Behavior Studies

Understanding Others' Regret: A fMRI Study

Nicola Canessa1,2,3,6, Matteo Motterlini1, Cinzia Di Dio5, Daniela Perani2,3,4,6, Paola Scifo2,3,4,6, Stefano F. Cappa1,2,3,6*, Giacomo Rizzolatti5

1 Centro di Ricerca in Epistemologia Sperimentale e Applicata (CRESA), Vita-Salute San Raffaele University, Milano, Italy, 2 Division of Neuroscience, San Raffaele Scientific Institute, Milano, Italy, 3 Cognitive Neuroscience Center (CNC), Vita-Salute San Raffaele University, Milano, Italy, 4 Nuclear Medicine Unit, San Raffaele Scientific Institute, Milano, Italy, 5 Department of Neuroscience, University of Parma, Parma, Italy, 6 National Institute of Neuroscience, Torino, Italy

Previous studies showed that the understanding of others' basic emotional experiences is based on a “resonant” mechanism, i.e., on the reactivation, in the observer's brain, of the cerebral areas associated with those experiences. The present study aimed to investigate whether the same neural mechanism is activated both when experiencing and attending complex, cognitively-generated, emotions. A gambling task and functional-Magnetic-Resonance-Imaging (fMRI) were used to test this hypothesis using regret, the negative cognitively-based emotion resulting from an unfavorable counterfactual comparison between the outcomes of chosen and discarded options. Do the same brain structures that mediate the experience of regret become active in the observation of situations eliciting regret in another individual? Here we show that observing the regretful outcomes of someone else's choices activates the same regions that are activated during a first-person experience of regret, i.e. the ventromedial prefrontal cortex, anterior cingulate cortex and hippocampus. These results extend the possible role of a mirror-like mechanism beyond basic emotions.

Am J Psychiatry 163:735-738, April 2006
doi: 10.1176/appi.ajp.163.4.735
© 2006 American Psychiatric Association

Use of fMRI to Predict Recovery From Unipolar Depression With Cognitive Behavior Therapy

Greg J. Siegle, Ph.D., Cameron S. Carter, M.D., and Michael E. Thase, M.D.

OBJECTIVE: In controlled treatment trials, 40%–60% of unmedicated depressed individuals respond to cognitive behavior therapy (CBT). The authors examined whether pretreatment neural reactivity to emotional stimuli accounted for this variation. METHOD: Unmedicated depressed individuals (N=14) and never depressed comparison subjects (N=21) underwent fMRI during performance of a task sensitive to sustained emotional information processing. Afterward, depressed participants completed 16 sessions of CBT. RESULTS: Participants whose sustained reactivity to emotional stimuli was low in the subgenual cingulate cortex (Brodmann’s area 25) and high in the amygdala displayed the strongest improvement with CBT. CONCLUSIONS: The presence of emotion regulation disruptions, which are targeted in CBT, may be the key to recovery with this intervention.

J Neurosci. 2009 Aug 12;29(32):10111-9.
Stressed memories: how acute stress affects memory formation in humans.

Henckens MJ, Hermans EJ, Pu Z, Joëls M, Fernández G.

Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, The Netherlands. marloes.henckens@donders.ru.nl

Stressful, aversive events are extremely well remembered. Such a declarative memory enhancement is evidently beneficial for survival, but the same mechanism may become maladaptive and culminate in mental diseases such as posttraumatic stress disorder (PTSD). Stress hormones are known to enhance postlearning consolidation of aversive memories but are also thought to have immediate effects on attentional, sensory, and mnemonic processes at memory formation. Despite their significance for our understanding of the etiology of stress-related mental disorders, effects of acute stress at memory formation, and their brain correlates at the system scale, remain elusive. Using an integrated experimental approach, we probed the neural correlates of memory formation while participants underwent a controlled stress induction procedure in a crossover design. Physiological (cortisol level, heart rate, and pupil dilation) and subjective measures confirmed acute stress. Remarkably, reduced hippocampal activation during encoding predicted stress-enhanced memory performance, both within and between participants. Stress, moreover, amplified early visual and inferior temporal responses, suggesting that hypervigilant processing goes along with enhanced inferior temporal information reduction to relay a higher proportion of task-relevant information to the hippocampus. Thus, acute stress affects neural correlates of memory formation in an unexpected manner, the understanding of which may elucidate mechanisms underlying psychological trauma etiology..

Biol Psychiatry. 2009 Oct 1;66(7):656-64. Epub 2009 Jul 9.
A functional magnetic resonance imaging study of deliberate emotion regulation in resilience and posttraumatic stress disorder.

New AS, Fan J, Murrough JW, Liu X, Liebman RE, Guise KG, Tang CY, Charney DS.

Mental Health Care Center, James J. Peters Veterans Affairs Medical Center, Bronx, New York, New York 10468, USA. antonia.new@mssm.edu

BACKGROUND: Sexual violence is an important public health problem in the United States, with 13% to 26% of women reporting a history of sexual assault. While unfortunately common, there is substantial individual variability in response to sexual assault. Approximately half of rape victims develop posttraumatic stress disorder (PTSD), while others develop no psychopathology (e.g., trauma-exposed non-PTSD). In this project, we examined the neural mechanisms underlying differences in response to sexual violence, focusing specifically on the deliberate modification of emotional responses to negative stimuli. METHODS: Using functional magnetic resonance imaging (fMRI) blood oxygenation level-dependent (BOLD) response, we examined the neural circuitry underlying effortful modification of emotional responses to negative pictures in 42 women: 14 with PTSD after sexual trauma, 14 with no psychiatric diagnosis after sexual trauma, and 14 nontraumatized control subjects. RESULTS: In response to deliberate attempts to downregulate emotional responses, nontraumatized healthy control subjects were more successful than either trauma-exposed group (PTSD or non-PTSD) in downregulating responses to the negative pictures as measured by subjective rating and BOLD response in regions of prefrontal cortex (PFC). In contrast, after deliberate attempts to upregulate emotional responses, regions of PFC were activated by trauma-exposed non-PTSD subjects more than by healthy control subjects or PTSD subjects. CONCLUSIONS: Successful downregulation of emotional responses to negative stimuli appears to be impaired by trauma exposure. In contrast, the ability to upregulate emotional responses to negative stimuli may be a protective factor in the face of trauma exposure and associated with resilience.

Neurocase. 2007 Oct;13(5):342-57.
The neurofunctional mechanisms of traumatic and non-traumatic memory in patients with acute PTSD following accident trauma.

Piefke M, Pestinger M, Arin T, Kohl B, Kastrau F, Schnitker R, Vohn R, Weber J, Ohnhaus M, Erli HJ, Perlitz V, Paar O, Petzold ER, Flatten G.

Department of Psychosomatics and Psychotherapeutic Medicine, University of the RWTH Aachen, Germany.

Neurofunctional alterations in acute posttraumatic stress disorder (PTSD) and changes thereof during the course of the disease are not well investigated. We used functional magnetic resonance imaging to assess the functional neuroanatomy of emotional memory in surgical patients with acute PTSD. Traumatic (relative to non-traumatic) memories increased neural activity in the amygdala, hippocampus, lateral temporal, retrosplenial, and anterior cingulate cortices. These regions are all implicated in memory and emotion. A comparison of findings with data on chronic PTSD suggests that brain circuits affected by the acute disorder are extended and unstable while chronic disease is characterized by circumscribed and stable neurofunctional abnormalities.

Aust N Z J Psychiatry. 2008 Jun;42(6):478-88.
Traumatic memories: bridging the gap between functional neuroimaging and psychotherapy.

Peres JF, McFarlane A, Nasello AG, Moores KA.

Neuroscience and Behavior, Institute of Psychology, University of São Paulo, São Paulo, Brazil. julioperes@yahoo.com

OBJECTIVE: Neuroimaging studies have highlighted important issues related to structural and functional brain changes found in sufferers of psychological trauma that may influence their ability to synthesize, categorize, and integrate traumatic memories. METHODS: Literature review and critical analysis and synthesis. RESULTS: Traumatic memories are diagnostic symptoms of post-traumatic stress disorder (PTSD), and the dual representation theory posits separate memory systems subserving vivid re-experiencing (non-hippocampally dependent) versus declarative autobiographical memories of trauma (hippocampally dependent). But the psychopathological signs of trauma are not static over time, nor is the expression of traumatic memories. Multiple memory systems are activated simultaneously and in parallel on various occasions. Neural circuitry interaction is a crucial aspect in the development of a psychotherapeutic approach that may favour an integrative translation of the sensory fragments of the traumatic memory into a declarative memory system. CONCLUSION: The relationship between neuroimaging findings and psychological approaches is discussed for greater efficacy in the treatment of psychologically traumatized patients.

Psychol Med. 2008 Dec;38(12):1771-80. Epub 2008 Feb 25.
Dissociative responses to conscious and non-conscious fear impact underlying brain function in post-traumatic stress disorder.

Felmingham K, Kemp AH, Williams L, Falconer E, Olivieri G, Peduto A, Bryant R.

Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital, Australia. kim_felmingham@wmi.usyd.edu.au

BACKGROUND: Dissociative reactions in post-traumatic stress disorder (PTSD) have been regarded as strategic responses that limit arousal. Neuroimaging studies suggest distinct prefrontal responses in individuals displaying dissociative and hyperarousal responses to threat in PTSD. Increased prefrontal activity may reflect enhanced regulation of limbic arousal networks in dissociation. If dissociation is a higher-order regulatory response to threat, there may be differential responses to conscious and automatic processing of threat stimuli. This study addresses this question by examining the impact of dissociation on fear processing at different levels of awareness. METHOD: Functional magnetic resonance imaging (fMRI) with a 1.5-T scanner was used to examine activation to fearful (versus neutral) facial expressions during consciously attended and non-conscious (using backward masking) conditions in 23 individuals with PTSD. Activation in 11 individuals displaying non-dissociative reactions was compared to activation in 12 displaying dissociative reactions to consciously and non-consciously perceived fear stimuli. RESULTS: Dissociative PTSD was associated with enhanced activation in the ventral prefrontal cortex for conscious fear, and in the bilateral amygdala, insula and left thalamus for non-conscious fear compared to non-dissociative PTSD. Comparatively reduced activation in the dissociative group was apparent in dorsomedial prefrontal regions for conscious fear faces. CONCLUSIONS: These findings confirm our hypotheses of enhanced prefrontal activity to conscious fear and enhanced activity in limbic networks to non-conscious fear in dissociative PTSD. This supports the theory that dissociation is a regulatory strategy invoked to cope with extreme arousal in PTSD, but this strategy appears to function only during conscious processing of threat.