A differential pattern of neural response toward sad versus happy facial expressions in major depressive disorder

Surguladze, Simon; Brammer, Michael; Keedwell, Paul Anthony; Giampietro, Vincent; Young, Andrew W.; Travis, Michael J.; Williams, Steven; Phillips, Mary L.

doi:10.1016/j.biopsych.2004.10.028

Cited by 575 publications

(461 citation statements)

References 34 publications

Supporting

Mentioning

394

Contrasting

Unclassified

Order By: Relevance

“…Thus, across studies using an identical paradigm, we have identified neurobiological markers that distinguish healthy transient mood effects from pathological depressive mood on executive function. A couple of studies , Surguladze et al, 2005, Fu et al, 2007 have reported different patterns of neural response to sad and happy facial expressions in MDD. Given the features of negative attentional bias and anhedonia (lack of pleasure) of MDD, one might predict that a happy stimulus might produce a less distractive effect on the performance of attentional targets detection in the MDD group relative to controls.…”

Section: Discussionmentioning

confidence: 99%

Prefrontal mechanisms for executive control over emotional distraction are altered in major depression

Wang

LaBar

Smoski

et al. 2008

Psychiatry Research: Neuroimaging

182

140

View full text Add to dashboard Cite

A dysfunction in the interaction between executive function and mood regulation has been proposed as the pathophysiology of depression. However few studies have investigated the alteration in brain systems related to executive control over emotional distraction in depression. To address this issue, 19 patients with major depressive disorder (MDD) and 20 healthy controls were scanned using functional magnetic resonance imaging. Participants performed an emotional oddball task in which infrequently presented circle targets required detection while sad and neutral pictures were irrelevant novel distractors. Hemodynamic responses were compared for targets, sad distractors, and for targets that followed sad or neutral distractors (Target-after-Sad and Target-after-Neutral). Patients with MDD revealed attenuated activation overall to targets in executive brain regions. MDD patients were also slower behaviorally in response to Target-after-Sad than Target-after-Neutral. Patients also revealed a reversed activation pattern from controls in the left anterior cingulate, insula, right inferior frontal gyrus (IFG), and bilateral middle frontal gyrus. Those patients who engaged the right IFG more during Target-after-Sad than Target-after-Neutral responded faster to targets, confirming a role of this region in coping with emotional distraction. The results provide direct evidence of the alteration in neural systems that interplay cognition with mood in MDD. (198 words) Keywords event-related fMRI; interaction of executive function and emotion; anterior cingulate cortex; inferior frontal cortex

show abstract

Section: Discussionmentioning

confidence: 99%

Prefrontal mechanisms for executive control over emotional distraction are altered in major depression

Wang

LaBar

Smoski

et al. 2008

Psychiatry Research: Neuroimaging

182

140

View full text Add to dashboard Cite

show abstract

“…To explore the role of antidepressant medication, patients were grouped into a low-dose group (medication level 1-2, n ¼ 12) and a high-dose group (medication level 3-4, n ¼ 16) (Surguladze et al, 2005). High-and low-dose group did not differ with respect to 5-HTTLPR risk group (w 2 (1) ¼ 0.0, p ¼ 1.0) and amygdala activity elicited by any masked emotion type (all p40.2).…”

Section: Role Of Medicationmentioning

confidence: 99%

5-HTTLPR Biases Amygdala Activity in Response to Masked Facial Expressions in Major Depression

Dannlowski

Ohrmann

Bauer

et al. 2007

Neuropsychopharmacol

163

108

View full text Add to dashboard Cite

The amygdala is a key structure in a limbic circuit involved in the rapid and unconscious processing of facial emotions. Increased amygdala reactivity has been discussed in the context of major depression. Recent studies reported that amygdala activity during conscious emotion processing is modulated by a functional polymorphism in the serotonin transporter gene (5-HTTLPR) in healthy subjects. In the present study, amygdala reactivity to displays of emotional faces was measured by means of fMRI at 3T in 35 patients with major depression and 32 healthy controls. Conscious awareness of the emotional stimuli was prevented via backward-masking to investigate automatic emotion processing. All subjects were genotyped for the 5-HTTLPR polymorphism. Risk allele carriers (S or L G ) demonstrated increased amygdala reactivity to masked emotional faces, which in turn was significantly correlated with life-time psychiatric hospitalization as an index of chronicity. This might indicate that genetic variations of the serotonin transporter could increase the risk for depression chronification via altering limbic neural activity on a preattentive level of emotion processing.

show abstract

“…21 A number of studies have demonstrated increased amygdalar responses in activation paradigms for those with mood disorders. [22][23][24] Interestingly, it has recently been reported that healthy carriers of the short (s) allele of the functional promoter polymorphism for the serotonin transporter gene (a finding that confers increased risk of depression) exhibit amygdalar hyperactivity. [25][26][27] One significant function of the amygdala is to evaluate the emotional valence-be it positive 28 or negative 29 -31 -of an experience.…”

Section: Functional Anatomy Of Mood Disordersmentioning

confidence: 99%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

135

View full text Add to dashboard Cite

Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

show abstract

A differential pattern of neural response toward sad versus happy facial expressions in major depressive disorder

Cited by 575 publications

References 34 publications

Prefrontal mechanisms for executive control over emotional distraction are altered in major depression

Prefrontal mechanisms for executive control over emotional distraction are altered in major depression

5-HTTLPR Biases Amygdala Activity in Response to Masked Facial Expressions in Major Depression

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Contact Info

Product

Resources

About