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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An obese patient with a ten year history of respiratory failure presented with insomnia and marked daytime somnolence. Respriatory failure had been attributed to obesity, respiratory centre insensitivity to carbon dioxide, and to diffuse airways obstruction. To investigate the possible role of episodic apnoea with frequent nocturnal arousals, continous recordings were obtained during sleep of arterial oxygen saturation, oesophageal pressure and the motions of the rib-cage and abdomen/diaphragm. Repeated episodes of hypoventilation and profound hypoxaemia were found which were due to intermittent obstruction of the upper airway rather than to cessation of breathing efforts. During the episodes of hypoxaemia, values of arterial O2 tension fell to as low as 24 mmHg. Episodic hypoxaemia was relieved but not abolished, by the use of a collar, designed to hold the mandible forward. Previous reports indicated that recognition of intermittent obstruction of the upper airway during sleep and treatment by a permanent tracheostomy, resulted in a significant long-term imporvement of pulmonary and cardiac function and relief of insomnia and day-time somnolence. When tracheostomy is inadvisable, as in the present patient, it is hoped that similar long-term benefits will result from a supportive collar.
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PMID:Intemittent obstruction of the upper airway during sleep causing profound hypoxaemia. A neglected mechanism exacerbating chronic respiratory failure. 107 82

The effects of 30-h sleep deprivation on cardiorespiratory function either at rest or in exercise were studied in 15 young healthy male volunteers. All subjects performed 1-min incremental exercise tests on a bicycle ergometer until exhaustion and endurance exercise tests at 3/4 of their maximal work rates. Arterialized venous blood samples were withdrawn at rest and during exercise tests to investigate the influence of sleep loss on blood gases. In addition, resting plasma catecholamine levels were also measured in ten subjects. The results showed that 1) resting heart rate, plasma catecholamine levels, and blood pH were decreased while minute ventilation (VI) and CO2 production (VCO2) were increased after 30 h of sleep loss (P less than 0.05), and 2) the maximal exercise performance was reduced by sleeplessness, as indicated by the decreases in the maximal heart rate, peak VI, peak VCO2, peak O2 consumption, and time to exhaustion (P less than 0.05). However, no significant changes in exercise endurance, arterialized venous pH, and PCO2 were found in exercise after sleep deprivation either. We therefore conclude that 30-h sleep loss alters cardiorespiratory function at rest and the ability to perform maximal exercise but not exercise endurance.
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PMID:Effects of 30-h sleep loss on cardiorespiratory functions at rest and in exercise. 190 33

The patient was 56-year-old female, who suffered from ataxia and then fell into coma on the next day after she had moved from the sea level to an altitude of 4,200 m. After she was brought to lower altitude, consciousness recovered within several hours. For about 2 days thereafter, disorientation was observed, and she was diagnosed as AMS (acute mountain sickness). Only insomnia continued in chronic stage. The results of X-ray computed tomography (CT) on 25th day after the onset of the disease revealed no abnormal finding except the slightly increasing uptake of contrast material. Symmetrical low density regions were seen in bilateral basal ganglia after one year, and the globus pallidus lesions were confirmed by magnetic resonance imaging. In the past, cerebral edema has been reported in most cases of AMS, and the neurotic symptoms of AMS have been attributed to cerebral edema, while the essential condition of this disease is not yet elucidated. In the present case, the globus pallidus lesions could be identified through the following-up of the central nervous system by X-ray CT and MRI as the first attempt for the case of AMS. There has been no report of globus pallidus lesions in the cases of AMS. Whereas low oxygen partial pressure is the primary cause of AMS, and it is highly probable that the disorders in globus pallidus as reported in the cases of carbon monoxide poisoning, anesthetic accident, etc. are related to the occurrence of AMS.
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PMID:[A case of acute mountain sickness with bilateral lesion of pallidum]. 222 57

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Workers exposed to carbon monoxide (CO) at a concentration of 26.8mg/m3 at an altitude of 2,300 metres above sea level were compared with a control group of local inhabitants. There were significant differences in symptoms of headache, vertige fatigue and weakness memory impairment, insomnia, palpitation and neurobehavioral functions. CO concentration in respiratory air and HbCO in blood was higher but partial pressure of oxygen (PO2) and saturation of oxygen (SaO2) in blood was lower in the exposed group than the control group. Self-comparison of CO in respiratory air and HbCO in blood was higher after work than before work. Neurasthenia rate was significantly higher but PO2 and SaO2 significantly lower at high altitude than in the plain. The results indicated that under same CO concentrations the hazards to workers at high altitude were greater than to those working in the plain. The author recommends that at high altitude the CO permissible level should be appropriately lowered.
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PMID:[Health effects on workers exposed to low concentration carbon monoxide at high altitude]. 835 10

Patients with severe chronic obstructive pulmonary disease (COPD) commonly complain of insomnia, but hypnotic drugs are generally not recommended due to their depressant effect on the respiratory centres. The aim of this study was, therefore, to compare the effects of a single dose of the benzodiazepine hypnotics, triazolam 0.25 mg and flunitrazepam 1 mg, and a new imidazopyridine compound, zolpidem 10 mg, in hypercapnic COPD patients. Twelve stable COPD patients (mean +/- SD arterial oxygen tension (PaO2) 9.3 +/- 0.8 kPa and arterial carbon dioxide tension (PaCO2) 5.9 +/- 1.9 kPa) were included in the study. The following measurements were performed before and 2 h after drug administration: PaO2 and PaCO2, minute ventilation (VE), mouth occlusion pressure (P0.1), rebreathing CO2 tests with ventilatory response to carbon dioxide stimulation (delta VE/delta PACO2) and mouth occlusion pressure response to carbon dioxide stimulation (delta P0.1/delta PACO2). The measurements were performed in a randomized, double-blind fashion, each patient receiving a single dose of each drug on three different days, separated by a one week interval. No difference was noted between control measurements and those taken 2 h after administration of zolpidem in the following parameters: PaCO2, PaCO2, VE, P0.1, delta VE/delta PACO2 and delta P0.1/PACO2. Two hours after administration of triazolam and flunitrazepam, a significant difference was noted in VE for triazolam and for flunitrazepam. After flunitrazepam administration, a significant decrease in PaCO2 (6 +/- 1.8 at baseline versus 7 +/- 0.4 kPa), and delta VE/PACO2 (0.44 +/- 0.20 at baseline versus 0.31 +/- 0.21 l.min-1 x kPa) were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of zolpidem, triazolam and flunitrazepam on arterial blood gases and control of breathing in severe COPD. 851 70

Cheyne-Stokes respiration (CSR) is a form of sleep-disordered breathing seen in approximately 40% of congestive heart failure patients with a left ventricular ejection fraction of < 40%. It is characterized by a crescendo-decrescendo alteration in tidal volume separated by periods of apnea or hypopnea. Sleep is generally disrupted, often with frequent nocturnal arousals. Clinical features include excessive daytime sleepiness, paroxysmal nocturnal dyspnea, insomnia, and snoring. Proposed mechanisms include the following: (1) an increased CNS sensitivity to changes in arterial PCO2 and PO2 (increased central controller gain); (2) a decrease in total body stores of CO2 and O2 with resulting instability in arterial blood gas tensions in response to changes in ventilation (underdamping); and (3) an increased circulatory time. In addition, hyperventilation induced hypocapnia seems to be an important determinant for the development of CSR. Mortality appears to be increased in patients with CSR compared to control subjects with a similar degree of left ventricular dysfunction. Therapeutic options include medically maximizing cardiac function, nocturnal oxygen therapy, and nasal continuous positive airway pressure. The role that other therapeutic modalities, such as inhaled CO2 and acetazolamide, might have in the treatment of CSR associated with congestive heart failure has yet to be determined.
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PMID:Cheyne-Stokes respiration during sleep in congestive heart failure. 904 98

The effect of sleep deprivation on male runners (age 18.1 +/- 0.35) and volleyball players (age 17.8 +/- 0.36) has not been investigated. Therefore, we studied the possible effect of sleep deprivation in the sportsmen. The athletes performed spirometric tests at rest and then incremental exercise test on ergometer following one night sleep and one night (25-30 h) sleeplessness. Several standard measurements of spirometric function showed no significant change following sleep loss. Sleep loss raised resting oxygen uptake (VO2) in the runners and resting carbon dioxide production (VCO2) in both the runners and the volleyball players (p < 0.05). However, it left heart rate (HR), respiratory quotient (R), minute ventilation (VE) and arterial oxygen saturation (SaO2) unchanged at rest in both groups. Sleep loss decreased time to exhaustion in the volleyball players (p < 0.01). In the runners and the volleyball players, sleep loss did not alter exercise values of HR, VO2, VCO2, R and SaO2, but it reduced exercise VE (p < 0.05). We suggest that one night sleep deprivation may reduce exercise performance by decreasing exercise VE and time to exhaustion. We also indicate that sleep loss may decrease more the performance of volleyball players than that of runners.
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PMID:Effects of sleep deprivation on cardiorespiratory functions of the runners and volleyball players during rest and exercise. 1926 40

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

The nature of the noradrenergic dysregulation in clinical anxiety disorders remains unclear. In panic disorder, the predominant view has been that central noradrenergic neuronal networks and/or the sympathetic nervous system was normal in patients at rest, but hyper-reactive to specific stimuli, for example carbon dioxide. These ideas have been extended to other anxiety disorders, which share with panic disorder characteristic subjective anxiety and physiological symptoms of excess sympathetic activity. For example, Generalized Anxiety Disorder is characterized by chronic free-floating anxiety, muscle tension, palpitation and insomnia. It has been proposed that there is chronic central hypersecretion of noradrenaline in Generalized Anxiety Disorder, with consequent hyporesponsiveness of central post-synaptic receptors. With regards to other disorders, it has been suggested that there is noradrenergic involvement or derangement, but a more specific hypothesis has not been enunciated. This paper reviews the evidence for noradrenergic dysfunction in anxiety disorders, derived from indirect measures of noradrenergic function in clinical populations.
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PMID:The role of central noradrenergic dysregulation in anxiety disorders: evidence from clinical studies. 2053 May 86


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