Increased amygdala response to shame in remitted major depressive disorder.
Proneness to self-blaming moral emotions such as shame and guilt is increased in major depressive disorder (MDD), and may play an important role in vulnerability even after symptoms have subsided. Social psychologists have argued that shame-proneness is relevant for depression vulnerability and is distinct from guilt. Shame depends on the imagined critical perception of others, whereas guilt results from one's own judgement. The neuroanatomy of shame in MDD is unknown. Using fMRI, we compared 21 participants with MDD remitted from symptoms with no current co-morbid axis-I disorders, and 18 control participants with no personal or family history of MDD. The MDD group exhibited higher activation of the right amygdala and posterior insula for shame relative to guilt (SPM8). This neural difference was observed despite equal levels of rated negative emotional valence and frequencies of induced shame and guilt experience across groups. These same results were found in the medication-free MDD subgroup (N = 15). Increased amygdala and posterior insula activations, known to be related to sensory perception of emotional stimuli, distinguish shame from guilt responses in remitted MDD. People with MDD thus exhibit changes in the neural response to shame after symptoms have subsided. This supports the hypothesis that shame and guilt play at least partly distinct roles in vulnerability to MDD. Shame-induction may be a more sensitive probe of residual amygdala hypersensitivity in MDD compared with facial emotion-evoked responses previously found to normalize on remission.
The University of Manchester and Manchester Academic Health Sciences Centre, School of Medicine, Neuroscience and Psychiatry Unit, Manchester, United Kingdom.
Erdem
E
Pulcu
The University of Manchester and Manchester Academic Health Sciences Centre, School of Medicine, Neuroscience and Psychiatry Unit, Manchester, United Kingdom ; The University of Manchester and Manchester Academic Health Sciences Centre, School of Psychological Sciences, Neuroscience and Aphasia Research Unit, Manchester, United Kingdom.
Karen
K
Lythe
The University of Manchester and Manchester Academic Health Sciences Centre, School of Medicine, Neuroscience and Psychiatry Unit, Manchester, United Kingdom.
Rebecca
R
Elliott
The University of Manchester and Manchester Academic Health Sciences Centre, School of Psychological Sciences, Neuroscience and Aphasia Research Unit, Manchester, United Kingdom.
Sophie
S
Green
Cognitive and Behavioral Neuroscience Unit, D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.
Jorge
J
Moll
The University of Manchester and Manchester Academic Health Sciences Centre, School of Medicine, Neuroscience and Psychiatry Unit, Manchester, United Kingdom.
John F W
JF
Deakin
The University of Manchester and Manchester Academic Health Sciences Centre, School of Psychological Sciences, Neuroscience and Aphasia Research Unit, Manchester, United Kingdom ; Institute of Psychiatry at King's College London, Department of Psychological Medicine, Centre for Affective Disorders, London, United Kingdom.
Roland
R
Zahn
D000679:Amygdala / Q000503:physiopathology*; D000928:Antidepressive Agents / Q000627:therapeutic use; D001931:Brain Mapping; D016022:Case-Control Studies; D003865:Major Depressive Disorder / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology; D006801:Humans; D008279:Magnetic Resonance Imaging; D012752:Shame
D000928:Antidepressive Agents