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In a 13-night sleep laboratory study, each of 18 normal young adult males twice received 1 cup of warm water, 1-, 2-, and 4-cup equivalents of regular coffee, a 4-cup equivalent of decaffeinated coffee, and a 4-cup equivalent of caffeine. All beverages were administered 30 min before bedtime according to a balanced Latin-square design. Regular coffee produced dose-related changes in most standard electroencephalogram-electrooculogram (EEG-EOG) sleep parameters, and the 4-cup equivalents of regular coffee and caffeine produced equivalent effects. Decaffeinated coffee had no effect. Regular coffee and caffeine caused rapid eye movement (REM) sleep to shift to the early part of the night and stages 3 and 4 sleep to shift to the later part. Coffee also produced dose-related changes in several subjects estimates of sleep characteristics. These results suggest that coffee and caffeine may be used in normal subjects to induce symptoms mimicking those of insomnia. Such a tool should promote further understanding of insomnia.

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We assessed the flow-impeding properties of nose and pharynx combined in four normals and five patients with occlusive sleep apnea (OSA) while awake by measuring supraglottic pressure and airflow at the nose. We calculated two indices of impedance presented by the supraglottic airway: the second coefficient (K2) of Rohrer's equation and supraglottic resistance (Rsg) at 0.4 l/s. The influence of posture and nasal mucosal circulation was evaluated by measuring these indices in sitting and supine position before and after administration of a nasal decongestant. The effects of changes in posture were similar in both normals and patients: K2 and Rsg values were significantly larger in supine than in sitting position. The nasal decongestant significantly decreased both values in sitting and supine positions for normals and patients but did not eliminate the posturally induced changes. Patients had significantly greater K2 and Rsg values than normals in all conditions. These results indicate supraglottic airway narrowing in OSA patients. This narrowing probably results from structural encroachment on the pharyngeal airway.

Fibrositis (fibromyalgia) patients were compared with normal controls in terms of electrophysiology (EEC), self-report indicants of awakening, quality of sleep, behaviourally signalled awakenings, and Symptom Check List 90R (SCL-90R) scores. The results differentiated fibrositis patients from normal controls in terms of SCL-90R scores, with fibrositis patients showing significantly more psychopathology. Fibrositis patients had more alpha EEG sleep and less REM and Stage 1 sleep. They were better able to recall their behaviourally signalled awakenings the following morning and reported qualitatively less satisfying sleep than the normal controls. The alpha EEG sleep anomaly may reflect a vigilant arousal state during nocturnal sleep and result in the daytime experience of unrefreshing sleep, psychologic distress, that re-enforces the perpetuation of the sleep-related symptoms.

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