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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific behavioral state. Yet, even without an understanding of what "causes" sleep, we may be able to develop pharmacological agents which permits discrete alteration of sleep mechanisms in a more physiological and specific manner. This potential for manipulation of sleep is of obvious importance in illnesses such as insomnia, narcolepsy, and sleep apnea (247, 248). In addition, it may be valuable in the treatment of such conditions as psychosis and depression, where sleep disturbances are an important component of the illness. For example, delirium tremens might be best understood as a psychotic episode which is the result of an aspect of sleep emerging into wakefulness. The range and breadth of both the basic questions and the potential application of sleep research portend an exciting future for this field.
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PMID:Neuroregulators and sleep mechanisms. 16 54

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.
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PMID:Narcolepsy. Diagnosis and treatment. 105 17

A 30-year-old man presenting with intellectual impairment and recurrent psychotic episodes was subsequently found to have suffered from a chronically untreated obstructive sleep apnoea syndrome. Polysomnography revealed sleep fragmentation, slow wave sleep deprivation and abnormal arterial oxygen desaturation. Tonsillectomy led to complete resolution of sleep apnoea and remission of psychosis at 2 years' follow-up, but his apparent intellectual impairment persisted. The limited literature on psychosis associated with sleep apnoea is briefly reviewed.
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PMID:Psychosis in sleep apnoea. 261 Jun 56

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

Narcolepsy is a disabling, chronic sleep-wake disorder that typically starts in a patient's second or third decade of life. Its key features are hypersomnia and cataplexy. Sleep paralysis, hallucinations, and disrupted sleep are nonspecific symptoms and are not always present. Disability relates primarily to sleepiness- related cognitive impairment, accidents, and psychosocial problems. Treatment, which includes counseling, scheduled napping, and pharmacologic intervention, is effective for most patients. Hypersomnia is best treated with such indirect sympathomimetics as mazindol, pemoline, methylphenidate, and amphetamine. Modafinil may become the drug of choice because it has fewer side effects. Cataplexy, sleep paralysis, and hallucinations may be ameliorated by compounds, including clomipramine and imipramine, that suppress rapid eye movement (REM) sleep. Regular follow-up visits enable the clinician to recognize uncommon but serious side effects (tolerance, substance abuse, psychosis, and hypertension) and additional sleep disturbances (sleep apnea, periodic limb movements in sleep, REM sleep behavior disorder), which can be specifically treated.
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PMID:Narcolepsy. 1109 16

A 52-yr-old man with a residual phase of schizophrenia developed sleep apnoea-hypopnoea syndrome (SAHS). After five days of continuous positive airway pressure (CPAP) treatment, the patient developed an aggressive mood with incoherence, prominent hallucinations and agitation, and attempted to hit his relatives. He was finally admitted to the hospital with an acute psychotic episode. Withdrawal of CPAP, and neuroleptic treatment controlled the episode, and clinical symptoms of SAHS reappeared 10 days later. Schizophrenia associated to sleep apnoea-hypopnoea syndrome has rarely been reported, but, to the authors' knowledge, the induction of a psychotic episode by continuous positive airway pressure treatment in a patient with sleep apnoea-hypopnoea syndrome and coexisting schizophrenia has never been previously reported.
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PMID:Acute psychosis after CPAP treatment in a schizophrenic patient with sleep apnoea-hypopnoea syndrome. 1133 36

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

Obesity and attention-deficit hyperactivity disorder (ADHD) are both increasing in prevalence. Childhood exposure to television has shown linkage to both ADHD and obesity with the former ascribed to dysfunctional cognitive hyperstimulation and the latter to altered patterns of diet and exercise. Empirical evidence has contradicted prior presumptions that the hyperactivity of ADHD would decrease the risk of obesity. Instead, obesity and ADHD demonstrate significant comorbidity. We propose that obesity and ADHD represent different manifestations of the same underlying dysfunction, a phenomenon we term environmental oversampling syndrome. Oversupply of information in the form of nutritional content and sensory content may independently predispose to both obesity and ADHD. Moreover, the pathogenic mechanisms of these conditions may overlap such that nutritional excess contributes to ADHD and cognitive hyperstimulation contributes to obesity. The overlapping effects of medications provide further evidence towards the existence of shared etiologic pathways. Metabolism and cognition may represent parallel systems of intelligence, and oversampling of content may constitute the source of parallel dysfunctions. The emerging association between psychiatric and metabolic disorders suggests a fundamental biologic link between these two systems. In addition, the immune system may represent yet another form of intelligence. The designation of syndrome X subsumes seemingly unrelated metabolic and inflammatory entities. Environmental oversampling syndrome may represent an even more inclusive concept that encompasses various metabolic, inflammatory, and behavioral conditions. Apparently disparate conditions such as insulin resistance, diabetes, hypertension, syndrome X, obesity, ADHD, depression, psychosis, sleep apnea, inflammation, autism, and schizophrenia may operate through common pathways, and treatments used exclusively for one of these conditions may prove beneficial for the others.
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PMID:Obesity and ADHD may represent different manifestations of a common environmental oversampling syndrome: a model for revealing mechanistic overlap among cognitive, metabolic, and inflammatory disorders. 1590 45

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

The Japanese Society of Mood Disorders (JSMD) published the "Treatment Guideline II: Major Depressive Disorder, 2012 Ver. 1" on July 26, 2012. This guideline (GL) is the first one published by an academic society in Japan. Presently in Japan, many people have depressive symptoms, and the socioeconomic loss (suicide, absence from work, etc.) induced by this condition cannot be overlooked. Although the Japanese society, including mass media and psychiatrists, has attempted to solve this public problem, a solution has not been found. JSMD regarded diagnosis and psychiatric management of depression, among other factors, as the key to solving this problem. For example, patients who meet the DSM-IV major depressive disorder (MDD) criteria still have numerous subtypes, and they often have other psychiatric comorbidities that a diagnosis of MDD alone cannot detect. Although the process for differential diagnosis and treatment planning is indispensable, its methodology has not been necessarily shared even among psychiatrists until today. In this GL, considering the research evidence and its limitations, JSMD suggests necessary steps for appropriate information intake, diagnosis, therapeutic alliance formation, psychoeducation, and treatment modality choice in every phase (acute and continuation/maintenance). This GL also considers pharmaco-, psycho-, and electroconvulsive therapy for major depressive subtypes (mild, moderate/severe, and psychotic). Simultaneously, psychiatrists are required to be alert to the risk from diffuse and multiple prescription of benzodiazepine receptor agonists (dependence, deterioration of sleep apnea, cognitive decline, paradoxical reaction, etc.), especially barbiturates. This GL will be revised on the basis of public comments, including criticism. In the future, treatment GLs for comorbid patients, return-to-work cases, primary care physicians, psychiatric residents, and patients with depressions other than MDD (subthreshold depression, dysthymic disorder, and adaptation disorder) may be needed.
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PMID:[Review of the new treatment guideline for major depressive disorder by the Japanese Society of Mood Disorders]. 2303 6


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