The hyperarousal hypothesis in psychophysiological insomnia

Study of default- mode network and its modification after CBT

Researcher(s)

Duration

01/01/2012 - 31/12/2015

Funding

FCT - Individual Fellowship

Primary Insomnia is the more prevalent sleep disorder both in clinical and community samples. One of the most frequent subtypes is psychophysiological insomnia (PI). The hyperarousal at different levels – biological, affective, cognitive, and behavioral – and the maladaptive conditioning between sleep related stimuli and arousal are two major features of PI. Since this is a disorder which assumes an important role in public health, we performed 4 empirical studies recurring to fMRI: In the first study, we compared neurobiological activation between a group of PI patients (n=5) and a sex- and age-matched control group (n=5) when they were exposed to words concerning to past/present worries, future worries and neutral words; in the second study, we explored the activity of default-mode network (DMN) and other brain resting states in the same groups as study 1; in the third and fourth studies, we repeated both experiments in a clinical group of patients with PI (N=2) after they underwent cognitive-behavioral therapy for insomnia (CBT-I). In general, it was observed that PI patients exhibited a generalized pattern of hyperarousal in several brain areas associated with DMN when they were confronted with affective stimuli and when they were resting in the fMRI scanner. In terms of activation of brain resting networks, we observed that the clinical group presented significant dysfunctions. After CBT-I, it was detected that the dysfunctional indicators observed in previous studies normalize, approaching the activation patterns typical of healthy individuals. The obtained results enhance the idea that the hyperarousal in PI is present during the 24-hours of the day; besides, the key role that cognitive arousal may be in the etiology and therapy of insomnia is also highlighted. In conclusion, this work contributes to a better understanding of neurobiology of insomnia and suggests that it might be possible to identify neural mechanisms underlying modifications accounted by CBT-I.