activation was observed in the elderly, suggesting frontal hyper-activation. These age-related differences in early sensory processing are discussed in terms of recent proposals that normal aging involves large-scale compensatory reorganization. Our results suggest that such compensatory mechanisms are not restricted to later higher-order cognitive processes but may also be a feature of early sensory-perceptual processes.

PUBLISHED, Mismatch negativity (MMN) is a negative-going event-related potential (ERP) component that occurs in response to intermittent changes in constant auditory backgrounds. A consistent finding across a large number of studies has been impaired MMN generation in schizophrenia, which has been interpreted as evidence for fundamental deficits in automatic auditory sensory processing. The aim of this study was to investigate the extent to which dysfunction in MMN generation might represent an endophenotypic marker for schizophrenia.

Background Variation at the dysbindin gene ( DTNBP1 ) has been associated with increased risk for schizophrenia in numerous independent samples and recently with deficits in general and domain-specific cognitive processing. The relationship between dysbindin risk variants and sensory-level deficits in schizophrenia remains to be explored. We investigated P1 performance, a component of early visual processing on which both patients and their relatives show deficits, in carriers and noncarriers of a known dysbindin risk haplotype. Methods Event-related potential responses to simple visual isolated-check stimuli were measured using high-density electrical scalp recordings in 26 individuals meeting DSM-IV criteria for schizophrenia, comprising 14 patients who were carriers of the dysbindin risk haplotype and 12 patients who were nonrisk haplotype carriers. Results Carriers of the dysbindin risk haplotype demonstrated significantly reduced P1 amplitudes compared with noncarriers. A large effect size of d=.89 was calculated for the difference in P1 amplitude over scalp sites where the deficit was maximal. Conclusions The P1 deficits associated with a dysbindin risk haplotype previously identified in our sample presents functional confirmation of its deleterious effect on brain activity. Building on evidence of dysbindin's role in higher cognitive function, these early visual processing deficits suggest a generalized role for dysbindin in brain function and is likely to be part of the mechanism by which illness susceptibility is mediated.