The Impact of Attentive System on Sleep Reactivity

Among sleep disorders, insomnia is the most common, with a prevalence around 10%. It is a debilitating disorder characterized by complaints of difficulty with sleep initiation, duration, consolidation, or quality, that occurs despite adequate opportunity for sleep, and that results in daytime impairment (i.e., fatigue, daytime sleepiness, mood disorders, cognitive deficits). For the diagnosis of chronic insomnia these symptoms need to occur at least three times a week for at least three months. Its precise etiology is still unknown and widely debated. One of the most valid hypotheses proposed is the hyperarousal model of insomnia. As insomnia is the result of predisposing, precipitating factors and perpetuating factors, this model asserts that one of these factors include an increased arousal (somatic, cognitive, and cortical activation). Subjects with an altered state of arousal tend to cognitively focus on their sleep problem or general distressful events through a mechanism known as rumination. Rumination contributes to strengthen ''learned sleep preventing associations''. Therefore, in this context is important to clarify the role of stress in impacting sleep. It's known that a single stressor can elicit different reactions across individuals, and this concern the wakefulness as well as sleep. For this reason, in sleep research contexts increasing attention is given to the construct of Sleep Reactivity.

Sleep Reactivity is defined as the degree to which a given amount of stress disrupts the sleep system, and it is consistent over time and across different type of stimuli. Sleep reactivity is a normal phenomenon under a certain threshold, but when it exceeds physiological threshold, this can lead to sleep disturbances that persist even following the removal of the stressor. Indeed, higher levels of sleep reactivity are associated to sleep quality depletion (i.e., increased sleep latency, reduced sleep efficiency and increased sleep fragmentation). The contribution of sleep reactivity in insomnia could be also related to altered (rapid eyes movement (REM)) REM sleep, since it plays a fundamental role in the elaboration of emotional and stressful stimuli, promoting a readjustment of the cognitive-emotional system. Hence, an alteration of REM after a stressor may prevent its proper processing and promote the disorder.

Moreover, the AIE (Attention-Intention-Effort) pathway model describe the fundamental role of attention during the falling asleep process. According to the model, healthy sleep is an automatic and involuntary process, and it can be inhibited by selectively directing attention to it. Thus, focusing on sleep promotes the development and maintenance of insomnia. Despite that, little consideration is given to the role of attention. A better understanding of these mechanisms could aid the management of sleep reactivity by promoting attentional shifting strategies to divert focus from stressors and sleep.

In order to, investigate this relationship this project aims to manipulate sleep reactivity to assess the differences between insomniacs and healthy controls, taking into account their attentional shifting performance and focusing on non-REM and REM sleep alterations.