![]() ![]() There have been many excellent and encompassing reviews of hyperarousal in insomnia since 2000 (see studies by Riemann, 11 Bonnet and Arand, 12 Roth et al, 13 Harvey et al, 14 Kay and Buysse, 15 Drummond et al, 16 and Vgontzas et al, 17 among others) therefore, we will attempt to not retread here. ![]() While this expansion both across and within domains has led to numerous important findings, it has also produced an ever-widening gap between researchers who are essentially studying the same construct. Thus, there has been an expansion in the scientific study of all aspects of sleep-related hyperarousal becoming practically as broad as the concept itself. Indeed, many conceptualizations exist that vary not only between but also within disciplines. Similar to terms such as stress, reactivity, and other broad constructs that cross the boundaries of psychology, physiology, and medicine, the term “hyperarousal” is difficult, if not impossible, to define without sufficient context. Note: Data were obtained from Ovid-MEDLINE database.Ī critical challenge for our current understanding of hyperarousal in insomnia is to synthesize these often-disparate findings both across and within these broad domains. Another contributing factor is the now wide availability and low cost of tools to study aspects of hyperarousal including its physiological, cognitive, and neuronal correlates.Īll published articles including keywords “sleep” and “insomnia” from 1990 to 2015. One factor is the near exponential rise of sleep science over the last 2 decades ( Figure 1). Several important factors have led to an increasing interest in this broadly defined area of sleep science. The concept of hyperarousal as an important etiological factor in insomnia has been long held, with serious scientific inquiry into this conceptualization, as well as the issue of cause and effect, undertaken more than 50 years ago. However, recent advances using hyperarousal and stress dysregulation models of insomnia have offered critical insights into insomnia disease processes. ![]() 10 Understanding the course of insomnia is difficult, in part, because its complex psychoneurobiology is not yet fully understood. 1, 2 Despite advances in pharmacological and behavioral interventions, 3– 8 many treated insomniacs relapse 9 and those with severe forms of insomnia are resistant to treatment. Insomnia is the most common sleep disorder in the US with prevalence rates estimated between 9% and 20% among adults. Future research on sleep reactivity is needed to identify its neurobiology, characterize its relationship with cognitive–emotional reactivity, and explore the potential clinical utility of sleep reactivity in treatment planning. We propose that sleep reactivity and cognitive–emotional reactivity may share a bidirectional relationship, conferring an insalubrious environment for sleep in response to stress. Importantly, stress-related cognitive–emotional reactivity (e.g., rumination, worry) may exploit the vulnerability of a highly reactive sleep system. Research points to genetics, family history of insomnia, gender, and environmental stress as factors that influence sleep reactivity. Premorbid sleep reactivity has been shown to identify individuals at risk for future insomnia disorder, such as highly reactive sleepers (whose sleep systems are sensitive to stress) who are at elevated disease risk. A trait characteristic, sleep reactivity is the degree to which stress disrupts sleep, manifesting as difficulty falling and staying asleep. In this report, we discuss evidence for hyperarousal in insomnia and explore the role of sleep reactivity. Similar basal arousal profiles between individuals with high vs low risk for insomnia in the absence of stress exposure suggest that dysregulated stress “response” rather than general hyperarousal may be a more pertinent marker of risk. Even so, mixed results regarding the specific mechanisms linking hyperarousal to sleep disturbance limit current etiological conceptualizations. ![]() Overall patterns in the literature suggest that over-active neurobiological and psychological systems contribute to difficulty sleeping. Hyperarousal is a key component in all modern etiological models of insomnia disorder. ![]()
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