Epilepsy and sleep disorders are considered by many to be common bedfellows. Several sleep phenomena may occur during nighttime taking a wide variety of forms and which can mimic seizures. Although most seizure sub-types have the potential to occur during sleep or wakefulness, sleep has a well-documented and strong association with specific epilepsy syndromes. Seizures in sleep also tend to occur during lighter stages of non-REM (NREM) sleep. The neurophysiologic process involved in the deepening of NREM sleep may also facilitate both seizures and IEDs. Epilepsy per se and/or seizures themselves promote sleep disruption and significantly affect the quality, quantity, and architecture of sleep. There are many causes of sleep disruption in patients with epilepsy, including inadequate sleep hygiene, coexisting sleep disorders, and circadian rhythm disturbances. Seizures themselves can disrupt sleep, even when they occur during wakefulness. Anti-epileptic drugs (AEDs) can also alter sleep in positive and negative ways, and these effects are independent of anticonvulsant actions. The end result of sleep disruption is excessive daytime sleepiness, worsening seizures, and poor quality of life. Screening for sleep disorders in the epilepsy population and appropriate intervention strategies will lead to overall improved quality of life and seizure control.
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http://dx.doi.org/10.1016/j.sleep.2010.01.012 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Cell Biology, Emory University, Atlanta, GA 30322.
To regulate brain function, peripheral compounds must traverse the blood-brain barrier (BBB), an interface between the brain and the circulatory system. To determine whether specific transport mechanisms are relevant for sleep, we conducted a BBB-specific inducible RNAi knockdown (iKD) screen for genes affecting sleep in . We observed reduced sleep with knockdown of solute carrier , a carnitine transporter, as determined by isotope flux.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
National Institute of Biological Sciences, Beijing 102206, China.
Sleep need accumulates during waking and dissipates during sleep to maintain sleep homeostasis (process S). Besides the regulation of daily (baseline) sleep amount, homeostatic sleep regulation commonly refers to the universal phenomenon that sleep deprivation (SD) causes an increase of sleep need, hence, the amount and intensity of subsequent recovery sleep. The central regulators and signaling pathways that govern the baseline and homeostatic sleep regulations in mammals remain unclear.
View Article and Find Full Text PDFSports Med Open
January 2025
Department of Physical Education, Tongji University, Shanghai, 200000, China.
Background: While the effects of sleep deprivation on cognitive function are well-documented, its impact on high-intensity endurance performance and underlying neural mechanisms remains underexplored, especially in the context of search and rescue operations where both physical and mental performance are essential. This study examines the neurophysiological basis of sleep deprivation on high-intensity endurance using electroencephalography (EEG). In this crossover study, twenty firefighters were subjected to both sleep deprivation (SD) and normal sleep conditions, with each participant performing endurance treadmill exercise the following morning after each condition.
View Article and Find Full Text PDFPaediatr Drugs
January 2025
Child and Maternal Health Division, Menzies School of Health Research, Charles Darwin University, Darwin, NT, Australia.
Despite significant global reductions in cases of pneumonia during the last 3 decades, pneumonia remains the leading cause of post-neonatal mortality in children aged <5 years. Beyond the immediate disease burden it imposes, pneumonia contributes to long-term morbidity, including lung function deficits and bronchiectasis. Viruses are the most common cause of childhood pneumonia, but bacteria also play a crucial role.
View Article and Find Full Text PDFJ Patient Rep Outcomes
January 2025
Sanofi US Services, Inc., Bridgewater, NJ, USA.
Background: Chronic rhinosinusitis (inclusive of subtypes with nasal polyps [CRSwNP], without nasal polyps [CRSsNP], and allergic fungal rhinosinusitis [AFRS]) causes inflammation of the nose mucosa and paranasal sinuses. Unfortunately, evidence supporting use of clinical outcome assessments (COAs) in regulated clinical trials to assess key measurement concepts of these conditions is limited.
Objective: To identify key disease-related symptoms and impacts, potential outcomes of interest for new treatments, and COAs available to measure those outcomes among adult and adolescent individuals living with CRSwNP, CRSsNP, and AFRS.
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