Sleep affects cortical source modularity in temporal lobe epilepsy: A high-density EEG study

•Sleep induces a spread of temporal interictal epileptiform discharges (IEDs) to a “sleep plus” zone, potentially signaling the epileptogenic zone and aid in the presurgical workup.•IEDs are naturally occurring, perturbing stimuli that interfere with brain oscillations.•Mesial and neocortical tempor...

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Published inClinical neurophysiology Vol. 126; no. 9; pp. 1677 - 1683
Main Authors Del Felice, Alessandra, Storti, Silvia Francesca, Manganotti, Paolo
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ireland Ltd 01.09.2015
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ISSN1388-2457
1872-8952
1872-8952
DOI10.1016/j.clinph.2014.12.003

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Summary:•Sleep induces a spread of temporal interictal epileptiform discharges (IEDs) to a “sleep plus” zone, potentially signaling the epileptogenic zone and aid in the presurgical workup.•IEDs are naturally occurring, perturbing stimuli that interfere with brain oscillations.•Mesial and neocortical temporal lobe epilepsy (TLE) react to IEDs with different EEG patterns in sleep, suggesting a state-dependent effect on cortical modularity. Interictal epileptiform discharges (IEDs) constitute a perturbation of ongoing cerebral rhythms, usually more frequent during sleep. The aim of the study was to determine whether sleep influences the spread of IEDs over the scalp and whether their distribution depends on vigilance-related modifications in cortical interactions. Wake and sleep 256-channel electroencephalography (EEG) data were recorded in 12 subjects with right temporal lobe epilepsy (TLE) differentiated by whether they had mesial or neocortical TLE. Spikes were selected during wake and sleep. The averaged waking signal was subtracted from the sleep signal and projected on a bidimensional scalp map; sleep and wake spike distributions were compared by using a t-test. The superimposed signal of sleep and wake traces was obtained; the rising phase of the spike, the peak, and the deflections following the spike were identified, and their cortical generator was calculated using low-resolution brain electromagnetic tomography (LORETA) for each group. A mean of 21 IEDs in wake and 39 in sleep per subject were selected. As compared to wake, a larger IED scalp projection was detected during sleep in both mesial and neocortical TLE (p<0.05). A series of EEG deflections followed the spike, the cortical sources of which displayed alternating activations of different cortical areas in wake, substituted by isolated, stationary activations in sleep in mesial TLE and a silencing in neocortical TLE. During sleep, the IED scalp region increases, while cortical interaction decreases. The interaction of cortical modules in sleep and wake in TLE may influence the appearance of IEDs on scalp EEG; in addition, IEDs could be proxies for cerebral oscillation perturbation.
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ISSN:1388-2457
1872-8952
1872-8952
DOI:10.1016/j.clinph.2014.12.003