EXAM QUESTION PLANS

Question 1

Describe and evaluate biological explanations of schizophrenia

Answer 1

Main Body

1. Genetic Factors (AO1)
   Twin studies: MZ twins ~48% concordance, DZ ~17%.
   -Family studies show increased risk in first-degree relatives.
   -Polygenic model – multiple genes involved (e.g., DISC1, COMT).

Evaluation (AO3)
Twin studies support genetic link but are not 100%.
Adoption studies support nature over nurture.
Genetics may interact with environment (diathesis-stress model).

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2. Dopamine Hypothesis (AO1)
   Classic: Overactivity of dopamine causes positive symptoms.
   Revised: Low dopamine in prefrontal cortex linked to negative symptoms.

Evaluation (AO3)
Antipsychotics (e.g., chlorpromazine) reduce dopamine and symptoms.
Not all respond to dopamine-targeting drugs.
Glutamate also likely involved – oversimplified model.

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3. Brain Structure Abnormalities (AO1)
   Enlarged ventricles, smaller hippocampus, and reduced grey matter.
   Commonly found in patients via brain imaging (MRI/CT).

Evaluation (AO3)
Structural abnormalities seen in some, not all, patients.
Hard to separate cause from effect – changes may result from illness or medication.
Confounding variables: substance use, comorbidity.

Conclusion
Biological explanations provide a strong foundation but not complete.
Most effective when integrated with psychological/social factors (diathesis-stress model

Question 2

Discuss the role of neurotransmitters in psychiatric disorders

Answer 2

Introduction
Neurotransmitters are brain chemicals that transmit messages across synapses.
Imbalances in neurotransmitters are linked to disorders like depression, schizophrenia, anxiety.

1. Dopamine – Schizophrenia
   Overactivity in mesolimbic areas → hallucinations, delusions.
   Antipsychotic meds block D2 receptors (e.g., haloperidol).

Evaluation
Treatment success supports dopamine role.
Doesn’t explain negative symptoms fully – other systems involved.

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2. Serotonin – Depression and Anxiety
   Low serotonin = low mood, anxiety, sleep disruption.
   SSRIs increase serotonin and reduce symptoms.

Evaluation
Evidence from effectiveness of SSRIs.
Delayed therapeutic effect suggests indirect mechanisms.
Not all patients respond.

3. GABA – Anxiety Disorders
   GABA = calming effect on brain.
   Low GABA → excessive activity → anxiety.
   Benzodiazepines enhance GABA and reduce symptoms.

Evaluation
Fast-acting drugs support GABA’s role.
Risk of dependence/side effects = concern.

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4. Glutamate – Emerging Theories (e.g., schizophrenia)
   Glutamate underactivity may explain negative and cognitive symptoms.
   NMDA receptor hypofunction hypothesis.

Evaluation
Animal and drug studies support this.
Still early in research – less evidence than for dopamine.

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Conclusion
Neurotransmitters play vital roles in mental disorders.
No single neurotransmitter explains everything – mental illness likely due to complex interactions.

Question 3

Compare and contrast models of attention

Answer 3

Introduction
Attention = cognitive process of selectively focusing on information.
Key models: Broadbent’s Filter Model, Treisman’s Attenuation Theory, and Late Selection Models.

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Main Body

1. Broadbent’s Filter Model (1958)
   Early selection: sensory input → selective filter → attended info processed.
   Dichotic listening task evidence.

Evaluation
Explains limited capacity well.
Can’t explain “cocktail party effect” (hearing own name in unattended ear).

2. Treisman’s Attenuation Model (1964)
   Modified Broadbent’s model: filter weakens (attenuates) unattended messages rather than blocks them.
   Words with meaning can be processed if threshold is low (e.g., name, important info).

Evaluation
Supported by shadowing tasks – explains cocktail party effect.
More flexible than Broadbent.

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3. Late Selection Models (Deutsch & Deutsch, 1963)
   All inputs processed for meaning before selection.
   Attention filters only after meaning is extracted.

Evaluation
Explains semantic intrusion.
But less efficient – seems implausible all inputs are processed fully.

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Comparison
All agree attention is selective, but differ on when filtering occurs.
Broadbent: early → Treisman: flexible → Deutsch & Deutsch: late.
Early models = more efficient; late models = more comprehensive.

Conclusion
No model explains all findings.
Treisman’s theory offers best balance – supported by evidence and accounts for flexible attention.

Question 4

Explain what attention disorders reveal about attention processes

Answer 4

Introduction
Attention disorders (e.g., ADHD, neglect syndrome) provide insight into normal attention by showing what happens when it breaks down.

1. ADHD (Attention Deficit Hyperactivity Disorder)
   Symptoms: inattention, impulsivity, hyperactivity.
   Suggests deficits in executive attention, sustained attention, and inhibition.
   Linked to dopamine dysfunction in frontal lobes.

Implications
Supports idea that attention = multi-component system.
Frontal cortex critical in controlling and directing attention.

2. Hemispatial Neglect (Often after stroke)
   Person ignores one side of space (usually left).
   Damage to right parietal lobe.
   Shows attention is not just about vision but about spatial awareness and conscious awareness.

Implications
Attention is lateralized in the brain.
Suggests attention = active process of prioritization.

3. Balint’s Syndrome
   Severe attentional disorder – patient sees individual objects but can’t perceive multiple objects together.
   Damage to parietal-occipital areas.

Implications
Attention necessary for binding features into unified perception.
Reinforces theories like Feature Integration Theory (Treisman).

Conclusion
Studying disorders reveals that attention is not a single process but a network of brain systems.
Different brain regions responsible for different types of attention (e.g., sustained, spatial, executive).