scholarly journals Continuous Spike-Wave during Slow Wave Sleep and Related Conditions

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Nilika Shah Singhal ◽  
Joseph E. Sullivan
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Treatment Strategies ◽  
Epileptic Encephalopathy ◽  
Related Condition ◽  
Age Related ◽  
Hormonal Therapies ◽  
Electroencephalogram Eeg ◽  
International League ◽  
Spike Wave

Continuous spike and wave during slow wave sleep (CSWS) is an epileptic encephalopathy that presents with neurocognitive regression and clinical seizures, and that demonstrates an electroencephalogram (EEG) pattern of electrical status epilepticus during sleep, as defined by the Commission on Classification and Terminology of the International League Against Epilepsy 1989. CSWS is an age-related condition, typically presenting in children around 5 years of age, with clinical seizures which progress within 2 years to a severe epileptic encephalopathy. The pathophysiology of CSWS is not completely understood, but the corticothalamic neuronal network involved in sleep patterns is thought to be involved. Genetic predisposition and injury in early development are thought to play etiological roles. Treatment strategies have involved traditional anticonvulsants, hormonal therapies, and other newer techniques. Outcomes are fair, and the thought is that earlier diagnosis and intervention preserve neurocognitive development, as in the case of other epileptic encephalopathies. Further understanding of the mechanisms of CSWS may lead to improved therapeutic options and thus outcomes of children with CSWS.

scholarly journals Epileptic Encephalopathies: An Overview

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Sonia Khan ◽  
Raidah Al Baradie
Keyword(s):  
Slow Wave Sleep ◽  
Epileptic Encephalopathy ◽  
Dravet Syndrome ◽  
Management Options ◽  
Epileptic Encephalopathies ◽  
Age Related ◽  
Ohtahara Syndrome ◽  
Cerebral Dysfunction ◽  
Epileptic Syndromes

Epileptic encephalopathies are an epileptic condition characterized by epileptiform abnormalities associated with progressive cerebral dysfunction. In the classification of the International League Against Epilepsy eight age-related epileptic encephalopathy syndromes are recognized. These syndromes include early myoclonic encephalopathy and Ohtahara syndrome in the neonatal period, West syndrome and Dravet syndrome in infancy, myoclonic status in nonprogressive encephalopathies, and Lennox-Gastaut syndrome, Landau-Kleffner syndrome, and epilepsy with continuous spike waves during slow wave sleep in childhood and adolescences. Other epileptic syndromes such as migrating partial seizures in infancy and severe epilepsy with multiple independent spike foci may be reasonably added. In this paper, we provide an overview of epileptic encephalopathies including clinical neurophysiological features, cognitive deterioration, and management options especially that these conditions are generally refractory to standard antiepileptic drugs.

scholarly journals Mr. Potato Head

2019 ◽  
pp. 468-487
Author(s):  
Nancy Foldvary-Schaefer ◽  
Thapanee Somboon ◽  
Zahreddin Alsheikhtaha
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Developmental Delay ◽  
Epileptic Encephalopathy ◽  
Electrode Placement ◽  
Age Related ◽  
Generalized Epilepsy ◽  
Patients With Epilepsy ◽  
Spike Wave

This case illustrates diagnostic challenges in patients with epilepsy and suspected sleep disorders. Specifically, the symptomatic generalized epilepsy Lennox-Gastaut syndrome is an age-related epileptic encephalopathy characterized by developmental delay; multiple seizure types, including tonic seizures in drowsiness and sleep; and generalized slow spike-wave complexes on electroencephalography (EEG). Tonic seizures in sleep can be unrecognized or can be confused with sleep disorders such as sleep apnea. The case demonstrates how to identify generalized epileptic abnormalities and seizures on the limited EEG montage used in routine polysomnography and expanded EEG using the 10-20 system of electrode placement.

The Cessation of Continuous Spike Wave in Slow-Wave Sleep Following a Temporal Lobectomy

2011 ◽  
Vol 27 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Brian D. Moseley ◽  
Radhika Dhamija ◽  
Elaine C. Wirrell
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Temporal Lobectomy ◽  
Spike Wave

Ghrelin promotes slow-wave sleep in humans

2003 ◽  
Vol 284 (2) ◽  
pp. E407-E415 ◽  
Author(s):  
J. C. Weikel ◽  
A. Wichniak ◽  
M. Ising ◽  
H. Brunner ◽  
E. Friess ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Wave Activity ◽  
Sleep Eeg ◽  
Endogenous Ligand ◽  
Plasma Gh ◽  
Electroencephalogram Eeg ◽  
Inverse Pattern ◽  
Ghs Receptor

Ghrelin, an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor, stimulates GH release, appetite, and weight gain in humans and rodents. Synthetic GHSs modulate sleep electroencephalogram (EEG) and nocturnal hormone secretion. We studied the effect of 4 × 50 μg of ghrelin administered hourly as intravenous boluses between 2200 and 0100 on sleep EEG and the secretion of plasma GH, ACTH, cortisol, prolactin, and leptin in humans ( n = 7). After ghrelin administration, slow-wave sleep was increased during the total night and accumulated δ-wave activity was enhanced during the second half of the night. Rapid-eye-movement (REM) sleep was reduced during the second third of the night, whereas all other sleep EEG variables remained unchanged. Furthermore, GH and prolactin plasma levels were enhanced throughout the night, and cortisol levels increased during the first part of the night (2200–0300). The response of GH to ghrelin was most distinct after the first injection and lowest after the fourth injection. In contrast, cortisol showed an inverse pattern of response. Leptin levels did not differ between groups. Our data show a distinct action of exogenous ghrelin on sleep EEG and nocturnal hormone secretion. We suggest that ghrelin is an endogenous sleep-promoting factor. This role appears to be complementary to the already described effects of the peptide in the regulation of energy balance. Furthermore, ghrelin appears to be a common stimulus of the somatotropic and hypothalamo-pituitary-adrenocortical systems. It appears that ghrelin is a sleep-promoting factor in humans.

scholarly journals Budgerigars have complex sleep structure similar to that of mammals

PLoS Biology ◽  
2020 ◽  
Vol 18 (11) ◽  
pp. e3000929
Author(s):  
Sofija V. Canavan ◽  
Daniel Margoliash
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Mammalian Species ◽  
Parallel Evolution ◽  
Bird Species ◽  
Sleep Architecture ◽  
Sleep Structure ◽  
Lighting Conditions ◽  
Order Of Magnitude ◽  
Electroencephalogram Eeg

Birds and mammals share specialized forms of sleep including slow wave sleep (SWS) and rapid eye movement sleep (REM), raising the question of why and how specialized sleep evolved. Extensive prior studies concluded that avian sleep lacked many features characteristic of mammalian sleep, and therefore that specialized sleep must have evolved independently in birds and mammals. This has been challenged by evidence of more complex sleep in multiple songbird species. To extend this analysis beyond songbirds, we examined a species of parrot, the sister taxon to songbirds. We implanted adult budgerigars (Melopsittacus undulatus) with electroencephalogram (EEG) and electrooculogram (EOG) electrodes to evaluate sleep architecture, and video monitored birds during sleep. Sleep was scored with manual and automated techniques, including automated detection of slow waves and eye movements. This can help define a new standard for how to score sleep in birds. Budgerigars exhibited consolidated sleep, a pattern also observed in songbirds, and many mammalian species, including humans. We found that REM constituted 26.5% of total sleep, comparable to humans and an order of magnitude greater than previously reported. Although we observed no spindles, we found a clear state of intermediate sleep (IS) similar to non-REM (NREM) stage 2. Across the night, SWS decreased and REM increased, as observed in mammals and songbirds. Slow wave activity (SWA) fluctuated with a 29-min ultradian rhythm, indicating a tendency to move systematically through sleep states as observed in other species with consolidated sleep. These results are at variance with numerous older sleep studies, including for budgerigars. Here, we demonstrated that lighting conditions used in the prior budgerigar study—and commonly used in older bird studies—dramatically disrupted budgerigar sleep structure, explaining the prior results. Thus, it is likely that more complex sleep has been overlooked in a broad range of bird species. The similarities in sleep architecture observed in mammals, songbirds, and now budgerigars, alongside recent work in reptiles and basal birds, provide support for the hypothesis that a common amniote ancestor possessed the precursors that gave rise to REM and SWS at one or more loci in the parallel evolution of sleep in higher vertebrates. We discuss this hypothesis in terms of the common plan of forebrain organization shared by reptiles, birds, and mammals.

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