The sleep–wake cycle in adult rats following pilocarpine-induced temporal lobe epilepsy (original) (raw)
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The sleep-wakefulness cycle of Wistar rats with spontaneous absence-like epilepsy
Possible interactions between the sleep-wakefulness cycle and a new kind of spontaneous epilepsy, expressed as absence-like seizures and spike-wave bursts in FMUSP rats, are evaluated. The electro-oscillograms of some cortical and subcortical regions of the brain were recorded, as well as head, rostrum/vibrissae and eye movements. Recordings were performed uninterruptedly during 24 hours. The seizures were mostly concentrated in the wakefulness state but they could occur in any other phase, including paradoxical sleep. After the seizure, the rats usually returned to the same phase that was interrupted, although they often returned to wakefulness. There was an intense fragmentation of the sleepwakefulness cycle. The incidence of each cycle phase was significantly reduced, except S III of synchronized sleep and paradoxical sleep, thus maintaining the overall duration and architecture of the sleep-wakefulness cycle. The fragmentation of the cycle seems to be due to an impairment of the very processes that generate sleep and wakefulness. Electrophysiological and behavioral profiles of the FMUSP rats recommend accurate and comprehensive study of the animal model owing to its resemblance to seizures in humans and also to discrepancies with existing genetic or experimental epilepsy models.
Clinical Neurophysiology, 2000
Objectives: A reciprocal effect is observed between sleep and epilepsy. Sleep effect on epilepsy is protective and facilitating. Reciprocally epilepsy alters sleep organization and microarchitecture. This interelationship is well established for some epilepsies but remains unde®ned for cryptogenic and symptomatic frontal and temporal lobe epilepsies. In order to research sleep in¯uence on seizures and epilepsy effects on sleep we carried out two studies in patients with cryptogenic/symptomatic frontal or temporal lobe epilepsies.
The roles of sleep-wake states and brain rhythms in epileptic seizure onset
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014
Editor's Note: These short, critical reviews of recent papers in the Journal, written exclusively by graduate students or postdoctoral fellows, are intended to summarize the important findings of the paper and provide additional insight and commentary. For more information on the format and purpose of the Journal Club, please see http://www.jneurosci.org/misc/ifa\_features.shtml.
The Relationship Between Sleep and Epilepsy
The Neurologist, 2008
The occurrence of seizures in the sleep state is observed in nearly one third of patients. This is caused by an intimate relationship between the physiological state of sleep and the pathological process underlying epileptic seizures. Both sleep and sleep deprivation influence the frequency of epileptiform discharges on electroencephalograms as well as the occurrence of clinical seizures, typically during nonrapid eye movement sleep. The relationship of epileptiform activity to nonrapid eye movement sleep is vividly shown in the syndrome of continuous spikes in slow-wave sleep and the Landau-Kleffner syndrome. Seizure semiology can also be influenced by sleep and sleep deprivation. Sleep disorders may influence seizure control, and effective treatment of sleep disorders can improve seizure control. Seizures, antiepileptic drugs, ketogenic diet, and vagus nerve stimulation all influence sleep quality, daytime alertness, and neurocognitive function.
Occurrence of Epilepsy at Different Zeitgeber Times Alters Sleep Homeostasis Differently in Rats
SLEEP, 2012
Epilepsy Alters Sleep Homeostasis-Yi et al INTRODUCTION According to the two-process model, sleep is regulated by two oscillatory processes: sleep homeostasis (process S) and the circadian pacemaker (process C). 1,2 The homeostatic process S mediates the rise of sleep propensity during waking and dissipates during sleep. Circadian process C is a clocklike mechanism which is independent of prior sleep-wake activities and determines the alteration of periods with high and low sleep propensity. 2 Slow wave activity (SWA) during slow wave sleep (SWS) and other factors that fluctuate with circadian rhythmicity (e.g., interleukin [IL]-1, tumor necrosis factor [TNF]-α, 3,4 corticotrophin-releasing hormone [CRH], 5,6 and growth hormone releasing hormone [GHRH] 7) may represent the homeostatic variable S. On the other hand, the circadian pacemaker, located in the suprachiasmatic nucleus (SCN) of the hypothalamus, coordinates daily oscillations in the transcription and
Time-frequency characteristics and dynamics of sleep spindles in WAG/Rij rats with absence epilepsy
Brain Research, 2014
Absence epilepsy WAG/Rij rats Continuous wavelet transform Instantaneous frequency dynamics a b s t r a c t In rat models of absence epilepsy, epileptic spike-wave discharges appeared in EEG spontaneously, and the incidence of epileptic activity increases with age. Spike-wave discharges and sleep spindles are known to share common thalamo-cortical mechanism, suggesting that absence seizures might affect some intrinsic properties of sleep spindles. This paper examines time-frequency EEG characteristics of anterior sleep spindles in non-epileptic Wistar and epileptic WAG/Rij rats at the age of 7 and 9 months. Considering non-stationary features of sleep spindles, EEG analysis was performed using Morlet-based continuous wavelet transform.
Updates in Sleep Neurology and Obstructive Sleep Apnea [Working Title], 2020
Complex interplay and reciprocal interactions between sleep and epilepsy have been known for centuries. However, newer technologies and in-depth studies have provided us with better understanding of this relationship. Nocturnal seizures can interrupt sleep, while a number of factors, including antiepileptic drugs and sleep disorders, can aggravate seizures. Interestingly, different epileptic syndromes may trigger increase in seizure frequency at a certain phases of the sleep-wake cycle, while others may not show any correlation with these phases. We aim to provide an overview of the interactions between sleep and epilepsy, and provide better understanding how knowledge of the relationship between these two conditions can help more effective management of both disorders.
Sleep Deprivation and Spike-Wave Discharges in Epileptic Rats
Sleep, 1995
The effects of sleep deprivation were studied on the occurrence of spike-wave discharges in the electroencephalogram of rats of the epileptic WAG/Rij strain, a model for absence epilepsy, This was done before, during and after a period of 12 hours of near total sleep deprivation. A substantial increase in the number of spikewave discharges was found during the first 4 hours of the deprivation period, whereas in the following deprivation hours epileptic activity returned to baseline values. Immediately after termination of deprivation, a decrease in the number of spike-wave discharges parallelled a rebound of rapid eye movement (REM) sleep and deep non-REM sleep. An initial increase in epileptic activity has also been reported during sleep deprivation of humans. This initial increase as well as the epileptogenic effects during the course of the sleep deprivation and during the recovery period after sleep deprivation can be interpreted in terms of changes in sleep-wake states. Although the epilepsy-provoking mechanisms are not yet understood, an explanation is suggested based on changes of transitions between sleepwake states and shifts in level of synchronization.
High-frequency oscillations recorded in human medial temporal lobe during sleep
Annals of Neurology, 2004
The presence of fast ripple oscillations (FRs, 200-500Hz) has been confirmed in rodent epilepsy models but has not been observed in nonepileptic rodents, suggesting that FRs are associated with epileptogenesis. Although studies in human epileptic patients have reported that both FRs and ripples (80-200Hz) chiefly occur during non-rapid eye movement sleep (NREM), and that ripple oscillations in human hippocampus resemble those found in nonprimate slow wave sleep, quantitative studies of these oscillations previously have not been conducted during polysomnographically defined sleep and waking states. Spontaneous FRs and ripples were detected using automated computer techniques in patients with medial temporal lobe epilepsy during sleep and waking, and results showed that the incidence of ripples, which are thought to represent normal activity in animal and human hippocampus, was similar between epileptogenic and nonepileptogenic temporal lobe, whereas rates of FR occurrence were significantly associated with epileptogenic areas. The generation of both FRs and ripples showed the highest rates of occurrence during NREM sleep. During REM sleep, ripple rates were lowest, whereas FR rates remained elevated and were equivalent to rates observed during waking. The predominance of FRs within the epileptogenic zone not only during NREM sleep, but also during epileptiformsuppressing desynchronized episodes of waking and REM sleep supports the view that FRs are the product of pathological neuronal hypersynchronization associated with seizure-generating areas.