Schizophrenia

Which of the following correctly distinguishes positive and negative symptoms of schizophrenia?

• APositive symptoms are pleasant experiences; negative symptoms are distressing ones
• BPositive symptoms are additional experiences beyond normal functioning (e.g. hallucinations); negative symptoms are a loss or reduction of normal functioning (e.g. avolition)✓
• CPositive symptoms always respond to drugs; negative symptoms never do
• DPositive symptoms are cognitive; negative symptoms are purely physical

Answer: Positive symptoms are additions to normal experience, such as hallucinations and delusions. Negative symptoms involve a loss or reduction of normal functioning, such as avolition (loss of motivation) and speech poverty. 'Positive/negative' refers to addition versus loss, not to whether the symptoms are pleasant.

Two clinicians using different diagnostic manuals reach different diagnoses for the same patient with schizophrenia. This is most directly a problem of:

• AConstruct validity
• BSymptom overlap with depression
• CReliability of diagnosis, specifically low inter-rater reliability✓
• DGender bias in diagnosis

Answer: When different clinicians fail to reach the same diagnosis for the same patient, this is a failure of inter-rater reliability (consistency of diagnosis between assessors). Validity concerns whether the diagnosis is accurate or measures a real condition, which is a separate issue.

Which finding provides the strongest support for a genetic explanation of schizophrenia?

• AAntipsychotic drugs reduce positive symptoms
• BConcordance rates are higher for monozygotic (MZ) twins than for dizygotic (DZ) twins✓
• CSchizophrenia is more common in cities than rural areas
• DHigh levels of expressed emotion predict relapse

Answer: Higher concordance for MZ twins (who share ~100% of genes) than DZ twins (who share ~50%) supports a genetic contribution, since the more genetically similar pair shows greater concordance. Drug effects relate to neurochemistry, and expressed emotion supports a psychological/family explanation.

The revised dopamine hypothesis proposes which pattern of dopamine activity in schizophrenia?

• AGlobally reduced dopamine throughout the brain
• BUniformly excessive dopamine in all brain regions
• CHyperdopaminergia in subcortical areas (e.g. excess D2 activity in the mesolimbic pathway) and hypodopaminergia in the prefrontal cortex✓
• DNormal dopamine levels but excess serotonin

Answer: The updated dopamine hypothesis proposes hyperdopaminergia in subcortical regions (excess dopamine/D2 activity in the mesolimbic pathway, linked to positive symptoms) combined with hypodopaminergia in the prefrontal cortex (linked to negative/cognitive symptoms). The original hypothesis claimed only excess dopamine.

Which of the following is a cognitive explanation for the symptoms of schizophrenia?

• AHigh levels of expressed emotion within the family
• BExcess dopamine in the mesolimbic pathway
• CThe double-bind theory of contradictory communication
• DDysfunctional information processing, such as impaired metarepresentation and central control, leading to symptoms like hallucinations and disorganised speech✓

Answer: Frith's cognitive account explains symptoms through dysfunctional thought processing, namely impaired metarepresentation (insight into one's own intentions) and impaired central control. Expressed emotion and the double-bind are family/psychological explanations; excess dopamine is biological.

How do typical antipsychotics (e.g. chlorpromazine) primarily act, compared with atypical antipsychotics (e.g. clozapine)?

• ATypical antipsychotics are dopamine agonists; atypical ones are antagonists
• BTypical antipsychotics mainly block dopamine D2 receptors; atypical antipsychotics also reduce dopamine but bind more temporarily to D2 and act on serotonin receptors too✓
• CTypical antipsychotics act only on serotonin; atypical ones act only on dopamine
• DBoth increase dopamine activity to reduce symptoms

Answer: Typical antipsychotics are dopamine antagonists that block D2 receptors. Atypical antipsychotics also reduce dopamine activity but tend to occupy D2 receptors more transiently and additionally act on serotonin (and other) receptors, which can improve negative symptoms and reduce side effects.

In family therapy for schizophrenia, what is the main therapeutic aim?

• ATo replace antipsychotic medication entirely
• BTo uncover repressed childhood conflicts through free association
• CTo reduce negative communication patterns and levels of expressed emotion within the family, thereby reducing the patient's stress and risk of relapse✓
• DTo challenge irrational delusional beliefs using reality testing

Answer: Family therapy aims to improve family communication and reduce expressed emotion (criticism, hostility, over-involvement), lowering stress and relapse rates. Challenging delusions through reality testing describes CBT, and free association describes psychoanalysis.

The diathesis-stress model, as used in the interactionist approach to schizophrenia, proposes that the disorder develops when:

• AStress alone is sufficient to cause schizophrenia in anyone
• BA genetic predisposition inevitably causes the disorder regardless of environment
• COnly biological factors, with no role for the environment, determine onset
• DA vulnerability (diathesis, e.g. genetic or early trauma) interacts with a stressor (e.g. an environmental or psychological trigger) to produce the disorder✓

Answer: The diathesis-stress model is interactionist: it argues schizophrenia develops when an underlying vulnerability (diathesis, which the modern model recognises can be genetic or psychological, such as early trauma) is triggered by a stressor. Neither the diathesis nor the stress alone is sufficient.