Insomnia

By | May 25, 2011

Occasional bouts of insomnia are of little consequence to a healthy adult; however, insomnia appears to be particularly problematic for those who are vulnerable to psychological problems or who have a co-morbid psychological disorder such as clinical depression. In the following sections we review what is known about the relationship between depression and insomnia, focusing specifically on the role of insomnia in the etiology and course of depression, issues related to treatment of depressed individuals with sleep problems, and possible implications of insomnia for relapse.

Epidemiology

Although occasional nights of insomnia are common, clinically significant insomnia is less common. Epidemiological studies show that in the general population approximately 6% to 12% report chronic problems initiating or maintaining sleep. The prevalence of insomnia in those with major depressive disorder is estimated to be 90% and is also likely to be high in other mood disorders such as dysthymia. The prevalence of comorbid insomnia also appears to change across the life span and is even higher in older adults. These epidemiological data indicate that insomnia is nearly always present in individuals with depression. Thus, it is important to carefully assess insomnia symptoms in patients with depression.

Diagnostic Criteria for Insomnia

Systems for classifying sleep disorders are presented in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994), in the International Classification of Sleep Disorders Revised (ICSD-R; American Academy of Sleep Medicine, 2001), and by the American Academy of Sleep Medicine (AASM). Each of these nosological systems classifies insomnia as a form of dyssomnia, or a disorder associated with getting too much or too little sleep. Insomnia is the most common dyssomnia and can be characterized as difficulty initiating sleep (early insomnia), difficulty maintaining sleep (middle insomnia), waking too early (terminal insomnia), or nonrestorative sleep despite adequate opportunity for sleep. In addition to a sleep-complaint these classification systems specify that clinically significant insomnia is also characterized by impairment in one or more area of daily living, and the common consensus is that symptoms must be present for at least 1 month. In recent years, there has been growing interest in further classifying the nature of sleep-related complaints. The AASM Work Group has proposed nine standard subtypes of insomnia to build on current definitions and has proposed that insomnia be further specified according to duration (acute or chronic), severity (mild, moderate, or severe), and presentation (sleep onset or sleep maintenance). Objective sleep data are not necessary to diagnose insomnia, and the discrepancy between objective and subjective sleep may be high. Overall, individuals with insomnia tend to underestimate their total sleep time. Individuals who consistently report poor or little sleep despite normal polysomnography (PSG) findings have been described as having sleep-state misperception or paradoxical insomnia, and the nature of these sleep-related complaints is not entirely understood. Current measures of sleep may be inadequate in quantifying these individual’s problems, or their symptoms may reflect other factors.

Assessment of Insomnia

Assessment of insomnia may be made by clinical interview. Diagnostic interviews should include all of the following information: symptoms, duration, frequency, and severity, other contributing factors (e.g., medication, substance use, psychological or medical disorders, environmental factors), and the presence of other sleep disorders should also be ruled out (see for best-practice assessment, Buysee, Ancoli-Israel, Edinger, Lichstein, & Morin, 2006). Insomnia symptoms can be assessed using a variety of assessment devices including structured interviews, self-report questionnaires, and sleep diaries. Sleep diaries are useful in assessing sleep hygiene and are often used in conjunction with treatment. Objective measures of sleep include actigraphy and polysomnography. An actigraph is a small wrist-worn device used to detect movement during sleep. Actigraphy has been validated against PSG with normal sleepers but may be less reliable in distinguishing between quiet wake and sleep. Nevertheless, actigraphy remains a useful and cost-effective adjunct to subjective measures. Polysomnography is not routinely used in the assessment of insomnia but may be useful in research settings to characterize specific sleep parameters (sleep onset latency or number of arousals) and should be used when the presence of other sleep disorders (e.g., sleep apnea or restless leg syndrome) are suspected.

The Role of Insomnia in the Etiology of Depression

The high comorbidity of depression and insomnia have led some to theorize that insomnia may have a causal role in the onset of depression. Insomnia symptoms often precede the onset of a depressive episode. Large, prospective epidemiological studies that control for a wide variety of demographic and health-related confounds have shown that chronic insomnia increases the risk of developing psychiatric disorders including major clinical depression. In fact, a recent meta-analysis documented that a person with insomnia is at 3.95 to 39.8 times higher risk of developing a mood disorder than someone without chronic sleep difficulties.

Insomnia and Depression: Linked Processes

The high comorbidity of depression and insomnia has led to theories that insomnia is related to depression in the following ways: as a causal agent, a diathesis, or that depression and insomnia share a common cognitive antecedent.

Insomnia and Mood

One obvious pathway between insomnia and depression is through changes in mood. Insomnia has been found to be related to higher daily negative affect, sleepiness and fatigue, and lower positive affect and feelings of alertness. Reduced sleep has been linked to more dysphoric affect, and chronic sleep deprivation is likely to be more troubling than acute sleep problems. Hamilton showed that multiple nights of experimental partial sleep deprivation produce a progressively worsened mood. Thus, across populations and research methodologies, sleep appears to have a direct prospective relationship with mood and emotional health.

Sleep and Stress

Sleep also appears to interact with the stress process and may serve as a cognitive resource. Adequate sleep serves as a biobehavioral resource that facilitates adaptive responses to stress and limits alostatic load. Consistent with these formulations, medical residents who were not able to obtain adequate sleep were found to have a heightened stress-response as well as reduced enjoyment of intellectually challenging tasks. Chronic pain patients with disrupted or inadequate sleep were more vulnerable to pain-related changes in mood. Furthermore, among patients with chronic pain, shorter sleep times inhibited full affective recovery from stress. Thus, insomnia may not have a direct effect on mood. Instead, insomnia may limit enjoyment of cognitively stimulating events while enhancing the emotional salience of, and preventing recovery from, negative events or unpleasant physical symptoms such as pain.

Cognitive Arousal, the Third Variable

In contrast with the previous models that postulate either a direct or indirect causal role for insomnia in the onset of depression, cognitive models of insomnia suggest that insomnia and depression are activated and maintained by similar cognitive processes. Cognitive arousal in the form of worry and excessive rumination about sleep, fear of the consequences of inadequate sleep, and unrealistic expectations about sleep are proposed to play a causal role in insomnia. Excessive negatively oriented cognitive activity triggers both autonomic arousal and emotional distress. The resulting anxious state is thought to trigger selective attention toward, and monitoring of, internal and external sleep-related threat cues. The combination of the anxious state and the attentional processes that are triggered by this state cause the individual to overestimate the extent of the perceived deficit in sleep and daytime performance. This process may explain why insomnia patients cannot always be differentiated from healthy sleepers using polysomnography. The unfortunate consequence of this process is that the excessive and escalating anxiety may cause a real deficit in sleep and daytime functioning.

Many of the cognitive processes involved in insomnia are also associated with depression and suggest a common cause. A number of studies have found that poor sleepers tend to engage in rumination about their sleep-related problems. Rumination is also a major cognitive risk factor for depression. It is thought that people with a high ruminative tendency may be especially vulnerable to depression when experiencing sleep disturbance because the mood symptoms associated with poor sleep could activate the ruminative process. Further, people with chronic insomnia tend to focus on their somatic symptoms as well as the consequences and daytime symptoms of their chronic sleep difficulties.

The causal association between cognitive processes in insomnia and risk for depression, however, is unclear. It is possible that cognitive arousal that results from sleepiness is itself a stressor that might trigger depressive episodes. Or, lack of restful sleep might magnify the appraisal of negative events, and fatigue might increase feelings of loss and helplessness that result in depression. Cognitive arousal, however, can also be a consequence of the depressive state. Careful longitudinal research would be needed to fully untangle causes from effects.

Although different in terms of the causal precedence assigned to cognition, emotion, sleep disturbance, and depression, these models illustrate the importance of attending to insomnia symptoms as a possible method to prevent the onset of a depressive episode. The next section focuses on the importance of attending to both insomnia and depression in the course of treatment.

Depression, Insomnia, and Intervention

The presence of insomnia may place a depressed patient at greater risk for negative outcomes. For instance, depressed patients with insomnia symptoms appear to be more impaired than those without insomnia. When depressed primary care patients with insomnia symptoms were compared to depressed patients without insomnia, patients with depression and insomnia reported more than twice the number of days in which social and occupational activities were limited because of illness. Insomnia may also indicate an increased risk for suicidality. Clinicians should carefully assess insomnia symptoms in patients with depression. The presence of insomnia also presents an added risk factor for patients with depression. Thus, it is important to evaluate treatment modalities as they relate to the course of both insomnia symptoms and depression.

Cognitive behavioral therapy (CBT) has been repeatedly validated as an effective treatment for both unipolar depressive disorders and insomnia. In fact, in randomized controlled trials, cognitive behavioral therapy produces either similar or larger effect sizes than most antidepressants for both the treatment of depression and insomnia and has more stable long-term results.

Similar to cognitive behavioral therapy for depression, cognitive behavioral therapy for insomnia (CBT-I) has been used effectively with a variety of populations with insomnia, including those in which insomnia is comor-bid with various medical and psychiatric conditions. Cognitive behavioral therapy for insomnia has repeatedly been found to be more effective than pharmacological treatment of insomnia. Cognitive behavioral therapy for insomnia is a modification of cognitive behavioral therapy for depression and therefore has similar therapeutic content and focus, although specific treatment is tailored to sleep disturbance. For example, both cognitive behavioral therapy for depression and cognitive behavioral therapy for insomnia target cognitive distortions and false beliefs. Additionally, both treatments include relaxation training and behavioral therapy that focuses on the areas of deficit. Cognitive behavioral therapy for insomnia differs from cognitive behavioral therapy in that it also includes behavioral interventions such as sleep-restriction and sleep hygiene that are specific to insomnia.

Given the observed comorbidity of depression and insomnia, and similarity in recommended treatment course, it may not be surprising that treating one disorder will often lead to improvements in the other. For instance, treatment of insomnia has been found to improve treatment outcomes for depression.

Although insomnia often disappears when depression is treated, sleep is physiologically abnormal in persons at risk for depression, and sleep disturbances frequently persist after remission of other depressive symptoms. In fact, insomnia is the most persistent residual symptom following treatment of depression and is present in approximately 44% of treatment completers. The persistence of insomnia after a depressive episode may indicate a continued vulnerability to depression, with patients being at risk for poorer clinical outcomes and higher rates of relapse. Thus, clinicians should be vigilant in treating both depression and insomnia.

Despite empirical findings that cognitive behavioral therapy for insomnia is the most effective long-term treatment for insomnia, medication usage is extremely common, with the most commonly prescribed medications being sedatives, hypnotics, and antidepressants. Historically, sedatives (barbiturates and benzodiazepines) and hypnotics (benzodiazepinelike agents and ethanol) have been the most commonly prescribed; however, these medications often cause daytime sleepiness, tolerance, and dependence. Thus, the number of sedatives and hypnotics prescribed for insomnia has decreased over the past 30 years.

The effects of antidepressant medications on sleep vary according to medication class. Tricyclic antidepressants (TCAs) are well known to produce side effects such as sedation and thus are often used as treatments for insomnia. However, TCAs are not uniform in how they affect sleep (see for a review of antidepressant medications on sleep physiology). Amitriptyline, doxepin, and nortriptyline, have been shown to reduce sleep-onset latency, improve the ability to remain asleep (sleep continuity), increase deep restorative sleep, and reduce REM sleep. Impirimine, desipramine, and clomipramine increase sleep-onset latency, may reduce continuity, but appear to increase the amount of deep restorative sleep and reduce REM sleep. In contrast, commonly used selective seratonin-reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, and sertraline appear to increase nighttime awakenings and also suppress REM sleep. Monoamine oxidase inhibitors, seratonin receptor modulators, and other classes of antidepressants also have been documented to affect the ability to fall asleep, stay asleep, and feel refreshed the next day. Given the documented effects of insomnia on treatment response and relapse rates, it is imperative for clinicians working with depressed patients to investigate whether patients’ medication regimens are improving or worsening insomnia symptoms.

Paradoxical Effects of Sleep Restriction

The link between insomnia and depression has been clearly established. Sleep disruption increases vulnerability to depression, and treatment of insomnia often improves depressive symptoms. Paradoxically, total sleep deprivation produces temporary but significant improvements in approximately 60% of all patients with affective disorders. Even higher rates of improvement are observed among patients with melancholic unipolar depression, among those with diurnal mood variability, and among those who have experienced only a single episode of depression. Unfortunately, the observed improvement in mood is transient and usually dissipates after a night of recovery sleep. In terms of treatment, however, there are some indications that even a single night of sleep deprivation may speed the therapeutic response to antidepressant medications for individuals with depression.

Although the effects of sleep deprivation are well documented and reliable, the phenomenon of mood improvement is not well understood. It has been theorized that the effects of sleep deprivation on improved mood are mediated by changes to the hypothalamic-pituitary-adrenal axis. Specifically, sleep restriction may increase secretion of growth hormone (hGh) and decrease secretion of cortisol. More recently, this theory was substantiated by laboratory studies showing that total sleep deprivation produces a significant decrease in circadian cortisol levels, increases in hGH during the recovery night, and also changes variability in both cortisol and hGH. Thus, total sleep deprivation may ameliorate depressive symptoms via the effects on the stress response.

Other theories focus on the effects of the serotonin system. Using nonhuman animal models, it has been documented that chronic partial sleep deprivation gradually reduces the sensitivity of the serotonin-1A autoreceptors. However, a single night of total sleep deprivation appears to decrease the sensitivity of presynaptic serotonin-1A autoreceptors, which ultimately increases the availability of serotonin within the synapse.

It is well documented that temporary sleep restriction immediately, albeit temporarily, relieves depression. Although sleep-restriction cannot be used for prolonged periods of time, clinical applications of sleep restriction warrant further study. Investigation of this phenomenon may lead to further understanding of the neurochemical profiles associated with both depression and insomnia.

Summary and Conclusions

The exact mechanism linking insomnia to depression is unknown. Although epidemiological data clearly show that insomnia often precedes onset of major depression, it is not known whether insomnia is part of the causal chain or whether it is a prodromal symptom or early warning sign. Nevertheless, it is possible that early intervention with insomnia could prevent onset of depression. More clear is the role of insomnia in the course of major depression. The data clearly indicate that successful treatment of depression does not always lead to remission of insomnia symptoms. Addition of CBTT or referral of a patient to therapist that specializes in cognitive behavioral therapy for insomnia may be an important aspect of relapse prevention that has not been fully appreciated by many depression researchers.

See also

Circadian Rhythms

Stressful Life Events