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Systematic review of the neural basis of social cognition in patients with mood disorders
Open accessAbstract
Background: This review integrates neuroimaging studies of 2 domains of social cognition — emotion comprehension and theory of mind (ToM) — in patients with major depressive disorder and bipolar disorder. The influence of key clinical and method variables on patterns of neural activation during social cognitive processing is also examined. Methods: Studies were identified using PsycINFO and PubMed (January 1967 to May 2011). The search terms were “fMRI,” “emotion comprehension,” “emotion perception,” “affect comprehension,” “affect perception,” “facial expression,” “prosody,” “theory of mind,” “mentalizing” and “empathy” in combination with “major depressive disorder,” “bipolar disorder,” “major depression,” “unipolar depression,” “clinical depression” and “mania.” Results: Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions. These results reveal an overall lack of inhibition by higher-order cognitive structures on limbic and emotion-related structures during social cognitive processing in patients with mood disorders. Critically, key variables, including illness burden, symptom severity, comorbidity, medication status and cognitive load may moderate this pattern of neural activation. Limitations: Studies that did not include control tasks or a comparator group were included in this review. Conclusion: Further work is needed to examine the contribution of key moderator variables and to further elucidate the neural networks underlying altered social cognition in patients with mood disorders. The neural networks underlying higher-order social cognitive processes, including empathy, remain unexplored in patients with mood disorders.
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In the paper
“A total of 65 studies met the appropriate criteria and were included in this review.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Results
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In the paper
“Other domains of social cognition, including empathy and moral reasoning, remain unexplored in these patients.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Introduction
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In the paper
“Other studies have reported evidence of a negative bias during facial expression recognition and detection tasks, 138,140,149-156 including a tendency to identify neutral faces as sad in patients with moderate to severe depressive symptoms compared with healthy controls.[157][158][159]”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of facial emotion processing
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
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In the paper
“By contrast, reduced amygdala activation in response to positive stimuli has been demonstrated across a small number of studies.71,99”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
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- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
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In the paper
“For example, level of depression severity has been shown to correlate negatively with the extent of activation in the fusiform gyrus, 43,47 anterior cingulate cortex 48 and amygdala 71,74 in response to happy and negative faces.62”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“Further analysis of data arising from the study by Keedwell and colleagues 61 showed that increased activity in the right visual cortex and subgenual cingulate to sad but not happy facial expressions in the first few weeks of treatment were predictive of a greater clinical recovery.65”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
What the sources say
- Not checked yetcites [65] source
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- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
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In the paper
“It should be noted, however, that an equal number of studies failed to find a significant association between level of depression and neural activity in response to facial emotions.41,49,59,67,69,72”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
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- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“Evidence from fMRI studies suggests that patients with acute MDD differ from healthy controls in the pattern of neural responding arising from exposure to a variety of emotional facial expressions (see Phillips and colleagues 162 ).”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites Phillips and colleagues 162
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- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“A recent report by Lee and colleagues 54 also demonstrated reduced activation in the DLPFC in response to the passive presentation of negative facial stimuli among patients with MDD.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [54] source
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- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
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In the paper
“This bias is accompanied by selective attention to negatively valenced faces depicting sadness 134,147,155,160 and anger.161”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of facial emotion processing
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- It may state two separate claims as one. 42
- Probably not a substantial claim. 12
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In the paper
“Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Abstract
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- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The neural networks under lying higher-order social cognitive processes, including empathy, remain unexplored in patients with mood disorders.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Abstract
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In the paper
“However, the same study group found that amygdala-DLPFC connectivity was significantly associated with illness severity, indicating that patients with MDD with reduced connectivity between these regions had a more pervasive and severe course of illness.58”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Illness burden
What the sources say
- Not checked yetcites [58] source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“A recent study by Victor and colleagues, 73 however, found that remitted patients with MDD showed exaggerated responses in the amygdala to masked sad faces and a lack of amygdalar response to masked happy faces compared with controls.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [73] source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“For example, a recent study by Fu and colleagues 43 examined responding to positive stimuli in patients with MDD compared with matched controls and found reduced activation in subcortical (basal ganglia), limbic (hippocampus) and extrastriate regions among acutely ill patients with MDD; this pattern was attenuated following treatment with fluoxetine.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
What the sources say
- Not checked yetcites [43] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“Preliminary findings by Norbury and colleagues 68 demonstrate elevated DLPFC activation in response to fearful faces in euthymic patients compared with controls.Levels of amygdala activation did not differ between patients and matched controls during the presentation of fearful faces.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [68] source
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
In the paper
“Similarly, Keedwell and colleagues 61 found that severely depressed patients showed increased visual cortex responses to sad faces and reduced neural response in these same regions to happy faces in the early stages of antidepressant treatment.Following continued antidepressant therapy and clinical improvement, these patterns were reversed.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
What the sources say
- Not checked yetcites [61] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
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In the paper
“Neuroimaging studies conducted in children and adolescents with MDD also show heightened activation in the amygdala 56,60,74 and OFC 74 in response to emotional facial expressions (for conflicting findings, see Thomas and colleagues 42 ).”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
- Rests on an assumption: fMRI activation in the brain regions examined is a valid index of social cognitive processing.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“to date, few studies have included separate groups with MDD and with bipolar disorder and have directly compared patterns of neural activation between these groups; most studies included relatively small samples of patients with MDD or bipolar disorder.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
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In the paper
“On average, neural activityis most commonly decreased in the DLPFC 30,59,68,76 and increased in the left amygdala, 55,74,76,79,98,99 the fusiform gyrus 82,93,98 and the inferior frontal gyrus 82,90,98 in patients with mood disorders.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
What the sources say
- Not checked yetcites [30] source
- Not checked yetcites [59] source
- Not checked yetcites [68] source
- Not checked yetcites [76] source
- Not checked yetcites [55] source
- Not checked yetcites [74]
- Not checked yetcites [79] source
- Not checked yetcites [98] source
- Not checked yetcites [99] source
- Not checked yetcites [82] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“To date, studies examining the neural correlates of ToM processing in patients with mood disorders have been confined to investigations of patients with bipolar disorder; 2 prelim inary investigations have examined euthymic patients with bipolar disorder.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Findings concerning the impact of symptom severity among actively ill patients have been less consistent and, on average, have failed to reveal a relation between severity of active illness and patterns of neural activation”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
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In the paper
“The effect of illness burden and age on neuronal activation during ToM performance in patients with mood disorders remains an underexplored area of research.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Illness burden, age
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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In the paper
“which may result in the misdiag nosis of bipolar depression as MDD, 37,38”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Introduction
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In the paper
“These models posit that prefrontal regions, such as the lateral prefrontal cortex, mPFC, OFC and dorsal anterior cingulate, modulate activity in subcortical (e.g., amygdala) and limbic regions.106,113”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of facial emotion processing
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In the paper
“Where possible, neuroimaging findings involving patients with mood disorders are contextualized based on several key variables, including illness burden (e.g., number of affective episodes), illness state (e.g., active v. remitted), medication status, age, cognitive load and comorbidity, thought to moderate cognitive performance in patients with mood disorders.29”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Introduction
What the sources say
- Not checked yetcites [29] source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Critically, key variables, including illness burden, symptom severity, comorbidity, medication status and cognitive load may moderate this pattern of neural activation.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
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In the paper
“For example, theoretical models propose that the ability to recognize another's emotion is critical to ToM, 8 with empirical evidence supporting this view.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Introduction
What the sources say
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In the paper
“Given the dearth of papers investigating the domains of ToM in patients with mood disorders, we adopted a liberal approach to the inclusion of relevant articles in these domains.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Methods
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In the paper
“These studies were likely not able to detect a relation between this illness variable and neuronal response because of their limited sample sizes and the inclusion of patients with varying levels of depression.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, these studies point toward a processing bias involving enhanced attention to and recognition of negatively valenced faces during active states of depression that may be accompanied by a tendency to mislabel positively valenced faces as sad and to misjudge (i.e., amplify) the amount of negative emotion conveyed in faces.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of facial emotion processing
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- Rests on an assumption: The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
In the paper
“Given the ubiquitous nature of facial expressions, the ability to recognize facial expressions is crucial for intact interpersonal functioning.123”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of facial emotion processing
What the sources say
- Not checked yetcites [123]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“it is possible that this null finding stemmed from the inclusion of first-episode patients in the mood disorders group.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [69] source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“whereas implicit processing of sad faces was associated with enhanced activation in the amygdala, anterior cingulate cortex, lateral temporal cortex and mPFC, explicit processing of sad faces was associated with attenuation of these same regions.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [188] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“a contrasting pattern of reduced amygdala and subgenual cingulate activation in response to sad but not happy facial expressions has been reported in conjunction with a mood-congruent deficit in recognizing sad facial affect.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [77] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“Depressed patients with bipolar disorder have also shown elevated activity in the amygdala 102 and attenuated responses in the OFC and DLPFC to neutral and negative (e.g., angry, fearful, sad) faces.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
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In the paper
“In euthymic patients with bipolar disorder compared with healthy controls, studies have demonstrated increased hippocampal activity 82 along with enhanced amygdala activity 76 and diminished DLPFC activation when viewing fearful faces 76,82,86”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, these results suggest that conventional antidepressants and novel treatments may dampen hyperactive responses to negative stimuli and enhance the salience of positive stimuli.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
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In the paper
“studies examining patients with bipolar disorder in a depressed phase of illness reveal a mood congruent bias in emotion perception tasks, including difficulties labelling happy faces 97,102 and a tendency to misinterpret neutral facial stimuli as sad 144,183 and happy faces as angry.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Facial emotion processing in patients with bipolar disorder
What the sources say
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In the paper
“Foland and colleagues 84 also found reduced functional connectivity between the ventrolateral prefrontal cortex and the amygdala during a facial emotional labelling task in line with reduced inhibitory frontal control over amygdala reactivity.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [84] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is plausible that the discrepant findings in subcortical activations in both actively ill and euthymic patients may stem from failure to account for comorbid disorders.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Severity of depressive or manic symptoms may influence neural response to affective facial stimuli in patients with bipolar disorder, although the evidence is inconsistent.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Evidence of greater left amygdala-OFC connectivity in response to sad faces and reduced bilateral connectivity between these same regions in response to happy faces has also been reported in depressed but not euthymic patients with bipolar disorder.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [97] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“In a sample of patients with bipolar disorder with mixed illness states, amygdala activity in response to happy faces was greater in unmedicated patients but lower in medicated patients compared with controls.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
What the sources say
- Not checked yetcites [80] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“emotionspecific impairments in the identification of sadness, 77 disgust 181 and fear 181 as well as a more generalized deficit in facial emotion recognition have been reported in actively manic patients.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Facial emotion processing in patients with bipolar disorder
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings indicate that the negative bias toward sad faces improves and a positive bias toward happy faces emerges with antidepressant treatment.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Medication status
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“Recent work has demonstrated significant associations between an earlier illness onset and both amygdala hyperactivity 86 and decreased activity within the DLPFC.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Mood state
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Thomas and colleagues 42 found that during passive viewing of fearful versus neural faces, patients with MDD showed hypoactivation of the right amygdala, whereas hyperactivation of this region was observed in patients with heterogeneous anxiety disorders (generalized anxiety disorder and/or panic disorder).”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Comorbidity
What the sources say
- Not checked yetcites [42] source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Hyperactivity in the amygdala in response to negative facial stimuli has been demonstrated across numerous studies of patients with MDD, and a small number of studies indicate hypoactivity in this region in response to positive facial stimuli.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Section summary
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None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, neuroimaging evidence also implicates the posterior superior temporal sulcus, which is involved in biological motion perception, 223,224 including socially relevant directional cues such as the eye gaze of others, 225,226 and the adjacent temporoparietal junction, which is involved in the attribution of beliefs to others, 227 as critical for ToM ability.7,228,229”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Theory of mind in patients with mood disorders
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“as neuroimaging studies are inherently under temporal constraint, a decreased number of trials may be used to shorten the scan duration, consequently decreasing the statistical power during between-and within-group comparisons.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“although patients with mood disorders may perform comparably to controls on behavioural measures, the neural processing of that information is extensively altered”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“During passive viewing paradigms, patients with bipolar disorder and those with MDD demonstrate hypoactivity in the DLPFC and OFC and hyperactivity in the amygdala and anterior cingulate (subgenual and pregenual), although evidence is less consistent for subcortical regions such as the amygdala and paralimbic regions.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Recognition of emotional prosody is thought to draw on multiple processing resources mediated by a complex neural network found primarily in the right superior temporal region.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Neural correlates of affective prosody recognition
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these different paradigms tend to converge on a pattern of decreased activation in prefrontal cortical regions associated with emotion regulation and cognitive control (e.g., DLPFC) and increased activation in prefrontal, limbic and subcortical regions associated with affective processing.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Influence of facial emotion processing paradigms
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Overall, these data suggest that patients with bipolar depression may be biased toward negative mood-congruent facial expressions, whereas those with unipolar depression have an attentional bias away from positive expressions.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Studies comparing patients with unipolar and bipolar depression
What the sources say
- Not checked yetcites [102] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rela tively small sample sizes and variable emotion processing paradigms employed in these studies may also have contributed to discrepant findings observed in subcortical regions, such as the amygdala, across mood states.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Comorbidity
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“A nascent literature suggests that youth with MDD and with bipolar disorder show impaired performance on tests of facial emotion processing, a finding underscored by studies demonstrating early alterations in the neuronal circuitry under lying social cognitive processing in these samples.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The theory of mind tasks used in the reviewed studies validly measure theory of mind ability.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these results point toward an overall lack of inhibition by higher-order cognitive structures on limbic and emotion-related structures during social cognitive processing in patients with mood disorders that is consistent across different social cognitive tasks, including recognition of emotion in faces and prosody, as well as ToM.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The functional neuroimaging measures used in the reviewed studies validly index the neural activity underlying social cognitive processing.
- Rests on an assumption: The core theory of mind network identified in healthy individuals applies to patients with mood disorders.
None of the sources cited for this claim have been checked yet.
In the paper
“patients with bipolar disorder do not show this normalization of function despite recovery (for exceptions following treatment with a mood stabilizer, see Hassel and colleagues 86 and Robinson and colleagues 90”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The functional neuroimaging measures used in the reviewed studies validly index the neural activity underlying social cognitive processing.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“social cognitive tasks that place high demands on cognitive processing resources (e.g., executive functioning, working memory) may engage higherorder cognitive regions to a greater extent than those social cognitive tasks having lower-order processing demands”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the inclusion of heterogeneous samples of patients with comorbid diag noses, particularly anxiety disorders, may limit the interpretability of findings.”
§ Systematic review of the neural basis of social cognition in patients with mood disorders > Conclusion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
The reviewed studies are sufficiently comparable in methods, tasks, and samples to be combined into a single pattern of neural activation.
“Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions.”
The paper relies on this without support.
fMRI activation in the brain regions examined is a valid index of social cognitive processing.
“Given that most studies using neuroimaging technology to examine the neural correlates of social cognitive processing in patients with mood disorders rely on functional magnetic resonance imaging (fMRI), we focused our review on this paradigm.”
The paper relies on this without support.
The included studies without control tasks or comparator groups still provide valid evidence for the review's conclusions.
“Studies that did not include control tasks or a comparator group were included in this review.”
The paper relies on this without support.
The functional neuroimaging measures used in the reviewed studies validly index the neural activity underlying social cognitive processing.
“Alterations in social cognitive functioning in patients with mood disorders are likely related to alterations in patterns of neuronal activation observed during performance of these tasks.”
The paper relies on this without support.
The theory of mind tasks used in the reviewed studies validly measure theory of mind ability.
“A small number of studies conducted in actively depressed patients with MDD suggest that these patients show impairments on ToM tasks that involve decoding mental states from available information, such as facial expressions, tone of voice, gestures and reasoning 232-234”
The paper relies on this without support.
The core theory of mind network identified in healthy individuals applies to patients with mood disorders.
“These regions have been shown previously to have strong functional connectivity with the temporoparietal junction and superior temporal sulcus, 241 regions thought to be crucial to ToM.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“There is well established evidence indicating structural and functional impairments in brain networks in depression that include abnormalities in regions that play a role in ToM such as ventromedial prefrontal and temporoparietal regions (Cusi et al., 2012).”
From Social functioning in major depressive disorder (2016) · cites this paper as Cusi et al., 2012
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Study showing elevated DLPFC activation is cited for decreased activation
MinorThe paper describes study 68 as finding elevated DLPFC activation in euthymic patients, but later includes that study among citations supporting decreased DLPFC activity.
“On average, neural activityis most commonly decreased in the DLPFC 30,59,68,76”
“Preliminary findings by Norbury and colleagues 68 demonstrate elevated DLPFC activation in response to fearful faces in euthymic patients compared with controls.”
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Social cognition and emotional processing in major depressive disorder
Fossati, P., & Hinfray, S. (2015) · Cambridge University Press eBooks · doi:10.1017/cbo9781139860567.008 · Cited by 2
Leutritz, A. L., Čolić, L., Borchardt, V., Cheng, X. M., Zhang, B., Lison, S., Frommer, J., Buchheim, A., Strauss, B. M., Fonagy, P., et al. (2019) · Psychology and Psychotherapy Theory Research and Practice · doi:10.1111/papt.12258 · Cited by 2
Fears, S. C., & Reus, V. I. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-410529-4.00104-2 · Cited by 2
The Neurophysiological Substrate of the Decision-Making Process in Depressed Patients
Laurentino, S. G., de Souza, S. L., & Sougey, É. B. (2020) · Open Journal of Depression · doi:10.4236/ojd.2020.93005 · Cited by 2
An Integrative Developmental Psychopathology Approach to Depression
Luyten, P., & Fonagy, P. (2021) · Depression and personality · doi:10.1007/978-3-030-77329-8_13 · Cited by 2
Cognition sociale et accident vasculaire cérébral : perspective neuropsychologique
Bertrand-Gauvin, C., Faucher, L., Bocti, C., Gagnon, M.-J., & Joanette, Y. (2014) · Revue de neuropsychologie · doi:10.3917/rne.062.0099 · Cited by 2
Chapter 6. Pharmacokinetics, Pharmacodynamics, and Pharmacogenomics
Goldberg, J. F. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as06 · Cited by 2
Mentalizing and Psychopathology in Schizophrenia, Depression, and Social Anxiety
Walter, H., & Mohnke, S. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-397025-1.00176-7 · Cited by 2
Structural Neuroimaging of Maltreatment and Inflammation in Depression
Redlich, R., Opel, N., Förster, K., Engelen, J., & Dannlowski, U. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811073-7.00016-7 · Cited by 2
Chapter 8. Personalized Medicine in Psychiatry
Perna, G., Alciati, A., & Nemeroff, C. B. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as08 · Cited by 2
Chapter 25. Classic Antipsychotic Medications
Nasrallah, H. A., & Tandon, R. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as25 · Cited by 2
Chapter 60. Treatment of Child and Adolescent Disorders
Wagner, K., & Pliszka, S. R. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as60 · Cited by 1
Chapter 14. Citalopram and Escitalopram
Shelton, R. C. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as14 · Cited by 1
Chapter 20. Duloxetine, Milnacipran, and Levomilnacipran
Jha, M. K., Mayes, T. L., & Trivedi, M. H. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as20 · Cited by 2
Schatzberg, A. F. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as17 · Cited by 1
Chapter 31. Ziprasidone and Asenapine
Newcomer, J. W., Lipsey, J., Strassnig, M., & Citrome, L. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as31 · Cited by 1
Chapter 11. Tricyclic and Tetracyclic Drugs
Nelson, J. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as11 · Cited by 2
Yang, Y. W.-H., & Marder, S. R. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as26 · Cited by 1
Buckley, P. F., & Foster, A. E. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as32 · Cited by 1
Chapter 29. Risperidone and Paliperidone
Lopez, L. V., Hill, M. B., & GOFF, D. C. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as29 · Cited by 1
Chapter 39. Carbamazepine, Oxcarbazepine, and Eslicarbazepine
Post, R. M., Wang, P. W., & Ketter, T. A. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as39 · Cited by 1
Mohnke, S., Walter, H., & Tantchik, W. (2018) · Nervenheilkunde · doi:10.1055/s-0038-1668316 · Cited by 1
Adolescent Social Cognitive DevelopmentPreprint
Williamson, V. G. (2021) · PsyArXiv (OSF Preprints) · doi:10.31234/osf.io/qd2vw · Cited by 2
Unravelling the Role of the Dopamine D1 Receptor in Anhedonia, Asociality, and Avolition
Witt, K. (2023) · doi:10.26686/wgtn.24646128 · Cited by 1
Chapter 63. Psychopharmacology During Pregnancy and Lactation
Newport, D. J., di Scalea, T. L., Richardson, E., Smith, T. L., Scott, N. P., & Stowe, Z. N. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as63 · Cited by 1
Chapter 3. Genetics and Epigenetics
Keverne, J., Czamara, D., & Binder, E. B. (2024) · American Psychiatric Association Publishing eBooks · doi:10.1176/appi.books.9781615375523.as03 · Cited by 1
Empathy, autism and the extreme female brain
Dinsdale, N. L. (2012) · Summit (Simon Fraser University)
Parlar, M. E. (2015) · MacSphere (McMaster University) · doi:10.71548/13583
Neuroimaging of Risk Factors of Depression and Cardiovascular Disease
Opel, N., Dannlowski, U., & Redlich, R. (2016) · Springer eBooks · doi:10.1007/978-3-319-32480-7_10
Bobrov, A. E., & Russian, P. (2014)
Holshausen, K. (2016) · QSpace (Queen's University Library)
Self-citationSocial Cognition in People with Bipolar Disorder
Bobyn, J. A. (2014) · Libraries and Cultural Resources (University of Calgary) · doi:10.11575/prism/27810
The Neuroimaging of Vicarious Pain
Terrighena, E. L., & Lee, T. M. C. (2017) · Springer eBooks · doi:10.1007/978-3-319-48046-6_16 · Cited by 1
Serra, L. (2017) · Gredos (University of Salamanca) · doi:10.14201/gredos.137135
Contextual influences on depressed interpersonal behavior
Girard, J. M. (2018) · D-Scholarship@Pitt (University of Pittsburgh)
Dualibe, A. L. (2018) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.17.2019.tde-19102018-095804
Kognitive Dysfunktionen bei unipolarer Depression
Kienzle, J., Listunova, L., Bartolovic, M., & Roesch-Ely, D. (2019) · Psychotherapie: Manuale · doi:10.1007/978-3-662-58182-7_3
Interpersonal hypersensitivity and Social Cognition in Borderline Personality Disorder
Sato, M. (2018) · UCL Discovery (University College London)
Metadata
- Authors
- Cusi, A. M., Nazarov, A., Holshausen, K., MacQueen, G. M., & McKinnon, M. C.
- Affiliations
- University of Calgary (CA)
- Venue
- Journal of Psychiatry and Neuroscience
- Publisher
- Canadian Science Publishing
- Published
- 2012-05
- Volume
- 37
- Issue
- 3
- Pages
- 154-169
- ISSN
- 1180-4882 (ISSN-L)
- 1488-2434
- PMC
- PMC3341408
- OpenAlex
- W2104541524
- Cited by
- 278
- References
- 265
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 73 · 2023: 11 · 2022: 8 · 2021: 17 · 2020: 15 · 2019: 13 · 2018: 25 · 2017: 16 · 2016: 15 · 2015: 20 · 2014: 29 · 2013: 19 · 2012: 7
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Psychiatry and Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Life Sciences › Neuroscience › Cognitive Neuroscience › Face Recognition and Perception
- Keywords
- social cognition, mood disorders, major depressive disorder, bipolar disorder, emotional understanding, theory of mind, mentalization, empathy, facial expressions, prosody, limbic system, frontal cortex, emotion regulation, moderators, disease burden, symptom severity, comorbidities, medication status, cognitive load
- MeSH terms
- Affect, Age Factors, Bipolar Disorder, Cognition, Major Depressive Disorder, Facial Expression, Humans, Magnetic Resonance Imaging, Psychotherapy, Social Behavior, Comorbidity, Cost of Illness, Mood Disorders, Theory of Mind
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