ABSTRACT
INTRODUCTION With the advent of the electroencephalographic study of sleep (1-3) and the more comprehensive methodology of polysomnography (4), the era of the objective assessment of sleep had arrived. Along with this technology, came the promise that sleep related complaints could be accounted for by abnormal physiologic function during sleep. That is, it was believed that the simultaneous and long duration monitoring of sleep continuity and sleep architecture along with pulmonary, cardiac, motor, and cortical function would reveal the abnormalities that account for sleep initiation and maintenance problems, the report of shallow and/or fragmented and/or nonrestorative sleep, and/or the diurnal complaints of sleepiness and fatigue. To a large extent this promise was realized for the complaint of shallow and/or fragmented and/or nonrestorative sleep, and/or the diurnal complaints of pathologic sleepiness. The polysomnographic study of sleep revealed that these complaints were, in large measure, directly related to sleep disordered breathing. The promise, however, was not realized for the complaint of insomnia (sleep initiation and maintenance problems). In fact, the very effort to objectively measure sleep continuity disturbance1 raised more questions than it answered. That is, the objective assessment of sleep with electroencephalography brought into sharp resolution that remarkable discrepancies existed between the subjective and objective measure of sleep latency, wake after sleep onset, number of awakenings, and total sleep time (4,5). Further, no evidence was obtained for physiologic abnormalities that clearly accounted for difficulty initiating or maintaining sleep (e.g., abnormal REM pressure, slow wave sleep deficiency, sleep onset related central apneic events, sleep induced cardiac or CNS irregularities, etc.). At best some of these factors were found to be indicative of “Secondary Insomnia” and particularly the sleep of patients with major depression (6,7).
