An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report
Major depressive disorder (MDD) is considered a highly heterogeneous clinical and neurobiological mental disorder. We employed a novel layered treatment design to investigate whether cortical thickness features at baseline differentiated treatment responders from non-responders after 8 and 16 weeks...
| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2020-01-01
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| Series: | NeuroImage: Clinical |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213158220300127 |
| _version_ | 1819092898620112896 |
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| author | Jee Su Suh Luciano Minuzzi Pradeep Reddy Raamana Andrew Davis Geoffrey B. Hall Jacqueline Harris Stefanie Hassel Mojdeh Zamyadi Stephen R. Arnott Gésine L. Alders Roberto B. Sassi Roumen Milev Raymond W. Lam Glenda M. MacQueen Stephen C. Strother Sidney H. Kennedy Benicio N. Frey |
| author_facet | Jee Su Suh Luciano Minuzzi Pradeep Reddy Raamana Andrew Davis Geoffrey B. Hall Jacqueline Harris Stefanie Hassel Mojdeh Zamyadi Stephen R. Arnott Gésine L. Alders Roberto B. Sassi Roumen Milev Raymond W. Lam Glenda M. MacQueen Stephen C. Strother Sidney H. Kennedy Benicio N. Frey |
| author_sort | Jee Su Suh |
| collection | DOAJ |
| description | Major depressive disorder (MDD) is considered a highly heterogeneous clinical and neurobiological mental disorder. We employed a novel layered treatment design to investigate whether cortical thickness features at baseline differentiated treatment responders from non-responders after 8 and 16 weeks of a standardized sequential antidepressant treatment. Secondary analyses examined baseline differences between MDD and controls as a replication analysis and longitudinal changes in thickness after 8 weeks of escitalopram treatment. 181 MDD and 95 healthy comparison (HC) participants were studied. After 8 weeks of escitalopram treatment (10–20 mg/d, flexible dosage), responders (>50% decrease in Montgomery-Åsberg Depression Scale score) were continued on escitalopram; non-responders received adjunctive aripiprazole (2–10 mg/d, flexible dosage). MDD participants were classified into subgroups according to their response profiles at weeks 8 and 16. Baseline group differences in cortical thickness were analyzed with FreeSurfer between HC and MDD groups as well as between response groups. Two-stage longitudinal processing was used to investigate 8-week escitalopram treatment-related changes in cortical thickness. Compared to HC, the MDD group exhibited thinner cortex in the left rostral middle frontal cortex [MNI(X,Y,Z=−29,9,54.5,−7.7); CWP=0.0002]. No baseline differences in cortical thickness were observed between responders and non-responders based on week-8 or week-16 response profile. No changes in cortical thickness was observed after 8 weeks of escitalopram monotherapy. In a two-step 16-week sequential clinical trial we found that baseline cortical thickness does not appear to be associated to clinical response to pharmacotherapy at 8 or 16 weeks. Keywords: Major depressive disorder, Cortical thickness, Structural neuroimaging, Antidepressant response, Clinical trial |
| first_indexed | 2024-12-21T23:02:56Z |
| format | Article |
| id | doaj.art-997e5e73ebcd4e20875b34d834f278fe |
| institution | Directory Open Access Journal |
| issn | 2213-1582 |
| language | English |
| last_indexed | 2024-12-21T23:02:56Z |
| publishDate | 2020-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | NeuroImage: Clinical |
| spelling | doaj.art-997e5e73ebcd4e20875b34d834f278fe2022-12-21T18:47:15ZengElsevierNeuroImage: Clinical2213-15822020-01-0125An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study reportJee Su Suh0Luciano Minuzzi1Pradeep Reddy Raamana2Andrew Davis3Geoffrey B. Hall4Jacqueline Harris5Stefanie Hassel6Mojdeh Zamyadi7Stephen R. Arnott8Gésine L. Alders9Roberto B. Sassi10Roumen Milev11Raymond W. Lam12Glenda M. MacQueen13Stephen C. Strother14Sidney H. Kennedy15Benicio N. Frey16Neuroscience Graduate Program, McMaster University, Hamilton, ON, Canada; Mood Disorders Program and Women's Health Concerns Clinic, St. Joseph's Healthcare Hamilton, Hamilton, ON, CanadaNeuroscience Graduate Program, McMaster University, Hamilton, ON, Canada; Mood Disorders Program and Women's Health Concerns Clinic, St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada; Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, CanadaRotman Research Institute, Baycrest Health Sciences; Department of Medical Biophysics, University of Toronto, Toronto, ON, CanadaDepartment of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, ON, CanadaDepartment of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, ON, CanadaDepartment of Computing Science, University of Alberta, Edmonton, AB, CanadaDepartment of Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Mathison Centre for Mental Health Research and Education, University of Calgary, Calgary, AB, CanadaRotman Research Institute, Baycrest Health Sciences; Department of Medical Biophysics, University of Toronto, Toronto, ON, CanadaRotman Research Institute, Baycrest Health Sciences; Department of Medical Biophysics, University of Toronto, Toronto, ON, CanadaNeuroscience Graduate Program, McMaster University, Hamilton, ON, Canada; Mood Disorders Program and Women's Health Concerns Clinic, St. Joseph's Healthcare Hamilton, Hamilton, ON, CanadaDepartment of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, CanadaDepartments of Psychiatry and Psychology, Queen's University and Providence Care Hospital, Kingston, ON, CanadaDepartment of Psychiatry, University of British Columbia, Vancouver, BC, CanadaDepartment of Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Mathison Centre for Mental Health Research and Education, University of Calgary, Calgary, AB, CanadaRotman Research Institute, Baycrest Health Sciences; Department of Medical Biophysics, University of Toronto, Toronto, ON, CanadaCanadian Biomarker Integration Network for Depression, St. Michael's Hospital, Toronto, ON, Canada; Department of Psychiatry, University of Toronto, Toronto, ON, CanadaNeuroscience Graduate Program, McMaster University, Hamilton, ON, Canada; Mood Disorders Program and Women's Health Concerns Clinic, St. Joseph's Healthcare Hamilton, Hamilton, ON, Canada; Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, Canada; Corresponding author at: 100 West 5th Street, Suite C124, Hamilton, ON L8N 3K7 Canada.Major depressive disorder (MDD) is considered a highly heterogeneous clinical and neurobiological mental disorder. We employed a novel layered treatment design to investigate whether cortical thickness features at baseline differentiated treatment responders from non-responders after 8 and 16 weeks of a standardized sequential antidepressant treatment. Secondary analyses examined baseline differences between MDD and controls as a replication analysis and longitudinal changes in thickness after 8 weeks of escitalopram treatment. 181 MDD and 95 healthy comparison (HC) participants were studied. After 8 weeks of escitalopram treatment (10–20 mg/d, flexible dosage), responders (>50% decrease in Montgomery-Åsberg Depression Scale score) were continued on escitalopram; non-responders received adjunctive aripiprazole (2–10 mg/d, flexible dosage). MDD participants were classified into subgroups according to their response profiles at weeks 8 and 16. Baseline group differences in cortical thickness were analyzed with FreeSurfer between HC and MDD groups as well as between response groups. Two-stage longitudinal processing was used to investigate 8-week escitalopram treatment-related changes in cortical thickness. Compared to HC, the MDD group exhibited thinner cortex in the left rostral middle frontal cortex [MNI(X,Y,Z=−29,9,54.5,−7.7); CWP=0.0002]. No baseline differences in cortical thickness were observed between responders and non-responders based on week-8 or week-16 response profile. No changes in cortical thickness was observed after 8 weeks of escitalopram monotherapy. In a two-step 16-week sequential clinical trial we found that baseline cortical thickness does not appear to be associated to clinical response to pharmacotherapy at 8 or 16 weeks. Keywords: Major depressive disorder, Cortical thickness, Structural neuroimaging, Antidepressant response, Clinical trialhttp://www.sciencedirect.com/science/article/pii/S2213158220300127 |
| spellingShingle | Jee Su Suh Luciano Minuzzi Pradeep Reddy Raamana Andrew Davis Geoffrey B. Hall Jacqueline Harris Stefanie Hassel Mojdeh Zamyadi Stephen R. Arnott Gésine L. Alders Roberto B. Sassi Roumen Milev Raymond W. Lam Glenda M. MacQueen Stephen C. Strother Sidney H. Kennedy Benicio N. Frey An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report NeuroImage: Clinical |
| title | An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report |
| title_full | An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report |
| title_fullStr | An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report |
| title_full_unstemmed | An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report |
| title_short | An investigation of cortical thickness and antidepressant response in major depressive disorder: A CAN-BIND study report |
| title_sort | investigation of cortical thickness and antidepressant response in major depressive disorder a can bind study report |
| url | http://www.sciencedirect.com/science/article/pii/S2213158220300127 |
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