Behavioural and neurocognitive responses to sad facial affect are attenuated in patients with mania

Lennox, Belinda; Jacob, Rebecca; Calder, Andrew J.; Lupson, Vicky; Bullmore, Edward T.

doi:10.1017/s0033291704002557

Cited by 183 publications

(137 citation statements)

References 25 publications

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“…We did not detect elevations in amygdala response in these BD participants to faces depicting negative emotional expressions, as have been noted in previous studies of BD participants (Yurgelun-Todd et al 2000, Lawrence et al 2004. Possible explanations include limitations in the power to detect differences owing to the small sample size, as well as the inclusion of BD participants with elevated mood symptoms, as attenuated amygdala response to faces depicting negative affect have been reported in association with manic symptoms in BD (Lennox et al 2004).…”

Section: Discussionsupporting

confidence: 57%

Preliminary evidence for medication effects on functional abnormalities in the amygdala and anterior cingulate in bipolar disorder

et al. 2005

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Rationale: Abnormal amygdala and frontocortical responses to emotional stimuli are implicated in bipolar disorder (BD) and have been proposed as potential treatment targets. Objectives: The aim of this study was to investigate amygdala and frontocortical responses to emotional face stimuli in BD and the influences of mood-stabilizing medications on these responses. Methods: Functional magnetic resonance imaging was performed while 17 BD participants (5 unmedicated) and 17 healthy comparison (HC) participants viewed faces with happy, sad, fearful, or neutral expressions. Results: The group by stimulus-condition interaction was significant (p<0.01) for amygdala activation, with the greatest effects in the happy face condition. Relative to HC, amygdala increases were greater in unmedicated BD, but lower in medicated BD. Rostral anterior cingulate (rAC) activation was decreased in unmedicated BD compared to HC; however, BD participants taking medication demonstrated rAC activation similar to HC participants. Conclusions: Although the sample sizes were small, these preliminary results suggest that BD is associated with increased amygdala and decreased rAC response to emotional faces. The findings also provide preliminary evidence that mood-stabilizing medications may reverse abnormalities in BD in the response of an amygdalafrontal neural system to emotional stimuli.

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Section: Discussionsupporting

confidence: 57%

Preliminary evidence for medication effects on functional abnormalities in the amygdala and anterior cingulate in bipolar disorder

et al. 2005

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“…11,12 Also, recent imaging studies have suggested the involvement of the subgenual cingulate cortex, together with prefrontal areas, in the neurobiology of bipolar disorder 31 and manic and hypomanic states. 32 These findings may suggest that the abnormal functioning of the brain regions implicated herein could be related to the expression of irritability not only in the context of depression, but also in that of manic and/or mixed states. 14 The pattern of increased activity in the BA 9 portion of the left dorsomedial prefrontal cortex, which was present during the presentation of irritability scripts relative to the neutral emotional state, is unlikely to be specifically related to the emergence of irritability emotions.…”

Section: Discussionmentioning

confidence: 78%

Cognitive control associated with irritability induction: an autobiographical recall fMRI study

Cerqueira

Almeida

Sato

et al. 2010

Rev. Bras. Psiquiatr.

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Objective: Despite the relevance of irritability emotions to the treatment, prognosis and classification of psychiatric disorders, the neurobiological basis of this emotional state has been rarely investigated to date. We assessed the brain circuitry underlying personal script-driven irritability in healthy subjects (n = 11) using functional magnetic resonance imaging. Method: Blood oxygen level-dependent signal changes were recorded during auditory presentation of personal scripts of irritability in contrast to scripts of happiness or neutral emotional content. Self-rated emotional measurements and skin conductance recordings were also obtained. Images were acquired using a 1,5T magnetic resonance scanner. Brain activation maps were constructed from individual images, and betweencondition differences in the mean power of experimental response were identified by using cluster-wise nonparametric tests. Results: Compared to neutral scripts, increased blood oxygen level-dependent signal during irritability scripts was detected in the left subgenual anterior cingulate cortex, and in the left medial, anterolateral and posterolateral dorsal prefrontal cortex (cluster-wise p-value < 0.05). While the involvement of the subgenual cingulate and dorsal anterolateral prefrontal cortices was unique to the irritability state, increased blood oxygen level-dependent signal in dorsomedial and dorsal posterolateral prefrontal regions were also present during happiness induction. Conclusion: Irritability induction is associated with functional changes in a limited set of brain regions previously implicated in the mediation of emotional states. Changes in prefrontal and cingulate areas may be related to effortful cognitive control aspects that gain salience during the emergence of irritability. Descriptors IntroductionSeveral imaging studies in healthy human subjects using positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) have been conducted during the provocation of specific emotional states, including happiness, sadness, fear, anger, anxiety, guilt or disgust. These studies have demonstrated the involvement of multi-focal brain circuits in emotional processing, frequently involving portions of the frontal and temporal neocortices, anterior cingulate gyrus, medial temporal structures, amygdala, insula and the basal ganglia.

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“…Structural MRI (sMRI) studies in bipolar adults find either increased or unchanged amygdala volume relative to controls (8)(9)(10), whereas functional MRI (fMRI) studies find that adults with BD, relative to controls, have either amygdala hyperactivation (11,37) or hypoactivation (12) in response to facial stimuli. In contrast to adult data, sMRI studies in bipolar children consistently document decreased amygdala volume in patients compared with controls (13)(14)(15)(16)(17).…”

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confidence: 99%

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

Rich

Vinton

Roberson‐Nay

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Reflecting a paradigm shift in clinical neuroscience, many chronic psychiatric illnesses are now hypothesized to result from perturbed neural development. However, most work in this area focuses on schizophrenia. Here, we extend this paradigm to pediatric bipolar disorder (BD), thus demonstrating traction in the developmental psychobiology perspective. To study amygdala dysfunction, we examined neural mechanisms mediating face processing in 22 youths (mean age 14.21 ؎ 3.11 yr) with BD and 21 controls of comparable age, gender, and IQ. Event-related functional MRI compared neural activation when attention was directed to emotional aspects of faces (hostility, subjects' fearfulness) vs. nonemotional aspects (nose width). Compared with controls, patients perceived greater hostility in neutral faces and reported more fear when viewing them. Also, compared with controls, patients had greater activation in the left amygdala, accumbens, putamen, and ventral prefrontal cortex when rating face hostility, and greater activation in the left amygdala and bilateral accumbens when rating their fear of the face. There were no between-group behavioral or neural differences in the nonemotional conditions. Results implicate deficient emotion-attention interactions in the pathophysiology of BD in youth and suggest that developmental psychobiology approaches to chronic mental illness have broad applicability.amygdala ͉ faces ͉ functional MRI R ecently, psychology and psychiatry have witnessed a major paradigm shift: virtually all chronic adult mental illnesses are now thought to result from long-term perturbations in neural development. Two lines of research support this perspective: family-based͞longitudinal studies and neurobiological studies. Family-based and longitudinal studies implicate developmental perturbations in a range of conditions, including behavior disorders, substance abuse, mood disorders, and psychoses (1-3). However, virtually all research on developmental neurobiology focuses on schizophrenia, where data implicate a neural circuit connecting the dorsolateral prefrontal cortex, striatum, and hippocampus (4, 5). Neurocognitive correlates of schizophrenia, such as deficient working memory, are thought to result from dysfunction in this circuit (6). An important next step is the extension of the developmental neurobiological approach to other mental illnesses and other neural systems associated with information processing and emotion regulation.For several reasons, bipolar disorder (BD) is an ideal illness in which to expand the emerging developmental paradigm by conducting neurobiologically oriented developmental research. BD causes marked disruption in social, academic, and family function. Major questions persist concerning the boundaries of the condition in children; neurobiological data might ultimately resolve them. Most importantly, research in adult patients and animals implicates a circuit encompassing the amygdala, striatum, and ventral prefrontal cortex (VPFC) in the pathophysiology of BD (7). This circu...

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Behavioural and neurocognitive responses to sad facial affect are attenuated in patients with mania

Cited by 183 publications

References 25 publications

Preliminary evidence for medication effects on functional abnormalities in the amygdala and anterior cingulate in bipolar disorder

Preliminary evidence for medication effects on functional abnormalities in the amygdala and anterior cingulate in bipolar disorder

Cognitive control associated with irritability induction: an autobiographical recall fMRI study

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

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