Madeleine M. Grigg-Damberger

Sleep and epilepsy: What we know, don't know, and need to know

Summary: Long-term video-EEG and, more recently, video-polysomnography, have provided the means to confirm and expand on the interconnections between sleep and epilepsy. Some of these relationships have become firmly established. When one of the authors (N.F.S.) presented part of this paper at a symposium on the Future of Sleep in Neurology at an American Clinical Neurophysiology Society annual meeting in 2004, the purpose was to summarize what we know, don’t know, and need to know about the effects of sleep on epilepsy and epilepsy on sleep. Here we seek to summarize some of the more firmly established relationships between sleep and epilepsy and identify intriguing associations that require further elucidation.

Roles of gender, age, race/ethnicity, and residential socioeconomics in obstructive sleep apnea syndromes.

Purpose of review Review recent research on the roles of gender, race/ethnicity, residential socioeconomics and age in obstructive sleep apnea syndromes (OSA) and their treatment. Recent findings Men have a higher prevalence of OSA than women and require higher continuous positive airway pressure (CPAP) pressures for treatment, given similar severity of OSA. When comparing age, women have less severe apnea at all ages. Menopause, pregnancy and polycystic ovarian syndrome increase the risk for OSA in women. Neck fat and BMI influence apnea–hypopnea index (AHI) severity in women; abdominal fat and neck-to-waist ratio do so in men. Obesity, craniofacial structure, lower socioeconomic status and neighborhood disadvantage may better explain ethnic/racial differences in the prevalence and severity of OSA. Ethnicity was no longer significantly associated with OSA severity when WHO criteria for obesity were used. Summary OSA has a male predominance; women have a lower AHI than men during certain stages of sleep; women require less CPAP pressure for treatment of similar severity of OSA, and there are ethnic/racial differences in the prevalence and severity of OSA but these may be due to environmental factors, such as living in disadvantaged neighborhoods.

Sleep and epilepsy.

Over a century of work has confirmed crucial links between sleep and epilepsy. Seizures and some antiepileptic drugs (AEDs) adversely affect the continuity of sleep. However, sleep is fragmented in the absence of seizures or medication, suggesting that sleep instability may be an inherent component of certain forms of epilepsy. In turn, sleep instability can promote seizures, thus forming a vicious cycle. Sleep deprivation provokes seizures and epileptiform discharges in some people with epilepsy. Synchronized nonrapid eye movement (NREM) sleep facilitates seizures, whereas desynchronized rapid eye movement (REM) sleep discourages seizure occurrence. The sleep electroencephalogram (EEG) is useful in the diagnosis and localization of epilepsy, as new epileptic foci can appear in sleep and REM sleep may demonstrate the narrowest localization of the primary focus. Polysomnography (PSG) with expanded EEG aids in the differentiation of seizures and parasomnias and in the diagnosis of primary sleep disorders, such as sleep apnea, that can exacerbate seizures. Treating sleep apnea may lead to improved seizure control. These observations underscore the importance of sleep in the diagnosis and treatment of people with epilepsy.

Prognostic significance of EEG triphasic waves in patients with altered state of consciousness.

Triphasic waves (TWs) are a distinctive, but nonspecific, EEG pattern found in metabolic encephalopathies and a variety of other neurologic conditions. The prognostic value of TWs was studied in 30 patients with altered state of consciousness. Patients were either comatose (18 patients) or very lethargic (12 patients). Triphasic waves were the dominant EEG pattern, present for at least 35% of the tracing. The etiology of their underlying encephalopathy was multiple metabolic derangements (12 patients), hepatorenal syndrome (5 patients), renal failure (4 patients), hypoxic encephalopathy (4 patients), hepatic failure (3 patients), hyponatremia (1 patient), and hypoglycemia (1 patient). Patients were followed up to 22 months. Fifty percent of the subjects died within 30 days of recording TWs. The overall mortality was 77%. Seven patients (23%) have survived, but only three patients (10%) are neurologically normal. In conclusion, TWs occur most often in patients with metabolic encephalopathies, cannot be used to distinguish different diagnostic entities, and indicate a poor prognosis for survival.

Why a Polysomnogram Should Become Part of the Diagnostic Evaluation of Stroke and Transient Ischemic Attack

Summary: Neurologists need to recognize, diagnose, and treat obstructive sleep apnea (OSA) in patients with stroke or transient ischemic attack (TIA). Increasing medical evidence suggests that OSA is an independent risk factor for stroke and TIA. Stroke (or TIA) is more likely a cause, rather than a consequence, of OSA because PSG studies have shown: 1) apneas in stroke are typically obstructive, not central or Cheyne-Stokes in type; 2) apneas are just as frequent and severe in patients with either TIA or stroke; 3) OSA severity is not influenced by the acuteness or location of the stroke; 4) untreated OSA patients have more strokes, stroke morbidity, and mortality than those who are treated. OSA alone can induce hypertension, especially in younger men. A causal relationship has recently been demonstrated between OSA and hypertension. A distinctive feature of OSA-induced hypertension is loss of the normal nighttime fall in blood pressure (“nondippers”). Data from the Sleep Heart Health Study showed a dose-response association between OSA severity and the presence of hypertension 4 years later. Hypertension or ischemic heart disease usually develops in untreated patients with OSA over time without particular worsening of OSA. Studies have shown sleep itself is not a risk factor for stroke because most stroke and TIAs begin between 6 am and noon, while the individual is awake. However, OSA promptly be considered in stroke beginning during sleep because 88% of strokes that develop during sleep occur in “nondippers.” Premature death in OSA patients is most often cardiovascular, but occurs while the patients are awake. The risk of myocardial infarction is increased 20-fold in untreated OSA. Treating OSA patients with continuous positive airway pressure can prevent or improve hypertension, reduce abnormal elevations of inflammatory cytokines and adhesion molecules, reduce excessive sympathetic tone, avoid increased vascular oxidative stress, reverse coagulation abnormalities, and reduce leptin levels. If all this can be achieved by a polysomnogram, then this test should become part of a neurologists armamentarium for stroke and TIA.

Non-respiratory indications for polysomnography and related procedures in children: An evidence-based review

OBJECTIVE This evidence-based review provides a systematic and comprehensive review of the literature regarding the utility of polysomnography for the evaluation of non-respiratory sleep disorders in children including hypersomnias, parasomnias, sleep-related movement disorders, and sleep in other special populations. METHODS A task force of pediatric sleep medicine experts performed a systematic review of the literature regarding the use of polysomnography for non-respiratory sleep disorders in children. They identified and graded 76 papers as evidence. RESULTS The main results include (1) polysomnography combined with the multiple sleep latency test is useful for evaluating disorders of excessive somnolence to objectively quantify sleepiness. The results have to be interpreted with consideration of the pubertal stage and regularity of the sleep patterns of the child; (2) polysomnography is indicated in children with parasomnias or sleep related movement disorders who have a high likelihood of having obstructive sleep apnea (OSA); (3) polysomnography is not routinely indicated in children with enuresis unless there is a high likelihood of OSA; (4) polysomnography can be helpful in evaluating children with restless legs syndrome (RLS) and when periodic limb movement disorder (PLMD) is suspected. CONCLUSIONS These findings suggest that, in children with non-respiratory sleep disorders, polysomnography should be a part of a comprehensive sleep evaluation in selected circumstances to determine the nature of the events in more detail or when the suspicion of OSA is relatively high.

Cognitive dysfunction and obstructive sleep apnea: from cradle to tomb.

Purpose of review To understand clinical characteristics and risk factors for cognitive impairment in patients with obstructive sleep apnea (OSA) syndromes. Recent findings Primary snoring increases the risk of neurocognitive impairment and lower intelligence quotients in infants and children. Middle-aged adults with severe OSA are at greater risk for cognitive impairment than young adults with apnea of equal severity. Older women with OSA are at increased risk for minimal cognitive impairment or dementia, 5 years later. Summary Certain age groups (younger and older) are particularly susceptible to the negative effects of OSA on cognition. Other influences that increase the risk for cognitive dysfunction in OSA include premature birth, apolipoprotein e4 allele status and other genetic polymorphisms, lower socioeconomic status, fewer years of education, and ethnicity.

The AASM scoring manual: a critical appraisal.

Purpose of review Summarize recently published studies and critiques evaluating the effects of the American Academy of Sleep Medicine (AASM) Sleep Scoring Manual. Recent findings Only a few retrospective studies have been published evaluating the new AASM Scoring Manual. These have shown that when scoring polysomnograms (PSGs) using the AASM rules compared to previous standards and guidelines: increased amount and percentage of sleep time in Non-Rapid Eye Movement Sleep (NREM) 1 (N1) and N3 sleep, and decreased NREM 2 (N2) sleep; improved interscorer reliability when scoring sleep stages in adults; large differences in apnea–hypopnea indexes (AHIs) using different hypopnea scoring definitions; and PSGs scored using the ‘recommended’ hypopnea definition in the new manual identified no significant sleep disordered breathing in 40% of lean individuals with symptomatic OSA (AHI ≥5/h by 1999 ‘Chicago’ criteria) and a favorable response to treatment. Summary Two years have passed since the AASM Scoring Manual was published, garnering less criticism than was feared by those who developed it. The improvement in interscorer reliability using the Manual is heartening since this goal shaped many of the choices made. The alternative hypopnea rule should be endorsed as a recommended option. The AASM Scoring Manual provides a foundation upon which we all can build rules and methods that quantify the complexity of sleep and its disorders. Multicenter validation and refinement of the Manual is encouraged.

Treatment strategies for complex behavioral insomnia in children with neurodevelopmental disorders.

Purpose of review This review describes recent research in pediatric behavioral insomnias in neurodevelopmental disorders and their treatment. Recent findings Insomnia in children with autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDDs) is typically complex, chronic, and difficult to adequately control. Abnormalities in genetic and/or epigenetic regulation of sleep/wakefulness and its timing predispose patients with NDD to insomnia, although poor sleep hygiene, maladaptive associations, and limit-setting are likely to contribute. Parents are agents for change in problematic sleep behaviors in patients with NDD. We review the benefits of behavioral therapies and melatonin to treat sleep problems in children with NDD. Problematic sleep is so prevalent in some neurodevelopmental syndromes (Rett, Angelman, Williams, and Smith–Magenis) that it is part of their diagnostic criteria. Summary Children and adolescents with neurological disorders frequently have complex sleep disorders that require treatment. Understanding the basic pathology and treatment strategies provides an opportunity to improve well being and quality of life in those affected by NDD and their families.

Sleep disorders in adults with epilepsy: past, present, and future directions.

Purpose of review To summarize recent studies on the complex relationships between sleep disorders, sleep, and epilepsy. Recent findings Insomnia in adults with epilepsy (AWE) warrants consideration of depression, anxiety, and suicidal ideation. Daytime sleepiness in AWE is more often due to undiagnosed sleep disorders. Sleep deprivation is an important provoker of seizures in juvenile myoclonic epilepsy. Abnormalities in frontal lobe executive function with difficulties making advantageous decisions may explain failure of juvenile myoclonic epilepsy patients to adhere to treatment recommendations and regulate their sleep habits. Sleep architecture in AWE is more likely to be abnormal if seizures are poorly controlled or occur during sleep. Obstructive sleep apnea is much more common in AWE who are man, older, heavier, or whose seizures are poorly controlled. Chronobiology and chronopharmacology of epilepsy is an emerging field worthy of future research and clinical applications. Summary 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.