Conservative method for vertical electrooculogram attenuation based on local suppression of ongoing EEG artifact templates.

Eye movement during blinking can be a significant artifact in Event-Related Potentials (ERP) analysis. Blinks produce a positive potential in the vertical electrooculogram (VEOG), spreading towards the posterior direction. Two methods are frequently used to suppress VEOGs: linear regression to subtract the VEOG signal from the electroencephalogram (EEG) and Independent Component Analysis (ICA). However, some information is lost in both. The present algorithm (1) statistically identifies the position of VEOGs in the frontopolar channels; (2) performs EEG averaging for each channel, which results in 'blink templates'; (3) subtracts each template from the respective EEG at each VEOG position, only when the linear correlation index between the template and the segment is greater than a chosen threshold L. The signals from twenty subjects were acquired using a behavioral test and were treated using FilterBlink for subsequent ERP analysis. A model was designed to test the method for each subject using twenty copies of the EEG signal from the subject's mid-central channel (with nearly no VEOG) representing the EEG channels and their respective blink templates. At the same 200 equidistant time points (marks), a signal (2.5 sinusoidal cycles at 1050 ms emulating an ERP) was mixed with each model channel and the respective blink template of that channel, between 500 to 1200 ms after each mark. According to the model, VEOGs interfered with both ERPs and the ongoing EEG, mainly on the anterior medial leads, and no significant effect was observed on the mid-central channel (Cz). FilterBlink recovered approximately 90% (Fp1) to 98% (Fz) of the original ERP and EEG signals for L = 0.1. The method reduced the VEOG effect on the EEG after ERP and blink-artifact averaging in analyzing real signals. The method is straightforward and effective for VEOG attenuation without significant distortion in the EEG signal and embedded ERPs.

Neurophysiological and behavioral correlates of alertness impairment and compensatory processes in ADHD evidenced by the Attention Network Test.

In Attention Deficit Hyperactivity disorder (ADHD), fMRI studies show asymmetric alterations: widespread hypoactivation in anterior cortical areas and hyperactivation in some posterior regions, and the latter is considered to be related to compensatory processes. In Posner's attentional networks, an important role is attributed to functional interhemispheric asymmetries. The psychophysiological Attention Network Test (ANT), which measures the efficiency of the alerting, orienting, and executive networks, seems particularly informative for ADHD. Potentials related to ANT stimuli (ANT-RPs) have revealed reduced cognitive potential P3 in ADHD. However, there are no studies associated with asymmetry of ANT-RPs. In the present study, conducted with 20 typically developing boys and 19 boys with ADHD, aged 11-13 years, the efficiency of the three Posner's networks regarding performance and amplitude asymmetries in ANT-RPs was evaluated according to the arithmetic difference of these parameters between different cue and target presentation conditions. The results were correlated to Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) scores. Regarding accuracy and intraindividual variation in reaction time, ADHD subjects showed lower efficiency of executive and alerting network, and this effect was correlated with DSM. Regarding alerting network, ANT-RPs in ADHD did not have the right-side amplitude prevalence in the temporal regions, which was observed in controls. In all ANT conditions, significantly higher asymmetries were observed in ADHD than in controls in the occipital regions 40-200 ms after target onset. Their amplitude in ADHD subjects was inversely proportional to DSM scores of inattentiveness and directly proportional to accuracy and efficiency of the executive network. The results suggest impaired alerting and executive networks in ADHD and compensatory occipital mechanisms.