Patients benefit from losing weight, lateral positioning during sleep, and avoidance of alcohol and other sedative drugs. Surgical correction of an upper airway defect may be helpful, but it is difficult to predict which patients will benefit. There are no clear guidelines for procedures such as uvulopalatopharyngoplasty and related surgeries or uvulectomy and tonsillectomy, except in children. These may obliterate snoring more than it ameliorates the sleep apnea. Oral alignment devices that are produced by dentists, aimed at advancing the mandible, have been helpful to some patients, especially for those who cannot tolerate positive pressure.
Those few patients with the most severe hypersomnia and cardiopulmonary failure who cannot tolerate nocturnal positive pressure ventilation require tracheostomy and nocturnal respirator care. (See Parkes for a fuller account of therapeutic measures.) Some patients with nonobstructive apnea may also benefit from nighttime treatment with CPAP, but the results are far less consistent than with the obstructive type. Curiously, treating obstructive sleep apnea has not reduced cardiovascular events in recent clinical studies (McEveoy et al).
In central apnea, any underlying abnormality, such as congestive heart failure or nasal obstruction, should, of course, be treated insofar as possible. Where no underlying cause can be found, one of several medications—acetazolamide, medroxyprogesterone, protriptyline, and particularly clomipramine—may be helpful in the short run (Brownell et al). However, drug treatment has proven generally unsatisfactory. Low-flow oxygen may also be useful in reducing central sleep apnea.
This clinical entity has long been known to the medical profession. Gélineau gave it the name narcolepsy in 1880, although several authors had described the recurring attacks of irresistible sleep even before that time. Gélineau had also mentioned that the sleep attacks were sometimes accompanied by falls (“astasias”), but it was Loewenfeld, in 1902, who first recognized the common association between the sleep attacks and the temporary paralysis of the somatic musculature during bouts of laughter, anger, and other emotional states; this was referred to as cataplectic inhibition by Henneberg (1916), and later as cataplexy by Adie (1926). The term sleep paralysis—used to designate the brief, episodic loss of voluntary movement that occurs during the period of falling asleep (hypnagogic, or predormital) or less often when awakening (hypnopompic, or postdormital)—was introduced by S.A. Kinnier Wilson in 1928. Actually, Weir Mitchell had described this latter disorder in 1876, under the title of night palsy.
Sometimes sleep paralysis is accompanied or just preceded by vivid and terrifying hallucinations (hypnagogic hallucinations), which may be visual, auditory, vestibular (a sense of motion), or somatic (a feeling that a limb or finger or other part of the body is enlarged or otherwise transformed). These four conditions—narcolepsy, cataplexy, hypnagogic paralysis, and hallucinations—constitute a clinical tetrad. Wilson has reviewed the historical aspects and early accounts of this subject. The most important observations regarding the pathophysiology of this process have been special relationship to a disordered pattern of REM sleep, and the more recent finding of abnormalities in hypothalamic substances that induce sleep, as discussed below.
Narcolepsy is encountered regularly by neurologists; Daly and Yoss recorded about 100 new cases a year at the Mayo Clinic. Dement and colleagues have estimated the prevalence at 50 to 70 per 100,000 in the San Francisco and Los Angeles areas. Men and women are affected equally.