Oxygen treatment of sleep hypoxaemia in Duchenne muscular dystrophy.

Patients with Duchenne muscular dystrophy develop progressive ventilatory muscle weakness and often die of respiratory complications. Recurrent, often profound, hypoxaemia has been shown in a previous study by this group to occur during rapid eye movement (REM) sleep in these patients before they develop sleep symptoms. In this study the efficacy and physiological effects of nocturnal oxygen in such patients have been assessed. Seven patients with Duchenne muscular dystrophy (age range 16-22 years; mean vital capacity 1.37 litres) with normal arterial blood gas tensions when awake were investigated by standard overnight polysomnography on an acclimatization night followed by two successive nights on which they received room air and nasal oxygen (2 litres/min) respectively in random order. Total sleep time, proportion of REM and non-REM sleep, and frequency and duration of arousals were similar on the two nights. When breathing air six of the seven subjects developed oxygen desaturation of more than 5% during REM sleep. With oxygen only one subject showed any oxygen desaturation exceeding 2.5%. Oxygen desaturation was associated with periods of hypopnoea or cessation of respiratory effort. The mean duration of episodes of hypopnoea and apnoea was prolonged during oxygen breathing by 19% and the mean duration of episodes during REM sleep by 33% (the proportion of REM sleep associated with hypopnoea and apnoea increased in all subjects). Heart rate in non-REM sleep fell by 9.3%; heart rate variation in REM and non-REM sleep was unchanged. These acute studies show that oxygen reduces the sleep hypoxaemia associated with respiratory muscle weakness; whether long term treatment will be possible or desirable is not clear as oxygen potentiates the underlying ventilatory disturbance.     

Sleep disordered breathing and pregnancy

Many changes in the respiratory system occur during pregnancy, particularly during the third trimester, which can alter respiratory function during sleep, increasing the incidence and severity of sleep disordered breathing. These changes include increased ventilatory drive and metabolic rate, reduced functional residual capacity and residual volume, increased alveolar-arterial oxygen gradients, and changes in upper airway patency. The clinical importance of these changes is indicated by the increased incidence of snoring during pregnancy, which is likely also to reflect an increased incidence of obstructive sleep apnoea/hypopnoea syndrome. For the respiratory physician asked to review a pregnant patient, the possibility of sleep disordered breathing should always be considered. This review first examines the normal physiological changes of pregnancy and their relationship to sleep disordered breathing, and then summarises the current knowledge of sleep disordered breathing in pregnancy.     

Transtracheal air in the treatment of obstructive sleep apnoea hypopnoea syndrome

A 49 year old woman with typical obstructive sleep apnoea hypopnoea syndrome underwent an unsuccessful trial with continuous positive airway pressure (CPAP) followed by uvulopalatopharyngoplasty with septorhinoplasty, treatment with protriptyline, and a second CPAP trial that was abandoned. Transtracheal air was then given and normalised sleep and breathing at a flow rate of 5 l/min. A sustained clinical improvement was observed at follow up visits. Transtracheal air could represent a simple and effective alternative to tracheotomy in patients with obstructive sleep apnoea hypopnoea syndrome in whom conventional treatments fail.     

Sleep apnoea in patients with quadriplegia.

BACKGROUND--This study was undertaken to establish the prevalence of, and the factors contributing towards, sleep disordered breathing in patients with quadriplegia. METHODS--Forty representative quadriplegic patients (time since injury > 6 months, injury level C8 and above, Frankel category A, B, or C; mean (SE) age 35.0 (1.7) years) had home sleep studies in which EEG, EOG, submental EMG, body movement, nasal airflow, respiratory effort, and pulse oximetry (SpO2) were measured. Patients reporting post traumatic amnesia of > 24 hours, drug or alcohol abuse or other major medical illness were excluded from the study. A questionnaire on medications and sleep was administered and supine blood pressure, awake SpO2, spirometric values, height, and neck circumference were measured. RESULTS--A pattern of sustained hypoventilation was not observed in any of the patients. Sleep apnoeas and hypopnoeas were, however, common. Eleven patients (27.5%) had a respiratory disturbance index (RDI, apnoeas plus hypopnoeas per hour of sleep) of > or = 15, with nadir SpO2 ranging from 49% to 95%. Twelve of the 40 (30%) had an apnoea index (AI) of > or = 5 and, of these, nine (75%) had predominantly obstructive apnoeas-that is, > 80% of apnoeas were obstructive or mixed. This represents a prevalence of sleep disordered breathing more than twice that observed in normal populations. For the study population RDI correlated with systolic and diastolic blood pressure and neck circumference. RDI was higher in patients who slept supine compared with those in other postures. Daytime sleepiness was a common complaint in the study population and sleep architecture was considerably disturbed with decreased REM sleep and increased stage 1 non-REM sleep. CONCLUSIONS--Sleep disordered breathing is common in quadriplegic patients and sleep disturbance is significant. The predominant type of apnoea is obstructive. As with non-quadriplegic patients with sleep apnoea, sleep disordered breathing in quadriplegics is associated with increased neck circumference and the supine sleep posture.     

Hypoxic ventilatory response after rocuronium-induced partial neuromuscular blockade in men with obstructive sleep apnoea

Obstructive sleep apnoea and residual neuromuscular blockade are, independently, known to be risk factors for respiratory complications after major surgery. Residual effects of neuromuscular blocking agents are known to reduce the hypoxic ventilatory response in healthy volunteers. Patients with obstructive sleep apnoea have impaired control of breathing, but it is not known to what extent neuromuscular blocking agents interfere with the regulation of breathing in such patients. In a physiological study in 10 unsedated men with untreated obstructive sleep apnoea, we wished to examine if partial neuromuscular blockade had an effect on hypoxic ventilatory response (isocapnic hypoxia to oxygen saturation of 80%) and hypercapnic ventilatory response (normoxic inspired carbon dioxide 5%). The hypoxic ventilatory response was reduced by 32% (p = 0.016) during residual neuromuscular block (rocuronium to train-of-four ratio 0.7), but the hypercapnic ventilatory response was unaffected. We conclude that neuromuscular blockade specifically depresses peripheral chemosensitivity, and not respiratory muscle function since the hypercapnic ventilatory response was unaffected.     

Respiratory muscle activity during rapid eye movement (REM) sleep in patients with chronic obstructive pulmonary disease.

BACKGROUND--In patients with chronic obstructive pulmonary disease (COPD) periods of hypopnoea occur during rapid eye movement (REM) sleep, but the mechanisms involved are not clear. METHODS--Ten patients with stable COPD were studied during nocturnal sleep. Detailed measurements were made of surface electromyographic (EMG) activity of several respiratory muscle groups and the accompanying chest wall motion using magnetometers. RESULTS--Hypopnoea occurred in association with eye movements during phasic rapid eye movement (pREM) sleep. During pREM sleep there were reductions in EMG activity of the intercostal, diaphragm, and upper airway muscles compared with non-REM sleep. Episodic hypopnoea due to partial upper airway occlusion ("obstructive" hypopnoea) was seen consistently in four subjects while the others showed the pattern of "central" hypopnoea accompanied by an overall reduction in inspiratory muscle activity. Although activity of the intercostal muscles was reduced relatively more than that of the diaphragm, lateral rib cage paradox (Hoover's sign) was less obvious during pREM-related hypopnoea than during wakefulness or non-REM sleep. CONCLUSIONS--Hypopnoea during REM sleep in patients with COPD is associated with reduced inspiratory muscle activity. The pattern of hypopnoea may be either "obstructive" or "central" and is generally consistent within an individual. Relatively unopposed action of the diaphragm on the rib cage during REM sleep is not accompanied by greater lateral inspiratory paradox.     

Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea

BACKGROUND: Previous studies have shown that changes in lung volume influence upper airway size and resistance, particularly in patients with obstructive sleep apnoea (OSA), and that continuous positive airway pressure (CPAP) requirements decrease when the lung volume is increased. We sought to determine the effect of a constant lung volume increase on sleep disordered breathing during non-REM sleep. METHODS: Twelve subjects with OSA were studied during non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. The increase in lung volume due to CPAP (at a therapeutic level) was determined with four magnetometer coils placed on the chest wall and abdomen. CPAP was then stopped and the subjects were studied for 1 hour in three conditions (in random order): (1) no treatment (baseline); (2) at "CPAP lung volume", with the increased lung volume being reproduced by negative extrathoracic pressure alone (lung volume 1, LV1); and (3) 500 ml above the CPAP lung volume(lung volume 2, LV2). RESULTS: The mean (SE) apnoea/hypopnoea index (AHI) for baseline, LV1, and LV2, respectively, was 62.3 (10.2), 37.2 (5.0), and 31.2 (6.7) events per hour (p = 0.009); the 3% oxygen desaturation index was 43.0 (10.1), 16.1 (5.4), and 12.3 (5.3) events per hour (p = 0.002); and the mean oxygen saturation was 95.4 (0.3)%, 96.0 (0.2)%, 96.3 (0.3)%, respectively (p = 0.001). CONCLUSION: An increase in lung volume causes a substantial decrease in sleep disordered breathing in patients with OSA during non-REM sleep.     

Induction of sleep apnoea with negative pressure ventilation in patients with chronic obstructive lung disease.

BACKGROUND: Negative pressure ventilation provides intermittent non-invasive ventilatory assistance for patients with advanced chronic obstructive lung disease. Upper airway obstruction during sleep, a reported complication of the technique, may, however, limit its clinical applicability. METHODS: The effects of nocturnal negative pressure ventilation on ventilation and on indices of sleep quality were investigated in five patients with severe chronic obstructive lung disease (mean (SE) FEV1 31% (3%) predicted) who had completed three months of nightly negative pressure ventilation. Subjects underwent overnight polysomnography on consecutive nights, the first night serving as a control and negative pressure ventilation being provided on the second night. Ventilators were adjusted to result in maximum suppression of the peak phasic electromyogram signal from the diaphragm. RESULTS: Negative pressure ventilation resulted in substantial increases in episodes of obstructive apnoea and hypopnoea (mean (SE)/h 59.3 (19.8) v 3.2 (1.3) on control nights). Most obstructive events, however, were associated with under 3% oxygen desaturation, and the lowest recorded values for overnight oxygen saturation were similar on the two study nights. Negative pressure ventilation was also associated with significant increases in the frequencies of movement arousals and changes in sleep stage. CONCLUSIONS: Negative pressure ventilation applied during sleep to patients with advanced chronic obstructive lung disease may result in the development of recurrent episodes of apnoea and hypopnoea as well as altered sleep quality, which could limit its clinical applicability.     

Effects of submental stimulation for several consecutive nights in patients with obstructive sleep apnoea.

BACKGROUND--It has previously been reported that short term submental stimulation can reduce the frequency of apnoea and improve sleep architecture in patients with obstructive sleep apnoea. The effects of submental stimulation during consecutive nights on apnoea or on daytime sleepiness have not, however, been studied. METHODS--Patients with obstructive sleep apnoea were studied by polysomnography on a control night, for five consecutive nights of submental stimulation, and on three following nights (n = 8). A multiple sleep latency test (MSLT) (n = 8) and measurement of the upper airway resistance (n = 5) were performed during the day after the polysomnographic study, on the control night, and on the fifth stimulation night. In an additional five patients with obstructive sleep apnoea, matched for age, sex, and weight, the effects of two nights of stimulation were examined for comparison. Submental stimulation began when an apnoea lasted for five seconds and stopped with the resumption of breathing as detected by oronasal flow. RESULTS--The apnoea index, the number of times per hour that SaO2 dropped below 85% (SaO2 < 85%/hour), and the total apnoea duration expressed as a percentage of total sleep time during stimulation nights decreased to approximately 50% of the corresponding values on the control night. This improvement persisted for at least two nights after the five consecutive stimulation nights, but not after the two consecutive stimulation nights. Sleep architecture and MSLT following the stimulation nights improved but upper airway resistance did not change. CONCLUSIONS--Submental stimulation for five consecutive nights in patients with obstructive sleep apnoea improved the breathing disturbance, sleep quality, and daytime sleepiness. The effect lasted for the following two nights, but did not completely abolish the sleep disordered breathing.     

Effects of acetazolamide in patients with the sleep apnoea syndrome.

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.     

Atrial natriuretic peptide levels in the sleep apnoea/hypopnoea syndrome.

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.     

Surgical correction of nasal obstruction in the treatment of mild sleep apnoea: importance of cephalometry in predicting outcome.

BACKGROUND--A study was undertaken to determine if cephalometric radiographs could identify those who will benefit from nasal surgery in patients with a sleep apnoea hypopnoea syndrome (SAHS) and chronic nasal obstruction. METHODS--Fourteen patients with SAHS were enrolled. Those with normal posterior airway space and mandibular plane to hyoid bone distances on preoperative cephalometric radiographs were matched with those with abnormal cephalometry for the frequency of sleep disordered breathing and body mass index. Polysomnographic studies (all subjects) and nasal resistance measurements (n = 10) were performed one to three months before and two to three months after surgery (septoplasty, turbinectomy, and polypectomy). RESULTS--There was no difference in the baseline results of the polysomnographic studies between the two groups of patients. Nasal resistance decreased from a mean (SE) value of 2.9 (0.3) cm H2O/l/s before surgery to 1.4 (0.1) cm H2O/l/s after surgery in the normal cephalometry group and from 2.7 (0.3) cm H2O/l/s to 1.3 (0.3) cm H2O/l/s in the other group. The apnoea + hypopnoea index returned to normal (< 10 breathing abnormalities/hour) in all but one subject with normal cephalometric measurements, and sleep fragmentation improved with a decrease in the arousal index from 23.9 (3.3)/hour at baseline to 10.6 (2.5)/hour after surgery. Both of these parameters remained unchanged after surgery in the patients with abnormal cephalometry. CONCLUSIONS--Normal cephalometry is helpful in identifying patients with mild SAHS and nasal obstruction who will benefit from nasal surgery. The presence of craniomandibular abnormalities makes it unlikely that nasal surgery will improve sleep related breathing abnormalities.     

Oestrogen and progesterone receptor expression in the female lower urinary tract, with reference to oestrogen status

OBJECTIVE: To assess the incidence and distribution of both oestrogen and progesterone receptors throughout the female lower urinary tract, and to compare receptor expression in women of varying oestrogen status. PATIENTS AND METHODS: The study included 90 women undergoing surgery for urogynaecological conditions; 33 were premenopausal, 26 postmenopausal and taking no oestrogen supplementation, and 31 postmenopausal and receiving some form of hormone-replacement therapy. Biopsies were taken during surgery from the bladder dome, trigone, proximal urethra, distal urethra, vagina and vesicovaginal fascia in the region of the bladder neck. All biopsies were routinely fixed and processed for histopathological assessment, and were then labelled immunohistochemically with monoclonal antibodies directed against human oestrogen (NCL-ERLH2) and progesterone (NCL-PGR) receptors. Both oestrogen and progesterone receptor expression were assessed in the epithelial, subepithelial and muscle/deeper fascial regions of all tissue for overall tissue positivity for each receptor, and by semiquantitative analysis of receptor concentration using histochemical scoring of the tissues. RESULTS: Oestrogen receptors were consistently detected in the squamous epithelia and were consistently absent in the urothelial tissues of the lower urinary tract of all women irrespective of oestrogen status; there was no significant variation in histological score. Progesterone receptor expression was more variable, being mostly subepithelial, and significantly lower in postmenopausal women receiving no oestrogen replacement. CONCLUSION: These findings confirm the female lower urinary tract to be a target organ for the action of oestrogen and progesterone, and shed further light on the areas of the lower urinary tract likely to respond to hormone-replacement therapy. This may have implications for the use of oestrogen supplementation in the treatment of lower urinary tract disorders of postmenopausal women.     

Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome.

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.     

Nasal pressure recording in the diagnosis of sleep apnoea hypopnoea syndrome

BACKGROUND: Nasal pressure tracing is now being used to measure breathing in ambulatory screening devices for sleep apnoea but it has not been compared with other methods of assessment. METHODS: Sleep induced breathing disorders were scored by three different methods of analysis (thermistry, inductive plethysmography, and nasal pressure tracing) in 193 consecutive patients referred to our sleep laboratory. With the conventional thermistry method an apnoea was defined as the absence of oronasal flow on the thermistor signal for >/=10 s and a hypopnoea as a 50% decrease in the sum signal of inductive plethysmography tracing for >/=10 s associated with an arousal and/or a 2% decrease in SaO2. Nasal pressure was measured via nasal prongs connected to a pressure transducer. Using the thermistor signal alone, a hypopnoea was defined as a 50% decrease in the signal for >/=10 s associated with an arousal and/or a 2% decrease in SaO2. A similar definition of apnoea and hypopnoea was used for nasal pressure, the fall in pressure being substituted for the thermistor reading. RESULTS: Impaired nasal ventilation prevented adequate measurements of nasal pressure in 9% of subjects. According to the conventional method of interpretation 107 subjects were identified as having the sleep apnoea hypopnoea syndrome (SAHS). The apnoea + hypopnoea index (AHI) was significantly lower using the thermistry method than with conventional analysis (mean difference -4.3/h, 95% CI -5.3 to -3.2, p<10(-4)); 39% of conventional hypopnoeic events were scored as apnoeas using nasal pressure scoring. Apnoeic and hypopnoeic events could also be observed without any change in thermistor and sum Respitrace signals that resumed with the occurrence of arousals or awakenings. The AHI was significantly higher with nasal pressure scoring than with the conventional method (mean difference 4.5, 95% CI 3.4 to 5.6, p<10(-4)). The mean difference in apnoea index between conventional and nasal pressure scoring was -7.5/h (95% CI -8.9 to -6.1). In the 78 patients who did not have SAHS according to the conventional method of analysis there was a significant positive relationship between the arousal index and AHI measured by nasal pressure tracing (R = 0.51, p<10(-4)). Seventeen of the 78 patients had an AHI of >15/h by the nasal pressure method of analysis. CONCLUSIONS: Nasal pressure recording provides a simple and reliable measurement of nocturnal breathing abnormalities and may identify breathing abnormalities associated with arousals that are missed by other diagnostic methods.     

Sleep. 4: Sleepiness, cognitive function, and quality of life in obstructive sleep apnoea/hypopnoea syndrome

Sleepiness, cognitive performance, and quality of life are overlapping aspects of daytime function that may be affected in patients with obstructive sleep apnoea/hypopnoea syndrome. The evidence is compatible with hypotheses that these deficits are reversible with treatment, particularly for patients with severe disease.     

Identification of sleep disruption and sleep disordered breathing from the systolic blood pressure profile.

BACKGROUND--Respiratory sleep studies are frequently performed to identify sleep disruption resulting from upper airway obstruction. Traditional polysomnographic studies may not detect brief recurrent sleep disruption and thus fail to recognise a significant problem when apnoea, hypopnoea, or arterial desaturation are not present. Arousal from sleep causes a transient blood pressure rise, and each inspiration causes a transient blood pressure fall. This study assesses whether these blood pressure changes are a useful indirect marker of disturbed sleep, obstructed sleep apnoea, and snoring related sleep disturbance. METHODS--Computer algorithms were developed to identify blood pressure falls caused by inspiration and rises related to arousal from 286 sleeping blood pressure samples of a consistent respiratory state drawn from 51 polysomnographic studies. From these samples, normal ranges for the number of arousal related systolic rises and the average size of the inspiratory falls were established. These were then applied prospectively to all night unedited blood pressure recordings from a further 20 subjects. RESULTS--The size of the inspiratory falls in blood pressure progressively increased from normal sleep, through snoring, to frank obstructive sleep apnoea. The 95th centile of normal was 12.5 mm Hg. The number of arousal related blood pressure rises also increased during obstructive sleep apnoea and periods of snoring with associated arousals, compared with normal undisturbed sleep, and all these periods of disturbed sleep included more than 30 such rises per hour. When these blood pressure features were examined in the 20 subjects studied prospectively, the six with a sleep related breathing disorder could all have been identified from their systolic blood pressure profile alone. CONCLUSIONS--The systolic blood pressure profile may be helpful in identifying patients with obstructive sleep apnoea, snoring with arousals, or other sleep disruption syndromes.     

Is there a familial association between obstructive sleep apnoea/hypopnoea and the sudden infant death syndrome?

BACKGROUND: One postulated cause of the sudden infant death syndrome (SIDS) is upper airway obstruction during sleep. Several studies have suggested that SIDS may be more common in families with obstructive sleep apnoea/hypopnoea syndrome (OSAHS), but were limited by uncertainty as to whether the deaths were due to SIDS. We have tested the hypothesis that parents of true SIDS cases have an increased frequency of apnoeas and hypopnoeas during sleep. METHODS: The parents of 269 rigorously determined SIDS cases were invited for single night polysomnography and daytime ventilatory control measurement. RESULTS: Parents of 198 cases were identified but 152 did not respond or declined. Fifty five parents of 34 cases were studied and matched for age, height, and weight to 55 subjects from general practice registers. There was no difference in breathing during sleep between the parents of SIDS cases (median (IQR) 5.9 (3.2, 10.7) apnoeas+hypopnoeas/h) and controls (6.7 (4.0, 12.2) apnoeas+hypopnoeas/h; p = 0.47), but the SIDS parents had lower minimum nocturnal oxygen saturation (median (IQR) 92 (89, 93)%) than controls (92 (90, 94)%; p = 0.048). There were no major differences in control of breathing when awake between SIDS parents and controls. CONCLUSIONS: These results provide no evidence to support an association between SIDS and OSAHS. However, the minor impairment of oxygenation during sleep in SIDS parents requires further study.     

Sleep. 1: Obstructive sleep apnoea/hypopnoea syndrome: definitions, epidemiology, and natural history

Arguments over the definition of obstructive sleep apnoea/hypopnoea syndrome (OSAHS) have still not been satisfactorily resolved. As a result, robust estimates of the prevalence of OSAHS are not possible. New approaches are needed to identify those who have "CPAP responsive" disease, enabling more accurate estimates to be made of the prevalence of the sleep apnoea syndrome in the community.     

Sleep. 2: pathophysiology of obstructive sleep apnoea/hypopnoea syndrome

The pathogenesis of airway obstruction in patients with obstructive sleep apnoea/hypopnoea syndrome is reviewed. The primary defect is probably an anatomically small or collapsible pharyngeal airway, in combination with a sleep induced fall in upper airway muscle activity.