Excessive daytime sleepiness is a common complaint in general medical practice (Table 18-2). Certainly, the most frequent causes are inadequate sleep and the use of any one of a large variety of medications. Abuse of alcohol and illicit drugs should also be included in this category. Most conditions associated with severe fatigue produce daytime sleepiness and a desire to nap. A survey of conditions giving rise to daytime sleepiness has been accumulated by Guilleminault and Dement (1977). A notable medical cause is infectious mononucleosis but many other viral infections have the same effect. Certain chronic neurologic conditions can produce fatigue and sleepiness, multiple sclerosis and Parkinson disease being the outstanding examples. Among general medical conditions, hypothyroidism and hypercapnia must always be considered when daytime sleepiness is a prominent feature. One must not overlook the possibility that excessive daytime drowsiness is the result of repeated episodes of sleep apnea, discussed below, or the disruption of nocturnal sleep by disorders such as the restless legs syndrome.
Once these causes of disrupted sleep have been addressed or excluded, sleep apnea remains the most important prevalent condition causing excessive daytime sleepiness. REM sleep is associated with irregular breathing, and this may include several brief periods of apnea up to 10 s in duration but these are not considered pathologic. The main features of sleep apnea are cyclic breathing during sleep with periods of apnea and hypoxemia. The condition is typically considered to have two varieties, sometimes coincident: obstruction of the upper airway (obstructive type) and loss of neurogenic drive for respiration (central type). Apneas occurring at the onset of sleep are not in themselves considered to be pathologic.
Apnea of the obstructive type in which the posterior pharyngeal muscles collapse and narrow the upper airway is far more common than the central variety. Obstructive apnea is associated with obesity and also accompanies acromegaly, hypothyroidism or myxedema, micrognathia. In children, more than in adults, adenotonsillar hypertrophy may be a factor. Instances occur as a result of neuromuscular diseases that weaken the posterior pharyngeal musculature; motor neuron disease is the most common example of this group. Obstructive sleep apnea is characterized by noisy snoring of a cyclic type. After a period of regular albeit noisy breathing, there occurs a waning of breathing efforts; then, despite repeated inspiratory efforts, airflow ceases. Following a prolonged period of apnea (10 to 30 s or even longer), the patient makes a series of progressively greater breathing efforts until breathing resumes, accompanied by very loud snorting sounds and a brief arousal.
Obstructive sleep apnea occurs during both REM and NREM sleep and the amount of apnea during REM exceeds that seen normally observed, as alluded to above. Just before the diaphragm contracts, the upper respiratory muscles (genioglossus, geniohyoid, tensor veli palatini, and medial pterygoid) normally contract to resist the collapse of the oropharynx. If the airway is obstructed or the muscles are weakened and then go slack, the negative intrathoracic pressure causes narrowing of this passage. Sedative medications, alcohol intoxication, excessive tiredness, a recent stroke, head trauma or other acute neurologic disease, and primary pulmonary disease may all exaggerate obstructive sleep apnea, particularly in the obese patient with a tendency to snore.
Hypoxia or perhaps other stimuli induce an arousal response, either a lightening of sleep or a very brief awakening, which is followed by an immediate resumption of breathing. The patient quickly falls asleep again and the sequence is repeated, several hundred times a night in severe cases, greatly disrupting the sleep pattern and reducing the total sleep time. Paradoxically, these patients are very difficult to rouse at all times during the night.