The purpose of the study is to evaluate the prevalence of epilepsy in children with surgically treated obstructive sleep apnea (OSA) and examine the associated healthcare utilization. This cross-sectional study included children aged 1-18 years diagnosed with moderate to severe OSA who were treated with adenoidectomy or adenotonsillectomy. A matched control group (1:3 ratio) without OSA was used for comparison. Data were obtained from Clalit Health Services, Israel's largest healthcare provider. The study analyzed the prevalence of epilepsy, hospital admissions for seizures, use of anti-seizure medications (ASMs), and outpatient visits to pediatric neurologists. Among 55,164 children (13,791 in the OSA group and 41,373 in the control group), the prevalence of epilepsy was higher in the OSA group (0.9% vs. 0.4%; odds ratio (OR) = 2.22, p < 0.001). The OSA group also exhibited higher rates of ASM use (1.1% vs. 0.5%; OR = 2.24, p < 0.001), emergency department visits (OR = 15.66, p < 0.001), hospital admissions (OR = 3.18, p < 0.001), and visits to pediatric neurologists (14% vs. 8.1%; OR = 1.85, p < 0.001). The usage of ASMs was significantly higher in the OSA group, particularly for levetiracetam (OR = 3.73, p < 0.001).

Children with surgically treated OSA had higher rates of epilepsy and greater healthcare utilization compared to their peers. These findings underscore the necessity for integrated care, including neurological assessments, for children with OSA. Further research is needed to examine the impact of OSA treatment on epilepsy outcomes.

• Obstructive sleep apnea (OSA) and epilepsy are prevalent neurological conditions in children, with evidence suggesting a bidirectional relationship between sleep disorders and epilepsy in adults. • OSA prevalence is notably higher in children with refractory epilepsy or those prescribed multiple anti-seizure medications (ASMs).

• This study demonstrates a twofold increase in epilepsy prevalence among children with surgically treated moderate-to-severe OSA compared to matched controls. • Pediatric patients with OSA exhibit significantly higher rates of epilepsy-related healthcare utilization, including hospital admissions, emergency visits, and consultations with pediatric neurologists.

Evaluate relationships between PSG-confirmed OSA and SUDEP risk using the revised SUDEP Risk Inventory (rSUDEP-7).

Identified adults with epilepsy (AWE) who underwent PSG 2004-2016 at Cleveland Clinic. OSA was defined as apnea-hypopnea index (AHI)- ≥-5/h sleep; moderate/severe OSA as AHI≥15. SUDEP risk was assessed using rSUDEP-7: higher rSUDEP-7 score, greater SUDEP risk. Associations between rSUDEP-7 score and OSA groups (AHI≥15 vs. <15) were evaluated using Wilcoxon rank-sum tests and multivariable linear models adjusting for age, sex, BMI, and smoking status. Spearman correlations measured relationships between rSUDEP-7 score with AHI and oxygen desaturation indices (ODI).

OSA was present in 134 (62.6 %) of 214 AWE; moderate/severe in 75 (35 %). AWE with AHI≥15 were more likely to be male and older, had higher BMI, greater frequency of tonic-clonic seizures (TCS), longer epilepsy duration, and more likely to have drug-resistant epilepsy (DRE) and sleep-related seizures (all p< 0.05). The median rSUDEP-7 score was 1 (0,3) but 37.4 % had a score ≥3 (high SUDEP risk), and 11.7 % ≥5 (highest SUDEP risk). rSUDEP-7 scores were higher in those with AHI≥15 (3 vs. 1, p = 0.001). Higher AHI and ODI 3% positively correlated with rSUDEP-7 (p=0.002 and p=0.016) while SpO2 nadir negatively correlated with rSUDEP-7 (p=0.007). After adjustments, AWE with AHI≥15 had mean rSUDEP-7 score 1.14 points (95% CI 0.55-1.72, p<0.001) higher than those with AHI<15.

AWE with PSG-confirmed moderate/severe OSA especially those who are older and have GTC had higher rSUDEP-7 scores potentially increasing their risk for SUDEP. Our findings support routine screening for OSA in AWE. Further studies confirming the significance and impact of OSA on SUDEP risk are needed.

The primary objective is to explore what causes slow-wave sleep loss in elderly patients with epilepsy. The secondary objective is to identify the PSG characteristics in elderly patients with epilepsy. The clinical demographics, sleep architecture, sleep-related events, and interictal epileptiform discharges are to be evaluated in the objectives.

The video electroencephalography (VEEG) and polysomnogram (PSG) data from 44 elderly patients with epilepsy and 52 elderly patients with sleep disorders but without definite central nervous system diseases were analysed. This was a case-control study. The differences in the PSG sleep architecture parameters (total sleep time (TST), sleep efficiency, wake after sleep onset, etc.) and sleep-related events (apnea hypopnea index, oxygen desaturation index (ODI), periodic limb movement index, etc.) between the epilepsy and control groups. As Additionally, these parameters were assessed within the elderly patients with epilepsy, comparing the slow-wave sleep existence and slow-wave sleep loss groups, using VEEG and PSG.

The epileptic group exhibited significantly lower TST (343.477 ± 96.3046min vs 389.115 ± 61.5727min, p < 0.05), rapid eye movement (%) (13.011 ± 7.5384 vs 16.992 ± 6.7025, p < 0.05), non-rapid eye movement stage 3 (%) (1.35[0,7.225] vs 3.65[0.425,13.75], p < 0.05), and sleep efficiency (%) (69.482 ± 14.1771% vs 77.242 ± 10.6171%, p < 0.05). Conversely, the ODI (25.6[9.825,51.775] events/hour vs 16.85[5.3,30.425] events/hour, p < 0.05) and spontaneous arousal index (4.0455[2.1805,6.9609] events/hour vs 2.9709[1.4747,5.0554] events/hour, p < 0.05) were significantly higher in elderly patients with epilepsy. The prevalence of obstructive sleep apnea-hypopnea syndrome (OSAHS) was significantly higher in the slow-wave sleep loss group than in the slow-wave sleep existence group (100% vs 77.8%, p < 0.05). The incidence of slow-wave sleep loss was lower in patients with epilepsy aged between 75 and 85 years compared to those aged between 65 and 75 years.

Elderly patients with epilepsy exhibit higher levels of ODI and spontaneous arousal index. Our findings indicate that OSAHS could be a contributing factor to slow-wave sleep loss in this population. The incidence of slow-wave sleep loss was lower in patients aged above 75 years among elderly patients with epilepsy.

The aim of this study was to determine whether patients with syndromic craniosynostosis (SCS) are at increased risk for epilepsy relative to patients with nonsyndromic craniosynostosis (NSCS).

A retrospective cohort study was completed using the Kids' Inpatient Database (KID). All patients diagnosed with craniosynostosis (CS) were included. The primary predictor variable was study grouping (SCS vs. NSCS). The primary outcome variable was a diagnosis of epilepsy. Descriptive statistics, univariate analyses and multivariate logistic regression were performed to identify independent risk factors for epilepsy.

The final study sample included a total of 10,089 patients (mean age, 1.78 years ± 3.70; 37.7% female). 9278 patients (92.0%) had NSCS, and the remaining 811 patients (8.0%) had SCS. A total of 577 patients (5.7%) had epilepsy. Not controlling for other variables, patients with SCS were at increased risk for epilepsy relative to patients with NSCS (OR 2.1, P < 0.001). After controlling for all significant variables, patients with SCS were no longer at increased risk for epilepsy relative to patients with NSCS (OR 0.73, P = 0.063). Hydrocephalus, Chiari malformation (CM), obstructive sleep apnea (OSA), atrial septal defect (ASD), gastro-esophageal reflux disease (GERD) were all independent risk factors (P < 0.05) for epilepsy.

Syndromic craniosynostosis (SCS) in itself is not a risk factor for epilepsy relative to NSCS. The greater prevalence of hydrocephalus, CM, OSA, ASD, and GERD, all of which were risk factors for epilepsy, in patients with SCS relative to patients with NSCS likely explains the greater prevalence of epilepsy in SCS relative to NSCS.

This study aimed to evaluate the relationship between status epilepticus (SE) and cardiorespiratory comorbidity in patients with epilepsy.

We conducted a population-based study using cloud-based aggregated electronic medical records from >53 million patients in the US (Explorys, IBM Watson; January 1999 to November 2020). During the study period, we identified patients with epilepsy with SE. Patients with a history of cardiac arrest, anoxic encephalopathy, and/or cerebrovascular disease were excluded. We reported the prevalences and prevalence ratios of cardiorespiratory and medical comorbidities using age- and sex-adjusted standardization.

We identified 494,790 patients with epilepsy and 19,190 had SE. Cardiovascular and respiratory diseases were statistically significantly more prevalent in patients with epilepsy with SE than in those without SE (adjusted prevalence ratio (APR) 1.13, prevalence 68.7% [95% confidence interval (CI): 67.6-69.9] vs 60.9% [95% CI: 60.7-61.1]) and (APR 1.25, 73.1% [95% CI: 71.8-74.3] vs 58.4% [95% CI: 58.1-58.6]), respectively. Aspiration pneumonia (APR 3.12, 0.47% [95% CI: 0.37-0.57] vs 0.15% [95% CI: 0.14-0.16]) and acute respiratory distress syndrome (APR 2.40, 0.47% [95% CI: 0.37-0.57] vs 0.20% [95% CI: 0.18-0.21]) were more prevalent in patients with epilepsy with SE. Common cardiovascular risk factors such as diabetes mellitus (APR 1.13, 17.1% [95% CI: 16.5-17.6] vs 15.1% [95% CI: 1.50-15.2]) and hypertension (APR 1.28, 10.6% [95% CI: 10.2-11.0] vs 8.31% [95% CI: 8.23-8.39]) were also more common in patients with epilepsy with SE.

In this population-based study, patients with epilepsy with SE had a statistically significantly higher prevalence of cardiorespiratory comorbidities than in those without SE.

Epilepsy is one of the most common but manageable neurological disorder. The relation between epilepsy, sleep, and health-related quality of life (HRQoL) in culturally distinct environment of Pakistan remains unclear. The purpose of this study was to determine prevalence and predictors of excessive daytime sleepiness (EDS), poor sleep quality (SQ), and to analyze their association with HRQoL in people with epilepsy (PWE).

A study was conducted among PWE attending two tertiary care hospitals of Islamabad and Rawalpindi, Pakistan. The EDS, SQ, and HRQoL were evaluated by Urdu versions of Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), and Quality of Life in Epilepsy-31 (QOLIE-31).

The study included 200 PWE and 51 healthy controls with mean (SD) ages of 33.1 ± 13.9, 32.9 ± 10.9, and a disease duration of 5.01 ± 6.17, respectively. The majority of the respondents (n = 130, 65%) had poor seizure control, and most of these (n = 88, 68%) were on combination antiepileptic drug (AED) therapy. In comparison to controls, a higher number of PWE had EDS by ESS (score ≥ 11, 10% vs. 40%, p-value 0.00), and poor SQ by PSQI (score > 5, 9% vs. 71%, p-value 0.00). A multiple logistic regression analysis reveals that the factors significantly associated with EDS were: female gender; increasing age; seizure control; duration of epilepsy; and combination AED therapy. A second multiple binary logistic regression analysis suggests that factors significantly associated with poor SQ were: increasing age; female gender; poor seizure control; and combination therapy. The Hierarchical multivariate analysis suggests that poor seizure control, EDS, and poor SQ were significant predictors of low HRQoL.

The findings suggest high prevalence of EDS and poor SQ in PWE in Pakistan. A significant negative association exists between sleep complaints and HRQoL. During routine clinical consultations, awareness about sleep hygiene practices must be provided to enhance HRQoL.

Sleep disturbances, such as insomnia, obstructive sleep apnea, and daytime sleepiness, are common in people diagnosed with epilepsy. These disturbances can be attributed to nocturnal seizures, psychosocial factors, and/or the use of anti-epileptic drugs with sleep-modifying side effects. Epilepsy patients with poor sleep quality have intensified seizure frequency and disease progression compared to their well-rested counterparts. A better understanding of the complex relationship between sleep and epilepsy is needed, since approximately 20% of seizures and more than 90% of sudden unexpected deaths in epilepsy occur during sleep. Emerging studies suggest that neuroinflammation, (e.g., the CNS immune response characterized by the change in expression of inflammatory mediators and glial activation) may be a potential link between sleep deprivation and seizures. Here, we review the mechanisms by which sleep deprivation induces neuroinflammation and propose that neuroinflammation synergizes with seizure activity to worsen neurodegeneration in the epileptic brain. Additionally, we highlight the relevance of sleep interventions, often overlooked by physicians, to manage seizures, prevent epilepsy-related mortality, and improve quality of life.

This targeted review addresses the best accepted and most intriguing recent observations on the complex relationships between sleep and epilepsy. Ten to 15% of all epilepsies are sleep-related. Included in these is sleep-related hypermotor epilepsy, renamed from nocturnal frontal lobe epilepsy by a 2016 consensus conference since 30% of cases are extra-frontal, seizures are related to sleep rather than clock time, and the predominant semiology is hypermotor. Stereo-EEG is providing crucial insights into network activation in sleep-related epilepsies and definition of the epileptogenic zone. Pathologic high-frequency oscillations, a promising biomarker for identifying the epileptogenic zone, are most frequent in NREM sleep, lowest in wakefulness and REM sleep, similar to interictal epileptiform discharges (IEDs). Most sleep-related seizures are followed by awakening or arousal and IEDs cause arousals and increase after arousals, likely contributing to sleep/wake complaints. Sleep/wake disorders are 2-3 times more common in adults with epilepsy than the general population; these comorbidities are associated with poorer quality of life and may impact seizure control. Treatment of sleep apnea reduces seizures in many cases. An emerging area of research is in circadian biology and epilepsy. Over 90% of people with epilepsy have seizures with circadian periodicity, in part related to sleep itself, and the majority of SUDEP cases occur in sleep. Recognizing these bidirectional relationships is important for patient and caregiver education and counseling and optimizing epilepsy outcomes.

Drug-resistant epilepsy accounts for approximately one third of all epilepsy cases; yet its exact etiopathogenesis still remains under intense exploration. Several factors have been advocated for predicting drug resistance in patients with epilepsy. Obstructive sleep apnea (OSA) is a commonly prevalent sleep disorder that exhibits a bidirectional and strong comorbidity with epilepsy. The exact pathophysiology of this comorbidity is not yet clearly explained. This study analyzes the relationship between drug-resistant epilepsy and OSA, and the findings indicate a strong role of rapid eye movement sleep (REMS) in the pathogenesis of this relationship. It also emerges from the study that REMS reduction is a prominent feature of OSA, and drug resistance in patients with epilepsy and treatment of OSA has been shown to restore REMS in several studies with concomitant improvement in seizure control.

In adult patients with epilepsy, treatment of comorbid obstructive sleep apnea syndrome (OSAS) by positive airway pressure (PAP) therapy results in improvements in the control of seizures. This is the first study investigating the long-term compliance with PAP therapy in patients with sleep-related epilepsy and OSAS.

In this longitudinal study, patients with sleep-related epilepsy and OSAS were followed-up for five years. The compliance with PAP therapy was defined as the use of PAP therapy for at least four hours per night for more than 70 % of nights.

A total of 58 patients with sleep-related epilepsy and OSAS completed study protocol. Eleven patients (19.0 %) refused PAP treatment for OSAS, and 13 patients (22.3 %) showed irregular use. Remaining 34 patients (58.7 %) were compliant with PAP therapy. Females were found to be more compliant than males (p = 0.027), while the age was not found to correlate with the compliance (p = 0.721). Epilepsy-related factors including the types of seizures, whether pure sleep-related or mixed (p = 0.403), localization (p = 0.920) or lateralization (p = 0.697) of discharges, showed no effect on the compliance with PAP therapy. On the other hand, patients with a lower number of seizures (p = 0.042) or with a lower seizure frequency (p = 0.048) showed better compliance with PAP therapy. Polysomnographic parameters including severity of OSAS failed to show a significant correlation.

Our findings showed that about two thirds of the study population was compliant with PAP therapy after a mean follow-up duration of almost three years. Newly-diagnosed patients, mostly females, with a lower number of total seizures and lower seizure frequency seem to be more compliant with PAP therapy, which implies the significance of investigation and treatment of OSAS as early as possible in the patients with sleep-related seizures.

Obstructive sleep apnoea (OSA) is a globally prevalent sleep disorder of significant health concern and confounded with several comorbidities resulting in adverse effect(s) on quality of life in patients afflicted with it. Of particular interest is the enigmatic high comorbidity of OSA with epilepsy, the exact underlying pathophysiology of which remains elusive despite a multitude of research performed in the last four decades. Hypoxaemia, which is an important characteristic feature found in OSA during apnoeic spells, has been implicated in the high comorbidity of OSA with epilepsy, the basis of which rests upon hypoxaemia-mediated brain damage, subcortical release phenomenon, oxidative stress and neuroinflammatory reactions. However, several studies present contradictory evidences that potentially refute the hypoxaemia-based mechanism. Additionally, the role of hypercapnia thatgenerally accompanies hypoxaemia during apnoeic spells, cannot be overlooked and is known to be potentially protective against neuronal hyperexcitability. Thus, hypoxaemia theory implicated in the high comorbidity of OSA and epilepsy appears weak and refutable. This brief paper studies and critically analyses the role of hypoxaemia in conjunction with hypercapnia in the underlying pathophysiology of the comorbidity.

Chronic intermittent hypoxia (CIH) is the most distinct feature of obstructive sleep apnea (OSA), a common breathing and sleep disorder that leads to several neuropathological consequences, including alterations in the hippocampal network and in seizure susceptibility. However, it is currently unknown whether these alterations are permanent or remit upon normal oxygenation. Here, we investigated the effects of CIH on hippocampal spontaneous network activity and hyperexcitability in vitro and explored whether these alterations endure or fade after normal oxygenation. Results showed that applying CIH for 21 days to adult rats increases gamma-band hippocampal network activity and aggravates 4-Aminopyridine-induced epileptiform activity in vitro. Interestingly, these CIH-induced alterations remit after 30 days of normal oxygenation. Our findings indicate that hippocampal network alterations and increased seizure susceptibility induced by CIH are not permanent and can be spontaneously reverted, suggesting that therapeutic interventions against OSA in patients with epilepsy, such as surgery or continuous positive airway pressure (CPAP), could be favorable for seizure control.

Sleepiness is among the most common complaints of people with epilepsy, but objective documentation is lacking. We systematically investigated subjective and objective sleepiness in an observational cross-sectional cohort of adults with epilepsy (AWE).

This is a prospective study of AWE consecutively recruited without foreknowledge of sleep/wake complaints. Polysomnography (PSG) with 18-channel electroencephalography (EEG) followed by multiple sleep latency testing (MSLT) was performed. Patients completed the Epworth Sleepiness Scale (ESS), a single-item question assessing excessive daytime sleepiness (EDS), and a 7-day sleep and seizure diary. Multivariable linear models were used to assess the association between MSLT mean sleep latency (MSL) and interests with adjustment of covariates of interest. Receiver operating characteristics (ROC) analysis was performed to evaluate the discrimination capability of ESS on MSL < 8 min and <5 min and investigate the optimal cutpoints.

Among 127 AWE (mean age: 38.7 ± 13.7 years), abnormal MSL (<8 min) was observed in 49.6% and MSL <5 min in 31.5%. While 78% reported feeling sleepy during the day on a single-item question, only 24% had elevated scores on the ESS (>10/24). The ESS score was associated with MSL even after adjusting for seizure frequency, antiseizure medication (ASM) standardized dose and number, age, gender, depression and insomnia symptom severity, and apnea-hypopnea index (HPI) and total sleep time on PSG (coefficients [95% confidence interval (CI)]: -0.26 [-0.48, -0.05], p = 0.018). The area under the curve (AUC) of the ESS ROC predicting MSL < 8 min and MSL < 5 min were similar: 0.62 (95%CI: 0.52-0.72) and 0.62 (95%CI: 0.51-0.74).

This is the largest prospective cross-sectional observational study to date using MSLT in AWE. We found subjective and objective daytime sleepiness highly prevalent in AWE and not explained by seizure frequency, ASM burden, symptoms of insomnia/depression, or PSG findings although those with MSL < 5 min were more likely to have obstructive sleep apnea (OSA). Pathologic sleepiness with MSL < 8 min was present in half of AWE. Nearly one-third of AWE unselected for sleep/wake complaints had MSL < 5 min, a range typical of narcolepsy.

The objective of this prospective study was to assess the effect of CPAP therapy on job productivity and work quality for patients with severe obstructive sleep apnea (OSA).

A convenience sample of patients diagnosed with severe OSA using polysomnography or polygraphy and with a therapeutic indication for CPAP was enrolled in our study. Patients completed two self-administered questionnaires: the first before CPAP therapy and the second during the first 6 months after CPAP treatment. OSA symptoms were evaluated through self-administered questionnaires assessing potential effects on occupational activity: excessive daytime sleepiness was rated by the Epworth Sleepiness Scale (ESS), emotional status was rated by the Hospital Anxiety and Depression (HAD) scale, work quality was rated by the Work Role Functioning Questionnaire (WRFQ).

Forty patients (30 men, mean age 47.3 ± 8.3, mean BMI 31.6 ± 7.4, mean apnea-hypopnea index 51.8 ± 16.3) showed a beneficial effect of CPAP therapy on ESS score (mean 11.6 to 8.2, p < 0.0001), the anxiety dimension (mean 57.5% to 20%, p = 0.0002), and the overall anxiety-depressive score (mean 50% to 22.5%, p = 0.0006). Mean WRFQ scores were significantly improved in the second questionnaire for the dimensions of timetable requirements (69.3% to 83.5%, p < 0.0001), productivity requirements (71.4% to 82.2%, p < 0.0001), mental requirements (72.0% to 84.3%, p < 0.0001), and social requirements (82.6% to 91.4%, p < 0.003).

We observed that adherence to CPAP therapy for patients with severe OSA mitigates the impact of symptoms on work including excessive daytime sleepiness, impairment of work ability, and anxiety and depressive disorders.

Co-morbid sleep disorders, including sleep apnea, insomnia, restless legs syndrome, and the parasomnias, occur frequently in people with epilepsy. This article reviews the cardinal presenting symptoms and diagnostic features of each of these disorders to enable epileptologists to readily screen and identify sleep co-morbidities in their patients. It summarizes current evidence concerning the reciprocal relationship between sleep disturbances and epilepsy and available treatment options for common sleep disorders in people with epilepsy. Several illustrative cases demonstrate the practical consequences of co-morbid sleep disorders in epilepsy patients and suggest diagnostic and treatment approaches that may improve daytime functioning, alertness, quality of life, and seizure burden.

Vagus nerve stimulation (VNS) can induce a sleep apnea syndrome (SAS), which in turn can worsen seizure control and represents a cardiovascular risk factor. Epidemiology of VNS-induced SAS has received little attention to date. The purpose of this study was to estimate the VNS-induced SAS prevalence and to explore clinical variables potentially correlating with its development.

We analyzed the computerized medical records of 18 consecutive adults treated for refractory epilepsy with VNS, implanted between May 2008 and October 2015. Patients underwent sleep polygraphy or polysomnography before and after VNS implantation. Between patients with and without SAS, we compared variables related to epilepsy type and device parameters.

Two patients had SAS and were treated before implantation; one improved after VNS, the other worsened. Four other patients developed SAS after VNS: induced/aggravated SAS occurred in 5/18 patients (prevalence: 27.8%). Only 2 of them had symptoms: one complained of important snoring, the other reported seizure worsening. All 5 patients were successfully treated by combinations of continuous positive airway pressure (cPAP), positional therapy, or VNS parameters modification. There was no statistically significant difference between potential predictors.

Despite the relatively modest clinical impact on epilepsy, in view of the associated cardiovascular risk factor development, easy treatment, and the relatively high SAS prevalence, routine screening for SAS before and after VNS implantation may represent a reasonable practice.

The objective of the present study was to evaluate the prevalence of obstructive sleep apnea (OSA) in patients with late-onset epilepsy (LOE) who were considered at higher risk of cardiovascular disease.

Polysomnography was performed on 27 patients with LOE. Berlin questionnaires and Epworth sleepiness score were performed on all patients. We compared clinical, demographic and anthropometric characteristics, questionnaire scores on the patients with no or mild OSA (group 1) and the patients with moderate or severe OSA (group 2). Patients eligible for continuous positive airway pressure (CPAP) therapy were reviewed in consultation.

Twenty-four patients (88.9%) had OSA and 55.6% had moderate or severe OSA. Patients in group 2 (n=15) were older than patients in group 1 (n=12). The two groups were similar in terms of body mass index (BMI), neck circumference, nocturnal seizure frequency, vascular cardiovascular risk factors and excessive daytime sleepiness. Leukoaraiosis in MRI was highly prevalent in our patients (40.7%), especially in group 2 patients. Eighty percent of the patients who had begun CPAP therapy experienced decreased seizure frequency.

Patients with LOE should be screened for the presence of OSA and treated accordingly.

The questions facing clinicians with patients with sleep disorder and epilepsy are addressed in this article. Both adult and child epilepsy are discussed in the context of the most typical questions a clinician would have, such as "Are parasomnias more common in people with epilepsy?", "Is sleep architecture abnormal in children with epilepsy", along with outcomes of numerous questionnaire-based, case-based, and double-blind placebo studies on such aspects as sleep duration, daytime sleepiness, anxiety and fears, limb movement, nocturnal seizures, agitation, behavioral disorders, and learning disorders.

Sleep and epilepsy are two well recognized conditions that interact with each other in a complex bi-directional way. Some types of epilepsies have increased activity during sleep disturbing it; while sleep deprivation aggravates epilepsy due to decreased seizure threshold. Epilepsy can deteriorate the sleep-related disorders and at the same time; the parasomnias can worsen the epilepsy. The secretion of sleep-related hormones can also be affected by the occurrence of seizures and supplementation of epileptic patients with some of these sleep-related hormones may have a beneficial role in controlling epilepsy.

Obstructive sleep apnea (OSA) is highly prevalent, affecting 25% of men and 10% of women. We recently reported a prevalence of OSA of 30% among 130 adults with epilepsy unselected for sleep disorder complaints, including 16% with moderate-to-severe disease, rates that markedly exceed general population estimates. Treatment of OSA with continuous positive airway pressure (CPAP) therapy or upper airway surgery reduces seizures in many cases. A single study reported a reduction in interictal spike rate with CPAP in 6 patients with OSA. We explored the effect of CPAP therapy on spike rate in 9 adults with epilepsy and OSA. Interictal epileptiform discharges were quantified during a diagnostic polysomnogram (PSG) and a second PSG using therapeutic CPAP. Spike rates were calculated for each recording during wake and sleep stages. Continuous positive airway pressure therapy was associated with significant reductions in median (quartiles) spike rate overall (77.9 [59.7-90.7] %), in wakefulness (38.5 [0.3-55] %), and in sleep (77.7 [54.8-94.7] %) but not in REM sleep. Continuous positive airway pressure therapy also produced a significant improvement in oxygen saturation and arousals. Our work extends a single prior observation demonstrating beneficial effects of CPAP therapy on interictal EEG in patients with epilepsy with comorbid OSA and supports the hypothesis that sleep fragmentation due to OSA contributes to epileptogenicity.

Previous studies suggest that treatment for obstructive sleep apnea (OSA) in patients with epilepsy can improve seizure control. We investigated the effect of positive airway pressure (PAP) therapy on seizures in adults with epilepsy referred to the Cleveland Clinic for polysomnography (PSG) from 1997 to 2010. Seizure outcome at baseline and 1 year later was compared in patients with no OSA (apnea-hypopnea index [AHI] <5), patients with PAP-treated OSA, and patients with untreated OSA. One hundred thirty-two subjects (age: 40.2±13 (18-76) years, 65.4% female) were included. Seventy-six (57.6%) subjects had OSA; of these, 43 (56.6%) were on PAP therapy, and 33 (43.4%) were not on PAP therapy (either PAP-intolerant or refused therapy). Of the group with PAP-treated OSA, 83.7% were adherent (use ≥4 h/night at least 5 nights/week). The percentage of subjects with ≥50% seizure reduction and the mean percentage of seizure reduction were significantly greater in the group with PAP-treated OSA (73.9%; 58.5%) than in subjects with untreated OSA (14.3%; 17.0%). There were significantly more subjects with successful outcomes (with ≥50% seizure reduction or seizure-free at both baseline and follow-up) in the group with PAP-treated OSA (83.7%) than in the groups with no OSA (53.6%) and untreated OSA (39.4%). After adjusting for age, gender, body mass index, AHI, and epilepsy duration, we found that the odds of successful outcomes in subjects in the group with PAP-treated OSA were 9.9 and 3.91 times those of the groups with untreated OSA and no OSA, respectively. The group with PAP-treated OSA had 32.3 times the odds of having a ≥50% seizure reduction compared with the group with untreated OSA and 6.13 times compared with the group with no OSA. Positive airway pressure therapy appears to produce beneficial effects on seizures in adult patients with epilepsy and OSA.

The ways in which sleep can affect epilepsy, and epilepsy can influence sleep and wakefulness, are described. Different forms of sleep disturbance have been reported in patients with epilepsy, depending on the type of seizure disorder. Confusions between epilepsy and non-epileptic parasomnias can be a particular diagnostic problem but they can be avoided. Untreated sleep disturbance is likely to have harmful psychological, physical and family effects. Screening for sleep disturbance should be routine, and leading, if indicated, to precise diagnosis of the underlying sleep disorder on which choice of advice and treatment depends.

The intimate relationship between sleep and epilepsy has long been recognized, yet our understanding of the relationship is incomplete. In this article we address four key issues in this area. First, we consider the reciprocal interaction between sleep and epilepsy. Sleep state clearly influences seizure onset, particularly in certain epilepsy syndromes. The converse is also true; epilepsy may disrupt sleep, either directly through seizures and epileptiform activity, or indirectly through medication-related effects. Unraveling the influences of sleep stage, epilepsy syndrome, and drug effects is challenging, and the current state of knowledge is reviewed. Secondly, accurate diagnosis of sleep-related epilepsy can be difficult, particularly the distinction of nocturnal frontal lobe epilepsy (NFLE) from arousal parasomnias. The challenges in this area, along with work from the authors, are discussed. Thirdly, we will explore the putative relationship between obstructive sleep apnea (OSA) and epilepsy, including the effect of OSA on quality of life; this will lead us to a brief exploration of the effects of OSA on neuroendocrine function. Finally, we will review the evidence surrounding the role of sleep in sudden unexpected death in epilepsy (SUDEP).

Although disturbed sleep has been frequently reported in patients with seizures, little is known about insomnia and epilepsy. The aims of this study were (1) to analyze the prevalence and degree of insomnia in patients with epilepsy, (2) to examine the clinical features and correlates of insomnia in these patients, and (3) to evaluate the impact of poor sleep on their quality of life.

One hundred-fifty-two patients with epilepsy (mean age 46 years) completed the following questionnaires: Insomnia Severity Index, Pittsburgh Sleep Quality Index, Beck Depression Inventory-II, Quality of Life in Epilepsy Inventory-31. Patients with other known sleep disorders, including obstructive sleep apnea, were excluded from the study. Regression analysis was conducted for adjusting for age, years since epilepsy onset, number of antiepileptic drugs, comorbidities, and depression scores.

More than half of the participants (55%) suffered from insomnia and more than 70% were "poor sleepers." Insomnia and poor sleep quality were significantly correlated with the number of antiepileptic medications and scores of depressive symptoms. After controlling for covariates, insomnia and poor sleep quality were significant predictors of lower quality of life.

These results suggest that insomnia and poor sleep are common in patients with epilepsy and may adversely impact quality of life. Further studies should examine whether improvements in sleep can improve seizure control and quality of life of these patients.

Sleep disordered breathing (SDB) is a common medical condition. Its manifestations of snoring, nocturnal choking, arousals, and sleep fragmentation can lead to excessive daytime sleepiness, neuropsychological slowing, lapses of consciousness, and accidents that can be misinterpreted as epileptic phenomena. Moreover, patients with documented epilepsy commonly exhibit similar symptomatology because of the undiagnosed coexistence of sleep apnea. Therefore, a large proportion of patients referred to the electroencephalogram (EEG) laboratory primarily to confirm or refute the diagnosis of epilepsy could suffer from latent sleep apnea and the routine EEG has the potential to divulge it. We retrospectively evaluated the reporting of sleep apnea symptomatology (snoring, choking, gasping/deep breath, apnea, desaturation, excessive drowsiness) in routine inpatient and outpatient adult EEG studies performed in our institution over the past 12 years (39,130 studies, approximately half of which recorded at least early stages of sleep). Comparisons were performed with the medical records to ascertain the coexistence of objectively diagnosed SDB with polysomnography before or after the EEG study and the importance of reporting variations in assisting with the diagnosis. Two illustrative examples are provided. Sixty-nine EEG studies were identified, performed primarily to confirm, or refute the diagnosis of epilepsy. The mean age of the subjects at EEG was 64 years (range 30-89), and 55 (80%) were male. 36% of them suffered from known epilepsy. Snoring was the most commonly reported sign in 48 (70%) of the studies, followed by arousals in 29 (42%), apnea in 16 (23%), excessive drowsiness in 13 (19%), gasping/deep breath in 9 (13%), and desaturation in 7 (10%). A sleep disorder was suggested in 25 (36%) of the interpretations and a direct recommendation for a sleep study was made in 22 of them (32%). This interpretation was included in the impression of the report in 21 (30%) of the cases, in the detail in 20 (30%) of the cases and in both in 28 (40%). Only 14 (20%) patients underwent polysomnography, and all of them were formally diagnosed with SDB. Seven (50%) of them were diagnosed with obstructive sleep apnea, 2 (14%) with central sleep apnea, 3 (22%) with both, 1 (7%) with upper airways resistance syndrome, and 1 (7%) with primary snoring. From these 14 patients, 9 (64%) were diagnosed with a sleep study performed after the EEG, 4 (29%) before the EEG interpretation, and 1 (7%) had a repeat study after the EEG. In the logistic regression model applied, with the exception of the presence of arousals (odds ratio = 4.63, P = 0.033), none of the aforementioned symptomatology or the reporting of suspicion for SDB or the location (impression vs. detail) of the reporting showed a statistically significant association with the completion of a sleep study. Routine EEG offers a unique opportunity of direct clinical observation along with electrophysiologic and cardiorespiratory monitoring. When sleep is recorded, it can help identify clinical and electrographic features of sleep apnea and prompt confirmation with a polysomnogram in the appropriate clinical context. It can therefore serve as a valuable, adjunctive tool for the diagnosis of SDB. Our data highlight that potential but unveil its decreased use in the neurology community. Increased awareness is required by the EEG technologists, interpreting neurologists, and referring physicians, regarding reporting and using sleep apnea features on the EEG.

Sleep-related breathing disruptions in children with epilepsy are common and can range from primary snoring to obstructive sleep apnea. Untreated obstructive sleep apnea can lead to significant morbidity. This study aimed to identify factors associated with its occurrence and severity in children with epilepsy. Children with epilepsy and sleep disruption were evaluated with polysomnography and diagnosed with obstructive sleep apnea or primary snoring. Statistical analyses were done to identify differences within both the groups and among the subjects in the obstructive sleep apnea group. Uncontrolled epilepsy was a risk factor for obstructive sleep apnea (80%) compared with primary snoring (47%, P = .02). Obstructive index increased with increasing number of antiepileptic drugs. In children with epilepsy and disturbed sleep, obstructive sleep apnea is associated with uncontrolled epilepsy and is more severe with polytherapy use. Children with uncontrolled seizures on antiepileptic polytherapy should be routinely screened for obstructive sleep apnea.

Obstructive sleep apnea (OSA) is highly prevalent, affecting 25% of men and 10% of women. Treatment reduces seizures in some patients. Awareness of the comorbidity of sleep disturbances in epilepsy has been increasing. No study has explored OSA predictors in patients unselected for epilepsy severity and sleep disorder symptoms. We assessed cross-sectional OSA prevalence and predictors (apnea-hypopnea index [AHI] ≥10) in 130 consecutive adults using structured interview, subjective assessments, and polysomnography. Obstructive sleep apnea prevalence was 30%, 16% having moderate-severe disease, rates that markedly exceed general population estimates. Obstructive sleep apnea predictors in multivariate modeling included age, dental problems, and standardized AED dose. Male gender, older age, higher BMI, hypertension, and dental problems were associated with higher AHI. Adults with epilepsy appear at increased risk for OSA, increasing with age and AED load, regardless of gender, BMI, and seizure frequency. These findings support the implementation of routine OSA screening in adult epilepsy clinics.

Obstructive sleep apnea (OSA) is prevalent in adults with epilepsy, especially refractory, but limited data exist in children with epilepsy.

We conducted a prospective pilot study in children with epilepsy to identify the prevalence of OSA and its relationship to the use of antiepileptic drugs (AEDs) and epilepsy types.

We used Michigan Pediatric Sleep Questionnaire (PSQ) in children with epilepsy. Patients were classified by seizures frequency as mild (0-1 seizure/month) or severe, refractory epilepsy (> 1 seizures/month). We used PSQ ≥ 0.33 as a cutoff point to assess the risk of OSA.

Of 84 children, 52 were classified as mild and 32 as severe. Prevalence of OSA was significantly higher in the severe (43.8%) vs the mild group (30.7%, P < 0.05). Children on >1 AED had significantly higher prevalence of OSA (45.8%) than children on ≤1 AED (30.6%, P < 0.05). There was no significant correlation between the prevalence of OSA and seizure types.

  OSA is more prevalent in refractory epilepsy and in children who are on multiple AEDs. While further studies are needed to confirm these findings and to assess the consequences of OSA, we believe it is important to screen the children with epilepsy for OSA.