Nonpharmacologic Treatment

Sleep experts universally recommend behavioral interventions, either alone or with adjunct medication, for the treatment of insomnia. When interventions such as keeping a regular sleep schedule; creating a dark, comfortable bedroom environment; and establishing a pre-bedtime ritual are effective, insomnia can be resolved without the expense of drugs or drug side effects. Specific interventions should be tailored to the type of sleep complaint. For example, eliminating alcohol for at least three to four hours before bedtime can alleviate fragmented sleep if alcohol is the cause. Avoiding exercise, heavy meals, or caffeine before bedtime can also benefit some patients. Light therapy is particularly beneficial for patients with circadian-rhythm sleep disorders, where an individual may delay sleep at night, then sleep in the next morning. Forcing the individual to awaken earlier, and exposing their face to 30–60 minutes of sunlight can “reset” the biologic clock so they naturally become sleepy earlier in the evening.

Mechanisms of Hypnotic Drugs

Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by increasing its affinity for its receptor. The benzodiazepine (BNZ) receptors also are known as omega-1, omega-2 and omega-3 receptors. The BNZ-1 receptors are located in areas of the brain that are involved in sedation, and BNZ-2 receptors are highly concentrated in areas responsible for cognition, memory, and psychomotor functioning. The BNZ-3 receptors are located in peripheral tissues and not involved in hypnotic efficacy. While benzodiazepines bind to at least these three omega receptor subtypes, zolpidem and zaleplon selectively bind to BNZ-1 receptors. Although hypnotic efficacy may not differ between benzodiazepines and the newer selective agents, the nonbenzodiazepine drugs theoretically should have less central adverse effects on cognition, memory, and psychomotor function. Compared to benzodiazepines, these agents have little effect on the normal stages of sleep, and few if any anxiolytic, anticonvulsant, or muscle relaxant properties.

Definition of Hypnotic Efficacy

Defining efficacy for a hypnotic drug is very difficult because efficacy is patient-dependent. Clinical trials evaluate hypnotic efficacy in a sleep laboratory, measuring time to sleep onset, frequency and duration of awakenings, total duration of sleep, and changes in sleep stages. None of these measurements can be accurately assessed in the usual treatment setting, so the clinician must rely exclusively on the patient’s self-report of his/her sleep before and after use of a hypnotic drug. Two pitfalls must be avoided in order to accurately evaluate hypnotic drug efficacy — inappropriate patient expectations and the patient reporting only his/her worst nights.

Clinicians must set an appropriate expectation for hypnotic effectiveness when a patient receives an initial prescription. Many patients believe the therapeutic endpoint of a hypnotic is a rapid onset of unconsciousness that is uninterrupted for eight hours. This expectation is unrealistic. A hypnotic is effective if it facilitates sleep that is both restful and restorative and allows usual functioning while awake. Normal sleep consists of some nights with occasional interruptions in sleep and some nights with six instead of eight hours of sleep. Counseling against unrealistic expectations may prevent patient-driven dose escalation, which increases the risk of adverse outcomes from hypnotic utilization.

In addition to setting appropriate expectations, the patient should be instructed to use a diary or journal to track sleep quality. This allows both patient and clinician to see averages over time. Without a diary, patients typically remember only their worst nights of sleep difficulty, which can lead to unnecessary increases in dosage.

In terms of dose-dependent hypnotic efficacy, the appropriate use of hypnotic agents has dramatically changed based upon lessons learned from triazolam. It was learned that 0.25 to 0.5 mg of triazolam was a significantly larger dose than was necessary to achieve optimal hypnotic effect, and withdrawal symptoms were significant. With doses of 0.125 to 0.25 mg, on the other hand, withdrawal effects are uncommon. A minimum effective dose for a hypnotic drug is usually not associated with significant rebound on withdrawal; rather, rebound insomnia upon withdrawal develops when doses are in excess of the therapeutic dose.

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