Changes in subcortical shape and cognitive function in patients with chronic insomnia

Koo, Dae Lim; Shin, Jeong Hee; Lim, Jae Sung; Seong, Joon Kyung; Joo, Eun Yeon

doi:10.1016/j.sleep.2017.04.002

Cited by 51 publications

(46 citation statements)

References 19 publications

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“…The reduced connectivity in the present study includes connections between frontal areas and classical limbic areas, such as amygdala, hippocampus and thalamus, and alterations in these regions have previously been reported in persons with Insomnia Disorder (Riemann et al, 2007;Huang et al, 2012;Koo et al, 2017). However, what is more pronounced is the reduced connectivity of frontal regions, including the orbitofrontal and medial frontal cortex with basal ganglia structures, such as the putamen, caudate and pallidum.…”

Section: Reduced Fronto-subcortical Connectivity In Insomnia Disordersupporting

confidence: 63%

“…Altered activity in basal ganglia structures has previously been associated with Insomnia Disorder. A recent study reported that structural changes of the putamen was related to higher arousal indices in participants with persistent insomnia (Koo et al, 2017).…”

Section: Reduced Fronto-subcortical Connectivity In Insomnia Disordermentioning

confidence: 98%

“…Other studies have approached the neurobiological basis of insomnia by looking at structural differences between persons with Insomnia Disorder and good sleeper controls with no sleep problems. In terms of grey matter alterations, neuroimaging studies have linked insomnia to grey matter decreases in the orbitofrontal cortex (Altena et al, 2010;Stoffers et al, 2012) and hippocampus (Riemann et al, 2007;Koo et al, 2017). In addition, two studies have used diffusion tensor imaging (DTI) to evaluate differences in white matter tracts in persons with Insomnia Disorder compared to matched controls.…”

mentioning

confidence: 99%

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Reduced structural connectivity in Insomnia Disorder

Jespersen

Stevner

Fernandes

et al. 2019

Preprint

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Insomnia Disorder is the most prevalent sleep disorder and it involves both sleep difficulties and daytime complaints. The neural underpinnings of Insomnia Disorder are poorly understood.Existing neuroimaging studies are limited by their focus on local measures and specific regions of interests. To address this shortcoming, we applied a data-driven approach to assess differences in whole-brain structural connectivity between adults with Insomnia Disorder and matched controls without sleep complaints. We used diffusion tensor imaging and probabilistic tractography to assess whole-brain structural connectivity and examined group differences using Network-Based Statistics. The results revealed a significant difference in the structural connectivity of the two groups. Participants with Insomnia Disorder showed reduced connectivity in a subnetwork that was largely left lateralized, including mainly fronto-subcortical connections with the insula as a key region. By taking a whole-brain network perspective, our study succeeds at integrating previous inconsistent findings, and our results reveal that reduced structural connectivity of the left insula and the connections between frontal and subcortical regions are central neurobiological features of Insomnia Disorder. The importance of these areas for interoception, emotional processing, stress responses and the generation of slow wave sleep may help guide the development of neurobiologybased models of the highly prevalent condition of Insomnia Disorder.

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Section: Reduced Fronto-subcortical Connectivity In Insomnia Disordersupporting

confidence: 63%

Section: Reduced Fronto-subcortical Connectivity In Insomnia Disordermentioning

confidence: 98%

mentioning

confidence: 99%

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Reduced structural connectivity in Insomnia Disorder

Jespersen

Stevner

Fernandes

et al. 2019

Preprint

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“…Moreover, in a recent multi-center study, both midlife and late-life terminal insomnia were associated with a higher risk of dementia [11].It is interesting to note that affected brain structures in people with disturbed sleep coincide with vulnerable areas in AD. Lower gray matter volume in hippocampus, precuneus, amygdala, and cingulate gyrus [12][13][14][15][16][17][18][19], and a higher degree of cortical atrophy have been described in cognitively-unimpaired insomnia patients [14,20]. A recent study performed in cognitively unimpaired adults aged between 45 and 75, found that insomnia patients presented decreases in grey matter volume in AD-related areas, that concur with other studies.…”

supporting

confidence: 77%

Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker

Lloret

Cervera‐Ferri

Nepomuceno

et al. 2020

IJMS

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In recent years, the idea that sleep is critical for cognitive processing has gained strength. Alzheimer's disease (AD) is the most common form of dementia worldwide and presents a high prevalence of sleep disturbances. However, it is difficult to establish causal relations, since a vicious circle emerges between different aspects of the disease. Nowadays, we know that sleep is crucial to consolidate memory and to remove the excess of beta-amyloid and hyperphosphorilated tau accumulated in AD patients' brains. In this review, we discuss how sleep disturbances often precede in years some pathological traits, as well as cognitive decline, in AD. We describe the relevance of sleep to memory consolidation, focusing on changes in sleep patterns in AD in contrast to normal aging. We also analyze whether sleep alterations could be useful biomarkers to predict the risk of developing AD and we compile some sleep-related proposed biomarkers. The relevance of the analysis of the sleep microstructure is highlighted to detect specific oscillatory patterns that could be useful as AD biomarkers.the risk of developing AD [9]. Similarly, Bubu and colleagues estimated in a meta-analysis that the risk of dementia in patients with sleep disorders was 1.68 times greater [10]. Moreover, in a recent multi-center study, both midlife and late-life terminal insomnia were associated with a higher risk of dementia [11].It is interesting to note that affected brain structures in people with disturbed sleep coincide with vulnerable areas in AD. Lower gray matter volume in hippocampus, precuneus, amygdala, and cingulate gyrus [12][13][14][15][16][17][18][19], and a higher degree of cortical atrophy have been described in cognitively-unimpaired insomnia patients [14,20]. A recent study performed in cognitively unimpaired adults aged between 45 and 75, found that insomnia patients presented decreases in grey matter volume in AD-related areas, that concur with other studies. Furthermore, they found greater volume in the left caudate in these subjects, which can also be seen in presymptomatic carriers of an AD genetic mutation [21]. Finally, a very recent study in middle-aged, cognitively unimpaired adults found lower grey matter volumes in the left angular gyrus, the bilateral superior frontal gyri, the thalami, and the right hippocampus in insomniac APOE-ε4 carriers (AD's main risk factor) when compared to non-carriers with or without insomnia [21].This temporal and anatomical relationship could suggest that sleep disturbances may influence or exacerbate AD pathology and that improving sleep may help slow down its progression [22,23]. Additionally, sleep alterations could be used to predict the risk of developing dementia and could also serve as early indicators of the disease. If sleep disorders constitute a risk factor to initiate or to accelerate the clinical course of AD, they could be used to develop disease biomarkers. Furthermore, a sleep biomarker with high sensitivity and specificity would be extremely useful, as electrophysiological re...

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“…Other studies have approached the neurobiological basis of insomnia by looking at structural differences between persons with Insomnia Disorder and good sleeper controls. In terms of greymatter alterations, neuroimaging studies have linked insomnia to grey-matter decreases in the orbitofrontal cortex (Altena, Vrenken, Van Der Werf, Van Den Heuvel, & Van Someren, 2010;Stoffers et al, 2012) and hippocampus (Koo, Shin, Lim, Seong, & Joo, 2017;Riemann et al, 2007). In addition, a few studies have used diffusion tensor imaging (DTI) to evaluate differences in white-matter tracts in persons with Insomnia Disorder compared with matched controls.…”

mentioning

confidence: 99%

Reduced structural connectivity in Insomnia Disorder

Jespersen

Stevner

Fernandes

et al. 2019

Journal of Sleep Research

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Insomnia Disorder is the most prevalent sleep disorder, and it involves both sleep difficulties and daytime complaints. The neural underpinnings of Insomnia Disorder are poorly understood. Several existing neuroimaging studies focused on local measures and specific regions of interests, which makes it difficult to judge their whole‐brain significance. We therefore here applied a data‐driven approach to assess differences in whole‐brain structural connectivity between adults with Insomnia Disorder and matched controls without sleep complaints. We used diffusion tensor imaging and probabilistic tractography to assess whole‐brain structural connectivity, and examined group differences using network‐based statistics. The results revealed a significant difference in the structural connectivity of the two groups (p = .014). Participants with Insomnia Disorder showed reduced connectivity in a sub‐network that included mainly fronto‐subcortical connections with the insula as a key region. By taking a whole‐brain network perspective, our study enables the integration of previous inconsistent findings. Our results reveal that reduced structural connectivity of the left insula and the connections between frontal and subcortical regions are central neurobiological features of Insomnia Disorder. The importance of these areas for interoception, emotional processing, stress responses and the generation of slow‐wave sleep may help guide the development of neurobiology‐based models of the prevalent condition of Insomnia Disorder.

show abstract

Changes in subcortical shape and cognitive function in patients with chronic insomnia

Cited by 51 publications

References 19 publications

Reduced structural connectivity in Insomnia Disorder

Reduced structural connectivity in Insomnia Disorder

Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker

Reduced structural connectivity in Insomnia Disorder

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