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Assessment is the initial step in management strategies. Assessment data should include documentation of predisposing factors, sleep patterns, emotional status, exercise and activity levels, diet, symptoms, medications, and caregiver routines. The diagnosis of insomnia is primarily based on a careful, detailed medical and psychiatric history. The American Academy of Sleep Medicine has produced guidelines for the use of polysomnography as an objective tool in evaluating insomnia. The routine polysomnogram includes the monitoring of electroencephalography, electro-oculography, electromyography, effort of breathing and air flow, oxygen saturation, electrocardiography, and body position.

Polysomnography is the major diagnostic tool in sleep disorders and is indicated in the evaluation of suspected sleep-related breathing disorders and periodic limb movement disorder, and when the cause of insomnia is uncertain or when behavioral or pharmacologic therapy is unsuccessful. One descriptive study [ 6 ] [Level of evidence: II] involving women with breast cancer used the General Sleep Disturbance Scale GSDS to identify three different sleep trajectories when self-reported sleep was evaluated beginning before surgery and continuing for 6 months.

Women in the group who were identified as having a more severe sleep disorder were significantly younger, had more comorbidities, had a lower performance status, and experienced hot flashes. Management of sleep disturbances should focus on treatment of problems with falling asleep, staying asleep, or early morning awakenings.

Other areas to manage include symptoms from cancer and its treatment, and the identification and management of environmental and psychological factors. When sleep disturbances are caused by symptoms of cancer or treatment, measures that control or alleviate symptoms are often the key to resolving sleep disturbances. Management of sleep disturbances combines nonpharmacologic and pharmacologic approaches individualized for the patient.

Many people who experience insomnia have been found to practice poor sleep hygiene such as smoking and drinking excessive alcohol just before bedtime , which can exacerbate or perpetuate insomnia. Sleep hygiene in an inpatient setting involves modifying the sleep environment to decrease sleep disruption. Minimizing noise, dimming or turning off lights, adjusting room temperature, and consolidating patient care tasks to reduce the number of interruptions can increase the amount of uninterrupted sleep.

Cognitive strategies include restructuring negative thoughts, beliefs, and attitudes related to sleep and preventing excessive monitoring or worrying about getting enough sleep. Both of these strategies seek to limit the time spent in bed that does not involve sleeping. Components of CBT-I include the following:. Relaxation therapy can be used to achieve both behavioral and cognitive outcomes, particularly when it is combined with imagery.

Educational objectives around sleep hygiene are also used to treat insomnia and include content on the following:[ 4 ]. Practice guidelines from the American Academy of Sleep Medicine clearly state that multicomponent therapy is recommended over single therapies. Because of insufficient evidence about its efficacy, sleep hygiene education should not be recommended as a single-modality management approach; other reviews state that sleep hygiene by itself is not effective.

Several trials and meta-analyses have shown CBT-I to be at least as effective as conventional pharmacological therapies in treating primary chronic insomnia but without side effects. A meta-analysis examining pharmacologic and behavioral studies for persistent insomnia found that pharmacologic and behavioral treatments did not differ in magnitude of benefit except for latency to sleep onset, in which greater reductions were found with behavioral therapy.

There are limited data evaluating elements of CBT-I in cancer survivors, and most of the data that exist are about women with breast cancer. However, there have been at least four randomized controlled trials of CBT-I in cancer survivors. One of these trials included patients with cancer diagnoses other than breast cancer,[ 16 ] and results did not differ by cancer diagnosis.

All studies showed improvements in numerous sleep parameters over time in the groups receiving CBT-I and demonstrated continued benefits 6 and 12 months later. Two of the four trials did not use active control arms. Studies using active control arms were in breast cancer survivors. One study compared CBT-I with sleep education and hygiene in 72 women,[ 15 ] while the other study used a healthy-eating education control group.

For example, the group receiving CBT-I improved by 30 minutes in time to fall asleep, compared with 11 minutes in the sleep education and hygiene group. In the study utilizing the healthy-eating education control, women were randomly assigned to a behavioral therapy group consisting of stimulus control, general sleep hygiene limiting naps, going to bed and rising at consistent times , and relaxation or to a healthy-eating education control group.

The interventions were delivered by trained nurses in person, 2 days before the initiation of chemotherapy and before each chemotherapy treatment and 30 days after the last chemotherapy treatment. The nurses worked with women assigned to behavioral therapy to individualize and reinforce the behaviors. Sleep quality significantly improved in the group receiving behavioral therapy, compared with the control group. These differences were also seen in data from the sleep diary and actigraph, with both showing significantly fewer awakenings in the behavioral therapy group.

In some places, patients may not have access to in-person, professionally delivered CBT-I because of limited resources. A randomized controlled trial conducted with breast cancer survivors demonstrated that CBT-I delivered via digital media can also produce meaningful clinical improvements, although improvements are not as robust as those produced with professionally delivered CBT-I. CBT delivered by psychologists has shown promise for the treatment of insomnia in patients with cancer.

Primary outcomes were sleep diary measures at baseline, posttreatment, and at 6-month follow-up. CBT was associated with significant and sustained improvements in several sleep aspects. These improvements were seen for both subjective sleep diary and objective actigraphy assessments. Additionally, CBT patients showed significant improvements in fatigue, anxiety, and depressive symptoms and reported improved quality of life, compared with patients who received treatment as usual.

A study conducted in cancer survivors demonstrated the benefits of a specialized yoga program to improve sleep quality and reduce medication use. A total of cancer survivors with moderate to severe sleep disturbances were randomly assigned to receive standard care or standard care plus a 4-week yoga intervention delivered in two weekly sessions by trained yoga instructors. The yoga participants showed significant improvement in sleep quality, daytime dysfunction, nighttime awakening, and sleep efficiency, compared with standard-care participants.

SLEEP LOSS

Two major limitations of this study were its limited population generalizability, as most study participants were female, white, married, and well-educated breast cancer survivors; and the lack of an adequate control group with respect to nonspecific effects such as group support and attention. Other actions or interventions that may promote rest in the hospital or extended-care setting include the following:[ 21 , 22 ].

Psychological interventions are directed toward facilitating the patient's coping processes through education, support, and reassurance. As the patient learns to cope with the stresses of illness, hospitalization, and treatment, sleep may improve. Relaxation exercises and self-hypnosis performed at bedtime can help promote calm and sleep. When cancer survivors experience sleep-wake disturbances, cognitive behavioral intervention counseling should be the first consideration for management. Refer to the Nonpharmacologic Management of Sleep Disturbances section of this summary for more information.


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It is acknowledged that resources for education and training in CBT may not be readily available in many cancer centers, and therefore community resources need to be investigated. In areas where CBT is not available or has been utilized but has not been successful, pharmacologic management can be considered. In addition, when patients have comorbidities contributing to sleep-wake cycle disturbances such as hot flashes, uncontrolled pain, anxiety, depression, or other mood disturbances ,[ 25 , 26 ] then pharmacologic management will probably be necessary.

Despite the lack of evidence in cancer populations, pharmacologic interventions are widely used by clinicians. Therefore, the following discussion of pharmacologic agents and recommendations for use is based on evidence from studies conducted in patients with primary insomnia and clinical experience. Several classes of medications are used to treat sleep-wake cycle disturbances:.

Drug characteristics that should be taken into account before a drug is chosen to treat an individual patient include the following:. These pharmacokinetic principles are important for the matching of agents to the type of sleep disturbance e. There are also safety issues to be considered, such as potentials for tolerance, abuse, dependence, withdrawal including risk of rebound insomnia , and drug-drug and drug-disease interactions.

Medications used to induce sleep are intended for the short-term management of sleep disorders. The use of these medications for longer periods is poorly studied. They are usually combined with lifestyle changes that will reinforce good sleep habits and negate the need for chronic hypnotic medications. Most research studies of current and historic hypnotic medications rarely exceed a duration of 12 to 16 weeks of study.

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Additionally, none of the current hypnotics re-create normal sleep architecture, and variations from normal periods of rapid eye movement REM sleep and non-REM sleep are common. It is important to taper hypnotic medications slowly, or the variations in normal sleep patterns can become even more pronounced, with the majority of time spent in REM sleep in a condition known as REM rebound. Table 2 lists the drug categories and specific medications, including doses, commonly used within those categories. All agents in this class are FDA approved for primary insomnia.

Unlike traditional benzodiazepines e. Zolpidem and zaleplon bind predominantly to the alpha-1 subtype of GABAA, and eszopiclone preferentially targets the alpha-3 receptor subtype. This selective receptor subtype targeting has both advantages and disadvantages. Conversely, because of the selective receptor subtype targeting, these agents have fewer effects on cognitive, psychomotor function and carry less risk of tolerance, dependence, and withdrawal especially physical withdrawal than do benzodiazepines. These agents may be preferred for use in patients with cancer, when only hypnotic effects are desired, and should be taken just before bedtime or even in bed because they enter the brain very quickly; some of these agents e.

Because of their longer-lasting effects, zolpidem extended-release and eszopiclone are preferred in the treatment of difficulties in staying asleep. Benzodiazepines are preferred when other effects such as antianxiety or muscle relaxant effects are desirable with or without the hypnotic effects. Benzodiazepines carry a much higher risk of tolerance, dependence, and withdrawal than do the nonbenzodiazepine receptor agonists.

Benzodiazepine withdrawal has been associated with the risk of seizures, delirium tremens , autonomic instability, and death. These agents should be used with extreme caution and with close monitoring in patients with histories of significant substance use because these patients are vulnerable to tolerance and dependence issues.

Disease Concept, Prevalence and Clinical Correlates of the REM Sleep Behavior Disorder

Benzodiazepines have also been associated with cognitive impairment and difficulties with motor coordination. Generally, benzodiazepines with longer half-lives e. Agents with shorter elimination half-lives e. Agents with longer half-lives e. All benzodiazepines are associated with risk of respiratory depression and should be used with caution in patients with preexisting respiratory disorders.

Ramelteon and tasimelteon work by binding to the melatonin receptor types MT1 and MT2. Ramelteon is useful only for the treatment of difficulties falling asleep and does not have any other effects, such as anxiolytic or myorelaxant effects, while tasimelteon is indicated for use in circadian sleep disorder. Diphenhydramine and hydroxyzine decrease arousal by blockading histamine receptors. Antihistamines are sold over the counter and are useful for treating difficulties in falling asleep only. There is limited evidence for the use of antihistamines to treat insomnia; these agents are used when traditional hypnotics or benzodiazepines are less suitable because of the risk of cross-dependence or other issues, such as vulnerability of a patient to addictions.

The anticholinergic properties of antihistamines may also be beneficial in the treatment of nausea and vomiting. The sedative and anticholinergic properties of these agents increase the risk of delirium, especially in older patients. These drugs include tricyclic antidepressants e. The sedating effects of tricyclic antidepressants are caused mainly by histamine receptor blockading and partially by blockading of 5-HT2 and muscarinic receptors. The sedating effects of mirtazapine are caused by its blocking of 5-HT2 and histamine receptors, while those of trazodone are caused by its blocking actions at the at histamine, 5-HT, and noradrenaline receptors.

Tricyclic antidepressants have a small therapeutic window and can be lethal in overdose, compared with second-generation antidepressants such as mirtazapine. Additionally, tricyclics carry other risks, such as risk of weight gain, anticholinergic side effects, and cardiovascular side effects and should be used under close supervision. This helps to avoid the side effects associated with higher doses while delivering the needed sedating effects. Tricyclics can also boost appetite and may be the treatment of choice for insomnia in patients with comorbid cachexia.

Certain tricyclics amitriptyline and nortriptyline can also be beneficial in the treatment of pain syndromes e. Low doses of antidepressants subtherapeutic for depression are frequently used to treat insomnia without any comorbidities. Mirtazapine, a second-generation antidepressant, also has appetite-stimulating and antiemetic properties in addition to sedating effects.

It is frequently used in insomniac patients with depression therapeutic dose for depression, 15—45 mg or without depression subtherapeutic doses for depression, 7. In low doses, trazodone 50— mg can promote sleep and is often combined with other antidepressants e. Antipsychotics such as quetiapine have sedating effects caused mainly by the blockade of histamine receptors. However, these agents should be considered as a last resort and as a short-term treatment because of their serious side-effect profile.

The use of antipsychotics has been associated with weight gain, metabolic syndrome, diabetes, cardiovascular risks, and the risk of extrapyramidal side effects, including tardive dyskinesia. Antipsychotics can be considered for treatment-refractory insomnia, especially with comorbid anxiety symptomatology. Chloral hydrate has sleep-promoting effects resulting from its effects on GABA systems.

It is associated with risk of withdrawal symptoms similar to those of benzodiazepines and is associated with rapid development of tolerance. Additionally, chloral hydrate carries the risk of gastric irritation and multiple drug-drug interactions, and it is lethal in overdose. Like antipsychotics, chloral hydrate is usually considered only in cases of treatment-refractory insomnia because of its serious side-effect profile and the availability of safer alternatives. Melatonin, a hormone produced by the pineal gland during the hours of darkness, plays a major role in the sleep-wake cycle and has been linked to the circadian rhythm.

However, these studies were not conducted in the context of cancer therapy. Evidence suggests that circulating melatonin levels are significantly lower in physically healthy older people and in insomniacs than in age-matched control subjects. In view of these findings, melatonin replacement therapy may be beneficial in the initiation and maintenance of sleep in elderly patients. However, melatonin replacement as a treatment for insomnia has not been studied in older people with cancer. Ramelteon and tasimelteon work via the melatonin receptor system: ramelteon to support the initiation of sleep, and tasimelteon to correct circadian sleep disorder.

Melatonin may interact with certain chemotherapeutic regimens via the cytochrome P enzyme and other systems. Clinical studies in renal, breast, colon, lung, and brain cancer suggest that melatonin exerts anticancer effects in conjunction with chemotherapy and radiation therapy; however, evidence remains inconclusive. Efforts by independent groups of investigators are under way to investigate these effects in carefully designed, randomized, blinded studies. No studies have been conducted to specifically evaluate the effects of Cannabis inhalation or other Cannabis products in patients with primary or secondary sleep disturbances.

Limited data from in vitro studies, animal studies, and small populations of healthy individuals or chronic Cannabis users are beginning to elucidate some of the relationships between various neurotransmitters and the sleep-wake cycle and related effects of Cannabis pharmacology. Cannabis -based medicines are under development as a treatment for chronic pain syndromes, including cancer-related pain. One such medication under investigation is nabiximols Sativex , an oromucosal formulation deltatetrahydrocannabinol and cannabidiol mixed in a ratio.

Studies conducted with nabiximols, primarily focusing on pain syndromes, have shown improvement in subjective sleep quality when sleep was measured as a secondary outcome. Concerns have been raised about the abuse and dependence potential of nabiximols, especially in the subpopulation of patients with histories of Cannabis use.

In the United States, it is only available for investigational use and is currently under investigation for the treatment of intractable cancer pain. Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available. Since enhanced pain control improves sleep, appropriate analgesics or nonpharmacologic pain management should be administered before introducing sleep medications.

Tricyclic antidepressants can be particularly useful for the treatment of insomnia in patients with neuropathic pain and depression. Patients on high-dose opioids for pain may be at increased risk for the development of delirium and organic mental disorders. Such patients may benefit from the use of low-dose neuroleptics as sleep agents e.

Evidence of the involvement of several brain stem structures mainly located in the pons, which include the ventral mesopontine junction, the pedunculopontine nucleus, the laterodorsal tegmental nucleus, the locus ceruleus LC and the peri-LC area, derives from animal models [ 50 , 51 ] and from neuropathological observations in human RBD [ 52 , 53 , 54 ]. The pedunculopontine nucleus and the LC, which represent the largest clusters of cholinergic and noradrenergic neurons within the brain stem reticular formation, respectively, are known to play a role in arousal, cortical activation and cognitive function, including attentional processes [ 55 , 56 , 57 , 58 ].

Therefore, a dysfunctioning cholinergic subcortical system might contribute to cognitive impairment and EEG slowing in iRBD patients. The fact that cholinergic activity promotes REM sleep, in which EEG slowing was observed in the studies described above [ 23 , 25 , 35 ], and that cholinergic denervation of the limbic cortex is a robust determinant of hyposmia [ 59 ], which was recognized in our study using threshold-discrimination-identification scores on Sniffin' Stick tests [ 35 ], might support this idea.

In vivo evaluation of some cholinergic circuits of the human brain has recently been introduced using a transcranial magnetic stimulation protocol that might yield information about the function of some cholinergic circuits in the human brain. This technique relies on short latency afferent inhibition SAI off the motor cortex [ 60 ]. In these patients, it can be increased by administration of acetylcholinesterase inhibitors [ 61 , 62 , 63 ].

Based on the hypothesis that cognitive performance and cortical activation in iRBD patients are associated with a dysfunctioning cholinergic system, Nardone et al. They found that mean SAI was significantly reduced in patients with iRBD compared with the controls, and that those SAI values correlated strongly with tests measuring episodic verbal memory and executive functions.

Sleep and Sleep Disorders in the Older Adult - Research on Aging

This finding also supports the hypothesis of cholinergic dysfunction in some patients with iRBD who develop cognitive impairment. Abnormalities in central cholinergic functions, as well as EEG slowing and cognitive decline in iRBD patients, might be caused either by cortical pathology or damage to the brain stem structure that regulates REM sleep and activates the neocortex [ 23 , 24 ]. Several neuropathological studies performed on iRBD patients have shown neural alterations in several brain stem nuclei i.

All of these brain stem structures have diffuse projections to the cerebral cortex, and perturbations in these neural networks might explain the presence of cognitive decline or EEG slowing. A diffusion tensor imaging study revealed microstructural changes in the white matter, particularly in the left superior temporal lobe and the right occipital lobe [ 66 ]. In addition, studies using voxel-based morphometry showed gray matter density anomalies in both hippocampi and the left parahippocampal gyrus in iRBD patients [ 67 , 68 ].

This evidence suggests that structural changes in the brain are responsible for EEG slowing and cognitive decline, although none of these studies simultaneously conducted cognitive function measurements and quantitative EEG analyses during both wakefulness and sleep. To date, few studies have examined longitudinal changes in the cognitive function of iRBD patients [ 14 , 69 , 70 ], and no conclusive information has been obtained. The scientific community interested in RBD requires further efforts to clarify this issue.

Inoue also reports an Intramural Research Grant 21B-4 for Neurological and Psychiatric Disorders from the National Center of Neurology and Psychiatry, but there is no conflict of interest for this study. Hirata and Dr. Sasai report no conflicts requiring disclosure. Distribution permitted for non-commercial purposes only.

Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions.

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Forgot your password? Institutional Login Shibboleth or OpenAthens For the academic login, please select your organization on the next page. Forgot Password? 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.

There are no specific therapies that relieve sleep-related symptoms caused by a stroke. Rather, treatments depend on the specific symptoms and are similar to the treatments of sleep disorders that arise indepen dent of a stroke. For example, CPAP is the treatment of choice for sleep disordered breathing, and insomnia and parasomnias are treated using similar temporary hypnotic drug therapies as typically used, zolpidem or benzo-diazepines.

However, treatments for hypersomnia are not always as effective following a stroke Bassetti, The syndrome is currently the third most common cause of infant death in the United States CDC, , responsible for approximately 3, infant deaths a year in this country NICHD, b. Although there are no known causes for SIDS , various hypotheses exist about the mechanisms underlying the syndrome. Infants who later die of SIDS have higher heart rates, narrower heart rate ranges, and problems with coordination of respiration, heart rate, and arterial blood pressure while sleeping Kemp and Thach, ; Schechtman et al.

This lack of coordination in the cardiorespiratory system may be a result of defects in the region of the brain responsible for controlling breathing and arousal Kinney et al. The chief risk factor for SIDS is a prone sleeping position, otherwise known as stomach sleeping Dwyer et al. Vulnerability to SIDS seems to depend on both gender and ethnicity. Finally, general measures of poor health form the final category of risk factors.

Smoking, drinking, or drug use by the mother during gestation are linked to an increased chance of SIDS -related deaths in infants, as is infant exposure to smoke Schoendorf and Kiely, ; AAP, ; Iyasu et al. A number of national intervention programs currently exist through various organizations. RLS is a neurological condition characterized by an irresistible urge to move the legs it also may affect the arms, trunk, or head and neck.

It is also associated with paresthesias—uncomfortable feelings—which individuals describe as creepy-crawly, jittery, itchy, or burning feelings. The symptoms are partially or completely relieved by movement. The urge to move and unpleasant sensations worsen during periods of rest or inactivity, espe cially in the evening and at night, causing most individuals difficulty falling asleep Michaud et al.

The discomfort associated with RLS also causes individuals to wake frequently during the night Montplaisir et al. Individuals with RLS often experience periodic limb movements; however, periodic limb movement disorder see below is not always associated RLS Michaud et al. This condition may be found in in adolescents and teenagers Kryger et al. RLS symptoms associated with pregnancy are caused by transient low levels of ferritin and folate; therefore, they typically disappear within 4 weeks after delivery Lee et al. In a cross-sectional survey of children, ADHD symptoms were almost twice as likely to occur with symptoms of RLS as would be expected by chance alone Chervin et al.

The exact cause of RLS is not completely understood. It likely results from altered dopamine and iron metabolism, and there is evidence for a genetic contribution. More than 50 percent of idiopathic cases are associated with a positive family history of RLS Ekbom, ; Walters et al. Susceptibility gene loci have been identified on chromosomes 12q Desautels et al. RLS commonly occurs in individuals with iron deficiency, including end-stage renal disease, iron-deficiency anemia, pregnancy, and gastric surgery.

Iron deficiency, for example caused by repeated blood donation, may also be associated with RLS Silber et al. It is hypothesized that low levels of iron impair transmission of dopamine signals, which contributes to RLS. Iron levels are reduced in the substantia nigra Allen et al. The iron deficiency is consistent with abnormal regulation of the transferrin receptor, which is responsible for transporting iron across cell membranes.

Iron in turn is necessary for the synthesis of dopamine and the activity of the D 2 dopamine receptor Turjanski et al. The association between dopamine, iron deficiency, and RLS is further supported by observations that dopamine antagonists usually make RLS symptoms worse Winkelmann et al. Idiopathic RLS is not associated with an increased mortality rate; however, in secondary cases of RLS, such as in individuals treated with long-term hemodialysis for end-stage renal disease, RLS is associated with a greater mortality risk Winkelman et al. There are both behavioral and pharmacological treatments for RLS ; however, there have been no clinical trials reporting the efficacy of non-pharmacological strategies to reduce RLS symptoms.

Mild to moderate symptoms can sometimes be treated by lifestyle changes, including maintaining a normal sleeping pattern, taking supplements to manage iron deficiencies, and minimizing consumption of alcohol, caffeine, and tobacco NINDS, RLS is primarily treated using one of four classes of prescription medications: dopaminergic agents, benzodiazepines, opioids, or anticonvulsants central nervous system depressants. Dopaminergic agents are the primary treatment option for individuals with RLS Hening et al. Medications include the dopamine precursor levodopa L-dopa. Although associated with some adverse effects, administration of L-dopa significantly reduces symptoms of RLS and periodic limb movements that occur throughout the night Brodeur et al.

However, dopaminergic agents can also have a stimulating effect that may exacerbate insomnia. Benzodiazepines are effective in improving sleep continuity and are therefore frequently prescribed in combination with dopaminergic agents. Opioids may be prescribed in patients with severe symptoms to help to induce relaxation and minimize pain Walters et al. However, opioids may also exacerbate sleep apnea; therefore, they should be used cautiously in patients who snore Montplaisir et al.

Anticonvulsants are commonly prescribed as an alternative to dopaminergic agents, owing to their ability to minimize leg pain Montplaisir et al. It is believed that anticonvulsants, such as carbamazepine and gabapentin, are less potent than dopaminergic agents; however, there have been no comparative studies performed. Furthermore, there have been a limited number of studies that have examined the safety and efficacy of these treatments in children and adolescents.

Periodic limb movement disorder is characterized by disruptions to sleep caused by periodic episodes of limb movements that occur during sleep, which cannot be explained by any other sleep disorder AASM, The periodic limb movements manifest themselves as rhythmic extensions of the big toe, dorsiflexions of the ankle, and occasional flexions of the knee and hip Coleman, These are scored using the periodic limb movements index, which examines over the course of an hour the number of movements that are 0.

How can I get enough sleep?

An overnight index score of 5 or greater in children and 15 or greater in adults is considered pathogenic AASM, Periodic limb movements typically occur in the lower extremities and may result in autonomic arousal, cortical arousal, or an awakening. However, typically the individual is unaware of the movements. They are more frequent in the beginning of the night and cluster together. These events are associated with a fast heart rate, followed by a period of slow heart rate Friedland et al. Periodic limb movements disorder is associated with above average rates of depression, memory impairment, attention deficits, oppositional behaviors, and fatigue AASM, Periodic limb movements are believed to be very common, especially in older persons, occurring in 34 percent of individuals over the age of 60 AASM, However, the disorder—periodic limb movements associated with sleep disruption—is not as common.

Periodic limb movements are very common in RLS , occurring in 80 to 90 percent of individuals. It is also observed in individuals with narcolepsy, REM sleep behavior disorder Folstein et al. Sleep-disordered breathing may be a modulator that increases the association between periodic limb movements and ADHD Chervin and Archbold, These sleep problems often result from pain or infection associated with the primary condition.

Although these are both known to cause problems with sleep-wake cycles, as will be shown below, very little is still known about the etiology. Pain is described as an acute or chronic unpleasant sensory and emotional experience that varies from dull discomfort to unbearable agony that is associated with actual or potential tissue damage. The symptoms depend on the type and severity of the pain. They include daytime fatigue and sleepiness, poor sleep quality, delay in sleep onset, and decreased cognitive and motor performance Table Bonnet and Arand, Chronic pain affects at least 10 percent of the general adult population Harstall, , of whom 50 percent complain of poor sleep Atkinson et al.

There are a number of clinical pain conditions that individuals report affect their sleep quality— RLS , irritable bowel, gastric ulcer, cancer, musculoskeletal disorders, dental and orofacial pain, spinal cord damage, burns, and other trauma Lavigne et al. Although progress has been made, there are still many unanswered questions about how pain affects regions of the brain responsible for regulating the sleep-wake cycle.

However, it is not known if hypocretin and other genes that regulate the circadian rhythms are affected by acute or chronic pain. Further, it is not known whether the hypothalamus, which is involved in sleep homeostasis, is affected by chronic pain Kshatri et al. Because little is known about the interaction between pain and the circuitry in the brain that is responsible for regulating the sleep-wake cycle, much of the management of sleep problems focuses on managing and alleviating the pain or sleep quality.

Infections caused by bacterial strains, viruses, and parasites may result in changes to sleep patterns. This is complicated by the unique effects that specific infections have on sleep patterns and the absence of a large body of clinical research. Alterations of sleep patterns can be affected by the type of bacterial infection Opp and Toth, For example, gram-negative bacteria induce enhanced sleep more rapidly than do gram-positive bacteria. Differences in the process and progression of the disease also affect the sleep-wake cycle. Viral infections also have effects on the sleep-wake cycle.

Individuals inoculated with rhinovirus or influenza virus report less sleep during the incubation period, while during the symptomatic period they slept longer Smith, However, compared to healthy individuals there were no reported difference in sleep quality and number of awakenings. The human immunodeficiency virus HIV also has been shown to alter sleep patterns.

Individuals spend increased time in SWS during the second half of night Darko et al. As the infection progresses to AIDS, individuals develop increased sleep fragmentation, significant reductions in SWS, and disruption to the entire sleep architecture Norman et al. Many patients with cancer also suffer pain or depression, which contributes to difficulty sleeping. These require treatment as in other patients with pain or depression as causes of insomnia. Excessive sleepiness may be caused by injury to the ascending arousal system due to brain metastases or by leptomeningeal carcinomatosis.

These signs often alert physicians to the need to treat the underlying spread of cancer to the central nervous system. Other patients with cancer may develop antitumor antibodies that attack the brain. In particular, anti-Ma-2 antibodies tend to cause hypothalamic lesions and may precipitate daytime sleepiness and even cataplexy Rosenfeld et al. Treatment of the underlying cancer may reverse the symptoms in some cases. Fungal and parasitic infections also can alter the sleep-wake cycle. For example, sleeping sickness, or African trypanosomiasis , commonly occurs in individuals who have been infected with the Trypanosoma brucei Tb parasite.

It is characterized by episodes of nocturnal insomnia and daytime sleep, but not hypersomnia Lundkvist et al. Sleeping sickness is found primarily in sub-Saharan African countries, where Tb is transmitted to humans as a result of bites received from tsetse flies Lundkvist et al. The prevalence of this disorder is not known; however, over 60 million people live in areas where the Tb parasite is endemic.

Sleeping sickness is associated with altered sleep architecture. EEG recordings of individuals with sleeping sickness from Gambia demonstrate periods of REM sleep that occur throughout the entire sleep-wake cycle, frequently without normal intermediate NREM periods Buguet et al. Circadian fluctuations of hormones—cortisol, prolactin, and growth hormone—are also altered in individuals with sleeping sickness Radomski et al.

Therefore, it has been hypothesized that sleeping sickness may be a circadian rhythm disease that affects the neural pathways that interconnect the circadian-timing and sleep-regulating centers Lundkvist et al. Numerous medical conditions are associated with a wide variety of sleep disorders including insomnia, hypersomnia, parasomnias, and sleep-related movement disorders. Although these disease-related sleep disorders have recently been receiving an increasing amount of attention, including addition to the latest International Classification of Sleep Disorders AASM, , the contribution that treatments for these medical conditions make to the development of sleep disturbances is less well appreciated.

However, many medical therapies have iatrogenic effects on sleep-wake regulatory systems causing disturbed sleep, daytime sleepiness, and other related side effects. For example, beta-antagonists, the mainstay of treatment for hypertension, are commonly associated with fatigue, insomnia, nightmares, and vivid dreams McAinsh and Cruickshank, Sleep disturbances appear to be more severe with lipophilic drugs e.

However, even atenolol, one of the most hydrophilic beta-blockers, has been shown to increase total wake time Van Den Heuvel et al. The mechanism underlying sleep disruption by beta-blocking agents may be their tendency to deplete melatonin, an important sleep-related hormone Garrick et al. Fatigue and somnolence have also been reported with other antihypertensive medications such as carvedilol, labetalol, clonidine, methyldopa, and reserpine Paykel et al. In contrast, angiotensin-converting enzyme inhibitors generally have very few effects on sleep Reid, Hypolipidemic drugs, including atorvastatin and lovastatin, have also been associated with reports of insomnia, but placebo-controlled clinical trials of lovastatin, simvastatin, and pravastatin did not appear to increase sleep disturbance Bradford et al.

Amiodarone, a widely use antiarrhythmic agent Hilleman et al. Patients with cancer receive multiple types of treatments designed at controlling the disease process including chemotherapy, biotherapy, radiotherapy, and medications. All can have important adverse effects on regulating the sleep-wake cycle. For example, sleep problems have been reported in patients undergoing chemotherapy Broeckel et al.

However, objective measures of sleep in the patients and analyses of clinical correlates are very limited. Thus, the mechanisms underlying these sleep problems are poorly understood. Menopausal symptoms arising from chemotherapy and hormonal therapy, especially those of a vasomotor type e. Nocturnal sleep disturbances and daytime sleepiness have also been reported in patients undergoing radiotherapy Beszterczey and Lipowski, ; Miaskowski and Lee, Cytokines biotherapy , a diverse group of peptide molecules that regulate cell functions, are sometimes used as adjunct therapy Dunlop and Campbell, Interferon, interleukin-2, and tumor necrosis factor are associated with a variety of side effects including daytime sleepiness, disturbed sleep, and depression Capuron et al.

Although very effective in reducing cancer-related pain, opioids often cause sleep disturbance and are associated with decreased REM and SWS Cronin et al. RLS , periodic limb movement disorder, sleep apnea, and excessive daytime sleepiness affect up to 70 percent of patients with end-stage renal disease receiving treatment with hemodialysis Parker et al.


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  6. Hemodialysis may alter biological systems controlling processes that regulate the sleep-wake cycle via several potential mechanisms. Several studies have reported an increase in cytokine production secondary to blood interactions with bioincompatible aspects of hemodialysis such as blood expo sure to membranes, tubing, and cellular mechanical trauma and backflow of endotoxins through the membrane Panichi et al.

    These substances have both somnogenic and pyrogenic properties and have been linked to a number of postdialytic symptoms Konsman et al. Dialysis -associated changes in melatonin levels and pattern of secretion and alterations in body temperature rhythm may also play a role in disrupting circadian systems Vaziri et al. Numerous other classes of medications can alter sleep and waking. Corticosteroids are a class of medications that are used to treat a variety of medical conditions including rheumatologic and immunologic disorders, cancer, and asthma.

    Sleep disturbances, insomnia, daytime hyperactivity, and mild hypomania are common side effects Wolkowitz et al. Theophylline, a respiratory stimulant and bronchodilator, is in the same class of medications as caffeine and can likewise disturb sleep—even in healthy subjects Kaplan et al. Nonsteroidal anti-inflammatory agents may also affect sleep as they decrease the production of sleep-promoting prostaglandins, suppress normal surge of melatonin, and alter the daily rhythm of body temperature Murphy et al.

    Pseudoephedrine and phenylpropanolamine, which have many of the same pharmacological properties of ephedrine, also cause sleep disruption—and many of these preparation are readily available over the counter Lake et al. Although the medications and treatments listed above are often necessary, it is essential for patients to be aware of potential side effects relating to the sleep-wake-related cycle.

    Unfortunately, patients often neglect to report such complaints as they think nothing can be done to alleviate the problems. However, numerous behavioral and pharmacological interventions are available to treat these iatrogenically induced problems with the sleep-wake cycle. In addition, administering treatment or medications at appropriate times of day in relationship to the sleep-wake schedule may potentially be beneficial and enhance clinical outcomes Levi, ; Bliwise et al. Research in this area is greatly needed.

    Circadian rhythm sleep disorders arise from chronic alterations, disruptions, or misalignment of the circadian clock in relation to environmental cues and the terrestrial light-dark cycle. The update of the International Classification of Sleep Disorders designated nine different circadian disorders, including delayed sleep phase type, advanced sleep phase type, nonentrained sleep-wake type, irregular sleep-wake type, shift work type, and jet lag type Box AASM, These disorders may be comorbid with other neurological or psychiatric disorders, making the diagnosis and treatment difficult Reid and Zee, Diagnosis with a circadian rhythm disorder requires meeting the following three criteria:.

    Shift Work Disorder and Jet Lag. Shift Work Disorder Shift work type circadian rhythm sleep disorder is characterized by complaints of insomnia or excessive sleepiness resulting from work hours that occur during the normal sleep period, including, night more The following sections will describe two of the nine more common types of circadian rhythm sleep disorders, delayed sleep phase type and advanced sleep phase type.

    The sleep pattern of individuals suffering from delayed sleep phase syndrome or delayed sleep phase type is characterized by sleep onset and wake times that are typically delayed 3 to 6 hours relative to conventional sleep-wake times Figure The impact of delayed sleep phase syndrome has not been fully investigated and is therefore limited.

    A second study investigated the impact of delayed sleep phase syndrome in 22 adolescents and found an association with increased daytime irritability, poor school performance, and mental disturbances Regestein and Monk, ; AASM, Representation of the temporal distribution of sleep. The exact prevalence of delayed sleep phase syndrome in the general population is unknown.

    It is unclear what the prevalence of this disorder is; however, it may be more prevalent in adolescents and young adults Weitzman et al. Night shift workers may be at higher risk for delayed sleep phase syndrome due to irregular circadian entrainment Santhi et al. Similarly, individuals who live in extreme latitudes and are exposed to extended periods of light may also be at increased risk of suffering from delayed sleep phase syndrome Lingjaerde et al. Biological, physiological, and genetic factors have been proposed to be responsible for causing delayed sleep phase syndrome.

    Furthermore, exposure to dim light in the late evening and at night, may also affect the circadian phase Zeitzer et al. Biological alterations to the endogenous circadian system also contribute to delayed sleep phase syndrome. Although levels of melatonin typically increase in the evening hours, individuals with this syndrome have a hypersensitivity to nighttime bright light exposure in the suppression of melatonin Czeisler et al.

    It has also been hypothesized that the disorder may result from a circadian phase that has a reduced sensitivity to photic entrainment, or the free-running period of the circadian cycle is prolonged Czeisler et al. Consistent with these hypotheses, polymorphisms in circadian genes influence the entraining and free-running period of the circadian cycle and may be associated with delayed sleep phase syndrome Takahashi et al.

    A recent study has also identified a candidate gene, human PER2 , that results in familial advanced sleep phase syndrome Xu et al. Treatment for delayed sleep phase syndrome requires resynchronizing to a more appropriate phase to the hour light-dark cycle. In addition to a structured sleep-wake schedule and good sleep hygiene practices, potential therapies include resetting the circadian pacemaker with bright light, melatonin, or a combination of both. However, studies that have investigated the efficacy of bright light have provided mixed results Pelayo et al.

    Consequently, there are no standard criteria for its use. Similarly, there have been no large-scale controlled studies examining the efficacy of melatonin, and as of yet it has not been approved by the Food and Drug Administration for this indication Reid and Zee, Advanced sleep phase syndrome or advanced sleep phase type is characterized by involuntary bedtimes and awake times that are more than 3 hours earlier than societal means Figure Reid and Zee, As is the case with delayed sleep phase syndrome, the amount of sleep is not affected, unless evening activities result in later bedtimes.

    Therefore, the syndrome is primarily associated with impaired social and occupational activities. The prevalence of advanced sleep phase syndrome is unknown; however, it has been estimated that as many as 1 percent of the middle-aged adults may suffer from it Ando et al. One of the challenges in determining its prevalence is that affected individuals typically do not perceive it as a disorder and therefore do not seek medical treatment Reid and Zee, The causes of this syndrome are not known; however, as with delayed sleep phase type, biological and environmental factors likely contribute to the onset of advanced sleep phase type.

    Several familial cases of this syndrome have been reported Jones et al. Polymorphisms in circadian clock genes have been identified in a family with advanced sleep phase syndrome Toh et al. Changes in the activity of genes involved in circadian biology are consistent with observations that individuals with this syndrome have circadian rhythms that are less than 24 hours. Treatment options for individuals with advanced sleep phase syndrome are limited. Bright light therapy in the evening has been used successfully in a limited study to reduce awakenings Campbell et al.

    It is also hypothesized that administration of low levels of melatonin in the early morning may also be used Lewy et al. Irregular sleep schedules frequently include significant disparities between sleep on week-days and weekends, which contribute to shifts in sleep phase and sleep problems. Turn recording back on. National Center for Biotechnology Information , U. Search term. Etiology and Risk Factors The causes of sleep loss are multifactoral.

    Sleep Loss Affects Health In the past 10 or more years, research has overturned the dogma that sleep loss has no health effects, apart from daytime sleepiness. The studies discussed in this section suggest that sleep loss less than 7 hours per night may have wide-ranging effects on the cardiovascular, endocrine, immune, and nervous systems, including the following: Obesity in adults and children. Sleep Loss Is Associated with Obesity When a person sleeps less than 7 hours a night there is a dose-response relationship between sleep loss and obesity: the shorter the sleep, the greater the obesity, as typically measured by body mass index BMI —weight in kilograms divided by height in meters squared.

    Sleep Loss Is Associated with Diabetes and Impaired Glucose Tolerance Two large epidemiological studies and one experimental study found an association between sleep loss and diabetes, or impaired glucose tolerance. Sleep Loss Is Associated with Cardiovascular Morbidity Sleep loss and sleep complaints are associated with heart attacks myocardial infarction and perhaps stroke, according to several large epidemiological studies Eaker et al.

    Sleep Loss and Disease Mortality Sleep loss is also associated with increased age-specific mortality, according to three large, population-based, prospective studies Kripke et al. Management and Treatment Management and treatment of sleep loss are rarely addressed by clinicians, despite the large toll on society Chapters 4 , 5 , and 7. Etiology and Risk Factors In simplest terms, OSA is caused by narrowing or collapse of the airway as a result of anatomical and physiological abnormalities in pharyngeal structures.


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    There are a number of risk factors for OSA , including: Obesity, male gender, and increasing age Table Young et al. It is unclear how incidence changes with older age; some data suggest that snoring and OSA may decline after age 65 years Young et al. The pathophysiological roles of these risk factors are not well understood, although evidence suggests that fat deposition in the upper airways, which is more likely in males, contributes to the physical narrow ing that causes OSA Robinson et al. Menopause also increases the risk of OSA Bixler et al.

    However, recent studies suggest that there may be a referral bias that results in a lower apparent rate of sleep apnea in females than in males Kapsimalis and Kryger, ; Shepertycky et al. Epidemiological evidence suggests that hormone replacement therapy lessens the risk of OSA Shahar et al. In children, the main risk factor for OSA is tonsillar hypertrophy, although OSA may also occur in children with congenital and neuromuscular disorders and in children who were born prematurely Rosen et al.

    Asthma, a common childhood respiratory illness, is also associated with OSA in children Sulit et al. In adolescents, risk factors may be more similar to those seen in adults and include obesity Redline et al. Being a minority is a risk factor for both increased prevalence and severity of sleep-disordered breathing in both children and adults Rosen et al.

    The prevalence of sleep-disordered breathing in the United States is approximately three times higher in middle-aged members of minority groups compared to non-Hispanic whites Kripke et al. African American children are at increased risk, even after adjusting for obesity or respiratory problems Redline et al. Familial and probably genetic factors strongly contribute to OSA Buxbaum et al.

    Patients with cardiovascular disease and diabetes are also at higher risk for developing both OSA and central sleep apnea Sin et al. Patients with impaired baroreflexes e. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion, and sympathetic activation during apnea may predispose to sudden death Somers et al.

    Advanced sleep phase disorder - Wikipedia

    The diagnostic criteria for primary insomnia include: Difficulty initiating or maintaining sleep or nonrestorative sleep. Causing clinically significant distress or impairment in social, occupational, or other important areas of functioning. Not due to the direct physiological effects of a substance or a medical condition APA, Etiology and Risk Factors The precise causes of insomnia are poorly understood but, in general terms, involve a combination of biological, psychological, and social factors.

    Treatment Insomnia is treatable with a variety of behavioral and pharmacological therapies, which may be used alone or in combination. Etiology and Risk Factors The etiological basis for the comorbidity of sleep disorders and psychiatric disorders is not well understood. Insomnia and Psychiatric Disorders As mentioned above insomnia is associated with depression, acting as both a risk factor and a manifestation Ford and Kamerow, ; Livingston et al. Excessive daytime sleepiness , defined as a background of constant sleepiness with sleep attacks leading to unintended napping during the day.

    In most cases, naps are refreshing, but the rested feeling only lasts a short time. When severe, sleepiness can manifest as automatic behavior, a continuation of activities in a semiautomatic manner when sleepy, with no subsequent memory. Cataplexy , which are sudden and brief bilateral episodes of muscle weakness triggered by a strong emotional stimulus, such as laughing.

    Sleep paralysis , or muscle paralysis akin to REM sleep atonia while awake, when falling asleep, or waking up. Insomnia , typically difficulty maintaining sleep. Autonomic behavior, or continue to function talking, putting things away, etc. Excessive daytime sleepiness occurs, as described above for narcolepsy, but in the typical form naps are unrefreshing. Excessive amounts of daily sleep, typically defined as more than 10 hours of sleep per day, as documented for long periods of time using daily logs and sleep studies. Sleep drunkenness sometimes referred to as sleep inertia —difficulty waking up and individual is foggy for long periods of time after wake onset.