The Evaluation and Management of the Anxious Insomniac

Karl Doghramji, MD


March 02, 2004

In This Article

Evaluation and Management of the Anxious Insomniac

When a patient presents with the primary symptoms of insomnia and anxiety, the first step should be to determine whether the difficulty represents primarily insomnia or an anxiety disorder. In the case of the former, the anxiety is typically associated with bedtime, increasing as bedtime approaches. Some of this may be due to anticipatory anxiety over the prospect of another sleepless night. These patients' minds race with random thoughts as they become focused upon, and brood over, their sleeplessness which, in turn, aggravates their insomnia even further. A situational pattern of insomnia is common, in which patients typically have greater difficulty falling asleep in their own bedrooms and are often amazed to find that they fall asleep more easily when away from home. This occurs because their own bedroom "triggers" the fear of sleeplessness and the cascade of anxiety.

In contrast, when the primary difficulty is an anxiety disorder, anxiety is present day and night. In addition, the patient's focus is usually not only the insomnia itself, but also ancillary aspects of the disorder, such as distressing nightmares in PTSD and compulsions in obsessive-compulsive disorder. Additionally, the situational aspects of primary insomnia are not seen.

If the determination is made that primary insomnia is the core issue, the optimal treatment is a combination of behavioral sleep-inducing strategies and pharmacologic agents. Pharmacologic agents have a rapid onset of action and can be withdrawn as behavioral measures (which have a delayed onset) begin to take effect.

For a review of behavioral treatments for insomnia, see Speilman et al.[12]

Principles of sleep hygiene include[5]:

  • Maintain regular wake time;

  • Avoid excessive time in bed;

  • Avoid naps, except if shift worker or elderly;

  • Expose yourself to bright light while awake;

  • Use the bed only for sleeping and sex;

  • Avoid nicotine, caffeine, and alcohol;

  • Exercise regularly early in the day;

  • Do something relaxing before bedtime;

  • Don't watch the clock; and

  • Eat a light snack before bedtime if hungry.

Relaxation training: Tension is reduced through electromyographic (EMG) biofeedback, abdominal breathing exercises, or progressive muscle relaxation techniques, among others.

Cognitive psychotherapy: This talk-therapy strives to identify and dispel thoughts that are tension-producing and that have a negative effect on sleep, such as the preoccupation with unpleasant work experiences or examinations at school.

Stimulus-control therapy: This is well suited for insomniacs who spend a great deal of time in bed brooding over sleeplessness. Patients are asked to use the bed only for sleep (not for reading or watching television) and to not stay in bed trying to sleep for more than 10-20 minutes at a time. Rather, they are urged to go into another room and to return to bed only after feeling sleepy.

Restriction of time spent in bed: This therapy is well suited for insomniacs who wake up repeatedly during the course of the night, such as the elderly. Sleep is monitored through sleep diaries and the sleep efficiency index is calculated by dividing the average daily time spent asleep over the average daily time spent in bed. The physician then asks the patient to lie in bed, on a daily basis, for the time that is equivalent to his total sleep time. The patient continues to fill out sleep logs, and calls the physician every 5 days with log data. If the sleep efficiency during the previous 5 days is less than 85%, no changes are made. However, if the sleep efficiency is greater than 85%, time in bed is increased by 15 minutes by allowing the patient to go to bed earlier. No changes are made to the morning awakening time. Patients avoid napping. Over the course of a few weeks, consolidation of sleep is noted along with an increase in quality and the sensation of restorative sleep.

Sedative-hypnotics are indicated primarily for short-term management of insomnia. Older preparations, such as chloral hydrate and the barbiturates, have a limited role due to side effects, such as daytime hangover, lightheadedness, malaise, ataxia, and nightmares. They are also more dangerous following overdose. More recently introduced agents have a better side-effect profile and are distinguished primarily by elimination half-life. Those with a long half-life include flurazepam and quazepam; those with an intermediate half-life include estazolam and temazepam. The short half-life hypnotics include triazolam, zolpidem, and zaleplon.[13] The longer half-life agents are associated with a greater potential for daytime carryover effects, such as daytime sedation, motor incoordination, amnesia, and slower reflexes. These may lead to performance decrements, auto accidents, and hip fractures in vulnerable individuals, such as the elderly. However, zaleplon, the shortest half-life agent, is the least likely to cause daytime carryover effects and, at 10-mg doses, the duration of its sedative effects is limited to 4 hours. Therefore, it can be administered in the middle of the night following nocturnal awakenings, as long as the patient is in bed for 4 hours following administration. Zaleplon is less suitable for patients who have sleep-interruption insomnia throughout the night and on a nightly basis.[14] A longer elimination half-life agent among the short half-life agents, such as zolpidem or triazolam, is more predictably efficacious for the entire duration of the night.[15] Ultimately, the choice of agent should take into consideration the patient's situation, preference, and effects of previous trials with similar agents.

Short elimination half-life hypnotics do not offer daytime anxiolysis in patients who are anxious during the daytime. Patients taking triazolam have been shown to exhibit rebound insomnia following abrupt discontinuation.[16] However, despite widespread concerns regarding both tolerance and rebound, neither property has been documented extensively. Nevertheless, both can be minimized by using the medication at the lowest effective dose and for brief periods of time. Additionally, rebound can be controlled by gradually tapering when discontinuing the drug. Both problems seem to be less prominent with the newest hypnotics, zolpidem and zaleplon. The former has been shown to lack tolerance or rebound following 6 weeks of continuous use in a controlled trial.[17] Guidelines for the use of hypnotics generally aim toward minimizing abuse, misuse, and addiction by discouraging chronic use.

Many agents not specifically indicated for insomnia are used for sleep induction. Alcohol may be one of the most widely used agents by insomniacs because it enhances sleepiness and allows for a more rapid onset of sleep. However, it is a poor choice inasmuch as it alters sleep quality. Alcohol can also result in further impairment in sleep-related respiration in patients with obstructive sleep apnea syndrome.[18] Antihistamines, such as doxylamine and diphenhydramine, can be sedating. However, they suffer from unpredictable efficacy and side effects, such as daytime sedation, confusion, and systemic anticholinergic effects.[19] Sedating antidepressants, used in low doses, are commonly used for the treatment of insomnias not associated with depression. Controlled studies have demonstrated the efficacy of trazodone 150-400 mg and doxepin 25-50 mg, yet further research is needed to confirm these results.[20,21] Antidepressants are also associated with side effects; in the case of trazodone, these include daytime sedation, orthostatic hypotension, and priapism.[22] The tricyclic antidepressants are also, as a class, associated with anticholinergic side effects, such as dry mouth, urinary flow difficulties, cardiac dysrhythmias, etc. Melatonin is a dietary supplement, used in doses of 0.5-3000 mg. Anecdotal reports indicate that it may be efficacious in certain subtypes of insomnia, such as shift work and jetlag and may restore circadian rhythms in the absence of proper sleep-wake regulation induced by blindness, delayed sleep-phase syndrome, and in the elderly. However, its efficacy has not been established conclusively and is in doubt. Additionally, concerns have been expressed regarding its side effects after the observation of coronary artery tissue stimulation in animals and regarding the purity of available preparations.[23,24]

If the determination is made that the underlying disorder is an anxiety disorder, then treatment should target the specific disorder (for a review, see Kaplan and Sadock[25]). The disorder most commonly confused with a primary insomnia is generalized anxiety disorder. Effective agents for this include older antidepressants, such as trazodone and imipramine, although the latter may be associated with a greater array of adverse effects than the newer serotonin reuptake inhibitors, such as venlafaxine extended-release, fluoxetine, paroxetine, sertraline, citalopram and escitalopram. Benzodiazepines are often effective, especially the longer-acting ones (eg, clonazepam and diazepam), yet these also introduce the possibility of tolerance and sedation. Other possible agents include buspirone and hydroxyzine. Recent evidence has suggested the efficacy of pregabalin and the GABA reuptake inhibitor tiagabine.[26] The treatment for PTSD is similar to that for generalized anxiety disorder, except that benzodiazepines are thought to have minimal utility in PTSD.

Although the above agents are effective for anxiety disorders, they often do not adequately address coexisting insomnia. In fact, the serotonin reuptake inhibitor antidepressants, possibly with the exception of citalopram, are known to cause further impairment in sleep architecture in the acute phases of treatment.[27] In such cases, it is important to effectively manage the sleep disturbance with the hypnotic agents discussed above. Although this introduces the possibility of enhanced adverse effects, most of the recently introduced hypnotics, such as zolpidem and zaleplon, have minimal potential for dangerous pharmacokinetic interaction with serotonin reuptake inhibitors.[28]


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