Damhoff ; Martin R. Authors Hajira Basit 1 ; Thomas C. Damhoff 2 ; Martin R. Huecker 3. Proper sleep is vital to maintain health and optimize overall functioning during periods of wakefulness.

Sleeplessness has been linked with several health problems, such as diabetes, obesity, and heart disease.

It is also linked to decreased work performance, traffic accidents, mood and relationship problems, and countless other issues. This activity will focus on the diagnosis and management of circadian rhythm sleep-wake disorders and explains the role of the interprofessional team in managing those with sleeplessness and circadian disorder.

Objectives: Identify the most common etiologies of sleep disorders. Outline the evaluation for each of the common sleep disorders. Summarize the common sleep disorders with the appropriate treatment recommendations. Review the importance of collaboration and communication among the interprofessional team in diagnosing and managing the different sleep disorders to improve the quality of life for those with this condition.

Access free multiple choice questions on this topic. Proper sleep is essential to maintain health and optimize overall functioning during wakefulness.

Sleeplessness has been linked with several health problems, including diabetes, obesity, and heart disease. Sleeplessness also leads to decreased work performance, traffic accidents, mood and relationship problems, and countless other issues.

The American Academy of Sleep Medicine International Classification of Sleep Disorders lists 7 broad categories of sleep disorders: insomnia, sleep-related breathing disorders, central disorders of hypersomnolence, circadian rhythm sleep-wake disorders, parasomnia, sleep-related movement disorders, and other sleep disorders.

This article will focus on circadian rhythm sleep-wake disorders. The circadian system regulates sleep consolidation and many other physiologic parameters necessary for health and optimal functioning.

The circadian system is an endogenous cycle entrained by external cues, most importantly light. The circadian rhythm can be measured by evaluating melatonin levels, cortisol levels, and core body temperature.

Structurally, the circadian rhythm exists within the suprachiasmatic nuclei of the hypothalamus. The suprachiasmatic nuclei receive direct information on illumination from ganglion cells in the retina. Ganglion cells contain a photopigment called melanopsin and transmit signals to the suprachiasmatic nuclei through the retinohypothalamic tract.

The suprachiasmatic nuclei then process this information and stimulate the pineal gland to release melatonin. Melatonin increases in the evening in response to dim light and peaks around 3 hours before waking.

Melatonin receptors are found primarily in the retina, the pars tuberalis of the pituitary gland, and the suprachiasmatic nuclei. This feedback onto the suprachiasmatic nuclei serves as a feedback mechanism that supports the circadian rhythm.

As sleep pressure accumulates during periods of wakefulness, the circadian rhythm system also works to maintain wakefulness. The circadian rhythm system has an intrinsic cycle, which on average, is just over 24 hours.

To compensate for the hour day, the system must undergo phase shifts. These shifts are driven by time cues called zeitgebers, of which the light-dark cycle is the most effective. The circadian rhythm system works in harmony with the sleep homeostatic system to ensure proper sleep.

Such a complex system that also relies on external stimuli is subject to dysfunction at many levels. Circadian rhythm system disorders can result from intrinsic dysfunction or the result of environmental factors.

Six recognized disorders will be discussed below. The diagnosis of sleeplessness and circadian rhythm disorders is primarily based on a thorough history. A comprehensive history helps in the differentiation of transient disorders from chronic disorders and primary disorders from secondary disorders, which also influences the direction of evaluation and treatment plans.

In cases of sleeplessness, it is essential to distinguish individuals with difficulty initiating sleep from those with trouble maintaining sleep, those with significant daytime impairment, and those with nonrestorative sleep.

The detailed history includes asking questions about the duration of symptoms, a pattern of the sleep-wake cycle, total sleep time, shift work, recent travel, psychological assessment, medication history, self-treatment attempts, environmental cues, and medical problems.

The physical examination supplements the history of patients with sleep disorders. The focus of the physical examination is on identifying risk factors for other conditions that may precipitate, augment, or mimic insomnia, which may include depression, obstructive sleep apnea OSA , and neurodegenerative disease.

The exam evaluates body mass index BMI , craniofacial morphology, chest examination, digital clubbing, and neurologic examination. Delayed Sleep-Wake Phase Disorder [4] [5]. This disorder is characterized by delayed sleep and wake times relative to what is desired or expected.

Not simply "night owls," those with delayed sleep-wake phase disorder may not prefer such a sleep schedule but find it difficult to adjust to desired sleep and wake times. Inadequate sleep and resultant daytime functional impairment are hallmarks of the condition. Relative to the optimal amount of sleep, on average, those affected lose at least 2 hours of sleep per night.

Those affected may have great difficulty waking up and require a significant amount of support to do so. Sleep inertia may lead to confusion and frustration upon waking.

When able weekends, days off , affected patients generally get a sufficient quantity and quality of sleep, but the delayed phase will remain, and patients may sleep well into the day. The incidence of delayed sleep-wake phase disorder peaks in adolescents and is often accompanied by depression.

Some evidence suggests adolescents have longer intrinsic circadian cycles, referred to as tau, that often exceed 24 hours, thus exacerbating the condition. While most adolescents prefer a later sleep cycle, delayed sleep-wake phase disorder represents a distinct condition detrimental to functioning well beyond the typical adolescent experience.

Diagnosis is based primarily on the history of persistent delayed sleep-wake cycles that interfere with desired daytime functioning. Sleep logs may aid in diagnosis.

Other causes of delayed sleep cycles, such as caffeine use and excessive evening light exposure from electronic devices, should be screened. Treatment consists of behavioral modification, including good sleep hygiene and gradually moving sleep and wake times earlier.

With strict adherence to deliberate sleep schedules, most patients can achieve reasonable success in the normalization of sleep schedules. Caffeine, alcohol, nicotine, and daytime naps should be avoided. Melatonin supplementation and circadian rhythm-light training may also be used if needed.

Advanced Sleep-Wake Phase Disorder [6] [7] [8]. This disorder is characterized by excessive evening sleepiness and early morning awakening. Patients may get adequate quality and quantity of sleep if no external pressures dictate that patients stay awake in the evening, but often patients are distressed and sleep deprived because societal obligations require patients to stay awake longer than desired in the evening.

Patients with advanced sleep-wake phase disorder will wake at the same early time whether they have forced themselves to stay up later, leading to sleep deprivation and daytime sleepiness. It is hypothesized that advanced sleep-wake phase disorder results from an intrinsic circadian cycle that is less than 24 hours.

Advanced sleep-wake phase disorder is more prevalent in older adults and males. Diagnosis is made with history and sleep logs.

Treatment is primarily achieved with evening bright light therapy. Pharmacotherapy is not indicated for this condition. This disorder represents a failure of the circadian rhythm system to consolidate sleep, leading to multiple short periods of sleep and wakefulness.

Diagnosis is made when no clear circadian rhythm pattern can be identified and at least 3 periods of wakefulness lasting at least one hour occur during an average hour period.

This disorder is generally found in patients with dementia and is attributed to dysfunction of the suprachiasmatic nuclei. Lack of exposure to external time cues zeitgebers may also contribute to this disorder. Furthermore, obesity also affects the severity of OSA. Significant weight loss in adolescents who underwent gastric bypass surgery mean, 58 kg was associated with a dramatic reduction of OSA severity Kalra et al.

In simplest terms, OSA is caused by narrowing or collapse of the airway as a result of anatomical and physiological abnormalities in pharyngeal structures. Apnea episodes cause hypoxemia insufficient oxygen in the blood and hypercapnia high concentration of blood carbon dioxide.

The episodes also increase the output of the sympathetic nervous system Narkiewicz and Somers, , the effect of which is to restore pharyngeal muscle tone and reopen the airway.

Although increased sympathetic activity is beneficial for restoring normal breathing and oxygen intake over the short term, it has long-term deleterious effects on vascular tone and blood pressure, among other effects Caples et al. These early events—which are mediated by a variety of chemoreceptors in the carotid body and brainstem—trigger pathophysiological changes that occur not only during the obstructive apneas, but also extend into wakeful states during the day.

For example, during daytime wakefulness, people with OSA have higher sympathetic activity Somers, et al. The full pathophysiology of OSA remains somewhat elusive, although research is piecing together the relationships between OSA and a range of the previously described long-term health effects.

The etiology of central sleep apnea, although also not well understood, is hypothesized to result from instability of respiratory control centers White, There are a number of risk factors for OSA , including:. Studies of patients at sleep clinics tend to show an association between sleep apnea and mortality He et al.

The subgroup experienced twice the risk of mortality Lindberg et al. In adults, OSA is most effectively treated with CPAP and weight loss Strollo et al.

The problem is that many patients are noncompliant with CPAP see Chapter 6. Other options, although less effective, include a variety of dental appliances Ferguson and Lowe, or surgery e. In children, the first-line treatment for most cases of OSA is adenotonsillectomy, according to clinical practice guidelines developed by the American Academy of Pediatrics Marcus et al.

Children who are not good candidates for this procedure can benefit from CPAP. Central apnea treatment is tailored to the cause of the ventilatory instability. Commonly used treatments include oxygen, CPAP, and acetazolamide, a drug that acts as a respiratory stimulant White, Insomnia is the most commonly reported sleep problem Ohayon, It is a highly prevalent disorder that often goes unrecognized and untreated despite its adverse impact on health and quality of life Benca, a see also Chapter 4.

The diagnostic criteria for primary insomnia include:. Insomnia symptoms are remarkably common, affecting at least 10 percent of adults in the United States Ford and Kamerow, ; Ohayon et al.

Prevalence is higher among women and older individuals Mellinger et al. Severe insomnia tends to be chronic, with about 85 percent of patients continuing to report the same symptoms and impairment months or years after diagnosis Hohagen et al. The comorbidity of sleep disorders with psychiatric disorders is covered later in this chapter.

The precise causes of insomnia are poorly understood but, in general terms, involve a combination of biological, psychological, and social factors. Insomnia is conceptualized as a state of hyperarousal Perlis et al.

Stress is thought to play a leading role in activating the hypothalamic-pituitary axis and setting the stage for chronic insomnia. A key study showed that adults with insomnia, compared with normal sleepers, have higher levels, over a hr period, of cortisol and adrenocorticotropic hormone ACTH , which are hormones released by the hypothalamic-pituitary-adrenal axis after stress exposure Vgontzas et al.

The hour pattern of cortisol and ACTH secretion is different, however, from that in individuals who are chronically stressed. Cognitive factors, such as worry, rumination, and fear of sleeplessness, perpetuate the problem through behavioral conditioning.

Other perpetuating factors include light exposure and unstable sleep schedules Partinen and Hublin, Insomnia patients often attribute their difficulty sleeping to an overactive brain. Several lines of evidence, from preclinical to sleep neuroimaging studies in insomnia patients, suggest that there are multiple neural systems arranged hierarchically in the central nervous system that contribute to arousal as well as insomnia complaints.

Disturbances in these systems may differ according to the nature of insomnia. Structures that regulate sleep and wakefulness, for example the brainstem, hypothalamus and basal forebrain, are abnormally overactive during sleep in primary insomnia patients Nofzinger et al.

In addition, limbic and paralimbic structures that regulate basic emotions and instinctual behaviors such as the amygdala, hippocampus, ventromedial prefrontal cortex and anterior cingulate cortex have been shown to be abnormally active during sleep in individuals with primary insomnia and secondary insomnias related to depression Nofzinger et al.

Abnormal activity in neocortical structures that control executive function and are responsible for modulating behavior related to basic arousal and emotions has been observed in individuals with insomnias associated with depression Nofzinger et al.

The two main risk factors of insomnia are older age and female gender Edinger and Means, One large, population-based study found that insomnia was nearly twice as common in women than men, although reporting bias cannot be ruled out as a contributing factor Ford and Kamerow, The reason behind the apparent higher prevalence in women is not understood.

Other risk factors for insomnia include family history of insomnia Dauvilliers et al. Although adolescent age is not viewed a risk factor, insomnia has rarely been studied in this age group. Insomnia is treatable with a variety of behavioral and pharmacological therapies, which may be used alone or in combination.

While the therapies currently available to treat insomnia may provide benefit, the NIH State of the Science Conference on the Manifestations and Management of Chronic Insomnia concluded that more research and randomized clinical trials are needed to further verify their efficacy, particularly for long-term illness management and prevention of complications like depression NIH, Behavioral therapies appear as effective as pharmacological therapies Smith et al.

Behavioral therapies, according to a task force review of 48 clinical trials, benefit about 70 to 80 percent of patients for at least 6 months after completion of treatment Morin et al.

The therapies are of several main types Table The major problem with current behavioral therapies is not their efficacy; rather it is lack of clinician awareness of their efficacy and lack of providers sufficiently trained and skilled in their use.

Other problems are their cost and patient adherence Benca, a. The most efficacious pharmacological therapies for insomnia are hypnotic agents of two general types, benzodiazepine or nonbenzodiazepine hypnotics Nowell et al.

Nonbenzodiazepine hypnotics are advantageous because they generally have shorter half-lives, thus producing fewer impairments the next day, but the trade-off is that they may not be as effective at maintaining sleep throughout the night Morin, ; Benca, a.

It is still unclear whether hypnotics lead to dependence. It is suggested that they should not be taken for more than 10 days in a row; however, recent studies suggest that hypnotics do not always lead to dependence Hajak et al.

There have been no large-scale trials examining the safety and efficacy of hypnotics in children and adolescents. Other pharmacological classes used for insomnia include sedating antidepressants, antihistamines, and antipsychotics, but their efficacy and safety for treating insomnia have not been thoroughly studied Walsh et al.

Sleep disturbances are common features of psychiatric disorders. The most frequent types of sleep disturbances are insomnia, excessive daytime sleepiness hypersomnia , and parasomnia. Sleep disturbances are so commonly seen as symptoms of certain psychiatric disorders that they are listed as diagnostic criteria under DSM-IV APA, For example, insomnia is a symptom used with others to diagnose major depression.

The comorbidity, or coexistence, of a full-blown sleep disorder particularly insomnia and hypersomnia with a psychiatric disorder is also common. Forty percent of those diagnosed with insomnia, in a population-based study, also have a psychiatric disorder Ford and Kamerow, Among those diagnosed with hypersomnia, the prevalence of a psychiatric disorder is somewhat higher— The reasons behind the comorbidity of sleep and psychiatric disorders are not well understood.

Comorbidity might be due to one disorder being a risk factor or cause of the other; they might both be manifestations of the same or overlapping physiological disturbance; one might be a consequence of the other. In some cases, the sleep disturbance can be both cause and consequence.

In generalized anxiety disorder, for example, the symptoms of fatigue and irritability used to diagnose it are often the result of a sleep disturbance, which itself is also a diagnostic symptom. Adolescents with major depressive disorders report higher rates of sleep problems and, conversely, those with sleep difficulties report increased negative mood or mood regulation Ryan et al.

In addition, sleep-onset abnormalities during adolescence have been associated with an increased risk of depression in later life Rao et al. The best studied and most prevalent comorbidity is insomnia with major depression.

Insomnia as a symptom of depression is highly common. On the basis of longitudinal studies, insomnia is now established as a risk factor for major depression. Not all people with insomnia have a depression diagnosis; however, studies have found that 15 to 20 percent of people diagnosed with insomnia have major depression Ford and Kamerow, ; Breslau et al.

Depressed individuals have certain abnormalities detected by polysomnography. One is shorter rapid eye movement REM latency a shorter period of time elapsing from onset of sleep to onset of REM sleep , an effect that persists even after treatment for depression. Other abnormalities include shortened initial REM period, increased REM density, and slow-wave deficits Benca, a.

Shorter REM latency and slow-wave sleep SWS deficits tend to run in families; these abnormalities are also found in first-degree relatives of people with major depression, but who are unaffected by depression Giles et al.

A variety of polysomnographic abnormalities have been found with other psychiatric disorders Benca, a. The etiological basis for the comorbidity of sleep disorders and psychiatric disorders is not well understood. Most potential mechanisms for sleep changes in psychiatric disorders deal specifically with insomnia and depression.

Possible mechanisms include neurotransmitter imbalance cholinergic-aminergic imbalance , circadian phase advance, and hypothalamic-pituitary-adrenal axis dysregulation Benca, a.

Recent evidence implicating regions of the frontal lobe has emerged from imaging studies using positron emission tomography. As they progress from waking to non- REM NREM sleep, depressed subjects have smaller decreases in relative metabolism in regions of the frontal, parietal, and temporal cortex when compared to individuals who are healthy Nofzinger et al.

Normally, the transition from waking to NREM sleep is associated with decreases in these frontal lobe regions.

What appears to occur with depression is that the decrease is less pronounced. Because the amygdala also plays a role in sleep regulation Jones, , this finding suggests that sleep and mood disorders may be manifestations of dysregulation in overlapping neurocircuits.

The authors hypothesize that increased metabolism in emotional pathways with depression may increase emotional arousal and thereby adversely affect sleep Nofzinger et al.

A major problem is underdiagnosis and undertreatment of one or both of the comorbid disorders. One of the disorders may be missed or may be mistakenly dismissed as a condition that will recede once the other is treated. In the case of depression, for example, sleep abnormalities may continue once the depression episode has remitted Fava, If untreated, residual insomnia is a risk factor for depression recurrence Reynolds et al.

Further, because sleep and psychiatric disorders, by themselves, are disabling, the treatment of the comorbidity may reduce needless disability. Insomnia , for example, worsens outcomes in depression, schizophrenia, and alcohol dependence. Another concern is that medication for one disorder might exacerbate the other e.

The choice of medica tion for psychiatric disorder or vice versa should be influenced by the nature of the sleep complaint e. As mentioned above insomnia is associated with depression, acting as both a risk factor and a manifestation Ford and Kamerow, ; Livingston et al.

Several studies done were longitudinal in design, including one that tracked more than 1, male physicians for 40 years Chang et al.

Another study, which followed 1, young adults at a health maintenance organization for 3. This figure is based on 16 percent of the sample who developed depression with a history of insomnia at baseline, as compared with 4.

Insomnia is also a predictor of acute suicide among patients with mood disorders Fawcett et al. Incidence of psychiatric disorders during 3. SOURCE: Breslau et al. The striking association between insomnia and depression in so many studies suggests that insomnia is also an early marker for the onset of depression, and the two may be linked by a common pathophysiology.

One hypothesis is that common pathways are the amygdala and other limbic structures of the brain Nofzinger et al. Another hypothesis is that chronic insomnia increases activity of the hypothalamic-pituitary-adrenal axis, which in turn contributes to depression Perlis et al.

The close association of insomnia and depression also raises the tantalizing possibility that treating insomnia may prevent some cases of depression Riemann and Voderholzer, , but limited data are available. The biological basis for the relationship between insomnia and new onset psychiatric disorders other than depression is also not known.

Narcolepsy and idiopathic hypersomnia are characterized by a clinically significant complaint of excessive daytime sleepiness that is neither explained by a circadian sleep disorder, sleep-disordered breathing, or sleep deprivation, nor is it caused by a medical condition disturbing sleep AASM, The diagnosis of narcolepsy and hypersomnia is based principally on the Multiple Sleep Latency Test MSLT , which objectively quantifies daytime sleepiness Box Carskadon et al.

Sleep logs or actigraphy a movement detector coupled with software that uses movement patterns to provide estimate sleep and wake times can also be used to exclude chronic sleep deprivation as a diagnosis prior to the MSLT. In many cases narcolepsy arises during the mid to late teenage years; however, frequently initial diagnosis is not correct, resulting in delays in diagnosis of 15 to 25 years after the onset of symptoms Broughton et al.

Onset of narcolepsy can also have a negative impact on school performance see Chapter 4. Narcolepsy is associated with a number of symptoms Anic-Labat et al.

Clinical Laboratory Findings in Narcolepsy and Hypersomnia. The Multiple Sleep Latency Test MSLT objectively quantifies daytime sleepiness.

It consists of five 20 minute daytime naps at 2-hour intervals. The amount of time it takes to fall asleep sleep more Narcolepsy can be diagnosed clinically, by using the MSLT , or by measuring cerebrospinal fluid CSF hypocretin-1 Box Idiopathic hypersomnia is classically separated into two subtypes.

The first, idiopathic hypersomnia with prolonged sleep time, is a rare disorder and is characterized by the following:. The second subtype of idiopathic hypersomnia, idiopathic hypersomnia without long sleep time, is characterized by a complaint of excessive daytime sleepiness and a short mean sleep latency on the MSLT.

In most sleep disorders clinics with experience in this area, approximately one-third of hypersomnia cases are diagnosed with this condition Aldrich, The prevalence is estimated to be around 0. In contrast, the prevalence of idiopathic hypersomnia without prolonged sleep time may be more substantial, as most patients are likely not diagnosed Arand et al.

Recurrent hypersomnia is periodic either in synchrony with menstruation menstruation-linked periodic hypersomnia or without any association and mostly in males with Klein-Levin syndrome Billiard and Cadilhac, ; Arnulf et al.

Klein-Levin syndrome is characterized by recurrent episodes of dramatic hypersomnia lasting from 2 days to several weeks. These episodes are associated with behavioral and cognitive abnormalities, binge eating or hypersexuality, and alternate with long asymptomatic periods that last months or years Arnulf et al.

Narcolepsy and hypersomnia can affect children, adolescents, adults, and older persons. In most cases these disorders begin in adolescence. The prevalence of narcolepsy with definite cataplexy has been documented in adults by numerous population-based studies and occurs in 0.

In contrast, very little is known about the prevalence of narcolepsy without cataplexy. Recent studies using the MSLT indicate that approximately 3. Secondary cases of narcolepsy or hypersomnia are also common, but the overall prevalence is not known Table International Classification of Sleep Disorders: Definitions, Prevalence, and Pathophysiology of Narcolepsy and Hypersomnias.

Similar to other sleep disorders, little is known about the pathophysiology and risk factors for narcolepsy and hypersomnia. Most of the knowledge in this area pertains to narcolepsy with cataplexy, which affects males and females equally.

Symptoms usually arise during adolescence. Approximately 70, hypothalamic neurons that are responsible for producing the neuropeptide hypocretin orexin are lost in individuals with narcolepsy with cataplexy Thannickal et al. Hypocretin is an excitatory neuropeptide that regulates the activity of other sleep regulatory networks.

Consequently, in some cases low levels of hypocretin-1 in the CSF , may be used to diagnose narcolepsy Kanbayashi et al. Less is known regarding the pathophysiology of narcolepsy without cataplexy.

The etiology is likely heterogeneous. An unknown portion may be caused by partial or complete hypocretin deficiency Kanbayashi et al. However, it has been hypothesized that some individuals with partial cell loss may have normal CSF hypocretin-1 Mignot et al. The pathophysiology of idiopathic hypersomnia is unknown.

When the disorder is associated with prolonged sleep time, it typically starts during adolescence and is lifelong. It is essential to exclude secondary causes, such as head trauma or hypersomnia owing to depression Roth, ; Billiard and Dauvilliers, Some cases with prolonged sleep times have been reported to be familial, suggesting a genetic origin.

Even less is known about idiopathic hypersomnia with normal sleep time. This condition is more variable and symptomatically defined. The cause of Kleine-Levin syndrome is unknown Arnulf et al. Treatment for these conditions is symptomatically based.

Even in the case of narcolepsy in which the disorder is caused by hypocretin deficiency, current treatment does not aim at improving the defective neurotransmission Mignot et al.

Behavioral measures, such as napping, support groups, and work arrangements are helpful but rarely sufficient. In most cases, pharmacological treatment is needed Nishino and Mignot, ; Lammers and Overeem, However, as with other pharmaceuticals designed to treat sleep problems, large-scale clinical trails have not examined the efficacy and safety of drugs to treat narcolepsy in children and adolescents.

In narcolepsy with cataplexy, pharmacological treatment for daytime sleepiness involves modafinil or amphetamine-like stimulants, which likely act through increasing dopamine transmission.

Cataplexy and abnormal REM sleep symptoms, sleep paralysis and hallucinations, are typically treated with tricyclic antidepressants or serotonin and norepinephrine reuptake inhibitors.

Adrenergic reuptake inhibition is believed to be the primary mode of action. Sodium oxybate, or gamma hydroxybutyric acid, is also used at night to consolidate disturbed nocturnal sleep.

This treatment is also effective on cataplexy and other symptoms. The treatment of narcolepsy without cataplexy and idiopathic hypersomnia uses similar compounds, most notably modafinil and amphetamine-like stimulants Billiard and Dauvilliers, Treatments, with the possible exception of lithium, of periodic hypersomnia and Kleine-Levin syndrome type are typically ineffective Arnulf et al.

Parasomnias are unpleasant or undesirable behaviors or experiences that occur during entry into sleep, during sleep, or during arousals from sleep AASM, They are categorized as primary parasomnias, which predominantly occur during the sleep state, and secondary parasomnias, which are complications associated with disorders of organ systems that occur during sleep.

Primary parasomnias can further be classified depending on which sleep state they originate in, REM sleep, NREM , or others that can occur during either state Table Parasomnias typically manifest themselves during transition periods from one state of sleep to another, during which time the brain activity is reorganizing Mahowald and Schenck, Activities associated with parasomnias are characterized by being potentially violent or injurious, disruptive to other household members, resulting in excessive daytime sleepiness, or associated with medical, psychiatric, or neurological conditions Mahowald and Ettinger, Disorders of arousal are the most common type of parasomnia, occurring in as much as 4 percent of the adult population Ohayon et al.

Typically the arousals occur during the first 60 to 90 minutes of sleep and do not cause full awakenings, but rather partial arousal from deep NREM sleep. Disorders of arousal manifest in a variety of ways, from barely audible mumbling, disoriented sleepwalking, to frantic bouts of shrieking and flailing of limbs Wills and Garcia, Individuals who experience confusional arousals exhibit confused mental and behavioral activity following arousals from sleep.

They are often disoriented in time and space, display slow speech, and blunted answers to questions AASM, Episodes of resistive and even violent behavior can last several minutes to hours. Confusional arousals are more than three to four times more prevalent in children compared to individuals 15 years or older around 3 percent Ohayon et al.

Sleepwalking is characterized by a complex series of behaviors that culminate in walking around with an altered state of consciousness and impaired judgment AASM, Individuals who are sleepwalking commonly perform routine and nonroutine behaviors at inappropriate times and have difficulty recalling episodic events.

Like confusional arousals, the prevalence of sleepwalking is higher in children than adults AASM, There appears to be a genetic predisposition for sleepwalking. Children who have both parents affected by sleepwalking are 38 percent more likely to also be affected Klackenberg, ; Hublin et al.

Sleep terrors are characterized by arousal from SWS accompanied by a cry or piercing scream, in addition to autonomic nervous system and behavioral manifestations of intense fear AASM, Individuals with sleep terrors are typically hard to arouse from sleep and, when they are awoken, are confused and disoriented.

There does not appear to be a significant gender or age difference in prevalence or incidence of sleep terrors AASM, REM sleep behavior disorder is characterized by a complex set of behaviors that occur during REM sleep, including mild to harmful body movements associated with dreams and nightmares AASM, The overall prevalence in the general population is estimated to be less than half a percent, slightly higher in older persons AASM, , and affecting men more frequently than women.

REM sleep behavior disorder is frequently associated with neurological disorders and it has been suggested that it could be an early sign of neurodegeneration Olson et al.

There are a number of effective pharmacological treatments, including a long-acting benzodiazepine Schenck and Mahowald, , clonazepam Schenck et al. Nightmare disorder is characterized by recurrent disturbances of dreaming that are disturbing mental experiences that seem real and sometimes cause the individual to wake up.

If awoken, individuals commonly have difficulty returning to sleep. Nightmares often occur during the second half of a normal period of sleep. Dream content involves a distressing theme, typically imminent physical danger. During nightmares, individuals experience increased heart and respiration rates Fisher et al.

Nightmares commonly affect children and adolescents and decrease in frequency and intensity as an individual grows older AASM, Drugs and alcohol can trigger nightmares.

Prevalence rates are also higher in individuals suffering from acute stress disorder and posttraumatic stress disorder.

Individuals suffering from dementia commonly experience sleep abnormalities. Typically, sleep is more fragmented, leading to more awakenings and consequently less time asleep, and REM may be decreased Petit et al. These sleep impairments usually worsen as the disease progresses.

Approximately one-quarter of these individuals have sleep disturbances Tractenberg et al. As a result of an increase in duration and number of awakenings, individuals spend an increased percentage of time in stage 1 sleep and a reduced percentage in stage 2 and SWS Prinz et al.

Associations with sleep disturbance and other behavioral symptoms have been identified, including aggressiveness Moran et al. However, the pathophysiology of this association is not known. Treatment options for demented individuals who suffer sleep disorders are typically the same as those received by individuals who do not have dementia.

The approach is to address the sleep disorder based on its symptoms while managing and treating the underlying medical or psychiatric disorder Petit et al.

It is characterized by trouble initiating walking and other movements, muscle tremor, a slow gait, and reduced facial expressions. During the day, many Parkinson patients have excessive sleepiness. Sleep disturbances typically increase with disease progression.

Individuals suffer from increased sleep latency and frequent awakenings, spending as much as 30 to 40 percent of the night awake Kales et al. This causes reduced time spent in stages 3 and 4 and REM sleep and increased duration in stages 1 and 2 Kales et al.

Sleep patterns are affected by abnormalities caused by neurodegeneration in regions of the brain that are involved in regulating the sleep-wake cycle.

Dopaminergic neurons in the substantia nigra are dramatically reduced in number, as are noradrenerics neurons in the locus coeruleus Jellinger, and cholinergic neurons in the pedunculopontine nucleus Zweig et al.

Braak and colleagues examined a large series of autopsy brains. The ability to ameliorate the symptoms of REM sleep behavioral disorder with dopaminergic agonist drugs suggests that it may be an early sign of damage to the dopaminergic system Trampus et al.

When used in low doses, these medications can promote sleep, but high doses may cause increased nocturnal wakefulness, decreased SWS , and decreased sleep continuity Leeman et al.

In contrast, excessive daytime sleepiness, including sleep attacks, has also been described in association with dopamine agonists Paus et al. All may potentially affect sleep Chrisp et al.

Epilepsy refers to a group of various disorders characterized by abnormal electrical activity in the brain that manifests itself in individuals as a loss of or impaired consciousness and abnormal movements and behaviors.

Sleep, sleep deprivation, and seizure activity are tightly intertwined. It is estimated that sleep-related epilepsy may affect as many as 10 percent or more of epileptic individuals AASM, Sixty percent of individuals who suffer partial complex localization related seizures— Similarly, sleep and sleep deprivation increase the incidence of seizure activity.

Sleep-related epilepsy normally presents with at least two of the following features: arousals, abrupt awakenings from sleep, generalized tonic-clonic movements of the limbs, focal limb movement, facial twitching, urinary incontinence, apnea, tongue biting, and postictal confusion and lethargy AASM, These features cause sleep fragmentation and daytime fatigue.

There are a number of common epileptic syndromes that manifest solely or predominately during the night, including nocturnal frontal lobe epilepsy, benign epilepsy of childhood with centrotemporal spikes, early-onset or late-onset childhood occipital epilepsy, juvenile myoclonic epilepsy, and continuous spike waves during non- REM sleep.

Nocturnal frontal lobe epilepsy is characterized by severe sleep disruption, injuries caused by involuntary movements, and occasional daytime seizures.

Juvenile myoclonic epilepsy is characterized by synchronous involuntary muscle contractions that often occur during awakening. Continuous spike waves during non-REM sleep epilepsy are commonly associated with neurocognitive impairment and sometimes with impairment of muscle activity and control.

Risk factors for sleep-related epilepsy include stress, sleep deprivation, other sleep disorders, and irregular sleep-wake rhythms. The etiologies for nocturnal seizures are not clearly understood. Genetic factors are likely important; however, as of yet no pathogenic markers have been associated with sleep-related epilepsy.

There are specific patterns of rhythmic activity among neurons within specific regions of the brain—the hypothalamus and brainstem—that regulate sleep and arousal. Association of specific neuronal activity between these different regions is important for regulating sleep, while bursts of disassociated neuronal activity may contribute to nocturnal seizures Tassinari et al.

Treatments for seizures caused by sleep-related epileptic syndromes are typically similar to those of other seizure disorders Dreifuss and Porter, Individuals with epilepsy are susceptible to nocturnal sleep disturbance and daytime sleepiness associated with commonly used medications.

However, daytime hypersomnolence is not always treatable with antiepileptic drugs Palm et al. In particular, phenobarbital, a mainstay of treatment for many years, causes daytime sedation in a dose depen dent manner Brodie and Dichter, Daytime sedation is also observed with other antiepileptic agents including carbamazepine, alproate, phenytoin, and primidone.

Some of the newer medication such as gabapentin, lamotrigine, bigabatrin, and zonisamide are often better tolerated Salinsky et al. In addition to daytime sedation, these drugs also cause increased nocturnal sleep time. Vagal nerve stimulation, however, has been reported to improve daytime alertness Rizzo et al.

Stroke results in a sudden loss of consciousness, sensation, and voluntary movement caused by disruption of blood flow—and therefore oxygen supply—to the brain. Insomnia is a common complication of stroke that may result from medication, inactivity, stress, depression, and brain damage.

The annual incidence of stroke is 2 to 18 per individuals, and sleep-wake disturbances are found in at least 20 percent of stroke patients Bassetti, In addition, over 70 percent of individuals who have suffered a mild stroke and are under 75 years of age suffer fatigue Carlsson et al.

Risk factors for stroke include heart disease, hypertension, alcohol abuse, transient ischemic attacks, and, as described above, possibly sleep-disordered breathing Diaz and Sempere, Studies investigating the association between sleep-disordered breathing and stroke found that 60 to 70 percent of individuals who have suffered a stroke exhibit sleep-disordered breathing with an apnea-hypopnea index of 10 or greater Dyken et al.

Sleep-disordered breathing has also been found in a high frequency of individuals with transient ischemic attacks McArdle et al. Circadian rhythm disorders - problems with the sleep-wake cycle. They make you unable to sleep and wake at the right times.

Parasomnia - acting in unusual ways while falling asleep, sleeping, or waking from sleep, such as walking, talking, or eating Some people who feel tired during the day have a true sleep disorder. What causes sleep disorders? There are different causes for different sleep disorders, including: Other conditions, such as heart disease , lung disease , nerve disorders , and pain Mental illnesses , including depression and anxiety Medicines Genetics Sometimes the cause is unknown.

There are also some factors that can contribute to sleep problems, including: Caffeine and alcohol An irregular schedule, such as working the night shift Aging. As people age, they often get less sleep or spend less time in the deep, restful stage of sleep.

They are also more easily awakened. What are the symptoms of sleep disorders? Some signs that you may have a sleep disorder include that: You regularly take more than 30 minutes each night to fall asleep You regularly wake up several times each night and then have trouble falling back to sleep, or you wake up too early in the morning You often feel sleepy during the day, take frequent naps, or fall asleep at the wrong times during the day Your bed partner says that when you sleep, you snore loudly, snort, gasp, make choking sounds, or stop breathing for short periods You have creeping, tingling, or crawling feelings in your legs or arms that are relieved by moving or massaging them, especially in the evening and when trying to fall asleep Your bed partner notices that your legs or arms jerk often during sleep You have vivid, dreamlike experiences while falling asleep or dozing You have episodes of sudden muscle weakness when you are angry or fearful, or when you laugh You feel as though you cannot move when you first wake up How are sleep disorders diagnosed?

The data includes: Brain wave changes Eye movements Breathing rate Blood pressure Heart rate and electrical activity of the heart and other muscles Other types of sleep studies may check how quickly you fall asleep during daytime naps or whether you are able to stay awake and alert during the day.

What are the treatments for sleep disorders? Treatments for sleep disorders depend on which disorder you have. They may include: Good sleep habits and other lifestyle changes, such as a healthy diet and exercise Cognitive behavioral therapy or relaxation techniques to reduce anxiety about getting enough sleep CPAP continuous positive airway pressure machine for sleep apnea Bright light therapy in the morning Medicines, including sleeping pills.

Usually, providers recommend that you use sleeping pills for a short period of time. Natural products, such as melatonin. These products may help some people but are generally for short-term use. Make sure to check with your health care provider before you take any of them.

Start Here. About Sleep Eunice Kennedy Shriver National Institute of Child Health and Human Development Also in Spanish Brain Basics: Understanding Sleep National Institute of Neurological Disorders and Stroke Also in Spanish What Are Sleep Deprivation and Deficiency?

National Heart, Lung, and Blood Institute Also in Spanish. Diagnosis and Tests. Sleep Studies National Heart, Lung, and Blood Institute Also in Spanish Sleep Study National Library of Medicine Also in Spanish. Treatments and Therapies. Melatonin American Academy of Family Physicians Also in Spanish Sleep Disorder Treatments National Heart, Lung, and Blood Institute Also in Spanish Sleep Disorders: In Depth National Center for Complementary and Integrative Health Sleep Education: Sleep Studies and Tests, Treatment, and Support American Academy of Sleep Medicine.

Related Issues. Jet Lag Disorder Mayo Foundation for Medical Education and Research Also in Spanish Kleine-Levin Syndrome National Institute of Neurological Disorders and Stroke Learn about Sleep Disorders American Academy of Sleep Medicine Narcolepsy National Heart, Lung, and Blood Institute Also in Spanish Narcolepsy National Institute of Neurological Disorders and Stroke Sleep Talking Somniloquy American Academy of Sleep Medicine Sleep Terrors Night Terrors Mayo Foundation for Medical Education and Research Also in Spanish Sleepwalking Mayo Foundation for Medical Education and Research Wake Up and Get Some Sleep: Improve the Quality of Your Sleep and Life as a Shift Worker National Highway Traffic Safety Administration What Are Circadian Rhythm Disorders?

Narcolepsy: MedlinePlus Genetics National Library of Medicine. Statistics and Research.