2013
DOI: 10.5665/sleep.2794
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Increased Rostral Anterior Cingulate Cortex Volume in Chronic Primary Insomnia

Abstract: Winkelman JW; Plante DT; Schoerning L; Benson K; Buxton OM; O'Connor SP; Jensen JE; Renshaw PF; Gonenc A. Increased rostral anterior cingulate cortex volume in chronic primary insomnia. 2013;36(7):991-998.

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Cited by 114 publications
(91 citation statements)
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“…These genes are enriched for expression in brain regions 9 (Supplementary Table 13), including the cerebellum (p=1.3 x 10 -6 ), frontal cortex (p=1.3 x 10 -5 ), anterior cingulated cortex (p=1.7 x 10 -5 ), hypothalamus (p=2.2 x 10 -5 ), basal ganglia (p=7.0 x 10 -4 ), amygdala (p=3.4 x 10 -4 ), and hippocampus (p=8.4 x 10 -4 ), in line with previous reports in the literature linking these brain regions to insomnia 21,22 . Integration of gene expression data with GWAS using transcriptomewide association analyses 23 identified 24 genes for which insomnia-SNPs influence gene expression in one or more of 14 tissue types tested, including eight brain regions, muscles, peripheral nerves, whole blood, pituitary, thyroid and adrenal gland tissue (Supplementary Table 16).…”
supporting
confidence: 78%
“…These genes are enriched for expression in brain regions 9 (Supplementary Table 13), including the cerebellum (p=1.3 x 10 -6 ), frontal cortex (p=1.3 x 10 -5 ), anterior cingulated cortex (p=1.7 x 10 -5 ), hypothalamus (p=2.2 x 10 -5 ), basal ganglia (p=7.0 x 10 -4 ), amygdala (p=3.4 x 10 -4 ), and hippocampus (p=8.4 x 10 -4 ), in line with previous reports in the literature linking these brain regions to insomnia 21,22 . Integration of gene expression data with GWAS using transcriptomewide association analyses 23 identified 24 genes for which insomnia-SNPs influence gene expression in one or more of 14 tissue types tested, including eight brain regions, muscles, peripheral nerves, whole blood, pituitary, thyroid and adrenal gland tissue (Supplementary Table 16).…”
supporting
confidence: 78%
“…6 The etiology of insomnia in the absence of any identifiable organic or psychiatric disorder is assumed to be multifac torial, involving cognitive factors (e.g., worry and rumina tion, selective attention for sleeprelated cues, dysfunctional attitudes and beliefs about sleep 7,8 ), maladaptive behaviours (e.g., extending time in bed or daytime napping 9 ) and in creased physiologic arousal. 10 From a neurobiological point of view, several subcortical and cortical regions, including the ascending reticular activating system, amygdala, hippo campus, caudate nucleus, anterior cingulate cortex (ACC), in sula and frontal cortex, [11][12][13][14][15][16][17][18][19][20] are thought to be involved in the pathophysiology of night and daytime symptoms in patients with insomnia.…”
Section: Introductionmentioning
confidence: 99%
“…MRI is an ideal tool to address whether variations in brain structure underlie these relationships, and MRI studies have linked primary insomnia with reduced volume of the orbitofrontal cortex (OFC), 4,5 hippocampus, 6,7 and precuneus, 4 and increased volume of the rostral anterior cingulate. 5 Although few studies have explored the relationship between sleep and brain structure in healthy individuals, crosssectional correlations have been reported between the volume of the OFC and early-morning awakening 8 and daytime sleepiness. 9 Furthermore, reduction in non-REM (NREM) slow wave activity (SWA) in older adults has been associated with age-related decreases in gray matter density within the medial prefrontal cortex (mPFC).…”
mentioning
confidence: 99%