Neurobiology of Depression in Relation to ECT. PJ Cowen Department of Psychiatry, University of Oxford

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1 Neurobiology of Depression in Relation to ECT PJ Cowen Department of Psychiatry, University of Oxford

2 Causes of Depression Genetic Childhood experience Life Events (particularly losses) Life Difficulties (social disadvantage) Neurotic temperament Dysfunctional attitudes (low self-esteem, perfectionism etc) Physical illness Substance misuse Previous history of depression

3 Pathophysiology of Depression Genetic- few current clues from molecular studies Abnormal cognitions (negative emotional bias) Cortisol hypersecretion Neurochemical- monoamines, glutamate and GABA Loss of synaptic plasticity and decreased neurogenesis- Volume loss of brain tissue Abnormalities in neural circuitry involved in experience and regulation of mood

4 From: Subtype-Specific Alterations of γ-aminobutyric Acid and Glutamate in Patients With Major Depression Arch Gen Psychiatry. 2004;61(7): doi: /archpsyc Figure Legend: Occipital cortex γ-aminobutyricacid (GABA) concentrations for all subjects in the combined data set brokendown by DSM-IV subtypes of major depressive disorder.boxed symbols represent subjects who also met the criteria for psychotic features. Date of download: 11/20/2014 Copyright 2014 American Medical Association. All rights reserved.

5 Effects of ECT and CBT on Brain GABA in Depressed Patients Measured by MRS Sanacora et al 2003; 2006

6 GABA and Depression Decreased GABA in brain measured by MRS Reduced levels of GABA interneurones in postmortem studies of depressed patients Increased cortical excitability (TMS) Increased resting state activity of midline brain neural networks ECT probably increases brain GABA Sanacora 2010

7 Brain Atrophy in Depression Atrophy of the Hippocampus in Depression Normal Depression Bremner JD, et al. Am J Psychiatry( 2000)

8 MRI Studies in Depression Meta-analysis by Arnone et al (2011) 101 studies-4000 patients This comprehensive meta-analysis of morphometric studies suggests that individuals with unipolar depression are characterised by volume reductions in the frontal cortex, orbitofrontal cortex, hippocampus, cingulate cortex and striatum, and an excess of white matter lesion volumes in comparison with healthy controls. Volume reductions were positively associated with length and severity of illness and age of onset

9 Cellular Pathology and Loss of Brain Volume Current theories associate loss of brain volume with cellular pathology including: Loss of neurones and glia (increased apoptosis) Decreased neuronal plasticity and synaptic density Decreased neurogenesis

10 Beyond Synapse: 5-HT and NA Aid BDNF Synthesis (Preclinical Evidence) = inhibitory Adapted from Manji HK, et al. Biol Psychiatry 2003;53(8): Tsankova NM, et al. Nat Neurosci 2006.

11 Arc mrna (fold change) Role of neural plasticity in depression pathophysiology (clinical imaging and post-mortem studies) Decreased hippocampal volume in depression Reduced neuron and glial cell density Decreased markers of plasticity (Arc, BDNF) Decreased synaptic numbers Neural plasticity marker in PFC Synapse density in PFC Control * Unmedicat ed Medicated Spine synapses per µm Control s MDD * *p<0.05 MDD, major depressive disorder Covington HE 3rd et al. J Neurosci 2010;30: ; Price JL, Drevets WC. Trends Cogn Sci 2012;16:61-71; Kang HJ et al. Nat Med 2012;18;1413-7

12 ECT and Neural Plasticity In experimental animals ECT increases markers of neuronal plasticity (BDNF and Arc) and increases neurogenesis in hippocampus. ECT increases serum BDNF in depressed patients Drivig et al, 2012; Taliaz et al, 2013; Brunoni et al 2014

13 ECT and Brain volume in Depression Dukart J et al. PNAS 2014;111: by National Academy of Sciences

14 Activity-dependent plasticity Neural plasticity hypothesis of antidepressant action Electroconvulsive therapy Psychotherapy Depression due to a failure in neural plasticity Antidepressants act by increasing neural plasticity Failure to trigger neural plasticity underlies treatment resistance Facilitation in neural plasticity leads to treatment augmentation General concept Castrén E. Nat Rev Neurosci 2005;6:241-6

15 Neural Circuitry in Depression- Functional Imaging Overactivity of limbic system (emotional perception and automatic appraisal) Underactivity of cortical regulatory regions (dorsolateral prefrontal cortex) Increased resting state activity of default mode network (medial temporal, medial cortical, posterior cingulate, parietal coretx).

16 Figure 1 Neural systems of relevance to major depressive disorder Key neural regions implicated in emotion and reward processing, and voluntary and automatic regulation of emotion are shown superimposed on a greyscale depiction of the human brain. DLPFC=d... David J Kupfer, Ellen Frank, Mary L Phillips Major depressive disorder: new clinical, neurobiological, and treatment perspectives The Lancet Volume 379, Issue

17 Connectivity map from the dorsal nexus to all of the voxels in the brain. Sheline Y I et al. PNAS 2010;107: by National Academy of Sciences

18 Functional connectivity in severely depressed patients before ECT (displayed in orange) and persisting connectivity after ECT (displayed in cyan), showing a substantial reduction in cortical connectivity after ECT treatment Perrin J S et al. PNAS 2012;109: by National Academy of Sciences

19 Conclusions Much is known about the social and personal antecedents of mood disorders but the neurobiology is only just starting to be elucidated. Scientific approaches to the neurobiology of depression have moved from the focus on a single neurotransmitter to notions of system level disruption based on deficient neuroplasticity accompanied by brain volume loss in regions critical to emotional regulation. This provides new ways of thinking about the action of ECT based on changes in neuroplasticity as well as effects mediated through changes in the connectivity of neural networks.

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