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Working memory (WM) plays a crucial role in human brain functions. The application of brain connectivity analysis helps to understand the brain network properties in WM. Combination of functional and effective connectivity can provide new insights for exploring network attributes. Nevertheless, few studies have combined these two modes in WM. Near-infrared spectroscopy was used to investigate the connectivity properties in the prefrontal cortex (PFC) during n-back (0-back and 2-back) tasks by combining functional and effective connectivity analysis. Our results demonstrated that the PFC network showed small-world properties in both WM tasks. The characteristic path length was significantly longer in the 2-back task than in the 0-back task, while there was no obvious difference in the clustering coefficient between two tasks. Regarding the effective connectivity, the Granger causality (GC) was higher for right PFC→left PFC than for left PFC→right PFC in the 2-back task. Compared with the 0-back task, GC of right PFC→left PFC was higher in the 2-back task. Our findings show that, along with memory load increase, long range connections in PFC are enhanced and this enhancement might be associated with the stronger information flow from right PFC to left PFC.

Objective. In electroencephalography (EEG) measurements, the signal of each recording electrode is contrasted with a reference electrode or a combination of electrodes. The estimation of a neutral reference is a long-standing issue in EEG data analysis, which has motivated the proposal of different re-referencing methods, among which linked-mastoid re-referencing (LMR), average re-referencing (AR) and reference electrode standardization technique (REST). In this study we quantitatively assessed the extent to which the use of a high-density montage and a realistic head model can impact on the optimal estimation of a neutral reference for EEG recordings. Approach. Using simulated recordings generated by projecting specific source activity over the sensors, we assessed to what extent AR, REST and LMR may distort the scalp topography. We examined the impact electrode coverage has on AR and REST, and how accurate the REST reconstruction is for realistic and less realistic (three-layer and single-layer spherical) head models, and with possible uncertainty in the electrode positions. We assessed LMR, AR and REST also in the presence of typical EEG artifacts that are mixed in the recordings. Finally, we applied them to real EEG data collected in a target detection experiment to corroborate our findings on simulated data. Main results. Both AR and REST have relatively low reconstruction errors compared to LMR, and that REST is less sensitive than AR and LMR to artifacts mixed in the EEG data. For both AR and REST, high electrode density yields low re-referencing reconstruction errors. A realistic head model is critical for REST, leading to a more accurate estimate of a neutral reference compared to spherical head models. With a low-density montage, REST shows a more reliable reconstruction than AR either with a realistic or a three-layer spherical head model. Conversely, with a high-density montage AR yields better results unless precise information on electrode positions is available. Significance. Our study is the first to quantitatively assess the performance of EEG re-referencing techniques in relation to the use of a high-density montage and a realistic head model. We hope our study will help researchers in the choice of the most effective re-referencing approach for their EEG studies., Journal of Neural Engineering, 12 (5), ISSN:1741-2560, ISSN:1741-2552

Background: Both Asperger's disorder and the social-emotional processing disorder (SEPD), a form of non-verbal learning disability, are associated with executive function deficits. SEPD has been shown to be associated with deficient saccadic inhibition. Objective: To study two executive functions in Asperger's disorder and SEPD, inhibition and task switching, using a single saccadic paradigm. Methods: 22 control subjects and 27 subjects with developmental social processing disorders—SEPD, Asperger's disorder, or both syndromes—performed random sequences of prosaccades and anti- saccades. This design resulted in four trial types, prosaccades and antisaccades, that were either repeated or switched. The design allowed the performance costs of inhibition and task switching to be isolated. Results: Subjects with both Asperger's disorder and SEPD showed deficient inhibition, as indicated by increased antisaccade errors and a disproportionate increase in latency for antisaccades relative to prosaccades. In contrast, task switching error and latency costs were normal and unrelated to the costs of inhibition. Conclusions: This study replicates the finding of deficient saccadic inhibition in SEPD, extends it to Asperger's disorder, and implicates prefrontal cortex dysfunction in these syndromes. The finding of intact task switching shows that executive function deficits in Asperger's disorder and SEPD are selective and suggests that inhibition and task switching are mediated by distinct neural networks.

Objectives: Recent transcranial magnetic stimulation (TMS) studies demonstrate that motor cortex excitability is increased in Alzheimer’s disease (AD) and that intracortical inhibitory phenomena are impaired. The aim of the present study was to determine whether hyperexcitability is due to the impairment of intracortical inhibitory circuits or to an independent abnormality of excitatory circuits. Methods: We assessed the excitability of the motor cortex with TMS in 28 patients with AD using several TMS paradigms and compared the data of cortical excitability (evaluated by measuring resting motor threshold) with the amount of motor cortex disinhibition as evaluated using the test for motor cortex cholinergic inhibition (short latency afferent inhibition) and GABAergic inhibition (short latency intracortical inhibition). The data in AD patients were also compared with that from 12 age matched healthy individuals. Results: The mean resting motor threshold was significantly lower in AD patients than in controls. The amount of short latency afferent inhibition was significantly smaller in AD patients than in normal controls. There was also a tendency for AD patients to have less pronounced short latency intracortical inhibition than controls, but this difference was not significant. There was no correlation between resting motor threshold and measures of either short latency afferent or intracortical inhibition (r = −0.19 and 0.18 respectively, NS). In 14 AD patients the electrophysiological study was repeated after a single oral dose of the cholinesterase inhibitor rivastigmine. Resting motor threshold was not significantly modified by the administration of rivastigmine. In contrast, short latency afferent inhibition from the median nerve was significantly increased by the administration of rivastigmine. Conclusions: The change in threshold did not seem to correlate with dysfunction of inhibitory intracortical cholinergic and GABAergic circuits, nor with the central cholinergic activity. We propose that the hyperexcitability of the motor cortex is caused by an abnormality of intracortical excitatory circuits.

Background: Rivastigmine enhances cholinergic activity and has been shown in clinical trials to decrease the rate of deterioration in Alzheimer's disease. It remains unclear where in the brain it exerts its effect. Functional magnetic resonance imaging (fMRI) can be used to measure changes in brain function and relate these to cognition. Objectives: To use fMRI to study brain activation with rivastigmine treatment. Methods: The effect on brain activation of a single dose of rivastigmine was tested in seven patients with mild Alzheimer's disease using fMRI during face encoding, and in five patients during a parametric working memory task. Results: During face encoding, rivastigmine increased bilateral activation in the fusiform gyrus. Brain activation was also enhanced in the prefrontal cortex in a simple working memory task. When working memory load was further increased, not only was increased activation seen, but in certain areas there was also decreased activation. Conclusions: These findings link the previously observed increase in cognitive performance in Alzheimer's disease after treatment with a cholinesterase inhibitor to altered brain activation. Although the results cannot be generalised to the Alzheimer's disease population at large, they provide evidence that in mild Alzheimer's disease, rivastigmine enhances brain activation in the fusiform and frontal cortices. This is compatible with the concept of cholinergic circuitry.

Objectives: We investigated the involvement of the basal ganglia in inhibiting ongoing responses in patients with Parkinson’s disease (PD). Methods: Thirty two patients with PD and 31 orthopaedic controls performed the stop signal task, which allows an estimation of the time it takes to inhibit an ongoing reaction (stop signal reaction time, SSRT). Results: Patients with PD showed significantly longer SSRTs than the controls. This effect seemed to be independent of global cognitive impairment and severity of PD. Furthermore, in the PD patients, there was no significant relation between general slowing and inhibitory efficiency. Conclusions: Our results provide evidence for involvement of the basal ganglia in the inhibition of ongoing responses.