A new brain imaging study reveals deficits in key networks involved in social functioning among individuals with schizophrenia.
The findings shed light on the underlying neural mechanisms that may contribute to impaired social skills in this psychiatric disorder.
Key Takeaways:
- Compared to healthy controls, schizophrenia patients showed altered activity in brain regions involved in processing social rewards and regulating emotions during social interactions. These regions included the striatum, orbitofrontal cortex, insula and amygdala.
- Schizophrenia patients exhibited reduced connectivity between two key social brain networks – the reward network and the emotional salience network.
- The abnormalities were not directly correlated with symptom severity or social functioning, suggesting complex relationships between brain activity patterns and real-world behavior.
- The findings point to dysfunctional social brain circuitry that may underlie the social interaction difficulties experienced by many individuals with schizophrenia.
Source: Brain Sci. 2023
Abnormal Brain Activation in Regions Involved in Social Cognition
The study, conducted by researchers in China, used resting-state functional magnetic resonance imaging (fMRI) to compare 60 subjects – 30 schizophrenia patients and 30 demographically matched healthy controls.
During rest, schizophrenia patients displayed altered spontaneous activity in several regions important for social cognition – the ability to understand others’ behaviors, intentions and emotions during social situations.
Specifically, patients showed heightened resting-state activity in the striatum, a set of structures including the caudate, putamen and pallidum.
The striatum plays key roles in experiencing pleasure, motivation and learning from reward.
Dysfunction in this dopamine-rich region may contribute to patients’ difficulties enjoying social interactions and integrating social feedback.
Patients also exhibited reduced resting activity in the insula.
This region is involved in emotional awareness, empathy and sensing cues from others’ voices, faces and gestures.
Insula deficits may relate to patients’ struggles reading social signals.
Together, the abnormal striatum and insula activity points to imbalances between social motivation and social perception circuits in schizophrenia.
Disrupted Connections Between Social Brain Networks
In addition to local activity changes, patients showed weaker connections between two complementary social brain systems – the reward network and the emotional salience network.
The reward network involves areas like the striatum, orbitofrontal cortex and amygdala.
It drives motivation to seek social rewards like acceptance and praise.
The emotional salience network, anchored by the anterior cingulate and insula, detects emotional importance and redirects attention to significant social events.
Specifically, patients exhibited reduced functional connectivity between the right orbitofrontal cortex and left amygdala.
This weaker link between systems for reward valuation and emotional processing may relate to patients’ social withdrawal and suspiciousness.
A dampened reward response and overly vigilant salience detection could make social interactions seem unappealing and potentially threatening.
No Direct Correlations with Symptoms or Functioning
Intriguingly, while schizophrenia patients showed aberrant social brain function compared to healthy controls, these specific brain activity measures did not directly correlate with symptom severity or a scale of psychosocial function.
This lack of linear relationships highlights the multifaceted, indirect links between neural activity and real-world behavior.
Symptoms likely emerge from complex interactions between various large-scale brain networks.
Future studies using more granular assessments of social skills during interactive tasks could help clarify brain-behavior relationships.
Examining how brain function tracks with symptom changes over time may also provide insights.
Overall, the dysfunctional social brain patterns likely represent key pathological processes in schizophrenia, even if not directly predictive of functioning scores at single timepoints.
Implications for Understanding and Treating Social Deficits
Social difficulties are a major source of disability for those with schizophrenia.
The findings help explain the brain basis of these challenges.
Dysfunctional social motivation, reward and salience circuits could make relationships feel unrewarding or unsafe.
This may lead patients to withdraw socially and have trouble re-engaging even when symptoms improve.
The results support social cognitive training and social skills groups targeting these specific circuits as add-on treatments.
Strengthening social motivation and emotional awareness could help patients pursue and enjoy social goals.
Brain stimulation techniques like tDCS could also be explored to enhance activity in underactive regions.
MRI-targeted stimulation of the insula and striatum may boost social capacities.
Additionally, future neuroscience studies on social functioning in schizophrenia could examine both task-based and resting-state brain activity.
This could clarify whether similar circuits show dysfunction during active social cognition vs. intrinsic connectivity at rest.
In summary, the researchers shed new light on the neural basis for social challenges in schizophrenia.
While complex brain-behavior relationships remain, the findings advance our models of socio-emotional dysfunction.
Targeting the identified social brain networks offers hope for improving social motivation and skills in this devastating illness.
References
- Study: Deficits in key brain network for social interaction in individuals with schizophrenia
- Authors: Yiwen Wu et al. (2023)
