ABSTRACT

Sleep-related breathing disorders (SRBDs) are an important public health problem associated with significant morbidity. Disorders of breathing during sleep exist along a spectrum of respiratory disturbances including conditions resulting in complete or partial upper airway obstruction, those that alter breathing patterns and those that lead to hypoventilation or hypoxemia. Initial descriptions of abnormal breathing during sleep can be traced to ancient historians. However, medical knowledge concerning SRBD dates back to the early 19th century, when the clinical observation of a pattern of breathing called Cheyne-Stokes was described (1,2). Subsequently, clinical descriptions of patients with obesity and excessive sleepiness were noted. In 1956, Burwell and colleagues applied the term “Pickwickian syndrome” to describe individuals with obesity, hypersomnolence, and chronic hypoventilation, because of the similar description of a character in the Dickens’ story, The Posthumous Papers of the Pickwick Club (3). Subsequent investigations of patients with the Pickwickian syndrome by Gastaut and coworkers in 1966 discovered that cessation of respiration during sleep in these patients was due to intermittent upper airway obstruction (4). This work is credited as the initial recognition of obstructive sleep apnea (OSA) as a distinct clinical syndrome. In subsequent years, the connection between nocturnal obstructive respiratory events and daytime sleepiness became generally accepted with Guilleminault and coworkers in 1976 describing the OSA syndrome as a disorder with daytime sleepiness and obstructive apneas on polysomnography (PSG) (5). This was followed shortly thereafter by reports indicating that partial airway obstruction or hypopneas during sleep could produce clinical symptoms identical to those previously attributed only to apnea (6,7). Consequently, OSA syndrome became known as obstructive sleep apnea hypopnea (OSAH) syndrome. More recently, Guilleminault and colleagues described a group of patients who had daytime sleepiness, but no apneas or hypopneas on PSG (8). More detailed physiologic investigation using esophageal manometry demonstrated episodes of increasingly negative intrathoracic pressure without reductions in tidal volume. These findings were evidence of periodic increased upper airways resistance. This led to the appellation of “upper airways resistance syndrome” (UARS) to describe these patients and the use of “respiratory effort-related arousals (RERAs)” as the corresponding nomenclature for these episodes of increased upper airways resistance.