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To determine the association of HLA DR2 in patients with narcolepsy without cataplexy, a case-control study was performed. Patients receiving the diagnosis of narcolepsy without cataplexy had excessive daytime sleepiness (EDS) and polysomnographic findings consistent with narcolepsy but no clinical evidence of cataplexy. Of 28 patients identified, 12 agreed to return for HLA typing. Respondents did not differ from nonrespondents in demographic, clinical, or sleep laboratory data. The comparison group was 503 individuals, those 30 years and older, on the Michigan Kidney Transplant Registry. The odds ratio obtained from logistic regression indicated a strong association between narcolepsy without cataplexy and HLA DR2. To control for potential confounding variables, multivariate models were constructed to explore the joint effects of HLA DR2 and each one of the covariates (age, sex, and race), their possible combinations, and the effect of all three covariates. The odds ratios decreased minimally and the association between the disease and HLA DR2 remained significant.

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In order to better characterize the subjective and polysomnographic findings in patients with narcolepsy, a follow-up questionnaire was mailed to all patients diagnosed with the disorder at the Henry Ford Hospital Sleep Disorders and Research Center. The questionnaire inquired regarding the present, previous, and change in status for the constellation of narcolepsy symptoms. Memory problems, problems of daytime function, and nocturnal sleep disturbance were included among the questions related to the symptomatic constellation. By definition, all patients were symptomatic of daytime sleepiness and were diagnosed with narcolepsy only if there were two or more rapid eye movement (REM) onsets documented on the polysomnographic evaluation. A high percentage of patients reported nocturnal sleep disturbance, which was one of the symptoms with the latest reported onset. Retrospective comparison of questionnaire responses to the clinical polysomnography revealed significantly more sleep maintenance difficulties in the group of patients reporting this symptom on the questionnaire. Patients with disturbed nocturnal sleep reported taking more naps during the day, although the Multiple Sleep Latency Test (MSLT) failed to show differences in sleep latency. Interestingly, this group of patients was found to have a significantly higher number of sleep onset REM episodes on the MSLT. Finally, the findings are discussed as they compare to studies that required the presence of cataplexy as part of their inclusion criteria.

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Patients with narcolepsy have more psychiatric symptoms than normal controls as measured by psychometric tests. However, it is unclear whether these findings are specific to narcolepsy, as some studies have suggested, or related to excessive daytime sleepiness (EDS) or to chronic illness. We compared a group of 56 narcoleptics to age- and sex-matched controls with EDS. A group of 48 individuals with normal sleep architecture was also used as an additional control group. Both the narcoleptic group and the EDS-control group had significantly greater scores on Minnesota Multiphasic Personality Inventory scales but were not different from each other. Our data suggest that the psychopathology associated with narcolepsy is not specific and may be generalized among patients with disorders of excessive sleepiness.

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Ninety-two consecutive patients with obstructive sleep apnea syndrome (OSAS) were studied before and six weeks after treatment with either nasal continuous positive airway pressure (CPAP) or uvulopalatopharyngoplasty (UPPP) (n = 46 per group). Assignment of patients to treatment was based on clinical considerations and patient preference. Patients were assessed by nocturnal polysomnography and performance on the Multiple Sleep Latency Test (MSLT) the following day. Before treatment, the CPAP and UPPP groups did not differ in sleep-related respiratory disturbance, oxygenation during sleep, fragmentation of sleep, or the level of excessive daytime sleepiness indicated by the MSLT. Both treatments produced significant improvement on all measures. However, improvement in UPPP patients was significantly less consistent than that of CPAP patients. To the extent that UPPP successfully reversed the respiratory disturbance (i.e., 50% reduction in respiratory events index), sleep continuity and daytime sleepiness were improved to a degree comparable to that of patients treated with CPAP.

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Although obstructive sleep apnea (OSA) has been studied in detail for over a decade, the mortality of this disorder is unclear. We calculated cumulative survival in 385 male OSA patients. We found that those with an apnea index (AI) greater than 20 had a much greater mortality than those with AI = less than 20. The probability of cumulative eight-year survival was .96 +/- 0.02 (SE) for AI = less than 20 vs. 63 +/- 0.17 for AI greater than 20 (p less than .05). This difference in mortality related to AI was particularly true in the patients less than 50 years of age in whom mortality from other causes is not common. None of the patients treated with tracheostomy or nasal CPAP died. Eight of the patients treated with uvulopalatopharyngoplasty (UPPP) died and the cumulative survival of the UPPP-alone treated group was not different from the survival curve of untreated OSA patients with an apnea index of greater than 20. We conclude that OSA patients with an apnea index of greater than 20 have a greater mortality than those below 20 and that UPPP patients be restudied after therapy. If the latter patients are found not to have marked amelioration of their AI, then they should be treated by nasal CPAP or tracheostomy.

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A polysomnographic assessment in healthy normal sleepers of possible dose relations for rebound insomnia was conducted. As an additional measure of rebound the study included a direct test of sleep/wake tendency during the night of drug discontinuation. Twelve, healthy men (21-30 years) each received placebo, 0.25 mg and 0.50 mg triazolam for 6 consecutive nights followed by a discontinuation night and 14 nights of recovery at home. The three conditions were presented, double-blind, in a latin square design. On night 6 of drug administration both doses increased total sleep time compared to placebo, but 0.50 mg did not improve sleep beyond 0.25 mg. On drug discontinuation (night 7) wake time over the 8 h recording and sleep latency after an experimental awakening (02.30 h) were increased with 0.50 mg compared to placebo and 0.25 mg. On these measures of rebound 0.25 mg did not differ from placebo. Thus rebound insomnia occurred only at a dose (0.50 mg) which produced no additional hypnotic efficacy in these normal sleepers. Whether tests of sleep/wake tendency make a useful measure of rebound insomnia needs further clarification.

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A new surgical procedure to treat obstructive sleep apnea by uvulopalatopharyngoplasty (UPPP) was evaluated in 66 patients, 63 men and 3 women, with objectively documented sleep apnea syndrome. Removal of redundant tissue in the oropharynx (UPPP) significantly improved excessive daytime sleepiness, reduced by half the frequency of apneas and hypoxia occurring during sleep, and improved the quality of sleep. Closer analysis indicated that all 66 patients did not benefit to the same degree. Among patients classified as responders, the frequency of apnea was reduced to a level seen in healthy adults of the same age, measures of sleep approached normal, and excessive daytime sleepiness was eliminated. In nonresponders, frequency of apnea and consequent disruption of sleep was not reduced, but nocturnal hypoxia was improved.

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The consistency of apneas from night to night was examined in 2 groups of patients. The first group had more than 100 apneas per night (frequent apnea) and the second group had less than 100 apneas per night (infrequent apnea). All patients underwent clinical polysomnography for 2 nights, with no significant weight change or treatment occurring between recordings. The frequent apnea group showed a consistent number of apneas on the 2 nights (r = 0.92, p less than 0.01), whereas the infrequent apnea group showed a highly variable number of apneas (r = 0.35, p greater than 0.10). The correlations on apnea index (apneas per hours of sleep) showed a similar result. Apnea duration and type were consistent in both groups of patients.

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A daytime nap procedure was used to evaluate the daytime sleepiness associated with antihistamines, as well as to assess their hypnotic potential. Healthy, normal subjects received diphenhydramine (150 mg), terfenadine (120 mg), and placebo and went to bed at 900, 1100, 2000, and 2200 h with the instruction to try to fall asleep. The remained in bed for 60 min while standard sleep recordings were made. Across all conditions latency to stage 1 sleep increased significantly from nap 1 to nap 4 and the amount of sleep (all nonstage 1 sleep) decreased significantly. Over the four naps the mean latency to stage 1 sleep with diphenhydramine was significantly shorter than terfenadine and placebo, which did not differ. On the other hand, there were no differences among the drug conditions in the amount of nonstage 1 sleep. In sum, diphenhydramine at this dose produces sleepiness but shows little potential as a hypnotic, and accumulated sleep across the day makes people progressively more alert.

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Triazolam is a new triazolobenzodiazepine drug that is indicated for the treatment of insomnia. The usual adult dosage is 0.25 to 0.5 mg; for geriatric patients a dose of 0.125 to 0.25 mg is recommended. Triazolam is readily absorbed and quickly eliminated with a half-life of 2-5 hours, making it the shortest acting benzodiazepine available in the United States. Sleep laboratory and non-laboratory clinical trials found triazolam 0.25 and 0.5 mg effective in inducing and maintaining sleep. It remained effective in laboratory studies of up to one month duration and non-laboratory studies of up to six months duration when the drug was administered nightly. On discontinuation disturbed sleep for one or two nights was observed in some studies. Triazolam impairs performance for several hours after administration. However, unlike benzodiazepines with long-acting metabolites, triazolam is relatively free of daytime residual effects, which is attributable to its short half-life. Overall, triazolam is an effective and safe compound for the symptomatic treatment of insomnia complaints.

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Polygraphic recordings of the sleep of patients complaining of insomnia has led to recognition of specific patterns of disturbed sleep corresponding to different etiologies of insomnia. This study presents results of polygraphic recordings of the sleep of 26 patients with chronic pain for which no physical cause can be found. All 26 also complained of insomnia. Sleep parameters of this group were compared with those to two other groups also complaining of insomnia: 12 patients whose disturbed sleep was judged secondary to psychiatric disorder, and 16 patients with the subjective complaint of insomnia in whom no objective evidence of sleep disturbance could be demonstrated. The three groups differed significantly in terms of their sleep parameters. The pain patients slept less than the subjective insomnia patients. The sleep disturbance of the psychiatric patients was more severe than that of the chronic patients. Several chronic pain patients showed evidence of nocturnal myoclonus; several also showed alpha rhythm intrusions into their sleeping electroencephalograms. The study verifies that chronic pain patients do experience significant sleep disturbance and raises several questions concerning relationships among chronic pain, sleep disturbance, and psychiatric illness, particularly depression.

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