K-complex-induced seizures in autosomal dominant nocturnal frontal lobe epilepsy

AP-HP, Epileptology Unit, Neurology 1 Department, La Pitié-Salpêtrière Hospital, Paris, France.
Clinical Neurophysiology (Impact Factor: 3.1). 09/2008; 119(10):2201-4. DOI: 10.1016/j.clinph.2008.07.212
Source: PubMed


To examine in detail the relations between seizures and K-complexes in autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE).
Prolonged continuous video-EEG recording and analysis of 30 seizures in an 18-year-old woman suffering from ADNFLE with a CHRNA4 gene mutation.
Twenty-seven of 30 recorded seizures started just after a K-complex. In nine cases a sound induced a K-complex that was immediately followed by the seizure. Most seizures preceded repetitive and brief ictal restarts.
Three new characteristics have been observed in this ADNFLE patient: a K-complex is almost invariably present at seizure onset; sounds trigger some seizures; ictal restarts occur often.
These new observations--the presence of K-complexes at seizure onset and occurrence of sound-triggered seizures--support the view that ADNFLE seizures may be initiated by K-complexes.

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    • "Other studies have found all NFLE episodes to occur during stage 2 NREM sleep (Derry and Johns, 2006; Montagna et al., 2008). The periodicity of the episodes was linked to different phasic events of NREM sleep (K-complexes and spindles) and to the CAP (Terzano et al., 1997; Picard et al., 1997; El Helou et al., 2008). The most striking observation is that the motor events, especially the smaller ones, follow the 20—40-s periodicity of the CAP (Terzano and Parrino, 2000). "
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    ABSTRACT: The article summarises the role of input and consequent phasic events in the dynamism of non-rapid eye movement (NREM) sleep and in homeostatic slow-wave economy during sleep. Then, an overview of the mechanism of how micro-arousals in NREM sleep gate epileptic events in absence epilepsy (AE) and in sporadic and autosomal dominant nocturnal frontal lobe epilepsy (NFLE/ADNFLE) is presented. The ictal type of generalised spike-wave discharges (SWDs) are associated with a special vigilance level in between NREM, rapid-eye movement (REM) and wake state. This transitional state is characterised by input-driven bidirectional fluctuations. Among them, SWDs are linked to A1 type A phases of CAP and therefore seem to be associated with shifts towards NREM sleep (sleep induction). In ADNFLE (and presumably in NFLE), micro-arousals release epileptic events in NREM sleep probably due to epileptic sensitisation of the cholinergic arousal system by the known acetylcholine (ACh) receptor mutations affecting the arousal system, giving rise to the epileptic (and also parasomniac) episodes. In both kinds of these system epilepsies (AE and NFLE), epileptic events can be released by phasic events during NREM sleep. The difference is that absences are activated in reactive states with a sleep-promoting, antiarousal effect, while in NFLE the epileptic disorder is interwoven with the cholinergic arousal function. The role of arousal/antiarousal in NFLE and AE fits nicely with the hypothesis that these epilepsies are disorders of two antagonistic thalamo-frontal systems involved in functions NREM sleep and wakefulness.
    Epilepsy research 08/2013; 107(1-2). DOI:10.1016/j.eplepsyres.2013.06.021 · 2.02 Impact Factor
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    • "Seizure manifestations have been reported to preceded by K-complexes [38], spindles [39]. This fits into a more global interrelationship with Cyclic Alternating Pattern (CAP) [24, 40]. "
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    ABSTRACT: Aims. To build up a coherent shared pathophysiology of NFLE and AP and discuss the underlying functional network. Methods. Reviewing relevant published data we point out common features in semiology of events, relations to macro- and microstructural dynamism of NREM sleep, to cholinergic arousal mechanism and genetic aspects. Results. We propose that pathological arousals accompanied by confused behavior with autonomic signs and/or hypermotor automatisms are expressions of the frontal cholinergic arousal function of different degree, during the condition of depressed cognition by frontodorsal functional loss in NREM sleep. This may happen either if the frontal cortical Ach receptors are mutated in ADNFLE (and probably also in genetically not proved nonlesional cases as well), or without epileptic disorder, in AP, assuming gain in receptor functions in both conditions. This hypothesis incorporates the previous "liberation theory" of Tassinari and the "state dissociation hypothesis" of Bassetti and Terzaghi). We propose that NFLE and IGE represent epileptic disorders of the two antagonistic twin systems in the frontal lobe. NFLE is the epileptic facilitation of the ergotropic frontal arousal system whereas absence epilepsy is the epileptic facilitation of burst-firing working mode of the spindle and delta producing frontal thalamocortical throphotropic sleep system. Significance. The proposed physiopathogenesis conceptualize epilepsies in physiologically meaningful networks.
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