Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with Cushing's syndrome (CS) frequently have sleep complaints. We evaluated sleep polysomnographically in 22 patients, including 17 with pituitary-ACTH-dependent Cushing's disease (CD) and five with CS from an adrenal tumor. Data were compared to healthy controls of comparable age. Seven patients (32%) demonstrated at least mild sleep apnea (> or = 9.4 events/hour), and four of 22 (18%) had > or = 17.5 events/hour. The apneic CD and CS patients had a trend for a greater complaint of excessive daytime sleepiness. Both apneic and nonapneic groups had considerable snoring and obesity. The electroencephalographic (EEG) sleep of nonapneic patients was compared to that of normal subjects. Nonapneic CD patients differed strikingly from healthy volunteers in sleep continuity and architecture, demonstrating lighter, fragmented sleep. Rapid eye movement (REM) sleep in CD patients bore many similarities to the sleep of patients with major depression, with REM latency being significantly shortened and REM density significantly increased. Continued examination of EEG sleep in CD patients may shed light on similarities in pathophysiology between CD and major depression, disorders which are characterized by both a dysfunction of the hypothalamic-pituitary-adrenal axis and alterations in mood.
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PMID:Sleep architecture and sleep apnea in patients with Cushing's disease. 133 12

The most predictable electroencephalographic sleep changes of major depression are a shortened first NREM sleep period, a prolonged first REM period (with increased density of rapid eye movements), sleep continuity disturbance, and diminished slow wave sleep (with shifting of delta activity from the first to the second NREM sleep period). The more rapid appearance of the first REM sleep period occurs in relation to sleep onset but not apparently in relation to clock time. The changes occurring in the first NREM-REM cycle of the night appear to be relatively specific to major (particularly endogenous) depression. Depressed men appear to have diminished nocturnal penile tumescence compared with healthy controls, but depressed patients generally do not have a higher incidence of sleep apnea or nocturnal myoclonus. The sleep physiologic changes of depression appear to persist into clinical remission, suggesting that they are trait-like. Published studies appear to support the conclusion that there is a close link between the regulation of sleep and the regulation of mood in affective illness.
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PMID:Sleep and affective disorders. A minireview. 333 19

Within the context of the comprehensive treatment of sleep disorders, which includes medical, neurologic, psychiatric, and social interventions, use of medication is often indicated. Among the three benzodiazepine hypnotics that are available in the United States for the treatment of insomnia, flurazepam is effective for both sleep induction and maintenance, and it retains most of its efficacy over a 4-week period of nightly administration; temazepam is effective only for sleep maintenance, and triazolam improves both sleep induction and maintenance with initial but not with continued administration. Rebound phenomena are more frequent and intense with the more rapidly eliminated drug, triazolam, and to a lesser degree with temazepam. Also, with triazolam, certain behavioral side effects, such as amnesia and psychotic-like symptoms, have been reported. With flurazepam, which is a slowly eliminated benzodiazepine, daytime sedation is more frequent than with the other two drugs. When insomnia is secondary to major depression, antidepressant medication should be administered. Methylphenidate, amphetamines, or other stimulant medications are used for the symptomatic treatment of the sleepiness and sleep attacks of narcolepsy and hypersomnia. For cataplexy and the other two auxiliary symptoms of narcolepsy, imipramine or other tricyclics are the drugs of choice. Protriptyline and medroxyprogesterone have been used in treating mild cases of obstructive sleep apnea, but their efficacy is limited. Similarly, for the treatment of central sleep apnea, medroxyprogesterone and acetazolamide have shown only limited effects. Medication for patients with sleepwalking, night terrors, or nightmares should be prescribed judiciously, and primarily when treatment of an underlying psychiatric condition is desired. The neuropharmacology of sleep should also consider drugs that may cause sleep disorders. Medications with sleep disturbing effects include various antihypertensives, bronchodilators, and the energizing antidepressants. Withdrawal of REM-suppressant drugs, such as the barbiturates, may cause nightmares in association with a REM rebound. Occasionally, a drug or a combination of drugs may produce somnambulistic-like activity in some patients.
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PMID:Clinical neuropharmacology of sleep disorders. 333 64

Sleep is disturbed in 90% of patients with major depression. Disordered sleep physiology may persist after clinical remission of depression, suggesting either that sleep disruption is a trait characteristic of recurrent depression or that depressed patients acquire new habits that perpetuate sleep-related problems. This article reviews the data suggesting a common pathophysiology between sleep and depression. It then focuses on a strategy for evaluating and treating sleep disruption in depressed patients. Treatment must have a conservative goal of restoring sleep quality to the pre-episode level. The treatment of sleep disruption relies primarily on optimal treatment of the depression itself. This includes evaluation and treatment of comorbid medical disorders, substance use (e.g., caffeine, alcohol), and sleep disorders (e.g., nocturnal myoclonus, sleep apnea). The effects of the different classes of antidepressant medications on sleep architecture are presented. Nonpharmacologic strategies for improving sleep, such as behavior modification, relaxation, and phototherapy, are discussed. Finally, the risks and benefits of hypnotic use in the depressed patient and a treatment algorithm for the acute and chronic use of hypnotics are considered.
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PMID:Treatment of sleep disturbances in depressed patients. 784 8

Our prospective, standardized cohort study was designed to assess the presence of alpha wave intrusions during non-rapid eye movement sleep (alpha-delta sleep) and its relationship to fibromyalgia, major depression, and chronic fatigue syndrome (CFS) in patients with a chief complaint of chronic fatigue. The study group comprised 30 consecutive patients seen at a university hospital referral clinic for evaluation of chronic fatigue. All patients had nocturnal polysomnography, dolorimetric tender point assessment for fibromyalgia, a comprehensive history, physical, and laboratory evaluation, and a structured psychiatric interview. Alpha-delta sleep was identified in 8 of the 30 patients (26%), major depression in 20 (67%), CFS in 15 (50%), and fibromyalgia in 4 (13%). Ten of the 30 patients (33%) had a primary sleep disorder (sleep apnea, periodic limb movements, or narcolepsy). Alpha-delta sleep was not significantly correlated with fibromyalgia, CFS, major depression, or primary sleep disorders, but was significantly more common among patients who had chronic fatigue without major depression. We conclude that primary sleep disorders are relatively common among patients with chronic fatigue and must be diligently sought and treated. Alpha-delta sleep is not a marker of fibromyalgia or CFS, but may contribute to the illness of nondepressed patients with these conditions.
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PMID:Alpha-delta sleep in patients with a chief complaint of chronic fatigue. 797 34

Our objectives were to determine the effects of nortriptyline and placebo on subjective and EEG sleep measures over 1 year of maintenance therapy in elderly depressed patients and to determine the relationship of such effects to recurrence in nortriptyline or placebo-treated patients during maintenance therapy. EEG and subjective sleep assessments were conducted before and during a maintenance therapy study of patients suffering from major depression. During acute treatment all patients received nortriptyline plus interpersonal psychotherapy (IPT). During maintenance treatment patients were randomly assigned to double-blind treatment in one of four cells: nortriptyline with IPT; nortriptyline with medication clinic (no IPT); placebo with IPT; or placebo with medication clinic. Sleep evaluations were conducted at one point before treatment, one point following remission during continuation nortriptyline/IPT treatment, and at three time points after random assignment to maintenance treatment. The setting was the sleep laboratory of the outpatient depression treatment clinic, and subjects were a convenience sample of media-recruited and clinically referred elderly outpatient depressed patients (n = 72). Complete sleep analyses were conducted for 21 nortriptyline- and 10 placebo-treated patients throughout 1 year of maintenance treatment. The main outcome measures were subjective and EEG sleep measures and the recurrence of major depression. Our results show that nortriptyline acutely and persistently decreased REM sleep, increased phasic REM activity, decreased sleep apnea, and had no effect on periodic limb movements during sleep. Recurrence on maintenance nortriptyline was associated with lower phasic REM activity during early continuation therapy, but EEG sleep measures did not predict recurrence during placebo maintenance therapy. Patients treated with nortriptyline had a lower recurrence rate than those treated with placebo. Better subjective sleep quality and maintenance IPT were associated with a lower rate of recurrence regardless of nortriptyline treatment. It seems that nortriptyline has persistent effects on REM sleep and sleep apnea in elderly depressed patients. Maintenance nortriptyline, maintenance IPT, good subjective sleep quality, and high-phasic REM activity are associated with a reduced likelihood of the recurrence of depression during maintenance therapy.
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PMID:Longitudinal effects of nortriptyline on EEG sleep and the likelihood of recurrence in elderly depressed patients. 892 92

Post-traumatic stress disorder (PTSD) overlaps major depression (MD) clinically, but differs with respect to treatment response and some biological markers. Sleep disturbances represent core features of PTSD and are also common in MD. Rapid eye movement sleep (REM) has been postulated to be involved in the pathophysiology of PTSD, and REM abnormalities occur in MD. Twenty-five patients with combat-related PTSD, 16 men with a principal diagnosis of MD, and 10 asymptomatic male controls were compared by polysomnography (PSG) under medication and substance-free conditions. Data were obtained from recordings made after an accommodation night. One subject from each group was excluded for significant apnea or limb movements. Sleep efficiency was decreased in the PTSD group compared to the MD and control groups. REM density was comparably increased in PTSD and MD groups, while the amount of REM sleep was reduced in PTSD compared to MD groups. These sleep measures were not significantly associated with co-morbid depression, substance-use disorder histories, or subclinical sleep apnea or limb movements within the PTSD group. These findings support sleep maintenance being impaired in chronic PTSD patients. Increased REM density in PTSD patients was replicated and was comparable to increases in the MD group. Divergence of REM time between these clinical groups suggests the possibility of different underlying mechanisms.
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PMID:A polysomnographic comparison of veterans with combat-related PTSD, depressed men, and non-ill controls. 913 Mar 34

Parkinson's disease is associated with classical Parkinsonian features that respond to dopaminergic therapy. Neuropsychiatric sequelae include dementia, major depression, dysthymia, anxiety disorders, sleep disorders, and sexual disorders. Panic attacks are particularly common. With treatment, visual hallucinations, paranoid delusions, mania, or delirium may evolve. Psychosis is a key factor in nursing home placement, and depression is the most significant predictor of quality of life. Clozapine may be the safest treatment for psychotic features, but more research is needed to establish the efficacy of antidepressant treatments. Dementia with Lewy bodies, the second most common dementia in the elderly, may present in association with systematized delusions, depression, or RBD. Early evidence suggests the utility of rivastigmine, donepezil, low-dose olanzapine, and quetiapine in treating DLB. Parkinson-plus syndromes generally lack a good response to dopaminergic treatment and evidence additional features, including dysautonomia, cerebellar and pontine features, eye signs, and other movement disorders. MSA is associated with dysautonomia and RBD. SND (MSA-P) is associated with frontal cognitive impairments, but dementia, psychosis, and mood disorders have not been strikingly apparent unless additional pathological findings are present. In SDS (MSA-A), impotence is almost ubiquitous; urinary incontinence is frequent; depression is occasional, and sleep apnea should be treated to avoid sudden death during sleep. OPCA neuropsychiatric correlates await further definition. Progressive supranuclear palsy neuropsychiatric features include apathy, subcortical dementia, pathological emotionality, mild depression and anxiety, and lack of appreciable response to donepezil. CBD usually is recognized by early frontal dementia with ideomotor apraxia, often in the right upper extremity, attended later by poorly responsive unilateral Parkinsonism, with additional signs including cortical reflex myoclonus, limb dystonia, alien limb, oculomotor apraxia when asked to look horizontally, depression, personality changes, and, occasionally, Kluver-Bucy syndrome. The neuropsychiatry of FTDP-17 involves apraxia, executive impairment, personality changes, hyperorality, and occasional psychosis. Future research in these Parkinsonian disorders should target the characterization of neuropsychiatric sequelae and their treatment.
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PMID:The neuropsychiatry of Parkinson's disease and related disorders. 1555 Feb 93

Modafinil is a wake-promoting agent that is pharmacologically different from other stimulants. It has been investigated in healthy volunteers, and in individuals with clinical disorders associated with excessive sleepiness, fatigue, impaired cognition and other symptoms. This review examines the use of modafinil in clinical practice based on the results of randomized, double-blind, placebo-controlled clinical trials available in the English language in the MEDLINE database. In sleep-deprived individuals, modafinil improves mood, fatigue, sleepiness and cognition to a similar extent as caffeine but has a longer duration of action. Evidence for improved cognition in non-sleep-deprived healthy volunteers is controversial.Modafinil improves excessive sleepiness and illness severity in all three disorders for which it has been approved by the US FDA, i.e. narcolepsy, shift-work sleep disorder and obstructive sleep apnoea with residual excessive sleepiness despite optimal use of continuous positive airway pressure (CPAP). However, its effects on safety on the job and on morbidities associated with these disorders have not been ascertained. Continued use of CPAP in obstructive sleep apnoea is essential. Modafinil does not benefit cataplexy.In very small, short-term trials, modafinil improved excessive sleepiness in patients with myotonic dystrophy. It was efficacious in fairly large studies of attention deficit hyperactivity disorder (ADHD) in children and adolescents, and was as efficacious as methylphenidate in a small trial, but has not been approved by the FDA, in part because of its serious dermatological toxicity. In a trial of 21 non-concurrent subjects, with 2-week treatment periods, modafinil was as effective as dexamfetamine in adult ADHD. Modafinil was helpful for depressive symptoms in bipolar disorder in a trial that excluded patients with stimulant-induced mania. A single dose of modafinil may hasten recovery from general anaesthesia after day surgery. A single dose of modafinil improved the ability of emergency room physicians to attend didactic lectures after a night shift, but did not improve their ability to drive home and caused sleep disturbances subsequently.Modafinil had a substantial placebo effect on outcomes such as fatigue, excessive sleepiness and depression in patients with traumatic brain injury, major depressive disorder, schizophrenia, post-polio fatigue and multiple sclerosis; however, it did not provide any benefit greater than placebo.Trials of modafinil for excessive sleepiness in Parkinson's disease, cocaine addiction and cognition in chronic fatigue syndrome provided inconsistent results; all studies had extremely small sample sizes. Modafinil cannot be recommended for these conditions until definitive data become available.Modafinil induces and inhibits several cytochrome P450 isoenzymes and has the potential for interacting with drugs from all classes. The modafinil dose should be reduced in the elderly and in patients with hepatic disease. Caution is needed in patients with severe renal insufficiency because of substantial increases in levels of modafinil acid. Common adverse events with modafinil include insomnia, headache, nausea, nervousness and hypertension. Decreased appetite, weight loss and serious dermatological have been reported with greater frequency in children and adolescents, probably due to the higher doses (based on bodyweight) used. Modafinil may have some abuse/addictive potential although no cases have been reported to date.
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PMID:Approved and investigational uses of modafinil : an evidence-based review. 1872 34

We report a case of central sleep apnea in a geriatric patient that was associated with treatment with aripiprazole for an episode of major depressive disorder with psychotic features. The patient was a 72-year-old man who was started on aripiprazole and developed central sleep apnea that improved significantly when the medication was stopped. A rechallenge with aripiprazole led to a worsening of the central sleep apnea, which again improved off the aripiprazole. We postulate that the central sleep apnea was due to aripiprazole. There have been numerous case reports in the literature of obstructive sleep apnea associated with atypical antipsychotics. To our knowledge, this is the first published case of central sleep apnea. We caution clinicians to be aware that there is potential risk of atypical antipsychotics like aripiprazole inducing or exacerbating central sleep apnea.
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PMID:Central sleep apnea in a geriatric patient treated with aripiprazole. 1930 45


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