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88) than automatic analysis (0.74) (p < 0.05).

Automatic cEEG analysis is a useful supplement to visual analysis, and provides additional cEEG diagnostic classifiers.

Automatic cEEG analysis provides useful information in septic patients.

Automatic cEEG analysis provides useful information in septic patients.

A major challenge that limits understanding and treatment of epileptic events from mesial temporal structures comes from our inability to detect and map interictal networks reproducibly using scalp electrodes. Here, we developed a novel approach to map interictal spike networks and demonstrate their relationships to seizure onset and lesions in patients with foramen ovale electrode implantations.

We applied the direct Directed Transfer Function to reveal interictal spike propagation from bilateral foramen ovale electrodes on 10 consecutive patients and co-registered spatially with both seizure onset zones and temporal lobe lesions.

Highly reproducible, yet unique interictal spike networks were seen for each patient (correlation 0.93 ± 0.13). Interictal spikes spread in both anterior and posterior directions within each temporal lobe, often reverberating between sites. Spikes propagated to the opposite temporal lobe predominantly through posterior pathways. Patients with structural lesions (N = 4), including tumors and sclerosis, developed reproducible spike networks adjacent to their lesions that were highly lateralized compared to patients without lesions. Only 5% of mesial temporal lobe spikes were time-locked with scalp electrode spikes. Our preliminary observation on two lesional patients suggested that along with lesion location, Interictal spike networks also partially co-registered with seizure onset zones suggesting interrelationship between seizure onset and a subset of spike networks.

This is the first demonstration of patient-specific, reproducible interictal spike networks in mesial temporal structures that are closely linked to both temporal lobe lesions and seizure onset zones.

Interictal spike connectivity is a novel approach to map epileptic networks that could help advance invasive and non-invasive epilepsy treatments.

Interictal spike connectivity is a novel approach to map epileptic networks that could help advance invasive and non-invasive epilepsy treatments.

The aim of this study was to determine the anesthesia-promoting effects of hydroxyzine on electroencephalograms during sevoflurane anesthesia and during propofol anesthesia.

We analyzed 40 patients scheduled for elective surgery under sevoflurane anesthesia (n = 20) or propofol anesthesia (n = 20). Anesthesia was adjusted at a bispectral index value of 50-60, and then 0.5 mg/kg of hydroxyzine was administered intravenously. We analyzed frontal electroencephalograms before and after hydroxyzine injection with power spectral and bicoherence analyses, which are suitable for assessing the anesthetic depth induced by γ-aminobutyric acid (GABA)ergic anesthetics.

Hydroxyzine increased the α bicoherence peaks in both sevoflurane anesthesia (mean difference, 11.2%; 95% confidence interval (CI), 7.6 to 14.8; P < 0.001) and propofol anesthesia (mean difference, 5.6%; 95% CI, 1.7 to 9.4; P = 0.008). Hydroxyzine increased the averaged δ bicoherence values in both sevoflurane anesthesia (mean difference, 5.5%; 95% CI, 2.1 to 8.8; P = 0.003) and propofol anesthesia (mean difference, 3.9%; 95% CI, 1.0 to 6.8; P = 0.011).

Hydroxyzine enhances both sevoflurane anesthesia and propofol anesthesia probably by facilitation of GABAergic neural circuit mechanisms.

The findings provide a new insight into the role of histaminergic neurons during general anesthesia in humans.

The findings provide a new insight into the role of histaminergic neurons during general anesthesia in humans.

Parietal lobe seizures (PLS) are characterized by multiple clinical manifestations including motor signs. (R)2Hydroxyglutarate The mechanisms underlying the occurrence of motor signs are poorly understood. The main objective of this work was to estimate the functional coupling of brain regions associated with this clinical presentation.

We retrospectively selected patients affected by drug-resistant epilepsy who underwent Stereoelectroencephalography (SEEG) for pre-surgical evaluation and in whom the seizure onset zone (SOZ) was located in the parietal cortex. The SOZ was defined visually and quantitatively by the epileptogenicity index (EI) method. Two groups of seizures were defined according to the presence ("motor seizures") or the absence ("non-motor seizures") of motor signs. Functional connectivity (FC) estimation was based on pairwise nonlinear regression analysis (h

coefficient). To study FC changes between parietal, frontal and temporal regions, for each patient, z-score values of 16 cortico-cortical interactions different than what is observed in PLS without motor semiology.

Our results indicate that preferential routes of coupling between parietal and premotor cortices are responsible for the prominent motor presentation during PLS.

Our results indicate that preferential routes of coupling between parietal and premotor cortices are responsible for the prominent motor presentation during PLS.

Neurofibromatosis type 1 (NF1)

is known to cause learning deficits in affected individuals. There has been evidence linking altered gamma-aminobutyric acid (GABA)

mediated inhibition to learning impairments in rodent models and humans with NF1. Still, evidence on the role of GABA in learning deficits associated with NF1 is inconclusive.

We examined procedural learning and motor cortex excitability through intracortical facilitation and short interval intracortical inhibition and its activity dependent modulation while performing a procedural sequence learning task in 16 asymptomatic NF1 gene carriers. We aimed to analyze potential brain-behavior correlations in a carefully selected sample of gene carriers in order to minimize confounding factors.

Gene carriers did not differ from healthy controls when learning the task with their non-dominant hand over three days of training. Electrophysiological data did not reveal alterations in patients' inhibitory function of the motor cortex.

In contrast with previous publications reporting various cognitive deficits in clinically asymptomatic individuals with NF1, here asymptomatic gene carriers did not show major neuropsychological or behavioral abnormalities.