Are Absence Epilepsy and Nocturnal Frontal Lobe Epilepsy System Epilepsies of the Sleep/Wake System?

Halász, Péter

doi:10.1155/2015/231676

Cited by 26 publications

(19 citation statements)

References 103 publications

(119 reference statements)

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“…The epileptic hyperexcitability is a sine qua non. Regarding absences, the activation of the sleep-promoting system may be a “reflex” seizure trigger ( 75 , 76 ).…”

Section: Absence Epilepsy (Ae) Is the Epilepsy Of The Nrem Sleep-prommentioning

confidence: 99%

Sleep and Epilepsy Link by Plasticity

Halász

Szücs

2020

Front. Neurol.

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We aimed to explore the link between NREM sleep and epilepsy. Based on human and experimental data we propose that a sleep-related epileptic transformation of normal neurological networks underlies epileptogenesis. Major childhood epilepsies as medial temporal lobe epilepsy (MTLE), absence epilepsy (AE) and human perisylvian network (PN) epilepsies - made us good models to study. These conditions come from an epileptic transformation of the affected functional systems. This approach allows a system-based taxonomy instead of the outworn generalized-focal classification. MTLE links to the memory-system, where epileptic transformation results in a switch of normal sharp wave-ripples to epileptic spikes and pathological high frequency oscillations, compromising sleep-related memory consolidation. Absence epilepsy (AE) and juvenile myoclonic epilepsy (JME) belong to the corticothalamic system. The burst-firing mode of NREM sleep normally producing sleep-spindles turns to an epileptic working mode ejecting bilateral synchronous spike-waves. There seems to be a progressive transition from AE to JME. Shared absences and similar bilateral synchronous discharges show the belonging of the two conditions, while the continuous age windows - AE affecting schoolchildren, JME the adolescents - and the increased excitability in JME compared to AE supports the notion of progression. In perisylvian network epilepsies - idiopathic focal childhood epilepsies and electrical status epilepticus in sleep including Landau-Kleffner syndrome - centrotemporal spikes turn epileptic, with the potential to cause cognitive impairment. Postinjury epilepsies modeled by the isolated cortex model highlight the shared way of epileptogenesis suggesting the derailment of NREM sleep-related homeostatic plasticity as a common step. NREM sleep provides templates for plasticity derailing to epileptic variants under proper conditions. This sleep-origin explains epileptiform discharges' link and similarity with NREM sleep slow oscillations, spindles and ripples. Normal synaptic plasticity erroneously overgrowing homeostatic processes may derail toward an epileptic working-mode manifesting the involved system's features. The impact of NREM sleep is unclear in epileptogenesis occurring in adolescence and adulthood, when plasticity is lower. The epileptic process interferes with homeostatic synaptic plasticity and may cause cognitive impairment. Its type and degree depends on the affected network's function. We hypothesize a vicious circle between sleep end epilepsy. The epileptic derailment of normal plasticity interferes with sleep cognitive functions. Sleep and epilepsy interconnect by the pathology of plasticity.

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“…The epileptic hyperexcitability is a sine qua non. Regarding absences, the activation of the sleep-promoting system may be a “reflex” seizure trigger ( 75 , 76 ).…”

Section: Absence Epilepsy (Ae) Is the Epilepsy Of The Nrem Sleep-prommentioning

confidence: 99%

Sleep and Epilepsy Link by Plasticity

Halász

Szücs

2020

Front. Neurol.

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“…However, whether and how somatostatin-positive interneurons, the main mediators of the dendritic inhibition-dependent regulation of input-output transformations in pyramidal neurons ( Lovett-Barron et al , 2012 ; Wilson et al , 2012 ; Lee et al , 2013 ), may contribute to absence seizure generation remains to be established. Moreover, somatostatin-positive interneurons in the somatosensory cortex are active during quiet wakefulness, the brain state where most absence seizures are expressed ( Halász, 2015 ) and their silencing increases burst firing in cortical pyramidal neurons ( Gentet et al , 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures

Crunelli

Lőrincz

McCafferty

et al. 2020

Brain

142

159

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Absence seizures in children and teenagers are generally considered relatively benign because of their non-convulsive nature and the large incidence of remittance in early adulthood. Recent studies, however, show that 30% of children with absence seizures are pharmaco-resistant and 60% are affected by severe neuropsychiatric comorbid conditions, including impairments in attention, cognition, memory and mood. In particular, attention deficits can be detected before the epilepsy diagnosis, may persist even when seizures are pharmacologically controlled and are aggravated by valproic acid monotherapy. New functional MRI-magnetoencephalography and functional MRI-EEG studies provide conclusive evidence that changes in blood oxygenation level-dependent signal amplitude and frequency in children with absence seizures can be detected in specific cortical networks at least 1 min before the start of a seizure, spike-wave discharges are not generalized at seizure onset and abnormal cortical network states remain during interictal periods. From a neurobiological perspective, recent electrical recordings and imaging of large neuronal ensembles with single-cell resolution in non-anaesthetized models show that, in contrast to the predominant opinion, cortical mechanisms, rather than an exclusively thalamic rhythmogenesis, are key in driving seizure ictogenesis and determining spike-wave frequency. Though synchronous ictal firing characterizes cortical and thalamic activity at the population level, individual cortico-thalamic and thalamocortical neurons are sparsely recruited to successive seizures and consecutive paroxysmal cycles within a seizure. New evidence strengthens previous findings on the essential role for basal ganglia networks in absence seizures, in particular the ictal increase in firing of substantia nigra GABAergic neurons. Thus, a key feature of thalamic ictogenesis is the powerful increase in the inhibition of thalamocortical neurons that originates at least from two sources, substantia nigra and thalamic reticular nucleus. This undoubtedly provides a major contribution to the ictal decrease in total firing and the ictal increase of T-type calcium channel-mediated burst firing of thalamocortical neurons, though the latter is not essential for seizure expression. Moreover, in some children and animal models with absence seizures, the ictal increase in thalamic inhibition is enhanced by the loss-of-function of the astrocytic GABA transporter GAT-1 that does not necessarily derive from a mutation in its gene. Together, these novel clinical and experimental findings bring about paradigm-shifting views of our understanding of absence seizures and demand careful choice of initial monotherapy and continuous neuropsychiatric evaluation of affected children. These issues are discussed here to focus future clinical and experimental research and help to identify novel therapeutic targets for treating both absence seizures and their comorbidities.

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“…Major epilepsies can be conceived as physiological systems in which an epileptic over-excitation (derailment) exaggerates the functions when they are activated. Sensory or praxis induced reflex epilepsies may be reinterpreted so [Szücs et al submitted], and certain nonsensory systems like sleep, arousal or the memory system might be additional examples [95].…”

Section: Discussionmentioning

confidence: 99%

Epilepsy as a derailment of sleep plastic functions may cause chronic cognitive impairment - A theoretical review

Halász

Ujma

Fabó

et al. 2019

Sleep Medicine Reviews

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We report on a peculiar way of chronic cognitive impairment associated with interictal epileptic activity during NREM sleep. We review three major groups of epilepsy: mesiotemporal epilepsy (MTLE) involving the epileptic derailment of the hippocampal declarative memory system; childhood developmental epileptic encephalopathies; and the spectrum disorders of the perisylvian communication network with the centrotemporal spike phenomenon, overarching child-and adulthood epilepsies, totaling up the majority of epilepsies in childhood.We outline high impact research-lines on the cognitive harm of epilepsy; causing specific or global cognitive decline through its interference with sleep plastic functions.We highlight the key role of interictal activity in the development of cognitive impairment and the fact that we are unarmed against this harm, antiepileptic pharmaco-therapy being ineffective against the interictal process marked by spikes and high frequency oscillations.

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Are Absence Epilepsy and Nocturnal Frontal Lobe Epilepsy System Epilepsies of the Sleep/Wake System?

Cited by 26 publications

References 103 publications

Sleep and Epilepsy Link by Plasticity

Sleep and Epilepsy Link by Plasticity

Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures

Epilepsy as a derailment of sleep plastic functions may cause chronic cognitive impairment - A theoretical review

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