A brain network model for depression: From symptom understanding to disease intervention

Abstract

Understanding the neural substrates of depression is crucial for diagnosis and treatment. Here, we review recent studies of functional and effective connectivity in depression, in terms of functional integration in the brain. Findings from these studies, including our own, point to the involvement of at least four networks in patients with depression. Elevated connectivity of a ventral limbic affective network appears to be associated with excessive negative mood (dysphoria) in the patients; decreased connectivity of a frontal-striatal reward network has been suggested to account for loss of interest, motivation, and pleasure (anhedonia); enhanced default mode network connectivity seems to be associated with depressive rumination; and diminished connectivity of a dorsal cognitive control network is thought to underlie cognitive deficits especially ineffective top-down control of negative thoughts and emotions in depressed patients. Moreover, the restoration of connectivity of these networks-and corresponding symptom improvement-following antidepressant treatment (including medication, psychotherapy, and brain stimulation techniques) serves as evidence for the crucial role of these networks in the pathophysiology of depression.

Disentangling the Neural Basis of Cognitive Behavioral Therapy in Psychiatric Disorders: A Focus on Depression

“…Such a finding may explain the generation of dysphoria (excessive negative mood) in depressed patients [13,18,19,20,21,22,23,24,25,26]. …”

Modulation of amygdala reactivity following rapidly acting interventions for major depression

“…Though encompassing different brain activation paradigms, based on meta‐analysis of standard pharmacological treatments (Delaveau et al, ; Ma, ), single ketamine administration in depression (Murrough et al, ; Reed et al, ) and in healthy subjects (Scheidegger et al, ; Scheidegger et al, ), we hypothesized that treatment‐related changes in neural activity would also occur in the larger corticolimbic‐striatal face emotion processing network, including in striatal, medial prefrontal/ACC regions, and insula for negative stimuli, and increases in medial prefrontal/ACC regions for positive stimuli. Since ketamine and ECT have different molecular mechanisms of action, are subject to different side effects and may target different symptoms, we also expected that some neural effects would diverge at the systems level especially in regions involved in cognition and memory (Li et al, ; Perrin et al, ; Yrondi, Peran, Sauvaget, Schmitt, & Arbus, ).…”

“…Though encompassing different brain activation paradigms, based on meta-analysis of standard pharmacological treatments (Delaveau et al, 2011;Ma, 2015), single ketamine administration in depression (Murrough et al, 2015;Reed et al, 2019) and in healthy subjects T A B L E 1 Participants demographic information with statistical differences at baseline, and clinical measures for both patient groups (ECT and ketamine) for baseline (TP1) and for after treatment (TP2; 24 to 72 hr after the fourth infusion of ketamine and after the last ECT session) , we hypothesized that treatment-related changes in neural activity would also occur in the larger corticolimbic-striatal face emotion processing network, including in striatal, medial prefrontal/ACC regions, and insula for negative stimuli, and increases in medial prefrontal/ACC regions for positive stimuli. Since ketamine and ECT have different molecular mechanisms of action, are subject to different side effects and may target different symptoms, we also expected that some neural effects would diverge at the systems level especially in regions involved in cognition and memory (Li et al, 2018;Perrin et al, 2012;Yrondi, Peran, Sauvaget, Schmitt, & Arbus, 2018 (Sackeim, 2001). To evaluate emotional processing within and across fast-acting therapies, 27 TRD patients received serial ketamine infusion and 17 patients received an index series of ECT using a nonrandomized naturalistic design.…”

Intrinsic activity temporal structure reactivity to behavioural state change is correlated with depressive symptoms

“…Interestingly, activity within intrinsic networks correlates with reported rumination and is modulated by rumination induced in a task (Berman et al, 2011;Zamoscik et al, 2014;Zhu et al, 2012). Together, these findings appear to point to a functional overlap between the properties of ongoing spontaneous activity and ruminative self-oriented thoughts related to depression (Li et al, 2018).…”