Fifty patients with chronic obstructive lung disease were questioned about their sleep quality and their responses were compared with those of 40 similarly aged patients without symptomatic lung disease. Patients with chronic obstructive lung disease reported more difficulty in getting to sleep and staying asleep and more daytime sleepiness than the control group. More than twice as many patients (28%) as controls (10%) reported regular use of hypnotics. In a subgroup of 16 patients with chronic obstructive lung disease (mean FEV, 0-88 (SD 0 44) 1) sleep, breathing, and oxygenation were measured to examine the relationship between night time hypoxaemia and sleep quality. Sleep architecture was disturbed in most patients, arousals occurring from three to 46 times an hour (mean 15 (SD 14)/h). Arterial hypoxaemia during sleep was common and frequently severe. The mean (SD) arterial oxygen saturation (Sao2) at the onset of sleep was 91% (7%). Nine patients spent at least 40% of cumulative sleeping time at an Sao2 of less than 90% and six of these patients spent 90% of sleeping time below this level. Only four of 15 patients did not develop arterial desaturation during sleep. The mean minimum Sao2 during episodes of desaturation was less in rapid eye movement (REM) sleep (72% (17%)) than in non-REM sleep (78% (10%); p < 0 05). The predominant breathing abnormality associated with desaturation was hypoventilation; only one patient had obstructive sleep apnoea. Arousals were related to oxygenation during sleep such that the poorer a patient's arterial oxygenation throughout the night the more disturbed his sleep (arousals/h v Sao2 at or below which 40% of the total sleep time was spent: r = 0-71, p < 0X01). Hypoxaemia during sleep was related to waking values of Sao2 and PaCo2 but not to other daytime measures of lung function.It is well recognised that sleep is associated with arterial oxygen desaturation in patients with chronic obstructive lung disease.' -6 Some physiological consequences of this desaturation, such as pulmonary hypertension, have been well investigated2 7 -9; reports of the consequences of arterial hypoxaemia in terms of quality of sleep and sleep related symptoms, however, are few and conflicting.'0'-4

We conducted a study of the prevalence of sleep-disordered breathing in subjects derived from a random sample of the population. A total of 2,202 subjects 35 to 69 yr of age were approached. Four hundred forty-one answered a questionnaire concerning their sleep symptoms, general health, and habits such as alcohol consumption, and they were monitored for sleep-disordered breathing (SDB). The sample was biased in favor of snorers and those with other subjective sleep complaints. Fifty-six percent of the subjects were men. Of the 441 subjects 79 (17.9%) had SDB (more than 15 episodes of apnea or hypopnea per hour: respiratory distress index [RDI] > or = 15), 289 were snorers but had RDI < 15, and 73 were nonsnorers. The prevalence of SDB in this sample was therefore at least 3.6% (79 of 2,204). The minimum prevalence in men was 5.7%, and in women it was 1.2%. Logistic regression identified only male sex as an independent predictor of snoring without SDB (adjusted odds ratio [OR], 3.24; 95% CI, 1.33 to 7.82), body mass index (adjusted OR for an increase of 5 kg/m2, 0.95; 95% CI, 0.85 to 1.05), and alcohol consumption (adjusted OR for an increase of 10 g/day, 1.05; 95% CI, 0.84 to 1.37) were not significant predictors of snoring. The independent predictors of SDB among snorers were age (adjusted OR for an increase of 5 yr, 1.26; 95% CI, 1.08 to 1.47) and neck circumference (adjusted OR for an increase of 2 cm, 1.53; 95% CI, 1.16 to 2.00).(ABSTRACT TRUNCATED AT 250 WORDS)

In order to determine whether measurement of arterial oxygen saturation (SaO2) could identify patients with obstructive sleep apnea (OSA), 98 consecutive patients referred for assessment of snoring and/or daytime somnolence were assessed clinically and then underwent both unsupervised oximetry in their homes and formal polysomnography. Clinical assessment identified patients with an apnea+hypopnea index (AHI) > or = 15 events per hour with a sensitivity of 79% and a specificity of 50%. Home oximetry analyzed by counting the number of arterial oxygen desaturations recorded was inferior to clinical assessment. For desaturations of 2% or more from baseline, desaturation index (DI) > or = 15 per hour identified patients with AHI > or = 15 with sensitivity 65% and specificity 74%; for 3% desaturations, sensitivity was 51% and specificity 90%; and for 4% desaturations, sensitivity was 40% and specificity 98%. From the oximetry data, the percentage of time spent at SaO2 below 90% (CT90) was also calculated. CT90 > or = 1% identified patients with AHI > or = 15 with sensitivity 93% and specificity 51%; for patients with AHI > or = 15 ultimately given nasal continuous positive airway pressure (CPAP), the sensitivity of a CT90 > or = 1% was 100%. We concluded that home oximetry with CT90 < 1% practically excludes clinically significant OSA. Conversely, home oximetry with DI > or = 15 for 4% desaturations makes OSA likely: the positive predictive value for OSA is 83% if the pretest probability of OSA is 30% and over 90% if the pretest probability is at least 50%.

We tested the hypothesis that hyperresponsiveness of the upper airway (UAHR) is present in patients with chronic cough of diverse etiology. We determined the frequency of bronchial hyperresponsiveness (BHR), hyperresponsiveness of the upper airway, sputum eosinophilia, pulmonary aspiration, and psychological symptoms in adults with chronic cough. Consecutive adults (n = 30) presenting to a tertiary referral clinic with chronic cough were compared with a group of 20 asymptomatic adults. Measurements included histamine provocation testing with measurement of flow volume curves to determine inspiratory and expiratory airflow obstruction; hypertonic saline induced sputum for analysis of eosinophils, mast cells and lipid-laden macrophages; and a validated psychological symptom questionnaire. Symptomatic rhinitis and gastroesophageal reflux were common causes of chronic cough. BHR occurred in seven patients (23%) and in no control subjects (p < 0.05). UAHR occurred in 40% of patients with cough and in four (20%) control subjects (p > 0.05). Eosinophils were present in the sputum of more patients with cough than control subjects (50% versus 19%; p < 0.05). High degrees of eosinophilia were present in six patients with cough, including three without BHR. No subject had significant lipid-laden macrophages. There was greater somatization in patients with chronic cough; ten subjects scored in the clinically significant range (p < 0.05). Abnormalities in one or more of these tests were 7.67-fold (95% CI 1.83-34.52) more likely to occur in cough patients than control subjects. We conclude that chronic cough is a nonspecific symptom that is associated with several apparently unrelated mechanisms. These include UAHR, somatization, BHR, and eosinophilic bronchitis. UAHR cannot be implicated as a single unifying mechanism. These findings emphasize the need to systematically evaluate several different causes of cough in patients who present with chronic cough.

SUMMARYThe aim of this study was to identify factors other than objective sleep tendency associated with scores on the Epworth Sleepiness Scale (ESS). There were 225 subjects, of whom 40% had obstructive sleep apnoea (OSA), 16% had simple snoring, and 4.9% had snoring with sleep disruption (upper airway resistance syndrome); 9.3% had narcolepsy and 7.5% had hypersomnolence without REM sleep abnormalities; 12% had chronic fatigue syndrome; 7.5% had periodic limb movement disorder and 3% had diurnal rhythm disorders. ESS, the results of overnight polysomnography and multiple sleep latency test (MSLT) and SCL-90 as a measure of psychological symptoms were recorded. The ESS score and the mean sleep latency (MSL) were correlated (Spearman =−0.30, P<0.0001). The MSL was correlated with total sleep time (TST) and with sleep efficiency but not with apnoea/hypopnoea index. There was no association between the MSL and any aspect of SCL-90 scores, except a borderline significant association with the somatisation subscale. The ESS was correlated with TST but not with sleep efficiency or apnoea/hypopnoea index. The ESS was correlated with all subscales of the SCL-90 except psychoticism. An ESS[10 had poor sensitivity and specificity as a predictor of MSL <10 min or MSL <5 min. We conclude that the MSLT and the ESS are not interchangeable. The ESS was influenced by psychological factors by which the MSL was not affected. The ESS cannot be used to demonstrate or exclude sleepiness as it is measured by MSLT.