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Orbitomedial Prefrontal Cortex and Beyond

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Orbitomedial Prefrontal Cortex and Beyond Neuroimaging markers of major depressive disorder: orbitomedial prefrontal cortex and beyond Citation for published version (APA): Samara, Z. (2015). Neuroimaging markers of major depressive disorder: orbitomedial prefrontal cortex and beyond. Boekenplan. https://doi.org/10.26481/dis.20151106zs Document status and date: Published: 01/01/2015 DOI: 10.26481/dis.20151106zs Document Version: Publisher's PDF, also known as Version of record Please check the document version of this publication: • A submitted manuscript is the version of the article upon submission and before peer-review. There can be important differences between the submitted version and the official published version of record. People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher's website. • The final author version and the galley proof are versions of the publication after peer review. • The final published version features the final layout of the paper including the volume, issue and page numbers. 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If the publication is distributed under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license above, please follow below link for the End User Agreement: www.umlib.nl/taverne-license Take down policy If you believe that this document breaches copyright please contact us at: [email protected] providing details and we will investigate your claim. Download date: 30 Sep. 2021 Neuroimaging Markers of Major Depressive Disorder: Orbitomedial Prefrontal Cortex and beyond Neuroimaging Markers of Major Depressive Disorder: Orbitomedial Prefrontal Cortex and beyond DISSERTATION to obtain the degree of Doctor at Maastricht University, on the authority of the Rector Magnificus,, Prof. Dr. L.L.G. Soete in accordance with the decision of the Board of Deans, to be defended in public on Friday 6th November 2015 at 10:00 o’clock by Zoe (Zoi) Samara born on the 16th of June 1977 in Thessaloniki, Greece Promotor: Prof. dr. J.G. Ramaekers (Maastricht University) Copromotors Dr. P. Stiers (Maastricht University) Dr. E.A.T. Evers (Maastricht University) Assessment Committee: Prof. dr. W. Riedel (chair; Maastricht University) Prof. dr. T. van Amelsvoort (Maastricht University) Prof. dr. R. Goebel (Maastricht University) Prof. dr. D. Margulies (Max Planck Institute) Prof. dr. S. Rombouts (Universiteit Leiden) © Zoe (Zoi) Samara, Maastricht 2015 Publisher Boekenplan, Maastricht ISBN 978 90 8666 391 0 All rights reserved Contents Chapter 1 Introduction 7 Chapter 2 Human orbitomedial prefrontal cortex: Intrinsic connectivity parcellation and functional organization 21 Chapter 3 Orbitomedial prefrontal cortex functional connectivity markers of Major Depression vulnerability and disease 69 Chapter 4 Altered face processing in Major Depression Vulnerability: Inhabiting different social worlds? 109 Chapter 5 Discussion 143 Summary 151 Addendum Knowledge valorization 153 Curriculum Vitae & Publications 156 Acknowledgements 158 Chapter 1 Introduction “What is depression like?” he whispered “It’s like drowning. Except you can see everyone around you breathing” 7 Chapter 1 1. Background Major Depressive Disorder syndrome Major Depressive Disorder (MDD) is a psychiatric syndrome affecting 4.7% of the population worldwide and women twice as often as men (Ferrari et al., 2013). According to DSM-IV TR (APA, 1994), MDD is diagnosed as the experience of episodes of persistent negative mood or anhedonia accompanied by at least four of the following somatic, affective or cognitive symptoms: significant weight changes, sleep disturbances, psychomotor agitation or retardation, fatigue, feelings of worthlessness or excessive guilt, indecisiveness and recurrent suicidal thoughts. The symptoms must be present for a minimum of 2 weeks, represent a marked change from previous functioning and cause significant distress. This definition of MDD emerged from efforts in psychiatry to formulate objective and reliable criteria to guide diagnosis in clinical and research settings. Although these diagnostic criteria are useful in practice, it should be emphasized that MDD is not the negative, pessimistic mood or anhedonic state per se; negative or "down" states are commonly experienced by otherwise healthy people during normal mood variations or in response to stressful experiences and significant life changes. Rather, MDD is better defined as a proclivity or susceptibility of the individual to enter such “down” states, coupled with an inability to successfully up- regulate his/her mood and disengage from the downward spiral of physiological and psychological events which subsequently unfolds (Holtzheimer & Mayberg, 2011). Subjectively, MDD presents as a negative view of the self, the world and the future (Beck’s famous cognitive triad; Beck, 2008) and negative, dysfunctional self-schemata (maladaptive internal representations of ideas or experiences related to one’ s self) are at the core of its clinical picture. The average age of MDD onset is around 32 years but MDD occurs also frequently in adolescent or early adulthood (Ferrari et al., 2013). The course of MDD can be episodic or chronic, with or without full symptomatic remission between the episodes, resulting in a quite variable clinical picture in each individual (Figure 1). MDD is associated with significant personal, societal and financial costs for both the sufferer and his/her immediate and extended social circle. It is projected to be the first overall contributor to the worldwide burden of disease in 2030 (Holtzheimer & Mayberg, 2011). MDD is often comorbid with other mental and physical health conditions (Ferrari et al., 2013), the most impactful of which is the decision of the sufferer to end his/her life, occurring 21% more often during depressive episodes (Holma et al., 2010). 8 Introduction Figure 1. Graphical depiction of the variable course of MDD. The horizontal axis plots the time-course over lifespan and the vertical axis plots clinically significant mood variations. a) Recurrent MDD with 2 episodes, b) dysthymic disorder, c) single MDD episode superimposed on antecedent dysthymic disorder (“double depression”), d) chronic MDD episode, e) MDD episode in partial remission and f) recurrent MDD with 2 episodes (similar to a) but without full inter-episode recovery. Figure originally published in Klein (2010). Early diagnosis and individually tailored treatment is instrumental for the alleviation of MDD. However, MDD patients frequently remain un- or misdiagnosed long past their first depressive episode (van Rijswijk et al., 2009), getting caught up amidst contradicting evaluations by general practitioners, psychologists, psychiatrists and health staff in general. Even when correctly diagnosed, MDD patients often undergo multiple unsuccessful treatment attempts. First-line MDD treatments are psychotherapy, predominantly cognitive-behavioral interventions and pharmacotherapy with various types of antidepressants. Efficacy rates of MDD treatment are sobering. Initial treatment response to the currently most commonly used antidepressant class, selective serotonin reuptake inhibitors, ranges between 40-60%. Full remission is achieved only by 30-45% of the treatment responders (Carvalho et al., 2007) while 1/3 of the patients under therapy develops recurrent symptoms (Souery et al., 2006). Given all these, it is common for MDD patients to have tried various kinds of treatments and several combinations of mono- and adjunct therapy. Alternative types of treatment for moderate depression include repetitive transcranial magnetic stimulation (rTMS) of the dorsolateral prefrontal cortex and lifestyle changes such as exercise, light therapy and dietary supplements. Severe, refractory MDD is treated with electroconvulsive therapy (see Figure 2 for the course of 9 Chapter 1 treatment attempts of MD patients). The efficacy of new treatments such as neuro-feedback therapy, vagus nerve stimulation and deep brain stimulation (DBS) in the subgenual cingulate and other brain regions is currently tested in randomized control trials. Figure 2. Average course of treatment attempts for MDD. SSRI (Selective Serotonin Reuptake Inhibitor); SNRI (Serotonin Norepinephrine Reuptake Inhibitor); NDRI (Norepinephrine Dopamine Reuptake Inhibitor); MAOI (Mono Amine Oxidase Inhibitor); TCA (Tricyclic Antidepressant); ECT (Electro Convulsive Therapy); VNS (Vagus Nerve Stimulation). Figure originally published in Kessler et al., (2005). MDD etiology and genetic influences The etiology of MDD is multifactorial but it has been established that genetic load influences the development of the syndrome. MDD heritability estimates in monozygotic twins range between 40% and 50% (Sullivan et al., 2000) while other first-degree relatives of MDD patients run a 2-5% higher risk of developing MDD themselves, depending on the severity and
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