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  1. Home
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  3. Sleepiness
  • Cited by 11
  • Edited by Michael J. Thorpy, Sleep-Wake Disorders Center, Montefiore Medical Center, Bronx, NY, USA, Michel Billiard, Guide Chauliac Hospital, Montpellier, France
Publisher:
Cambridge University Press
Online publication date:
February 2011
Print publication year:
2011
Online ISBN:
9780511762697
DOI:
https://doi.org/10.1017/CBO9780511762697
Subjects:
Psychiatry and Clinical Psychology, Neurology and Clinical Neuroscience, Medicine, Psychiatry
Information

Book description

Written and edited by leading clinicians and researchers in sleep medicine, this is the first book to focus on the causes, consequences and treatment of disorders of excessive sleepiness. Extensive coverage is provided for all known causes of sleepiness, including sleep deprivation, obstructive sleep apnea syndrome, narcolepsy and other hypersomnias of central origin, shift work, and medical and psychiatric disorders. Since many causes of sleepiness are difficult to differentiate from each other, and treatment modalities can vary greatly from one disorder to another, this book helps the clinician to formulate a differential diagnosis that will ultimately lead to the correct diagnosis. Epidemiology, evaluation of the sleepy patient, diagnostic investigations including neuroimaging, subjective and objective testing, cognitive effects of sleepiness, motor vehicle driving issues, medico-legal aspects of sleepiness, and therapy are also discussed in detail. This is an essential resource for neurologists, psychiatrists and sleep specialists.

Reviews

'… an excellent reference for sleep clinicians and sleep researchers, providing an extensive review of the causes, consequences, and treatment of excessive sleepiness.'

Source: Doody's Notes

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Contents

Page 2 of 2

Contents
  • Chapter 21 - Time-zone transitions and sleepiness
    pp 225-237
  • View abstract

    Summary

    This chapter provides an overview of idiopathic hypersomnia together with a discussion on the nosological limits of the condition. It presents the history, clinical features, diagnostic procedures, treatment and differential diagnosis of idiopathic hypersomnia. All efforts to clarify demographics, pathophysiology and treatment have been hampered by the nosological uncertainty on the borders of idiopathic hypersomnia. The latest International Classification of Sleep Disorders confirmed the distinction of two forms of idiopathic hypersomnia and used a new wording of idiopathic hypersomnia with long sleep time and idiopathic hypersomnia without long sleep time. The diagnosis of idiopathic hypersomnia with long sleep time is mainly based on clinical features and on the absence of associated symptoms such as snoring or cataplexy. However, polysomnography and the multiple sleep latency test (MSLT) are indispensable to rule out other conditions. Further research is necessary to specify the limits of idiopathic hypersomnia with and without long sleep time.
  • Chapter 22 - Restless legs syndrome and periodic limb movements and excessive sleepiness
    pp 238-248
  • View abstract

    Summary

    Kleine-Levin syndrome (KLS) is a rare neurological disorder primarily affecting young subjects. The first episode usually begins within a few hours, with patients becoming extremely tired, generally after an identifiable triggering event, such as a banal infection in most cases, alcohol intake, or a head trauma. The symptomatic periods involve hypersomnia, and cognitive, behavioral and psychological problems, and last from two days to several weeks. The most difficult differential diagnoses are psychiatric disorders (psychosis and depression), hence many patients are sent to the psychiatric department before the diagnosis of KLS is made. Recent methods of investigation such as SPECT indicate that the brain dysfunction could be larger than expected, and would encompass both cortical and subcortical (and especially thalamus and hypothalamus) areas. This general picture and the fluctuating symptoms in KLS are consistent with the possibility of an autoimmune mediation of the disorder.
  • Chapter 23 - Long sleepers
    pp 249-261
  • View abstract

    Summary

    This chapter reviews what is known about menstrual-related hypersomnia, a rare disorder of recurrent hypersomnia that is temporally linked with menses. In light of the rareness of cases of menstrual hypersomnia, the chapter also discusses the influence of the menstrual cycle on levels of daytime sleepiness in women during normal cycles and in those with premenstrual syndrome. Evidence indicates that ovulation is necessary for hypersomnia episodes to appear in affected individuals. Hypersomnia episodes were associated with ovulatory but not anovulatory cycles, as monitored with basal temperature measurements, in one patient, and prevention of ovulation with oral contraceptive treatment effectively alleviates the hypersomnia. Women experience increased feelings of sleepiness and fatigue around the time of menstruation. Laboratory findings show that women with premenstrual syndrome (PMS) are able to maintain wakefulness under soporific conditions despite their subjective sleepiness.
  • Chapter 24 - Sleepiness in children
    pp 262-276
  • View abstract

    Summary

    This chapter addresses the prevalence of sleepiness in obstructive sleep apnea syndrome (OSA) and the potential confusion with fatigue, depression and attentional deficits. In clinical practice, sleepiness is in most cases evaluated by the Epworth Sleepiness Scale (ESS). Sleep fragmentation and other sleep structure disturbances are classically considered the main causes of daytime sleepiness in OSA patients. Sleepiness, regardless of its cause, affects driving ability through increased reaction time, inattentiveness or microsleep episodes. Obstructive sleep apnea syndrome (OSAS) and hypertension are linked in a dose-response fashion. This is true even when taking into account confounding factors such as age, alcohol, tobacco consumption, and body mass index (BMI). The beneficial continuous positive airway pressure (CPAP) effect is obtained after only a few weeks of treatment, with quality of life returning to normal. CPAP treatment restores normal alertness except in some patients with residual excessive sleepiness.
  • Chapter 25 - Depression and sleepiness: a chronobiological approach
    pp 279-291
  • View abstract

    Summary

    This chapter evaluates whether insomnia patients are sleepier than healthy controls without insomnia. In order to assess whether insomnia patients suffer from sleepiness, the authors assessed the extent to which treatments for insomnia improved some measure related to daytime sleepiness. The current literature suggests that insomnia is frequently associated with greater self-reported daytime sleepiness than is seen in healthy individuals without sleep complaints. The multicomponent cognitive-behavioral therapy had a significant advantage over the control therapy in decreasing number of naps per week. Some have hypothesized that this mismatch reflects a hyperarousal state in insomnia that prevents the daytime sleepiness that they experience from becoming manifest in objective daytime sleepiness. The findings of treatment studies provide preliminary evidence that insomnia patients have some degree of daytime sleepiness that can be improved with treatment.
  • Chapter 26 - Aging, Alzheimer's disease and sleepiness
    pp 292-300
  • View abstract

    Summary

    This chapter discusses the symptom of sleepiness in two of the most common circadian rhythm sleep disorders: advanced sleep phase disorder (ASPD) and delayed sleep phase disorder (DSPD). The personality disorders are diagnosed more frequently in those with DSPD compared with other sleep disorder populations, including ASPD. In ASPD, an individual's circadian sleep tendency is advanced relative to the (societally) desired clock time. A number of investigators have recently reported age-related changes in the circadian timing system that may be associated with the sleep patterns often observed in older subjects. The effective use of current interventions in the treatment of DSPD and ASPD, as well as the development of new approaches, depends largely on the findings obtained from this type of analytic approach. This is emphasized by the results of several studies showing successful phase shifts of the circadian system, without any improvement in sleep quality.
  • Chapter 27 - Excessive daytime sleepiness in Parkinson's disease
    pp 301-315
  • View abstract

    Summary

    Shift work disrupts circadian and homeostatic sleep regulation and is probably the most common cause of sleepiness in society. This chapter talks about the shift work disorder, and presents survey studies of sleepiness, physiological sleepiness and momentary subjective sleepiness. EEG measures give some indication of the pattern of sleepiness in relation to shift work, that is, incidents of sleep intrusions are frequently seen during the second half of a night shift. If sleepiness is as pronounced as suggested in connection with night work, there should be a link with performance errors and accidents. Shift work that includes night shifts causes high levels of sleepiness that may constitute a major safety risk, particularly in transport work, but also in health care and industry. The chapter discusses the individual differences, the diagnosis shift work disorder, and possible ways of counteracting or treating intolerance to shift work.
  • Chapter 28 - Myotonic dystrophy and sleepiness
    pp 316-328
  • View abstract

    Summary

    This chapter reviews the manner in which sleep deprivation and circadian misalignment lead to impaired performance among healthcare providers. Several sleep and circadian factors affect the performance of physicians-in-training as well as other healthcare providers. In addition to acute sleep restriction, residents suffer chronic sleep restriction. Extended-duration work shifts also increase the likelihood of fatigue-related, self-reported medical errors. As learning is central to medical residency, any factor impairing resident learning is of concern. The only randomized evidence regarding elimination of 30-h shifts, and substitution with 16-h shifts, suggests that errors could in fact decrease by more than double this amount with widespread implementation of a 16-h shift limit. Lab- and field-based studies show us that extended resident shifts impair cognition and likely impair learning. Such impairment translates into error, poor patient care, and resident harm.
  • Chapter 29 - Post-traumatic sleepiness
    pp 329-334
  • View abstract

    Summary

    The challenge for any ancient military strategist who wanted to deprive his enemy of sleep would have been figuring out how to do so without exacting a comparable toll on his own troops. In this context, there is probably no better example of a strategy that achieved such an outcome than that employed by Alexander the Great at the Battle of Gaugamela. This chapter illustrates the manner in which sleep/sleepiness has remained a militarily relevant factor in modern times. This is best highlighted by the presumed military strategy of the former USSR/Warsaw Pact nations during the Cold War. Military sleep researchers have mostly been dedicated to performing studies with an ultimate aim of sustaining the military effectiveness (ability to perform those tasks required to successfully achieve mission objectives) of sleepy soldiers. The Walter Reed Army Institute of Research (WRAIR) is a comprehensive sleep/performance management system (SPMS).
  • Chapter 30 - Genetic disorders and sleepiness
    pp 335-350
  • View abstract

    Summary

    In this chapter, travel fatigue and jet lag are treated as a subjective assessment that is synonymous with fatigue and lack of alertness. The symptoms of travel fatigue include a general weariness, and travellers often nap during the journey. The circadian rhythms tend to fall into two groups: those that peak during the daytime and are associated with the active phase of the individual; and those that peak during nocturnal sleep and are associated with fasting and recuperation. The suprachiasmatic nuclei (SCN), paired groups of cells in the base of the hypothalamus, are the site of the body clock in mammals. The body clock transmits its rhythmic output to regions of the brain controlling temperature regulation, hormone release, feeding and sleep. Measured circadian rhythms are combined effects from a body clock (endogenous component) and the environment (exogenous component) that are normally in synchrony.
  • Chapter 31 - Brain tumors, infections, and other CNS causes of sleepiness
    pp 351-363
  • View abstract

    Summary

    Restless legs syndrome and periodic limb movement disorder are common neurological entities that may be associated with insomnia and excessive daytime sleepiness. This chapter reviews the clinical features, natural history, laboratory investigations, genetics, pathology, and management of primary restless legs syndrome (RLS) and periodic limb movement disorder (PLMD). Large epidemiological surveys have shown that self-reported symptoms of RLS were correlated with sleepiness. Electrodiagnostic testing with nerve conduction studies and electromyography are useful to detect subtle peripheral neuropathies. Several factors suggest that impaired dopaminergic function and iron homeostasis underlie the pathophysiology of RLS. One study demonstrated that dopaminergic treatment of RLS patients improved both RLS severity and sleepiness as measured by multiple sleep latency test (MSLT) score. Considerable research has been directed towards elucidating the basic mechanisms and optimizing the management of RLS and PLMD.
  • Chapter 32 - Hypothyroidism and other endocrine causes of sleepiness
    pp 364-374
  • View abstract

    Summary

    This chapter focuses on formulating an integrated position on sleepiness in long sleepers. It reviews studies conducted through a pathology lens, where long sleepers frequently include individuals in poor physical or psychological health, who are often older and experience poor nocturnal sleep quality, including insomnia. Most epidemiological studies investigating sleepiness and the behavioral and psychological characteristics of long sleepers have examined the extremes of sleep duration relative to each other. Existing empirically supported models of sleep regulation postulate that duration and timing of sleep are regulated by an interaction between a circadian pacemaker, which programs daily cycles in sleep propensity, and a sleep homeostat, which tracks increases in sleep pressure. Investigations conducted outside the U-shaped pathology lens have also found that long sleepers who do not have insomnia are no sleepier than midrange sleepers.
  • Chapter 33 - Toxic and metabolic causes of sleepiness
    pp 375-385
  • View abstract

    Summary

    Hypersomnia is characterized by recurrent episodes of excessive daytime sleepiness (EDS) or prolonged nighttime sleep that affects the everyday life of the patient. Clinical surveys have reported EDS as a complaint in up to 68% of normal high-school children. Causes of EDS are divided into three categories: insufficient nighttime sleep, fragmented nighttime sleep, and an increased need of sleep. Pediatric daytime sleepiness scale (PDSS) is a recently introduced validated measure for assessing sleepiness in children. Management of disorders that may coexist with hypersomnia of central origin such as obstructive sleep apnea, psychiatric disorders, medications, and circadian rhythm disorders will require specific therapeutic interventions, but need to be done for optimal outcome in children with narcolepsy. The general approach to the treatment of childhood narcolepsy and other hypersomnias of central origin is based on the adult experience.
  • Chapter 35 - Amphetamines, methylphenidate and excessive sleepiness
    pp 401-407
  • View abstract

    Summary

    This chapter highlights studies on excessive daytime sleepiness (EDS) and depression within the framework of human sleep and chronobiology. It provides an outlook of chronobiological underpinnings of this relationship in order to provide insights and candidates for chronobiological management. Sleepiness may reflect the waning of processes maintaining wakefulness and/or may result from distinct neural systems acting to promote sleep. Recent imaging studies have shed new light on the neurobiological basis of depression. Clinical rating scales measuring depression often inquire about fatigue and tiredness. On a pharmacological domain, there is emerging evidence that the circadian system is implicated in some of the treatment mechanisms, such as lithium therapy for bipolar depression. Insights on the link among EDS, depression and chronobiology can provide a better comprehension of this sleep-wake disturbance, together with promising therapeutic managements.
  • Chapter 36 - Modafinil/armodafinil in the treatment of excessive daytime sleepiness
    pp 408-420
  • View abstract

    Summary

    This chapter makes a distinction between studies of sleepiness and studies of napping. In considering difficulties with excessive daytime sleepiness among older adults, one key factor is poor quality nighttime sleep. Many studies have found that depression is associated with excessive daytime sleepiness (EDS), with some of those studies focusing specifically on older adults. One key treatment consideration in the management of daytime sleepiness among older adults is to address primary sleep disorders that disrupt nighttime sleep. One such example is a randomized controlled trial of the effect of treatment of sleep apnea on daytime functioning in patients with Alzhiemer's disease (AD). Studies show that patients with dementia, particularly with AD, commonly suffer from daytime sleepiness. Studies also highlight that increased exposure to bright light, particularly when combined with efforts to reduce time in bed during the day, may be an effective method for decreasing daytime sleepiness.
  • Chapter 37 - Sodium oxybate for the treatment of excessive sleepiness
    pp 421-429
  • View abstract

    Summary

    Dopamine cell death attending Parkinson's disease (PD) profoundly alters the sleep-wake state which can be classified into disturbances of: nocturnal movement, and thalamocortical arousal state. Diurnal rhythms in the content, turnover, release and behavioral responsiveness of the brain's principal dopamine systems are well established. Clinicians have long relied upon the wake-promoting effects of dopaminomimetics inclusive of traditional psychostimulants. Apart from the neurobiological substrates governing PD, genetic and disease factors may also influence expression of sleepiness and sleep onset rapid-eye-movement sleep (SOREMs). The utility of the multiple sleep latency test (MSLT), and other objective and subjective measures of sleepiness in PD has been reviewed. The clinician treating sleepiness in the parkinsonian patient is in the unenviable position of weighing the potential positive impact of dopaminomimetics upon sleep as it relates to daytime motor function, against the real possibility of adverse effects upon daytime alertness.
  • Chapter 38 - Caffeine and other alerting agents
    pp 430-443
  • View abstract

    Summary

    Myotonic dystrophy type I (DM1) is one of the most variable of all human disorders, with virtually all body systems affected in some way, and age at disease onset varies from fetal life to old age. The character of DM1-related excessive daytime sleepiness (EDS) is that of a persistent sleepiness unaffected by naps, the latter being long, unrefreshing and without any associated dream. This chapter presents the scores of DM1 patients with and without EDS on the eight Short-Form 36-item Health Survey subscales, a frequently used generic health-related quality of life (HRQoL) questionnaire. It describes the personality and cognitive characteristics of 200 DM1 patients with and without EDS. The chapter discusses the habitual sleep-wake schedule and sleep-related complaints of 200 DM1 patients with and without EDS. Sleep-disordered breathing (SDB), hypercapnia, and nocturnal desaturation are all frequent in DM1. Psychostimulant drugs are increasingly used to treat EDS in DM1.
  • Chapter 39 - Histamine receptor (H3R) antagonists, hypocretin agonists, and other novel alerting agents
    pp 444-451
  • View abstract

    Summary

    This chapter discusses the post-traumatic sleep-wake disturbances and post-traumatic sleepiness. Two prospective studies on post-traumatic sleep-wake disturbances identified excessive daytime sleepiness (EDS) as the most common symptom after traumatic brain injury (TBI), but other symptoms also frequently occur. A study found sleep-wake disturbances in 46% of the examined population, with post-traumatic sleepiness as the most common finding. TBI patients often ask their doctors whether or not their enhanced sleep drive and their increased sleep need will ameliorate over time. The interview and scales should consist not only of sleepiness questions, but should also include questions on fatigue and hypersomnia, because these symptoms may be related. Sleep-wake disturbances likely result from and contribute to multiple factors associated with the brain injury, all of which complicate recovery and resolution of symptoms. To create evidence, larger multicenter trials are currently being undertaken to study the effect of modafinil and armodafinil on post-traumatic sleepiness.
  • Chapter 40 - Behavioral and psychiatric treatments for sleepiness
    pp 452-461
  • View abstract

    Summary

    This chapter reviews the type and prevalence of sleep problems including daytime sleepiness in a range of commonly presenting genetic syndromes and diseases. It covers the chromosomal abnormalities and genetic programming malformations of the nervous system. The chapter discusses the inherited metabolic disorders and heredodegenerative diseases. It describes the neurodevelopmental syndromes with genetic compound, and reviews the genetically based neuromuscular diseases. Excessive daytime sleepiness (EDS) is the most common sleep-related symptom in the Prader-Willi syndrome. Smith-Magenis syndrome is a severe neurodevelopmental disorder characterized by mental retardation with distinctive behavioral characteristics, dysmorphic features and an abnormal circadian pattern of melatonin ascribed to an intersticial deletion of chromosome 17. Neuromuscular diseases include a wide spectrum of motor unit diseases starting with the affection of motor neuron in the brainstem and spinal cord, continuing through myasthenic syndromes, muscle dystrophies and congenital myopathies, myotonic syndromes and ending with hereditary motor and sensory polyneuropathies (HMSN).

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