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Structural Neuroimaging in Anorexia ...

Miles, Amy E.

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Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls./
Author:	Miles, Amy E.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:	198 p.
Notes:	Source: Dissertations Abstracts International, Volume: 80-06, Section: B.
Contained By:	Dissertations Abstracts International80-06B.
Subject:	Neurosciences. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10937369
ISBN:	9780438684324

Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls.
Miles, Amy E.

Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 198 p.

Source: Dissertations Abstracts International, Volume: 80-06, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2018.

This item must not be sold to any third party vendors.

Background: Anorexia nervosa (AN) is a heritable psychiatric disorder characterized by starvation and emaciation. Although AN is widely considered a brain-based disease, its neuroanatomical correlates are poorly understood. As such, we aim to characterize cortical surface architecture and white matter microstructure in acute and remitted patients (acAN, recAN), their unaffected sisters (sibAN), and unrelated healthy controls (HC). Methods: Neuroimaging and assessment data was collected from 84 women (24 acAN, 24 recAN, 12 sibAN, 24 HC). T1/diffusion-weighted MRI data was acquired on a 3T GE scanner with 60 gradient directions, and it was processed with Freesurfer and FSL pipelines. Group differences in vertex/voxel-wise cortical thickness (CT), cortical surface area (CSA), local gyrification index (LGI), fractional anisotropy (FA), and mean diffusivity (MD) were tested with separate univariate analyses of covariance. Relationships among vertex/voxel-wise CT, CSA, FA, and MD and empirical measures of clinical and cognitive impairment were tested with separate linear regressions. Results: We detected significant group differences in CT in frontal and temporal regions (acAN < recAN, HC), LGI in frontal and frontoparietal regions (recAN < acAN, HC; acAN HC). We also detected significant associations between CSA in frontotemporal regions and an index of psychosocial impairment (r = -0.617) and FA in major white matter tracts and an index of cognitive impairment (r = -0.561). Conclusions: Site-specific cortical thinning and hypogyrification appear state-dependent and starvation-driven, and we propose cellular remodeling as a mechanism of action. Site-specific dysgyrification and white matter impairment appear trait-based and developmental in origin, and we propose atypical cortical expansion, altered myelination, and systemic inflammation as mechanisms of action. Variations in cortical surface architecture and white matter microstructure in regions subserving affective and cognitive processing could contribute to AN vulnerability and manifestation.

ISBN: 9780438684324Subjects--Topical Terms:

588700
Neurosciences.

Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls.
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245 1 0 $a Structural Neuroimaging in Anorexia Nervosa: Cortical Surface Architecture and White Matter Microstructure in Acute and Remitted Patients, their Unaffected Sisters, and Unrelated Healthy Controls.
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300 $a 198 p.
500 $a Source: Dissertations Abstracts International, Volume: 80-06, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
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502 $a Thesis (Ph.D.)--University of Toronto (Canada), 2018.
506 $a This item must not be sold to any third party vendors.
520 $a Background: Anorexia nervosa (AN) is a heritable psychiatric disorder characterized by starvation and emaciation. Although AN is widely considered a brain-based disease, its neuroanatomical correlates are poorly understood. As such, we aim to characterize cortical surface architecture and white matter microstructure in acute and remitted patients (acAN, recAN), their unaffected sisters (sibAN), and unrelated healthy controls (HC). Methods: Neuroimaging and assessment data was collected from 84 women (24 acAN, 24 recAN, 12 sibAN, 24 HC). T1/diffusion-weighted MRI data was acquired on a 3T GE scanner with 60 gradient directions, and it was processed with Freesurfer and FSL pipelines. Group differences in vertex/voxel-wise cortical thickness (CT), cortical surface area (CSA), local gyrification index (LGI), fractional anisotropy (FA), and mean diffusivity (MD) were tested with separate univariate analyses of covariance. Relationships among vertex/voxel-wise CT, CSA, FA, and MD and empirical measures of clinical and cognitive impairment were tested with separate linear regressions. Results: We detected significant group differences in CT in frontal and temporal regions (acAN < recAN, HC), LGI in frontal and frontoparietal regions (recAN < acAN, HC; acAN HC). We also detected significant associations between CSA in frontotemporal regions and an index of psychosocial impairment (r = -0.617) and FA in major white matter tracts and an index of cognitive impairment (r = -0.561). Conclusions: Site-specific cortical thinning and hypogyrification appear state-dependent and starvation-driven, and we propose cellular remodeling as a mechanism of action. Site-specific dysgyrification and white matter impairment appear trait-based and developmental in origin, and we propose atypical cortical expansion, altered myelination, and systemic inflammation as mechanisms of action. Variations in cortical surface architecture and white matter microstructure in regions subserving affective and cognitive processing could contribute to AN vulnerability and manifestation.
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