Schizophrenia A-level Revisions Notes

Schizophrenia Mock Exam Mark Scheme

Biological explanations

Biological explanations for schizophrenia: genetics and neural correlates, including the
dopamine hypothesis.

The biological approach asserts that schizophrenia is a physical illness resulting from organic malfunctions.

This perspective focuses on three primary areas:

• Genes: the inheritance of specific gene clusters.
• Dopamine: dysregulation of this neurotransmitter.
• Brain Structure: abnormalities within the brain’s physical architecture.

---

Genetic Explanations: Heritability and Polygenicity

Genetic theories propose that schizophrenia is a heritable condition.

Since no single gene is responsible, researchers call schizophrenia polygenic, meaning many genes contribute. It is also aetiologically heterogeneous: different genetic combinations can produce the same symptoms in different people.

Concordance Rates and Family Studies

To separate nature from nurture, psychologists use concordance rates, which measure the probability that two people will both have the disorder.

• Twin Studies: Gottesman (1991) identified a 48% concordance rate for monozygotic (MZ) twins, who share 100% of their DNA. In contrast, dizygotic (DZ) twins showed only a 17% concordance.
• Adoption Studies: Kety and Ingraham (1992) found that the risk of schizophrenia was ten times higher among biological relatives than adoptive relatives. This suggests that the genetic link remains potent even when the individual is raised in a different environment.

Genome-Wide Association Studies (GWAS)

Modern molecular biology has identified specific locations on the human genome associated with the disorder.

Ripke et al. (2014)

---

Dopamine Hypothesis

Dopamine is a neurotransmitter that facilitates communication between neurons in the brain.

The dopamine hypothesis argues that an imbalance in this chemical messenger drives the symptoms of schizophrenia.

Hyperdopaminergia (Excess)

The original hypothesis focused on high dopamine activity in the subcortex and the mesolimbic pathway.

Excess dopamine is believed to cause positive symptoms like auditory hallucinations. It may arise from over-active neurons or an overabundance of D2 receptors.

Hypodopaminergia (Deficit)

A more recent revision focuses on low levels of dopamine in the pre-frontal cortex (the mesocortical pathway).

This deficit is linked to negative symptoms, such as avolition and cognitive impairment.

Empirical Validation: Dopamine

Curran et al. (2004)

---

Neural Correlates: Structural Brain Abnormalities

The neural correlates explanation suggests that specific brain structures function or appear differently in schizophrenic patients.

Ventricular Enlargement

Ventricles are fluid-filled cavities in the brain.

Research has consistently shown that schizophrenic patients often have significantly larger ventricles than healthy controls.

This enlargement suggests that the surrounding brain tissue has shrunk or failed to develop, particularly in the pre-frontal cortex.

Regional Activation and Symptoms

Neuroimaging allows researchers to link specific brain regions to specific symptoms:

• Auditory Hallucinations: Allen et al. (2007) found lower activation levels in the superior temporal gyrus and anterior cingulate gyrus during hallucinatory episodes.
• Speech Poverty: Reduced activity in Wernicke’s area (the region responsible for speech comprehension) is negatively correlated with the severity of thought disorders.

---

Critical Evaluation of Biological Models

The Issue of Causation

A major weakness in biological research is the “direction of causality” problem.

Brain scans show enlarged ventricles. However, it is unclear whether these changes caused schizophrenia or resulted from it. The long-term stress of the disorder, or the medication used to treat it, may have caused the brain damage.

Biological Reductionism

Critics argue that these theories are too simplistic.

By focusing only on dopamine, researchers may overlook the role of other neurotransmitters like glutamate and serotonin.

Biological models also ignore the diathesis-stress model. It says a genetic vulnerability only produces schizophrenia when stress triggers it. Biology alone cannot explain why some people with high genetic risk never develop the disorder.

Environmental Influence

MZ twins have only a 48% concordance rate, not 100%. This proves that biology is not destiny.

Environmental factors, such as dysfunctional family dynamics or urban living, must interact with biological vulnerabilities to trigger the onset of the illness.

Contemporary Research

Genetic research has moved on since Ripke et al. (2014) found 108 loci. A far larger study by Trubetskoy et al. (2022) now offers the fullest map of risk genes.

With 287 loci involved, risk is clearly spread across many genes, as the polygenic account predicts. Heritability is estimated at 60 to 80%. That still leaves room for environmental stress, the other half of the diathesis-stress model.

Psychological Explanations

Psychological explanations for schizophrenia: family dysfunction and cognitive explanations,
including dysfunctional thought processing.

Psychological theories of schizophrenia emphasize that environmental stressors and cognitive deficits drive the disorder’s development. One example is dysfunctional thought processing, meaning breakdowns in how the brain monitors and controls its own thoughts.

Researchers focus on how specific social interactions and internal processing errors create and sustain psychotic symptoms.

Family Dysfunction as a Social Stressor

Family dysfunction refers to maladaptive patterns of communication and high levels of interpersonal conflict within the domestic environment.

These stressors often serve as the primary environmental triggers for individuals with an underlying genetic vulnerability.

The Schizophrenogenic Mother

Fromm-Reichmann (1948) identified the “schizophrenogenic mother” as a primary cause of paranoid delusions.

This term describes a parent who is simultaneously cold, rejecting, and overly controlling of her child’s behavior.

Such parenting creates a climate of secrecy and tension, leading to profound distrust in the developing child.

Without emotional security, the child eventually breaks from reality.

Double Bind Theory

Bateson et al. (1956) proposed the Double Bind Theory to explain disorganized thinking.

A double bind is a communication paradox where a person receives two or more conflicting messages. For example, a parent may verbally express love while pulling away with cold body language.

The child cannot resolve the contradiction. They fear punishment whatever they do.

Study: Bateson et al. (1956)

High Expressed Emotion (EE)

Expressed Emotion (EE) measures the quality of the emotional environment directed toward a patient by their caregivers.

It consists of three main elements: verbal criticism, hostility, and emotional over-involvement.

High EE environments serve as a powerful psychological stressor that frequently triggers symptomatic relapse.

Study: Vaughn and Leff (1976)

Theoretical Limitations

Despite practical successes, the family dysfunction model faces significant scrutiny regarding its scientific validity and ethical impact.

Critics argue that the theory often confuses the consequences of the illness with its causes.

The Direction of Causality

Establishing a clear cause-and-effect relationship remains the primary challenge for this theory.

Most research is correlational, meaning researchers cannot confirm if family conflict triggers schizophrenia or if the stress of managing a symptomatic child disrupts the family.

Study: Mischler and Waxler (1968)

Methodological Validity and Retrospective Data

Much evidence relies on retrospective data, which refers to memories of past events reported by patients during adulthood. This method is notoriously unreliable in clinical populations.

Positive symptoms like delusions can distort a patient’s perception of their upbringing.

Furthermore, early researchers lacked objectivity, often seeking “crazy-making” traits in parents to confirm their existing biases.

Social Sensitivity and Ethical Guilt

The family dysfunction explanation is highly socially sensitive because it identifies parents as the source of their child’s suffering.

Terms like “schizophrenogenic mother” impose a heavy burden of guilt on families already struggling with a crisis.

This psychological pressure can increase domestic tension, inadvertently triggering the very relapses the theory seeks to explain.

The Interactionist Perspective

Focusing solely on the family is considered a form of environmental reductionism, as it ignores biological foundations.

Schizophrenia is now largely understood through the Diathesis-Stress Model.

This interactionist approach posits that a biological vulnerability (diathesis) must be present, which is then activated by a social stressor (stress).

Without the genetic predisposition, even the most dysfunctional family environment is unlikely to produce the disorder.

---

Cognitive Explanations of Schizophrenia

The cognitive approach suggests that schizophrenia results from dysfunctional thought processing and impaired mental mechanisms.

It focuses on how the brain filters information and interprets internal versus external stimuli.

Attentional Bias

Bentall (1994) argued that sufferers possess an attentional bias, which is a tendency to focus excessively on threatening stimuli.

This hyper-vigilance causes individuals to misinterpret mundane events as personal threats or persecutory plots.

A person might focus on a stranger’s hand in their pocket and conclude they are concealing a weapon.

Dysfunctional Thought Processing

Christopher Frith (1992) identified two specific cognitive systems that fail in those with schizophrenia.

These failures directly correlate to the positive and disorganized symptoms observed in clinical settings.

• Metarepresentation: This is the cognitive ability to reflect on our own thoughts and identify them as internal. Dysfunction here leads to “thought insertion,” where patients believe their own thoughts are being placed there by others.
• Central Control: This refers to the ability to suppress automatic responses and perform deliberate actions. If central control fails, the individual cannot stop tangential thoughts from intruding into speech, resulting in word salad or derailment.

Study: Stirling et al. (2006)

Theoretical Limitations

A major limitation of cognitive theories involves the “direction of causality” problem.

These models effectively explain proximal causes: the immediate cognitive failures that produce symptoms. They often overlook distal causes.

Proximal vs. Distal Etiology

Proximal causes refer to the current cognitive deficits, such as impaired metarepresentation, that explain why a patient hears voices.

In contrast, distal causes refer to the initial origins of the condition, such as genetic inheritance or neurochemical imbalances.

Integration with Biological Factors

It is highly probable that structural brain abnormalities or dopamine dysregulation represent the true root causes of the disorder.

These biological factors likely create the faulty cognitions observed by psychologists.

Consequently, cognitive explanations are often viewed as incomplete because they describe the symptoms’ mechanisms rather than the disorder’s primary source.

---

Drug Therapy: Biological Treatments for Schizophrenia

Drug therapy: typical and atypical antipsychotics.

Antipsychotics are drugs that reduce psychotic symptoms such as hallucinations and delusions. Typical (first-generation) drugs came first. Atypical (second-generation) antipsychotics act on a broader range of brain chemicals and cause fewer movement side effects.

Typical Antipsychotics

Typical antipsychotics, or first-generation antipsychotics, have served as the primary pharmacological intervention for schizophrenia since the mid-20th century.

These conventional medications, such as Chlorpromazine and Haloperidol, are administered via tablets, syrups, or intramuscular injections to manage acute psychotic episodes.

Mechanism of Action: The Dopamine Hypothesis

Typical antipsychotics function as dopamine antagonists, which are chemicals that reduce the activity of a neurotransmitter by blocking its receptors.

These drugs target D2 receptors in the mesolimbic pathway, a brain region associated with reward and sensory perception.

By binding to roughly 60% to 70% of these receptors, the medication prevents dopamine from stimulating the postsynaptic neuron.

This blockade arrests overactive dopaminergic signaling. Researchers believe that overactivity is the primary cause of positive symptoms like hallucinations.

Beyond their primary neurological target, many typical antipsychotics influence histamine receptors.

This secondary interaction produces a powerful sedative effect. Clinicians therefore use the drugs to calm highly anxious or aggressive patients.

---

Empirical Support and Economic Utility

The widespread adoption of drug therapy is supported by extensive meta-analytic data and practical financial advantages.

These treatments allow for a level of patient independence that was historically impossible before the 1950s.

Study: Thornley et al. (2003)

Study: Leucht et al. (2012)

Typical antipsychotics are also highly cost-effective compared to specialized psychological interventions like Cognitive Behavioral Therapy (CBT).

Because they require minimal patient effort, they are often more accessible for individuals suffering from severe cognitive impairment or a lack of motivation.

---

Physiological Risks and Ethical Constraints

While effective at symptom reduction, typical antipsychotics are non-selective, meaning they block dopamine throughout the entire brain.

This lack of precision leads to significant neurological side effects and raises concerns about patient autonomy.

Limited Scope

Typical antipsychotics only treat the positive symptoms of schizophrenia and are largely ineffective at addressing negative symptoms, such as avolition or speech poverty.

Extrapyramidal Side Effects

The most common complications are extrapyramidal symptoms, which are physical movement disorders resulting from dopamine blockade in the motor pathways.

Mild issues include lethargy or dry mouth, but chronic use can lead to tardive dyskinesia.

This condition involves involuntary facial movements, such as grimacing or rapid eye blinking, and is often irreversible even after medication ceases.

Neuroleptic Malignant Syndrome (NMS)

A rare but potentially fatal risk is Neuroleptic Malignant Syndrome (NMS).

This occurs when dopamine blockage affects the hypothalamus, leading to high fever, muscle rigidity, and autonomic instability.

High Dropout Rates

While the drugs are effective, the severity of the side effects means that the costs can sometimes outweigh the benefits.

The unpleasant side effects lead many patients to abandon their medication. This creates a “revolving door” effect in which they inevitably suffer a severe relapse.

The “Chemical Straightjacket” Debate

Ethical concerns persist regarding the use of these drugs for sedation rather than therapy.

Critics like Healy (2012) argue that drug efficacy data may be misleading.

Instead of curing the underlying pathology, the drugs may simply sedate patients into a state of compliance.

This has led to the term “chemical straightjacket.” It describes medication used to make patients easier for hospital staff to manage rather than improving the patient’s internal experience.

The Treatment-Aetiology Fallacy

A drug that relieves symptoms does not prove the theory behind it is correct. Assuming otherwise is the treatment-aetiology fallacy.

Antipsychotics reduce positive symptoms, which fits the dopamine hypothesis. Yet relief could occur through a mechanism unrelated to what first caused the disorder. Drug therapy therefore treats symptoms, not necessarily the underlying cause.

---

Atypical Antipsychotics

Atypical antipsychotics, or second-generation antipsychotics, represent a pharmacological advancement designed to treat schizophrenia with greater precision.

Developed in the 1970s, these medications aim to suppress a wider range of symptoms while reducing the motor-function side effects associated with earlier drugs.

The table contrasts the two drug classes. Each row restates points developed in the sections that follow.

Feature	Typical (first-generation)	Atypical (second-generation)
Examples	Chlorpromazine, haloperidol	Clozapine, risperidone
Brain chemistry	Block dopamine (D2) receptors, mainly in the mesolimbic pathway	Block dopamine and also modulate serotonin; clozapine acts as a glutamate agonist
Symptoms treated	Mainly positive symptoms	A wider range, including some effect on negative symptoms
Main side effects	Movement problems (extrapyramidal), including tardive dyskinesia	Metabolic problems such as weight gain; agranulocytosis risk with clozapine

Multifaceted Mechanism of Action

Atypical antipsychotics operate through a broader neurochemical profile than their predecessors.

While they still function as dopamine antagonists, they also modulate serotonin and glutamate activity to balance brain chemistry.

Clozapine

Clozapine is a potent antagonist for dopamine and serotonin receptors, while also acting as an agonist for glutamate.

An agonist is a substance that initiates a physiological response when combined with a receptor.

This unique interaction helps alleviate “negative symptoms,” such as avolition (a total lack of motivation) and speech poverty.

Clozapine is also frequently used to treat comorbid depression. This is because of its impact on serotonin. Comorbid depression affects approximately 50% of schizophrenia patients.

Risperidone

Risperidone was developed to provide a safer alternative to Clozapine by targeting dopamine and serotonin receptors with higher affinity.

Affinity refers to the strength with which a drug binds to its target receptor.

Because it binds so strongly to D2 receptors, Risperidone is effective in significantly smaller doses.

Lower doses typically mean milder side effects for many patients.

---

Empirical Validation and Economic Benefits

Atypical medications are often the preferred clinical choice due to their superior performance in treatment-resistant cases and their lower dropout rates among patients.

Study: Bagnall (2003)

Study: Meltzer (2012)

Beyond clinical metrics, these drugs provide substantial economic utility.

By stabilizing both positive and negative symptoms, they facilitate a patient’s return to the workforce.

This reduces the financial burden on public health systems by preventing expensive, long-term institutionalization.

Contemporary Research on Antipsychotics

Huhn et al. (2019) compared 32 oral antipsychotics side by side. It is a far wider comparison than the earlier reviews above.

The authors rated their confidence in the evidence as often low. The rankings therefore need cautious reading. They do support the cost-benefit judgment that clinicians must make for each patient.

---

Physiological Risks and Clinical Management

Despite their advantages, atypical antipsychotics are not without significant medical risks.

Clinicians must perform a rigorous cost-benefit analysis before prescribing these potent chemical agents.

Metabolic Side Effects

While atypical drugs reduce the risk of movement disorders, they increase the likelihood of metabolic complications.

Patients frequently experience significant weight gain, which can lead to secondary conditions like Type 2 diabetes and cardiovascular disease.

These physical health risks can diminish a patient’s quality of life and discourage continued adherence to the medication.

Agranulocytosis

Clozapine carries a specific and life-threatening risk known as agranulocytosis.

Agranulocytosis is a severe form of leukopenia, a condition where the white blood cell count drops to dangerously low levels.

This leaves the patient highly vulnerable to infection.

Consequently, any patient prescribed Clozapine must undergo mandatory and regular blood monitoring to ensure their safety.

Relapse and Quality of Life

The presence of side effects can severely reduce a patient’s quality of life.

This can lead to patients stopping their treatment entirely, which then results in them experiencing a relapse of their schizophrenic symptoms.

Because of these risks, clinicians must weigh the benefits of symptom reduction against the costs of side effects. They make this cost-benefit judgment for each individual patient.

Positive Economic Implications

By successfully reducing the severity of a patient’s symptoms, atypical antipsychotics can have significant economic benefits.

Effective drug therapy lets individuals potentially return to work. It also prevents frequent hospital readmissions and the need for full-time institutional care. This reduces the negative financial impact on the economy and public health services.

---

CBT and Family Therapy for Schizophrenia

Cognitive behavior therapy and family therapy as used in the treatment of schizophrenia.

Drugs are not the only treatment. Psychological therapies target the thoughts and family stress that keep symptoms going. Both are used alongside antipsychotic medication, not instead of it.

CBT for Psychosis (CBTp)

Cognitive behavior therapy for psychosis (CBTp) targets the irrational beliefs and cognitive biases that sit behind positive symptoms. It does not target their biological roots directly. Patients learn to test their beliefs against the evidence.

A therapist typically works in four ways:

• Examine Beliefs: The patient identifies an irrational belief, such as “my carers intend to harm me”, and weighs the evidence for it.
• Alternative Explanations: The therapist offers less threatening interpretations of the same events.
• Thoughts and Behavior: The patient sees how a belief produces fear, which then drives safety behaviors such as locking doors.
• Coping Strategies: The therapist explains that voices may be the patient’s own misattributed inner speech. Distraction and “talking back” can help.

Evaluating CBTp means judging both effectiveness and appropriateness.

• Effectiveness: CBTp modestly reduces positive symptoms. Evidence is weaker for negative symptoms and long-term relapse prevention.
• Appropriateness: It needs real engagement and thinking capacity, which acute psychosis or severe avolition can make difficult. It is also slower and costlier than medication.

Jauhar et al. (2014) pooled randomized trials to test how strong the evidence really is. Effect sizes were small: 0.33 for overall symptoms (34 studies), 0.25 for positive symptoms (33 studies) and 0.13 for negative symptoms (34 studies).

The effect shrank further in trials where assessors did not know which patients had received therapy. CBTp helps, but the benefit is modest.

Family Therapy

Family therapy builds directly on expressed emotion research. Because high-EE homes predict higher relapse, therapy aims to lower expressed emotion and improve family communication and problem-solving.

Sessions usually combine three elements:

• Psychoeducation: Relatives learn that symptoms are not the patient’s fault and are not within their control.
• Communication Training: Families practice calmer, clearer ways of talking and solving problems together.
• Structured Sessions: Therapists often run multi-family groups that treat the family as a resource to support, not a cause to blame.

This is a deliberate break from the schizophrenogenic mother and double bind theories. It also eases the burden on relatives themselves.

• Effectiveness: Family intervention has a robust evidence base for reducing relapse and hospital readmission. Benefits tend to persist at follow-up.
• Appropriateness: It depends on an involved, available family. It also demands sustained commitment from relatives who are already under strain.

Drug Therapy Compared With Psychological Therapies

Exam answers often compare treatments. The table summarizes the main contrasts between drug therapy and the psychological therapies.

Feature	Drug therapy	CBTp and family therapy
Speed and cost	Faster and cheaper	Slower and more resource-intensive
Effort needed	Little patient motivation	Greater engagement from patient and family
Physical costs	Heavier side-effect burden	Avoid antipsychotics’ physical costs
Patient role	Less active role	More empowering: active tools for managing relapse risk
Main target	Symptoms, not any psychosocial cause	Thoughts, communication and stress that maintain illness
Best timing	Acute episodes	Usually once antipsychotics have stabilized the patient

Contemporary treatment guidance favors combining drug and psychosocial approaches rather than choosing between them. Each approach covers some of the other’s weaknesses. That is itself a strong evaluation point, and it leads directly to the interactionist approach.

---

Interactionist Approach: The Diathesis-Stress Model

The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis-stress model.

The interactionist approach combines biological, psychological and environmental factors. No single explanation accounts for schizophrenia on its own.

Why Single Explanations Fall Short

Every single-factor explanation in this topic has a clear limitation:

• Biological: Roughly half of identical twin pairs are discordant. They share their genes, yet only one twin has schizophrenia.
• Family Dysfunction: Poor communication may be a reaction to the illness rather than its cause. Correlational evidence cannot rule this out.
• Cognitive: These explanations describe proximal mechanisms, the immediate failures behind a symptom. They do not explain the distal origin, such as why the vulnerability arose.

The interactionist approach does not pick a winner. It treats biological vulnerability and psychosocial stress as jointly necessary.

Biological explanations tend to ignore stress, while psychological explanations tend to ignore biology. Each explanation then becomes one part of a larger account instead of a rival to the others.

The Diathesis-Stress Model

In the diathesis-stress model, a person inherits a vulnerability, not the disorder itself. This vulnerability is the diathesis. It may be genetic risk or another biological predisposition.

Schizophrenia appears only when a sufficient stressor is also present. Examples include a traumatic life event, family conflict or drug use. The stress must push the person past a threshold.

Neither factor is enough alone.

Someone with high genetic risk in a stable, low-stress environment may never develop the disorder. Someone with lower risk but severe, sustained stress might.

Vulnerability is a matter of degree, not an all-or-nothing trait.

This explains the twin data. Identical twins share almost all their genes but not the same life stressors. A concordance rate well below 100% is what the model predicts.

Treatment Implications and Evaluation

If both a biological diathesis and a stress component are necessary, treating only one side is unlikely to be best. That logic supports combining antipsychotic medication with CBTp or family therapy.

Medication targets the biological diathesis. The psychological therapies target the stress and its psychosocial maintenance. The interactionist approach is therefore both an explanation and the justification for combined, whole-person care.

• Strength: The model is integrative. It does not deny any evidence base but explains why each, taken alone, is incomplete. It also has testable treatment implications.
• Limitation: It is underspecified. It does not say how much diathesis or stress is needed, or which stressors matter most for which people.

Critics therefore see it as a broad organizing framework rather than a tightly predictive model.

---

Exam Technique for Schizophrenia

Schizophrenia is only one of three Option 2 topics in Paper 3. Confirm which topic your class studied. You cannot fall back on another mid-exam.

How Paper 3, Section C Is Assessed

Paper 3 (Issues and Options in Psychology) lasts 2 hours and is worth 96 marks, which is 33.3% of the A-level. It has four sections of 24 marks each:

• Section A: Issues and debates in psychology (compulsory).
• Section B: One Option 1 topic: relationships, gender, or cognition and development.
• Section C: One Option 2 topic: schizophrenia, eating behavior, or stress.
• Section D: One Option 3 topic: aggression, forensic psychology, or addiction.

Questions mix multiple-choice, short-answer and extended-writing formats. Each is marked against three assessment objectives:

• AO1: Accurate knowledge of a symptom, diagnostic issue, explanation or treatment, such as outlining what comorbidity means.
• AO2: Applying that knowledge to a case study, such as spotting which of a person’s symptoms are positive and which are negative.
• AO3: Evaluating an explanation or treatment.

Effectiveness Versus Appropriateness

Paper 3 adds one explicit expectation. You must evaluate therapies and treatments in terms of both appropriateness and effectiveness. These are two different angles:

• Effectiveness: Does it work? Look for reduced symptoms, relapse or readmission, backed by meta-analyses, trials and effect sizes.
• Appropriateness: Should it be used, and for whom? Weigh side effects, ethics, cost, access, and how much patient or family engagement it demands.

Mark schemes credit the two separately. An answer covering only one tends to stall in the mid-band.

Apply both angles to every treatment. For drug therapy, effectiveness covers the meta-analyses above, while appropriateness covers side effects, dropout and the chemical straightjacket debate.

For CBTp and family therapy, appropriateness turns on the patient’s capacity to engage and on whether an involved family is available. Effectiveness turns on symptom and relapse evidence.

AO2: The Two-Sentence Technique

AO2 questions give you a short case study. State the relevant knowledge in one sentence. Then name the specific detail from the case that it explains.

Avolition is a negative symptom involving a marked reduction in self-initiated, goal-directed activity (AO1). In the scenario, Aisha cannot get out of bed to look for work, even though she says she wants a job. This illustrates avolition rather than laziness, because her drive is impaired, not her desire (AO2).

Full marks need the link to the person’s own presentation. A generic description of CBT will not score well on a case-study question. Name the symptom, then the evidence.

Practice the pattern with each symptom, therapy and diagnostic issue in this topic. For more practice, see our guide to answering AO2 questions.

Comparison Questions and Specification Changes

In a compare question, outlining both explanations is not enough. You must set them against each other directly, or the answer is capped below the top band. Good comparison points include:

• Role of the Family: Biological explanations involve the family only passively, through heredity. Family dysfunction explanations hold the family actively responsible.
• Social Sensitivity: A family-behavior framing risks stigmatizing relatives. A biological framing blames them less.
• Treatments: Both explanations led to effective treatments: medication and family intervention.
• Causality: Neither can establish cause and effect, because the supposed cause may be a consequence of the illness.
• Wider Dimensions: Determinism, reductionism, ethics and nomothetic versus idiographic approaches are also creditable. They connect to issues and debates.

Check older past papers for specification changes. Token economies appeared in earlier schizophrenia questions but are no longer in the current specification. Treat them as background only.

---

References

Allen, P., Amaro, E., Fu, C. H. Y., Williams, S. C. R., Brammer, M. J., Johns, L. C., & McGuire, P. K. (2007). Neural correlates of the misattribution of speech in schizophrenia. British Journal of Psychiatry, 190(2), 162–169. https://doi.org/10.1192/bjp.bp.106.025700

Andreasen, N. C. (1982). Negative symptoms in schizophrenia. Archives of General Psychiatry, 39(7). https://doi.org/10.1001/archpsyc.1982.04290070020005

Bagnall, A.-M., Jones, L., Ginnelly, L., Lewis, R., Glanville, J., Gilbody, S., Davies, L., Torgerson, D., & Kleijnen, J. (2003). A systematic review of atypical antipsychotic drugs in schizophrenia. Health Technology Assessment, 7(13). https://doi.org/10.3310/hta7130

Bateson, G., Jackson, D. D., Haley, J., & Weakland, J. (1956). Toward a theory of schizophrenia. Behavioral Science, 1(4), 251–264. https://doi.org/10.1002/bs.3830010402

Buckley, P. F., Miller, B. J., Lehrer, D. S., & Castle, D. J. (2009). Psychiatric comorbidities and schizophrenia. Schizophrenia Bulletin, 35(2), 383–402. https://doi.org/10.1093/schbul/sbn135

Cochrane, R. (1977). Mental illness in immigrants to England and Wales: An analysis of mental hospital admissions, 1971. Social Psychiatry, 12(1), 25–35. https://doi.org/10.1007/BF00578979

Curran, C., Byrappa, N., & McBride, A. (2004). Stimulant psychosis: Systematic review. British Journal of Psychiatry, 185(3), 196–204. https://doi.org/10.1192/bjp.185.3.196

Fromm-Reichmann, F. (1948). Notes on the development of treatment of schizophrenics by psychoanalytic psychotherapy. Psychiatry, 11(3), 263–273. https://doi.org/10.1080/00332747.1948.11022688

Gara, M. A., Minsky, S., Silverstein, S. M., Miskimen, T., & Strakowski, S. M. (2019). A naturalistic study of racial disparities in diagnoses at an outpatient behavioral health clinic. Psychiatric Services, 70(2), 130–134. https://doi.org/10.1176/appi.ps.201800223

Healy, D. (2012). Pharmageddon. University of California Press. https://doi.org/10.1525/9780520951815

Huhn, M., Nikolakopoulou, A., Schneider-Thoma, J., Krause, M., Samara, M., Peter, N., Arndt, T., Bäckers, L., Rothe, P., Cipriani, A., Davis, J. M., Salanti, G., & Leucht, S. (2019). Comparative efficacy and tolerability of 32 oral antipsychotics for the acute treatment of adults with multi-episode schizophrenia: A systematic review and network meta-analysis. The Lancet, 394(10202), 939–951. https://doi.org/10.1016/S0140-6736(19)31135-3

Jauhar, S., McKenna, P. J., Radua, J., Fung, E., Salvador, R., & Laws, K. R. (2014). Cognitive–behavioural therapy for the symptoms of schizophrenia: Systematic review and meta-analysis with examination of potential bias. British Journal of Psychiatry, 204(1), 20–29. https://doi.org/10.1192/bjp.bp.112.116285

Kety, S. S., & Ingraham, L. J. (1992). Genetic transmission and improved diagnosis of schizophrenia from pedigrees of adoptees. Journal of Psychiatric Research, 26(4), 247–255. https://doi.org/10.1016/0022-3956(92)90031-I

Leucht, S., Tardy, M., Komossa, K., Heres, S., Kissling, W., Salanti, G., & Davis, J. M. (2012). Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: A systematic review and meta-analysis. The Lancet, 379(9831), 2063–2071. https://doi.org/10.1016/S0140-6736(12)60239-6

Loring, M., & Powell, B. (1988). Gender, race, and DSM-III: A study of the objectivity of psychiatric diagnostic behavior. Journal of Health and Social Behavior, 29(1). https://doi.org/10.2307/2137177

Meltzer, H. Y. (2012). Clozapine. Clinical Schizophrenia & Related Psychoses, 6(3), 134–144. https://doi.org/10.3371/CSRP.6.3.5

Schizophrenia Working Group of the Psychiatric Genomics Consortium. (2014). Biological insights from 108 schizophrenia-associated genetic loci. Nature, 511(7510), 421–427. https://doi.org/10.1038/nature13595

Stirling, J., Hellewell, J., Blakey, A., & Deakin, W. (2006). Thought disorder in schizophrenia is associated with both executive dysfunction and circumscribed impairments in semantic function. Psychological Medicine, 36(4), 475–484. https://doi.org/10.1017/S0033291705006884

Thornley, B., Rathbone, J., Adams, C. E., & Awad, G. (2003). Chlorpromazine versus placebo for schizophrenia. Cochrane Database of Systematic Reviews, Article CD000284. https://doi.org/10.1002/14651858.CD000284

Trubetskoy, V., Pardiñas, A. F., Qi, T., Panagiotaropoulou, G., Awasthi, S., Bigdeli, T. B., Bryois, J., Chen, C.-Y., Dennison, C. A., Hall, L. S., Lam, M., Watanabe, K., Frei, O., Ge, T., Harwood, J. C., Koopmans, F., Magnusson, S., Richards, A. L., Sidorenko, J., . . . O’Donovan, M. C. (2022). Mapping genomic loci implicates genes and synaptic biology in schizophrenia. Nature, 604(7906), 502–508. https://doi.org/10.1038/s41586-022-04434-5

Vaughn, C. E., & Leff, J. P. (1976). The influence of family and social factors on the course of psychiatric illness. British Journal of Psychiatry, 129(2), 125–137. https://doi.org/10.1192/bjp.129.2.125