An fMRI Study of Facial Emotion Processing in Patients With Schizophrenia

Gur, Raquel E.; McGrath, Claire; Chan, Robin M.; Schroeder, Lee F.; Turner, Travis H.; Turetsky, Bruce I.; Kohler, Christian G.; Alsop, David C.; Maldjian, Joseph A.; Ragland, J. Daniel; Gur, Ruben C.

doi:10.1176/appi.ajp.159.12.1992

Cited by 465 publications

(320 citation statements)

References 39 publications

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“…Aversive faces also activated posterior OFC on the right, lateral frontal cortex, and temporal poles on both sides, occipital and extrastriate regions, particularly fusiform gyrus, again broadly consistent with other studies (Keightley et al, 2003;Lange et al, 2003;Gur et al, 2002;Abel et al, 2003;Surguladze et al, 2003;Sprengelmeyer et al, 1998).…”

Section: Covert Face Emotion Recognitionsupporting

confidence: 90%

The Effect of Citalopram Pretreatment on Neuronal Responses to Neuropsychological Tasks in Normal Volunteers: An fMRI Study

Del-Ben

Deakin

McKie

et al. 2005

Neuropsychopharmacol

237

184

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Changes in serotonin neurotransmission have also been implicated in the etiology and treatment of impulse control disorders, depression, and anxiety. We have investigated the effect of enhancing serotonin function on fundamental brain processes that we have proposed are abnormal in these disorders. In all, 12 male volunteers received citalopram (7.5 mg intravenously) and placebo pretreatment in a single-blind crossover design before undertaking Go/No-go, Loss/No-loss, and covert (aversive) face emotion recognition tasks during functional magnetic resonance imaging (fMRI). Blood oxygenation level dependent responses were analyzed using Statistical Parametric Mapping (SPM2). The tasks activated prefrontal and subcortical regions generally consistent with literature with lateral orbitofrontal cortex (BA47) common to the three tasks. Citalopram pretreatment enhanced the right BA47 responses to the No-go condition, but attenuated this response to aversive faces. Attenuations were seen following citalopram in the medial orbitofrontal (BA11) responses to the No-go and No-loss (ie relative reward compared with Loss) conditions. The right amygdala response to aversive faces was attenuated by citalopram. These results support the involvement of serotonin in modulating basic processes involved in psychiatric disorders but argue for a process-specific, rather than general effect. The technique of combining drug challenge with fMRI (pharmacoMRI) has promise for investigating human psychiatric disorders.

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Section: Covert Face Emotion Recognitionsupporting

confidence: 90%

The Effect of Citalopram Pretreatment on Neuronal Responses to Neuropsychological Tasks in Normal Volunteers: An fMRI Study

Del-Ben

Deakin

McKie

et al. 2005

Neuropsychopharmacol

237

184

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“…Behaviourally, the only notable group difference found across studies employing non-facial baseline conditions was a slowed response in patients [42,47,49,[54][55][56], although one study found patients to be less accurate than controls at identifying all emotions[41].…”

Section: Findings For An Attentional Bias Towards Negative Stimuli Inmentioning

confidence: 99%

Psychobiology of threat appraisal in the context of psychotic experiences: A selective review

2015

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A key factor in the transition to psychosis is the appraisal of anomalous experiences as threatening.Cognitive models of psychosis have identified attentional and interpretative biases underlying threatbased appraisals. While much research has been conducted into these biases within the clinical and cognitive literature, little examination has occurred at the neural level. However, neurobiological research in social cognition employing threatening stimuli mirror cognitive accounts of maladaptive appraisal in psychosis. This review attempted to integrate neuroimaging data regarding social cognition in psychosis with the concepts of attentional and interpretative threat biases. Systematic review methodology was used to identify relevant articles from Medline, PsycINFO and EMBASE, and PubMed databases. The selective review showed that attentional and interpretative threat biases relate to abnormal activation of a range of subcortical and prefrontal structures, including the amygdala, insula, hippocampus, anterior cingulate, and prefrontal cortex, as well as disrupted connectivity between these regions, when processing threatening and neutral or ambiguous stimuli.Notably, neural findings regarding the misattribution of threat to neutral or ambiguous stimuli presented a more consistent picture. Overall, however, the findings for any specific emotion were mixed, both in terms of the specific brain areas involved and the direction of effects (increased/decreased activity), possibly owing to confounds including small sample sizes, varying experimental paradigms, medication, and heterogeneous, in some cases poorly characterised, patient groups. Further neuroimaging research examining these biases by employing experimentally-induced anomalous perceptual experiences and well-characterised large samples is needed for greater aetiological specificity.

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“…Deficits of the neural mechanism involved in attribution of emotional salience in schizophrenics (Kohler et Table 2) and electrophysiological (Pfefferbaum et al, 1989) studies, employing various natural probes ranging from odors to facial images and aversive vs neutral scenes (Taylor et al, 2002(Taylor et al, , 2005Gur et al, 2002;Paradiso et al, 2003;Takahashi et al, 2004;Williams et al, 2004).…”

Section: Abnormal Dopaminergic Function Impairs Wanting Processes In mentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

131

142

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Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

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An fMRI Study of Facial Emotion Processing in Patients With Schizophrenia

Cited by 465 publications

References 39 publications

The Effect of Citalopram Pretreatment on Neuronal Responses to Neuropsychological Tasks in Normal Volunteers: An fMRI Study

The Effect of Citalopram Pretreatment on Neuronal Responses to Neuropsychological Tasks in Normal Volunteers: An fMRI Study

Psychobiology of threat appraisal in the context of psychotic experiences: A selective review

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

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