Br. J. Anaesth. (1989), 63, 477-488

OBSTRUCTIVE SLEEP APNOEA C. D. HANNING Obstructive sleep apnoea (OSA) is the most common disorder of breathing during sleep. It is characterized by repetitive episodes of upper airway obstruction which result in disruption of sleep and hypoxaemia. The condition has been described in various forms in the past, but its true nature was described in 1966 by Gastaut [26]. Charles Dickens, well recognized in his own time as an astute observer of medical conditions, captured the essentials of the condition in "Joe, the Fat Boy" in Pickwick Papers (fig. 1). The condition is often referred to as the "Pickwickian syndrome," but this title is best reserved for those patients who are obese and have developed right heart failure. Aetiology The cause of OSA is partial or complete collapse of the pharynx during inspiration. Partial collapse with fluttering of the pharyngeal walls and palate results in the common symptom of snoring. There is a spectrum of disease from occasional snorers through heavy, persistent snorers to the various degrees of OSA. The collapse may occur at any point from the soft palate to the hypopharynx posterior to the tongue [49]. The collapsing force is the sub-atmospheric pressure in the airway which is opposed normally by the dilating action of the upper airway muscles which contract in synchrony with the muscles of ventilation [68]. The tone in the pharyngeal muscles diminishes during Stage 4 and REM sleep, making collapse more likely in those phases of sleep [94]. Any anatomical factor which narrows the airway, such as tonsillar or adenoidal hypertrophy, obesity or THK K.\T BOY ASIJ.KI' AliAIN mandibular hypoplasia, increases the likelihood of Pidnriek collapse. Abolition of mucosal sensation in the mouth [67] and nose [112] with topical analgesia FIG. 1. "The Fat -Boy asleep again" by Harry Furniss. also promotes OSA. The pharyngeal mucosa In: The Posthumous Papers of the Pickwick Club, by Charles becomes thickened, oedematous and lax in long- Dickens. London: The Educational Book Company, 1910. C. D. HANNING, B.SC, M.B., B.S., F.F.A.R.C.S., Sleep Disorders

Clinic, University Department of Anaesthesia, Leicester General Hospital, Leicester LE5 4PW.

standing cases, further exacerbating the obstruction. Cigarette smoking is also a factor in causing pharyngeal wall thickening [4]. Any factor which

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increases nasal airway resistance enhances the always eliminated by tracheostomy [106] or sub-atmospheric inspiratory intra-pharyngeal effective nasal continuous positive airway pressure pressure and worsens or induces collapse [78, (nCPAP) [103]. These cardiovascular changes are the main 105]. In the author's experience this latter precipitating factor is the most common cause of cause of the excess mortality in patients with OSA. In a recent survey of nearly 400 men, the OSA in the United Kingdom. predicted 8-yr survival was 63 % for subjects with Normal sleep itself has effects on respiration, decreasing minute ventilation and causing a small severe OSA of all ages and 53 % for those aged increase in PaCOl and decrease in PaOj [102]. > 50 yr [45]. Mortality was related to age and Ventilatory control is diminished also, particu- severity of the condition. Epidemiological studies of snoring have shown consistently a decrease in larly during REM sleep [87]. the proportion of snorers in the population aged Consequences > 70 yr [3,12]. The inescapable conclusion is that Sleep fragmentation and hypoxaemia result in snoring and OSA are a risk to health, although the several serious consequences. Systemic and pul- significance of snoring alone has been challenged monary arterial pressures are increased markedly [108]. The surveys have also shown a considerable during the episodes of apnoea [16] and are thought male predominance, of the order of 10-20:1, both to be the principal cause of the systemic hyper- for snoring and OSA. tension which is often found in these patients There has been speculation as to whether or [98]. In epidemiological studies, significantly not patients with OSA die predominantly at night higher systolic and diastolic arterial pressures during an apnoea or whether the deaths are caused have been noted in heavy snorers compared with by effects on the cardiovascular system and could non-snorers [61,71]. The consequence of hyper- occur at any time during the day. Understandably, tension (angina and stroke) are also commoner there is little direct evidence, although Guillemiin snorers [60, 80]. Surveys of patients with nault, van den Hoed and Mitler [38] recorded that hypertension have shown a high incidence of OSA three of 10 patients who declined treatment died [57]; the severity of the hypertension and its during sleep within 6 months, a further two resistance to treatment was related to the severity patients had severe cardiac failure and another of the OSA. had a myocardial infarction during sleep. The Pulmonary hypertension is an uncommon find- contrary view has been proposed by Gonzalezing and probably occurs only when there is Rothi, Foresman and Block [30], but the condition associated daytime hypoxaemia [7]. Clinically, it in their patients was probably not as severe as in is more common in the severely obese—the true those of Guilleminault. The consensus view is "Pickwickian". Right heart failure occurs eventu- that patients with severe OSA may die suddenly ally and is the mode of presentation in many during sleep and thus the institution of appatients [40]. Correction of the OSA may result in propriate therapy must be regarded as a priority complete resolution of the heart failure and [79]. electrocardiographic signs of right ventricular Polycythaemia is found only in approximately strain. 7 % of patients with OSA without lung disease, Cardiac arrythmias commonly accompany the despite profound desaturation during sleep [33]. episodes of apnoea [2,52]. Tachycardia and It would appear that the presence of normal bradycardia may occur and OSA may be diag- oxygenation during the day prevents the excessive nosed from 24-h ECG monitoring by a charac- production of erythropoietin, as most cases are teristic repetitive R-R interval variability during associated with daytime hypoxaemia secondary to sleep. The severity of the bradycardia is related to lung disease. This need not be severe, as there is the degree of hypoxaemia [115] and is probably a evidence that erythropoietin production is stimuresult of both hypoxaemia and baroreceptor lated by an 5aOj less than 92% [55] and any response from the increasing systemic arterial patient with unexplained polycythaemia should pressure. Ventricular ectopic beats and, rarely, undergo overnight oximetry [74,109]. Correction ventricular tachycardia have been recorded also of the hypoxaemia leads to resolution of the and are more common in those patients in whom polycythaemia. the oxyhaemoglobin saturation (SaoJ decreases to The fragmentation of sleep by the frequent less than 60% [35]. The arrythmias are almost arousals results in unrefreshing sleep and ex-

OBSTRUCTIVE SLEEP APNOEA TABLE I. Symptoms of obstructive sleep apnoea

Snoring Sudden arousals with choking Excessive daytime sleepiness Unrefreshing sleep Fatigue Lethargy Depression Morning dry throat Morning headaches Impotence Enuresis Nocturnal sweating

cessive daytime sleepiness (EDS). This may be difficult to assess, as the subjective complaint of sleepiness depends upon personality and the importance and stimulation of the tasks undertaken. An objective measure can be obtained with the multiple sleep latency test (MSLT). The subject is placed in a comfortable, darkened room and the EEG is monitored. The time from " lights out" to the onset of sleep is recorded. The subject is then woken and the test repeated at 2-h intervals. The mean time to onset of sleep in normal subjects is 10-15 min and patients with OSA and narcolepsy generally have times of less than 5 min. EDS may manifest in many ways. Falling asleep while driving is common, and patients with OSA have a higher accident rate than normal subjects [22,27,45]. General feelings of fatigue and tiredness are common, as are complaints of poor memory and automatic behaviour, and have been linked to nasal obstruction for more than a century [111]. Depression appears to be a common complaint, but is probably related to the feelings of fatigue and the difficulty many patients have experienced in persuading their medical attendants to treat their complaints seriously. A large number of other symptoms have been reported (table I). Severe sweating, sudden arousals with a choking feeling, restlessness, chest and limb pains and a dry mouth in the morning are relatively common. Enuresis is uncommon and may be related to hypoxic convulsions. Morning headaches are an indication for early investigation, as they may indicate carbon dioxide retention. Impotence is a rare complaint in men with OSA, but spermatic dysfunction has been described and may be caused by the reduction of growth hormone secretion secondary to the sleep deprivation [93]. Similar studies have not been conducted in women, but it is notable that menstrual

4?9

and ovulatory irregularities and infertility are common in obese young women. Clinical picture

The most constant features of OSA are a history of heavy snoring and EDS. The history of snoring, which is the most likely presenting symptom, depends upon complaints from the sleeping partner or neighbours and thus may not be present in those living alone. The partner may describe episodes of silence followed by a loud snort often referred to as an "heroic" snore, and may express the fear that the patient has stopped breathing. Some patients describe occasional awakenings with a choking feeling, particularly at sleep onset. The history of EDS may be difficult to elicit, since individuals vary greatly in their response to sleep deprivation and the gradual onset of symptoms often leads them to attribute the tiredness and fatigue to advancing age. The most common manifestations are a need for afternoon and evening naps and a tendency to fall asleep during non-stimulating activities such as driving on motorways, sitting in committee or watching television. Clinical examination is directed at both the cause of the OSA and its consequences. The nasal airway is examined and an objective measure

FIG. 2. Typical pharyngeal appearance in a patient with OSA.

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TABLE II. Conditions associated with obstructive sleep apnoea. The list is not exhaustive

Nasal obstruction [21,78,105,111] Tonsillar and adenoidal hypertrophy [6,49,104,110] Obesity [26,47,76] Mandibular hypoplasia [15,49,89,95] (e.g. Bird-like-face, Pierre Robin syndromes) Down's syndrome [14] Storage diseases [83,97,100] (e.g. Hurler, Hunter, Schie syndromes) Hypothyroidism [32] Acromegaly [70] Achondroplasia [101] Neurological disorders [34,36] (e.g. Shy-Drager, poliomyelitis, myotonic dystrophy, dysautonomia) Chronic renal failure [59]

made of its airway resistance such as the peak inspiratory flow rate [29]. The pharynx often has a characteristic appearance, with reddened and thickened mucosa, with redundant folds and a long thickened soft palate and uvula (fig. 2). It has a reduced cross-sectional area and is more compliant than normal [6]. The gag reflex is often diminished and in the author's experience is a valuable sign. An assessment is made of the length of the lower jaw. The patient is weighed and the

distribution of fat noted, in particular the presence of jowls, which indicate the presence of pharyngeal fat pads. Hypertension is a common consequence of OSA and the cardiovascular system should be examined carefully. OSA has been described in association with a number of medical conditions. A brief list, which is by no means exhaustive, is given in table II. Investigations

The diagnosis is usually self evident in the majority of patients, and an overnight study of sleep is necessary only to determine the severity of the condition. In these cases oximetry alone or, preferably, combined with respiratory monitoring suffices [42]. Full polysomnography including EEG, EOG and EMG recording for sleep staging is necessary in those patients in whom the diagnosis is in doubt. OSA is classified from the oximetry trace [66] (fig. 3). Minor reductions in SaOz without repetitive desaturations is the least severe class (Grade 0) and may progress to periods of repetitive desaturation because of apnoea in some sleep phases (Grade 1). Most subjects fall within these groups, but some progress to repetitive

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FIG. 3. Classification of obstructive sleep apnoea from the recording of oxyhaemoglobin saturation. Tracings taken from the analogue output of a pulse oximeter (Ohmeda Biox III). A = Grade 0; B = Grade 1; c = Grade 2; D = Grade 3 (as defined in text).

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desaturations throughout sleep but with return of the SaO2 to baseline with arousals (Grade 2). Very few fall within the worst category (Grade 3) where the 5aOj remains low between apnoeas, signifying hypoventilation. Radiology of the upper airway is helpful in determining treatment. Lateral cephalometry suffices in many patients, but CT scanning of the naso-, oro- and hypopharynx is invaluable if it is available. Treatment Simple measures suffice for many minor cases. Weight loss, avoidance of alcohol, sleeping on the side with head and shoulders raised and stopping smoking should be advised. Intraoral devices may be of value in mild cases [11,43]. A naso=pharyngeal airway may be tolerated both as a short term expedient and for longer term management [75,100]. Surgery to improve the nasal airway and remove excess tonsillar and adenoidal tissue is necessary in many cases. Uvulopalatopharyngoplasty (UPPP) was described by Ikematsu [51] and popularized by Fujita [25] and has been used widely. The free edge of the soft palate and uvula is excised, together with any tonsillar tissues and redundant mucosal folds. The procedure is restricted to subjects in whom the site of pharyngeal collapse is at the level of the palate and not posterior to the tongue. These subjects may be identified from radiological studies of the airway [44] or by fibreoptic endoscopy during sleep. Symptomatic improvement is to be expected in appropriate subjects, but objective reduction in the severity of the OSA is often less impressive [86,107] and, more importantly, nCPAP is no longer effective. The procedure is thus reserved for patients with Grades 0 and 1 disease who are not obese [107]. A recent survey has shown that the life expectancy of patients who have undergone UPPP is no different from untreated patients with OSA [45]. Patients with severe disease and those unsuitable for UPPP are best managed with nCPAP [103]. Purpose designed masks, breathing circuits and pumps are used and pressures of 5-15 cm H2O are adequate for most patients (fig. 4). The technique can also be adapted for children [39]. The subject is admitted to the laboratory and the lowest pressure necessary to abolish the apnoea is determined. Restoration of normal sleep is associated with a rebound of excessive Stage 4 and REM sleep during the first night, which in the

FIG. 4. Nasal CPAP pump, mask and single hose tubing system ("Sleep-Easy I I " pump with Sanders circuit, Respironics).

occasional subject may lead to hypoxaemia [54]. Long term acceptance rates of 60-80 % may be achieved with close follow up and attention to detail. Tracheotomy is the only other surgical treatment where complete abolition of apnoea may be expected. However, the long term complications are such that it is reserved for those patients in whom nCPAP is impractical or intolerable and as an emergency measure in those patients with life threatening cardiac failure. Mandibular advancement and elevation hyoidplasty have been advocated for those patients with a narrow posterior air space behind the tongue, in whom UPPP alone is unlikely to be successful [88]. Laryngeal incompetence has been reported as a complication of this procedure and it is probably best reserved for those patients who do not comply with CPAP and refuse tracheotomy. A large number of remedies have been suggested in the past for the management of snoring. Several hundred have been patented in the past century [5]. Most have worked by ensuring nasal rather than mouth breathing (fig. 5) or by persuading the sufferer to sleep in the lateral position. More recently, electronic devices have been described which wake the snorer with an electric shock when snoring is detected. The rationale of disturbing the sleep of an individual whose sleep is already fragmented is doubtful and the devices, if at all effective, work by training the subject to sleep in the lateral position. The same

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c. H. JOHNSTON

2,528,370

DEVICE TO PREVENT I50UTH BREATHING Filed Oct. 18. 1948

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FIG. 5. An example of the many devices patented for the management of snoring by ensuring nasal breathing.

effect can be achieved with a tennis ball placed in the small of the back. Drug treatment for OSA and snoring has been disappointing. Oxygen therapy does not influence the degree of the episodic decreases in Sa0^ but increases apnoea duration by delaying the arousal caused by hypoxaemia [1]. Respiratory stimulants have little effect, principally because tolerance to their effects develops rapidly. Modification of the sleep pattern may be helpful in those mild cases where the OSA occurs only in REM sleep. Protryptilline decreases the amount of REM sleep and may be helpful in mild cases, but the side effects are often troublesome [10]. Long acting tissue lubricants, such as phosphocholinamin, which prevent the pharyngeal walls from adhering to each other, have been shown to have a small effect in mild cases [48].

anaesthetists will suffer from the condition. Sleep deprivation is often cited as a possible factor in the inattention which may cause or precipitate a critical incident during anaesthesia. The deprivation is usually caused by excessive hours of wakefulness and often thought to affect principally junior anaesthetists. Chronic sleep fragmentation in senior colleagues with undiagnosed OSA may be just as likely.

The patient with OSA The anaesthetic agents, sedatives and opioid analgesics worsen OSA by several mechanisms. First and most important, they tend to reduce pharyngeal muscle tone to a greater degree than skeletal muscle tone and thus increase the likelihood of upper airway collapse. Second, they reduce the arousal responses to hypoxaemia, hypercapnia and airway obstruction [84]. Third, they reduce the ventilatory response to hypoxia Implications for the Anaesthetist and hypercapnia. Personal There are few controlled studies of the effects of OSA is a common disorder, affecting approxi- drugs on OSA, with the exception of alcohol [53, mately 1 % of the population [19,23,28,65]. It is 96], the effects of which are well known to every commonest in middle age and older males and it suffering partner of a chronic snorer. The lack of is not unreasonable to suspect that a number of studies is not surprising in view of the many case

OBSTRUCTIVE SLEEP APNOEA reports detailing the deleterious effects in individual patients [20,37,69]. The preferential reduction in upper airway muscle tone [90] has been shown for anaesthetic agents [50,77], alcohol [63], opioid analgesics [91], inorganic solvents [72], neuromuscular blocking drugs [81] and the benzodiazepines [114]. It is of interest to note that zolpidem, an imidazopyridine which acts preferentially at the BD1 receptors, appears to have a lesser myorelaxant effect compared with the benzodiazepines [114] and little propensity to worsen sleep-disordered breathing [Rhodes, Parry and Hanning, in preparation]. The effect of drugs on arousal from sleep has been even less well studied. Flurazepam has been shown to attenuate the arousal caused by hypoxia and hypercapnia [46] and it is likely that other agents would have a similar effect. Other aspects of care may also worsen OSA, for example the habit of nursing many patients on their back and the reduction of the nasal airway by a nasogastric tube. Patients with OSA often have arterial hypertension and associated ischaemic heart disease which may complicate anaesthetic management. Of more importance and often more difficult to assess is the patient with right heart failure. Obesity may make the ECG difficult to interpret and the presence of oedema difficult to assess. It is probably wise to assume right heart failure in any patient with daytime hypoxaemia and to be suspicious of very obese patients with Grades 2 and 3 OSA. The ultimate experience with patients of this type is that of a patient weighing 430 kg [76]. Children with enlarged tonsils and adenoids seem to be particularly at risk [8,104] and Wilkinson reported a 3 % incidence of right heart strain on preoperative ECG tracings [113]. The condition may not have been diagnosed before surgery and may become apparent only during anaesthesia [110].

483 Induction of anaesthesia

I.v. induction of anaesthesia is preferable, even in children. A gaseous induction may be difficult and airway obstruction may occur early [73]. CPAP may be instituted when the face mask can be firmly applied. It is thus important to use a system which lends itself to this technique. Tracheal intubation may be difficult in many subjects, particularly children, because of anatomical abnormalities such as a receding jaw [15, 89,95], short "bull neck" and a relatively large tongue [97], and appropriate steps should be taken to prepare for this eventuality [13]. Awake intubation with local anaesthesia using a fibreoptic instrument has been advocated [18]. Recovery

The recovery period is the most dangerous for the patient with OSA [58]. Residual anaesthetic agents and analgesics are combining to worsen the apnoea at a time when vigilance is diminishing. Snoring is such a common phenomenon on the postoperative ward that the episodes of apnoea are generally overlooked. Clinical detection of hypoxaemia is acknowledged to be poor and will pass unnoticed. Fortunately, most patients survive apparently unscathed, but the role of OSA in the genesis of postoperative myocardial infarction demands investigation. It has been demonstrated that the incidence of arrhythmias is as great in the postoperative period as during the operation [31]. Arrhythmias commonly accompany OSA which has been shown to occur in the postoperative period even in apparently asymptomatic subjects [24]. The patient with known severe OSA should be managed on the Intensive Care Unit or similar high dependancy area. Any patient who normally requires nCPAP should be restarted on therapy at the earliest opportunity and it should be considered in any other patient with recurrent apnoea. Premedication Continuous monitoring of oxygenation with pulse oximetry warns of apnoea and enables appropriate Sedative drugs are best avoided in the patient action. An alternative approach is to monitor with proven severe OSA. A number of episodes of complete upper airway obstruction following airflow at the mouth and nose with a capnograph premedication have been described [47,85,92, or thermistors. 99]. If premedication is required, the patient should be observed closely in an area close to the Analgesia Local analgesia is the preferred method of pain operating theatre and monitored with a pulse oximeter. The anaesthetist should be prepared to control in the patient with OSA. Systemic opioids intervene to maintain the airway if obstruction should be used with extreme caution and the dose kept to a minimum. Extradural opioids have been occurs.

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advocated [82], but have been associated with an serious complication, because a tracheostomy is exacerbation on at least one occasion [64]. Keta- often the only possible management thereafter. Postoperative swelling may cause considerable mine proved useful in one subject [9]. worsening of the OSA following UPPP and Surgical Procedures for OSA careful observation is mandatory [56]. A nasoNasal surgery pharyngeal tube may be left in place in the postoperative period [17]. Nasal surgery requiring bilateral packing may The importance of careful preoperative evalube hazardous for some patients [21] and packing around nasopharyngeal tubes should be con- ation is illustrated by the following case history. The patient, an obese 24-yr-old male, was sidered. The anaesthetic technique should use the minimum of long acting sedatives and the referred to the ENT surgeons with a history of patients should be monitored carefully in the difficulty in nasal breathing and heavy snoring. A history of enuresis was elicited and he was referred recovery area until fully awake. to a neurologist for investigation of possible Tonsillectomy nocturnal epilepsy. This was felt to be unlikely, Airway management may be difficult in these but right heart strain was found and a cardiac patients, particularly if an inhalation induction is catheterization was requested which showed pulchosen. The improvement in the airway following monary hypertension. He was referred to the surgery results in less risk of OSA than before chest physicians for overnight oximetry. OSA of Grade 3 was found, with the lowest Sa.o approxisurgery. mately 20%. He was referred back to "the ENT Palatal surgery surgeons for nasal surgery and tonsillectomy. The nasal airway was improved and packed around Palatal surgery in children with cleft palates may create OSA. Velopharyngeal repair has been pharyngeal tubes and a UPPP performed. He was associated with sudden death in the postoperative admitted to the ITU where he was noted to be period and such children should be observed desaturating to an S&o^ less than 50%, associated closely [62]. Temporary or permanent tracheo- with bradycardia (fig. 6A). This persisted despite stomy may be required in a few individuals [41]. removal of the packs. He was reviewed and found UPPP requires a careful anaesthetic technique, to have persistent severe OSA caused in part by a as coughing and straining may result in disruption small posterior airspace secondary to a small jaw. of the sutures and healing with stenosis. This is a Nasal CPAP was ineffective because of the UPPP

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FIG. 6. Oxyhaemoglobin saturation in a patient with severe (Grade 2) OSA on the first nights following (A) uvulopalatopharyngoplasty and (B) subsequent tracheotomy. Tracing taken from the trend facility of a monitoring system (Spacelabs).

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15. Coccagna G, Di Donato G, Verucchi P, Cirignotta F, Mantovani M, Lugaresi E. Hypersomnia with periodic apneas in acquired micrognathia (a bird-like face syndrome). Archives of Neurology 1976; 33: 769—776. 16. Coccagna G, Mantovani M, Brignani F, Parchi C, Lugaresi E. Continuous recording of the pulmonary and Conclusions systemic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing. Bulletin de PhysioObstructive sleep apnoea is a common condition pathologie Respiratoire 1972; 8: 1217-1227. which has many implications for the anaesthetist. 17. Colman M. The use of a nasopharyngeal tube after A clear appreciation of the nature of the condition palatopharyngoplasty in patients with sleep apnea. Laryngoscope 1985; 95: 609-610. is essential for successful management and the 18. Craddock M, Lees DE. Anesthesia for obstructive sleep avoidance of complications. apnea patients: risks, precautions and management. 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BRITISH JOURNAL OF ANAESTHESIA parative pharmacology of zolpidem and other hypnotics and sleep inducers. In: Sauvant JP, Langer SZ, Morselli PL, eds. Imidazopyridines in Sleep Disorders. New York: Raven Press, 1988; 97-109. 115. Zwillich C, Devlin T, White D, Douglas NJ, Weil J, Martin R. Bradycardia during sleep apnea: Characteristics and mechanism. Journal of Clinical Investigation 1982; 69: 1286-1292. FURTHER READING Fairbanks DNF, Fujita S, Ikematsu T, Simmons FB, eds. Snoring and Obstructive Sleep Apnea. New York: Raven Press, 1987. Guilleminault C, ed. Sleep and its Disorders in Children. New York: Raven Press, 1986. Guilleminault C, Dement WC, eds. Sleep Apnea Syndromes New York: Alan Liss, 1978. Home JA. Why We Sleep. Oxford: Oxford University Press, 1988. Kryger MH, Roth T, Dement WC, eds. Principles and Practise of Sleep Medicine. Philadelphia: W. B. Saunders, 1989. Orem J, Barnes GD, eds. Physiology in Sleep. New York: Academic Press, 1980. Parkes JD. Sleep and Its Disorders. London: W.B. Saunders, 1985. Saunders NA, Sullivan CE, eds. Sleep and Breathing; Vol. 21: Lung Biology in Health and Disease (Lenfant C, ed.) New York: Marcel Dekker, 1984. Thawley SE, ed. Sleep apnea disorders. Medical Clinics of North America 1985; 69.