Effect of sleep on interictal spikes and distribution of sleep spindles on electrocorticography in children with focal epilepsy

Asano, Eishi; Mihaylova, Temenuzhka; Juhász, Csaba; Sood, Sandeep; Chugani, Harry T.

doi:10.1016/j.clinph.2007.02.021

Cited by 29 publications

(35 citation statements)

References 38 publications

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“…The excessive brief wakes of DS mice, occurring exclusively during NREM sleep, illustrate both the abnormal fragmentation in NREM sleep and the resistance of REM sleep to brief wakes. The appearance of numerous interictal spikes exclusively during NREM sleep is consistent with results of several clinical and animal studies that lead to the idea that NREM sleep promotes the generation of epileptiform discharges via thalamocortical synchronous activity, whereas REM sleep is resistant to both brief wakes and interictal spikes (Asano et al, 2007; Kotagal and Yardi, 2008; Matos et al, 2010; Zhou et al, 2007). This result is also consistent with the idea that interictal spikes are a signature clinical feature of DS and suggests that evaluations of EEG interictal spikes during NREM sleep would increase the yield and accuracy of diagnostic exams (Arzimanoglou, 2009).…”

Section: Discussionsupporting

confidence: 87%

Sleep impairment and reduced interneuron excitability in a mouse model of Dravet Syndrome

Kalume

Oakley

Westenbroek

et al. 2015

Neurobiology of Disease

105

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Dravet Syndrome (DS) is caused by heterozygous loss-of-function mutations in voltage-gated sodium channel NaV1.1. Our genetic mouse model of DS recapitulates its severe seizures and premature death. Sleep disturbance is common in DS, but its mechanism is unknown. Electroencephalographic studies revealed abnormal sleep in DS mice, including reduced delta wave power, reduced sleep spindles, increased brief wakes, and numerous interictal spikes in Non-Rapid-Eye-Movement sleep. Theta power was reduced in Rapid-Eye-Movement sleep. Mice with NaV1.1 deleted specifically in forebrain interneurons exhibited similar sleep pathology to DS mice, but without changes in circadian rhythm. Sleep architecture depends on oscillatory activity in the thalamocortical network generated by excitatory neurons in the ventrobasal nucleus (VBN) of the thalamus and inhibitory GABAergic neurons in the reticular nucleus of the thalamus (RNT). Whole-cell NaV current was reduced in GABAergic RNT neurons but not in VBN neurons. Rebound firing of action potentials following hyperpolarization, the signature firing pattern of RNT neurons during sleep, was also reduced. These results demonstrate imbalance of excitatory vs. inhibitory neurons in this circuit. As predicted from this functional impairment, we found substantial deficit in homeostatic rebound of slow wave activity following sleep deprivation. Although sleep disorders in epilepsies have been attributed to anti-epileptic drugs, our results show that sleep disorder in DS mice arises from loss of NaV1.1 channels in forebrain GABAergic interneurons without drug treatment. Impairment of NaV currents and excitability of GABAergic RNT neurons are correlated with impaired sleep quality and homeostasis in these mice.

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Section: Discussionsupporting

confidence: 87%

Sleep impairment and reduced interneuron excitability in a mouse model of Dravet Syndrome

Kalume

Oakley

Westenbroek

et al. 2015

Neurobiology of Disease

105

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“…Overall IED rate may be increased during sleep with spindles, but the spatial distribution of spike frequency appears similar during wakefulness and sleep in children with intractable focal seizures. Thus sleep with spindles may decrease the threshold of emergence of IED activity diffusely rather than focally [88]. These EEG clinical observations are consistent with spindles representing a series of depolarizations of lower (type I) or higher (type II) firing capacity (riding on top of a DC negativity) and so constitute a state of relatively higher cortical excitability (see chapter 2.1.).…”

Section: Spindles and Epilepsysupporting

confidence: 60%

Sleep Spindles – As a Biomarker of Brain Function and Plasticity

Urakami¹,

Ioannides²,

Kostopoulos³

2012

Advances in Clinical Neurophysiology

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“…This would suggest that EEG spindles are generated by a distributed source. Distributed sources decrease relatively little from the cortical surface to the scalp [Nunez and Silberstein, 2000], and this can be inferred to be the case from combined recordings of ECOG and scalp EEG spindles, although this has not been systematically quantified [Asano et al, 2007; Nakabayashi et al, 2001]. Thus, the fact that EEG and MEG spindles can occur independently, as well as their relative amplitudes with respect to each other and to cortical recordings, are consistent with the possibility that MEG is recording from scattered focal asynchronous generators whereas EEG is recording from a highly distributed and coherent generator.…”

Section: Discussionmentioning

confidence: 99%

Emergence of synchronous EEG spindles from asynchronous MEG spindles

Dehghani¹,

Cash²,

Halgren³

2011

Human Brain Mapping

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Sleep spindles are bursts of rhythmic 10–15 Hz activity, lasting ~0.5–2 s, that occur during Stage 2 sleep. They are coherent across multiple cortical and thalamic locations in animals, and across scalp EEG sites in humans, suggesting simultaneous generation across the cortical mantle. However, reports of MEG spindles occurring without EEG spindles, and vice versa, are inconsistent with synchronous distributed generation. We objectively determined the frequency of MEG-only, EEG-only, and combined MEG-EEG spindles in high density recordings of natural sleep in humans. About 50% of MEG spindles occur without EEG spindles, but the converse is rare (~15%). Compared to spindles that occur in MEG only, those that occur in both MEG and EEG have ~1% more MEG coherence and ~15% more MEG power, insufficient to account for the ~55% increase in EEG power. However, these combined spindles involve ~66% more MEG channels, especially over frontocentral cortex. Furthermore, when both MEG and EEG are involved in a given spindle, the MEG spindle begins ~150 ms before the EEG spindle and ends ~250 ms after. Our findings suggest that spindles begin in focal cortical locations which are better recorded with MEG gradiometers than referential EEG due to the biophysics of their propagation. For some spindles, only these regions remain active. For other spindles, these locations may recruit other areas over the next 200 ms, until a critical mass is achieved, including especially frontal cortex, resulting in activation of a diffuse and/or multifocal generator that is best recorded by referential EEG derivations due to their larger leadfields.

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Effect of sleep on interictal spikes and distribution of sleep spindles on electrocorticography in children with focal epilepsy

Cited by 29 publications

References 38 publications

Sleep impairment and reduced interneuron excitability in a mouse model of Dravet Syndrome

Sleep impairment and reduced interneuron excitability in a mouse model of Dravet Syndrome

Sleep Spindles – As a Biomarker of Brain Function and Plasticity

Emergence of synchronous EEG spindles from asynchronous MEG spindles

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