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 1,062 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disorders can be divided into those producing insomnia, those causing daytime sleepiness, and those disrupting sleep. Transient insomnia is extremely common, afflicting up to 80% of the population. Chronic insomnia affects 15% of the population. Benzodiazepines are frequently used to treat insomnia; however, there may be a withdrawal syndrome with rapid eye movement (REM) rebound. Two newer benzodiazepine-like agents, zolpidem and zaleplon, have fewer side effects, yet good efficacy. Other agents for insomnia include sedating antidepressants and over-the-counter sleep products (sedating antihistamines). Nonpharmacologic behavioral methods may also have therapeutic benefit. An understanding of the electrophysiologic and neurochemical correlates of the stages of sleep is useful in defining and understanding sleep disorders. Excessive daytime sleepiness is often associated with obstructive sleep apnea or depression. Medications, including amphetamines, may be used to induce daytime alertness. Parasomnias include disorders of arousal and of REM sleep. Chronic medical illnesses can become symptomatic during specific sleep stages. Many medications affect sleep stages and can thus cause sleep disorders or exacerbate the effect of chronic illnesses on sleep. Conversely, medications may be used therapeutically for specific sleep disorders. For example, restless legs syndrome and periodic limb movement disorder may be treated with dopamine agonists. An understanding of the disorders of sleep and the effects of medications is required for the appropriate use of medications affecting sleep.
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PMID:Medications for the Treatment of Sleep Disorders: An Overview. 1501 9

Excessive daytime sleepiness (EDS) is a common but underrecognized and preventable cause of traffic accidents. It creates a problem of particular importance for professional drivers. We performed the Epworth Sleepiness Scale (ESS) and questionnaire related to their history of traffic accidents to 118 professional taxi drivers to determine the EDS and its effects on driving performance in taxi drivers. There were 58 (49.2%) subjects with loud snoring, 8 (5.9%) subjects with cardinal symptoms due to obstructive sleep apnea syndrome (OSAS) and 28 (23.7%) subjects with ESS > or =10 in the group of taxi drivers. Eighty (67.8%) drivers had been involved in a traffic accident. We found a significant relation between the number of traffic accident and EDS, witnessed apnea, cardinal symptom related to OSAS but not with snoring. The present data that sleepiness is a common symptom in taxi drivers and may be related to traffic accident.
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PMID:[The evaluation of excessive daytime sleepiness in taxi drivers]. 1514 86

Sleep disorders occur commonly in patients with epilepsy, and can be responsible for symptoms of daytime somnolence and also can contribute to the intractability of epilepsy. The most important aspect of treating sleep disorders, especially sleep apnea, is the recognition of the problem. In a busy clinical practice, symptoms of sleep disorders are frequently overlooked or mistaken. Whenever sleep disruption or excessive daytime somnolence is potentially problematic, the patient should be referred to a sleep specialist and, if indicated, diagnostic testing performed (usually polysomnography with or without multiple sleep latency tests). The author also recommends that all patients receive basic counseling about sleep hygiene, because its principles are often helpful to patients in general. Even in the absence of a sleep disorder, the choice of an anticonvulsant can be partly tailored to the sleep needs of the patient, with alerting drugs (lamotrigine and felbamate) dosed early in the day and relatively sedating agents (phenobarbital and phenytoin) dosed later or at bedtime.
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PMID:Sleep, Sleep Apnea, and Epilepsy. 1515 11

Excessive daytime sleepiness, hallucinations and REM sleep behavior disorder are symptoms reported in both dementia with Lewy bodies (DLB) and narcolepsy. Considering the demonstration of low hypocretin-1/orexin A levels in the cerebrospinal fluid (CSF) of most patients with narcolepsy, we hypothesized the presence of a deficient hypocretinergic transmission in DLB. Hypocretin-1 was tested in the CSF of 10 DLB patients. Levels were found to be in the normal range (mean 521 pg/ml, range 382-667) when compared to controls (n = 20, mean 497 pg/ml, range 350-603) and Alzheimer's disease patients (n = 7, mean 474 pg/ml, range 333-564). In DLB, excessive daytime sleepiness, hallucinations and REM sleep behavior may occur in the absence of a detectable hypocretin deficiency.
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PMID:Normal CSF hypocretin-1 (orexin A) levels in dementia with Lewy bodies associated with excessive daytime sleepiness. 1525 27

To investigate the prevalence and severity of excessive daytime somnolence (EDS) in Japanese patients with Parkinson's disease (PD) and to examine the main cause of EDS. Fifty-three Japanese patients with PD (PDs: 32 females and 21 males) and 17 controls (10 females and seven males) were evaluated using the Epworth Sleepiness Scale (ESS). The severity of the disease was evaluated by Unified Parkinson's disease Rating Scale (UPDRS), and information about quality and quantity of medications was collected. The correlations amongst EDS and age, severity of PD, duration of illness and medications were analyzed. The mean ESS score was significantly higher in advanced PDs than in controls, and correlated with the UPDRS score (r(s) = 0.743, P < 0.0001). Age, duration of illness and the dose of levodopa weakly correlated with ESS score. The intake of dopamine agonists did not affect the severity of EDS. The mean ESS score in PDs was lower than that reported in PD in European and American studies. EDS in Japanese patients with PD was milder compared with Caucasian patients, which might be due to the lower doses of the medications used in Japan. The results suggest that EDS in PD is mainly because of neuropathological changes of the disease itself.
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PMID:Excessive daytime somnolence in Japanese patients with Parkinson's disease. 1527 98

Excessive daytime sleepiness (EDS) has recognized detrimental consequences such as road traffic accidents, impaired psychological functioning and reduced work performance. EDS can result from multiple causes such as sleep deprivation, sleep fragmentation, neurological, psychiatric and circadian rhythm disorders. Treating the underlying cause of EDS remains the mainstay of therapy but in those who continue to be excessively sleepy, further treatment may be warranted. Traditionally, the amphetamine derivatives, methylphenidate and pemoline (collectively sympathomimetic) psychostimulants were the commonest form of therapy for EDS, particularly in conditions such as narcolepsy. More recently, the advent of modafinil has broadened the range of therapeutic options. Modafinil has a safer side-effect profile and as a result, interest in this drug for the management of EDS in other disorders, as well as narcolepsy, has increased considerably. There is a growing school of thought that modafinil may have a role to play in other indications such as obstructive sleep apnea/hypopnea syndrome already treated by nasal continuous positive airway pressure but persisting EDS, shift work sleep disorders, neurological causes of sleepiness, and healthy adults performing sustained operations, particularly those in the military. However, until adequately powered randomised-controlled trials confirm long-term efficacy and safety, the recommendation of wakefulness promoters in healthy adults cannot be justified.
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PMID:Pharmacotherapy for excessive daytime sleepiness. 1533 35

Excessive daytime sleepiness (EDS) or somnolence is common in our patients and in society in general. The most common cause of EDS is "voluntary" sleep restriction. Other common causes include sleep-fragmenting disorders such as the obstructive sleep apnea syndrome. Somewhat less familiar to the clinician are EDS conditions arising from central nervous system dysfunction. Of these so-called primary disorders of somnolence, narcolepsy is the most well known and extensively studied, yet often misunderstood and misdiagnosed. Idiopathic hypersomnia, the recurrent hypersomnias, and EDS associated with nervous system disorders also must be well-understood to provide appropriate evaluation and management of the patient with EDS. This review summarizes the distinguishing features of these clinical syndromes of primary EDS. A brief overview of the pharmacological management of primary EDS is included. Finally, in view of the tremendous advances that have occurred in the past few years in our understanding of the pathophysiology of canine and human narcolepsy, we also highlight these discoveries.
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PMID:Narcolepsy and syndromes of primary excessive daytime somnolence. 1544 20

Excessive daytime sleepiness (EDS) is now recognized as an important problem in Parkinson's disease (PD), and its detection and treatment are clinically relevant. Several methods are available to evaluate EDS. Subjective methods consist of questionnaires to be filled out by the patient and include, among others, the Stanford Sleepiness Scale, the Karolinska Sleepiness Scale, and the Epworth Sleepiness Scale. These are entirely dependent on the patients' perception of their problems. Objective methods evaluate sleepiness indirectly, measuring the time it takes for the subject to fall asleep when placed in a soporific situation. Two types can be further identified: those using electrophysiologic measures [the Multiple Sleep Latency Test (MSLT) and the Maintenance of Wakefulness Test (MWT)] and those measuring performance (e.g., the Oxford Sleep Resistance test). The Epworth Sleepiness Scale and the MSLT have been used repeatedly in PD and, in spite of their limitations, they are, together with the MWT, the best available methods to measure EDS in these patients.
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PMID:How to evaluate excessive daytime sleepiness in Parkinson's disease. 1550 38

Excessive daytime sleepiness and abnormal sleep-wake patterns are becoming increasingly pervasive in modern society. The major causes of excessive daytime sleepiness include pathologic abnormalities of the central nervous system, such as narcolepsy and idiopathic hypersomnia; deficiencies in quality or quantity of sleep, such as those caused by sleep apnea and poor sleep hygiene; disturbances to the body's natural circadian rhythm, such as those caused by shift work or jet lag; and drugs, which can increase sleepiness either therapeutically or as a side effect. Determining the cause of daytime sleepiness is the first step in treating it. Setting appropriate and realistic treatment goals with the patient and initiating treatment are the next steps. Although the medications available to improve daytime wakefulness (e.g., amphetamines, methylphenidate, pemoline, and modafinil) are effective, they are not a substitute for sleep. Finally, timely follow-up is necessary to monitor treatment adherence, response, and side effects.
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PMID:Pharmacologic management of daytime sleepiness. 1557 5

The association between excessive daytime somnolence (EDS) and idiopathic Parkinson's disease (PD) is often reported but still debated. The possible role of antiparkinsonian therapy or primarily of PD on excessive diurnal sleepiness is controversial. We describe the case of a 61-year-old patient affected by PD who experienced sleep episodes (SE) occurring during pramipexole plus L-Dopa therapy. Polysomnographic sleep studies and subjective evaluations of daytime sleepiness (Epworth Sleepiness Scale) were carried out under administration of pramipexole plus L-Dopa, L-Dopa monotherapy and cabergoline plus L-Dopa. The polysomnography revealed two sleep events during pramipexole plus L-Dopa. Moreover, the polysomnographic data showed an increase of both diurnal and nocturnal sleep under pramipexole plus L-Dopa compared with cabergoline plus L-Dopa and L-Dopa as monotherapy. In addition, while Epworth Sleepiness Scale (ESS) Score showed a mild sleepiness under pramipexole (ESS score=11), ESS scores were normal under both L-Dopa and cabergoline plus L-Dopa. Sleep episodes also disappeared under both L-Dopa and cabergoline plus L-Dopa (2- and 12-month follow-up). We hypothesize that an individual susceptibility to specific antiparkinsonian drug may play a significant role in the genesis of sleepiness in our PD patient.
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PMID:Sleep episodes and daytime somnolence as result of individual susceptibility to different dopaminergic drugs in a PD patient: a polysomnographic study. 1560 3


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