The efficacy of zolpidem, a non benzodiazepine hypnotic agent with a short elimination half life, was reviewed, analysing more than 50 international clinical trials published since 1986. The hypnotic activity of zolpidem has been explored in different patient populations including normal volunteers, general practice outpatients and psychiatric out- or in-patients with varying sleep disorders; both transient and chronic. Assessment methods used have included objective and subjective measures of hypnotic efficacy for different treatment durations, with results confirming that 10 mg is superior to placebo. Zolpidem was shown to be superior in most trials on sleep parameters such as total sleep time, sleep onset latency and nocturnal awakenings, but total REM sleep and REM latency were usually unmodified. Zolpidem maintained normal sleep physiology as demonstrated by the preservation of slow wave stages and no, or minimal, effects on sleep architecture after abrupt discontinuation. Consequently, 10 mg is the recommended dose for the short-term treatment of insomnia in the non-elderly; in elderly patients 5 mg has been shown to be effective at inducing sleep whilst giving an optimum safety profile.

The potential effects of zolpidem, a non-benzodiazepine hypnotic, on cognitive and psychomotor functions have been explored in more than 30 placebo controlled studies, and in many cases in comparison with benzodiazepine reference hypnotics (ie flunitrazepam, nitrazepam, triazolam). Daytime impact of drug administration on alertness has been studied with the Multiple Sleep Latency Test, and no significant clinical impairment has been found after zolpidem 5 to 10 mg, unlike benzodiazepines. Evaluation of the effects of zolpidem on attention and psychomotor skills (critical flicker fusion threshold, substitution or copying tests, choice reaction times or driving tests, etc) indicate that zolpidem at recommended doses (5 mg in elderly and 10 mg in adults) is unlikely to produce significant detrimental residual effects on daytime vigilance, concentration and coordination performances on the morning after intake. In accordance with its pharmacokinetic and pharmacodynamic properties, the effects on zolpidem on memory functions were limited to the first hours after administration and no significant difference was observed between zolpidem (5–10 mg) and placebo 6 hours after administration; longer memory impairment was observed with flunitrazepam or triazolam. Various groups of subjects were included in these studies, both young adults and elderly subjects, healthy volunteers and insomniac patients, and duration of treatment varied between one single dose and 28 days of repeated intake. In conclusion, experimental evidence demonstrates a satisfactory safety profile of zolpidem (5–10 mg) on daytime cognitive functions as compared to other hypnotics.

The different aspects of general safety of zolpidem are reviewed after analysing the safety data obtained in adults as well as in elderly patients. The low incidence of reported adverse events during the first three years of utilisation of zolpidem have corroborated the results of the clinical studies. The most frequent adverse effects are central nervous system (CNS) related but they can be largely prevented by respecting the recommended doses and prescription rules. In cases of acute overdoses, no severe complications have been attributed to zolpidem taken alone. In most of the studies carried out within the recommended treatment duration, abrupt treatment discontinuation was not associated with clinically significant rebound insomnia, and the available pre-clinical and clinical data indicate that the risk of abuse or dependence is minimal when prescribed according to the recommended doses of 10 mg in adults and 5 mg in elderly. Thus, with now well-established arguments on a large patient basis going in the same direction, the safety of zolpidem can authorise and justify its wide prescription in the short-term treatment of insomnia.

A growing number of people are concerned about their sleep in the United States. There are an estimated 40 million US citizens with chronic sleep disorders. The cost to society of sleep disorders has been estimated at greater than $90 billion US dollars. Despite this enormous cost to society, there remains a pervasive lack of attention provided to medical management of this problem. This is compounded by inadequate funding of sleep disorders research. There are treatments available to improve insomnia. These include different behavioral and pharmacologic regimes that can be used separately or in combination. Successful treatment requires thorough knowledge of the differential diagnosis of insomnia. The greatest public health challenge in the management of insomnia is how to develop effective educational programs that will allow the general public to improve their sleep. This will require greater cooperation from primary care providers and the government. Sleep disorders are the most important public health problem not being addressed in the United States.

Insomnia affects about one-third of the population, and is associated with increased morbidity and mortality, reduced production and higher rates of accidents. This suggests that insomnia may burden society with significant cost. However, a precise economic analysis of insomnia is a challenge. Insomnia is part of a very complex interplay of physical and psychological illness, functioning both as a cause and as a consequence. In this paper, some of the methodological issues related to an economic analysis of insomnia are discussed. Data is presented using an economic analysis as an organizer, thus illustrating what conclusions can be drawn, and where further research is needed.