Investigating the Role of Hyperarousal in Sleep-Onset Insomniacs

Devon A. Grant

Chronic insomnia is estimated to affect up to 25% of the U.S. population. Insomnia has been linked to several causal factors including life events, poor sleep hygiene, medical conditions, and hyperarousal. Of these, hyperarousal is the most widely accepted theory for the cause and maintenance of primary insomnia. However, there is continuing debate over whether the hyperarousal is general (i.e., present all the time) or bedtime-specific. One reason why this debate remains unresolved is that stable insomnia subtypes – sleep-onset and sleep-maintenance insomnia – are not usually differentiated in insomnia research, thereby ignoring the possibility of distinct mechanisms. Insomniacs typically report daytime functional impairment, but waking neurobehavioral impairment has been difficult to demonstrate objectively. It is possible that hyperarousal masks objective impairment, and exposure to total sleep deprivation (TSD) could potentially unmask it. The purpose of this dissertation is to examine the role of hyperarousal in sleep-onset insomnia. In Chapter 1, we present results of the validation of two portable versions of the Psychomotor Vigilance Test (PVT) in healthy normals, and demonstrate their utility for measuring neurobehavioral impairment during TSD. In Chapter 2, we present data on the neurobehavioral performance of sleep-onset insomniacs under conditions of TSD, and show that there is profound impairment in neurobehavioral performance relative to healthy normal sleepers as wakefulness is extended. The results indicate that hyperarousal, if present, does not provide protection against further sleep loss, and that hyperarousal may be bedtime-specific in sleep-onset insomniacs. In Chapter 3, we investigate the role of hyperarousal in relation to physiological reactivity to stressors. We find a blunted, rather than heightened, physiological response in sleep-onset insomniacs, which we also observe in healthy normal sleepers exposed to TSD. Hyperarousal does not explain the exacerbated performance impairment during TSD and the blunted stressor reactivity in sleep-onset insomniacs. Rather, sleep-onset insomniacs may be under allostatic load from prior chronic sleep restriction. This novel finding may have important implications for the treatment of sleep-onset insomniacs.

Investigating the Role of Hyperarousal in Sleep-Onset Insomniacs

Files and links (1)

Abstract

Metrics

Details