The relationship between sleep and epilepsy: Evidence from clinical trials and animal models

Matos, Gabriela; Andersen, Mônica Levy; Valle, Angela C.; Tufik, Sérgio

doi:10.1016/j.jns.2010.05.003

Cited by 67 publications

(45 citation statements)

References 79 publications

(98 reference statements)

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“…The role of sleep deprivation in eliciting epileptiform activity has been recognized more than 50 years ago (Rodin et al, 1962) and then repeatedly documented (reviewed by Kotagal, 2001; Matos et al, 2010). In certain types of epileptic syndromes seizures predominantly occur after sleep deprivation (Derry and Duncan, 2013).…”

Section: Epilepsy and The Glycogen Hypothesis Of Sleepmentioning

confidence: 99%

Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?

et al. 2014

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Epilepsy is a family of brain disorders with a largely unknown etiology and high percentage of pharmacoresistance. The clinical manifestations of epilepsy are seizures, which originate from aberrant neuronal synchronization and hyperexcitability. Reactive astrocytosis, a hallmark of the epileptic tissue, develops into loss-of-function of glutamine synthetase, impairment of glutamate-glutamine cycle and increase in extracellular and astrocytic glutamate concentration. Here, we argue that chronically elevated intracellular glutamate level in astrocytes is instrumental to alterations in the metabolism of glycogen and leads to the synthesis of polyglucosans. Unaccessibility of glycogen-degrading enzymes to these insoluble molecules compromises the glycogenolysis-dependent reuptake of extracellular K+ by astrocytes, thereby leading to increased extracellular K+ and associated membrane depolarization. Based on current knowledge, we propose that the deterioration in structural homogeneity of glycogen particles is relevant to disruption of brain K+ homeostasis and increased susceptibility to seizures in epilepsy.

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Section: Epilepsy and The Glycogen Hypothesis Of Sleepmentioning

confidence: 99%

Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?

et al. 2014

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“…Reducing sleep time is a common route in a notoriously busy society, but prolonged sleep loss will cause (among other defects) impaired metabolism, impaired immune function, impaired cognitive function, and will, ultimately, lead to death [149]. Many pathophysiological states, such as lethargic encephalitis [190], insomnia [47], narcolepsy [114], apnoea [186], cataplexy [126], or epilepsy [104], are related to disturbances in the mechanisms of sleep induction or maintenance.…”

Section: Introductionmentioning

confidence: 99%

The sleep relay—the role of the thalamus in central and decentral sleep regulation

Coulon

Budde

Pape

2011

Pflugers Arch - Eur J Physiol

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Surprisingly, the concept of sleep, its necessity and function, the mechanisms of action, and its elicitors are far from being completely understood. A key to sleep function is to determine how and when sleep is induced. The aim of this review is to merge the classical concepts of central sleep regulation by the brainstem and hypothalamus with the recent findings on decentral sleep regulation in local neuronal assemblies and sleep regulatory substances that create a scenario in which sleep is both local and use dependent. The interface between these concepts is provided by thalamic cellular and network mechanisms that support rhythmogenesis of sleep-related activity. The brainstem and the hypothalamus centrally set the pace for sleep-related activity throughout the brain. Decentral regulation of the sleep-wake cycle was shown in the cortex, and the homeostat of non-rapid-eye-movement sleep is made up by molecular networks of sleep regulatory substances, allowing individual neurons or small neuronal assemblies to enter sleep-like states. Thalamic neurons provide state-dependent gating of sensory information via their ability to produce different patterns of electrogenic activity during wakefulness and sleep. Many mechanisms of sleep homeostasis or sleep-like states of neuronal assemblies, e.g. by the action of adenosine, can also be found in thalamic neurons, and we summarize cellular and network mechanisms of the thalamus that may elicit non-REM sleep. It is argued that both central and decentral regulators ultimately target the thalamus to induce global sleep-related oscillatory activity. We propose that future studies should integrate ideas of central, decentral, and thalamic sleep generation.

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“…Although most studies on this issue are based on clinical trials, experimental studies are of great significance for understanding this relationship (13). Most experimental techniques for selective REM sleep deprivation are based on the single platform method of Jouvet (37,38), which was modified by Susic and Markovic (33).…”

Section: Sleep and Epilepsy: Bidirectional Relationshipmentioning

confidence: 99%

“…There is a complex interplay between sleep and epilepsy. This interplay is of special interest for neuroscientists because it is still only poorly understood (12,13). Additionally, the relationship between physical exercise and epilepsy is quite intriguing, especially the mechanism underlying this relationship.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Epileptic Activity in Rats: Focus on Sleep, Physical Exercise and Nitric Oxide–mediated Neurotransmission in a Model of Homocysteine Thiolactone–induced Seizures

Hrnčić

Rašić-Marković

Šušić

et al. 2014

Serbian Journal of Experimental and Clinical Research

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Epilepsy is a chronic neurological disorder characterised by recurrent epileptic seizures. Understanding the mechanisms by which it initiates and develops, as well as its modulating factors, are of great scientifi c interest. Experimental models of epilepsy are useful for understanding these mechanisms.Homocysteine, an amino acid endogenously generated in the body, together with its reactive metabolite, homocysteine thiolactone (HCT), is recognised as a risk factor for a variety of diseases. HCT-induced seizures are a model of generalised epilepsy in which the coexistence of two types of epileptic activity has been documented. Th e complex interplay between sleep and epilepsy is still only poorly understood. Additionally, the relationship between physical exercise and epilepsy is quite intriguing, especially the mechanism underlying this relationship. Th e role of nitric oxide (NO)-mediated neurotransmission in the development of epileptic activity is highly debated in the existing scientifi c literature .In this review article, we described the modulation of epileptic activity in rats and focused on sleep, physical activity and NO-mediated signalling. First, we explain the characteristics of the experimental models of epileptic activity and the unique features of HCT-induced seizures. Second, the modulating eff ects of sleep and regular physical exercise training on epileptic activity, along with works from the authors, are discussed. Finally, the anticonvulsive eff ects of NO that is produced via nNOS and iNOS in HCT-induced seizures are reviewed. SAŽETAKEpilepsija je hronično neurološko oboljenje koje karakteriše rekurentna pojava epileptičnih napada. Razumevanje menahizama nastanka i širenja epileptične aktivnosti, kao i foktora modulacije ovih procesa, od izuzetnog je naučno-stručnog značaja. Eksperimentalni modeli epilepsije su značajni za razumevanje upravo ovih mehanizama. Homocistein, aminokiselina koja se endogeno sintetiše u organizmu, zajedno sa svojim reaktivnim metabolitom homocistein tiolaktonom (HCT), je prepoznat kao faktor rizika za nastanak različitih bolesti. Epilepsije izazvane HCT-om predstavljaju model generalizovane epileptične aktivnosti u kome je pokazana koegzistencija dva tipa napada. Složeni uzajamni odnos između spavanja i epilepsije još uvek nije dovoljno razjašnjen. Takođe, međuodnos fi zičke aktivnosti i epilepsije je krajnje interesantan, naročito mehanizmi ovih odnosa. Uloga neurotransmisije posredovane azot monoksidom (NO) u nastanku epileptične aktivnosti je vrlo kontradiktorna u postojećoj literaturi. Predmet ovog rada bila je modulacija epileptične aktivnosti kod pacova sa posebnim osvrtom na spavanje, fi zičku aktivnost i neurotransmisiju posredovanu NO. Najpre su razmotreni koncepti eksperimentalnih modela epileptične aktivnosti sa osobenostima HCT epilepsija. Zatim su diskutovani modulatorni efekti spavanja i regularnog fi zičkog veržbanja na epileptičnu aktivnost zajedno sa rezultatima radova autora. Na posletku, dat je osvrt na antikonvulzivnu ulogu NO i doprinos nNOS i...

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The relationship between sleep and epilepsy: Evidence from clinical trials and animal models

Cited by 67 publications

References 79 publications

Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?

Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?

The sleep relay—the role of the thalamus in central and decentral sleep regulation

Modulation of Epileptic Activity in Rats: Focus on Sleep, Physical Exercise and Nitric Oxide–mediated Neurotransmission in a Model of Homocysteine Thiolactone–induced Seizures

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