Room 151 AG

16:00 - 18:00

Moderators:

Stefan Sunaert, Steven C. R. Williams

Han Yuan¹, Vadim Zotev¹, Raquel Phillips¹, Kymberly D. Young¹, Masaya Misaki¹, and Jerzy Bodurka^1,2
1Laureate Institute for Brain Research, Tulsa, OK, United States, ²College of Engineering, University of Oklahoma, Norman, OK, United States

We acquired simultaneous EEG and BOLD fMRI in groups of major depressive (MDD) and healthy control subjects. We developed a multimodal analysis approach to investigate the abnormal resting-state default model network (DMN) connectivity in MDD. Our study revealed increased connectivity in the left superior frontal cortex, bilateral middle temporal gyri, and medial prefrontal cortex and decreased connectivity in the posterior cingulate cortex. Furthermore, joint analysis with EEG found that, in the regions with abnormal DMN connectivity, MDD subjects’ score of depression severity are positively correlated with the EEG-microstates-associated BOLD activity, but not with the DMN activity derived from BOLD alone.

Vincent A. Magnotta^1,2, Casey P. Johnson¹, Robin Follmer², Simon Roh¹, and John A. Wemmie^2
1Radiology, The University of Iowa, Iowa City, IA, United States, ²Psychiatry, The University of Iowa, Iowa City, IA, United States

The purpose of this study is to evaluate functional T1rho imaging in panic disorder. We used a visual flashing checkerboard to assess dynamic changes in the T1ρ relaxation parameter within the occipital cortex. In addition, BOLD and 31P spectroscopy were obtained using a similar paradigm. We found a significant increase in T1ρ relaxation in panic subjects as compared to controls during the visual activation task within the cuneus bilaterally and a significant decrease in the anterior cingulate bilaterally. In subjects with panic disorder, we found a significant relationship between the magnitude of the T1rho response and symptoms as measured with the Beck Anxiety Inventory. BOLD imaging did not reveal any significant relationships with symptoms.

Xun Yang¹, Keith Maurice Kendrick², Taolin Chen¹, Bochao Cheng¹, Li Yao¹, Shiguang Li¹, Xiaoqi Huang¹, and Qiyong Gong^1
1Huaxi MR Research Center (HMRRC), West China Hospital of Sichuan University, Chengdu, Sichuan, China, ²Key Laboratory for Neuroinformation, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, Sichuan, China

How to distinguish shyness from social anxiety and trait anxiety has been of great concern to both clinicians and researchers. We assume that shyness should be contributed to by structural and functional changes in the brain and addressed this issue by using voxel-based sMRI and rfMRI to test correlations between brain structure, functional connectivity and shyness and social anxiety. Our results have indeed confirmed the presence of extensive structural and functional connectivity changes in cortical and limbic regions involved with processing social stimuli in shy individuals. And these changes are not associated with social or trait anxiety despite both having some behavioral correlation with shyness.

Yuan Xiao¹, Su Lui¹, Li Yao¹, Teng Xie², Yong He², and Qiyong Gong^1
1Department of Radiology, Huaxi MR Research Center,West China Hospital, Chengdu, Sichuan, China, ²State Key Laboratory of Cognitive Neuroscience and Learning,Beijing Normal University, Beijing, Beijing, China

Synopsis:Cortical thickness was measured to investigate the anatomical deficit in antipsychotic naive first episode schizophrenia. 128 patients and 141 healthy controls were recruited. We employed CIVET software to extract cortical thickness measurements from T1-weighted MRI images. The cortical thinning, especially, the right dorsolateral prefrontal cortex, may be resulted from neuroprogression in schizophrenia. Cortical thickening in bilateral temporal poles and other cortices were also revealed and may result from the compensatory mechanism or abnormal neurodevelopment at early stage of schizophrenia. In addition, a strong link between PANSS scores and cortical thickness displayed a consensus between cerebral structure and clinical manifestations.

David Shin¹, Jerod Rasmussen², Burak Ozyurt¹, Juan Bustillo³, Theodorus GM Van Erp², Jatin Vaidya⁴, Daniel Mathalon⁵, Bryon Mueller⁶, James Voyvodic⁷, Douglas Greve⁸, Judith Ford⁵, Gary H. Glover⁹, Gregory Brown¹, Steven Potkin², and Thomas Liu^1
1University of California, San Diego, La Jolla, CA, United States, ²University of California, Irvine, Irvine, CA, United States, ³University of New Mexico, Albuquerque, NM, United States, ⁴University of Iowa, Iowa City, IA, United States, ⁵University of California, San Francisco, San Francisco, CA, United States, ⁶University of Minnesota, Twin Cities, Minneapolis, MN, United States, ⁷Duke University, Durham, NC, United States, ⁸Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, United States, ⁹Stanford University, Stanford, CA, United States

In this multisite ASL study, we used a standardized FAIR protocol to measure baseline CBF in 112 healthy controls and gender/age matched 122 schizophrenic patients across 6 sites. CBF processing and group analysis were performed by the CBFBIRN Data Analysis and Processing Pipeline (https://cbfbirn.ucsd.edu). Whole-brain gray matter CBF was significantly lower in patients (52.03±1.36 ml/100g-min) compared to healthy controls (55.12±1.36 ml/100g-min). In standard space, voxel-level analysis, schizophrenia was associated with 12 brain regions characterized by hypoperfusion (p<0.01, corrected) including right insula. In contrast, CBF in right putamen was found to be higher with schizophrenia (41.27±1.72 vs. 34.27±1.62 ml/100g-min).

Najib Allaïli^1,2, Romain Valabregue², Malgorzata MarjanskaA^3,4, Pauline Delaveau¹, Éric Bardinet², Maritza Jabourian⁵, Judith LAREDO⁵, Philippe Fossati^1,6, and Stéphane Lehéricy^2,7
1USR 3246, CNRS, Paris, Île-de-France, France, ²Centre de Neuroimagerie de Recherche - CENIR, Institut du Cerveau et de la Moelle épinière - ICM, Paris, Île-de-France, France, ³Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States, ⁴Department of Radiology, University of Minnesota, Minneapolis, MN, United States, ⁵Institut de Recherches Internationales Servier - IRIS, Courbevoie, Île-de-France, France, ⁶Psychiatry, APHP - GH Pitié Salpêtrière, Paris, Île-de-France, France, ⁷UMR-S975 ; Inserm, U975 ; CNRS, UMR 7225, Paris, France, CRICM, Université Pierre et Marie Curie, Paris, Île-de-France, France

In this study, we sought to identify spectroscopic correlates of depressive state and of response to Agomelatine, a new antidepressant with melatonin agonist and 5-HT2C antagonist properties. 21 patients diagnosed with major depressive disorder and 15 matched healthy controls underwent a spectroscopic examination in the left hippocampus before starting a 6-week treatment with Agomelatine. Clinical symptoms were assessed at W0 and W7.

Peiying Liu¹, Bryon Adinoff^2,3, Carol Tamminga², Francesca Filbey⁴, and Hanzhang Lu^1
1Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, Texas, United States, ²Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas, United States, ³VA North Texas Health Care System, Dallas, Texas, United States, ⁴Center For Brain Health, University of Texas at Dallas, Dallas, Texas, United States

Long-term cocaine use is known to negatively impact neural systems. Cerebral metabolic rate of oxygen (CMRO2) is thought to be a direct index of neural activity, but no measurements of brain oxygen metabolism in cocaine-addicted patients has been reported. We used a non-invasive, fast and reliable MR method to examine impact of long-term cocaine use on CMRO2. We sought to answer three questions: 1) is CMRO2 in cocaine-addicted participants significantly different from that in healthy controls? 2) is there a relationship between cocaine use and the severity of metabolic deficit? 3) does the degree of CMRO2 deficit predict cognitive ability?

Milan Scheidegger^1,2, Alexander Fuchs¹, Mick Lehmann², Simone Grimm^2,3, Heinz Boeker², Erich Seifritz², and Anke Henning^1,4
1Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland, ²Clinic of Affective Disorders and General Psychiatry, University Hospital of Psychiatry Zurich, Zurich, Switzerland, ³Cluster Languages of Emotion, Freie Universität Berlin, Berlin, Germany, Germany, ⁴Max Planck Institute for Biological Cybernetics, Tübingen, Germany

Ketamine is a potent glutamatergic NMDA receptor antagonist with rapid antidepressant properties at subanaesthetic doses, thus providing a valuable research tool for the investigation of the neurobiology of major depressive disorder (MDD). This double-blind, randomized, placebo-controlled 1H-MRS study in 13 healthy subjects reveals the neuropharmacological effects of a single intravenous subanaesthetic ketamine infusion on prefrontal aspartate, glutamine and GABA levels in the 3-4 hour post-infusion interval. Our findings are in line with a shift in the excitatory-inhibitory balance following ketamine administration that may play an important role in restoring parts of the disrupted neurometabolic homeostasis in MDD patients.

Steffen Bollmann^1,2, Carmen Ghisleni^1,2, Ruth L. O'Gorman^1,2, Simon S. Poil^1,2, Peter Klaver^2,3, Lars Michels^1,4, Juliane Ball⁵, Dominique Eich-Höchli⁶, Ernst Martin^1,2, and Daniel Brandeis^5,7
1Center for MR-Research, University Children‘s Hospital, Zürich, Switzerland, ²Center for Integrative Human Physiology (ZIHP), University of Zürich, Zürich, Switzerland, ³Institute of Psychology, University of Zürich, Zürich, Switzerland, ⁴Institute of Neuroradiology, University of Zürich, Zürich, Switzerland, ⁵Department of Child & Adolescent Psychiatry, University of Zürich, Zürich, Switzerland, ⁶Psychiatric University Hospital, University of Zürich, Zürich, Switzerland, ⁷Central Institute of Mental Health Mannheim, Medical Faculty Mannheim/ Heidelberg University, Mannheim, Germany

Since working memory deficits play an important role in ADHD we developed a spatial working memory task to examine differences in brain activity between adults and children with ADHD and controls. In a fMRI study we investigated adults and children with and without ADHD to understand the underlying developmental deficits seen in ADHD. Our results suggest that the working memory networks are not yet fully developed in children and that ADHD subjects do not recruit a larger network to handle increased working memory demand, unlike control subjects.

Chun S. Zuo¹, Brent Forester¹, Fei Du¹, and Perry F. Renshaw^2
1McLean Hospital, Belmont, MA, United States, ²The Brain Institute, Dept. of Psychiatry, University of Utah, Salt Lake City, UT, United States

To address possible altered energy metabolism in bipolar disorder (BPD), this study evaluated the effects of an 8-week trial of oral CoEnzyme Q10 for ten individuals with BPD stable on concurrent psychiatric medication using 31P MRS at 4T and weekly clinical mood assessment. CoQ10 treatment was associated with a statistically significant improvement in mood at week 2 and week 4 of treatment. The 31P MRS scan at week 8 found that CoQ10 resulted in an uptrend of creatine kinase activity, measured by kfor, and an increase in the PME/PDE ratio, suggesting alterations in membrane metabolites in bipolar patients.