Evaluation and Management of Insomnia in the Psychiatric Setting

Of the general adult population, 35% experience insomnia during the course of 1 year (8). Half experience the problem as severe, and 20.1% of adults are dissatisfied with their sleep or take medication for sleeping difficulties (9).

Studies on the prevalence of insomnia in adults have yielded discrepant results, largely owing to differences in defining insomnia. In a recent study (10) insomnia was divided into four categories: 1) difficulty in initiating and maintaining sleep or nonrestorative sleep; 2) insomnia symptoms accompanied by daytime consequences; 3) dissatisfaction with sleep quality or quantity; and 4) insomnia diagnosis based on definitions established by DSM-IV-TR or International Classification of Sleep Disorders (ICSD) (11). The first category revealed a prevalence of 30%–48%. This dropped to 16%–12% when frequency modifiers were added to symptoms such as the presence of symptoms on at least 3 nights a week or “often” or “always.” When severity criteria were added to insomnia symptoms, the prevalence of insomnia ranged from 10% to 28%. The prevalence of insomnia based on insomnia symptoms with daytime consequences (category 2) was approximately 10%. The prevalence of insomnia based on dissatisfaction with sleep quality and quantity (category 3) was 8%–18% with a higher prevalence being consistently being reported in females. The prevalence of insomnia based on DSM-IV-TR classification varied from 4.4% to 6.4%. Primary insomnia was the most frequent diagnosis, its prevalence ranging between 2% and 4%.

There are fewer studies in the pediatric population, but they show a similar prevalence. One of the earliest studies in preadolescent children showed that 14% of an outpatient pediatric population between the ages of 6 and 12 had insomnia with a mean duration of 5 years (12).

Insomnia is more common in women by a factor of 1.5:1 (13). In women, its prevalence peaks during pregnancy and in the peri- and postmenopausal years. It is also more common in adolescents (ages 11–14) than in younger girls (30.4% versus 16.8%) (14). Its prevalence also increases with advancing age and it affects more than one-third of the population aged 65 and older (15). The risk of insomnia is based on levels of inactivity, dissatisfaction with social life, and the presence of organic and mental disorders, without which the risk of insomnia in healthy seniors is similar to that of younger individuals.

Insomnia is more common in shift workers than in individuals working fixed schedules (20.1% versus 12.0%) (16), and its prevalence increases in proportion to the number of shifts worked (17). Working the night or third shift may not only acutely cause insomnia but may also have a persistent deleterious effect on sleep quality even after the individual has reverted to working a day or evening shift (18).

Unemployment, lower socioeconomic status (15, 16), marital status (being divorced, widowed, or single) (10), poor mental and physical health (19), noisy environments (20), medical problems (depressive disorders, anxiety disorders, substance abuse, schizophrenia, congestive heart failure, obstructive airway disease and other respiratory illnesses, back and hip problems, and prostate problems) are also associated with an increased prevalence of insomnia (21–25).

Seasonal differences have been reported in patients with chronic insomnia. In Norway a survey done among a representative sample of 14,667 adults living in the municipality of Tromsø, north of the Arctic Circle, revealed increased incidence of complaints of insomnia during the dark period of the year (26).

Insomnia is associated with decreased quality of life (directly related to the severity of insomnia), greater use of health care resources, functional decrements (27–29), and cognitive deficits (30, 31). A fundamental methodological issue in many studies examining the impairments associated with insomnia has been the inclusion of insomniacs with a wide variety of comorbid conditions. Nevertheless, a limited number of recent studies revealed psychomotor performance deficits in primary insomniacs when responding to challenging reaction time tasks.

One of two studies conducted over the course of 6 years revealed an increased mortality rate and the other revealed no increase in insomniacs (32, 33). A more recent study in older adults with a mean follow-up of 12.8 years revealed that participants who had baseline sleep latencies of greater than 30 minutes had a 2.14 times greater mortality risk and those with sleep efficiency <80% had a 1.93 times greater risk of death (34). Mechanisms that may underlie an association between insomnia and mortality are unclear, yet a study showing an association between difficulties falling asleep and mortality due to coronary artery disease in men (35) may provide some clues into this question. The existence and continuation of insomnia also confer a risk for the future occurrence of new psychiatric disorders (see below).

Insomnia causes a significant burden for the health care system (36) and also for employers of insomniacs in both direct and indirect expenses including medical expenses, ramifications of accidents, and reduced productivity due to absenteeism and decreased work efficiency (29). Insomnia costs the American public $92.5–$107.5 billion annually (37).

Studies in insomnia reveal evidence of hyperarousal, an overly active arousal system. This is evident not only in the environment and timing of sleep but also during the day, as insomniacs display enhanced alertness or a decreased ability to fall asleep during the daytime nap opportunities of the multiple sleep latency test compared with normal sleepers (38). Hyperarousal is also evident in the following areas in patients with primary insomnia:

Other neurophysiologic models indicate the importance of the circadian system in the genesis of insomnia, pointing to various circadian rhythm disorders such as delayed sleep phase syndrome and advanced sleep phase syndrome, which are associated with difficulty in falling asleep and early awakening, respectively. In these disorders, the circadian system is disturbed, causing sleep/wakefulness, melatonin, cortisol, and presumably other endogenous rhythms to be either delayed or advanced in relation to the environmental light/dark cycle. Recent findings of a genetic basis for these disorders in at least some individuals [a mutation in a human clock gene (Per2) was shown to produce advanced sleep phase syndrome, and a functional polymorphism in Per3 is associated with delayed sleep phase syndrome] further support genetic models of insomnia (44).

One study noted that the correlation between insomnia was greater with monozygotic than in dizygotic twins (0.47 versus 0.15) (45). Other studies have shown similar genetic mutations and genotypes in a rare form of insomnia, fatal familial insomnia (46).

Although a variety of psychoanalytic models have been proposed throughout the past century, the one most widely recognized is that of Sigmund Freud. This construct proposed, in essence, that insomnia represents a failure of dream work (47). Dreams, according to Freud, are created by a combination of daily events (“residue”) and conflictual, anxiety-producing, unconscious wishes. These are, in turn, transformed into dreams through a series of mental processes, including displacement, condensation, symbolic representation, and secondary elaboration, which are collectively subsumed under the rubric of “dream work.” Freud further hypothesized that successful dream work is necessary for the preservation of sleep. However, in insomnia, “evil, repudiated wishes become active precisely at night and disturb us during sleep” (48). Dream work is unsuccessful because of the intensity of the anxiety caused by the underlying conflict, resulting in the awakening of the dreamer and the complaint of insomnia.

Cognitive/behavioral constructs in the genesis of insomnia rely on the importance of sleep-related thoughts and associated behaviors. Cognitive and emotional arousal due to traumatic events and stressors can precipitate insomnia in most individuals. However, insomniacs are theorized to have a predisposition for an exaggerated reaction to such stressors, requiring less activation to achieve high levels of arousal, which, in turn, lead to disturbed sleep. This predisposition is supported by studies indicating that insomniacs report difficulty relaxing, feeling tense and anxious, being overly preoccupied with a myriad of thoughts, being worried, and being depressed more frequently than control subjects (49). Other predisposing factors, such as distorted beliefs about sleep itself, including the belief that poor sleep is inevitable, that the lack of a full night of sleep will inevitably lead to disastrous health consequences, and that a minimum of 8 hours of sleep per day is critical to maintain health, can induce further emotional and cognitive arousal. Such catastrophizing is encouraged by many nights of poor sleep, which can foment cognitive rumination and worry about not falling asleep and about the potential for disastrous next-day consequences of sleeplessness. Therefore, such a cycle of apprehension and worry can perpetuate insomnia and make future sleep even less likely. Finally, insomniacs are prone to excessive cognitive monitoring at bedtime, which can further perpetuate insomnia; insomniacs carefully monitor mental and body sensations as well as external cues such as the bedroom clock and environmental noises.

Arousal at bedtime can also be a learned response. The repeated experience of poor sleep promotes an association between sleeplessness and both presleep activities and the sleep setting. Once these connections are established, the bedtime rituals and environment become contextual cues for arousal rather than for sleep (59). The interaction between predisposing, precipitating, and perpetuating factors in the genesis and progression of insomnia are depicted in Figure 2.

In primary insomnia, no coexisting disorder has been identified (51). Primary insomnia can also be referred to as an insomnia syndrome, presumed to be an independent disorder, which does not preclude the possibility that other medical, psychiatric, or sleep disorders can coexist with primary insomnia. However, they are not thought to contribute to the insomnia complaint.

This category includes insomnia disorders that are comorbid with other medical and psychiatric conditions and other sleep disorders. It represents the vast majority of insomnia. Historically, this has also been referred to as “secondary insomnia.” However, a recent National Institutes of Health State of the Science Conference statement recommended the use of term “comorbid insomnia,” noting that the limited understanding of mechanistic pathways in insomnia precludes drawing firm conclusions about the nature of the associations between insomnia and comorbid conditions or the direction of causality.

Insomnia can be associated with a host of medical, psychiatric, and sleep disorders. Some of these are listed in Table 1 (52). Table 2 lists some of the commonly encountered comorbid insomnia disorders and their defining symptoms (53). A variety of medications can also cause the complaint of insomnia, including anticholinergic agents, antihypertensives, antineoplastics, CNS stimulants, hormones, antidepressants, and antipsychotics as well as withdrawal from sedating agents (52). Anxiety and mood disorders represent some of the most commonly encountered disorders in psychiatric practice and are highly associated with insomnia.

There is a strong association between insomnia and mood disorders. The complaint of insomnia is voiced by most patients with major depression. Sleep patterns include difficulty falling asleep, frequent nocturnal awakenings, early morning awakening, nonrestorative sleep, decreased total sleep, and disturbing dreams. Daytime fatigue is also common (54). Insomnia is also a common complaint in bipolar patients in the depressed phase, yet hypersomnia is also a frequent complaint, with extended nocturnal sleep periods, difficulty awakening, and excessive daytime sleepiness (55). Hypersomnia is also common in seasonal affective disorder during episodes of winter depression. During manic periods, however, patients usually report significantly reduced amounts of total sleep, often with a subjective sense of a decreased need for sleep.

Conversely, 14%–20% of individuals with significant complaints of insomnia show evidence of major depression, whereas rates of depression are less than 1% in those without sleep complaints (8, 56). Although clinical wisdom suggests that insomnia is a consequence of mood disorders, longitudinal studies indicate that insomnia is more likely to emerge before rather than after the onset of the acute phase of a mood disorder (57). Indeed, the complaint of insomnia also confers an increased risk for the development of new psychiatric disorders over the course of the ensuing year, a risk that diminishes if the insomnia resolves (56). Other studies have noted an enhanced risk for mood disorders for a median of 34 years after the complaint of insomnia (57). Thus, insomnia in early adulthood was associated with an increased risk of depression some 17–30 years later. Other studies have shown that the occurrence and persistence of insomnia confers an enhanced risk for the future occurrence of anxiety and substance use disorders (36, 59). From a clinical standpoint, these data suggest that the presence of chronic insomnia should alert the clinician to the possibility of the future emergence of a mood, anxiety, or substance use disorder. In addition, the lack of sufficient response to the treatment of presumed primary insomnia should alert the clinician to the possibility of an underlying, disguised, mood, substance use, or anxiety disorder that may warrant independent management.

Polysomnographic studies have revealed a constellation of findings during major depressive episodes (54, 59). These are listed in Table 3.

The clinical relevance of these findings is not straightforward. They have, however, been used historically in research settings to establish a diagnosis of depression during the acute phase of a depressive episode, to identify individuals in the population who may be vulnerable for the future development of depression, to predict relapse, and to predict response to treatment. They have also been used to support various neurophysiological formulations regarding the pathophysiology of depression (61).

The treatment of disturbed sleep in mood disorders should start with the management of the underlying mood disorder. The short-term subjective effects of some of the more commonly used pharmacological agents are listed in Table 4 (61). It should be noted that antidepressant medications are not approved by the U.S. Food and Drug Administration (FDA) for the treatment of insomnia.

Nonpharmacological treatments directed primarily at the mood disorder can also diminish sleep disturbances, yet their effects may be more modest than those of antidepressants. Clinical wisdom suggests that effective management of the underlying mood disorder should provide relief from related sleep disturbances. However, pharmacological treatment studies indicate that less than 20% of full responders to antidepressant treatment are free of all major depressive disorder symptoms (62) and nearly half of responders have persistent sleep disturbances. Therefore, it is often necessary to supplement antidepressants with sleep-specific treatments such as hypnotic medications and insomnia-specific cognitive behavior therapy, described in greater detail below.

Insomnia and anxiety are closely related in a variety of ways. These symptoms coexist frequently in the clinical practice of medicine and may even involve common etiologies. Both can be symptomatic manifestations of other comorbid conditions. In addition, both can represent distinct primary conditions or syndromes in their own right. Anxiety disorders represent the most frequent psychiatric disorder in individuals with insomnia (16). As noted above, insomnia often precedes the onset of an anxiety disorder. However, unlike the situation in mood disorders, insomnia is more likely to emerge at the same time (>38%) or after (>34%) the onset of the anxiety disorder (57).

The comorbidity of generalized anxiety disorder (GAD) and insomnia is more frequent than that for all other anxiety disorders (63). Objective studies in GAD reveal a longer sleep latency and an increase in the frequency of awakenings compared with those in control subjects. However, unlike in patients with major depression, patients with GAD appear to have normal REM latency (64).

Insomnia is one of the core symptoms of PTSD and is thought to be a reflection of increased psychological and physiologic arousal (DSM-IV-TR) associated with the original experience of the traumatic event or its reexperiencing. Another core symptom of PTSD is distressing dreams and nightmares, reflections of the reexperiencing of the traumatic event. As with insomnia, their presence early in the aftermath of trauma is a strong predictor of the later development of PTSD itself (65, 66). Nightmares may incorporate elements of or the entirety of the actual traumatic event and its affective correlates. However, the latent content of the dream (i.e., the traumatic event and its psychic correlates) may be disguised so that dreams may be affectively charged yet lack the factual recollection of the actual event or may not be remembered at all. Evidence is emerging to suggest that in the aftermath of trauma, the latter experience carries a more positive prognosis. Mellman et al. (67) reported that within 6 weeks of traumatic events reports of dreams rated as “highly similar” to the traumatic experience and as distressing were associated with concurrent and subsequent PTSD severity. On the other hand, lack of dream recall or dreams that did not depict actual memories of the traumatic event were more characteristic of the group of individuals exposed to trauma who did not subsequently develop PTSD, although their dreams did contain some threatening scenarios. The authors theorized that dreams with highly replicative content represent a failure of adaptive emotional memory processing that is a normal function of REM sleep and dreaming.

Polysomnographic studies in PTSD have not revealed consistent findings in sleep initiation and maintenance, possibly because of the diversity in the nature of the populations examined and in the temporal relationship between the development of PTSD symptoms and the traumatic event itself. Some studies have shown an enhancement of phasic activity and eye movement density during REM sleep in those with PTSD as well as reports of nightmares and awakenings from REM sleep even early in the development of the disorder (68).

Insomnia is not one of the diagnostic symptoms of panic disorder. However, insomnia, characterized by both impaired sleep initiation and maintenance, is more commonly reported in those with panic disorder than in normal individuals (69). Insomnia can be related to episodes of panic, which can arise during sleep and result in the complaint of insomnia. The first awareness of panic in most people with this disorder is a somatic symptom such as racing heart or shortness of breath (70), which results in sudden awakening with a feeling of physical intensity. Taylor et al. (71) found that major spontaneous panic attacks clustered during the sleep period between 1:30 and 3:30 a.m. Contrary to popular belief, they generally do not occur in REM sleep. They have been observed to occur in slow-wave sleep and during the transition from stage 2 to slow-wave sleep (66). Dreams are not commonly reported preceding panic episodes. Not all patients with panic disorder experience panic episodes during sleep.

Insomnia can also arise from recurrent sleep panic attacks, which, in turn, can create a state of anticipatory anxiety and apprehension over the prospect of yet another night of sleeplessness followed by another day of fatigue. A vicious cycle can then ensue in which excessive focus on sleep and trying to sleep causes greater tension and even greater impairment in sleep initiation and maintenance, thereby resulting in a second comorbid condition, i.e., psychophysiologic insomnia (see above).

Nonpharmacologic treatments for anxiety disorders include cognitive behavior therapy (CBT) and exposure therapy alone, in combination, or combined with relaxation training. These therapies share some similarities with the nonpharmacologic treatments for insomnia, described in greater detail below. Preliminary studies indicate that when used for the management of anxiety disorders, these therapies can also ameliorate insomnia. GAD-specific CBT can ameliorate insomnia when used for the treatment of GAD (72), and imagery rehearsal for the nightmares of patients with PTSD can improve sleep, presumably as a secondary consequence of diminished nightmares (73).

The benzodiazepine receptor agonists (GABA_A receptor agonists) are effective for both anxiety and insomnia symptoms in patients with comorbid insomnia and anxiety disorders, although individual agents may not have an FDA-approved indication for both conditions. Antidepressants can also ameliorate insomnia in various anxiety disorders, as noted above, and, if insomnia persists after the management of the underlying anxiety disorder, the addition of hypnotic agents can be helpful.

Essential elements of the history are outlined in Table 5. The hallmark symptoms of the various disorders described above should be asked for (Table 2). Collateral information from bed partners can be useful in obtaining information that the patient may not be aware of, such as snoring; breathing pauses during sleep, limb movements, and the extent and frequency of naps. The history should also include the past medical history, history of medications and substance use, family history [certain sleep disorders, such as restless leg syndrome and obstructive sleep apnea syndrome (OSAS), can have a familial basis and the genetic bases of insomnia and certain circadian rhythm disorders are discussed above], and social and occupational history for entities that can contribute to irregular sleep/wake habits.

A physical examination is essential; for example, a neck circumference of 16 in. or greater in women and 17 in. or greater in men, is associated with an increased risk for sleep-related breathing disorders. Useful scales and inventories include the Insomnia Severity Index, the Fatigue Severity Scale, the Epworth Sleepiness Scale, sleep diaries, and the Mallampati Airway Classification (53). General serum laboratory tests including thyroid function studies can be considered if data are not current. Polysomnography or a referral to a sleep medicine specialist should be considered if the evaluation raises the suspicion of OSAS or periodic limb movement disorder, if the patient reports violent or potentially injurious nocturnal behaviors, for the diagnosis of paroxysmal arousals or other sleep disruptions thought to be seizure related, if the office-based evaluation is not fruitful, or if the patient does not respond appropriately to treatment of the presumed disorder.