Sleep disorders in adults with epilepsy

Grigg-Damberger, Madeleine; Ralls, Frank M.

doi:10.1097/mcp.0000000000000101

Cited by 31 publications

(10 citation statements)

References 96 publications

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“…This is in accordance with the few data in the literature reporting frequencies of insomnia similar to ours 4,11,19. After all, it is well known that there are several factors which can cause insomnia in patients with epilepsy: sleep fragmentation due to recurrent seizures, the effect of some AEDs, as well as the simultaneous presence of mood disorders.…”

Section: Discussionsupporting

confidence: 93%

“…Insomnia is usually present in 30–40% of patients. While the frequency of OSAS ranges from 10% to 30%, and that of RLS from 10% to 33%4,10,11 It is possible that the alterations between the different studies investigating sleep disorders in patients with epilepsy are partially related to biases in the selection of patients, but also to the use of different tests, different sample sizes as well as to differences in the type of treatment (mono-poly-therapy) 12. In fact, many studies have focused their attention only on a population of patients with focal epilepsy undertaking a multidrug treatment.…”

Section: Introductionmentioning

confidence: 99%

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Excessive Daytime Sleepiness and Sleep Disorders in a Population of Patients with Epilepsy: a Case-Control Study

Gammino

Zummo²,

Bue

et al. 2016

J Epilepsy Res

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Background and PurposeThere are several primary causes for excessive daytime sleepiness (EDS) and sleep disorders in patients with epilepsy. Up to now, studies in the literature report conflicting data in terms of both prevalence and aetiology. The aim of our study was therefore to evaluate the prevalence of EDS and some sleep disorders in a population of patients with epilepsy treated with no more than two antiepileptic drugs (AEDs). We also investigated the role of the depression of mood as a variable that can negatively affect EDS.MethodsWe prospectively and consecutively recruited 99 patients with a diagnosis of epilepsy, sleep disorders and EDS, belonging to the Centre for Epilepsy of the Department of Experimental Biomedicine and Clinical Neurosciences of the University of Palermo. 61.6% of patients recruited were suffering from focal epilepsy, and 38.3% from generalized epilepsy. 68.6% were undertaking monotherapy and 27.2% were drug resistant. Patients were matched for sex and age (+/− 5 years) with 96 non epileptic controls recruited from high school students, college students, relatives and friends of the medical team that conducted the study. EDS was found in 11.1% of patients with epilepsy. Clinical evaluation of sleep disorders was performed using validated questionnaires to investigate excessive daytime sleepiness (EDS), insomnia, Restless Legs Syndrome (RLS) and Obstructive Sleep Apnoea Syndrome (OSAS). In a second phase of the study, 43 of the investigated patients and 34 controls - after giving their consent - underwent a polysomnographic examination by “Compumedics Somtè”.ResultsOur study shows a statistically significant difference between cases and controls with regard to the prevalence of RLS (p = 0.022) and severity of OSAS with an increased risk in moderate-severe forms of epilepsy (odd ratio [OR] 2.5) most significantly associated with male gender (p = 0.04) and focal epilepsy (OR 3.8) with PSG seizures (0.02). Moreover, a statistically significant difference was demonstrated about mood disorders (p = 0.001) among patients with epilepsy and non epileptic controls. Sleepiness in patients with epilepsy seems to be particularly related to both the depression of mood (p = 0.01) and the presence of OSAS (p = 0.03), as well as to a higher mean age (p = 0.006) and a longer duration of illness (p = 0.04).ConclusionsOur results confirm that drowsiness trouble frequently complained by patients with epilepsy, is particularly related not only to the presence of OSAS but also to the depression of mood.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Excessive Daytime Sleepiness and Sleep Disorders in a Population of Patients with Epilepsy: a Case-Control Study

Gammino

Zummo²,

Bue

et al. 2016

J Epilepsy Res

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“…In an excellent atlas, the Gibbses ( 1 ) described the NREM sleep enhancement of interictal epileptic discharges (IEDs). Several authors ( 2 – 4 ) summarized the related data, mainly on the distribution of spikes and seizures across sleep stages in different epilepsies. The growing knowledge about sleep physiology in the end of the last century increased the interest in sleep grapho-elements and their role in epilepsies.…”

Section: Introductionmentioning

confidence: 99%

Sleep and Epilepsy Link by Plasticity

Halász

Szücs

2020

Front. Neurol.

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We aimed to explore the link between NREM sleep and epilepsy. Based on human and experimental data we propose that a sleep-related epileptic transformation of normal neurological networks underlies epileptogenesis. Major childhood epilepsies as medial temporal lobe epilepsy (MTLE), absence epilepsy (AE) and human perisylvian network (PN) epilepsies - made us good models to study. These conditions come from an epileptic transformation of the affected functional systems. This approach allows a system-based taxonomy instead of the outworn generalized-focal classification. MTLE links to the memory-system, where epileptic transformation results in a switch of normal sharp wave-ripples to epileptic spikes and pathological high frequency oscillations, compromising sleep-related memory consolidation. Absence epilepsy (AE) and juvenile myoclonic epilepsy (JME) belong to the corticothalamic system. The burst-firing mode of NREM sleep normally producing sleep-spindles turns to an epileptic working mode ejecting bilateral synchronous spike-waves. There seems to be a progressive transition from AE to JME. Shared absences and similar bilateral synchronous discharges show the belonging of the two conditions, while the continuous age windows - AE affecting schoolchildren, JME the adolescents - and the increased excitability in JME compared to AE supports the notion of progression. In perisylvian network epilepsies - idiopathic focal childhood epilepsies and electrical status epilepticus in sleep including Landau-Kleffner syndrome - centrotemporal spikes turn epileptic, with the potential to cause cognitive impairment. Postinjury epilepsies modeled by the isolated cortex model highlight the shared way of epileptogenesis suggesting the derailment of NREM sleep-related homeostatic plasticity as a common step. NREM sleep provides templates for plasticity derailing to epileptic variants under proper conditions. This sleep-origin explains epileptiform discharges' link and similarity with NREM sleep slow oscillations, spindles and ripples. Normal synaptic plasticity erroneously overgrowing homeostatic processes may derail toward an epileptic working-mode manifesting the involved system's features. The impact of NREM sleep is unclear in epileptogenesis occurring in adolescence and adulthood, when plasticity is lower. The epileptic process interferes with homeostatic synaptic plasticity and may cause cognitive impairment. Its type and degree depends on the affected network's function. We hypothesize a vicious circle between sleep end epilepsy. The epileptic derailment of normal plasticity interferes with sleep cognitive functions. Sleep and epilepsy interconnect by the pathology of plasticity.

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“…Often, these disruptions manifest in the form of increased latency to sleep or premature waking, suggesting that dysfunction of the circadian clock may underlie some sleep issues. Conversely, disruptions in sleep are known to alter neurological symptoms, including those common to MEs such as seizure frequency and cognitive ability, and metabolic function in diseases such as type II diabetes (Suzuki et al, 1997, Grigg-Damberger and Ralls, 2014, Jain and Kothare, 2015, Nedeltcheva and Scheer, 2014, Guarnieri and Sorbi, 2015). Additionally, it has recently been shown that sleep deprivation alters mitochondrial function and gene expression in response to oxidative stress in Drosophila (Rodrigues et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Sleep and circadian defects in a Drosophila model of mitochondrial encephalomyopathy

Fogle

Mobini

Paseos

et al. 2019

Neurobiology of Sleep and Circadian Rhythms

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Mitochondrial encephalomyopathies (ME) are complex, incurable diseases characterized by severe bioenergetic distress that can affect the function of all major organ systems but is especially taxing to neuromuscular tissues. Animal models of MEs are rare, but the Drosophila ATP61 mutant is a stable, well-characterized genetic line that accurately models progressive human mitochondrial diseases such as Maternally-Inherited Leigh Syndrome (MILS), Neuropathy, Ataxia, and Retinitis Pigmentosa (NARP), and Familial Bilateral Striatal Necrosis (FBSN). While it is established that this model exhibits important hallmarks of ME, including excess cellular and mitochondrial reactive oxygen species, shortened lifespan, muscle degeneration, and stress-induced seizures, it is unknown whether it exhibits defects in sleep or circadian function. This is a clinically relevant question, as many neurological and neurodegenerative diseases are characterized by such disturbances, which can exacerbate other symptoms and worsen quality of life. Since Drosophila is highly amenable to sleep and circadian studies, we asked whether we could detect disease phenotypes in the circadian behaviors of ATP61. Indeed, we found that day-time and night-time activity and sleep are altered through disease progression, and that circadian patterns are disrupted at both the behavioral and neuronal levels. These results establish ATP61 as an important model of sleep and circadian disruption in ME that can be studied mechanistically at the molecular, cellular, and behavioral level to uncover underlying pathophysiology and test novel therapies.

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Sleep disorders in adults with epilepsy

Abstract: Identifying and treating unrecognized sleep disorders and understanding the impact of circadian rhythms on epilepsy can improve quality of life and seizure control in AWE.

Cited by 31 publications

References 96 publications

Excessive Daytime Sleepiness and Sleep Disorders in a Population of Patients with Epilepsy: a Case-Control Study

Excessive Daytime Sleepiness and Sleep Disorders in a Population of Patients with Epilepsy: a Case-Control Study

Sleep and Epilepsy Link by Plasticity

Sleep and circadian defects in a Drosophila model of mitochondrial encephalomyopathy

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