Schizophrenia

Classification and Diagnosis of Schizophrenia AO1 (there is no AO3 for this)

The nature of schizophrenia:

Schizophrenia is a type of psychosis, a sever mental disorder in which thoughts and emotions are so impaired that the individual loses touch with external reality

Prevalence:

• Affects 1% of the population at some point.

• Most common between ages 15-35.

• Men and women affected equally.

Diagnosing schizophrenia:

To make a diagnosis of schizophrenia, a clinician would use a diagnostic manual such as DSM-V. DSM (The Diagnostic and Statistical Manual of Psychiatric Disorders) is a classification and description of over 200 mental disorders, grouped in terms of their common features. Version 5 (DSM-V) is the most recent update. DSM is mostly used in the US, whereas in Europe ICD (International Classification of Diseases) is more commonly used. The most recent update of ICD is ICD-11.

Positive symptoms:

The symptoms of schizophrenia are typically divided into positive symptoms and negative symptoms.

Positive symptoms are those that appear to reflect an excess or distortion of normal functions. They include the following:

• Hallucinations - bizarre, unreal perceptions of the environment that are usually auditory (hearing voices that other people can’t hear) but may also be visual (seeing lights, objects or faces that other people can’t see), olfactory (smelling things that other people cannot smell) or tactile (e.g. feeling that bugs are crawling on or under the skin or something touching the skin).

• Delusions - bizarre beliefs that seem real to the person with schizophrenia, but they are not real.

• Disorganised speech – the result of disordered thinking, where the individual has problems organising their thoughts and this shows up in their speech (e.g. word salad, gibberish).

• Disorganised or Catatonic behaviour - includes the inability or motivation to initiate a task, or to complete it once it is started, which leads to difficulties in daily living and can result in decreased interest in personal hygiene. The individual may dress or act in ways that appear bizarre to other people, such as wearing heavy clothes on a hot summer’s day. Catatonic behaviours are characterised by a reduced reaction to the immediate environment, rigid postures or aimless motor activity.

Negative symptoms:

The negative symptoms of schizophrenia are those that appear to reflect a reduction or loss of normal functions, which often persist even during periods of low (or absent) positive symptoms.

Negative symptoms weaken the person’s ability to cope with everyday activities, affecting their quality of life and their ability to manage without significant outside help.

Enduring negative symptoms are sometimes referred to as the ‘deficit syndrome’, characterised by the presence of at least two negative symptoms for 12 months or longer.

Negative symptoms include:

• Alogia (speech poverty) - Lessening of speech fluency and productivity, thought to reflect slowed or blocked thoughts.

• Avolition - Reduction of interests and desires, and inability to initiate or persist in goal-directed behaviour (e.g. sitting idle for hours). LACK OF MOTIVATION.

• Affective flattening - Reduction in the range and intensity of emotional expression including facial expression, voice tone, eye contact, and body language.

• Anhedonia – The inability to experience pleasure.

Reliability and Validity in the diagnosis and classification of schizophrenia AO1

Reliability:

One issue with the classification and diagnosis of schizophrenia is reliability, which refers to the consistency of a diagnosis.

For a diagnosis to be reliable, different psychiatrists should reach the same conclusion when assessing the same patient - known as inter-rater reliability.

However, research has shown that agreement between psychiatrists is often low. For example, in the DSM-5 field trials, the diagnosis of schizophrenia had a kappa score of only 0.46 (Regier et al., 2013).

Test–retest reliability is also an issue, as the same psychiatrist may not reach the same diagnosis at different times, further reducing diagnostic consistency.

In terms of classification of schizophrenia, reliability is an issue because, for example, the DSM requires at least one positive symptom for diagnosis whereas ICD allows for diagnosis with only negative symptoms.

Validity:

Another issue with the classification and diagnosis of schizophrenia is validity, which concerns how accurate and meaningful a diagnosis is. So, whether the system measures what it claims to measure.

If schizophrenia is validly diagnosed, the label should represent a distinct and real disorder separate from other conditions. However, symptoms overlap, as many symptoms of schizophrenia (such as hallucinations or avolition) also appear in other disorders like bipolar disorder and depression.

Ellason and Ross found that patients with dissociative identity disorder (DID) were sometimes diagnosed with schizophrenia, showing that overlapping symptoms make accurate (valid) diagnosis difficult.

Reliability and Validity:

Reliability and validity are closely linked, as if scientists cannot consistently agree on who has schizophrenia (low reliability), then any claims about what schizophrenia actually is (validity) become meaningless.

If you get a 16 marker like “Discuss issues of reliability and validity associated with the classification and/or diagnosis of schizophrenia”, then all of the above is your AO1.

BUT if the 16 marker is like “With reference to _________, outline and evaluate issues of reliability and validity associated with the classification and/or diagnosis of schizophrenia”, then you still use all the above AO1 but you also need to include a bit about the _________.

This _________ can be culture bias, gender bias, co-morbidity, or symptom overlap.

Culture bias:

Culture bias threatens reliability. This is because psychiatrists from different cultural backgrounds may interpret behaviours differently, leading to inconsistent diagnoses across cultures.

For example, hearing voices may be considered a symptom of schizophrenia in Western cultures but in some non-Western cultures it may be considered a normal spiritual experience.

Additionally, there are cultural inconsistencies in terms of how different cultures experience schizophrenia. For example, a study showed that African and Indian ps reported positive experiences with the voices they heard, whereas US ps reported violent, hateful voices. This shows that classification systems are not applied consistently across cultures.

Gender bias:

Gender bias threatens reliability. This is because clinicians may interpret symptoms differently depending on the gender of the patient, leading to inconsistent diagnoses across genders.

For example, Broverman et al. (1970) found that US clinicians equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour. As a result, women were more likely to be perceived as mentally ill when displaying behaviours that deviated from this male norm.

Additionally, diagnostic criteria may be biased towards pathologising one gender more than the other. This can result in overdiagnosis in men or underdiagnosis in women, depending on how symptoms are expressed and interpreted.

There are also gender differences in how schizophrenia is experienced and responded to. For instance, parents tend to be less tolerant of schizophrenic sons than daughters, which may contribute to earlier diagnoses in males. This shows that classification systems are not applied consistently across genders.

Co-morbidity:

Co-morbidity is when two disorders occur together, such as schizophrenia and depression. This threatens validity because this makes it difficult to determine whether symptoms are due to schizophrenia itself or another condition. This reduces the accuracy of diagnosis and challenges the reliability of classification systems.

For example, Buckley et al. (2009) found that 50% of patients with schizophrenia also experience co-morbid depression, and 47% have a lifetime diagnosis of substance abuse. This means that many individuals could receive multiple diagnoses, raising questions about whether schizophrenia is being identified consistently.

Additionally, schizophrenia frequently co-occurs with obsessive-compulsive disorder (OCD). Swets et al. (2014) reported that at least 12% of patients with schizophrenia also met the diagnostic criteria for OCD, and around 25% displayed significant obsessive-compulsive symptoms.

This overlap suggests that the boundaries between disorders are not clear-cut.

Overall, co-morbidity undermines the validity of schizophrenia diagnosis because it blurs distinctions between disorders and makes it harder to apply classification systems consistently.

Symptom overlap:

Symptom overlap threatens validity. This is because many of the symptoms used to diagnose schizophrenia are also found in other mental disorders, making it difficult to distinguish between conditions. As a result, patients may be misdiagnosed or receive multiple diagnoses, reducing the accuracy of classification systems.

For example, Ellason and Ross (1995) found that people with dissociative identity disorder (DID) actually displayed more schizophrenic symptoms than those diagnosed with schizophrenia. This highlights how overlapping symptoms blur diagnostic boundaries.

Additionally, Read (2004) reported that most individuals diagnosed with schizophrenia also have sufficient symptoms to meet the criteria for at least one other disorder, such as depression or bipolar disorder. This shows that classification systems are not applied consistently across different conditions.

Overall, symptom overlap undermines the validity of schizophrenia diagnosis because it makes it unclear whether symptoms belong uniquely to schizophrenia or to another disorder.

Reliability and Validity in the diagnosis and classification of schizophrenia AO3

There is research support for reliability being an issue in the diagnosis and classification of schizophrenia. This is because when 50 senior US psychiatrists were asked to distinguish between bizarre and non-bizarre delusions, the inter-rater reliability score was only 0.40, showing poor agreement between the psychiatrists. This suggests that even trained professionals struggle to apply diagnostic criteria in the same way, indicating that classification systems, such as the DSM-V, allow too much subjectivity when identifying symptoms such as delusions. As a result, patients may receive different diagnoses depending on who assesses them. Therefore, this research supports the view that reliability is an issue, as the diagnosis of schizophrenia is not consistent across psychiatrists.

Support for validity being an issue in the classification and diagnosis of schizophrenia comes from research showing that the diagnosis of schizophrenia has little predictive validity. Studies have found that people diagnosed with schizophrenia rarely share the same outcomes as around 20% recover to their previous level of functioning, 10% show lasting significant improvement, and 30% show some improvement with intermittent relapse. This shows that the diagnosis of schizophrenia does not accurately predict how individuals will progress or respond to treatment, and thus it lacks predictive validity. This means the diagnosis may not represent a single, distinct disorder, thus highlighting that the way schizophrenia is currently classified lacks validity (as the system may not be measuring what it claims to measure).

Support for the idea that reliability and validity are issues in the classification and diagnosis of schizophrenia comes from research by Rosenhan (1973). In his study “On Being Sane in Insane Places,” Rosenhan sent eight psychologically healthy confederates (pseudo-patients) to psychiatric hospitals, all claiming to hear the same fake symptom (the words “empty,” “hollow,” and “thud”). Despite showing no further signs of abnormality once admitted, all but one were diagnosed with schizophrenia and kept in hospital for 7-52 days. This demonstrates a lack of reliability in the diagnostic system as one ps was not diagnoses despite having the same symptoms as the other pseudo-patients. This also shows poor validity as the diagnoses did not accurately reflect the true mental state of the individuals. Therefore, Rosenhan’s findings show how the classification and diagnosis of schizophrenia has reliability and validity issues.

A culture bias AO3 point:

There is support for the idea that culture bias affects reliability of the classification and diagnosis of schizophrenia. Copeland et al. (1971) gave a description of the same patient to both American and British psychiatrists and found that 69% of the American psychiatrists diagnosed schizophrenia, compared to only 2% of the British psychiatrists. This demonstrates that there are clear cultural differences in how symptoms are interpreted, suggesting that the diagnostic systems are not applied consistently across cultures. It shows that what is considered abnormal in one culture might be viewed as normal in another, which reduces inter-rater reliability and questions the validity of the diagnosis. Therefore, Copeland’s study provides strong empirical support for the idea that cultural bias leads to unreliable and invalid diagnoses, showing that classification systems such as the DSM and ICD may not be universally applicable.

A gender bias AO3 point:

There is research support for the idea that gender bias reduces the reliability of schizophrenia diagnosis. Loring and Powell (1988) found that when psychiatrists were presented with identical case vignettes, 56% diagnosed schizophrenia when the patient was described as male or gender-unspecified, but only 20% did so when the patient was described as female. This bias was more pronounced among male psychiatrists. This suggests that diagnostic decisions are not based solely on symptoms, but are influenced by stereotypes and assumptions about gender. If clinicians interpret the same behaviour differently depending on the patient’s gender, then the diagnosis lacks consistency and objectivity. Therefore, gender bias undermines the reliability of schizophrenia diagnosis, as it leads to inconsistent outcomes based on non-clinical factors.

Biological explanations for schizophrenia AO1

Genetic factors

Family studies:

Family studies have established that schizophrenia is more common among biological relatives of a person with schizophrenia, and that the closer the degree of genetic relatedness, the greater the risk.

In Gottesman's (1991) meta-analysis of 40 studies, the findings showed that the greater the genetic relatedness, the higher the concordance rate for schizophrenia. For example, a finding was that children with two schizophrenic parents had a concordance rate of 46%

Twin studies:

If monozygotic (MZ – genetically identica and share 100% of their genesl) twins are more concordant than dizygotic (DZ – who share only 50% of their genes), then this suggests that the greater similarity is due to genetic factors.

Joseph (2004) found that concordance rate for MZ twins was 40.4%, whereas the concordance rate for DZ twins was 7.4%.

Gottesman et al (1972) found MZ concordance rate to be 42% and DZ concordance rate to be 9%.

So essentially, MZ concordance rate is 40% meaning if you have schizophrenia, there is a 40% that your MZ twin will too.

Adoption studies:

Adoption studies look at genetically related twins who have been reared apart.

Using adoption studies is beneficial because they control for the fact that people who share the same genes also tend to share the same environment.

An example of an adoption study comes from Tienari et al. (2000) in Finland:

• Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis

• Compared to just 4 (2%) of the 197 control adoptees (born to non-schizophrenic mothers)

Neural correlates:

Dopamine hypothesis:

The dopamine hypothesis claims that an excess of dopamine in certain brain regions is associated with the positive symptoms of schizophrenia. Schizophrenics are thought to have abnormally high numbers of D₂ receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.

Two key sources of evidence support this…

Drugs that increase dopaminergic activity:

Amphetamine is a dopamine agonist. So, it stimulates dopamine-containing nerve cells, flooding the synapse with dopamine.

Normal individuals exposed to large doses of amphetamines can develop schizophrenia-like symptoms, which typically disappear with abstinence.

Drugs that decrease dopaminergic activity:

Antipsychotic drugs are dopamine antagonists. So, they block dopamine activity in the brain.

By reducing dopamine in neural pathways, these drugs eliminate symptoms like hallucinations and delusions, reinforcing dopamine’s role in schizophrenia.

The revised dopamine hypothesis

Davis and Kahn (1991) proposed:

• Positive symptoms stem from excess dopamine in subcortical areas, especially the mesolimbic pathway.

• Negative and cognitive symptoms arise from dopamine deficits in the prefrontal cortex (mesocortical pathway).

So dopamine is one neural correlate, but you need to know at least one other just in case a question asks for neural correlates. The easiest one is enlarged ventricles because it’s 2 sentences!

Enlarged ventricles:

Ventricles are brain cavities filled with cerebrospinal fluid.

Individuals with schizophrenia often show enlarged ventricles compared to the general population.

Biological explanations for schizophrenia AO3

Genetic factors:

A limitation of the biological explanation is that twin studies may exaggerate the role of genetics. Although monozygotic (MZ) twins show higher concordance rates for schizophrenia than dizygotic (DZ) twins, the concordance is never 100%. Joseph (2004) argued that this difference may reflect environmental factors, since MZ twins are often treated more similarly than DZ twins, due to their identical appearance, and thus encounter more similar environments. This means that higher concordance in MZ twins might not be purely genetic, but influenced by environmental similarity. Therefore, biological explanations cannot fully account for schizophrenia without considering environmental influences.

A limitation of the biological explanation is that adoption studies may be biased due to selective placement. These studies assume that adoptees are randomly placed into adoptive families, regardless of their biological background. However, Joseph (2004) argues that it is highly unlikely that children born to mothers with schizophrenia were placed into the same type of adoptive families as those without such a background. This is because adoption agencies may have considered the child’s psychiatric risk or the mother’s mental health history when choosing adoptive placements. As a result, environmental differences between adoptive families could influence outcomes, undermining the assumption that genetic factors alone explain the development of schizophrenia. Therefore, conclusions drawn from adoption studies may overstate the role of biology.

Neural correlates:

The dopamine hypothesis is supported by evidence from Parkinson’s disease treatment. Individuals with Parkinson’s have low levels of dopamine and are treated with L-dopa to increase dopamine activity. However, a known side effect of L-dopa is the emergence of schizophrenic-like symptoms, such as hallucinations and delusions. This supports the dopamine hypothesis, which claims that excess dopamine is linked to the positive symptoms of schizophrenia. The fact that artificially raising dopamine can induce these symptoms strengthens the biological explanation by showing a clear biochemical link.

A limitation of the biological explanation is that the dopamine hypothesis lacks consistent supporting evidence. Moncrieff (2009) argues that while drugs like cocaine and amphetamines raise dopamine and can induce schizophrenic symptoms, they also affect other neurotransmitters, so dopamine may not be the sole cause. Additionally, post-mortem studies do not always show excess dopamine in schizophrenic patients, suggesting individual differences. Confounding factors such as smoking, which increases dopamine, may also explain why schizophrenics appear to have elevated dopamine levels. This undermines the idea of a direct causal link and suggests the biological explanation may be overly simplistic.

The biological explanation is supported by evidence from drug treatments. Leucht et al. (2013) conducted a meta-analysis of 212 studies and found that antipsychotic drugs were significantly more effective than placebos in treating both positive and negative symptoms of schizophrenia. These drugs work by reducing dopamine activity, which supports the dopamine hypothesis — the idea that excess dopamine contributes to the disorder. The consistency of these findings across a large number of studies strengthens the biological explanation and highlights the practical value of dopamine-targeting treatments.

Psychological explanations for schizophrenia AO1

There are two psychological explanations for schizophrenia: family dysfunction and cognitive explanations.

Family dysfunction:

A psychological explanation of schizophrenia is family dysfunction, which suggests that problems within family communication and relationships contribute to the development of the disorder.

Bateson et al. (1956) proposed the double bind theory, which suggests that children who frequently receive contradictory messages from parents, for example a mother telling her son she loves him yet at the same time turning away in disgust, are prevented from developing an internally coherent understanding of reality, increasing vulnerability to schizophrenic symptoms like disordered thinking.

Another aspect of family dysfunction is expressed emotion (EE), which refers to family a communication style involving criticism, hostility, and emotional over-involvement within the patient. Research has shown that patients returning to high EE environments are at greater risk of relapse, with Linszen et al. (1997) finding that such individuals were four times more likely to relapse than those in low EE families.

Early theorists also proposed the idea of the schizophrenogenic mother (Fromm-Reichmann, 1948), describing a cold, rejecting, and controlling mother who creates an atmosphere of tension and mistrust, thought to contribute to the onset of schizophrenia in vulnerable children.

Cognitive explanations:

The cognitive approach suggests that schizophrenia results from dysfunctional thought processing, meaning individuals process information in a distorted or biased way compared to neurotypical controls. This is especially evident in positive symptoms like delusions and hallucinations.

Delusions can be explained by egocentric bias, where individuals perceive themselves as the central focus of events and make faulty conclusions about external stimuli. For example, muffled voices are interpreted as people criticising them or flashes of light are interpreted as divine signals.

Hallucinations are linked to hypervigilance in terms of excessive attention to auditory stimuli.

• Individuals have a high expectancy for hearing voices, which biases their perception.

• Aleman (2001) suggests they struggle to distinguish between internal imagery and external sensory input.

  • For example, a thought like “What do people think of me?” may be misattributed as an external voice saying “He is not a good person.”

• These misattributions are not corrected because patients lack effective reality testing — they don’t check external sources to verify what they’ve perceived

NOTE:

You could be asked a 16 marker on only one of the explanations, so you would write the AO1 just on the explanation asked for, then write an AO3 point on the other explanation. E.g. if asked a 16 marker on family dysfunction, one of your AO3 points can be about how there’s an alternative explanation - the cognitive explanation.

You can be asked for both though, in which case maybe don’t bother with double bind statements for family dysfunction.

Psychological explanations for schizophrenia AO3

You do unfortunately have to learn all of these!

Family dysfunction:

A limitation of family dysfunction as an explanation is that there is an alternative, potentially better psychological explanation. This is the cognitive explanation, which argues that symptoms arise from dysfunctional thought processing rather than maladaptive family relationships. For example, delusions can be explained by egocentric bias, while hallucinations result from failures in reality testing and hypervigilance. This explanation has greater practical value as its therapy, CBT, has been shown in research to be more successful than family therapy, which is the therapy from the family dysfunction explanation. This therefore suggests that the cognitive explanation has higher credibility in explaining schizophrenia.

(^ this is for if AO1 was JUST family dysfunction)

There is research support for the family dysfunction explanation of schizophrenia. Tienari et al. (2000) conducted an adoption study in Finland, investigating children who had biological mothers with schizophrenia. They found that these adoptees were more likely to develop schizophrenia compared to those with non-schizophrenic biological mothers, but only if they were adopted into families rated as disturbed. In contrast, those raised in healthy, supportive families rarely developed the disorder. This suggests that while a genetic vulnerability may increase the risk of schizophrenia, it is the presence of family dysfunction that can act as a trigger, supporting the idea that maladaptive family environments play a crucial role in the onset of the disorder.

A strength of the double bind theory as an explanation of schizophrenia is that there is research support for it. Berger (1965) found that individuals with schizophrenia reported a higher recall of double-bind statements from their mothers compared to non-schizophrenic controls. This supports the idea that exposure to contradictory and confusing parental communication may contribute to the development of schizophrenic symptoms such as disorganised thinking and paranoia. However, this evidence relies on retrospective self-reports, which may not be reliable, as individuals with schizophrenia could have impaired recall or distorted memories due to their condition. Therefore, while Berger’s findings provide some support for the role of dysfunctional family communication, the validity of this evidence is limited, reducing the overall credibility of the double bind theory.

A weakness of the expressed emotion (EE) explanation is that there are significant individual differences in vulnerability to high-EE environments. Research has shown that not all individuals who live in families high in criticism, hostility, or emotional over-involvement go on to develop schizophrenia, and likewise, not all patients who return to high-EE families experience relapse. This suggests that some people are more resilient or less biologically sensitive to family stress than others. Therefore, the relationship between EE and schizophrenia is not straightforward, as individual differences in stress responses or genetic vulnerability likely moderate this effect. This means that EE alone cannot fully explain the development or relapse of schizophrenia, limiting the explanatory power of family dysfunction as a universal account.

Cognitive explanations:

A strength of the cognitive explanation is that it may be more credible than alternative psychological explanations such as family dysfunction. Family dysfunction theories, like Bateson’s double bind or high expressed emotion, emphasise maladaptive family communication, but they struggle to explain the specific mechanisms underlying symptoms. In contrast, the cognitive approach directly accounts for how delusions arise from egocentric bias and hallucinations from failures in reality testing and hypervigilance. The cognitive explanation also has greater practical value, as CBT based on cognitive principles has been shown to be more effective than family therapy, which derives from the family dysfunction explanation. Therefore, compared to family dysfunction, the cognitive explanation offers both stronger explanatory power and more successful treatment outcomes, increasing its credibility.and in guiding successful treatment.

(^ this is for if AO1 was JUST cognitive explanations)

A limitation of the cognitive explanation is that it focuses mainly on positive symptoms of schizophrenia. It explains hallucinations and delusions through mechanisms like egocentric bias and failures in reality testing. However, it neglects negative symptoms such as avolition or speech poverty, which are equally debilitating and central to the disorder. This means the cognitive explanation provides only a partial account of schizophrenia and lacks full explanatory power.

A limitation is the issue of causality within the cognitive explanation. It assumes that cognitive dysfunction causes schizophrenia, but it may be that schizophrenia itself leads to cognitive deficits. Without longitudinal evidence showing that cognitive biases precede the disorder, it’s unclear whether they are a cause or a consequence. This weakens the validity of the cognitive explanation, as it may be describing symptoms rather than explaining their origin.

A limitation is that cognitive deficits are not unique to schizophrenia. Studies of brain-damaged patients show similar cognitive issues, such as attention problems, yet these individuals do not develop schizophrenia. This suggests that cognitive dysfunction alone is insufficient to cause the disorder and other factors, such as biochemical abnormalities, may be involved. Therefore, the cognitive explanation is unlikely to be a complete account of schizophrenia on its own.

There is research support for cognitive explanations. For example, Sarin and Wallin (2014) found that positive symptoms such as delusions and hallucinations originate from faulty cognition. This is because patients showed egocentric thought patterns, biased information processing, and failures in reality testing. This demonstrates that dysfunctional thought processing directly contributes to the development of schizophrenia’s core symptoms, giving the cognitive explanation strong scientific credibility. Therefore, the cognitive explanation is a well-supported account of schizophrenia, backed by evidence of how faulty cognition underlies positive symptoms.

Drug therapy for schizophrenia AO1

Drug therapy for schizophrenia uses antipsychotic medication to reduce symptoms by acting on dopamine systems in the brain.

There are two types of antipsychotics: typical and atypical.

• Typical antipsychotics combat positive symptoms.

• Atypical antipsychotics also combat positive symptoms but may help with negative symptoms also.

Typical antipsychotics (first-generation), such as chlorpromazine, work as dopamine antagonists by binding to D₂ receptors in the mesolimbic pathway without activating them. This blocks dopamine transmission, reducing positive symptoms like hallucinations and delusions. However, because they also block dopamine in other brain areas, they can cause side effects such as tardive dyskinesia (involuntary movements).

Atypical antipsychotics (second-generation), such as clozapine, also block D₂ receptors but temporarily, because they rapidly dissociate, allowing normal dopamine transmission and reducing movement-related side effects. They additionally act on serotonin receptors (5-HT₂), which may help with negative symptoms (e.g., social withdrawal) and cognitive impairment. Atypical drugs are often used for treatment-resistant patients and have a lower risk of extrapyramidal side effects compared to typical antipsychotics.

Drug therapy for schizophrenia AO3

A strength of antipsychotics as a treatment for schizophrenia is that they have passed placebo-controlled trials. Leucht et al. (2012) conducted a meta-analysis involving 6000 participants, comparing antipsychotics with placebos. They found that 64% of those given a placebo relapsed, compared to 27% who stayed on antipsychotic medication, showing that antipsychotics are significantly more effective than placebos. This supports the effectiveness of drug therapy for schizophrenia, increasing confidence in its use as a treatment.

Top tip: For any evaluation on any drug treatment, you can always say that the drug ‘came out on top’ in placebo trials. We know this is always the case because for a drug to be available to patients it HAD to pass placebo trials. So there you have it, an easy-to-remember eval point for all essays on drug treatment.

A weakness of drug therapy for schizophrenia is that it can lead to motivational deficits. Ross and Read (2004) argue that being prescribed medication ‘reinforces the fact that there is something biologically wrong with you’. This belief may reduce the patient’s motivation to seek out other potential triggers of their schizophrenia that need to be addressed, such as stress, family problems, or social factors. Therefore, drug therapy might discourage holistic treatment approaches, limiting recovery.

A weakness of drug therapy for schizophrenia is that typical antipsychotics are associated with severe side effects, creating ethical concerns. These drugs affect the extrapyramidal brain area responsible for motor control, often causing tardive dyskinesia, which involves uncontrollable movements of the lips, tongue, face, or hands. Around 30% of patients on typical antipsychotics develop this condition, and in 75% of cases it is irreversible. This raises an ethical dilemma: should clinicians keep medication doses low to reduce side effects, risking symptom relapse, or increase dosage for symptom control, which heightens the chance of serious, untreatable side effects? Such risks and ethical issues undermine the appropriateness of drug therapy as a sole treatment for schizophrenia.

A limitation of drug therapy for schizophrenia is that it often provides only a short-term fix. When patients stop taking medication, relapse into a schizophrenic state is highly likely. This suggests that antipsychotic drugs do not address the underlying causes of schizophrenia, meaning long-term recovery may require additional treatments such as psychological therapy. Therefore, drug therapy alone may not be sufficient for sustained symptom management.

Another weakness is that the effectiveness of drug therapy is limited by patient compliance. Because of their delusions, individuals with schizophrenia are often reluctant to take medication. This non-compliance reduces the overall success of drug therapy, as symptoms persist or worsen without consistent treatment. Therefore this undermines the appropriateness of drug therapy as the sole treatment for schizophrenia.

Cognitive Behaviour Therapy (CBT) as a treatment for schizophrenia AO1

Cognitive Behavioural Therapy for Psychosis (CBTp) is a psychological treatment recommended by NICE for individuals with schizophrenia, usually alongside antipsychotic medication.

Its main aim is to correct distorted or irrational beliefs that contribute to psychotic symptoms such as delusions. For example, a person may believe their behaviour is controlled by external forces or that they are being followed by the FBI.

In CBTp, therapy often begins with assessment, where the patient shares their thoughts and experiences so the therapist can understand their symptoms and set realistic goals. This is followed by engagement, which focuses on building trust and a collaborative relationship through empathy and validation, helping the patient feel supported.

CBTp helps patients challenge irrational beliefs by using the LEP approach, which stands for Logical, Empirical, and Pragmatic questioning. This involves asking:

• Logical: “Does it make sense that the FBI would follow me?”

• Empirical: “Is there any actual evidence that supports this belief?”

• Pragmatic: “Is thinking this way helpful for me in my daily life?”

By systematically questioning the validity and usefulness of these thoughts, patients learn to replace irrational interpretations with more balanced and realistic explanations.

Techniques also include setting behavioural homework tasks, such as keeping a diary to reflect on alternative explanations (e.g., the patient may write “a car followed me home” but then after reflecting they add “it might have been my neighbour”).

CBTp can be delivered in groups but is more commonly provided one-to-one, and NICE recommends at least 16 sessions.

Cognitive Behaviour Therapy (CBT) as a treatment for schizophrenia AO3

A strength of CBT is that it offers advantages over standard care (drug therapy). For example, a NICE review (2014) compared CBT with standard care using antipsychotics and found that patients receiving CBT had lower relapse rates and reduced symptom severity. However, many studies in this review involved patients who were receiving both CBT and antipsychotics, making it difficult to isolate the effects of CBT alone. This means the improvement could be due to the combination of treatments rather than CBT by itself. Therefore, while research suggests CBT is effective for schizophrenia, its benefits may have been overstated, as the positive outcomes might reflect the combined effect of CBT and medication rather than CBT alone.

A weakness of CBT is that it is expensive and therefore inaccessible to many people who could benefit from it. Research shows that only 1 in 10 individuals who could benefit from CBTp actually receive it, highlighting a significant gap in availability. Even when therapy is offered, attendance rates are often low because patients with schizophrenia may experience negative symptoms such as avolition, which reduces motivation to attend sessions, or delusional thinking, which can lead to distrust of the therapist. These barriers mean that CBTp is not widely implemented in practice, and as a result, we may not know its true effectiveness because so few people complete the full course of therapy. This raises concerns about its practicality as a large-scale treatment option compared to more accessible interventions like medication.

A weakness of CBT for schizophrenia is that its effectiveness depends on the stage of the disorder. Research by Addington et al. found that during the initial acute phase of schizophrenia, the self-reflection component of CBT is not particularly useful because patients are often too disoriented or distressed to engage meaningfully with therapy. However, in the later stages of the disorder, once psychotic symptoms have been stabilised through antipsychotic medication, patients are better able to benefit from CBT techniques such as self-reflection, especially in group-based settings. This suggests that CBT is not universally effective across all stages of schizophrenia and may only be suitable as a complementary treatment after medication has reduced acute symptoms, limiting its applicability as a standalone intervention.

A weakness of CBT as a treatment for schizophrenia is that its benefits may have been overstated due to flawed research. For example, meta-analyses that suggest CBT is effective often fail to account for study quality, which can lead to biased findings (Juni et al., 2001). Specifically, some studies do not mask the treatment condition when assessing later symptoms, meaning psychiatrists may know which patients received CBT, introducing observer bias. Additionally, some studies fail to randomly allocate participants to CBT and control conditions, reducing internal validity. More methodologically rigorous meta-analyses indicate that CBTp effectiveness may be lower than originally thought. Therefore, these methodological issues suggest that the reported benefits of CBT for schizophrenia may not be as strong as previously believed, reinforcing the idea that its effectiveness could be overstated in research.

Family therapy AO1

Family therapy (FT) is a psychological intervention designed to support individuals with schizophrenia by improving the family environment and reducing factors that contribute to relapse.

It focuses on lowering family levels of expressed emotion (EE), which is characterised by criticism, hostility, and emotional over-involvement, because research shows that patients returning to high EE families are up to four times more likely to relapse.

NICE guidelines recommend FT for all individuals with schizophrenia who live with or have regular contact with family members.

The therapy typically lasts between 3 and 12 months and involves at least 10 sessions.

A key component of FT is psychoeducation, which helps family members understand schizophrenia and its symptoms so they can provide better support.

The therapist acts as a mediator during sessions, encouraging open communication where the patient can express their needs and identify what worsens their condition.

FT employs strategies such as forming alliances with relatives, reducing the emotional climate within the family, and enhancing relatives’ ability to anticipate and solve problems. It also aims to reduce expressions of anger and guilt, maintain reasonable expectations, and encourage relatives to set appropriate boundaries.

Overall, FT seeks to create a calmer, more supportive family environment that minimises stress and negative interactions, thereby reducing relapse risk and improving long-term outcomes for the patient.

Family therapy AO3

A strength of family therapy is that research evidence supports its effectiveness in improving outcomes for individuals with schizophrenia. Pharoah et al. (2010) conducted a meta-analysis and found that family therapy significantly improved patients’ mental state and social functioning compared to standard care. This suggests that family therapy can play an important role in reducing relapse rates and enhancing quality of life by creating a more supportive family environment. However, its effectiveness may partly be due to increased medication compliance because patients who engage in family therapy are more likely to take their antipsychotic medication. This makes it difficult to determine whether improvements are due to the therapy itself or the medication (or both), which limits the ability to draw firm conclusions about its independent effectiveness.

An ethical concern with family therapy is that it can imply the family is to blame for the individual’s schizophrenia, even when this may not be the case. Family therapy often focuses on reducing expressed emotion (EE) and improving communication within the family. While these changes can be helpful, the emphasis on family dynamics as a contributing factor may lead relatives to feel guilt or responsibility for the illness. This can create unnecessary emotional distress for family members who may already be struggling to support their loved one. It risks damaging relationships and could even discourage families from engaging with therapy if they feel blamed. Therefore, while family therapy aims to improve outcomes, it must be delivered sensitively to avoid reinforcing stigma or guilt, ensuring that families understand schizophrenia is a complex condition with multiple causes, not simply the result of their behaviour.

A limitation of family therapy is that it may not be appropriate for all individuals with schizophrenia. Family therapy is most effective when schizophrenia symptoms are linked to high levels of expressed emotion (EE) within the family. If a person comes from a supportive and low-stress family environment, the therapy is unlikely to provide significant benefits. This means family therapy is not a universal treatment and its applicability depends on the underlying causes and context of the individual’s condition. For those without problematic family dynamics, other interventions such as medication or cognitive therapies may be more suitable. Therefore, while family therapy can be highly beneficial for some, its limited scope reduces its overall usefulness as a treatment for schizophrenia.

A strength of family therapy is that research supports its positive impact on patients and their families. For example, Lobban et al. (2013) reviewed 50 family therapy studies and found that 60% reported significant benefits, such as reductions in expressed emotion (EE) and improvements in relationship quality within the family. This suggests that family therapy not only helps manage symptoms but also enhances the overall family dynamic, creating a more supportive environment that can reduce relapse rates and improve long-term outcomes. Therefore, the consistent evidence of positive changes in family functioning and emotional climate highlights family therapy as an effective intervention for individuals with schizophrenia.

A limitation of family therapy is that some psychologists argue it is more of a management therapy rather than a direct treatment for schizophrenia. Family therapy primarily focuses on reducing expressed emotion (EE), improving communication, and creating a supportive environment rather than addressing the core symptoms of schizophrenia such as hallucinations or delusions. This means that while family therapy can help reduce relapse rates and improve social functioning, it does not directly treat the biological or cognitive causes of schizophrenia. Instead, it manages external stressors that may exacerbate symptoms, making it more of a complementary approach rather than a standalone treatment. Therefore, family therapy may be best viewed as part of a broader treatment plan alongside medication and other psychological interventions, rather than as an independent cure for schizophrenia.

A limitation of family therapy research is that many studies lack proper blinding, which can introduce significant bias. In several studies, the assessors who rate whether patients have improved after therapy are aware of which treatment the patient received, for example, whether they had family therapy or an alternative intervention. This lack of blinding means that raters’ expectations about the effectiveness of family therapy could influence their judgments. Such observer bias can artificially inflate the reported success of family therapy because improvements may reflect the assessor’s beliefs rather than actual changes in the patient’s condition. This undermines the internal validity of the research and makes it harder to draw firm conclusions about the true effectiveness of family therapy. Therefore, the absence of blinding in many studies suggests that findings supporting family therapy should be interpreted with caution, as the results may not accurately represent its real impact.