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Brain Activation Changes in Insomnia: A Review of Functional Magnetic Resonance Imaging Studies

Chronobiology in Medicine 2020년 2권 3호 p.103 ~ 108
황윤지, 김석주,
소속 상세정보
황윤지 ( Hwang Yun-Jee ) - Sungkyunkwan University School of Medicine Samsung Medical Center Department of Psychiatry
김석주 ( Kim Seog-Ju ) - Sungkyunkwan University School of Medicine Samsung Medical Center Department of Psychiatry

Abstract


Numerous studies have examined factors associated with the occurrence of insomnia. With recent advances in brain imaging studies, neurobiological substrates of insomnia have received attention. In this review, we explore changes in brain activity in insomnia and their clinical and neurobiological interpretation by examining previous functional magnetic resonance imaging (fMRI) studies of insomnia. First, the question of whether insomnia may be related to attentional bias toward sleep-related stimuli has been an issue. Although controversies persist, previous fMRI studies have supported attentional bias to sleep-related stimuli in insomnia patients. Second, many studies have investigated which brain regions are involved in impaired cognitive performance of insomnia using fMRI. The prefrontal cortex or caudate nucleus has been implicated in cognitive impairment with insomnia. Third, we focused on the question of which brain regions are involved in emotional dysregulation in insomnia and its origins. Previous studies using fMRI suggested that sleep disturbance may occur due to abnormal brain function, such as reduced functional connectivity between the amygdala and other areas. Besides these factors, a variety of interconnected factors may have an impact on sleep disturbances, especially the interplay of stress and insomnia; this requires further research. Future fMRI studies of insomnia based on various theoretical models or novel imaging technologies might reveal the neurobiological pathways underpinning the development and maintenance of insomnia.

키워드

Insomnia; fMRI; Attentional bias; Cognitive impairment; Emotional dysregulation

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