Usefulness of polysomnography in epilepsy patients

We reviewed the records of 63 adult epilepsy patients who underwent polysomnograms in our laboratory since 1985 to determine the indications for polysomnography and the results of testing. Reasons for referral included excessive daytime sleepiness, suspected obstructive sleep apnea (OSA), and characterization of nocturnal spells. The most common polysomnographic diagnosis was OSA, although we also found narcolepsy, insufficient sleep syndrome with possible idiopathic hypersomnolence, and previously unrecognized nocturnal seizures. We treated OSA with continuous positive airway pressure in 28 patients, 15 of whom were using the device at follow-up appointments. The majority of patients treated for OSA or other disorders reported an improvement in sleepiness or seizure control. Polysomnography, when indicated, is beneficial in epilepsy patients.     

The Epworth Sleepiness Scale may not reflect objective measures of sleepiness or sleep apnea

OBJECTIVE: To assess the validity of the Epworth Sleepiness Scale score (ES) as a measure of sleepiness among patients suspected or confirmed to have obstructive sleep apnea syndrome. BACKGROUND: The ES is used with increasing frequency as a measure of excessive daytime sleepiness in part because several studies suggested that the ES correlates with mean sleep latency (MSL) on the Multiple Sleep Latency Test and with severity of sleep apnea among patients with that disorder. However, associations identified between the ES and other measures were not strong or consistent. METHODS: The authors used regression models and retrospective data from a relatively large series of 237 patients to restudy how ES relates to MSL, to a simple self-rating of problem sleepiness (available for 141 patients), and to two polysomnographic measures of sleep apnea severity: the number of apneas or hypopneas per hour of sleep and the minimum recorded oxygen saturation. RESULTS: The ES had a statistically significant association with self-rated problem sleepiness but not with MSL or measures of sleep apnea severity. Male gender, adjusted for potential confounding variables, had considerably more influence on the ES than did MSL or measures of sleep apnea severity. CONCLUSIONS: Our data suggest that the subjectively derived ES cannot be used as a surrogate for the objectively determined MSL.     

Idiopathic hypersomnia

Idiopathic hypersomnia is not as well delineated as narcolepsy and its history is much more recent. There are at least two forms of the disorder: (1) a polysymptomatic form, characterized by excessive daytime sleepiness, nocturnal sleep of abnormally long duration, and signs of sleep drunkenness on awakening, and (2) a monosymptomatic form that manifests only by excessive daytime sleepiness. The most widely used laboratory procedures are nocturnal polysomnographic recording following by an MSLT demonstrating a mean sleep latency of less than 10 minutes. At least in the polysymptomatic form, however, continuous polysomnography on an ad lib protocol deserves to be performed to catch the abnormally long major sleep episode and the long unrefreshing naps. Idiopathic hypersomnia is probably one of the most overdiagnosed sleep disorders. Several other disorders must be excluded before the diagnosis can be considered conclusive. Treatment of idiopathic hypersomnia relies on stimulants, which are frequently less effective and less well tolerated than in narcolepsy.     

Psychotherapeutic agents in older adults. Sedative hypnotics and sleep

Complaints about sleep are prominent among geriatric patients. Insomnia is a prominent feature of many psychiatric and general medical conditions. The physiologic effects of aging and primary sleep disorders also contribute to insomnia, sleep pattern changes, daytime sleepiness, and dozing. The clinical approach to insomnia requires a thorough diagnostic assessment as well as study of sleep habits and hygiene. Hypnotic agents may be useful in providing short-term relief. Pharmacologic intervention is best combined with nonpharmacologic approaches that improve the efficiency of sleep.     

Sleepiness and sleep disorders. Causes and consequences

Sleepiness and sleep disorders are prevalent in our society. Symptoms of sleepiness and complaints referable to sleep disorders have generally--and incorrectly--been discounted as being of minor importance and are often thought to be manifestations of psychological problems or character defects. It is now apparent that the cost to the American public--both to individuals and the larger society--is substantial. Sleep medicine has become established as an independent field, and knowledge of sleep, sleepiness, and sleep disorders has grown dramatically. This knowledge, when applied to individuals, will enhance the lives of patients with sleep disorders, and when applied to society as a whole, will have important socioeconomic implications.     

Obstructive sleep apnea and related disorders

OSAS, a common cause of disrupted sleep and EDS, result from repetitive closure of the upper airway during sleep. It probably represents the most severe syndrome related to obstruction of the upper airway; less severe forms include UARS, a syndrome characterized by the need for increased effort to breath but no prominent apneas or hypopneas, and primary snoring. Initial clues to the presence of OSAS and related disorders are derived from the history and include loud snoring, EDS or insomnia, and witnessed apneas. Some patients, especially women, may complain mostly of tiredness or fatigue, and children may present with behavioral abnormalities. Obesity, a large neck circumference, and a crowded oropharynx are common on physical examination. Nonobese patients, in particular, often have retrognathia, a high-arched narrow palate, macroglossia, enlarged tonsils, temporomandibular joint abnormalities, or chronic nasal obstruction. The clinical suspicion of obstructed nocturnal breathing is confirmed by overnight polysomnography, and an MSLT may be used to assess sleepiness. Esophageal manometry during polysomnography facilitates diagnosis of UARS. Treatment most commonly consists of nasal CPAP or BPAP, although problems with compliance make surgical treatment preferable in some cases. Although UPPP eliminates sleep apnea only in a minority of patients, combining UPPP with maxillofacial procedures appears to improve outcomes. Other treatments such as the use of dental appliances or medications, weight loss, and positional therapy may be useful as adjunctive therapy for moderate to severe OSAS or as primary treatments for UARS or mild OSAS.     

Effect of anatomical and physiological factors on the indirect blood pressure measurement: identification of nurses'' knowledge

Sleep disorders are major syndromes that can interfere with falling to sleep or maintaining sleep, or produce excessive daytime sleepiness. Sleep disorders are rarely diagnosed in the elderly due to age-related changes in sleep patterns. Gerontological nurses can assist the elderly client to achieve improved sleep through increased awareness of sleep disorders, related assessment tools, and interventions.     

Understanding sleep ontogeny to assess brain dysfunction in neonates and infants

The ontogenetic framework onto which a child's sleep is constructed undergoes significant developmental alterations during early life. Sleep state behaviors, in large part, reflect continuities from fetal through neonatal time periods. Major changes in sleep organization subsequently occur throughout infancy. Maturational expressions of sleep behaviors must be understood by the pediatric neurologist before specific physiologic phenomena can be assessed as transient sleep disturbances or clinically relevant sleep disorders. The first part of this two-part review article focuses on the major aspects of developmental sleep physiology in the first few months of life. Recognition of age-specific electroencephalographic/polysomnographic patterns will facilitate the child neurologist's evaluation of the newborn with suspected seizures and interictal encephalopathies, as well as the prediction of neurologic sequelae.     

Wake disorders. I. Primary wake disorders

Primary wake disorders encompass various conditions of excessive daytime sleepiness and/or increased nighttime sleep, of unknown origin beginning most often in adolescence and of chronic or recurrent natural history. The best known of these conditions is narcolepsy associating two major clinical features, irresistible episodes of sleep, sleep onset REM periods and an almost constant association with HLA DR2-DQ1. The prevalence of the condition is close to the one of multiple sclerosis but positive diagnosis requires most often over 10 years to be made. The treatment of excessive daytime sleepiness has recently benefited from a new non-amphetamine awakening compound, modafinil, active in 60 to 70 p. 100 of the cases. The treatment of cataplexy still relies on antidepressants, tricyclics or selective serotonin reuptake blockers. Major advances in pathophysiology and pathogeny have been obtained through a natural model of the disease, canine narcolepsy. Pharmacological studies point to the importance of alpha-1 b adrenergic mechanisms in cataplexy, while dopaminergic systems seem more involved in excessive daytime sleepiness. As concerns genetics, the HLA DQB1*0602 gene predisposes to narcolepsy. In the canine model it is mirrored by an autosomal recessive gene showing a strong homology with the human immunoglobulin gene mu-switch. Familial studies have shown that besides typical phenotypes, attenuated forms of the condition characterized by isolated recurrent daytime naps and/or lapses into sleep do exist. In addition one or several other genes may be involved. Narcolepsy is multifactorial, including one or several genes as well as environmental factors. Idiopathic hypersomnia is noted for very long night sleep, difficulty waking up and more or less constant excessive daytime sleepiness. In contrast with narcolepsy sleep in not refreshing. There is no polysomnographic or immunogenetic special feature. Idiopathic hypersomnia is 10 times less frequent than narcolepsy. It is often overdiagnosed due to insufficient knowledge of other causes of excessive daytime sleepiness such as the upper airway resistance syndrome. Modafinil is also of great value in the treatment of idiopathic hypersomnia. In the absence of an animal model, pathophysiology and pathogeny are still poorly understood. Even rarer is the Kleine-Levin syndrome which is easily distinguishable through its recurrent character and its tendency to progressively disappear. It mainly occurs in early adolescent males. Its main features are episodes of sleep of a week duration recurring at a several months' interval along with disturbances of alimentary and sexual behavior. There is no satisfactory treatment of hypersomniac episodes. On the other hand a prophylactic treatment with carbamazepine or lithium may be active. Pathophysiology remains unsettled in spite of some evidence of a hypothalamic functional disturbance.     

Sleep apneas

In its most frequent form, in which obstructive apneas are predominant, the sleep apnea syndrome appears more and more as a frequent disorder. Clinically, it can be easily suspected in a patient presenting with snoring and daytime sleepiness, provided that these symptoms are systematically sought. A firm diagnosis relies on polysomnographic recordings. Beyond these symptoms, which are social and professional handicaps, the severity of the disorder is related to its cardiovascular long-term complications. The standard treatment is based upon nasal continuous positive airway pressure, which is safe and efficient but constraining. Surgical treatments, which are not as safe nor as efficient, can be proposed when continuous positive airway pressure is not accepted.     

Sleep disorders in children.

Many children experience some type of sleep problem. Often, these are transient problems with no long-lasting sequelae. But in certain cases, sleep problems may significantly impact on functioning and well-being. Sleep disorders in children can be classified into 2 major categories. Dyssomnias include those disorders that result in difficulty either initiating or maintaining sleep or involve excessive sleepiness. Parasomnias are disorders that disrupt sleep after it has been initiated but do not result in complaints of insomnia or excessive sleepiness. Even though sleep disorders in children are common, not enough is known. This article reviews the dyssomnias and parasomnias experienced by children, discusses methodological limitations of the studies reviewed, and presents future directions for research in this field. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Obstructive sleep apnea

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.     

In vivo 1H MRS of normal breast and breast tumors using a dedicated double breast coil

OBJECTIVE: To characterize sleep patterns of patients with juvenile rheumatoid arthritis (JRA). METHODS: Sixteen patients with JRA aged 12+/-4 years and 9 controls aged 11+/-3 years underwent a comprehensive evaluation by self-report questionnaire and formal all night polysomnographic recordings. Multiple sleep latency test was performed in 7 patients. RESULTS: Patients had 90% more arousals and awakenings (p<0.01) and the median length of occurrences of uninterrupted sleep in stages 2 and 3 and rapid eye movement (REM) sleep was 60% shorter than in controls (p<0.01). The overall amount of sleep stage shift from deeper to lighter sleep was 23.5+/-10.8 events in patients compared to 14.9+/-4.0 in controls (p<0.05). In 15 of 16 patients 15% of non-REM sleep consisted of alpha-delta (alpha-rating) sleep, compared with less than 1% in controls (p<0.001). Multiple sleep latency test for patients was 10.3+/-2.6 min. There were no differences between JRA and controls in self-reported questions. However, patients reported longer afternoon naps, 1.8+/-1.3 h compared to 0.3+/-0.8 h in controls (p<0.05). CONCLUSION: Objective polysomnographic evidence of abnormal sleep has been confirmed in patients with JRA. Sleep disturbance was associated with daytime sleepiness as evidenced by abnormal multiple sleep latency test and longer afternoon naptime.     

Epstein-Barr virus lacking glycoprotein gp42 can bind to B cells but is not able to infect

Sleep consists of two complex states--NREM and REM sleep--and disturbances of the boundaries between the states of sleep and wakefulness may result in violence. We investigated our population for reports of violence associated with sleep. REM behavior disorder is rarely associated with injury to the sufferer or others. NREM sleep related nocturnal wandering associated with self-inflicted injuries has variable etiologies. In the elderly, it is associated with dementia. In young individuals, it may be associated with mesio-temporal or mesio-frontal foci and an indication of a complex partial seizure. It also may be related to abnormal alertness and is associated with excessive daytime sleepiness, micro-sleeps, and hypnagogic hallucinations in sleep disorders such as narcolepsy or sleep disordered breathing.     

Increased prevalence of sleep disturbances and daytime sleepiness in subjects with bronchial asthma: a population study of young adults in three European countries

The aim of this study was to investigate whether asthma is associated with decreased quality of sleep and increased daytime sleepiness. The study involved a random population of 2,202 subjects supplemented by 459 subjects with suspected asthma, aged 20-45 yrs. The subjects were from Reykjavik (Iceland), Uppsala and G?teborg (Sweden) and Antwerp (Belgium), and participated in the European Community Respiratory Health Survey. The investigation included a structured interview, methacholine challenge, skinprick tests and a questionnaire on sleep disturbances. Participants in Iceland and Sweden also estimated their sleep times and made peak expiratory flow (PEF) recordings during a period of 1 week. Asthma was defined as self-reported physician-diagnosed asthma with current asthma-related symptoms (n = 267). Difficulties inducing sleep (DIS) and early morning awakenings (EMA) were about twice as common, and daytime sleepiness 50% more common, in asthmatics compared with subjects without asthma. After adjusting for possible confounders, a positive association was found between asthma and: DIS (odds ratio (OR) = 1.8); EMA (OR = 2.0); daytime sleepiness (OR = 1.6); snoring (OR = 1.7); and self reported apnoeas (OR = 3.7). Allergic rhinitis, which was reported by 71% of subjects with asthma, was independently related to DIS (OR = 2.0) and daytime sleepiness (OR = 1.3). A significant correlation was found between the number of asthma-related symptoms and sleep disturbances (p < 0.001). Asthma is associated with decreased subjective quality of sleep and increased daytime sleepiness. Concurrent allergic rhinitis may be an important underlying cause of sleep impairment in asthmatic patients.     

Cell adhesion molecules in vasculitis

Daytime sleepiness is a common complaint in blind subjects. Abnormally timed melatonin has been invoked as a possible cause of both daytime sleepiness and nighttime awakening. In free-running blind individuals, there is an opportunity to assess the relationship between endogenous melatonin rhythms and subjective sleepiness and naps. The aim of this study was to characterize melatonin rhythms and simultaneously to evaluate subjective napping. A total of 15 subjects with no conscious light perception (NPL) were studied for 1 month. Prior to the study, sleep disorders were assessed using the Pittsburgh Sleep Quality Index. Cosinor and regression analysis revealed that 9 of the 15 NPL subjects had free-running 6-sulphatoxymelatonin (aMT6s) rhythms (period [tau] range = 24.34 to 24.79 h), 3 were entrained with an abnormal phase, and 3 were normally entrained. Most of the subjects (13 of 15) had daytime naps; the 2 individuals who did not made conscious efforts not to do so. Subjects with abnormal aMT6s rhythms had more naps of a longer duration than did those with normal rhythms. Free-running nap rhythms occurred only in subjects with free-running aMT6s rhythms. The 2 abnormally entrained subjects who napped did so at times that coincided with high levels of aMT6s (mean aMT6s acrophase [phi] +/- SD = 14.30 +/- 1.08 h, 20.30 +/- 0.62 h; mean nap time +/- SD = 14.01 +/- 3.60 h, 18.23 +/- 3.20 h, respectively). Regardless of aMT6s rhythm abnormality, significantly more naps occurred with a 4-h period before and after the estimated aMT6s acrophase. In 4 free-running subjects, aMT6s acrophase (phi) passed through an entire 24-h period. When aMT6s was in a normal phase position (24:00 to 06:00 h), night-sleep duration tended to increase with a significant reduction in the number and duration of naps. Sleep onset and offset times tended to advance and delay as the aMT6s rhythms advanced and delayed. Our results show a striking relationship between the timing of daytime production of melatonin and the timing of daytime naps. This suggests that abnormally timed endogenous melatonin may induce sleepiness in blind subjects.     

Characteristics of apneas and hypopneas during sleep and relation to excessive daytime sleepiness

STUDY OBJECTIVES: One of the most important symptoms in patients evaluated for possible obstructive sleep apnea syndrome is excessive daytime sleepiness, but the measures of apnea severity and of sleepiness used most commonly have not generally shown strong associations. We explored whether information recorded during standard polysomnography, other than the overall rate of apneas and hypopneas per hour of sleep (AHI), might help explain the measured severity of sleepiness. DESIGN: Observational SETTING: A clinical sleep laboratory in a university hospital PATIENTS: N = 1,146 patients evaluated for suspected sleep-disordered breathing with nocturnal polysomnograms and multiple sleep latency tests. RESULTS: The AHI during supine sleep (recorded in a subgroup of n = 169 subjects), the rate of apneas (n = 1,146), and the rate of obstructive apneas (n = 1,146) were particularly useful in explaining variation in measured levels sleepiness; rates of hypopneas and central apneas were less useful (n = 1,146). In addition, the minimum recorded oxygen saturation (n = 1,097) was as important as the AHI to the level of sleepiness. CONCLUSIONS: In an attempt to explain excessive daytime sleepiness among patients evaluated for sleep-disordered breathing, additional insight is provided by observation of supine sleep during polysomnography, by emphasis on apneas rather than hypopneas, by emphasis on obstructive rather than central events, and by consideration of the minimum oxygen saturation.     

Child sleep disorders: Associations with parental sleep duration and daytime sleepiness.

This study examined the associations between childhood sleep disorders and mothers' and fathers' sleep duration and daytime sleepiness. One hundred seven families of children (ages 2-12 years) presenting to a pediatric sleep disorders clinic completed questionnaires assessing the sleep symptoms of the mother, father, and child. Parents of children with more than 1 type of sleep disorder experienced more daytime sleepiness than parents of children with a single sleep disorder. The pattern of results suggested more associations between maternal and child sleep than between paternal and child sleep. Within families, mothers reported significantly more daytime sleepiness than fathers, although there were no parental differences in sleep duration. Results provide preliminary evidence for an association between child sleep problems and parental daytime sleepiness, which may, in turn, extend previous research linking young children's sleep problems and parental functioning. Implications for treatment of both children and adults with sleep problems are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sleep of sleep research personnel--results of the Munster Congress survey

Due to different knowledge of sleep and sleep disorders (i.e. focussing) sleep quality of sleep-researchers may be better or worse than the sleep of other scientists. On the Münster Congress for Sleep-research and Sleep medicine in March 1994 we investigated this question using the Pittsburger Sleep Quality Index (PSQI). 46 sleep researchers, 52 practitioners and 103 scientists of other disciplines from the Münster University filled out the questionnaire. Results show no difference in overall sleep quality between the three groups, but only sleep quality in the group of sleep researchers shows a bimodal distribution suggesting a subpopulation with more serious sleep problems. 10 to 15% of the total academic population can be regarded as "poor" sleepers. Especially the group of practitioners, in which we found the highest values of daytime sleepiness, seems to be a risk-population for sleep disorders.     

Sleep disorders in neurology. Hypersomnia

Hypersomnia (excessive sleepiness) accompanies many diseases. 14% of the total Austrian population regularly have problems staying awake during the day or are prone to taking spontaneous naps. Hypersomnia is a symptom of the sleep apnea syndrome, which is a risk factor for cerebrovascular disorders. Daytime sleepiness is also a characteristic symptom of narcolepsy, idiopathic hypersomnia, episodic hypersomnia, and many more neurological or psychiatric disorders; it can also be drug induced. Involvement of brain structures which are essential for the regulation of the sleep wake cycle as a result of neurological disorders can likewise lead to hypersomnia. Symptomatic treatment is necessary when treatment of the causal factors is not possible or no improvement has been achieved.