Cortical Thinning and Abnormal Structural Covariance Network After Three Hours Sleep Restriction.
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SUBMITTER: Wang C
PROVIDER: S-EPMC8329354 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Study objectivesRecent studies have suggested that structural abnormalities in insomnia may be linked with alterations in the default-mode network (DMN). This study compared cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia (PI) and good sleepers (GS).MethodsThe current study used a clinical subsample from the longitudinal community-based Korean Genome and Epidemiology Study (KoGES). Cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia symptoms (PIS; n = 57) were compared to good sleepers (GS; n = 40). All participants underwent MRI acquisition. Based on literature review, we selected cortical regions corresponding to the DMN. A seed-based structural covariance analysis measured cortical thickness correlation between each seed region of the DMN and other cortical areas. Association of cortical thickness and covariance with sleep quality and neuropsychological assessments were further assessed.ResultsCompared to GS, cortical thinning was found in PIS in the anterior cingulate cortex, precentral cortex, and lateral prefrontal cortex. Decreased structural connectivity between anterior and posterior regions of the DMN was observed in the PIS group. Decreased structural covariance within the DMN was associated with higher PSQI scores. Cortical thinning in the lateral frontal lobe was related to poor performance in executive function in PIS.ConclusionDisrupted structural covariance network in PIS might reflect malfunctioning of antero-posterior disconnection of the DMN during the wake to sleep transition that is commonly found during normal sleep. The observed structural network alteration may further implicate commonly observed sustained sleep difficulties and cognitive impairment in insomnia.
| S-EPMC4678334 | biostudies-literature
Project description:Background: Hyperuricemia is the cause of gout. The antioxidant and neuroprotective effects of uric acid seem to benefit some patients with central nervous system injury. However, changes in the brain structure have not been discovered in patients with gout. Object: Clarify the changes in cortical thickness in patients with gout and the alteration of the structural covariance networks (SCNs) based on cortical thickness. Methods: We collected structural MRIs of 23 male gout patients and 23 age-matched healthy controls. After calculating and comparing the difference in cortical thickness between the two groups, we constructed and analyzed the cortical thickness covariance networks of the two groups, and we investigated for any changes in SCNs of gout patients. Results: Gout patients have thicker cortices in the left postcentral, left supramarginal, right medial temporal, and right medial orbitofrontal regions; and thinner cortices were found in the left insula, left superior frontal, right pericalcarine, and right precentral regions. In SCN analysis, between-group differences in global network measures showed that gout patients have a higher global efficiency. In regional network measures, more nodes in gout patients have increased centrality. In network hub analysis, we found that the transfer of the core hub area, rather than the change in number, may be the characteristic of the gout's cortical thickness covariance network. Conclusion: This is the first study on changes in brain cortical thickness and SCN based on graph theory in patients with gout. The present study found that, compared with healthy controls, gout patients show regional cortical thinning or thickening, and variation in the properties of the cortical thickness covariance network also changed. These alterations may be the combined effect of disease damage and physiological compensation. More research is needed to fully understand the complex underlying mechanisms of gout brain variation.
| S-EPMC8481804 | biostudies-literature
Project description:ObjectiveThe structural covariance network (SCN) alterations in patients with temporal lobe epilepsy and comorbid sleep disorder (PWSD) remain poorly understood. This study aimed to investigate changes in SCNs using structural magnetic resonance imaging.MethodsThirty-four PWSD patients, thirty-three patients with temporal lobe epilepsy without sleep disorder (PWoSD), and seventeen healthy controls underwent high-resolution structural MRI imaging. Subsequently, SCNs were constructed based on gray matter volume and analyzed via graph-theoretical approaches.ResultsPWSD exhibited significantly increased clustering coefficients, shortest path lengths, transitivity, and local efficiency. In addition, various distributions and numbers of SCN hubs were identified in PWSD. Furthermore, PWSD networks were less robust to random and target attacks than those of healthy controls and PWoSD patients.ConclusionThis study identifies aberrant SCN changes in PWSD that may be related to the susceptibility of patients with epilepsy to sleep disorders.
| S-EPMC10605209 | biostudies-literature
Project description:Benign childhood epilepsy with centrotemporal spikes (BECTS) is associated with cognitive and language problems. According to recent studies, disruptions in brain structure and function in children with BECTS are beyond a Rolandic focus, suggesting atypical cortical development. However, previous studies utilizing surface-based metrics (e.g., cortical gyrification) and their structural covariance networks at high resolution in children with BECTS are limited. Twenty-six children with BECTS (15 males/11 females; 10.35 ± 2.91 years) and 26 demographically matched controls (15 males/11 females; 11.35 ± 2.51 years) were included in this study and subjected to high-resolution structural brain MRI scans. The gyrification index was calculated, and structural brain networks were reconstructed based on the covariance of the cortical folding. In the BECTS group, significantly increased gyrification was observed in the bilateral Sylvain fissures and the left pars triangularis, temporal, rostral middle frontal, lateral orbitofrontal, and supramarginal areas (cluster-corrected p < 0.05). Global brain network measures were not significantly different between the groups; however, the nodal alterations were most pronounced in the insular, frontal, temporal, and occipital lobes (FDR corrected, p < 0.05). In children with BECTS, brain hubs increased in number and tended to shift to sensorimotor and temporal areas. Furthermore, we observed significantly positive relationships between the gyrification index and age (vertex p < 0.001, cluster-level correction) as well as duration of epilepsy (vertex p < 0.001, cluster-level correction). Our results suggest that BECTS may be a condition that features abnormal over-folding of the Sylvian fissures and uncoordinated development of structural wiring, disrupted nodal profiles of centrality, and shifted hub distribution, which potentially represents a neuroanatomical hallmark of BECTS in the developing brain.
| S-EPMC5807981 | biostudies-literature
Project description:BackgroundPrevious neuroimaging studies have detected abnormal activation and intrinsic functional connectivity of the thalamus after total sleep deprivation. However, very few studies have investigated age-related changes in the dynamic functional connectivity of the thalamus and the abnormalities in the thalamic shape following partial sleep deprivation.MethodsFifty-five participants consisting of 23 old adults (mean age: 68.8 years) and 32 young adults (mean age: 23.5 years) were included in current study. A vertex-based shape analysis and a dynamic functional connectivity analysis were used to evaluate the age-dependent structural and functional abnormalities after three hours of sleep restriction.ResultsShape analysis revealed the significant main effect of deprivation with local atrophy in the left thalamus. In addition, we observed a significant age deprivation interaction effect with reduced variability of functional connectivity between the left thalamus and the left superior parietal cortex following sleep restriction. This reduction was found only in young adults. Moreover, a significantly negative linear correlation was observed between the insomnia severity index and the changes of variability (post-deprivation minus pre-deprivation) in the functional connectivity of the left thalamus with the left superior parietal cortex.ConclusionsThe results indicated that three hours of sleep restriction could affect both the thalamic structure and its functional dynamics. They also highlighted the role of age in studies of sleep deprivation.
| S-EPMC7845526 | biostudies-literature
Project description:Study objectivesTo determine the association between self-reported sleep duration and cortical thinning among older adults.MethodsWe studied 122 cognitively normal participants in the Baltimore Longitudinal Study of Aging with a mean age = 66.6 y (range, 51-84) at baseline sleep assessment and 69.5 y (range, 56-86) at initial magnetic resonance imaging (MRI) scan. Participants reported average sleep duration and completed a mean of 7.6 1.5-T MRI scans (range, 3-11), with mean follow-up from initial scan of 8.0 y (range, 2.0-11.8).ResultsIn analyses adjusted for age, sex, education, race, and interval between sleep assessment and initial MRI scan, participants reporting > 7 h sleep at baseline had thinner cortex in the inferior occipital gyrus and sulcus of the left hemisphere at initial MRI scan than those reporting 7 h (cluster P < 0.05). In adjusted longitudinal analyses, compared to those reporting 7 h of sleep, participants reporting < 7 h exhibited higher rates of subsequent thinning in the superior temporal sulcus and gyrus, inferior and middle frontal gyrus, and superior frontal sulcus of the left hemisphere, and in the superior frontal gyrus of the right hemisphere; those reporting > 7 h of sleep had higher rates of thinning in the superior frontal and middle frontal gyrus of the left hemisphere (cluster P < 0.05 for all). In sensitivity analyses, adjustment for apolipoprotein E (APOE) e4 genotype reduced or eliminated some effects but revealed others. When reports of < 7 h of sleep were compared to reports of 7 or 8 h combined, there were no significant associations with cortical thinning.ConclusionsAmong cognitively normal older adults, sleep durations of < 7 h and > 7 h may increase the rate of subsequent frontotemporal gray matter atrophy. Additional studies, including those that use objective sleep measures and investigate mechanisms linking sleep duration to gray matter loss, are needed.
| S-EPMC4835311 | biostudies-literature
Project description:The highly convoluted shape of the adult human brain results from several well-coordinated maturational events that start from embryonic development and extend through the adult life span. Disturbances in these maturational events can result in various neurological and psychiatric disorders, resulting in abnormal patterns of morphological relationship among cortical structures (structural covariance). Structural covariance can be studied using graph theory-based approaches that evaluate topological properties of brain networks. Covariance-based graph metrics allow cross-sectional study of coordinated maturational relationship among brain regions. Disrupted gyrification of focal brain regions is a consistent feature of schizophrenia. However, it is unclear if these localized disturbances result from a failure of coordinated development of brain regions in schizophrenia. We studied the structural covariance of gyrification in a sample of 41 patients with schizophrenia and 40 healthy controls by constructing gyrification-based networks using a 3-dimensional index. We found that several key regions including anterior insula and dorsolateral prefrontal cortex show increased segregation in schizophrenia, alongside reduced segregation in somato-sensory and occipital regions. Patients also showed a lack of prominence of the distributed covariance (hubness) of cingulate cortex. The abnormal segregated folding pattern in the right peri-sylvian regions (insula and fronto-temporal cortex) was associated with greater severity of illness. The study of structural covariance in cortical folding supports the presence of subtle deviation in the coordinated development of cortical convolutions in schizophrenia. The heterogeneity in the severity of schizophrenia could be explained in part by aberrant trajectories of neurodevelopment.
| S-EPMC4481329 | biostudies-literature
Project description:Anhedonia is a common symptom in schizophrenia and is closely related to poor functional outcomes. Several lines of evidence reveal that the orbitofrontal cortex plays an important role in anhedonia. In the present study, we aimed to investigate abnormalities in structural covariance within the orbitofrontal subregions, and to further study their role in anticipatory and consummatory anhedonia in schizophrenia. T1 images of 35 schizophrenia patients and 45 healthy controls were obtained. The cortical thickness of 68 cerebral regions parcellated by the Desikan-Killiany (DK) atlas was calculated. The structural covariance within the orbitofrontal subregions was calculated in both schizophrenia and healthy control groups. Stepwise linear regression was performed to examine the relationship between structural covariance and anhedonia in schizophrenia patients. Patients with schizophrenia exhibited higher structural covariance between the left and right medial orbitofrontal thickness, the left lateral orbitofrontal thickness and left pars orbitalis thickness compared to healthy controls (p < 0.05, FDR corrected). This results imply that the increased structural covariance in orbitofrontal thickness may be involved in the process of developing anhedonia in schizophrenia. The result indicated that the increased structural covariance between the left and right medial orbitofrontal thickness might be a protective factor for anticipatory pleasure (B' = 0.420, p = 0.012).
| S-EPMC10073085 | biostudies-literature
Project description:Neuroimaging studies of patients with amyotrophic lateral sclerosis (ALS) have shown widespread alterations in structure, function, and connectivity in both motor and non-motor brain regions, suggesting multi-systemic neurobiological abnormalities that might impact large-scale brain networks. Here, we examined the alterations in the topological organization of structural covariance networks of ALS patients (N = 60) compared with normal controls (N = 60). We found that structural covariance networks of ALS patients showed a consistent rearrangement towards a regularized architecture evidenced by increased path length, clustering coefficient, small-world index, and modularity, as well as decreased global efficiency, suggesting inefficient global integration and increased local segregation. Locally, ALS patients showed decreased nodal degree and betweenness in the gyrus rectus and/or Heschl's gyrus, and increased betweenness in the supplementary motor area, triangular part of the inferior frontal gyrus, supramarginal gyrus and posterior cingulate cortex. In addition, we identified a different number and distribution of hubs in ALS patients, showing more frontal and subcortical hubs than in normal controls. In conclusion, we reveal abnormal topological organization of structural covariance networks in ALS patients, and provide network-level evidence for the concept that ALS is a multisystem disorder with a cerebral involvement extending beyond the motor areas.
| S-EPMC6411656 | biostudies-literature
Project description:Here we test the hypothesis that the neurodegenerative process in Parkinson's disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n?=?105) and matched controls (n?=?57) underwent T1-MRI at entry and 1 year later as part of the Parkinson's Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical thinning is correlated to connectivity (measured functionally or structurally) to a "disease reservoir" evaluated by MRI at baseline. The atrophy pattern in the ventral frontal lobes resembles one described in certain cases of Alzheimer's disease. Our findings suggest that disease propagation to the cortex in PD follows neuronal connectivity and that disease spread to the cortex may herald the onset of cognitive impairment.
| S-EPMC5750227 | biostudies-literature