EEG anomalies in adult ADHD subjects performing a working memory task.

Functional imaging studies have revealed differential brain activation patterns in attention deficit hyperactivity disorder (ADHD) adult patients performing working memory (WM) tasks. The existence of alterations in WM-related cortical circuits during childhood may precede executive dysfunctions in this disorder in adults. To date, there is no study exploring the electrophysiological activation of WM-related neural networks in ADHD. To address this issue, we carried out an electroencephalographic (EEG) activation study associated with time-frequency (TF) analysis in 15 adults with ADHD and 15 controls performing two visual N-back WM tasks, as well as oddball detection and passive fixation tasks. Frontal transient (phasic) theta event-related synchronization (ERS, 0-500 msec) was significantly reduced in ADHD as compared to control subjects. Such reduction was equally present in a task-independent manner. In contrast, the power of the later sustained (∼500-1200 msec) theta ERS for all tasks was comparable in ADHD and control groups. In active WM tasks, ADHD patients displayed lower alpha event-related desynchronization (ERD, ∼200-900 msec) and higher subsequent alpha ERS (∼900-2400 msec) compared to controls. The time course of alpha ERD/ERS cycle was modified in ADHD patients compared to controls, suggesting that they are able to use late compensatory mechanisms in order to perform this WM task. These findings support the idea of an ADHD-related dysfunction of neural generators sub-serving attention directed to the incoming visual information. ADHD cases may successfully face WM needs depending on the preservation of sustained theta ERS and prolonged increase of alpha ERS at later post-stimulus time points.

Individual classification of mild cognitive impairment subtypes by support vector machine analysis of white matter DTI.

BACKGROUND AND PURPOSE: MCI was recently subdivided into sd-aMCI, sd-fMCI, and md-aMCI. The current investigation aimed to discriminate between MCI subtypes by using DTI. MATERIALS AND METHODS: Sixty-six prospective participants were included: 18 with sd-aMCI, 13 with sd-fMCI, and 35 with md-aMCI. Statistics included group comparisons using TBSS and individual classification using SVMs. RESULTS: The group-level analysis revealed a decrease in FA in md-aMCI versus sd-aMCI in an extensive bilateral, right-dominant network, and a more pronounced reduction of FA in md-aMCI compared with sd-fMCI in right inferior fronto-occipital fasciculus and inferior longitudinal fasciculus. The comparison between sd-fMCI and sd-aMCI, as well as the analysis of the other diffusion parameters, yielded no significant group differences. The individual-level SVM analysis provided discrimination between the MCI subtypes with accuracies around 97%. The major limitation is the relatively small number of cases of MCI. CONCLUSIONS: Our data show that, at the group level, the md-aMCI subgroup has the most pronounced damage in white matter integrity. Individually, SVM analysis of white matter FA provided highly accurate classification of MCI subtypes.

Aging effects on selective attention-related electroencephalographic patterns during face encoding.

Previous electrophysiological studies revealed that human faces elicit an early visual event-related potential (ERP) within the occipito-temporal cortex, the N170 component. Although face perception has been proposed to rely on automatic processing, the impact of selective attention on N170 remains controversial both in young and elderly individuals. Using early visual ERP and alpha power analysis, we assessed the influence of aging on selective attention to faces during delayed-recognition tasks for face and letter stimuli, examining 36 elderly and 20 young adults with preserved cognition. Face recognition performance worsened with age. Aging induced a latency delay of the N1 component for faces and letters, as well as of the face N170 component. Contrasting with letters, ignored faces elicited larger N1 and N170 components than attended faces in both age groups. This counterintuitive attention effect on face processing persisted when scenes replaced letters. In contrast with young, elderly subjects failed to suppress irrelevant letters when attending faces. Whereas attended stimuli induced a parietal alpha band desynchronization within 300-1000 ms post-stimulus with bilateral-to-right distribution for faces and left lateralization for letters, ignored and passively viewed stimuli elicited a central alpha synchronization larger on the right hemisphere. Aging delayed the latency of this alpha synchronization for both face and letter stimuli, and reduced its amplitude for ignored letters. These results suggest that due to their social relevance, human faces may cause paradoxical attention effects on early visual ERP components, but they still undergo classical top-down control as a function of endogenous selective attention. Aging does not affect the face bottom-up alerting mechanism but reduces the top-down suppression of distracting letters, possibly impinging upon face recognition, and more generally delays the top-down suppression of task-irrelevant information.

Visual sensory processing deficit in the occipital region in children with attention-deficit / hyperactivity disorder as revealed by event-related potentials during cued continuous performance test.

AIMS OF THE STUDY: Recent studies described several changes of attention-related components of late frontal event-related potentials (ERPs) during Go/NoGo paradigm in children with attention-deficit/hyperactivity disorder (ADHD). We aimed to determine whether ERP components corresponding to earlier encoding of visual incoming information are also modulated by attentional disorders. METHODS: We recorded high-resolution EEG in 15 children meeting DSM-IV criteria for ADHD, comprising 15 age-matched control groups during an equiprobable Go/NoGo task in a cued continuous performance test (CPT-AX) paradigm. Both P100 and N200 ERP components were measured in response to both Go and NoGo stimuli. We analyzed both components with SwLORETA in order to localize their brain sources. RESULTS: A low rate of Go correct response and high rate of omission errors were observed in ADHD children. When compared to controls, these displayed delayed P100 and N200 latency, and lower P100-NoGo amplitude. In addition, the P100 latency was delayed for NoGo compared to Go condition. The source of P100 was located in occipital area. A sizable decrease in early electrical activity was found in ADHD, especially in the NoGo condition. CONCLUSION: Our results suggest an early deficit in visual sensory integration within the occipital cortex in children with ADHD.

Working memory load-related electroencephalographic parameters can differentiate progressive from stable mild cognitive impairment.

Recent studies described several changes of endogenous event-related potentials (ERP) and brain rhythm synchronization during memory activation in patients with Alzheimer's disease (AD). To examine whether memory-related EEG parameters may predict cognitive decline in mild cognitive impairment (MCI), we assessed P200 and N200 latencies as well as beta event-related synchronization (ERS) in 16 elderly controls (EC), 29 MCI cases and 10 patients with AD during the successful performance of a pure attentional detection task as compared with a highly working memory demanding two-back task. At 1 year follow-up, 16 MCI patients showed progressive cognitive decline (PMCI) and 13 remained stable (SMCI). Both P200 and N200 latencies in the two-back task were longer in PMCI and AD cases compared with EC and SMCI cases. During the interval 1000 ms to 1700 ms after stimulus, beta ERS at parietal electrodes was of lower amplitude in PMCI and AD compared with EC and SMCI cases. Univariate models showed that P200, N200 and log% beta values were significantly related to the SMCI/PMCI distinction with areas under the receiver operating characteristic curve of 0.93, 0.78 and 0.72, respectively. The combination of all three EEG hallmarks was the stronger predictor of MCI deterioration with 90% of correctly classified MCI cases. Our data reveal that PMCI and clinically overt AD share the same pattern of working memory-related EEG activation characterized by increased P200-N200 latencies and decreased beta ERS. They also show that P200 latency during the two-back task may be a simple and promising EEG marker of rapid cognitive decline in MCI.

Frontal theta event-related synchronization: comparison of directed attention and working memory load effects.

Early studies showed that long-term encoding and retrieval of new information is associated with modulation of the theta rhythm. More recently, changes in theta power amplitude over frontal electrode sites were reported during working memory, yet their relative significance in regard to attentional and memory processes remains unclear. Event-related synchronisation responses in the 4-7.5 Hz theta EEG frequency band was studied in 12 normal subjects performing four different tasks: two working memory tasks in which load varied from one (1-back task) to two (2-back task) items, an oddball detection (attention) task and a passive fixation task. A phasic theta increase was observed following stimulus apparition on all electrode sites within each task, with longer culmination peak and maximal amplitude over frontal electrodes. Frontal theta event-related synchronization (ERS) was of higher amplitude in the 1-back, 2-back and detection tasks as compared to the passive fixation task. Additionally, the detection task elicited a larger frontal and central theta ERS than the 2-back task. By analyzing theta ERS characteristics in various experimental conditions, the present study reveals that early phasic theta response over frontal regions primarily reflects the activation of neural networks involved in allocation of attention related to target stimuli rather than working memory processes.

Aging and working memory: early deficits in EEG activation of posterior cortical areas.

Using the n-back task, we recently identified, in young subjects, a positive-negative event related potential component (PN(wm)) in a time-range window between 140 and 280 ms after stimulus onset representing an electrophysiological correlate of working memory load. To evaluate age-related electrophysiological changes in working memory processing, we applied the same neuropsychological paradigm and compared densities of the PN(wm) component in 17 young (mean age: 26) and 17 healthy elderly individuals (mean age: 75). Both age groups displayed a PN(wm) component during the two working memory tasks. For the 1-back task, densities were similar in both young and elderly individuals. In contrast, PN(wm) densities increased with higher memory load (2-back>1-back) in the younger but not in the older group. This difference was mainly observed over parietal electrodes suggesting an impaired activation of neural generators within this brain region. The present results are consistent with the hypothesis of decreased brain reserve in the elderly and provide evidence for age-related deficits in the recruitment of posterior cortical neurons with increasing working memory load.

Automatic attentional shifts induced by a noradrenergic drug in Alzheimer's disease: evidence from evoked potentials.

Prior research showed that attentional deficits are observed in Alzheimer's disease (AD). These deficits can further impair other cognitive processes. The present experiment was designed to study the shifts in attention induced by a noradrenergic drug (S 12024-2) through their electrophysiological correlates in 12 outpatients with mild AD, using an auditory oddball paradigm. The P3a component, known to be related to automatic attentional processing, was increased by the drug, whereas no changes occurred either in PN or in P3b, which are considered to reflect conscious processing. These results point to an involvement of the noradrenergic system in the modulation of automatic attentional processing, and provide evidence for weakening of the orienting reflex in AD, due to a possible noradrenergic deficit in patients with mild AD.