🤖 Autism Biological Explanation- Amygdala Flashcards

(16 cards)

1
Q

Structure of the Amygdala

Q: What is the amygdala, and where is it located?

A
  • A cluster of 13 nuclei (grey matter) in the medial temporal lobe, part of the limbic system.
  • There are two amygdalae, one in each brain hemisphere.
  • Highly interconnected with the hypothalamus, prefrontal cortex, hippocampus, and other brain regions.
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2
Q

Functions of the Amygdala

Q: What key behaviors does the amygdala influence?

A

Motivation, emotion, threat detection, and social interaction due to its widespread neural connections.

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3
Q

Amygdala Development in ASD

Q: How does amygdala development differ in children with ASD?

A
  • 2+ years old: 6–9% larger volume in ASD (Nordahl et al., 2012).
  • Typical children: Amygdala grows later (adolescence).
  • Adulthood: No size difference, but early overgrowth in ASD may disrupt neural organization/function.
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4
Q

Amygdala as the “Social Brain”

Q: Why is the amygdala called the “social brain”?

A
  • Leslie Brothers coined the term due to its role in social behavior.
  • Baron-Cohen (2000): Abnormal amygdala development → social deficits in ASD (e.g., emotion recognition, social perception).
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5
Q

Baron-Cohen’s Eye Task Study (1999)

Q: What did Baron-Cohen’s study reveal about amygdala function in ASD?

A
  • Compared ASD adults vs. matched controls.
  • Viewed photos of eyes showing emotions; fMRI measured brain activity.
  • ASD group performed worse at emotion recognition.
  • Left amygdala activated in controls but not in ASD participants.
  • Suggests amygdala dysfunction impairs reading emotions from eyes.
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6
Q

Flashcard 6: Neural Connections in ASD

Q: How might abnormal amygdala development lead to ASD symptoms?

A
  • Early overgrowth disrupts connections to frontal cortex, impairing:
  • Social perception (e.g., understanding facial expressions).
  • Processing social information.
  • Emotional inference (e.g., “mind-reading”).
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7
Q

Critical Period Hypothesis

Q: Why is the timing of amygdala growth important in ASD?

A

Early overgrowth (before age 2) may “wire” the brain atypically, causing lasting social deficits even after size normalizes in adulthood.

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8
Q

Key Study Support

Q: What evidence supports the link between amygdala dysfunction and ASD?

A
  • Nordahl (2012): Early amygdala overgrowth in ASD children.
  • Baron-Cohen (1999): Left amygdala inactivity during emotion-recognition tasks in ASD.
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9
Q

Evaluation: Support from Clinical Studies

Q: How does research on amygdala damage (e.g., patient SM) support the amygdala dysfunction theory of ASD?

A
  • Kennedy et al. (2009): SM (with amygdala damage) showed reduced personal space preference, mirroring ASD social deficits.
  • Implication: Amygdala dysfunction may underlie impaired social behavior in ASD.
  • Limitation: Correlational—doesn’t prove causation; other brain areas may contribute.
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10
Q

Evaluation: Inconsistent Findings on Amygdala Volume

Q: Why are inconsistent findings about amygdala volume problematic for the theory?

A
  • Howard et al. (2000): Increased amygdala volume in ASD adults.
  • Pierce et al. (2001): Decreased volume.
  • Nordahl vs. Herbert (children): Conflicting results (increase vs. decrease).
  • Conclusion: No clear pattern → weakens theory. Methodological differences may explain discrepancies.
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11
Q

Evaluation: Indirect Effects via Anxiety

Q: How might amygdala dysfunction indirectly cause ASD symptoms?

A
  • Amygdala regulates anxiety/fear responses.
  • Ollendick et al. (2009): High anxiety in ASD may disrupt social interactions.
  • Limitation: Doesn’t explain ASD cases without anxiety, suggesting other factors (e.g., genetics, prefrontal cortex).
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12
Q

Evaluation: Danger of Oversimplification

Q: Why is focusing solely on the amygdala an oversimplification?

A
  • Paul et al. (2010): Isolated amygdala damage (e.g., SM) caused milder deficits than full ASD.
  • Implication: ASD likely involves multiple brain regions (e.g., hippocampus, prefrontal cortex).
  • Conclusion: A network-based approach (connectivity) is needed.
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13
Q

Key Criticism – Lack of Causality

Q: What’s the main limitation of clinical studies like SM’s case?

A
  • Shows correlation, not causation.
  • ASD is heterogeneous; amygdala dysfunction may not apply to all cases.
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14
Q

Alternative Explanations

Q: What other brain areas might contribute to ASD symptoms?

A
  • Prefrontal cortex: Decision-making/social cognition.
  • Mirror neuron system: Imitation/empathy deficits.
  • Hippocampus: Memory/context processing.
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15
Q

Evaluation: Future Research Directions

Q: How could future studies address current limitations?

A
  • Longitudinal studies: Track amygdala development in ASD vs. controls.
  • Advanced imaging: Examine connectivity between amygdala and other regions.
  • Genetic studies: Explore links between amygdala function and ASD risk genes.
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16
Q

Summary of Evaluation

Q: What’s the overall strength of the amygdala dysfunction theory?

A

âś… Supported by:

Clinical cases (SM) and some volume studies.
Role in anxiety/social processing.
❌ Limited by:
Inconsistent findings.
Oversimplification (ignores other brain areas).
Indirect effects complicate causality.