Introduction

Excessive sleepiness represents a major, albeit poorly recognized public safety and health problem (1). Countless motor vehicle and work-related accidents directly result from sleepiness. Sleepiness contributes to such accidents via inattention, response slowing, or unexpected lapses into sleep. Sleepiness is the normal physiological consequence of sleep loss, sleep disruption, or diminished sleep integrity. Sleepiness can also arise from central nervous system alterations produced by brain lesions, medications, or disease. Severe sleepiness is the hallmark symptom of several sleep disorders, including narcolepsy, obstructive sleep apnea, behaviorally induced insufficient sleep syndrome, and idiopathic hypersomnia with or without long sleep time (2). Excessive sleepiness may occur secondary to psychiatric, neurological, medical, and substance abuse conditions. Therefore, a careful evaluation of sleepiness is both clinically relevant and important. Results of such evaluation must be interpreted within the context of sleep schedule, napping, diet, comorbid illnesses, and concurrent medication.

As a hypothalamic physiologically motivated state, sleepiness may be viewed as an appetite. This appetite promotes a behavioral action designed to alleviate a "drive" state. Thus, in response to hunger we eat, in response to thirst we drink, and in response to sleepiness we sleep. Sleepiness, however, has an additional layer of complexity in as much as it is the net balance between physiological systems promoting sleep and other systems promoting wakefulness. The two-factor model, as proposed by Borbely (3) posits increasing sleepiness in response to sustained wakefulness (Factor S) and fluctuating sleepiness in response to an internal biological clock (Factor C). At least one current model views the circadian (C) factor as an alerting signal opposing the wakefulness-driven rising sleep load. The alerting signal is further countered by oscillating melatonin levels (that provide the brain an internal signal for darkness) but melatonin itself can be suppressed by bright light. These interwoven systems governing sleepiness and alertness are further complicated by autonomic nervous system (ANS) influences. ANS sympathetic activation can increase alertness and reduce sleepiness. Thus, sleepiness may be viewed as a composite of at least three (and maybe more) physiological systems. Consequently, it is easy to appreciate the difficulty encountered when attempts are made to measure it as a unitary phenomenon.

When we ask, "how sleepy are you?" are we asking (i) how do you feel? (ii) how quickly could you fall asleep? or (iii) how difficult would it be for you to remain awake? To better delineate issues, Carskadon and Dement (4) proposed characterizing sleepiness as introspective, physiological, and manifest. This approach provides a potentially useful framework for understanding measurement similarities and differences (Fig. 1). "Introspective sleepiness" indexes an individual's self-assessment of their internal state, or more simply, how they feel. By contrast,

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