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Researchers outline strategies to improve recognition, diagnosis, treatment of insomnia

Wednesday, December 12 2007 | Comments

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What's This? Although insomnia is estimated to affect 40 million to 70 million Americans, it remains underrecognized, underdiagnosed, and undertreated, according to a panel of experts.

For physicians, the process of recognizing and diagnosing insomnia is complicated by a lack of patient awareness. People with insomnia often fail to recognize their symptoms or they underestimate the importance of their sleep problems; as a result, few patients spontaneously discuss sleep problems with their health care provider, according to Dr. Ruth Benca with the University of Wisconsin School of Medicine and Public Health.

This process is further complicated by the clinical profile of insomnia. The disorder frequently occurs with comorbid conditions, its symptoms may be mistaken for those of depression, and a substantial proportion of patients with insomnia (as many as one third to half) endorse a sleep-state misperception with subjective complaints that are not substantiated by objective polysomnography (PSG) assessments, according to Dr. Benca.

The successful recognition, diagnosis, and treatment of insomnia, she noted, involves collecting a comprehensive medical, psychiatric, and sleep history (including sleep diary data); evaluating subjective and objective assessments of sleep and daytime function; considering patient-specific variables and preferences; and realizing that there are multiple treatment paths that can lead to normal, healthy sleep.

To underscore the patient-centered approach, Dr. Benca and colleagues illustrated the process of diagnosing and treating insomnia in 2 case study analyses.

The first case described a woman aged 38 years with primary insomnia. During the consultation, the patient explained that she wanted a "quick fix" for her sleep problem, but she had concerns about addiction and next-morning residual effects. She worked in the health care field and, given her knowledge of possible treatment options, was curious about initiating treatment with either quetiapine or trazodone to improve her sleep.

Dr. Xavier Preud'homme of Duke University Medical Center endorsed a medication-only approach in this scenario. He advised that treatment should begin with education about the known efficacy and adverse event profiles of currently available insomnia treatments using evidence-based medicine. In so doing, it is possible to explain why certain insomnia agents would be preferable to quetiapine or trazodone, while simultaneously addressing the patient's concerns about addiction and next-day effects. If the patient's response to drug therapy is suboptimal, consider adding cognitive-behavioral therapy (CBT), he added. If the patient still does not respond to therapy, Dr. Preud'homme recommended rethinking the diagnosis of insomnia (considering a possible circadian pathology) and requesting an overnight PSG to rule out the possibility of other sleep disorders.

By contrast, Dr. Mugdha Thakur of Duke University Medical Center advocated an approach for this patient that combined the rapid relief of pharmacotherapy with the long-term benefits of CBT.

Dr. Thakur cited recent research suggesting CBT is at least as effective as drug therapy for the short-term treatment of insomnia with effects that persist after active treatment is discontinued. She also noted that recent studies have suggested CBT plus drug therapy is more effective than hypnotic therapy alone. Moreover, Dr. Thakur asserted, studies indicate that CBT can be effective in primary care settings, in group settings, and after as few as 2 sessions.

In the second case study, Drs. Benca and Thakur proposed possible approaches for treating a woman aged 48 years with a diagnosis of moderate, recurrent major depressive disorder with comorbid insomnia. Although she reported fatigue, she had little daytime sleepiness (Epworth Sleepiness Scale score of 3).

Dr. Thakur suggested a "wait-and-watch" approach to treating this woman's insomnia (ie, treat the depression and wait for the insomnia to improve as a result), with the rationale being that insomnia is a core symptom of depression, which responds to treatment with antidepressants. Dr. Thakur recommended initiating treatment with a sedating antidepressant, such as mirtazapine. If the insomnia does not improve with the depressive symptoms, then consider treating the insomnia directly, she added.

Dr. Benca, however, recommended a combined approach to target the depression and insomnia simultaneously, particularly if it is possible that antidepressants are exacerbating a patient's insomnia. She noted that insomnia may also aggravate depression and it is the most likely symptom to persist after others resolve.

The treatment of insomnia in this patient, Dr. Benca argued, could be accomplished with pharmacotherapy, CBT, or both. The evidence for CBT in patients with comorbid insomnia, she noted, can be found in a review conducted by the American Academy of Sleep Medicine (AASM) in which the academy concluded that "CBT is effective for insomnia associated with psychiatric disorders, although to a lesser extent than medical disorders or primary insomnia." As a result of this review, Dr. Benca noted, the AASM made a standard-level recommendation in 2006 supporting the use of psychological and behavioral interventions "in the treatment of secondary insomnia."

Evidence supporting the use of pharmacotherapy in patients with comorbid insomnia comes, in part, from recent research with zolpidem and eszopiclone, Dr. Benca added. Zolpidem data suggest the drug significantly improves insomnia symptoms caused by selective serotonin reuptake inhibitors, while eszopiclone research indicates that the addition of eszopiclone to fluoxetine may significantly improve antidepressant response rates and time response onset.

Lastly, if drug therapy will play a role in the treatment of a patient's insomnia, it is important for a physician to consider the drug's mechanism of action and pharmacokinetic properties as these will determine how the drug affects sleep parameters, according to Dr. David Nutt, head of the psychopharmacology department at the University of Bristol in England. For example, among drugs that target gamma-aminobutyric acid-a receptors, such as benzodiazepines and nonbenzodiazepine receptor antagonists, there are substantial differences in drug half-lives. Some, such as zaleplon and zolpidem, have short half-lives (<4 hr) such that these agents may induce sleep onset but the benefit of the drug will likely wear off before an individual gets a full night's sleep (although the controlled-release formulation of zolpidem appears to extend the drug's duration of action).

Others, such as flurazepam and nitrazepam, have much longer half-lives (>10 hr), which may lead to next-day hangover effects, he said. By contrast, drugs such as zopiclone have a half-life intermediate between these 2 extremes (approximately 4 to 6 hours), which may be ideal for sleep onset and maintenance.

This information concerns uses that have not been approved by the Food and Drug Administration.

By Courtneay Parsons

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