ASERINSKY and KLEITMAN [5], in the early 1950s, revealed the presence of slow and rapid eye movement (REM) during sleep, and they observed that REM is associated with a lightening of sleep, dreaming and a number of cardiovascular and respiratory phenomena. The association of REM sleep with muscle relaxation was later made by JOUVET et al. [6]. During the late 1950s and early 1960s, several different clinical reports described the causative associations between obesity, chronic hypoventilation, pulmonary hypertension and cor pulmonale, but the excessive sleepiness was typically attributed to hypercarbia and depression of the respiratory centre. Cor pulmonale was associated with tonsillar and adenoidal hypertrophy and micrognathia in other reports, but the underlying aetiology was not clarified. In 1965, GASTAUT et al. [7] provided the first comprehensive account of OSAS, describing polysomno- graphy in obese hypersomnolent patients with frequent nocturnal apnoeas. During the following decade, the clinical and pathophysiological features of OSAS were described, and it became clear that the pathophysiological basis of obstructive apnoea fundamentally relates to a narrowing of the upper airway, which is partly genetic in origin, but to which acquired factors, such as obesity, also contribute. This narrowing compromises the balance between collapsing forces affecting the upper airway during inspiration and the counteracting forces of upper airway dilating muscles. Although early research focused on clinical and pathophysiological aspects, recent research has increasingly focussed on genetic and molecular aspects, particularly in the development of comorbid conditions, such as cardiovascular and metabolic disease. OSAS is now recognised to be highly prevalent in disorders such as congestive heart failure, systemic hypertension and renal failure. Although much has been learnt, substantial knowledge deficits remain, and the basic mechanisms and consequences of OSAS represent an exciting area for future research. The relatively recent clinical and pathophysiological descriptions of OSAS are surprising given that the disorder is now widely recognised and highly prevalent, affecting o4% of adult males and o2% of adult females in the developed world, and with this prevalence growing in parallel with the growing prevalence of obesity. However, most of these cases are clinically unsuspected, since the two most common symptoms of loud snoring and a tendency to fall asleep during the daytime are often considered normal variants, and patients frequently do not seek medical attention. Unfortunately, many patients who do seek medical attention are dismissed as having no significant illness, without formal assessment, and it is very common for patients who have been symptomatic for many years to present to sleep clinics. The failure to recognise clinically significant OSAS is particularly unfortunate for many reasons. First, the condition carries significant morbidity and mortality, and is associated with an increased risk of heart attack and stroke [8], in addition to a significant risk of automobile accidents and injury in the workplace as a consequence of excessive sleepiness [9]. Secondly, the condition is very treatable, and severe forms of OSAS can respond dramatically well to the continued home use of nocturnal nasal continuous positive airway pressure (CPAP) therapy. Additional clinical challenges in the assessment and management of OSAS include the presentation of OSA without sleepiness and the clinical spectrum of OSA in the elderly and in females. Although OSAS has traditionally been regarded as a disease affecting males, there is increasing recognition that the disease is also prevalent in females, particularly after the menopause, and that the clinical manifestations may differ from those in males [10]. OSA is prevalent in the elderly population, but affected patients appear to be relatively less symptomatic, and the disorder may have less severe clinical consequences in this age group [11]. Treatment approaches to OSAS have evolved in parallel with the increased pathophysiological understanding. Most treatment modalities have been mechanistic, with nasopharyngeal airways and tracheostomy being used as a means of bypassing the site of obstruction in the upper airway in the 1970s [12]. However, these treatments were neither indicated nor acceptable to patients without very severe disease. Surgical approaches to enlargement and/or stiffening of the upper airway were also developed, the most widely used being uvulopalatopharyngoplasty, which was described by FUJITA et al. [13] in 1981. The development by SULLIVAN et al. [14], in 1981, of CPAP viii INTRODUCTION