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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal subjects may present central-type apneas or periodic respiration during sleep (stages I and II and paradoxical sleep). The importance of these respiratory disorders increases with age. Hypersomniac patients can manifest either similar or more significant sleep respiratory disorders than normal subjects. The presence of cataplexy or obesity does not permit the prediction of the existence of respiratory arrhythmias or of their type. Sleep respiratory arrhythmias of central type are not likely to cause hypersomnia; however, an aggravating role may be played by obstructive apneas.
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PMID:Sleep respiratory arrhythmias in control subjects, narcoleptics and non-cataplectic hypersomniacs. 7 98

Although narcolepsy is rarely diagnosed before adulthood, symptoms often begin much earlier and can easily mimic psychiatric disorders in children and adolescents. Clinical experience from a pediatric sleep center is reviewed in 16 consecutive cases of polysomnographically proven narcolepsy with onset of symptoms by age 13 years. Only 1 of the 16 patients presented with the classic clinical tetrad of symptoms (sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis). Behavioral and emotional disturbances were present in 12 of 16 cases, with four patients appearing to have been misdiagnosed with a psychiatric disorder before recognition of the narcolepsy. Obesity appeared as an unexpected association in this case series, with 11 of the 16 narcoleptic patients found to be overweight at the time of diagnosis. The varied clinical presentations, polysomnographic findings, family history, and associated psychiatric symptoms are described. The importance of considering narcolepsy in the differential diagnosis of any child or adolescent with excessive sleepiness is emphasized.
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PMID:A clinical picture of child and adolescent narcolepsy. 808 40

Narcolepsy is a derangement of the normal sleep-wakefulness rhythms. Originally, narcolepsy was thought to be a form of epilepsy; however, with the development and subsequent refinement of the electroencephalograph, this notion is no longer accepted. The disorder is characterized by inappropriate intrusions of rapid eye movement sleep into the wakeful state and multiple disruptions of the sleep cycles. Narcolepsy usually has its onset anytime between the ages of 10 years and 50 years, with the greatest majority of patients first reporting noticeable symptoms between the ages of 15 and 35 years. Patients with narcolepsy may exhibit excessive daytime sleepiness, cataplexy, hypnogogic and/or hypnopompic hallucinations, and sleep paralysis. The cause of narcolepsy is presently unknown. Recent research has identified a possible genetic contribution via chromosome 6, but some form of environmental influence appears to be necessary for the disorder to be manifested. There is no cure for narcolepsy; however, symptomatic relief may be achieved through a trial-and-error combination of amphetamines and tricyclic antidepressants. The nature of narcolepsy often forces the individual to undergo some rather dramatic lifestyle changes and can lead to the development of other associate disorders, such as depression and obesity.
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PMID:Anesthesia considerations for patients with narcolepsy. 1048 78

An overweight patient (body mass index of 34 kg/m(2)) with narcolepsy associated with cataplexy is described. Polysomnography did not indicate obstructive sleep apnea. Her obesity was treated with sibutramine, a norepinephrine, serotonin and dopamine reuptake inhibiting medication and her severe cataplexy remitted. Clinicians must be aware that sibutramine may suppress cataplexy when evaluating excessive daytime sleepiness in an overweight patient taking this anti-obesity medication. Therefore a negative history of cataplexy in these cases may be misleading and narcolepsy may be overlooked in the differential diagnosis. Sibutramine should be discontinued before polysomnography and multiple sleep latency testing but may be a useful medication in the management of obese narcoleptic patients with cataplexy. With the discovery of decreased hypocretin 1 levels in humans with narcolepsy, a neuropeptide that modulates sleep and feeding, the association between narcolepsy and obesity requires more attention.
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PMID:Narcolepsy and obesity: remission of severe cataplexy with sibutramine. 1115 84

Narcolepsy is characterized by excessive daytime sleepiness and abnormal manifestations of rapid eye movement sleep such as cataplexy. The authors review the clinical features of narcolepsy, including epidemiology, symptoms, diagnosis, and treatment, in detail. Recent findings show that a loss of hypocretin-producing neurons lies at the root of the signs and symptoms of narcolepsy. The authors review the current state of knowledge on hypocretin anatomy, physiology, and function with special emphasis on the research regarding the hypocretin deficiency in narcolepsy, which may also explain associated features of the disorder, such as obesity. Lastly, they discuss some future perspectives for research into the pathophysiology of sleep/wake disorders, and the potential impact of the established hypocretin deficiency on the diagnosis and treatment of narcolepsy.
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PMID:Narcolepsy: clinical features, new pathophysiologic insights, and future perspectives. 1143 2

A few examples of hypothalamic, peptidergic disorders leading to clinical signs and symptoms are presented in this review. Increased activity of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) and decreased activity of the vasopressin neurons in the biological clock and of the thyroxine-releasing hormone (TRH) neurons in the PVN contribute to the signs and symptoms of depression. In men, the central nucleus of the bed nucleus of the stria terminalis (BSTc) is about twice as large and contains twice as many somatostatin neurons as in women. In transsexuals this sex difference is reversed, pointing to a role of this structure in gender. Luteinizing hormone-releasing hormone (LHRH) neurons are formed in the fetal olfactory placade and migrate along the terminal nerve fibers into the hypothalamus. In Kallmann's syndrome the migration process of the LHRH (gonadotropin-releasing hormone) neurons is aborted, which explains the joint occurrence of hypogonadotropic hypogonadism and anosmia in this syndrome. In postmenopausal women, the neurons of the infundibular nucleus hypertrophy and become hyperactive because of the disappearance of the estrogen feedback and contain hyperactive peptidergic neurons. Climacteric flushes may be caused by hyperactivity of the neurokinin-B or LHRH neurons in this nucleus. The hypocretin (orexin) neurons in the perifornical area are involved in sleep. In narcolepsy with cataplexy, a loss of these neurons, probably due to an autoimmune process, is found. Obese subjects with a mutation in the gene that encodes for leptin, the preproghrelin gene, or the alpha-melanocyte-stimulating hormone (alpha-MSH) gene have been described. Decreased numbers and activity of the oxytocin neurons in the PVN may be responsible for the absence of satiety in Prader-Willi syndrome. Moreover, a glucocorticoid receptor polymorphism is associated with obesitas and dysregulation of the hypothalamus-pituitary-adrenal axis. In contrast, two single nucleotide polymorphisms (SNPs) of the AGRP gene have been associated with anorexia nervosa.
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PMID:Neuropeptides in hypothalamic neuronal disorders. 1554 16

Four patients with clinically and genetically confirmed Prader-Willi syndrome (PWS) underwent nocturnal polysomnograpy (PSG), multiple sleep latency test (MSLT), human leukocyte antigens (HLA) typing and estimation of cerebrospinal fluid (CSF) hypocretin-1 (Hcrt-1) level to investigate if a role of hypothalamic dysfunction and sleep disturbance might be functionally connected through the hypocretin (orexin) system. In all four patients physical examination confirmed extreme obesity (increasing with age) with dysmorphogenetic features. Excessive daytime sleepiness (EDS) was manifested in only two subjects without any imperative feature. None of the patients under study suffered from cataplexy. Nocturnal PSG revealed fragmented sleep with low efficiency, the hypopnea and apnea indexes increasing from borderline up to very high values in direct proportion to the patients' age. MSLT latency was shortened in two patients with clinically expressed EDS, only one sleep onset rapid eye movements (REM) period (SOREM) was found. HLA typing showed DQB1*0602 positivity in two patients; the further two were negative. Mean value of CSF Hcrt-1 in the patients group was down to 164 +/- 46.8 pg/ml (in comparison with 265.8 +/- 48.8 pg/ml in 10 young healthy subjects, P=0.02). The deficiency of CSF Hcrt-1 level correlated in PWS patients with their EDS severity.
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PMID:Hypocretin deficiency in Prader-Willi syndrome. 1561 51

In children, narcolepsy may be the symptom of a brain lesion or genetic disease. The authors report two cases with severe narcolepsy-cataplexy emerging in childhood in close temporal association with obesity and precocious puberty.
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PMID:Narcolepsy-cataplexy associated with precocious puberty. 1671 24

Narcolepsy is a chronic disease commonly diagnosed in middle adulthood. However, the first symptoms often appear in childhood and/or adolescence. Pediatric cases of narcolepsy are among the most often underrecognised and underdiagnosed diseases. This fact raises questions about the reasons for such diagnostic delay from the clinical point of view, and what kind of help can be expected from auxiliary diagnostic examinations. The aim of the review is to stress some specific features of the clinical picture in children, to discuss the role of auxiliary examinations at the onset of the disease including sleep studies, tests for human leukocyte antigens (HLAs), and cerebrospinal fluid hypocretin (Hcrt) measurement, and to draw attention to the most common cases of pediatric misdiagnosis. Frequent cataplectic attacks at an early age should lead to detailed clinical, neuroimaging and genetic examinations to rule out a secondary etiology. Beside the typical symptoms (excessive daytime sleepiness, cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations), some additional features including obesity and nocturnal bulimia can appear. Also poor school performance and emotional disorder are common complaints. Treatment should start as early as possible to avoid the development of problems with progress at school, and close cooperation between school and family should be maintained.
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PMID:Narcolepsy in childhood. 1915 53

Fatalities resulting from popular use of gamma hydroxybutyrate (GHB) have previously been reported. We report three deaths associated with use of Xyrem (sodium oxybate), a pharmaceutical preparation of GHB initially approved for treatment of narcolepsy with cataplexy. One death appears associated with Xyrem abuse, with extremely high postmortem blood GHB levels documented. Although postmortem blood GHB levels in two other deaths are consistent with therapeutic levels, cause and effect cannot be established. We discuss these cases and factors which may have exerted contributory respiratory depressant effects, singly or in combination, including concurrent use of sedative hypnotics, obstructive sleep apnea, and obesity.
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PMID:Three deaths associated with use of Xyrem. 2064 79


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