The increased prevalence of insomnia in older adults is partly explained by the higher incidence of physical health problems with aging. Changes in sleep patterns associated with the normal developmental process must be differentiated from those exceeding age-related changes. Although polysomnography is of limited value in the routine evaluation of in- somnia, it may be more useful in the differential diagnosis among older adults because the etiologies of insomnia (e.g., sleep apnea) are more often identifiable in older individuals.
While the risk and prognostic factors discussed in this section increase vulnerability to in- somnia, sleep disturbances are more likely to occur when predisposed individuals are ex- posed to precipitating events, such as major life events (e.g., illness, separation) or less severe but more chronic daily stress. Most individuals resume normal sleep patterns after the initial triggering event has disappeared, but others—perhaps those more vulnerable to insomnla—continue experiencing persistent sleep difficulties. Perpetuating factors such as poor sleep habits, irregular sleep scheduling, and the fear of not sleeping feed into the in- somnia problem and may contribute to a Vicious cycle that may induce persistent insomnia.
Temperamental. Anxiety or worry-prone personality or cognitive styles, increased arousal predisposition, and tendency to repress emotions can increase vulnerability to insomnia.
Environmental. Noise, light, uncomfortably high or low temperature, and high altitude may also increase vulnerability to insomnia.
Genetic and physiological. Female gender and advancing age are associated with in- creased vulnerability to insomnia. Disrupted sleep and insomnia display a familial dispo- sition. The prevalence of insomnia is higher among monozygotic twins relative to dizygotic twins; it is also higher in first-degree family members compared with the general population. The extent to which this link is inherited through a genetic predisposition, learned by observations of parental models, or established as a by-product of another psy- chopathology remains undetermined.
Course modifiers. Deleterious course modifiers include poor sleep hygiene practices (e.g., excessive caffeine use, irregular sleep schedules).
Insomnia is a more prevalent complaint among females than among males, with first onset often associated with the birth of a new child or with menopause. Despite higher preva- lence among older females, polysomnographic studies suggest better preservation of sleep continuity and slow-wave sleep in older females than in older males.
Polysomnography usually shows impairments of sleep continuity (e.g., increased sleep la- tency and time awake after sleep onset and decreased sleep efficiency [percentage of time in bed asleep] and may show increased stage 1 sleep and decreased stages 3 and 4 sleep.
The severity of these sleep impairments does not always match the individual’s clinical presentation or subjective complaint of poor sleep, as individuals with insomnia often un- derestimate sleep duration and overestimate wakefulness relative to polysomnography.
Quantitative electroencephalographic analyses may indicate that individuals with insom- nia have greater high—frequency electroencephalography power relative to good sleepers both around the sleep onset period and during non—rapid eye movement sleep, a feature suggestive of increased cortical arousal. Individuals with insomnia disorder may have a tive sleep laboratory measures compared with individuals without sleep disorders.
Other laboratory measures show evidence, although not consistently, of increased arousal and a generalized activation of the hypothalamic-pituitary-adrenal axis (e.g., in- creased cortisol levels, heart rate variability, reactivity to stress, metabolic rate). In general, findings are consistent with the hypothesis that increased physiological and cognitive arousal plays a significant role in insomnia disorder.
Individuals with insomnia disorder may appear either fatigued or haggard or, con- versely, overaroused and ”wired.” However, there are no consistent or characteristic abnormalities on physical examination. There may be an increased incidence of stress- related psychophysiological symptoms (e.g., tension headache, muscle tension or pain, gastrointestinal symptoms).