Nouvelle version 22/04/2009 1 Chronic and treatment-resistant depression : a study using arterial spin labeling perfusion MRI at 3 tesla. Bérengère Duhameau a and Jean-Christophe Ferré b , Pierre Jannin d,e,f , Jean-Yves Gauvrit b , Marc Vérin c , Bruno Millet a , Dominique Drapier a Departments of Psychiatry a , Neuroradiology b and Neurology c , CHU Rennes, France INSERM, U746, Faculté de Médecine CS34317, F-35043 d , Rennes, France INRIA, VisAGeS Unité/Projet, F-35042 e , Rennes, France Université Rennes I, CNRS, UMR6074, IRISA, F-35042 f , Rennes, France 1. Introduction Chronicity in depressive illness is estimated at 20%, and to this day, despite the development of new antidepressant drugs, failures are observed in approximately 30% of treated cases (Thase, 2001). Treatment-resistant depression is defined as a major depressive disorder (MDD) which fails to respond to antidepressant treatment or which does not evolve favorably under the influence of this treatment (Thase et al., 2001). Treatment resistance is currently studied using a multi-dimensional approach. Several levels of resistance have been defined, on the basis of the number of antidepressant trials the class of drugs, and their administration in adequate doses and for sufficient durations (Drevets, 2000). Physical treatment by electroconvulsive therapy is also taken into account. Recent studies using neuroimaging techniques have led to a better understanding of the depressive disease pathophysiology and have redefined the neurobiological hypothesis of depression (Brody et al., 2001a; Drevets, 2000; Tekin and Cummings, 2002). This hypothesis is based on the existence of dysfunctional cortico-subcortical circuits. The anterior cingulate cortex (ACC) has become a particular area of interest in depression research. Morphological and functional imaging studies using positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) with the blood oxygen level dependent (BOLD) effect have revealed dysfunction in this region (Ballmaier et al., 2004; Drevets et al., 1997; George et al., 1997; Liotti et al., 2002; Mayberg et al., 1997). Some studies have identified the subgenual ACC (sACC) as the focus of this dysfunction. The sACC is the ventral part of the ACC, located beneath the genu of the corpus callosum, and corresponds primarily to Brodmann’s area (BA) 25. This area is also called Cg 25. In addition to showing reduced inserm-00546501, version 1 - 14 Dec 2010 Author manuscript, published in "Psychiatry Research / Psychiatric Research 2010;182(2):111-6" DOI : 10.1016/j.pscychresns.2010.01.009