Narcolepsy is a neurological condition with a prevalence of up to 1 per 1,000 that is characterized by irresistible bouts of sleep. Associated features include the pathological manifestations of rapid-eye-movement (REM) sleep: cataplexy, sleep paralysis, hypnagogic hallucinations, and abnormal sleep-onset REM periods and disturbed nocturnal sleep. The condition is strongly associated with the HLA-DR2 and DQw1 phenotype. The phenomenology of narcolepsy is discussed, and diagnostic procedures are reviewed. Treatment modalities involving central nervous system stimulants for somnolence and tricyclic drugs for REM-sleep abnormalities are discussed. Sleep laboratory studies on the treatment efficacy of methylphenidate, pemoline, dextroamphetamine, protriptyline, and viloxazine are presented. Data suggest that: (1) methylphenidate and dextroamphetamine objectively improve somnolence; (2) pemoline, at doses up to 112.5 mg, is less effective in controlling somnolence but may improve certain aspects of performance; and (3) protriptyline and viloxazine are effective anticataplectic agents that produce little improvement in somnolence.

A survey was conducted on 10 polysomnographic studies on the pharmacologic treatment of the sleepiness of narcolepsy. Three studies employed the MSLT and 7 employed the MWT as their polygraphic measure of sleep tendency. Statistically and clinically significant therapeutic changes were apparent for pemoline, modafinil, dextroamphetamine and methylphenidate. Codeine, ritanserin and protriptyline did show statistically significant effects. The common feature among the drugs that did produce clinically significant improvements seems to be facilitatory action on central catecholaminergic transmission. Within this group of drugs, only methylphenidate and dextroamphetamine brought MWT sleep latencies to approximately 70% of normal levels.

A sample of 4,920 disease-related deaths from New York City for 1979 (8.7 percent of all relevant data from New York City's files) showed a 60 percent rise in death rate beginning at 2 A.M. and reaching a peak at 8 A.M. A smaller peak was also noted at 6 P.M. The rise in human mortality beginning at 2 A.M. and peaking at 8 A.M. might be explained by: artifact of deaths occurring anytime during the night that are discovered after daybreak, effect of less efficient health care between 2 A.M. and 8 A.M., and disease processes that somehow increase risk of death between 2 A.M. and 8 A.M. An attempt was made to differentiate among these possibilities by comparing time of death for various subsamples. The bimodal pattern appeared only in the temporal distribution of deaths of persons over 65 years of age; deaths of persons under 65 did not show significant temporal concentration. There were also prominent differences in the distribution of deaths for different reported causes of death. Ischemic heart disease, which numerically accounted for over 50 percent of the sample, showed peak mortality at 8 A.M. for both males and females. Hypertensive disease showed a significant peak in mortality at 1 A.M. for females only. Cerebrovascular disease peaked significantly at 6 A.M. with a significant peak only for males. The age and disease specificity of the 2 A.M. to 8 A.M. rise in death is consistent with a disease-related explanation for the bimodal circadian pattern in mortality. The quality and efficiency of health care could be improved with more precise information on peak periods of risk for specific morbid conditions.