Approach to the Patient with Insomnia
Jeffrey B. Weilburg
Insomnia is a problem of major proportions. Up to 50% of US adults complain of transient difficulty with sleep, and between 4% and 22% of the population have insomnia (depending on which of the various different insomnia criteria are used). Up to 35% of primary care patients have insomnia. The prevalence of insomnia is four to six times higher in patients with comorbid psychiatric conditions (depression, anxiety, or substance abuse) and three to five times higher in patients with comorbid medical conditions (hypertension, diabetes, breathing and sleep-related breathing problems, GI and GU problems, and cancer) compared to patients with no comorbid conditions. Other risk factors include depression, gender (females are twice as likely to have insomnia), advancing age, low socioeconomic status, marital status (higher prevalence in divorced or separated people), and race (African Americans at higher risk than Whites).
Patients with insomnia suffer significant reduction in quality of life, with a level of impairment similar to that for congestive heart failure, and they have significantly elevated risks for depression and motor vehicle accidents. The cost of health care services provided for the treatment of insomnia exceeds $12 billion/year in the United States, with medications accounting for more than $2 billion/year. An estimated $63 billion is wasted each year in the United States because of insomnia-driven workplace difficulties.
Given the extent and significance of the problem, it is essential that the primary care physician be skilled in the assessment and basic treatment of insomnia.
Definition
Insomnia is defined as persistent global dissatisfaction with sleep, occurring despite an adequate opportunity for sleep, that produces clinically significant impairment of social, occupational, or other daytime function. Persistence can be defined as sleep disturbance occurring at least three nights a week for at least 3 months. Note that insomnia actually persists for greater than 1 year in 70% of patients, with greater than 3 years in 50%. Global dissatisfaction with sleep can be defined as complaints of difficulty initiating or maintaining sleep (e.g., frequent or prolonged awakenings with difficulty returning to sleep), earlymorning awakening, and/or of sleep that is nonrestorative.
Clinical Presentations
Insomnia-associated daytime manifestations include fatigue, low energy, cognitive impairment (disturbance of attention, concentration, and/or memory), daytime sleepiness, and mood disturbance (dysphoria, irritability). In children, sleep dissatisfaction may present as resistance going to bed; daytime manifestations include behavioral problems such as hyperactivity, aggression, and impulsivity.
Sleep Physiology and Pathophysiology
Sleep physiology can be examined by polysomnography, continuous all-night recording of respiration, electroencephalogram (EEG), electrocardiogram, and the monitoring of eye movements, muscle tone, and blood oxygen saturation. It helps to differentiate normal from disturbed sleep.
Normal Sleep
Normal sleep has two basic phases: rapid eye movement (REM) sleep and non-REM (NREM) sleep.
REM Sleep.
REM sleep is a state of mental and physical activation. Pulse and respiration are increased, but muscle tone is diminished; little body movement occurs. The brain is active, and the EEG shows a pattern similar to that seen during waking. Most dreaming occurs during REM sleep.
Non-REM Sleep.
In contrast, this is a time of deep rest. Pulse, respiration, and EEG all slow, and the patient goes from light sleep, called stage N1 to deeper stages, called N2 (with spindles and K-complexes on EEG) and deep or delta sleep, designated stage N3.
REM sleep and NREM sleep normally cycle in a reciprocal pattern, giving a typical “architecture” to the polysomnogram. The entire cycle lasts about 90 minutes and is repeated four or five times during the night. The ventrolateral preoptic area (VLPO), located in the anterior hypothalamus, appears to be a key “sleep center.” Reciprocal inhibition between the VLPO and “wake and alertness” centers such as the tuberomammillary nucleus (TMN) in the posterior hypothalamus and other areas in the forebrain and brainstem produces alternating periods of sleep and waking.
The alternation of sleep and wake, that is, the sleep cycle, may be regulated by a “biologic clock”—the suprachiasmatic nucleus (SCN)—located in the hypothalamus. The absence of light appears to be one of the signals that prompts the SCN to stimulate the pineal gland to secrete melatonin, which may inhibit the stimulation of wake centers by the SCN, allowing the VLPO to promote sleep. Information is emerging regarding subtypes of melatonin receptors (MT1 and 2), stimulation of which may have different aspects of sleep and awakening.
VLPO neurons express inhibitory neurotransmitters such as γ-aminobutyric acid (GABA) and galanin (most available insomnia medications stimulate GABA receptors). TMN neurons secrete histamine, which, along with the serotonin, noradrenaline, and acetylcholine secreted by the brainstem and other centers, may stimulate the cortex and thalamus to promote alertness and wakefulness. Medications such as antihistamines, antidepressants, and stimulants may produce insomnia or sedation by affecting these neurotransmitters. Adenosine accumulates in the brain during waking. Increasing concentrations of adenosine may inhibit wake and alertness centers; caffeine may promote wake and may produce insomnia because it is a potent adenosine receptor antagonist.
Not all persons who sleep less than the average amount each night have insomnia. Natural short sleepers are persons who regularly have less than 7 hours of well-maintained sleep yet suffer no problems in daytime function. Normal aging is associated with reductions in total sleep time, sleep continuity, and slow-wave sleep but does not produce insomnia or other formal sleep disorders. Anxiety and discomfort related to these normal changes may respond to counseling but not to medication or other treatment, so it is important to distinguish normal sleep changes from the specific symptoms of insomnia.
Insomnia
Insomnia has no single or pathognomonic polysomnographic pattern. Some insomniacs have sleep times that are slightly shorter than normal, some have less stage delta sleep, and some have repeated arousals. However, the degree of gross polysomnographic change is often not concordant with the degree of subjective distress.
At present, the precise etiology and underlying pathophysiology of insomnia remains obscure. Patients with at risk for insomnia may have high levels of physiologic arousal, perhaps driven by the overactivity in brain alertness and wake centers during both sleep and waking observed in functional imaging research studies. Such patients may, when stressed, develop maladaptive psychological responses to this arousal. The response and the arousal itself may persist, leading to chronic insomnia.
Classification: Types of Insomnia
Definitions and classifications of insomnia are found in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, fifth edition, (DSM-V); the American Academy of Sleep Medicine’s International Classification of Sleep Disorders, second edition (ICSD-2); and the World Health Organization’s International Statistical Classification of Diseases and Related Health Problems, tenth revision.
The insomnia section of DSM-V incorporates recent data and provides a new, perhaps more useful approach to classification. It drops the etiologic assumptions, such as “primary insomnia” and “insomnia due to a general medical condition,” and drops various insomnia subtypes used in ICSD and earlier versions of the DSM (e.g., psychophysiologic, paradoxical insomnia), creating instead a single “insomnia disorder.” These changes highlight insomnia as a problem independent of, albeit often coexisting with, psychiatric and medical disorders and reinforce a bidirectional interaction between insomnia and depression, substance abuse, and anxiety, as well as between insomnia and comorbid medical problems. This may help clinicians focus clinical attention on insomnia itself. The result is movement from thinking about causes to considering comorbidities (see Tables 232-1 and 232-2).
Psychiatric disorders, substance abuse, and medical conditions may present with insomnia as a major complaint.
Situational and Psychiatric Disorders
At least 50% of patients with insomnia disorder have comorbid psychiatric problems. Patients experiencing severe acute psychosocial or situational stresses are subject to severe short-term insomnia, having difficulty falling asleep. More sustained difficulty occurs in patients with anxiety and obsessive disorders, who report chronic difficulty falling asleep because they lie in bed and ruminate. Patients with character disorders such as narcissistic or borderline character disorders may feel angry about not being able to get the sleep they feel they are entitled to. The anger at failed efforts to sleep may produce arousal and make it increasingly difficult for them to fall asleep. Active psychosis of any type (e.g., schizophrenia) produces disturbed sleep and accounts for the other 10% of psychiatric insomnia. Hallucinations, delusions, and other signs and symptoms of psychotic illness present with the insomnia, facilitating recognition.
Patients with major depression complain of either difficulty falling asleep or of waking in the early morning and being unable to return to sleep. Diurnal variation of mood is often noted. Severe depression with agitation may lead to markedly diminished total sleep and overall exhaustion (see Chapter 227). It is important to recognize that insomnia may be the presenting symptom of major depression, and patients with insomnia are at risk for developing depression. Insomnia may also persist after other symptoms of depression resolve.
TABLE 232-1 Insomnia Causes/Comorbidities | ||||||||||||||
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Patients with dysthymic disorder (a variant of depression) often complain of feeling tired and irritable, have difficulty falling asleep, and report that they cannot get enough sleep to feel rested. Sometimes, they deny feeling sad or depressed and focus only on their physical complaints. Patients in the manic phase of a bipolar affective disorder may report difficulty falling asleep or staying asleep, but they do not report feeling tired during waking times.
It is important to recognize the significant bidirectional relationship between insomnia and depression. Patients with insomnia but without current depression are much more likely to develop future depression than are those without insomnia. Successful treatment of insomnia in depressed patients predicts better outcomes for the depression and lower rates of depression relapse.
TABLE 232-2 Medications and Substances Associated with Insomnia | |
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Drugs and Substance Abuse (see also Chapter 235)
Drugs and alcohol are present in about 10% to 15% of all patients with insomnia and may be its cause. Alcohol induces sedation, but the resulting sleep is often shallow, fragmented, and not restorative. Alcoholics can have prematurely “aged” sleep (i.e., shallow and short) during and for months after the cessation of drinking. Sedatives, especially barbiturates, when used on a regular longterm basis lead to shallow, fragmented sleep. Rebound insomnia and rebound anxiety prompt reuse, and tolerance leads to dose escalation, and so patients get caught in a vicious cycle. Sedatives and alcohol depress respiratory function, which can lead to sleep of very poor quality in patients with sleep apnea.
Stimulant drugs, such as amphetamines, activating antidepressants, and the phenylpropanolamine found in many overthe-counter decongestants, can induce significant difficulty in falling asleep. The caffeine and other stimulant xanthines found in tea, coffee, cola drinks, and chocolate are well recognized and often used for their ability to keep one awake. In those who are sensitive, even small amounts can prevent sleep. Nicotine and other substances found in cigarette smoke disrupt sleep induction and continuity. Bronchodilators such as aminophylline and β-agonists can make sleep difficult when given before bedtime.
Medical Problems
Approximately 10% of patients with insomnia disorder have comorbid medical problems. Chronic pain is a leading, although often overlooked, factor (e.g., that experienced by elderly persons with degenerative joint disease). Delirium is another important cause in the elderly, resulting from unrecognized infection or medication toxicity (as from anticholinergic agents used in over-the-counter sleep remedies). Cardiopulmonary dysfunction may contribute by causing orthopnea, paroxysmal nocturnal dyspnea, or nocturnal angina. Urinary frequency due to infection, prostatism, diabetes, or poor timing of diuretic use is another important disrupter of sleep. Often, it is the nocturia and disturbed sleep that causes the patient with prostatism finally to seek definitive therapy. Nocturia has also been noted to be a consequence of sleep apnea.
Primary Sleep Disorders
Circadian rhythm disorders.
Circadian rhythm disorders may present with insomnia. In the delayed sleep phase syndrome subtype, the patient falls asleep later than the usual bedtime, sleeps well, and gets up later than is socially acceptable. This common disturbance often presents in adolescents. Shift-work disorder or jet travel across time zones (jet lag), in which the inability to rapidly reset one’s circadian rhythm to local time, may produce insomnia. For travel westward across time zones, the typical experience is awakening in the middle of the night local time (morning at home) and being unable to fall back to sleep despite feeling tired. Restful sleep is not achieved. Moreover, there is marked afternoon or early-evening sleepiness (bedtime at home). The inability to attain restful sleep culminates in exhaustion, and the patient requests help for insomnia. Endogenous disruptions of the brain’s internal circadian rhythm setter can produce a similar picture.
Restless legs syndrome.
Restless legs syndrome is another motor disturbance associated with insomnia. Characteristic features include the urge to move the legs when awake and periodic leg movements when asleep (see Appendix 232-1-232-232). Only the
waking symptoms define the syndrome; polysomnography is not required.
waking symptoms define the syndrome; polysomnography is not required.
Sleep apnea.
Sleep apnea is a disorder characterized by repeated apneic periods due to soft tissue upper airway obstruction followed by disruption of sleep. In severe cases, behavioral changes, pulmonary hypertension, cardiac arrhythmias, and death can occur. Up to 50% of patients with sleep apnea complain of insomnia as well as of daytime sleepiness (see Chapter 46).
Since the goal of management is improving daytime functioning and ameliorating global sleep dissatisfaction, the initial workup should focus on discovery of predisposing, precipitating, and perpetuating factors (the “3 Ps”).
History
In addition to getting a good description of the sleep problem, it is important to elucidate any predisposing factors such as prior episodes of stress-related insomnia and a family history of insomnia; precipitating factors such as medical, psychosocial, or environmental problems; and any perpetuating factors such as feelings of frustration, anger, anxiety, or despair related to difficulty sleeping. A full description of the problem may be facilitated by having the patient keep a sleep log or diary, which includes time in bed, estimate of time asleep, any awakenings, time of morning arousal, estimate of sleep quality, and comments on unusual events and any associated symptoms (e.g., orthopnea, urinary frequency, pain, palpitations). Entries are recorded by the patient directly on getting up each morning. Paradoxically and dysfunctionally, the patient may spend more time in bed — sleep beliefs should be explored. Note that insomnia patients may increase their time in bed in hopes of increasing sleep; however this can paradoxically worsen insomnia if time in bed exceeds sleep capacity. This maladaptive behavior is addressed in a component of cognitive behavioral therapy for insomnia called sleep restriction. The history should include beliefs about sleep: fear of not meeting the widely held ideal of 8 hours per night can itself contribute to insomnia. Close attention must also be given to use of sedatives, hypnotics (including over-the-counter preparations), and stimulants (see Table 232-2). Screening for abuse of alcohol and other substances is essential (see Chapters 228 and 235).
It is most important to listen carefully for and inquire directly about symptoms of depression, bipolar disease, anxiety disorder, and psychosis (see Chapters 226 and 227). Occupational and travel patterns should be noted. Whenever possible, interviewing the spouse, bed partner, or family member is of great value, particularly for symptoms suggestive of sleep apnea (e.g., excessive snoring, apneic episodes, disturbed sleep). Family members may also bring to light covert substance use or abuse that patients may minimize or deny. Past and family medical and psychiatric histories are sometimes revealing. Perimenopausal women should be asked about hot flashes.
Physical Examination
The pertinent physical examination is a function of the history. One checks for upper airway soft tissue obstruction in the patient with suspected sleep apnea; for jugular venous distention, rales, wheezes, heaves, and gallops when there is concern about a cardiopulmonary etiology; for moist skin, tachycardia, proptosis, goiter, and tremor when hyperthyroidism is under consideration; and for prostatic enlargement in the elderly male with sleep-disturbing nocturia. Any reported sources of pain should be evaluated and confirmed by physical examination. A careful mental status examination helps in the detection of neuropsychiatric disease (see Chapters 169, 226, 227, 228, and 235).
Laboratory Testing
Testing should be limited, selective, and based on evidence from the history and physical examination (e.g., thyroid-stimulating hormone for suspected hyperthyroidism, chest x-ray for cardiopulmonary disease, toxic screen for substance abuse). Polysomnography is generally not indicated in the evaluation of insomnia in primary care settings.
PRINCIPLES OF MANAGEMENT (8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30 and 31)
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