In the last two decades, several models have been proposed to understand the etiology and pathophysiology of insomnia and most of them have emphasized the importance of the joint effect of stress and psychological factors in the pathogenesis of insomnia.14 The characteristic psychological profile of patients with insomnia, consisting of cognitive-emotional hyperarousal (i.e., obsessive, anxious, ruminative, and dysthymic personality traits) and emotion-oriented coping strategies,14-16 is thought to be present pre-morbidly and play a key role in the etiology of the disorder.14,17-20 Insomnia is associated with precipitating life events21 and cognitive-emotional arousal14 and is perceived by the patient as stressful on its own. Thus, insomnia should be expected to be associated with activation of the stress system.
Stress has been associated with the activation of the hypothalamic-pituitary-adrenal (HPA) and the sympatho-adrenal-medullary axes, whereas corticotropin-releasing hormone (CRH) and cortisol (products of the hypothalamus and adrenals, respectively), and catecholamines (products of the sympathetic system) are known to cause arousal and sleeplessness to humans and animals. On the other hand, sleep and particularly deep sleep appears to have an “anti-stress” effect as it is associated with an inhibitory effect on the stress system including its main two components, the HPA axis and the sympathetic system.