Affect and Arousal in Insomnia: Through a Lens of Neuroimaging Studies

Abstract

Purpose of Review Previous research has struggled with identifying clear-cut, objective counterparts to subjective distress in insomnia. Approaching this discrepancy with a focus on hyperarousal and dysfunctional affective processes, studies examining brain structures and neural networks involved in affect and arousal are reviewed and conclusions for an updated understanding of insomnia are drawn. Recent Findings Recent studies found that amygdala reactivity, morphometry and adaptation in insomnia are altered, indicating that processing of negative stimuli is intensified and more lasting. Also, patients with insomnia show aberrant connectivity in the default mode network (DMN) and the salience network (SN), which is associated with subjective sleep disturbances, hyperarousal, maladaptive emotion regulation and disturbed integration of emotional states. The limbic circuit is assumed to play a crucial role in enhanced recall of negative experiences. Summary There is reason to consider insomnia as a disorder of affect and arousal. Dysregulation of the limbic circuit might perpetuate impaired connectivity in the DMN and the SN. However, the interplay between the networks is yet to be researched.

Alterations of Subcortical Brain Structures in Paradoxical and Psychophysiological Insomnia Disorder

“…Comparing two patients groups showed that although various subcortical regions undergo structural changes in psychophysiological insomnia, it is mainly associated with shrinkage in thalamus, amygdala, and hippocampus. This is in line with the hyperarousal model of insomnia and emotional memory impairment in ID (14,45). This model suggests that ID is characterized by increased arousal at the physiological, endocrine, cognitive or emotional levels and increased amygdala activity (17).…”

“…The amygdala plays a key role in processing negative emotional arousal and fear-inducing stimuli and therefore is involved in the hyperarousal model of ID (14,45). Gong et al also reported atrophy in the left superficial and right basolateral nucleus of amygdala, the association of insomnia severity with shape of the right centromedial nucleus, and the link between anxiety and shape of the basolateral nucleus of amygdala (16).…”

“…Several neuroimaging studies revealed widespread structural and functional cortical changes (12)(13)(14) including gray matter atrophy in the orbitofrontal cortex, dorsolateral prefrontal, pericentral cortices, temporal cortex, and precuneus, but increased gray matter volume in the anterior cingulate cortex (ACC). For review see (13,14). The role of subcortical brain regions in pathophysiology of ID was previously examined, although the results were inconsistent and difficult to replicate.…”

“…The role of subcortical brain regions in pathophysiology of ID was previously examined, although the results were inconsistent and difficult to replicate. For review see (13,14). A surface-based shape analysis of 27 patients with ID revealed that poor sleep quality and higher arousal are associated with subcortical atrophy including the hippocampus, amygdala, basal ganglia, and thalamus that was linked with impaired cognitive functions (15).…”

Editorial: The Interplay Between Sleep and Emotion: What Role Do Cognitive Processes Play?

“…Neuroimaging studies are also supporting this view. As recently summarized by Schiel et al (2020), insomnia is related to altered amygdala reactivity, morphometry, and adaptation. Moreover, insomnia is associated with aberrant connectivity in the default mode network, alterations in the salience network associated with hyperarousal, maladaptive emotion regulation, and disturbed integration of emotional states.…”