Exercise can help reduce insomnia, although not necessarily within a few hours before sleep.

Developing a relaxing evening routine that includes soothing activities as bedtime approaches is a good way to combat insomnia.

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Advise the patient to use the bedroom for sleep and sex only. This helps build strong and positive associations of one’s bed.

Exposure to extreme temperatures, disturbing light, and disruptive noises when trying to sleep should be avoided, although absolute silence can be counterproductive.

Relaxation techniques. The underlying principle behind relaxation techniques is that they reduce physiologic and cognitive arousal at bedtime, which can make falling asleep easier. Available techniques include progressive muscle relaxation, biofeedback, breathing exercises, yoga, and meditation. These activities should be practiced at a time other then bedtime. Once mastered, such techniques will more readily help the body and mind prepare for sleep.

Stimulus-control therapy. This strategy is aimed at helping patients break associations of their bed with wakefulness. Stimulus-control therapy combines deconditioning with slight sleep deprivation to promote going to bed with a successful sleep onset. Patients should be cautioned not to go to bed until they think they can fall asleep; if they do not fall asleep within 10 minutes of getting into bed, they should get up and go to another room and engage in another activity. Regardless of the time of slumber, a regular wake-up time must be maintained and napping avoided.31

Sleep-restriction therapy. This approach also seeks to break the negative association of the bed with wakefulness. Patients are instructed to limit the time spent in bed to the estimated total sleep time while maintaining the same wake-up schedule. After reporting more than 90% of their time spent in bed asleep, a patient can then retire a little earlier.32

Psychotherapy. In some instances, insomnia develops because of issues and circumstances in the person’s life that are not effectively dealt with. A cognitive-behavioral therapy approach to insomnia will incorporate education about sleep hygiene and elements of other nonpharmacologic strategies.39

A meta-analysis of 59 insomnia studies revealed that patients who received one or more of these nonpharmacologic interventions fell asleep more easily and maintained their sleep better. The most effective strategies in this meta-analysis were stimulus control and sleep restriction.39

Pharmacologic therapy

OTC agents. Approximately 25% of patients suffering from some form of insomnia attempt to address the issue initially with OTC sleep aids from a local pharmacy or supermarket. Dietary supplements and herbal preparations touted as sleep aids include such ingredients as valerian root, kava kava, melatonin, chamomile, and passiflora. However, because herbals are not regulated in the same manner and to the same degree as pharmaceuticals, little is known about the efficacy, purity, or safety of most of these products.5

Melatonin is one of the few dietary supplements promoted to treat insomnia that has been studied extensively. However, results have been ambiguous regarding its efficacy.5

People who resort to OTC remedies often delay seeking proper medical attention for insomnia. This can postpone effective therapy as well as the diagnosis and treatment of any underlying medical conditions or disorders.5

OTC antihistamines are also used to combat insomnia. Diphenhydramine is the most common ingredient in OTC and prescription antihistamines. This agent is well absorbed and widely distributed through the CNS and has an elimination half-life of about eight hours. Its principal mechanism of action is postsynaptic blockade of H1-receptors, which promotes sleep onset.5

Despite its OTC availability, diphenhydramine can cause more problems than some prescription sleep aids. In addition to being a postsynaptic H1-receptor antagonistic, it is also a postsynaptic muscarinic-receptor antagonist. Therefore, diphenhydramine can cause anticholinergic side effects that include dry mouth, blurred vision, constipation, urinary retention, memory impairment, confusion, and delirium.5

Also, since diphenhydramine has a long half-life, it may cause the patient to wake up feeling groggy.5

Antipsychotics. Antipsychotic agents can be mildly to moderately sedating and have minimal abuse potential. These agents are beneficial in patients with insomnia who also have schizophrenia, bipolar disorder, or another comorbid psychiatric disorder. Antipsychotic drugs are fairly long-acting and can result in residual daytime sedation.

Selective serotonin reuptake inhibitors and other sedating antidepressants. Many patients with depression also have trouble sleeping. A sedating antidepressant can be a good treatment choice; however no antidepressant has an FDA indication for insomnia.5,40

Often prescribed for insomnia, selective serotonin reuptake inhibitors (SSRIs) do very little to promote sleep. In fact, SSRIs are mildly stimulating and can undermine sleep quality. Other antidepressants that are sometimes prescribed include trazodone (Desyrel, Oleptro), nefazodone (Serzone), and mirtazapine (Remeron).

Trazodone is prescribed for insomnia more often than any other medication indicated for the condition, including the hypnotics. Trazodone facilitates sleep primarily through postsynaptic blockade of 5HT-2A and H1 receptors.5,40,41

A number of adverse affects are associated with trazodone. Because of its relatively long half-life (five to 12 hours, depending on the person’s metabolism), it often causes residual sedation. Trazodone is an alpha1-receptor blocker and can cause orthostatic hypotension or dizziness in patients with hypotension. It may also cause arrhythmias, as well as priapism in men.5,40,41

Trazodone , in conjunction with other serotonergic medications, has been implicated in causing serotonin syndrome, which is rarely brought on by a single medication. The initial symptoms of serotonin syndrome include agitation, restlessness, and confusion, which could progress to incoordination, myoclonus, hyper-reflexia, diaphoresis, shivering, fever, and in the most extreme cases, coma and death.41

Sedative hypnotics. The eight agents with an indication for insomnia include five older benzodiazepines (estazolam [ProSom], flurazepam [Dalmane], quazepam [Doral], temazepam [Restoril], and triazolam [Halcion]) and three newer, non-benzodiazepine medications (eszopiclone [Lunesta, Lunestar], zaleplon [Sonata], and zolpidem [Ambien, Edluar]). All of these drugs work by enhancing gamma-aminobutyric acid (GABA) activity.

The GABAA receptor complex is involved in the production of sedating, hypnotic effects. Each type of GABA receptor complex can be further divided into subunits, each of which has a number of subtypes. The five benzodiazepines are nonselective, which means they interact with many of the GABAA subunit subtypes. The three newer agents, however, are more selective for the alpha1 subtype. GABAA1 subtype is highly correlated with sedation and amnesia.5,40,41

Because the elimination half-lives of sedative hypnotics vary tremendously, so does their duration of action. Half-lives range from one hour for zaleplon to several days for flurazepam. Medications in this class can hasten sleep onset, reduce the number of awakenings, and increase total sleep time. If discontinued abruptly, however, sedative hypnotics may produce some rebound insomnia. The benzodiazepines can decrease slow-wave and REM sleep.5,40,41

The non-benzodiazepines appear to have less abuse potential than the benzodiazepines, but all agents in this class have some potential for abuse and are classified as Schedule IV drugs by the Drug Enforcement Administration.5,40,41

The FDA indication for the two older non-benzodiazepines (zaleplon and zolpidem) is for short-term difficulty in falling asleep, whereas the newest, eszopiclone, is indicated for the treatment of insomnia. Long-term use of zaleplon or zolpidem may be equally safe as long-term use of eszopiclone.5,40,41

Zaleplon has the shortest duration of action (three to four hours) of all three of the hypnotics. This drug is best suited for patients whose main difficulty is with falling asleep. It may be less helpful in reducing the number of awakenings later in the night. One advantage of zaleplon is that it has no lingering effects the next morning. Zolpidem has a half-life of 2.5 hours. Zolpidem can increase the duration of sleep and decrease sleep latency.42

Eszopiclone is a slightly modified version of zoplicone. It is the first sedative-hypnotic to have been studied in long-term, double-blind, placebo-controlled clinical trials. The half-life of eszopiclone is approximately six hours. Because of its long duration of action, it may have lingering morning after effects.42-44

Selective melatonin MT1/MT2-receptor agonists. The FDA approved ramelteon (Rozerem) in 2005 for the treatment of insomnia characterized by sleep-onset difficulty. This agent acts on the SCN rather than the CNS globally. Because it is not a CNS depressant, ramelteon has no sedating properties and no abuse liability, and is the first insomnia medication not designated as a controlled substance by the DEA.45

Ramelteon does not interact with the GABA system, histamine receptors, opioid receptors, noradrenergic receptors, or acetylcholine receptors. Rather, it interacts with melatonin MT1 and MT2 receptors, functioning as an agonist. The MT1 receptors have a sleep-promoting function, and the MT2 receptors are thought to be involved in the timing of circadian rhythms. Therefore, the mechanism of action can be classified as a chronobiotic effect. The drug’s affinity for both MT1 and MT2 receptors is significantly greater than that of melatonin itself.

Although no significant endocrinopathies are associated with the use of ramelteon, there have been reports of mild increase in prolactin production in women.45,46