Authors: Levi Pouwer, Keaton Helquist
Mentors: Jared Nielsen
Insitution: Brigham Young University
OBJECTIVE:
To identify brain regions and networks underlying acquired-brain-injury-induced insomnia.
BACKGROUND:
In patients of tertiary-level mental healthcare facilities, symptoms of chronic insomnia are prevalent in 78.2% of the population. Additionally, among those who suffer from acquired brain injury, few symptoms are as generally pervasive as that of chronic insomnia. Meta-analyses of insomnia patients with fMRI data have failed to identify consistently affected brain regions. Individual studies have suggested several brain regions are involved in insomnia, including the anterior cingulum, orbitofrontal cortex, the insula, caudate nucleus, and the anterior capsula interna. However, few regions have consistently been implicated in the pathophysiology of insomnia. Moreover, little is known regarding the collective brain networks involving insomnia.
DESIGN/METHODS:
A comprehensive systematic literature review was conducted to identify case studies of individuals afflicted with acquired brain injury-induced insomnia (N=53). The review process was facilitated by employing Cadima, specialized literature review software. To establish a reference baseline for comparison, a substantial cohort of resting-state functional MRI (fMRI) scans from healthy control subjects (N=1000) was meticulously acquired. Subsequently, lesion network mapping analysis, as outlined by Fox et al. in 2018, was applied to the lesions observed in the 53 patients. This method allowed us to assess the impact on functional connectivity and analyze its implications by comparing the patients' lesion networks with the baseline scans obtained from healthy controls.
RESULTS:
In the context of lesion network mapping analysis, our study revealed that 45 out of 53 patients diagnosed with acquired brain injury-induced insomnia exhibited brain lesions that were functionally connected to both the left amygdala and the left anterior insula. Moreover, in 39 out of 57 patients, the lesion networks also included bilateral anterior insula and the hypothalamus. Comparative analysis of these lesions with a normative database unveiled a substantial disparity in functional connectivity to the left amygdala and left anterior insula in patients suffering from acquired brain injury-induced insomnia. This finding underscores the relevance of tissue within these regions and tissues functionally connected to these areas in relation to the onset of lesion-induced insomnia.
CONCLUSION:
The observed functional network connectivity among the left amygdala and the left insular region in relation to insomnia introduces a potentially more intricate mechanism underlying the onset of insomnia, in addition to the previously proposed factors such as hyperarousal in cortical regions and subcortical neuropathologies. Our findings highlight the possibility of a deeper connection between the initiation of insomnia and limbic structures, specifically emphasizing their role in emotion and sleep regulation. This suggests that the neural mechanisms influencing anxiety may have interrelated effects on the mechanisms influencing insomnia. It is evident that further investigation, particularly among psychiatric patients afflicted with insomnia, is warranted to delve into the activities occurring in these regions and to elucidate the potential interplay between anxiety and insomnia. This research paves the way for a deeper understanding of the complex relationship between neural pathways and the development of insomnia, ultimately offering valuable insights for future clinical and therapeutic considerations.