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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep pattern and breathing in humans are altered following cerebrovascular accidents involving the brainstem. Sleep apnea is a well-established complication of stroke involving the brainstem. On the other hand, the effect of cerebral stroke on sleep and breathing has not been well defined. The diffuse cerebral symptoms such as cognitive deficits, depression or fatigue, after hemispheric stroke mimic those present in patients with sleep apnea. To define the breathing pattern in patients with stroke involving cerebral hemispheres without brainstem lesion and without the prior history of sleep-disordered breathing, we studied 10 patients within 1 year of their stroke. The data collected during polysomnography from the stroke patients were compared with a group of subjects matched for age, body mass index, presence of hypertension, and smoking history without stroke. Patients with stroke had an abnormal sleep architecture with significantly lower slow wave sleep and rapid eye movement (REM) sleep when compared with controls. Sleep was fragmented because of the presence of increased respiratory disturbances. Stroke patients had a respiratory disturbance index of 52 +/- 10 events per hour when compared with 3 +/- 1 in controls (p < .05). Majorities of respiratory events were obstructive apneas and were associated with arterial oxygen desaturations and arousals. The pathogenic mechanism of sleep-disordered breathing in patients with hemispheric stroke seems to be related to the physiological effect of sleep on already compromised upper airway muscle control. Patients with stroke and diffuse cerebral symptoms should be investigated for the possibility of sleep-disordered breathing.
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PMID:Sleep apnea in patients with hemispheric stroke. 781 Nov 79

It has long been known, that irregular, heavy snoring and daytime sleepiness are common features of acromegaly. Only recently has the high incidence (30-60%) and clinical relevance of the sleep apnoea underlying these symptoms been recognized. Both diseases have a group of common symptoms and prognostic features: Increased cardiovascular and respiratory mortality, elevated incidence of hypertension, daytime sleepiness, decreased vitality, headaches and depression. These are very prominent in sleep apnoea and often reversible under treatment. In acromegaly their etiology has been widely unexplained and they commonly persist even when human growth hormone (hGH) levels remain normal after operative treatment. We report on 2 patients presenting with excessive daytime sleepiness and severe obstructive sleep apnoea caused by acromegaly. Both had macroglossia and hypertrophy of hypopharyngeal tissues regressive after surgical therapy. The average hGH-levels were 20 and 31 ng/ml before and 3 and 1.7 ng/ml several months after operation respectively. Apnoea indices and minimal oxygen saturations (SO2) were 59/h and 55/h, and 60% and 58% initially and improved postoperatively to 40/h and 50/h, and 72% and 70%. Polysomnographic parameters were normalized by NCPAP-therapy pre- and postoperatively and daytime sleepiness improved dramatically. In one patient the NCPAP-pressure could be decreased postoperatively. Since patients with sleep apnoea have an increased perioperative risk of hypoxia and because transsphenoidal operation and postoperative nasal tamponade were performed, both patients were tracheostomized perioperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnoea in acromegaly--prevalence, pathogenesis and therapy. Report on two cases. 783 Dec 13

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

38 male patients with obstructive sleep apnea were asked to complete 2 weeks of rating symptoms, physical examination, diagnostic polysomnography, and MMPI testing prior to being placed on nasal continuous positive airway pressure (CPAP) therapy. Six months later, 26 (72.2%) of the 36 subjects available for follow-up showed continued compliance. A regression analysis conducted with those 28 subjects who completed all pretreatment measures showed that continued therapy was predicted by such pretreatment measures as patients' body mass index, ratings of daytime sleepiness and nocturnal sleep quality, and MMPI Depression and Hypochondriasis scale scores (R2 = 0.63). Eventual compliers had a higher Body Mass Index, reported less daytime sleepiness and better nocturnal sleep quality, and scored lower on the MMPI D and Hs scales prior to treatment than did the noncompliers. A linear discriminant function analysis with analog cross-validation showed these five predictors would identify approximately 80% of eventual noncompliers and 97% of those who display compliance. It was concluded that subjective report and personality measures may be useful in predicting long-term use. Additional studies are needed to assess the clinical significance of the noted MMPI scale elevations among sleep apnea patients in general and among those patients who display eventual noncompliance.
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PMID:Psychological status, syndromatic measures, and compliance with nasal CPAP therapy for sleep apnea. 793 34

Impaired vigilance performance has been reported in older subjects with sleep apnea syndrome (SAS). The current study is an attempt to extend these findings and to investigate additional factors that might have implications for vigilance in the older adult. Fifty-nine older adults [age: 62 +/- 5 (mean +/- SD), range 54-75 years; respiratory disturbance index (RDI): 8.8 +/- 14.4 (mean +/- SD), range 0-67.5] were categorized as SAS or NotSAS, based on various classification criteria [i.e. apnea index (AI) > or = 5, and 10, RDI > or = 5, 10 and 15], and were compared on their vigilance performance as assessed by the computer program "Steer Clear". Vigilance performance did not discriminate the groups, independent of how they were formed. Groups were then formed based on vigilance performance (HiVig vs. LowVig) and compared on assorted sleep variables, periodic leg movements, and self-reported hypersomnolence and depression. Only age discriminated vigilance performance (an inverse relationship), accounting for 31% of the observed variance. Our findings suggest that subject selection may unintentionally bias findings regarding the neuropsychological functioning of individuals with SAS, that vigilance may be impaired only in relatively more "severe" SAS, and that severity of SAS in older adults may not be well characterized by current classification standards. Age clearly impacted vigilance performance, despite the constricted age range sampled, and should be taken into account in future research.
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PMID:Sleep apnea and vigilance performance in a community-dwelling older sample. 793 25

In postnatal infants, there is similarity between the time course of transient gonadal steroid secretion and the age-related incidence of sudden infant death syndrome (SIDS). The cause of death in SIDS is generally thought to be a ventilatory arrest, but the mechanism responsible for such an event remains unknown. Testosterone has been demonstrated to depress ventilatory drive and increase sleep apnea in adult men. We tested the hypothesis that the gonadal steroid testosterone depresses infant ventilatory drive during sleep. Three newborn male infant primates were gonadectomized after birth. Ventilation was observed and quantified for each animal during completely natural unencumbered sleep by plethysmography for an average of 16 wk. Ventilatory patterns were recorded, and ventilatory drive was challenged with hypercapnia and hypoxia during quiet sleep on the night before and the night after testosterone administration. Hypercapnic ventilatory drive during sleep was significantly depressed by an average of 33.6% on the night after compared with the night before testosterone administration. Depression of the response to hypercapnia after testosterone was not accompanied by any change in resting minute ventilation measured during quiet sleep. Hypoxic ventilatory drive, incidence of apneic events, and length of apnea were not different after testosterone. The effects of injecting a placebo on ventilatory patterns and drive were tested by giving the placebo to all animals on several test weeks. Placebo injections produced no significant change in any measured parameters. These results support the hypothesis that testosterone depresses hypercapnic ventilatory drive during sleep in the infant primate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Depression of hypercapnic ventilatory drive by testosterone in the sleeping infant primate. 804 60

The objective of the study was to evaluate the relation between every-night (habitual) snoring, sleep apnea and cognitive complaints (concentration and memory problems) in an adult population-based sample. In the Dan-MONICA (MONItoring trends in CArdiovascular diseases) 1,504 males and females aged 30, 40, 50 and 60 years were classified according to their snoring habits. Nocturnal respiration was measured in 748 participants. The following measures were regarded as potential confounders: age, gender, unintended sleepiness, insomnia, depression, hypnotic use, alcohol and tobacco consumption by questionnaire, body mass index (BMI) and blood pressure. Concentration and memory problems were both related to depression, insomnia and unintended sleepiness. Snoring and sleep apnea (defined as a respiratory distress index - RDI > or = 5), were associated with concentration problems and unintended sleepiness. The odds ratios (95% confidence intervals) between snoring, concentration and memory problems, calculated by logistic regression analysis after adjustments of the above confounders, were 1.90 (1.23-2.91, p < 0.01) and 1.38 (0.97-1.99, NS). For those with sleep apnea, the odds ratios were 3.53 (1.42-8.73, p < 0.001) and 1.51 (0.81-2.14, NS) for concentration and memory problems, respectively. The main conclusion drawn from this study is that cognitive complaints show a high correlation to mood, insomnia, and hypersomnia. Habitual snoring and sleep apnea show a correlation to concentration problems, but not to memory complaints. This suggests that part of the association between snoring, sleep apnea and cognitive dysfunction is related to the presence of sleep disturbances and daytime sleepiness.
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PMID:Self-assessed cognitive function in snorers and sleep apneics. An epidemiological study of 1,504 females and males aged 30-60 years: the Dan-MONICA II Study. 808 78

Ten patients undergoing major abdominal surgery under general anaesthesia were monitored with a pulse oximeter, electroencephalogram, electromyogram, electrocardiogram and eye and hand movement sensors two nights before and three nights after surgery. Episodic hypoxaemic events were increased significantly after surgery (P < 0.05). Rapid eye movement (REM) sleep decreased significantly on the first night after operation (P < 0.05). Seven patients had increased amounts of REM sleep (rebound) on the second, third or both nights after operation compared with the preoperative night. Slow wave sleep was depressed significantly on the first two nights after operation (P < 0.05). REM sleep-associated hypoxaemic episodes for individual patients increased about three-fold on the second and third nights after operation compared with the night before operation (P < 0.05). We conclude that postoperative sleep pattern is disturbed severely with early depression of REM and slow wave sleep and with rebound of REM sleep on the second and third nights. Postoperative rebound of REM sleep may contribute to the development of sleep disordered breathing and nocturnal episodic hypoxaemia.
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PMID:Late postoperative nocturnal episodic hypoxaemia and associated sleep pattern. 811 May 63

Patient-controlled iv delivery of opioids for postoperative pain management is a popular alternative to the traditional im route of administration. However, occasional patients receiving opioids in this manner develop severe respiratory depression. The purpose of this paper is to determine the incidence of, and factors contributing to, the development of this complication. To do this, the Office of Medical Quality Improvement retrospectively searched for reports of respiratory depression in a database compiled from the charts of approximately 1600 patients who had received PCA at the University of Alberta Hospitals in 1992. Eight cases of serious respiratory depression were detected. Factors associated with the occurrence of respiratory depression included the concurrent use of a background infusion, advanced age, concomitant administration of sedative/hypnotic medications, and pre-existing sleep apnoea syndrome. No cases were attributed to operator error or equipment malfunction. In conclusion, the risk of respiratory depression with patient-controlled opioid administration is similar to that observed when opioids are delivered by the traditional im or spinal routes. The safe and effective use of patient-controlled analgesia depends upon knowledgeable medical and nursing staff, clearly defined nursing policy and procedures, and frequent patient follow-up.
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PMID:Respiratory depression associated with patient-controlled analgesia: a review of eight cases. 790 32

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53


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