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1.  Sleep‐disordered breathing after stroke: a randomised controlled trial of continuous positive airway pressure 
Background
Sleep‐disordered breathing (SDB) is common after stroke, but it is unclear whether it should be treated.
Objective
To conduct a randomised controlled trial of continuous positive airway pressure (CPAP) after stroke.
Methods
Patients with stroke with ⩾30 apnoeas and hypopnoeas per hour ((A+H)/h) with predominant obstructive sleep apnoea or hypopnoea were randomised to either CPAP treatment or conservative treatment for 8 weeks. Outcomes were measured blind to treatment allocation at 8 weeks and 6 months after the stroke. The primary outcome was physical function on the Nottingham Extended Activities of Daily Living Scale.
Results
Of 658 patients with stroke screened, only 71 (10.7%) were eligible and consented to a sleep study 14–19 days after stroke. 66 patients completed the sleep study (21 women; mean age 72 years), 33 (50%) had ⩾30 (A+H)/h that were predominantly obstructive. 15 were randomised to CPAP treatment and 15 to conventional treatment. Despite intensive efforts, objective use of CPAP was poor, averaging 1.4 h a night. CPAP treatment resulted in no significant improvements (p>0.1) in the primary outcome or in neurological function or sleepiness, and in poorer health status on some measures.
Conclusions
This trial showed no benefit from CPAP treatment, the relevance of the observed detrimental effects is questionable. Even in our highly selected patients with stroke, use of CPAP was poor. At present, CPAP treatment should be advocated for patients with stroke only if they have symptoms of SDB.
doi:10.1136/jnnp.2005.086686
PMCID: PMC2077531  PMID: 16772358
2.  Effect of chronic continuous positive airway pressure (CPAP) therapy on upper airway size in patients with sleep apnoea/hypopnoea syndrome. 
Thorax  1996;51(2):190-192.
BACKGROUND: There is evidence to suggest that chronic continuous positive airway pressure (CPAP) therapy may produce reversible changes in upper airway morphology and function in patients with sleep apnoea/hypopnoea. This study was designed to examine the effect of chronic CPAP therapy on upper airway calibre. METHODS: Twenty four men with the sleep apnoea/hypopnoea syndrome (mean (SE) apnoea/hypopnoea index 37 (5)) underwent lateral cephalometry with measurement of posterior airway space performed before and at least three months after initiation of CPAP therapy. RESULTS: There was no weight change between the two assessments and mean CPAP use was 4.8 (0.4) hours per night. Posterior airway space (PAS) was measured in erect and supine postures. PAS supine increased with CPAP therapy from a mean (SE) of 11.8 (0.8) mm to 13.4 (0.8) mm, but PAS erect did not. Correlation of the change in PAS (dPAS) before and after CPAP therapy showed an increase with increasing CPAP compliance measured as machine run time both for dPAS supine (r = 0.68) and dPAS erect (r = 0.47). CONCLUSIONS: Patients with the sleep apnoea/hypopnoea syndrome regularly using CPAP for more than four hours per night all showed an increase in dPAS supine. The use of chronic CPAP increases PAS supine probably by a reduction in upper airway oedema, and the change in size is dependent on CPAP use.
PMCID: PMC473036  PMID: 8711654
3.  Comparison of polysomnography with ResCare Autoset in the diagnosis of the sleep apnoea/hypopnoea syndrome. 
Thorax  1995;50(11):1201-1203.
BACKGROUND--Increasing referral numbers make the development of simplified accurate methods of diagnosing the sleep apnoea/hypopnoea syndrome highly desirable. The accuracy of one such system--the ResCare Autoset--has been examined. METHODS--Thirty one consecutive patients assessed by polysomnography had simultaneous monitoring of their respiratory pattern using the Autoset system. The Autoset detects episodes of flattening of the flow/time profile using nasal cannulae. RESULTS--There was a good correlation (r = 0.85) between the number of apnoeas+hypopnoeas/hour in bed recorded using polysomnography and the Autoset system. The median difference in such events was 3.1 (95% confidence interval 8.4 to -1.6)/hour in bed. In two patients the Autoset scored 70 apnoeas+hypopnoeas/hour in bed compared with 34 apnoeas+hypopnoeas with 35 arousals/hour in bed by polysomnography; however, this did not alter the diagnostic category of either patient. Autoset gave a sensitivity of 100%, specificity of 92%, positive predictive value of 92%, and negative predictive value of 100%, which was better than oximetry alone. A sleep study using the Autoset system costs 14 pounds compared with 126 pounds for polysomnography. CONCLUSIONS--The Autoset is clinically useful for diagnosing the sleep apnoea/hypopnoea syndrome.
PMCID: PMC475095  PMID: 8553279
4.  Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome. 
Thorax  1994;49(3):263-266.
BACKGROUND--Continuous positive airway pressure (CPAP) therapy is the treatment of choice for the sleep apnoea/hypopnoea syndrome. Compliance with this relatively obtrusive therapy has not been well studied. METHODS--Usage of CPAP was investigated in 54 patients with sleep apnoea/hypopnoea syndrome (median 36 (range 7-129) apnoeas + hypopnoeas/hour slept) over the first 1-3 months after starting CPAP therapy. In all cases CPAP usage was monitored by hidden time clocks that indicated for how long the machines were switched on--that is, the CPAP run time. In 32 patients the time at which the CPAP mask pressure was at the therapeutic level of CPAP pressure set for that patient--that is, the mask time--was also monitored. In all patients objective daytime sleepiness was assessed by multiple sleep latency before and after CPAP therapy. RESULTS--The mean (SE) nightly CPAP run time was 4.7 (0.4) hours. There was no correlation between run time and severity of the sleep apnoea/hypopnoea syndrome as assessed by apnoea + hypopnoea frequency or multiple sleep latency, and no correlation between CPAP usage and improvement in multiple sleep latency. Thirty two patients in whom mask time was recorded had therapeutic CPAP pressures for 89% (3%) of their CPAP run times. Patients who experienced side effects from CPAP used their CPAP machines significantly less than those who did not. CONCLUSIONS--Patients with sleep apnoea/hypopnoea syndrome used CPAP for less than five hours/night on average with no correlation between severity of sleep apnoea/hypopnoea syndrome and CPAP usage. Patients who complained of side effects used their CPAP therapy less. It is recommended that, as a minimum, CPAP run time should be regularly recorded in all patients receiving CPAP therapy.
PMCID: PMC1021157  PMID: 8202884
5.  Role of inflammation in nocturnal asthma. 
Thorax  1994;49(3):257-262.
BACKGROUND--Nocturnal airway narrowing is a common problem for patients with asthma but the role of inflammation in its pathogenesis is unclear. Overnight changes in airway inflammatory cell populations were studied in patients with nocturnal asthma and in control normal subjects. METHODS--Bronchoscopies were performed at 0400 hours and 1600 hours in eight healthy subjects and in 10 patients with nocturnal asthma (> 15% overnight fall in peak flow plus at least one awakening/week with asthma). The two bronchoscopies were separated by at least five days, and both the order of bronchoscopies and site of bronchoalveolar lavage (middle lobe or lingula with contralateral lower lobe bronchial biopsy) were randomised. RESULTS--In the normal subjects there was no difference in cell numbers and differential cell counts in bronchoalveolar lavage fluid between 0400 and 1600 hours, but in the nocturnal asthmatic subjects both eosinophil counts (median 0.11 x 10(5) cells/ml at 0400 hours, 0.05 x 10(5) cells/ml at 1600 hours) and lymphocyte numbers (0.06 x 10(5) cells/ml at 0400 hours, 0.03 x 10(5) cells/ml at 1600 hours) increased at 0400 hours, along with an increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid (3.0 micrograms/ml at 0400 hours, 2.0 micrograms/l at 1600 hours). There were no changes in cell populations in the bronchial biopsies or in alveolar macrophage production of hydrogen peroxide, GM-CSF, or TNF alpha in either normal or asthmatic subjects at 0400 and 1600 hours. There was no correlation between changes in overnight airway function and changes in cell populations in the bronchoalveolar lavage fluid. CONCLUSIONS--This study confirms that there are increases in inflammatory cell populations in the airway fluid at night in asthmatic but not in normal subjects. The results have also shown a nocturnal increase in eosinophil cationic protein levels in bronchoalveolar lavage fluid, but these findings do not prove that these inflammatory changes cause nocturnal airway narrowing.
PMCID: PMC1021156  PMID: 8202883
6.  Evaluation of a computerised polysomnography system. 
Thorax  1993;48(3):280-283.
BACKGROUND: Manual analysis of sleep, breathing, and oxygenation records is the "gold standard" for diagnosing sleep abnormalities but is time consuming and cumbersome. The accuracy and cost of a computerised sleep analysis system have therefore been investigated. METHODS: Manual and computerised (CNS Sleep Lab) scores from 43 consecutive clinical sleep studies were prospectively compared for accuracy and the time and costs were recorded. RESULTS: There were good correlations and no systematic differences between manual and computer scoring for total sleep time, sleep onset latency, and duration of REM sleep. There was a small but clinically insignificant systematic difference in breathing pattern analysis, the number of hypopnoeas/hour being lower with manual than with computer scoring (13 (SE 3) v 15 (SE 3)/hour). There was no difference between computer and manual scoring of the frequency of apnoeas, so the frequency of apnoeas + hypopnoeas was clinically insignificantly higher with computer scoring with a highly significant correlation between the two techniques. The time taken to perform the analyses was not different between the two methods (manual 83 (SE 8) v computer 86 (SE 8) minutes). The computer system was six times more expensive than the manual system and annual running costs, including full maintenance contract and 15% depreciation, were twice as great. CONCLUSION: The CNS Sleep Lab is sufficiently accurate for use in clinical sleep studies but is significantly more expensive and does not save technician time.
PMCID: PMC464370  PMID: 8497829
7.  Salmeterol in nocturnal asthma: a double blind, placebo controlled trial of a long acting inhaled beta 2 agonist. 
BMJ : British Medical Journal  1990;301(6765):1365-1368.
OBJECTIVE--To determine whether inhaled salmeterol, a new long acting inhaled beta adrenergic agonist, reduces nocturnal bronchoconstriction and improves sleep quality in patients with nocturnal asthma. DESIGN--Randomised, double blind, placebo controlled crossover study. SETTING--Hospital outpatient clinics in Edinburgh. SUBJECTS--Twenty clinically stable patients (13 women, seven men) with nocturnal asthma, median age 39 (range 18-60) years. INTERVENTIONS--Salmeterol 50 micrograms and 100 micrograms and placebo taken each morning and evening by metered dose inhaler. Rescue salbutamol inhalers were provided throughout the run in and study periods. MAIN OUTCOME MEASURES--Improvement in nocturnal asthma as measured by peak expiratory flow rates and change in sleep quality as measured by electroencephalography. RESULTS--Salmeterol improved the lowest overnight peak flow rate at both 50 micrograms (difference in median values (95% confidence interval for difference in medians) 69 (18 to 88) l/min) and 100 micrograms (72 (23 to 61) l/min) doses twice daily. While taking salmeterol 50 micrograms twice daily patients had an objective improvement in sleep quality, spending less time awake or in light sleep (-9 (-4 to -44) min) and more time in stage 4 sleep (26 (6-34) min). CONCLUSIONS--Salmeterol is an effective long acting inhaled bronchodilator for patients with nocturnal asthma and at a dose of 50 micrograms twice daily improves objective sleep quality.
PMCID: PMC1664533  PMID: 1980220
8.  Use of home sleep studies for diagnosis of the sleep apnoea/hypopnoea syndrome 
Thorax  1997;52(12):1068-1073.
BACKGROUND: A study was undertaken to test the hypothesis that unsupervised domiciliary limited sleep studies do not impair the accuracy of diagnosis when used to investigate the sleep apnoea/hypopnoea syndrome (SAHS) and can be cheaper than laboratory polysomnography. METHODS: For validation, 23 subjects with suspected SAHS underwent laboratory polysomnography and a home study (EdenTec 3711) on successive nights. All subjects with > 15 apnoeas + hypopnoeas (A + H)/hour on polysomnography showed > 30 A + H/hour on their home study. Thereafter, in a prospective trial 150 subjects had a home study as the initial investigation and studies showing > 30 events/hour were regarded as diagnostic of SAHS. Those showing fewer events were investigated with polysomnography if necessary. Time to treatment, outcome, and costs of this protocol were compared with those of 75 patients investigated initially with polysomnography. RESULTS: Of the prospective trial subjects, 29% had > 30 A + H/hour and proceeded directly from home study to treatment; 15% without daytime sleepiness were not investigated further. Polysomnography was undertaken to establish a diagnosis in 56% of cases, including 18% whose home studies were unsuccessful. Compared with the 75 control patients, this protocol gave a diagnosis faster (median 18 (range 0-221) versus 47 (0-227) days, p < 0.001) and more cheaply (mean (SD) 164 pounds (104) versus 210 pounds (0), p < 0.001). The proportions offered CPAP (61% versus 67%) and subsequent objective CPAP usage (mean 4.7 (2.4) versus 5.0 (2.4) hours/night) were not different. CONCLUSIONS: Use of home sleep studies has benefits in time and cost. For diagnostic reliability a further sleep study was required in 56% of cases. 



PMCID: PMC1758463  PMID: 9516901
9.  Effect of CPAP therapy on daytime function in patients with mild sleep apnoea/hypopnoea syndrome 
Thorax  1997;52(2):114-119.
BACKGROUND: Continuous positive airway pressure (CPAP) is an effective treatment in patients with moderate and severe sleep apnoea/hypopnoea syndrome (SAHS), but the minimum illness severity at which patients obtain benefit from CPAP is unclear. A study was therefore undertaken to investigate whether CPAP improves symptoms and daytime function in patients with mild SAHS. METHODS: Sixteen consecutively recruited patients with mild SAHS (5.0-14.9 apnoeas + hypopnoeas per hour slept and two or more symptoms of SAHS) participated in a prospective placebo controlled randomised crossover trial to assess the effects of CPAP on symptoms and daytime function. Patients spent four weeks on placebo and four weeks on CPAP, undergoing assessments of sleepiness, symptoms, cognitive performance, and well being on the last day of each treatment. Data from the placebo and CPAP assessments were compared. RESULTS: The mean (SE) objective effective use of CPAP was 2.8 (0.7) hours per night. Significant improvements in symptom score (-1.7 (0.5), p < 0.01), mental flexibility (-14 (5) seconds, p = 0.02), and depression rating (-1.6 (0.8), p = 0.03) on CPAP were observed. However, no significant differences in subjective or objective sleepiness were found. Ten of the 16 patients preferred CPAP and opted to continue with this treatment, although this proportion was non- significant (p > 0.4). The eight patients with best CPAP use showed an additional CPAP related improvement in quality of life (-4.4 (1.8), p = 0.03). Those who complied better with CPAP therapy also had a higher average microarousal frequency (p < 0.01) and apnoea+hypopnoea index (p = 0.02) than the poorer compliers. CONCLUSIONS: The results of this study provide evidence for improvements in symptoms and daytime function for patients with mild SAHS treated with CPAP. 



PMCID: PMC1758499  PMID: 9059469
11.  Morbidity in nocturnal asthma: sleep quality and daytime cognitive performance. 
Thorax  1991;46(8):569-573.
Most patients with asthma waken with nocturnal asthma from time to time. To assess morbidity in patients with nocturnal asthma nocturnal sleep quality, daytime sleepiness, and daytime cognitive performance were measured prospectively in 12 patients with nocturnal asthma (median age 43 years) and 12 age and intellect matched normal subjects. The median (range) percentage overnight fall in peak expiratory flow rate (PEF) was 22 (15 to 50) in the patients with nocturnal asthma and 4 (-4 to 7) in the normal subjects. The patients with asthma had poorer average scores for subjective sleep quality than the normal subjects (median paired difference 1.1 (95% confidence limits 0.1, 2.3)). Objective overnight sleep quality was also worse in the asthmatic patients, who spent more time awake at night (median difference 51 (95% CL 8.1, 74) minutes), had a longer sleep onset latency (12 (10, 30) minutes), and tended to have less stage 4 (deep) sleep (-33 (-58, 4) minutes). Daytime cognitive performance was worse in the patients with nocturnal asthma, who took a longer time to complete the trail making tests (median difference 62 (22, 75) seconds) and achieved a lower score on the paced serial addition tests (-10 (-24, -3)). Mean daytime sleep latency did not differ significantly between the two groups (2 (-3, 7) minutes). It is concluded that hospital outpatients with stable nocturnal asthma have impaired sleep quality and daytime cognitive performance even when having their usual maintenance asthma treatment.
PMCID: PMC463276  PMID: 1926025
13.  Posture and nocturnal asthma. 
Thorax  1989;44(7):579-581.
To investigate whether the supine posture caused sustained bronchoconstriction and could thus contribute to the development of nocturnal asthma, nine patients with nocturnal asthma were studied on two consecutive days, lying supine for four hours on one day and sitting upright for four hours on the other, the order of the two postures being randomised. Peak expiratory flow (PEF), forced expiratory volume in one second (FEV1), and forced vital capacity (FVC) were measured immediately before and after the four hours and over the subsequent hour. There was no significant difference between the erect and supine posture for PEF (248 v 248 l/min), FEV1 (1.31 v 1.22 l), or FVC (2.34 v 2.28 l) at the end of the four hours, nor did any significant change develop subsequently. Thus the supine posture is not associated with prolonged bronchoconstriction. As each patient had previously shown an average overnight fall in PEF of more than 20%, this study strongly suggests that the supine posture is not an important cause of overnight bronchoconstriction.
PMCID: PMC461961  PMID: 2772857
14.  Is nocturnal asthma caused by changes in airway cholinergic activity? 
Thorax  1988;43(9):720-724.
A randomised, double blind, placebo controlled crossover trial of high dose nebulised ipratropium was carried out in 10 asthmatic patients with documented nocturnal bronchoconstriction. Patients received nebulised saline or ipratropium 1 mg at 10 pm and 2 am on two nights. Absolute peak flow (PEF) rates were higher throughout the night after the patients had received ipratropium (at 2 am, for example, mean (SEM) PEF was 353 after ipratropium and 285 l/min after placebo). The fall in PEF overnight, however, was similar with ipratropium and placebo. Patients were given a further 1 mg nebulised ipratropium at 6 am on both nights. There was a significant overnight fall in PEF on the ipratropium night even when comparisons were made between the times that maximal cholinergic blockade would be expected, PEF falling between 11.30 pm and 7.30 am from 429 to 369 l/min. The percentage increase in PEF, though not the absolute values, was greater after ipratropium at 6 am than at 10 pm. These results confirm that ipratropium raises PEF throughout the night in asthmatic patients, but suggest that nocturnal bronchoconstriction is not due solely to an increase in airway cholinergic activity at night.
PMCID: PMC461462  PMID: 2973665
15.  Breathing patterns during sleep in patients with nocturnal asthma. 
Thorax  1987;42(8):600-603.
Breathing patterns early and late in the night, at the same sleep stage, were compared in six healthy subjects and 15 adults with nocturnal asthma, to try to identify changes of overnight bronchoconstriction, and breathing patterns at different sleep stages, to see whether there were changes related to sleep stages that were indicative of bronchoconstriction. Despite an average 31% fall in FEV1 overnight in the patients with asthma, neither breathing frequency nor expiratory time, which might be expected to change during bronchoconstriction, was different early in the night from late in the night, nor did they differ between sleep stages. There was no evidence of asynchronous movement of the chest and abdomen in any patient. This study did not identify any abnormality of breathing pattern that would indicate the development of nocturnal asthma without the need to awaken the patient.
PMCID: PMC460860  PMID: 3509951
16.  Accuracy of inpatient oxygen administration. 
Thorax  1989;44(12):1036-1037.
The accuracy of supplemental oxygen delivery was assessed in two medical units. Only 90 of 206 patients (44%) were receiving oxygen as prescribed. The ward oxygen rotameters were inaccurate at normal clinical flow rates, the range of flows being delivered as a percentage of the indicated flow varying from 15% at 8 l/min to 40% at 1 and 2 l/min.
PMCID: PMC1020881  PMID: 2617443
17.  Effect of sustained release terbutaline on symptoms and sleep quality in patients with nocturnal asthma. 
Thorax  1987;42(10):797-800.
The effect of an oral sustained release beta 2 agonist on symptoms, sleep quality, and peak flow rates has been studied in nine patients with nocturnal asthma. Patients received oral terbutaline 7.5 mg twice daily or placebo for seven days in a double blind crossover study and spent the last two nights of each limb in a sleep laboratory. Oral terbutaline improved morning peak flow (259 v 213 l min-1) and decreased nocturnal inhaler usage (1.3 v 1.9) with no alteration in sleep quality as assessed electroencephalographically. The study shows that oral sustained release terbutaline can be useful in the treatment of nocturnal asthma without impairment of sleep quality.
PMCID: PMC460955  PMID: 3321540
18.  Effect of sleep deprivation on overnight bronchoconstriction in nocturnal asthma. 
Thorax  1986;41(9):676-680.
Nocturnal cough and wheeze are common in asthma. The cause of nocturnal asthma is unknown and there is conflicting evidence on whether sleep is a factor. Twelve adult asthmatic subjects with nocturnal wheeze were studied on two occasions: on one night subjects were allowed to sleep and on the other they were kept awake all night, wakefulness being confirmed by electroencephalogram. Every patient developed bronchoconstriction overnight both on the asleep night, when peak expiratory flow (PEF) fell from a mean (SE) of 418 (40) 1 min-1 at 10 pm to 270 (46) 1 min-1 in the morning, and on the awake night (PEF 10 pm 465 (43), morning 371 (43) 1 min-1). The morning values of PEF were, however, higher (p less than 0.1) after the awake night and both the absolute and the percentage overnight falls in PEF were greater when the patients slept (asleep night 38% (6%), awake night 20% (4%); p less than 0.01). This study suggests that sleep is an important factor in determining overnight bronchoconstriction in patients with nocturnal asthma.
PMCID: PMC460429  PMID: 3787554
19.  Do asthmatics suffer bronchoconstriction during rapid eye movement sleep? 
Many patients with asthma are troubled by nocturnal wheeze. The cause of this symptom is unknown, but sleep is an important factor. A study was carried out to determine whether nocturnal bronchoconstriction is related to any specific stage of sleep. Eight asthmatics with nocturnal wheeze and eight control subjects performed forced expiratory manoeuvres immediately after being woken from rapid eye movement (REM) or non-REM sleep, wakings being timed to differentiate temporal effects from those related to the stage of sleep. The control subjects showed no significant temporal bronchoconstriction or bronchoconstriction related to the stage of sleep. All patients showed bronchoconstriction overnight, the mean peak expiratory flow rate falling from 410 (SEM 50) 1/min before sleep to 186 (49)1/min after sleep. After the patients had been woken from REM sleep the forced expiratory volume in one second was on average 300 ml lower (p less than 0.02) and peak expiratory flow rate 45 1/min lower (p less than 0.03) than after they had been woken from non-REM sleep. As wakenings from REM sleep were 21(8) minutes later in the night than those from non-REM sleep multivariate analysis was performed to differentiate temporal effects from those related to the stage of sleep. This showed that the overnight decreases in forced expiratory volume in one second and peak expiratory flow rate were significantly related both to time and to REM sleep. This study suggests that asthmatics may suffer bronchoconstriction during REM sleep.
Images
PMCID: PMC1340176  PMID: 3085766
20.  Sustained release choline theophyllinate in nocturnal asthma. 
Nocturnal wheeze is common in patients with asthma, and slow release theophyllines may reduce symptoms. As theophyllines are stimulants of the central nervous system the effect of 10 days' twice daily treatment with sustained release choline theophyllinate or placebo on symptoms, overnight bronchoconstriction, nocturnal oxygen saturation, and quality of sleep were studied in a double blind crossover study in nine stable patients with nocturnal asthma (five men, four women, age range 23-64 years; forced expiratory volume in one second (FEV1) 0.85-3.8 1; vital capacity 1.95-6.1 1). When treated with the active drug all patients had plasma theophylline concentrations of at least 28 mmol/l (5 micrograms/ml) (peak plasma theophylline concentrations 50-144 mmol/l (9-26 micrograms/ml]. Morning FEV1 was higher when treated with sustained release choline theophyllinate (2.7 (SEM 0.3) 1) than placebo (2.1 (0.3) 1) (p less than 0.01). Both daytime and nocturnal symptoms were reduced when the patients were treated with sustained release choline theophyllinate and subjective quality of sleep was improved (p less than 0.002). When treated with the active drug, however, quality of sleep determined by electroencephalography deteriorated with an increase in wakefulness and drowsiness (p less than 0.05) and a reduction in non-rapid eye movement sleep (p less than 0.005). Treatment with choline theophyllinate had no effect on either the occurrence or the severity of transient nocturnal hypoxaemic episodes or apnoeas or hypopnoeas. In conclusion, sustained release choline theophyllinate prevents overnight bronchoconstriction, but impairs quality of sleep defined by electroencephalography.
PMCID: PMC1418455  PMID: 3935204
21.  Bronchodilatation and the site of airway resistance in severe chronic bronchitis. 
Thorax  1979;34(1):51-56.
Twenty-one patients with severe chronic bronchitis and emphysema (FEV1 less than 1 1) inhaled 80 microgram of the atropine-like agent ipratropium or placebo in a double-blind study and three hours later inhaled 200 microgram salbutamol. After 80 microgram ipratropium, mean FEV1 was significantly greater than after 200 microgram salbutamol (P less than 0.025), but the difference was only 40 ml and the clinical significance of this difference is unproved. There was no correlation between the patient's response to ipratropium and the response to salbutamol. When salbutamol was administered three hours after ipratropium, the FEV1 rose to higher levels than after either agent alone (P less than 0.01). Studies breathing 80% helium/20% oxygen suggest that ipratropium dilates both large and small airways. There was no correlation between the response to helium/oxygen and the response to either bronchodilator. The results suggest that in severe chronic bronchitis and emphysema ipratropium is at least as effective as salbutamol, and that such patients should have reversibility studies with salbutamol alone, ipratropium alone, and after both agents together. The combination of ipratropium and salbutamol may be clinically useful.
PMCID: PMC471007  PMID: 155891
22.  Self assessment of daytime sleepiness: patient versus partner. 
Thorax  1995;50(9):994-995.
BACKGROUND--Patients with the sleep apnoea/hypopnoea syndrome (SAHS) and their spouses often differ in their assessment of the patient's sleepiness. A study was therefore undertaken to investigate whether either the patient's or partner's rating on the Epworth sleepiness scale (ESS) was better related to illness severity. METHODS--Nocturnal variables (apnoeas+hypopnoeas/hour (AHI) and arousals/hour) and patient and partner ESS scores were compared in 103 new patients attending the sleep clinic. RESULTS--Mean patient and partner ESS scores were not different. In the whole population neither patient nor partner ESS variables correlated with AHI or arousal frequency. In the patients with SAHS (AHI > or = 15), partner ESS correlated weakly with AHI, but patient ESS did not. CONCLUSIONS--This study suggests that neither patient nor partner ESS ratings are strong predictors of SAHS severity.
PMCID: PMC1021317  PMID: 8539684
24.  Atrial natriuretic peptide levels in the sleep apnoea/hypopnoea syndrome. 
Thorax  1994;49(9):920-921.
BACKGROUND--Patients with the sleep apnoea/hypopnoea syndrome have increased salt and water excretion at night which has been reported to be associated with an increase in plasma levels of atrial natriuretic peptide (ANP). A study was performed to determine whether any rise in plasma ANP levels was related to nocturnal hypoxaemia. METHODS--Nine patients with sleep apnoea/hypopnoea syndrome were studied on two nights, one breathing air and the other 28% oxygen, the order being randomised. Venous levels of ANP, aldosterone, and renin activity were measured. RESULTS--No decrease in plasma ANP levels on oxygen was seen, and, indeed, there was no evidence of an overnight increase in ANP levels. CONCLUSION--Oxygen therapy does not diminish nocturnal plasma ANP levels in patients with sleep apnoea/hypopnoea syndrome.
PMCID: PMC475196  PMID: 7940435
25.  Computerised polysomnography. 
Thorax  1994;49(5):528.
PMCID: PMC474892  PMID: 8068098

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