Clinical manifestations

Presentation and course

Chronic insomnia is defined as difficulty with initiating or maintaining sleep with resulting daytime sequelae, occurring at least three nights per week and lasting over 3 months (04). Chronic insomnia includes a variety of drivers that were previously considered distinct diagnoses, but these were combined as evidence demonstrated the distinction is less clear. The diagnosis of chronic insomnia can be categorized into subtypes, one of which is psychophysiological insomnia. The subtype of psychophysiological is characterized by heightened arousal and learned associations that prevent or interfere with sleep. These patients often have trouble sleeping in their usual sleep environments but may fall asleep in a different setting or when not trying to fall asleep. The symptoms of insomnia cannot be explained by inadequate opportunity or circumstances for sleep. In addition, the symptoms cannot be best explained by another sleep disorder, medical disorder, mental disorder, or medication/substance use.

Psychophysiological insomnia includes focused attention on the inability to sleep, which is perceived to be the only source of distress. Patients typically repress or deny awareness of stress factors and are unable to find any reason for the insomnia. This concept was analyzed and at least partially confirmed by using tests for attentional bias (the visual dot-probe test [VDP] and an emotional Stroop test [EST]) (79). It was further strengthened in subjects with primary insomnia by their delayed disengagement to the clock during the normal sleep period, a finding that fits in with the “attention-intention-effort” model (87). Another study found that when tasked with a facial expression recognition task in the early evening, patients with psychophysiological insomnia described expressions displaying sadness and fear as significantly less emotionally intense than good sleepers (49). This suggests that patients with psychophysiological insomnia may present with a difference in response to emotional stimuli than control subjects. Another cognitive model of insomnia suggests that individuals with insomnia have a sleep-specific expectancy bias. When study participants with high rates of insomnia were given a reaction time task with different sleep related scenarios, those with insomnia were more likely to solve sleep related scenarios with negative outcomes compared to those with low rates of insomnia (24).

Acute insomnia symptoms typically emerge when underlying precipitating factors are present, such as stress. After a few days of sleeping poorly, the patient becomes concerned about his or her inability to sleep, trying harder and harder to get to sleep. The inability to sleep itself then causes arousal and further aggravates insomnia symptoms. Maladaptive behaviors and thought patterns that occur as a result of insomnia symptoms may act as perpetuating factors that can result in persistent or chronic insomnia symptoms regardless of the status of the precipitating event/stressor. The stimuli surrounding the bedtime event (such as the bed itself, the bedroom, etc.) may become conditioned triggers to arousal. This can present as patients having severe problems with sleeping in their own bedroom but improved sleep in other environments.

Daytime symptoms can include fatigue, negative mood, cognitive impairment, and a decline of quality of life. These symptoms are correlated with perceived poor quality of sleep. Cognitive deficits, such as difficulty with attention and episode memory, have been found to be significantly higher in patients with insomnia. However, it is difficult to tease out whether this is associated with sleep deficits or to dysfunctional belief or attitudes about sleep (34).

Prognosis and complications

If untreated, psychophysiological insomnia can continue for decades. Overall quality of life, as measured by the Short Form-36 Health Status Survey, is greatly impaired by chronic insomnia (02). When compared to healthy controls and to patients with obstructive sleep apnea or narcolepsy, the subjects with psychophysiological insomnia, similar to ones with sleep apnea or narcolepsy, performed poorer than healthy controls on standardized attention tests but scored as normal on daytime alertness tests (73).

Other complications are those of any serious insomnia: excessive use of hypnotics, self-treatment with alcohol, treatment of ensuing daytime somnolence by stimulants, and daytime tension with tranquilizers. Psychological complications can include a passive and defeatist attitude and other maladaptive behaviors as well as cognitive and memory impairment. Prospective epidemiological studies have found links between insomnia and suicide risk. Notably, catastrophizing and the sense of defeat have been identified as potential cognitive pathways through which insomnia aggravates suicidality in patients with chronic pain (85).

Insomnia, when coupled with short sleep duration, is also a predictor of hypertension, diabetes, and overall mortality (82) in men independent of age, obesity, other sleep disorders, and other risk factors. More studies have shown that both reduced sleep hours and increased sleep hours exceeding more than 10 hours per day were associated with increased mortality, which was most evident in women (92). Moreover, insomnia (objectively defined via polysomnography) with features of hyperarousal (characterized by a latency to sleep on a multiple sleep latency test of more than 14 minutes) resulted in a significant risk of hypertension (53). A retrospective review of patients stroke-free at baseline showed association of insomnia with an increased risk of stroke (71). This association was stronger in those under 50 years of age. More work is needed on the effects of insomnia on psychiatric and somatic morbidity and mortality. More work is needed on the effects of insomnia on psychiatric and somatic morbidity and mortality.

Clinical vignette

A 70-year-old female was referred to the Sleep Disorders Center reporting that she had “not slept a full night in 30 years.” Her psychiatric history was significant for depression. Her medical history was significant for fibromyalgia, hypothyroidism, hypertension, and irritable bowel syndrome. The patient identified the death of her husband 30 years ago as the precipitating factor for her insomnia. She was subsequently left to run their successful business and raise the three children on her own. The patient reported that over the next 30 years, she developed habits surrounding sleep. Behavioral changes included spending excessive time in bed. She would get into bed at 7:30 p.m. to meditate. She got out of bed at 6:30 a.m. She also drank three glasses of wine before bed. The patient reported that she was “careful” about her sleep. She thought about her sleep throughout the day, and her anxiety level increased as bedtime approached. The patient underwent six sessions of cognitive behavioral therapy for insomnia, which focused on addressing perpetuating factors such as spending excessive time in bed and alcohol use for sleep. Cognitive therapy focused on her dysfunctional beliefs and increased anxiety about sleep. The patient’s sleep efficiency gradually increased over the six sessions, and she became less focused on her sleep.

Biological basis

Etiology and pathogenesis

A few nights of disturbed sleep, as the result of factors such as stress, is a universal human experience. In the majority of cases, the trouble is short lived and resolves spontaneously. Three types of factors play a role in the development of psychophysiological insomnia: (1) predisposing or constitutional factors: the tendency to worry excessively about anticipated danger and the tendency to be generally hyperaroused, both metabolically and cognitively; (2) precipitating factors: a transient stressor; and (3) perpetuating factors, ie, maladaptive behaviors and thought patterns that can result in continued insomnia symptoms despite resolution of the original stressor.

In some patients with psychophysiological insomnia, no precipitating stress is found. Rather, poor sleep may have gradually developed as an occasionally occurring disturbed night leads to increased concern, causing sleep to deteriorate until it becomes the patient's chief concern. There may be a familial contribution to the development of insomnia; however, it is unclear if this pattern is genetic versus other determinants, such as shared environments or learned behaviors (04).

The interaction of personality traits, affective disorders, and insomnia is also important. Studies have suggested the comorbidity prevalence between insomnia and psychiatric disorders may range from 40% to 50% (33). Insomnia has been shown to be more frequent in adults with major depressive disorder, generalized anxiety disorder, alcohol dependence, cannabis dependence, and tobacco use (43). It is known that insomnia is a risk factor for future depression (03) and that adverse childhood experiences are a significant risk factor for sleep disturbances in later life (19). Moreover, the number of diagnoses of depression and anxiety early in life has been associated with future insomnia (36).

Growing evidence shows that insomnia has organic components. The pathogenesis and pathophysiology of psychophysiological insomnia is presumed to be moderate hyperarousal or imbalance of the sleep-wake system towards alertness. Physiological hyperarousal is documented in many types of insomnia and implies an overactive wake mechanism. Hyperarousal (13) characterized by difficulty initiating sleep on a nap opportunity also appears to be present during the daytime in patients with psychophysiological insomnia (64).

A study that examined responses to questionnaires regarding cognitive and emotional experience prior to sleep in subjects with psychophysiological insomnia revealed that trait hyperarousal was associated with higher levels of both negative and positive emotionality, as well as negative beliefs about sleep in both genders. Among women, high pre-sleep arousal was associated with negative emotionality, whereas in men greater pre-sleep arousal was associated with cognitions about their control over sleep (38).

A large-scale study of twins from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (n = 7500) examined the genetic overlap of insomnia and other psychopathology. The study found significant overlap between latent additive genetic influences of insomnia with major depressive disorder (56% for females, 74% for males) and generalized anxiety disorder (100%). Only modest genetic overlap with alcohol abuse or dependence (18%) was present (55). The presence of anxiety also appears to be involved in objective sleep parameters. Polysomnographic characteristics in 1083 patients undergoing sleep studies showed prolonged sleep onset latency was associated with state anxiety while alterations in REM sleep were associated with trait anxiety (41).

There may also be a mechanism of dysfunctional homeostatic sleep contributing to insomnia symptoms. In response to cognitive-behavioral therapy, Krystal and Edinger described a more rapid decline in delta power overnight in a group of insomniacs, suggesting an increase or restoration of normal homeostasis with treatment of the underlying insomnia (47).

Patients with insomnia display faster heart rates, higher body temperature, and higher electromyogram activity. Heart rate at sleep onset, in addition to brain-derived neurotrophic factor (BDNF) levels, has been identified as a possible biomarker for insomnia (27). Insomnia patients are also as alert or more alert than controls during the day. Multiple Sleep Latency Tests show increased sleep latency in insomnia subjects as compared to controls (80).

By electroencephalographic criteria, patients with insomnia tend to have a higher percentage of faster frequencies both in waking and in NREM sleep (48; 23) and lower theta power in the waking EEG (86). Lamarche and Ogilvie compared patients with psychophysiological insomnia to patients with insomnia associated with psychiatric disorders and to normal controls. Electroencephalographic activity showed higher cortical arousal in the psychophysiological insomniacs versus the other two groups, which did not differ from each other significantly (51). Corsi-Cabrera and colleagues found similar results when they compared beta and gamma power in primary insomniacs versus healthy controls. They were particularly interested in explaining the nonrestorative quality of sleep reported by many insomniacs. Compared to pre-sleep, the primary insomniacs showed increased beta and gamma power with increased synchronization in anterior and posterior regions of the brain, suggesting that these electrophysiological differences might account for the report of nonrestorative sleep (23). Buysse and colleagues found that women with primary insomnia had greater EEG spectral activity during NREM sleep, particularly in the earlier hours of sleep, than did normal sleepers (16).

A study using event-related potentials showed enhanced excitatory and reduced inhibitory processes of auditory stimuli during sleep in patients with primary insomnia, giving further credence to the hyperarousal theory (09). Another study, however, found no difference in changes in EEG activity following evoked K-complexes between patients with psychophysiological insomnia and a good sleeper control group (32). Spontaneous K-complex density was slightly higher in the insomnia group. If K-complexes are hypothesized to be protective of sleep, then the lack of changes between the insomnia group and normal controls suggests that impairment of a protective K-complex does not contribute to the development of psychophysiological insomnia.

Some studies have shown a positive correlation between objective sleep disturbance and the activity of both limbs of the stress system (the hypothalamic-pituitary-adrenal axis and the sympathetic system) and increased serum levels of ACTH and cortisol in a group of chronic insomniacs (39). The cortisol awakening response is the change in cortisol concentration that occurs in the first hour after waking from sleep. Adults with insomnia have shown a significantly greater cortisol awakening response independent of depression and anxiety. Additionally, both adults and adolescents with worse insomnia had higher cortisol levels in the late evening (10:00 pm) (91). In another study, nocturnal melatonin production was significantly diminished in insomniac patients compared to healthy controls (68).

Single photon emission computed tomography neuroimaging during NREM sleep has shown decreased perfusion in the basal ganglia and other areas of the brain in primary insomniacs compared to normal controls (77). Proton magnetic resonance spectroscopy studies have shown inconsistent results regarding altered levels of gamma amino butyric acid (GABA) in patients with primary insomnia. Resting-state functional magnetic resonance imaging (fMRI) of chronic insomnia patients showed decreased connectivity between the anterior cingulate cortex and the bilateral precuneus gyrus. This decrease positively correlated with Self-Rating Anxiety Scale scores (84).

COVID-19 and psychophysiological insomnia

In 2020, there was a rise in insomnia, anxiety, and depression rates, particularly in first-line health care workers in response to the COVID-19 pandemic. As early as January 2020, a high symptom prevalence of depression, anxiety, and combination of depression and anxiety (48.3%, 22.6%, and 19.4%, respectively) was identified by an online survey of 5000 healthcare workers. Although the prevalence of insomnia was low overall, slightly more front-line workers than second-line workers (10.5% vs. 4.0%, p < 0.001) had moderately severe insomnia on the Insomnia Severity Index (50). Similar results were found in Oman, where as many as 30% of physicians and nurses who treated patients with COVID-19 experienced moderate to severe anxiety (08). Studies have shown reduced sleep duration (22), reduced sleep quality, and increased nightmares in both community members (54) and front-line workers (76).

Epidemiology

Little data are available regarding the prevalence of psychophysiological insomnia. The third edition of the International Classification of Sleep Disorders (ISCD) identifies chronic insomnia as occurring in about 10% of the population (04). Of this, psychophysiological insomnia is only a portion. Several investigators suggest a point prevalence and in-clinic prevalence rates for psychophysiological insomnia of 1% to 2% and 12% to 15%, respectively. Of insomniacs who seek help at sleep centers, about 11.3% to 15% were diagnosed with psychophysiological insomnia in several large studies of sleep disorders centers. In a sample of 881 patients over 60 years of age in Korea, the prevalence of psychophysiological insomnia was 20.5%. Of those patients with psychophysiological insomnia, 53.7% had subsyndromal depression (44). Chronic insomnia was also found to be prevalent in 36.2% of 142 Japanese older adults over 75 years of age. Of those patients, the Geriatric Depression Scale scores were higher (40).

Prevention

It was first suggested in 1999 that patients who are prone to somatization and who deny emotional stress may be at risk for psychophysiological insomnia (12).

Bruck and colleagues found that both young and older individuals may have unrealistic expectations about sleep, such as sleeping without awakenings (15). Education and reassurance about “normal healthy” sleep may aid in a prevention program. Sleep education may also help to lessen patient fears regarding consequences of insomnia. Access to self-help resources may also be beneficial as patients may not always seek professional consultations at symptom onset. Many individuals may first initiate self-help treatments, particularly when daytime impairments such as fatigue become more noticeable.

A useful tool in the identification and possible prevention of worsening psychophysiological insomnia is the Ford Insomnia in Response to Stress Test (FIRST). This test has been used to identify who is at risk for insomnia. In a study, responders who had “highly reactive sleep systems” also reported longer sleep onset latencies (FIRST ≥ 16: 65 min; FIRST ≥ 18: 68 min) compared to those with “nonreactive insomnia” (FIRST < 16: 37 min; FIRST < 18: 44 min) (42).

Other scales may also help to identify those at risk for psychophysiological insomnia. Insomnia rumination scores on an insomnia-specific measurement scale predicted insomnia even after controlling for depression (17). Sleep disturbance while transitioning from inpatient alcohol detoxification treatment to the outpatient environment may predict relapse after discharge (14). Surprisingly, higher dysfunctional beliefs about sleep were associated with lower rates of relapse (78).

Key features of psychophysiological insomnia include worry, dysfunctional beliefs, somatic arousal, selective attention, and monitoring of sleep and safety behaviors. These five types of cognitive processes are key treatment targets as they may affect remission of insomnia over time (61). These ruminations about sleep are problematic not only at night, but also in the daytime in psychophysiological insomnia (63), suggesting that insomnia is a 24-hour disorder. A clinical history to help identify these key features of psychophysiological insomnia can help to prevent the evolution of insomnia symptoms to the chronic level.

Differential diagnosis

Confusing conditions

Psychophysiological insomnia lies on a continuum with a number of other diagnostic categories.

Idiopathic insomnia is diagnosed if the predisposition towards poor sleep by itself is severe enough to cause insomnia. Psychophysiological insomnia is assumed to start with a somewhat milder predisposition towards poor sleep that usually develops into insomnia only with the occurrence of some other, identifiable stressor acting as the trigger.

Paradoxical insomnia, sleep state misperception, is when the patient sleeps adequately but does not perceive it as sleep.

Circadian rhythm disorders occur when the patient sleeps well but not at socially acceptable times.

Inadequate sleep hygiene is diagnosed if insomnia is maintained primarily by neglecting sleep hygiene, eg, drinking too much coffee, lacking exercise, napping, staying in bed too long. To the extent that the insomnia is independent of the precipitating causes and also independent of the quality of sleep hygiene, psychophysiological insomnia is the preferred diagnosis.

Medical causes of insomnia may include, but are not limited to, propriospinal myoclonus, restless legs syndrome, cardiorespiratory disorders, pain, degenerative disorders, prostatic hypertrophy, and obstructive sleep apnea disorder.

Drug-related insomnia may include, but is not limited to, stimulants, theophylline, prednisone, selective serotonin reuptake inhibitors, withdrawal from sedative medication, idiosyncratic reactions to other medications, and toxin-related causes such as alcohol or other recreational substance abuse, carbon monoxide, or inorganic mercury.

Associated or underlying disorders

Generalized anxiety disorder is the preferred diagnosis if anxiety permeates most aspects of a patient's functioning (anxiety in social interactions, about job performance, etc.). This may be difficult to disentangle as insomnia has been found in 40% of patients with symptoms of anxiety and depression symptoms (58). There are also clear associations between characteristics of obsessive-compulsive disorder and symptoms of insomnia (67). Psychophysiological insomnia is preferred if the anxiety is focused almost exclusively on poor sleep and its consequences on daytime functioning.

Affective disorders are sometimes difficult to separate from psychophysiological insomnia because a dysphoric mood that is ascribed to the effects of poor sleep often accompanies psychophysiological insomnia. It is especially difficult to distinguish dysthymia from psychophysiological insomnia in cases of "masked" depression, ie, when the patient denies overt sadness or hopelessness. Often, the discrimination can be made on other "vegetative signs," such as loss of appetite or libido or the typical diurnal fluctuation of depression (morning being worse). In the final analysis, the diagnostician's sense is important whether depression is still driving the insomnia, or whether the insomnia is driven by maladaptive sleep habits learned during a previous depression. Also, dysthymic patients may typically show depressive traits before the insomnia developed.

Diagnostic workup

The diagnosis of psychophysiological insomnia is typically made by interview, paying attention to learned associations preventing sleep and to the patient's display of somatized tension. Typical clinical inquiries might include whether the patient sleeps better away from home, has excessive focus or anxiety about sleep, has difficulty sleeping in their bed but not in other locations, has mind racing, and has somatic tension when trying to sleep. In addition, a sleep diary or log may help track the patient’s sleep pattern and help elucidate possible underlying contributors to the insomnia, such as circadian variation or relation to work, stress, or other activities or substances. Certain standardized questionnaires like the Insomnia Severity Index are sometimes used to screen for insomnia and determine its severity.

A psychiatric interview can be helpful to rule out psychiatric disorders. There can be a close relationship between insomnia and mood disorders. One systematic analysis found a reciprocal relationship between subjective sleep variables (sleep quality, sleep duration, and sleep latency) and daytime affective states over the short term (46).

A general medical evaluation rules out physical problems, such as other medical or neurologic disorders, medication effects, or substance abuse (75). For most patients with insomnia, polysomnography is not needed. Polysomnography may be useful for those who may have findings suggestive of sleep-related breathing disorders or movement disorders. Typically, polysomnography demonstrates increased sleep latency, increased wakefulness after sleep onset, decreased sleep efficiency, or a combination of these disturbances. There may also be increased stage N1 sleep. These features, however, are simply the hallmarks of poor sleep in general. No polysomnographic features are specifically diagnostic of psychophysiological insomnia; however, some patients with psychophysiological insomnia may actually sleep better in the laboratory. Polysomnography in patients with suspected psychophysiological insomnia seems necessary only when other sleep disorders are suspected such as sleep apnea or sleep state misperception, when treatment has failed, or if the cause of insomnia is uncertain (75).

Actigraphy has been evaluated as a potential tool to help identify insomnia, although results have not been positive. A case control designed study showed significant group differences of total sleep time and sleep efficiency, but there was significant overlap of individual patients and control subjects (69). This study suggests that actigraphy may be unable to show any difference on actigraphy between individual insomnia patients and controls. Actigraphy may be helpful in patients with complaints such as "I don't sleep at all" and should be supplemented with subjective sleep logs.

Management

Management for psychophysiological insomnia may include cognitive behavioral treatment for insomnia (CBTI), hypnotic medication, or a combination of the two (60). CBTI is an effective non-pharmacological intervention that typically includes sleep restriction therapy, sleep hygiene education, stimulus control therapy, and correcting distorted perceptions of sleep. According to Edinger and colleagues, all components of CBTI have evidence to support their use as single-component therapies for chronic insomnia, except sleep hygiene (29).

CBTI is now considered first-line treatment for insomnia according to the American College of Physicians (66). Brain activity reduction after CBTI has been found via imaging techniques, specifically in the left middle temporal and left middle occipital gyrus. This was evidenced in a small sample of patients with psychophysiological insomnia who were tested with MRI before and after CBTI (45). Adjunctive approaches to treating psychophysiological insomnia have included using mindfulness and acceptance (62; 21). A randomized controlled trial of older adults found that mindful awareness practices to improve sleep quality were significantly more helpful for sleep, depression, and fatigue compared to a sleep hygiene intervention alone (11). Mindfulness-based stress reduction and mindfulness-based therapy for insomnia have been found to be well accepted by patients (57) and may also be an effective treatment for insomnia in breast cancer survivors (52). Even just providing relaxation and sleep hygiene can be more helpful for insomnia compared to treatment as usual in postmenopausal women (28). An effectiveness trial of acceptance and commitment therapy (ACT) compared to CBTI was completed among women veterans. Similar effectiveness was reported with ACT being noninferior in all four of the key outcome variables (56).

Specific questionnaires used in CBTI, such as the dysfunctional beliefs and attitudes about sleep scale (DBAS), can be particularly helpful for patient engagement and adherence to therapy components in patients with psychophysiological insomnia (25). Although both behavioral and cognitive therapy components of CBTI reduce dysfunctional beliefs, cognitive therapy appears to be more powerful of an intervention to reduce the strength of dysfunctional believes (30).

In addition to behavioral therapies, moderate intensity exercise can be used to reduce pre-sleep anxiety and improve sleep. In one study, exercise was associated with increasing the total sleep time by 18% and reducing sleep latency by 55%.

Both psychological and pharmacological treatments can be effective for the treatment of insomnia, although the benefits of CBTI may be more durable than medications (59). CBTI is a combination of cognitive and behavioral therapies typically lasting between four to eight sessions. In a study that examined insomnia-related worry before and 1 year after completion of CBTI, there were reductions in insomnia-related worry, which was associated with improvements in insomnia severity, sleep continuity, and depression (81).

Clinicians may consider whether CBTI for psychophysiological insomnia is the most beneficial treatment option in patients with significant psychiatric comorbidities. The data have been somewhat mixed on its efficacy in a comorbid population. One study examining 60 patients with logistic regression analyses showed that the presence of psychiatric comorbidity was strongly predictive for negative treatment outcome (83). On the other hand, a meta-analysis of the efficacy of CBTI for psychiatric and medical comorbidities found that CBTI was helpful, with larger effect sizes for comorbid psychiatric conditions. Post-treatment assessments found that 36% of patients who underwent CBTI were in remission from insomnia compared to 16% in the control conditions (88). There is growing evidence to suggest the benefits of targeting insomnia even in the context of other disorders (18).

Multiple delivery methods for CBTI are available (eg, individual, group, internet, self-help, etc). CBTI is well adapted to be delivered via telemedicine (07) and Internet-based platforms (72; 89). Several mobile apps have very good data to support their effectiveness for improving sleep and mood (20; 26). Telemedicine has been particularly useful during the COVID-19 pandemic with the reduction of in-person visits. Given the overlap between COVID anxiety and insomnia, one study emphasized addressing “cognitive reappraisal” to better help prepare nurses to alleviate mental health problems and sleep difficulties that are related to COVID-19 (90). One study showed that effects of digital CBTI were sustained in the intervention group (74).

Pharmacotherapy can be used as an adjunct to CBTI or used independently for the treatment of insomnia (10; 70). Although a detailed review of all sleep aids is outside the scope of this review, there are several reviews available on medications for insomnia in adults (35) and in older adults (01).

The American Academy of Sleep Medicine guideline for the pharmacologic treatment of chronic insomnia in adults identifies only a weak recommendation for the use of eszopiclone, zaleplon, and zolpidem for sleep-onset insomnia. The recommendation is similar for agents such as ramelteon and doxepin. Agents such as trazodone, diphenhydramine, and melatonin have a recommendation for no use as treatment for sleep-onset insomnia. The use of medications for insomnia is typically indicated for the short term. A retrospective cohort data review found that in about 4000 individuals analyzed who were prescribed a hypnotic medication, 59.6% were prescribed hypnotics for only 1 month, 11.3% were prescribed hypnotics for two consecutive months, and 10.1% of patients received prescriptions for the entire 12-month observation period (31).

As noted above, the American College of Physicians recommends CBTI as the first-line treatment for insomnia. As a result, some patients are encouraged to add CBTI as an approach to assist with sleep medication taper. CBTI has been shown to be helpful in the process of hypnotic withdrawal with improved sleep over time (10; 37). With only sleep hygiene and psychosocial support, Puustinen and colleagues found that at 3 years after withdrawal from benzodiazepine agonists (BZDA) the number of BZDA-free participants had decreased (65). One-third of the subjects remained BZDA-free, and one-third had reduced their use. Although sleep hygiene and psychosocial support can be helpful, CBTI is preferred for long-term benefit.

Special considerations

Pregnancy

Pregnancy may aggravate psychophysiological insomnia, especially in the first and third trimesters.