Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
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PMID:Central sleep apnea. 393 82

Chronic congestive heart failure is a highly prevalent and progressive disorder associated with excess morbidity and mortality; it has huge economic impact. Left heart failure may be systolic or may occur as isolated diastolic dysfunction. The diastolic form predominates in older people. Sleep disorders are frequent in both types. Most systematic studies have been performed in patients with systolic heart failure. Prospective studies show the presence of obstructive and central sleep apnea, periodic limb movements, and significant alterations in sleep architecture, characterized by poor efficiency, excess stage 1 and arousals, and lack of deep sleep. Both obstructive sleep apnea and central sleep apnea occur in patients with heart failure and have been shown to be associated with excess mortality. Obstructive sleep apnea is best treated with continuous positive airway pressure (CPAP) devices. Central sleep apnea is also best treated with CPAP, but only about 50% of the patients are considered responders. Survival improves when heart failure patients are effectively treated with CPAP for both central and obstructive sleep apnea. A new positive airway pressure device, a pressure support servo-ventilator, is the next best choice for heart failure patients whose central sleep apnea does not respond to CPAP. Nocturnal oxygen should be used for patients whose central sleep apnea does not respond to positive pressure devices. Both periodic limb movements and insomnia could have adverse hemodynamic consequences for the failing heart. There are no guidelines or long-term studies regarding treatment of these conditions in heart failure. For restless legs syndrome with or without periodic limb movements, pramipexole and ropinirole have been approved. Treatment of insomnia comorbid with heart failure depends on the cause. In the absence of any known cause, a trial of ramelteon is the first choice.
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PMID:Sleep dysfunction in heart failure. 1878 5

Central sleep apnoea (CSA) is characterized by the cessation of breathing during sleep due to absent ventilatory drive and may be associated with symptoms of insomnia, excessive daytime sleepiness or frequent arousals. Central apnoeas occur through two pathophysiologic patterns, either post- hyperventilation or post-hypoventilation. The prevalence of CSA is dependent on the population being studied, the predominant risk factors being elderly age group and co-morbid conditions.Data regarding the racial distribution of this disorder are very limited. CSA may be a clinical marker of underlying medical disorders, including cardiac or neurological disease, with resultant significant morbidity and mortality. Given that the underlying pathogenesis remains poorly understood, therapeutic options are currently limited to empiric treatment with PAP devices and rudimentary attempts at pharmacologic therapy with respiratory stimulant drugs and/or oxygen/carbon dioxide gas supplementation as well as treating the underlying cause. The long-term impact of CSA on health and mortality needs further clarification. Future research should be aimed at elucidating the physiologic determinants and consequences of central breathing instability in populations of different age groups, gender and racial descent, as a prerequisite to the development of novel therapeutic interventions in the different populations.
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PMID:Central sleep apnoea. 2030 40

Central sleep apnea is not uncommon in children with neurologic disorders. The mechanisms include increased ventilatory chemosensitivity to carbon dioxide level. Conventional treatments include oxygen, noninvasive ventilation, and in patients with heart failure, improving cardiac output. Here, we present a case of a 9-year-old male with Angelman syndrome, epilepsy, insomnia, and central sleep apnea. The patient was initially evaluated for nighttime awakenings and pauses in breathing. Sustained-release melatonin was used to improve his nighttime awakenings. A polysomnography confirmed central sleep apnea. We saw a reduction in arousals and improvement in insomnia with sustained-release melatonin. On a repeat study, central sleep apnea was improved. We hypothesize that sustained-release melatonin, by improving sleep continuity and reducing arousals, might improve central sleep apnea. Studies are needed to test the hypothesis.
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PMID:Central sleep apnea: does stabilizing sleep improve it? 2322 Jul 92

A number of autoantibodies, some paraneoplastic, are associated with sleep disorders. Morvan syndrome and limbic encephalitis, associated with voltage-gated potassium channel-complex antibodies, principally against CASPR2 and LGI1, can result in profound insomnia and rapid eye movement sleep behavior disorder (RBD). Patients with aquaporin-4 antibodies and neuromyelitis optica may develop narcolepsy in association with other evidence of hypothalamic dysfunction, sometimes as the initial presentation. Central sleep apnea and central neurogenic hypoventilation are found in patients with anti-N-methyl-d-aspartate receptor antibody encephalitis, and obstructive sleep apnea, stridor, and hypoventilation are prominent features of a novel tauopathy associated with IgLON5 antibodies. In addition, paraneoplastic diseases may involve the hypothalamus and cause sleep disorders, particularly narcolepsy and RBD in those with Ma1 and Ma2 antibodies. Patients with antineuronal nuclear autoantibodies type 2 may develop stridor. Several lines of evidence suggest that narcolepsy is an autoimmune disorder. There is a strong relationship with the human leukocyte antigen (HLA) DQB1*06:02 haplotype and polymorphisms in the T-cell receptor alpha locus and purinergic receptor P2Y11 genes. Patients with recent-onset narcolepsy may have high titers of antistreptococcal or other antibodies, although none has yet been shown to be disease-specific but, supporting an immune basis, recent evidence indicates that narcolepsy in children can be precipitated by one type of vaccination against the 2009-2010 H1N1 influenza pandemic.
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PMID:Autoimmune sleep disorders. 2711 85