![]() Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops as well as potential targets for prevention and treatment. ![]() It should also explain the discrepancy between subjective (self-report) and objective (polysomnography ) measures of insomnia symptoms reported by some individuals with insomnia (see Reference 13 for a review). ![]() To be comprehensive, an etiologic or pathophysiologic model of insomnia should explain features such as the heterogeneity of symptoms and the risk insomnia confers for other comorbid conditions, such as depression and cardiometabolic syndrome. This may be related to the heterogeneity of insomnia, its highly comorbid nature, or differences in what level of analysis the models use, from phenomenology to physiology. 9Īlthough progress has been made in recent years regarding our understanding of the nature, etiology, and pathophysiology of insomnia, 6, 10- 12 there is still no universally accepted model. 4, 5, 7, 8 Insomnia is a chronic problem in 31% to 75% of patients, 1, 6, 7 with more than two-thirds of patients reporting symptoms for at least 1 year. ![]() 3- 6 Most reports suggest prevalence rates of insomnia disorder at 5% to 15%. 1 Prevalence estimates of insomnia vary, with 30% to 43% of individuals reporting at least one nighttime insomnia symptom. Insomnia is differentiated from sleep deprivation by difficulty sleeping despite having adequate opportunity to sleep. 1, 2 The disorder is also characterized by significant distress or impairment in functioning, and daytime symptoms including fatigue, daytime sleepiness, impairment in cognitive performance, and mood disturbances. Insomnia disorder is characterized by dissatisfaction with sleep quantity or quality, associated with difficulty falling asleep, frequent nighttime awakenings with difficulty returning to sleep, and/or awakening earlier in the morning than desired. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with difficulty falling asleep, frequent nighttime awakenings with difficulty returning to sleep, and/or awakening earlier in the morning than desired.
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