Lecture 10 - Social cognition (Cognitive Neuroscience, UU)

Our brains may have grown in size because we are social animals.

The orbitofrontal cortex plays a role in social functioning.

• OFC damage: over-reliance on perceptual cues to guide behavior
• Difficulty placing appropriateness of behavior in context
• Lack awareness of whether their own/other’s behavior is appropriate

Somatic marker hypothesis

• Fast activation of ANS by affective associations: somatic states are induced
• Potential threats or rewards are signaled before conscious knowledge of such a threat / reward
• Sort through behavioral options to limit choice

vmOFC: associates a ‘gut-feeling’ with each choice – helps sort through available options.

Patients with vmOFC damage: the somatic marker does not cause the SCR reflects to be a learned association.

The somatic marker occurs when you’re about to do something risky.

The default mode network may be involved in self-referential processing.

Most people think they are better than average: the better than average effect.

• More medial and lateral OFC recruitment leads to more realistic evaluations of self compared to others.

Processing others’ thoughts (theory of mind) can be measured using the false-belief test.

The TPJ is specifically involved in processing stories on other people’s thoughts. Why is this active?

• Role: enables shifts of attention
• In vision: attention shifts to other locations
• Hypothesis: TPJ enables shifts of attention to other viewpoints in social reasoning.

Mirror neurons and mimicry also play a role.

These mechanisms may be deficient in autism. For example, the higher the autism quotient, the lower the mimicry.

People with autism look at the eyes way less than healthy controls.

High testosterone prenatally: low scores on the reading the eyes in the mind task.

Oxytocin: bonding hormone. Oxytocin enhances fixations on eye region and improves reading mind from eye.

Summary:

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