Rapid eye movement (REM) sleep and seizure control in idiopathic generalized epilepsy

Hamdy, Mohamed M.; Elfatatry, Amr; Mekky, Jaidaa; Hamdy, Eman

doi:10.1016/j.yebeh.2020.107064

Cited by 11 publications

(5 citation statements)

References 23 publications

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“…Moreover, epileptiform discharges have been found to be enhanced during sleep in both mice haploinsufficient for the murine orthologue of SYNGAP1 and patients with pathologic mutations [ 21 ]. It has been hypothesized that abnormal epileptic discharges might disrupt normal sleep architecture leading to sleep disorders [ 22 , 23 ]. The enhanced night-time epileptiform discharges might explain the more severe sleep abnormalities observed in patients with SYNGAP1 mutations and warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Sleep Abnormalities in the Synaptopathies—SYNGAP1-Related Intellectual Disability and Phelan–McDermid Syndrome

et al. 2021

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Neurodevelopmental disorders are frequently associated with sleep disturbances. One class of neurodevelopmental disorders, the genetic synaptopathies, is caused by mutations in genes encoding proteins found at the synapse. Mutations in these genes cause derangement of synapse development and function. We utilized a validated sleep instrument, Children’s Sleep Habits Questionnaire (CSHQ) to examine the nature of sleep abnormalities occurring in individuals with two synaptopathies—Phelan–McDermid syndrome (PMD) (N = 47, male = 23, female = 24, age 1–46 years) and SYNGAP1-related intellectual disability (SYNGAP1-ID) (N = 64, male = 31, female = 33, age 1–64 years), when compared with unaffected siblings (N = 61, male = 25, female = 36, age 1–17 years). We found that both PMD and SYNGAP1-ID have significant sleep abnormalities with SYNGAP1-ID having greater severity of sleep disturbance than PMD. In addition, sleep disturbances were more severe for PMD in individuals 11 years and older compared with those less than 11 years old. Individuals with either disorder were more likely to use sleep aids than unaffected siblings. In conclusion, sleep disturbances are a significant phenotype in the synaptopathies PMD and SYNGAP1-ID. Improved sleep is a viable endpoint for future clinical trials for these neurodevelopmental disorders.

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Section: Discussionmentioning

confidence: 99%

Sleep Abnormalities in the Synaptopathies—SYNGAP1-Related Intellectual Disability and Phelan–McDermid Syndrome

et al. 2021

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“…indicating REM sleep has a protective effect related to epileptic seizures [13,14]. Disruptions in sleep architecture experienced by patients with epilepsy affect mainly REM sleep [15], which is regulated by melanin-concentrating hormone neurons and GABAergic neurons in the hypothalamus. The center of the pontine tegmentum excites the cortical and limbic regions of the brain and inhibits neurons in the ventral medulla through the glutamatergic-GABAergic and cholinergic systems, thereby hindering skeletal muscle activity [16].…”

Section: Resultsmentioning

confidence: 99%

Effects of lateralized interictal epileptiform discharges on the sleep architecture of people with epilepsy: a case-control study

Wang

et al. 2023

Preprint

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Background: Disruption of sleep architecture occurs in patients with epilepsy, with interictal epileptiform discharge (IED) being one possible cause. IED lateralization may exert different effects on sleep architecture, and different types of IEDs may affect the sleep architecture of patients with epilepsy. Therefore, we investigated the sleep architecture of people with epilepsy to determine the effects of IED lateralization on sleep architecture. Methods: A total of 119 patients with epilepsy who sought medical attention at our hospital between March 2018 and March 2022 and 106 healthy control participants were selected for this study. Patients with epilepsy were grouped based on the IED source determined by nocturnal scalp electroencephalography as left-sided, right-sided, simultaneous bilateral, and alternating bilateral. Polysomnography was performed to compare the effects of IED lateralization on sleep architecture among the different groups. Normally distributed data were tested for differences using the t test; the Mann–Whitney U test was used to analyze data with a non-normal distribution or heterogeneity of variance. Count data were compared using the chi-squared test, and comparisons of multiple groups were performed using analysis of variance. Results: Compared with the control group, the epilepsy group showed a statistically significant decrease in the percentage of rapid eye movement (REM) sleep (R%) and REM sleep time. The left-sided and right-sided IED groups exhibited significant decreases in R%, and the left-sided IED group showed a significant decrease in REM sleep time. Multiple linear regression analysis showed that the IED index was correlated positively withcomorbid hypertension, non-REM stage 1 (N1) sleep time, and sleep latency. Conclusions: An increase in the IED index correlates positively with comorbid hypertension, N1 sleep time, and sleep latency. Therefore, a worthwhile consideration for neurologists to reduce the IED index in clinical practice is to adopt methods that include sleep improvement techniques for patients with epilepsy.

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“…Sleep issues are common in NDDs including autism and epilepsy. In particular for epilepsy, it has been hypothesized that abnormal epileptic discharges might disrupt normal sleep architecture leading to sleep disorders 16 . This is potentially most relevant for SYNGAP1 as >90% of individuals with pathogenic SYNGAP1 mutations develop epilepsy and have abnormal interictal epileptiform discharges 4,6 .…”

Section: Discussionmentioning

confidence: 99%

Sleep Abnormalities in the Synaptopathies – SYNGAP1-related Intellectual Disability and Phelan-McDermid syndrome

Smith‐Hicks

McCormack

Stowe

et al. 2020

Preprint

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Neurodevelopmental disorders are frequently associated with sleep disturbances. One class of neurodevelopmental disorders, the genetic synaptopathies, is caused by mutations in genes encoding proteins found at the synapse. Mutations in these genes cause derangement of synapse development and function. We utilized a validated sleep instrument, Childrens Sleep Habits Questionnaire (CSHQ) to discover what sleep abnormalities occur in individuals with two synaptopathies Phelan-McDermid syndrome (PMD) and SYNGAP1-related Intellectual Disability (SYNGAP1-ID) when compared with healthy controls. We found both PMD and SYNGAP1-ID have significant sleep abnormalities with SYNGAP1-ID having greater severity of sleep disturbance than PMD. We found that sleep disturbances were more severe for both disorders in individuals 10 years and older compared with those less than 10 years old. Individuals with either disorder were more likely to use sleep aids than healthy controls. Furthermore, review of polysomnography studies for individuals with SYNGAP1-ID revealed significant reduction in rapid eye movement (REM) sleep content and delayed REM latency demonstrating abnormalities in sleep architecture. In conclusion, sleep disturbances are a significant phenotype in the synaptopathies PMD and SYNGAP1-ID. Improved sleep is a viable clinical endpoint for future clinical trials for these neurodevelopmental disorders.

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Rapid eye movement (REM) sleep and seizure control in idiopathic generalized epilepsy

Cited by 11 publications

References 23 publications

Sleep Abnormalities in the Synaptopathies—SYNGAP1-Related Intellectual Disability and Phelan–McDermid Syndrome

Sleep Abnormalities in the Synaptopathies—SYNGAP1-Related Intellectual Disability and Phelan–McDermid Syndrome

Effects of lateralized interictal epileptiform discharges on the sleep architecture of people with epilepsy: a case-control study

Sleep Abnormalities in the Synaptopathies – SYNGAP1-related Intellectual Disability and Phelan-McDermid syndrome

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