Clinical reviewThe hyperarousal model of insomnia: A review of the concept and its evidence
Introduction
Insomnia as a diagnostic entity is defined as a complaint of prolonged sleep latency, difficulties in maintaining sleep, the experience of non-refreshing or poor sleep coupled with impairments of daytime functioning, including reduced alertness, fatigue, exhaustion, dysphoria and other symptoms. The complaints have to endure for at least 4 weeks to be diagnosed as insomnia. The Diagnostic and Statistical Manual of the American Psychiatric Association (DSM)1 classifies insomnias into primary insomnia (PI), insomnia related to a medical or mental disease and insomnia related to the intake or abuse/dependency from substances. The International Classification of Sleep Disorders (ICSD) 2 goes beyond that approach and specifies 11 insomnia subtypes encompassing among others acute, psychophysiological, paradoxical, idiopathic and substance-induced insomnia.
Insomnia as a symptom is a highly prevalent health complaint afflicting up to 50% of the general population depending on criteria applied. Estimates for the prevalence of PI as a diagnostic entity in the general population range from 3 to 5%.3 Research diagnostic criteria for insomnia4 now provide operationalized and standardized criteria for the diagnosis of insomnia and its subtypes.
Polysomnographic research on insomnia revealed a remarkable discrepancy between the subjective experience of insomnia and polysomnographically rather undisrupted sleep in many patients with primary insomnia.5, *6 Thus, polysomnography (PSG), in contrast to other fields of clinical sleep medicine, has not become the via regia to the diagnosis of insomnia.7 Insomnia diagnosis and assessment is based on subjective reports (sleep questionnaires) of sleep behavior and relies on sleep diaries filled out every evening and morning (for an overview of relevant instruments see8, 9).
The effectiveness of cognitive-behavioral treatment for insomnia (CBT-I)10, 11, 12 compared to the risks inherent with pharmacological insomnia treatment (e.g., benzodiazepines13) may have added to the conceptualization of PI as primarily a psychological disorder and negligence to study its biological aspects (compared to other sleep disorders or other disorders in the field of mental health).
The “hyperarousal” perspective of insomnia14, 15, *16 has gained widespread attention as an integrative approach to the pathophysiology of insomnia (especially primary insomnia (PI) or psychophysiological insomnia), assuming an interplay between psychological and physiological factors in the etiology and perpetuation of chronic insomnia. Accordingly, acute episodes of insomnia are triggered by acute stressors (“threat”, i.e., psychosocial, medical, drug factor). In many cases, with the cessation of the influence of the stressor, the sleep complaint resolves. Only a subpopulation of afflicted patients develops persistent, chronic insomnia which becomes independent of the initial stressors.17
The hyperarousal concept postulates that subjects who tend to focus cognitively on the insomnia and start to ruminate about their sleep complaint are prone to develop “learned sleep preventing associations” which explain the chronicity of the disorder. Maladaptive behaviors (i.e., prolongation of bedtime, daytime napping, increased alcohol consumption, etc.) are postulated to contribute additionally to the perpetuation of insomnia. The hyperarousal concept from early on encompassed physiological phenomena as it was demonstrated that chronic insomnia is accompanied by indices of increased autonomic activity.14, 18 The term “psychophysiological” insomnia as it was coined by Hauri19 indicated that “psychophysiological insomnia… develops secondary to chronic, somatized tension and negative conditioning”. Yet, 20 years later, when considering the description of psychophysiological insomnia in the ICSD-2,2 not much knowledge seems to have been accumulated concerning the “physiological” (=somatized tension) aspect.
It is the aim of the present article to review the hyperarousal concept of primary insomnia and to discuss the underlying evidence with an emphasis on neurobiological studies. Furthermore we aim to integrate these findings with neuroscientific knowledge on sleep–wake regulation.
Section snippets
The hyperarousal concept of insomnia
Perlis and colleagues*16, *20 provided a comprehensive review of the hyperarousal perspective including neurobiological variables which they termed “neurocognitive” theory of insomnia (modified version see Fig. 1).
The model is based on the behavioral perspective that insomnia occurs acutely in association with predisposing and precipitating factors (for example psychosocial stressors), and chronically in association with perpetuating factors17 (for example extension of time in bed). The
(Molecular-)genetic studies
As in other areas of medicine the ultimate goal of this line of research is to delineate one or several genes whose presence/absence is highly predictive that a given subject will develop a certain disorder/disease. As sleep and sleep disorders are complex phenotypes, regulated by many genes, gene interactions, environment and gene–environment interactions, it is extremely unlikely that there is a clear-cut single gene relationship for insomnia.23 It seems more likely that several genes and
The neurobiology of sleep–wake regulation: consequences for the understanding of insomnia
Based on the early work of von Economou146 and Moruzzi and colleagues147 it is widely acknowledged that the ascending reticular activating systems (ARAS), originating in the brainstem, plays a major role in the regulation of sleep–wake states and is the major source of cortical arousal. Saper and colleagues*148, 149 have elegantly summarized up to date knowledge about the neurobiology and neurochemistry of sleep–wake regulation. In short, according to their model (see Fig. 2), wakefulness
Synthesis
Till recently, insomnia, especially primary insomnia, was mainly conceptualized as a psychological disorder caused by psychosocial stress and maintained by maladaptive behaviors and conditioned arousal leading to the subjective experience of disturbed sleep which could, however, not be corroborated by objective measures of sleep like polysomnography. It was the aim of this review to demonstrate that by basing our theoretical reasoning on the concept of hyperarousal and linking it with the
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