Clinical reviewHyperarousal and insomnia: State of the science
Section snippets
Evidence for physiological arousal in patients with primary insomnia
Extensive physiological differences between good and poor sleepers were first reported by Monroe,4 who found increased rectal temperature, heart rate, basal skin resistance, and phasic vasoconstrictions 30 minutes prior to and during sleep in poor sleepers as compared to normal sleepers. In the 20 years that followed, several additional differences were reported when patients with insomnia were compared with normal sleepers. Poor sleepers had increased secretion of corticosteroids and adrenaline,
Animal model
The diagnosis of insomnia is based upon the subjective complaint of poor sleep that is sometimes corroborated by EEG recordings. The requirement of a complaint, of course, makes an animal model of insomnia difficult, but studies of poor sleep in animals in response to expected stressors can add unique insight to human work. In a recent model, rats were placed in a cage previously occupied by a male rat (odor exposure). This is a species specific model that produces an acute stress response.
Genetic studies
Basal level of sympathetic nervous system activity, like many other attributes, could be seen as normally distributed in the population. This would mean that some individuals would probably have a genetic predisposition to greater sympathetic activation and therefore a greater predisposition to develop associated disorders such as insomnia. A good deal of evidence suggests that insomnia is under strong genetic influence.66 A recent twin study showed a heritability estimate of 57% for insomnia
Cause versus effect
Despite the fact that there is now pervasive evidence of physiological arousal in numerous systems during sleep in patients with insomnia, none of the literature cited, except, perhaps the rat stress-induced model, comments on causality. Insomnia is typically accompanied by numerous changes including cognitive arousal/stress, dysphoria or degraded mood, depression or anxiety and fatigue in addition to the numerous physiological changes described previously. It has always been difficult to
Medical implications of hyperarousal
Insomnia has been considered an acute disorder often secondary to other medical pathology such as depression or pain. However, more recently an NIH review of insomnia and treatments has concluded that insomnia can be a primary or comorbid chronic disorder.79 Many studies have shown that insomnia is a predictor for the later development of depression.80 In addition, much evidence has accumulated showing abnormal levels of arousal in patients with depression and other mood disorders.81
Treatment of hyperarousal as treatment for insomnia
Although the concept of physiological arousal as a basis for insomnia dates to early studies of poor sleep,4 treatment strategies have continued to focus on changes in EEG sleep latency and sleep efficiency. Relatively few studies have documented changes in other physiological measures with therapy and even fewer have attempted therapies that target the entire night and day. It is known that benzodiazepines, for example, directly decrease metabolic rate87 and body temperature88 and therefore
Summary
In the last few years, increasingly sensitive measures of central nervous system function have provided a much clearer view of the neurophysiology of insomnia both in man and in newly developing animal models. These new data strongly support the view that primary insomnia is a true conflict between the sleep system and inappropriate activation of central nervous system. Identification of specific sites of brain activation with lesion study confirmation should allow development of increasingly
Acknowledgements
Supported by the Dayton Department of Veterans Affairs Medical Center, Wright State University School of Medicine, and the Sleep–Wake Disorders Research Institute.
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