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Signal Attenuation as a Rat Model of Obsessive Compulsive Disorder
Published on: January 9, 2015
Hippocampal and amygdala subfield volumes in obsessive-compulsive disorder by medication status
Ziphozihle Ntwatwa1, Christine Lochner2, Annerine Roos2
1From the Department of Psychiatry & Mental Health, Neuroscience Institute, University of Cape Town, Cape Town, South Africa (Ntwatwa, Roos, Sevenoaks, van Honk, Groenewold, Stein, Ipser); the SAMRC Unit on Risk & Resilience in Mental Disorders, Department of Psychiatry, Stellenbosch University, Stellenbosch, South Africa (Lochner); the Department of Psychology, Utrecht University, Utrecht, The Netherlands (van Honk); the Department of Psychiatry and Department of Anatomy & Neuroscience, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands (Veltman, van den Heuvel); the Compulsivity Impulsivity and Attention program, Amsterdam Neuroscience, Amsterdam, The Netherlands (Veltman, van den Heuvel); the Bellvitge Biomedical Research Institute-IDIBELL, Department of Psychiatry, Bellvitge University Hospital, Department of Clinical Sciences, Bellvitge Campus, Universitat de Barcelona-UB, CIBERSAM, Carlos III Health Institute, Madrid, Spain (Menchón); the Bellvitge Biomedical Research Institute-IDIBELL, Department of Psychiatry, Bellvitge University Hospital, Department of Social Psychology and Quantitative Psychology, Institute of Neurosciences, Universitat de Barcelona-UB, CIBERSAM, Carlos III Health Institute, Madrid, Spain ( Soriano-Mas); the Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Mataix-Cols); the Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden (Mataix-Cols); the Department of Clinical Sciences, Lund University, Lund, Sweden (Mataix-Cols); the Department of Psychiatry, Graduate School of Medical Science, Kyoto Prefectural University of Medicine (Nakamae); the Institute of Human Behavioral Medicine Psychiatry, Department of Psychiatry, Seoul National University College of Medicine, Seoul, South Korea (Choi, Kim, Kwon); the Department of Brain and Cognitive Sciences, Seoul National University College of Natural Sciences, Seoul, Republic of Korea (Choi); the Department of Psychiatry, Faculty of Medicine, University of São Paulo, São Paulo, Brazil (Batistuzzo, Hoexter, Miguel); the Department of Methods and Techniques in Psychology, Pontifical Catholic University, São Paulo, SP, Brazil (Batistuzzo); the SAMRC Unit on Risk & Resilience in Mental Disorders, Department of Psychiatry, University of Cape Town, Cape Town, South Africa (Stein) ziphozihle.ntwatwa@uct.ac.za.
Background:
Although it has been suggested that the hippocampus and amygdala (HA) are involved in the neurobiology of obsessive-compulsive disorder (OCD), volumetric findings have been inconsistent, and little work has been undertaken on the volumetry of the heterogeneous anatomic units of HA, with their specific functions and cytoarchitecture, in OCD. We sought to explore potential sources of heterogeneity in brain volumes by performing a separate analysis for people with and without psychotropic medication use, as well as the association of subfield volumes with OCD symptom severity.
Methods:
We segmented T 1-weighted images from people with OCD and healthy controls in the OCD Brain Imaging Consortium to produce 12 hippocampal subfields and 9 amygdala subfields using Free-Surfer 6.0. We assessed between-group differences in subfield volume using a mixed-effects model adjusted for age and quadratic effects of age, sex, site, and whole HA volume. We also performed subgroup analyses to examine subfield volume in relation to comorbid anxiety and depression, medication status, and symptom severity. We corrected all analyses for multiple comparisons using the false discovery rate (FDR).
Results:
We included images from 381 people with OCD and 338 healthy controls. These groups did not significantly differ in HA subfield volumes. However, medicated people with OCD had significantly smaller volumes in the hippocampal dentate gyrus (p FDR = 0.04, d = -0.26) and molecular layer (p FDR = 0.04, d = -0.29), and larger volumes in the lateral (p FDR = 0.049, d = 0.23) and basal (p FDR = 0.049, d = 0.25) amygdala subfields, than healthy controls. Unmedicated people with OCD had significantly smaller volumes in the hippocampal cornu ammonis sector 1 (p FDR = 0.02, d = -0.28) than controls. We did not detect associations between any subfield volume and OCD severity.
Limitations:
We used cross-sectional data, which limits the interpretation of our analysis.
Conclusion:
Differences in HA subfields between people with OCD and healthy controls are dependent on medication status, in line with previous work on other brain volumetric alterations in OCD. This emphasizes the importance of considering psychotropic medication in neuroimaging studies of OCD.
