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

The objective of this questionnaire-based survey was to evaluate the prevalence and causes of sleep disturbances in 90 nondepressive patients with Parkinson's disease (PD) and 71 age-matched healthy subjects. We also assessed the prevalence and characteristics of excessive daytime sleepiness (both groups) and excessive fatigue (PD patients). A high prevalence of sleep disturbances in PD patients was found; this is to a large extent probably the result of aging. As compared with controls, patients had a more severely disturbed sleep maintenance because of nycturia, pain, stiffness, and problems with turning in bed. The prevalence of excessive dreaming is similar in both groups, but altered dream experiences almost exclusively occurred in PD. Patients rated themselves more often to be morning-types than controls. This finding may account for the reported adaptation effects in experimental settings and the reduced REM latency in PD patients. The prevalence of daytime sleepiness was similar in both groups. Excessive daytime sleepiness showed a clear diurnal pattern with a peak in the early afternoon. As for excessive fatigue, the majority of the patients did not report a preferential time for this symptom. Our findings further argue against an association of fatigue with any circadian factor, and instead suggest a relationship with the motor deficits of PD.
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PMID:Sleep, excessive daytime sleepiness and fatigue in Parkinson's disease. 836 3

Eighteen narcoleptic patients were treated in a single-blind study with brofaromine, a new selective and reversible MAO-A-inhibitor. After a drug-free period of seven days, brofaromine was administered for two weeks. Patients were treated with 75 mg brofaromine for the first week and with 150 mg brofaromine for the second week of the study. After an adaptation night nocturnal sleep EEGs were recorded under placebo before brofaromine was given, one week later under 75 mg, and another week later under 150 mg brofaromine. Excessive daytime sleepiness (EDS) was evaluated under placebo at the beginning of the study, under 75 mg at the end of the first week, and under 150 mg brofaromine at the end of the second week by means of the Multiple Sleep Latency Test (MSLT) and the Maintenance of Wakefulness Test (MWT). The number of cataplexies was protocolled by the patients. Compared to placebo the administration of 150 mg brofaromine led to a significant increase of sleep latency in the MLST as well as in the MWT. REM sleep was significantly suppressed in the nocturnal sleep EEG, in the MSLT and in the MWT. The number of cataplexies protocolled by the patient was significantly decreased under 150 mg of brofaromine compared to placebo. Improvement of vigilance and cataplexy occurred in dose-dependent manner. No serious side effects were observed. The results of the present single-blind study indicate that brofaromine seems to be a well-tolerated and effective drug for the treatment of excessive daytime sleepiness and cataplexy in narcoleptic patients.
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PMID:Treatment of narcolepsy-cataplexy syndrome with the new selective and reversible MAO-A inhibitor brofaromine-a pilot study. 1060 1

Seventeen children and young adults with the Prader-Willi syndrome were investigated. Twelve of 17 subjects had excessive daytime sleepiness as determined by their own or parental report, a high Epworth Sleepiness Scale score or a short mean sleep latency. Night sleep disturbances were reported in seven subjects with snoring, mouth-breathing, breath-holding and occasional nocturnal enuresis. Polysomnography showed abnormalities of sleep structure with rapid eye movements without reduction in muscle tone at sleep onset in 12 subjects, and a high respiratory event index with frequent brief apnoeas, particularly in REM sleep, in 16 subjects. Most apnoeas were not accompanied by arousals. Seven subjects, all of whom were obese, were considered to have symptomatic sleep apnoea and were treated with continuous positive airway pressure (CPAP) but this was poorly tolerated in two. Five subjects continued CPAP over a 6-month period resulting in subjective improvement in excessive daytime sleepiness in 3. Excessive daytime sleepiness occurs in approximately two-thirds of subjects with the Prader-Willi syndrome. It is mainly of central origin but obstructive sleep apnoea may increase sleepiness, particularly in obese subjects.
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PMID:Sleep apnoea in the Prader-Willi syndrome. 1060 16

Narcolepsy syndrome is a common, although often misdiagnosed, neurological disorder, whose clinical features are excessive daytime somnolence with sleep attacks, caplexy, sleep paralysis and hypnagogic hallucinations. The clinical manifestation have been interpreted as the expression of a sudden intrusion of dissociated REM phenomena in wakefulness. Sometimes the clinical manifestations may include only some of the symptoms: in particular, the cases in which the only symptom is excessive daytime somnolence may be difficult to diagnose. The etiopathogenesis of narcolepsy syndrome is still poorly understood. Recent experimental evidences suggest that a protein, called "orexin", which is supposed to play a role in the control mechanisms of both sleep and eating behaviour, is involved in its pathogenesis. The treatment of narcolepsy has been, up to now, exclusively symptomatic, and in some way empirical and unsatisfactory, especially regarding to daytime sleepiness. Recently, new pharmacological agents, acting on the serotoninergic and/or noradrenergic systems, allow a better control of the cataplectic attacks. The recent development of modafinil, a central nervous system stimulant, devoid of the serious side effects of amphetamines and other compounds, allows to hope in a better control of daytime somnolence and sleep attacks. The aim of the paper is to describe the recent advances in the diagnosis and treatment of narcolepsy.
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PMID:[New perspectives in the diagnosis and therapy of narcolepsy]. 1114 20

Pharmacological therapies are presented for two typical neurological sleep-wake disorders, restless legs syndrome (RLS) and narcolepsy. The individual discomfort caused by RLS and the accompanying problems with initiating and maintaining sleep often require a therapy with L-dopa and dopamine agonists. Positive treatment effects on sensory and motor symptoms have been shown in open trials and controlled studies. Development of time shift and/or augmentation of symptoms is a problem of L-dopa therapy. Further efficient drugs are opioids and benzodiazepines. The therapy of narcolepsy depends on its severity and the pattern of the symptoms. Excessive daytime sleepiness and sleep attacks are the most impairing symptoms, which are difficult to treat. These symptoms require an optimal combination of CNS stimulants with regular napping. Cataplexy and other REM sleep associated symptoms are effectively treated with REM sleep suppressing antidepressants.
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PMID:[Treatment of the neurological sleep disorders restless legs syndrome and narcolepsy]. 1123 89

Parkinson's disease (PD) is associated with sleep disorders which are attributed mainly to dopamine deficiency, nocturnal akinesia, drug therapy, and cofactors such as age and depression. These disturbances affect the macro- and microstructure of both REM and non-REM sleep and motor, respiratory, and autonomic functions. Excessive daytime sleepiness and the interactions between sleep and daytime motor performance in PD are not yet completely understood. Correct diagnosis and treatment of sleep disorders is essential due to the risk of harm to the patient and others and due to their effect on quality of life for all concerned. As sleep disorders in PD are extremely common (about 70%) and may have severe consequences, a systematic sleep history and specific therapy should be considered integral to treatment in every PD patient.
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PMID:[Pathophysiology, clinical aspects and therapy of sleep disorders in Parkinson disease]. 1143

A patient in stage 3-4 of the Unified Parkinson's Disease Rating Scale (UPDRS), or in stage 4-5 of Hoehn and Yahr staging scale, or a patient with 0-50% activities of daily living scale of Schwab and England is considered a Late Parkinson's Disease (LPD) patient. The prevalence of disturbed sleep in Parkinson's Disease (PD) was found to vary according to an objective rating, from 60 to 98%. The factors predicting the quality of life in PD patients are: depression, sleep disturbances and dependence. The present article proposes the insertion of the following items as a chapter in a revised UPDRS based on updated knowledge in sleep arousal disturbances in PD. V. SLEEP-AROUSAL DISTURBANCES: Sleep disturbances 43. Light fragment sleep (LFS) 44. Sleep-related breathing disorders (SRBD) 45. Restless legs-periodic leg movements during sleep (RLS-PLM) 46. REM behavioral disorders (RBD) 47. Sleep-related hallucinations (SRH) 48. Sleep-related psychotic behavior (SRPB) Arousal disturbances 49. Sleep attacks (SA) 50. Excessive daytime sleepiness (EDS). Approaching the treatment of disturbed sleep in LPD means postponement of the institutionalization of the LPD patient, allowing the spouse or the caregiver a quiet nights sleep. This approach consists of three steps, each one of major importance. (1) Correct diagnosis based on detailed anamnesis of the patient, of the spouse or of the caregiver; a one week recording on a symptom diary (log) by the patient or the caregiver; excluding co morbidities. Then choosing the most appropriate sleep test, if necessary: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), actigraphy or video-PSG. This first step allows the diagnosis of one of the above mentioned sleep-arousal disturbances. (2) The non-specific therapeutic approach consists of: (a) checking the sleep effect on motor performance: beneficial, worse or neutral. (b) Dopaminergic adjustment is necessary due to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals which alter the normal modulator mechanisms of motor centers in LPD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and non-REM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates LPD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. L-Dopa has also an arousal effect on Non-REM sleep, repeatedly awakening the patient and enhancing the fragmentation due to the involuntary movements. (c) Socio-physical assistance. (3) The specific therapy consists of: LFS-Sinemet CR, Tolcapone, Intranasal Desmopressin, Domperidon, Cisapride and neurosurgery; SRBD-CPAP, UPPP, nasal interventions, losing weight; RLS-PLM-Benzodiazepine (Clonazepam), Opioid, Apomorphine infusion; RBD-Clonazepam and dopaminergic agonists; SRH-Clozapine, Risperidone; SRPD-Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual LPD patient.
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PMID:Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS. 1148 77

Narcolepsy is a disabling sleep disorder characterized by excessive daytime somnolence (EDS), cataplexy and REM sleep-related abnormalities. It is a frequently-occurring but under-diagnosed condition that affects 0.02 to 0.18% of the general population in various countries. Although most cases occur sporadically, familial clustering may be observed; the risk of a first-degree relative of a narcoleptic developing narcolepsy is 10-40 times higher than in the general population. The disorder is tightly associated with the specific human leukocyte antigen (HLA) allele, DQB1*0602 [most often in combination with HLA-DR2 (DRB1*15)]. Genetic transmission is, however, likely to be polygenic in most cases, and genetic factors other than HLA-DQ are also likely to be implicated. In addition, environmental factors are involved in disease predisposition; most monozygotic twins pairs reported in the literature are discordant for narcolepsy. Narcolepsy was reported to exist in canines in the early 1970s. Both sporadic and familial cases are also observed in this animal species. A highly-penetrant single autosomal recessive gene, canarc-1, is involved in the transmission of narcolepsy in Doberman pinschers and Labrador retrievers. Positional cloning of this gene is in progress, and a human homologue of this gene, or a gene with a functional relationship to canarc-1, might be involved in some human cases. Human narcolepsy is currently treated with central nervous system (CNS) stimulants for EDS and antidepressants for cataplexy and abnormal REM sleep. These treatments are purely symptomatic and induce numerous side effects. These compounds disturb nocturnal sleep in many patients, and tolerance may develop as a result of continuous treatment. The canine model is an invaluable resource for studying the pharmacological and physiological control of EDS and cataplexy. Experiments using canine narcolepsy have demonstrated that increased cholinergic and decreased monoaminergic transmission are likely to be at the basis of the pathophysiology of the disorder. Pharmacological studies have shown that blockade of norepinephrine uptake mediates the anticataplectic effect of currently prescribed antidepressants, while blockade of dopamine uptake and/or stimulation of dopamine release mediates the awake-promoting effect of CNS stimulants. Studies in canine narcolepsy also suggest that mechanisms and brain sites for triggering cataplexy are not identical to those regulating REM sleep. It may thus be possible to develop new pharmacological compounds that specifically target abnormal symptoms in narcolepsy, but do not disturb physiological sleep/wake cycles. (See also postscript remarks).
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PMID:Narcolepsy: genetic predisposition and neuropharmacological mechanisms. REVIEW ARTICLE. 1253 Nov 61

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

Recent studies provide valid criteria that help differentiate idiopathic narcolepsy from other disorders of excessive daytime somnolence [3]. Research to date suggests that idiopathic narcolepsy might properly be considered a disorder of excessive sleepiness with dysfunctional REM-sleep mechanisms, clinically evidenced as cataplexy and electrophysiologically recognized as SOREMPs. Given these criteria, a diagnosis can generally be made using a combination of history, PSG, and MSLT. Traditionally, the medical treatment of idiopathic narcolepsy has centered on a two-drug regimen (stimulants for sleepiness and TCAs for cataplexy and auxiliary symptoms). Some newer medications are proving efficacious for sleepiness with minimal adverse effects, whereas others may provide a single-drug regimen that simultaneously addresses sleepiness and cataplexy [18]. New research has allowed some experts to hypothesize that idiopathic narcolepsy may be the result of a genetic predisposition to autoimmune disease [176]. It is possible that aberrant genetic coding of elements in the hypocretin/orexin systems allows a sensitivity to inducible and possibly virally mediated changes, which leave cells in the lateral hypothalamus susceptible to autoimmune attack [96]. As such, genetic screening of high-risk individuals might eventually rationalize the prophylactic use of immunosuppressants in some instances. In the future, for atypical cases(poorly responsive to therapy), genetic, CSF, and brain imaging studies, and possibly even neuronal transplantation may prove beneficial in the assessment and treatment of idiopathic narcolepsy.
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PMID:Narcolepsy and disorders of excessive somnolence. 1593 92


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