Schizophrenia - Paper 3 Flashcards

Paper 3

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1
Q

How is Schizophrenia classified?

A
  • The DSM-5 (The Diagnostic and Statistical Manual of Mental Disorders) published by the American Psychiatric Association (APA)
  • The ICD – 10 (International Classification of Diseases) produced by the World Health Organisation (WHO).
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2
Q

What is criterion A for the classification of schizophrenia?

A

Two (or more) of the following symptoms must be present for a significant portion of time during a 1-month period.

At least one of these should include an active symptom (1- 3).

  1. Delusions
  2. Hallucinations
  3. Disorganised speech
  4. Grossly disorganised or catatonic behaviour
  5. Negative symptoms (i.e. diminished emotional expression or avolition)
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3
Q

What is criterion B for the classification of schizophrenia?

A

There should be a reduction in one or more major areas of functioning such as work, interpersonal relations or self-care.

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4
Q

What is criterion C for the classification of schizophrenia?

A

Continuous signs of the disturbance must persist for at least 6 months, during which the patient must experience at least 1 month of active symptoms.

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5
Q

What are the positive symptoms of schizophrenia?

A

Hallucinations and delusions

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6
Q

What are hallucinations?

A

These are unusual sensory experiences (visual, auditory, smell, touch or taste). About 70% of people with schizophrenia suffer from auditory hallucinations. Typically, the person hears a voice. This voice/voices may critically comment on their behaviour, warn them of future dangers, accuse them of something they did not do, or give orders

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7
Q

What are delusions?

A

There are irrational beliefs that have no basis in reality. Delusions can make a sufferer of schizophrenia behave in ways that make sense to them but seem bizarre to others.

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8
Q

What are delusions of persecution?

A

This is the belief that they are being spied on or plotted against by others such as the government.

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9
Q

What are delusions of grandeur?

A

This is when a person believes they are an important historical or religious figure, such as the queen or the pope.

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10
Q

What are the negative symptoms of schizophrenia

A

Speech poverty and avolition

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11
Q

How can you remember the difference between positive and negative symptoms?

A

Positive - behavioural excess
Negative - behavioural deficit

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12
Q

What is speech poverty?

A

This is a decrease in speech fluency and productivity. They produce fewer words in a given time on a task of verbal fluency (e.g. name as many animals as you can in 1 minute). This is not due to less verbal ability than people without schizophrenia, but more a difficulty spontaneously producing them. Patients will often slur their responses, not pronouncing consonants clearly and their words might trail off into a whisper.

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13
Q

What is avolition?

A

: A reduction of interests and desires as well an inability to initiate and persist in goal-directed behaviour. For example, sitting in the house for hours every day, doing nothing. Avolition is distinct from poor social functioning, which can be the result of other circumstances (e.g. having no friends and family available to have social contact with). To be classed as avolition, there must be a reduction in self-initiated involvement in activities that are available to the patient.

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14
Q

What is reliability in diagnosis and classification of schizophrenia?

A

Consistency in diagnosis. Whether there is agreement in the diagnosis of SZ by different psychiatrists across time and cultures. This is inter-rater reliability. It can be seen in whether diagnostic tests are consistent on different occasions - test-retest

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15
Q

What is a criticism of reliability of classification?

A

DSM and ICD tools are routinely used with a high level of reliability by mental health clinicians. Cheniaux (2009) asked two psychiatrists to independently diagnose 100 patients using both the DSM and the ICD. Inter-rater reliability was poor, for example, using the DSM, one psychiatrist diagnosed 26 patients with schizophrenia whilst the other only diagnosing 13. This a weakness of the diagnostic systems as they failed to produce consistent results and therefore shows that the reliability of diagnosing schizophrenia is poor.

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16
Q

What is co-morbidity? (reliability)

A

The presence of one or more additional disorders or diseases simultaneously occurring with SZ. substance abuse (47%), Anxiety/panic disorder (15%), symptoms of depression (50%). If a sufferer can experience simultaneous disorders this suggests that schizophrenia may not actually be a separate disorder. This could lead to different medical professionals giving different diagnoses of the same patient.

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17
Q

What is an evaluation point of comorbidity?

A

There is a large body of evidence to suggest that many sufferers do also have issues of substance abuse. Buckley (2009) found that around 50% of patients with schizophrenia also have depression or substance abuse. Alcohol, cannabis and cocaine are substances that can be abused by people with schizophrenia (possibly as a way of self-medicating) and not only does such co-morbid substance abuse make a reliable diagnosis of schizophrenia difficult to achieve, it also leads to lower levels of functioning, increased hospitalisations and lower compliance with medication, which makes effective treatment more difficult to achieve. This is a strength because it demonstrates the complexities involved in giving a reliable diagnosis if the person with schizophrenia is also using recreational drugs. Sufferers who use recreational drugs may find it difficult to achieve a reliable diagnosis as it’s difficult to know what symptoms are a direct effect of having schizophrenia and what are the symptoms of substance abuse.

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18
Q

What is culture bias in diagnosis and classification of SZ?

A

Culture bias reduces the validity of the diagnostic system. Both the ICD and DSM were developed by Western clinicians and are criticised for lacking cultural relativism. Therefore, people who show behaviours such as hearing voices, which may be normal in their own culture, are sometimes classified as having schizophrenia.
Culture bias can also affect the reliability of the diagnostic system. Research suggests there is a significant variation between cultures when it comes to diagnosing schizophrenia.
Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. 60% of the US psychiatrists diagnosed schizophrenia, but only 2% of British ones did, showing diagnosis was unreliable across different cultures.

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19
Q

What is an evaluation point of culture bias in classification of SZ?

A

Research suggests that the diagnosis of schizophrenia is affected by culture bias. Pinto and Jones (2008) reported that in Haiti some people believe that voices are communications from ancestors. British people of African – Caribbean origin are up to nine times more likely to receive a diagnosis than white British people, although people living in African – Caribbean countries are not, ruling out a genetic vulnerability. This is a weakness of the diagnostic system because it highlights that the difference in diagnostic statistics of some cultural groups is due to the biased overinterpretations of symptoms by some psychiatrists.

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20
Q

What is validity in diagnosis and classification of SZ?

A

This is the extent to which the methods used to measure schizophrenia are accurately measuring schizophrenia. For example, the patient may have hallucinations but is not suffering with schizophrenia (symptom overlap and comorbidity) or it may be that psychiatrists are misinterpreting the behaviour of the patient (gender/culture bias). Additionally, different assessment systems (ICD/DSM) may arrive at completely different diagnoses. We can assess validity by using predictive validity - if a diagnosis leads to successful treatment, then diagnosis is seen as valid. The research findings on whether the diagnosis of schizophrenia is valid are very mixed. Some researchers report that when you match patients diagnosed with schizophrenia to the DSM criteria there is a good correlation (Hollis, 2000), suggesting that diagnosis is valid.

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21
Q

What is an evaluation point of validity in classification of SZ?

A

A threat to the validity of diagnosing schizophrenia is highlighted by the fact that in the same way that people diagnosed with schizophrenia rarely share the same symptoms, likewise there is no evidence that they share the same outcomes. The prognosis for patients diagnosed with schizophrenia varies with about 20% recovering their previous level of functioning. 10% achieving significant and lasting improvement, and about 30% showing some improvement with intermittent relapses. This is a problem because a diagnosis therefore, has little predictive validity because some people never appear to recover from the disorder, while many do.

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22
Q

What is the issue of gender bias in classification of SZ?

A

Gender bias in the diagnosis of schizophrenia occurs when the accuracy of diagnosis is dependent on the gender of an individual; the diagnostic criteria may be gender-biased or clinicians may base their judgments on stereotypical beliefs about gender.

Gender bias refers to the differential treatment of males and females in the diagnoses of schizophrenia. Statistically, since the 1980s, men are diagnosed with schizophrenia more often than women. It may be that due to genetic factors, women are genetically less vulnerable than men. However, it seems more likely that women are underdiagnosed because they are more likely to have support around them and therefore function better than men.

Cotton (2009) found that in patients with schizophrenia that female patients function better than male patients. E.g., they are more likely to work, and have good family relationships. This may explain why women are not diagnosed with schizophrenia as frequently as men. It appears that their better interpersonal functioning may bias clinicians to under-diagnose schizophrenia in women. This also explains why the age of onset tends to be much younger in males than in females.

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23
Q

What is an evaluation point of gender bias in sz?

A

Research suggests that gender bias is a problem in the diagnosis of schizophrenia and subsequent treatment offered. Evidence shows that males could be more likely to be committed to psychiatric institutions (referred to as being hospitalised) when they show mild signs of schizophrenia, due to the risk of socially deviant behaviour (e.g. violence). Females, on the other hand, are likely to be voluntary patients (even though they too spend some time in hospital) because they are more likely to seek help earlier. This is a strength as it supports the idea that gender differences in diagnosis exist. It appears that their better interpersonal functioning may bias clinicians to under-diagnose schizophrenia in women. This therefore threatens the validity of the diagnostic system because people may get an incorrect or no diagnosis based on their gender, rather than their symptoms.

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24
Q

What is symptom overlap?

A

This occurs when symptoms of schizophrenia are also found in other disorders. For example, positive symptoms, such as delusions and negative symptoms such as avolition occur in both schizophrenia and bipolar disorder. This makes it difficult for clinicians to accurately decide which particular disorder someone is suffering from when diagnosing.

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25
Q

What is the evaluation of symptom of overlap?

A

Research suggests symptom overlap can cause issues when accurately and reliably diagnosing schizophrenia.
Ophoff (2011) found a genetic overlap between bipolar disorder and schizophrenia. Three of the seven gene locations on the genome associated with schizophrenia were also associated with bipolar disorder. Both schizophrenia and bipolar disorder involve positive symptoms (such as delusions) and negative symptoms (such as avolition). This highlights the problem when trying to distinguish schizophrenia from other illnesses and in terms of classification this suggests that schizophrenia and bipolar disorder may not be two different conditions but variations of single condition.

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26
Q

What is a general evaluation point about the reliability and validity of classification and diagnosis of SZ?

A

A major consequence of invalid or unreliable diagnosis of SZ relates to the social stigma carried by being incorrectly labelled: Such inaccurate diagnosis can have a long-lasting negative impact on the lives of those diagnosed. Despite these problems, the classification systems do at least allow professionals to share a common language which helps in communicating ideas and also allows greater opportunities for research which can lead to a better understanding of schizophrenia.

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27
Q

What are biological explanations of SZ?

A

Dopamine hypothesis, enlarged ventricles, genetics

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28
Q

What is the dopamine hypothesis?

A

This biochemical explanation suggests that the positive symptoms of schizophrenia are the result of the overactive transmission of the neurotransmitter dopamine. Sufferers of Sz are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. Dopamine neurons play a key role in guiding attention, so disturbances in this process may well lead to the problems relating to attention, perception and thought found in people with schizophrenia.

An excess of dopamine has been found in the Broca’s area. As the Broca’s area is responsible for speech production, an excess of dopamine in this area may be responsible for auditory hallucinations.

Recent versions of the dopamine hypothesis have focused on abnormal dopamine levels in the pre-frontal cortex (outer layer of the brain). For example low levels in the prefrontal cortex (responsible for thinking and decision making) are linked to the negative symptoms of schizophrenia. Therefore, it appears that both high and low levels of dopamine, in different brain regions, are involved in schizophrenia.

29
Q

What are the positive evaluation points of the dopamine hypothesis?

A

PET scans: Wong found an increase in the number of dopamine receptors in several brain regions in patients with schizophrenia.
This is a strength because it supports the view that schizophrenia is caused by unusually high levels of these receptors, increasing the validity of the dopamine hypothesis.

Drug use: Drugs such as cocaine and amphetamines increase dopamine levels in the brain, causing schizophrenic-like symptoms in normal people. Additionally, Parkinson’s disease is caused by a lack of dopamine in the brain and a drug called L-dopa is used to increase these levels. However, if the dosage is too high, patients suffer from schizophrenic-like side effects.
These examples are a strength because they lend further support to the view that dopamine is the primary cause of many schizophrenic symptoms.

Practical applications: It led to the creation of anti-psychotic drugs, such as chlorpromazine, which reduce the amount of dopamine in the brain and therefore reduce positive symptoms of schizophrenia.
This is a strength because the success of these drugs strengthens the validity of the dopamine hypothesis as an explanation for Schizophrenia i.e. if the drugs help reduce the symptoms of schizophrenia by reducing the levels of dopamine this suggests the symptoms are caused by high levels of dopamine.

30
Q

What are enlarged ventricles?

A

Early research was focused on people with schizophrenia having enlarged ventricles (the fluid-filled gaps between brain areas). Enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex, which recent scanning studies have also linked to the disorder. Early research focused on sufferers of schizophrenia having enlarged ventricles and these were associated with the negative symptoms of schizophrenia such as avolition and speech poverty. There are neural correlates for both negative and positive symtpoms

31
Q

What are neural correlates of negative symptoms?

A

one negative symptom is avolition, this is the loss of motivation. Motivation is the anticipation of receiving a reward, one area of the brain ventral striatum is involved in anticipation. It is therefore logical that abnormality of this area may be involved in the development of avolition.
Juckel (2006) measured the activity levels in the ventral striatum in schizophrenics and found lower levels of activity than those in the control group. They observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms. Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia.

32
Q

What are the neural correlates of positive symptoms?

A

positive symptoms also have neural correlates. Allen (2007) scanned the brains of patients experiencing auditory hallucinations and compared them to the control group brains whilst they identified pre-recorded speech as theirs or others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucinations group, who also made more errors than the control group. Therefore, reduced activity in these two areas of the brain is a neural correlate of auditory hallucinations.

33
Q

What are the positive evaluation points of enlarged ventricles?

A

Yoon et al., (2013) used fMRI scans to examine the brains of 18 patients with schizophrenia and 19 people without schizophrenia performing a memory task. Schizophrenic participants had decreased activity in the prefrontal cortex and diminished connectivity between other parts of the brain (the striatum), the stronger the symptoms of schizophrenia were.
This suggests that abnormal functioning of the prefrontal cortex-basal ganglia brain circuit may be related to the cognitive deficits experienced by schizophrenics.
The use of objective, replicable, brain scans as evidence for this explanation has increased the scientific credibility of this explanation for schizophrenia as it has allowed for a direct objective comparison of the neurological differences between brains of patients with the disorder and those without schizophrenia.

34
Q

What are the negative evaluation points of enlarged ventricles as a cause for SZ?

A

As much of the evidence to support neural correlates is correlational, it is impossible to establish causation.
For example, it is possible that schizophrenic symptoms cause changes in the brain (rather than the other way round).
Furthermore, not all patients with schizophrenia have evidence of enlarged brain ventricles and some people have enlarged ventricles but do not suffer with schizophrenia
This is a weakness because it makes it difficult to draw firm conclusions about the role of neural correlates in the causes of schizophrenia, thus reducing the validity of this theory and clearly demonstrating how using the enlarged ventricles theory alone to explain the cause of all types of schizophrenia is not possible.

35
Q

What is an overall evaluation point for neural correlates as an explanation for the cause of SZ?

A

The neural correlates explanation is no longer accepted as a complete explanation of schizophrenia. According to the diathesis-stress model, faulty levels of dopamine alone are unlikely to cause the disorder. Instead, it would suggest that while faulty dopamine levels may make a person vulnerable to developing schizophrenia, the onset of the condition must be triggered by a stressful life events such as family problems or drug abuse.

36
Q

What are the genetic explanations of SZ?

A

it is argued that schizophrenia is passed on from one generation to the next through genetic inheritance. Therefore, in theory, the more closely related the family member is to the person with schizophrenia, the greater their chance of developing the disorder. No single gene is thought to be responsible for the development of schizophrenia and it is more likely that different combinations of genes make individuals more vulnerable to the disorder and so schizophrenia is believed to be ‘polygenic’.

Much of the evidence for this explanation comes from family studies, twin studies and adoption studies. These studies are used to establish a concordance rate (or the degree to which relatives share the same disorder). For example, identical (monozygotic) and non-identical (dizygotic) twins where one of each twin pair has schizophrenia can be compared to see how often the other twin also shows the illness. If schizophrenia is genetic then it is argued that monozygotic (MZ) twins should have higher concordance rates for the disorder than dizygotic (DZ) twins.

Gottesman found that children with two schizophrenic parents had a concordance rate of 46%, children with one schizophrenic parent a rate of 13%, and siblings (where a brother or sister had schizophrenia) a concordance rate of 9%.

37
Q

What are the positive evaluation points for genetic explanations of SZ?

A

Twin studies: There is strong support for a genes as a cause of schizophrenia. Twin studies have found a concordance rate of 40% for MZ twins compared to only just over 7% for DZ twins (Joseph, 2004). This suggests a genetic cause of schizophrenia since the MZ twins share 100% of their genes and had the higher concordance rates for the disorder compared to the DZ twins who share only 50% of their genes (a difference of 33%). However, if schizophrenia is caused by genetic factors alone then the concordance rates would be expected to be 100% for identical twins (MZ) since they have the exactly the same genetic makeup. Furthermore, some critics have claimed that the higher concordance rates for MZ twins compared to DZ twins is because they are more likely to be treated similarly and have the same environmental experiences. This suggests that the genetic explanation of schizophrenia may not provide a complete explanation.

Family studies: Evidence to support the genetic explanation for schizophrenia has been provided from family studies. Varma (1997) found 16% of the first degree relatives of someone with schizophrenia developed schizophrenia compared to only 7% of the controls. This is a strength of the genetic explanation because it demonstrates that the closer the genetic relatedness to someone with schizophrenia, the greater the chance of developing the disorder. However, it is possible that the increased rate of schizophrenia amongst those with parents with schizophrenia was due to environmental rather than genetic influences. This means that it is not possible to firmly conclude that schizophrenia is caused by maladaptive genes.

Adoption studies: Tienari et al (2004) compared adopted children whose biological mothers had SZ compared to a control group of adoptees without any genetic risk. He found a much higher rate of SZ amongst those whose biological mothers had SZ. This is a strength because even when the environmental influence of the biological mother was removed, the genetic risk was still evident therefore supporting the theory that genetic factors cause schizophrenia. However, it was found that a ‘healthy’ adoptive family could protect against those with a high genetic risk developing schizophrenia suggesting the environment does play a role in schizophrenia onset as well.
(You could talk about the Diathesis-stress explanation here)
A reasonable conclusion is that schizophrenia is caused by a complex interaction of both genetic and environmental factors and it is not possible to say with certainty which contributes the most. Most psychologists believe that genes predispose certain individuals toward schizophrenia BUT this will only become apparent under particular environmental conditions (diathesis–stress model).

38
Q

What are some general evaluation points for biological explanations of SZ?

A

All biological explanations of schizophrenia (neural correlates and genetics) is that they could be said to be deterministic. This means that the disorder is inevitable in those with the wrong genes (genes influence neurotransmitters and how the brain develops). Nobody would try to argue that a person with schizophrenia has free will and choice in their experience of suffering with the illness but taking a deterministic view when explaining an illness can be controversial.

This deterministic view of the cause of Sz could be viewed both positively and negatively. On the one hand, biological explanations could be said to be more humane because the sufferer is not blamed for their illness as it is not something they can control.

On the other hand, a biologically deterministic explanation could have a negative impact because a sufferer may feel that they are ‘sick’ and that there is little they can do to recover from this disorder.

However, the diathesis-stress model doesn’t claim a deterministic view. It suggests people with genetic abnormalities may have a predisposition (an increased risk). If a person reduces their risk factors they can influence whether they develop schizophrenia or not.

Furthermore, biological explanations could also be said to be reductionist because they focus wholly on one level of explanation i.e internal factors (e.g. genes and neurochemistry) and ignore environmental factors. Indeed, there are psychological explanations of schizophrenia such as family explanations which argue that the way parents treat their child is the main influence on schizophrenia onset or that poor people are more at risk of schizophrenia. As a result, biology alone may not explain all aspects of schizophrenia.

39
Q

What are the 2 types of biological treatment for SZ?

A

Atypical and Typical antipsychotics

40
Q

What are Typical Antipsychotics?

A

Chlorpromazine is a dopamine antagonist that works to reduce the effects of dopamine. They achieve this by binding to dopamine receptors (particularly the D2 receptors) but not stimulating them, thus blocking their action. By reducing the effect of dopamine, the positive symptoms of schizophrenia, such as hallucinations and delusions are reduced. These symptoms are linked to the excesses of dopamine and are reduced.

41
Q

What are Atypical Antipsychotics?

A

Atypical Antipsychotic drugs such as Clozapine and Risperidone are the ‘newer’ types of drug treatments. Clozapine acts on the dopamine system by blocking D2 receptors. Unlike the typical antipsychotics, these drugs only temporarily block dopamine receptors before dissociating to allow normal dopamine transmission. The effect being that it reduces the positive symptoms of schizophrenia and the temporary effect on the D2 receptors leads to less extra-pyramidal side effects (movement disorders). Atypical antipsychotics also affect serotonin (5-HT) receptors in the brain, particularly the 5-HT2A receptors which are considered to be vital in the role of the negative symptoms of schizophrenia. The atypical drugs help improve patients’ mood and improve cognitive functioning.

42
Q

What are the supportive evaluation points for drug therapy as treatment for SZ?

A

There is a wealth of supporting research for the effectiveness of typical antipsychotic drugs in the treatment of Schizophrenia. Thornley (2003) reviewed studies comparing the effects of Chlorpromazine to reduce symptoms. Some sufferers were given the drug and others were given a placebo The data included over 1,000 participants and found that Chlorpromazine was associated with better overall functioning and reduced symptoms and also that the relapse rate was lower when the drug was taken, compared to the placebo group. This quantitative data shows clear support for the effective use of typical anti-psychotics, and has also used a scientific way of conducting the research with control group comparisons. Antipsychotics are effective, relatively cheap to produce, easy to administer and have positive effects on many sufferers, allowing them to live normal lives outside of mental institutions. Less than 3% of people with schizophrenia in the UK live permanently in hospital. This further supports the use of antipsychotics as they have practical applications and benefits to the economy.

There is also a wealth of supporting research for the effectiveness of atypical antipsychotic drugs when treating Schizophrenia.
(Example) In a review, Meltzer (2012) concluded that Clozapine (an atypical antipsychotic) was more successful in treatment resistant cases of schizophrenia than typical antipsychotics (30-50% more effective). This is clear support for the use of atypical antipsychotic medication to treat schizophrenia and supports the idea that Schizophrenia is caused by a chemical imbalance as the drugs correct the imbalance of neurotransmitters. However, Critics have argued that there are serious flaws with the evidence showing drug therapy is an effective treatment for schizophrenia. Healy (2012) claims most studies only focus on short term effects and the positive effects have been exaggerated because the data has been published numerous times. This means that caution should be observed when evaluating the success of drug therapy as an effective treatment for schizophrenia.

43
Q

What are the negative evaluation points for biological treatments of SZ?

A

One major issue with using drugs to treat schizophrenia is that serious sides effects can occur.
(Example) Serious side effects of typical antipsychotics can lead to movement disorders (extrapyramidal side effects) such as Tardive Dyskinesia. This is characterised by involuntary chewing and sucking, jerky movements and twisting of the mouth and face, all of which can be permanent. About 30% of people taking antipsychotic medication go on to develop tardive dyskinesia. This side effect is irreversible in 75% of cases (Hill, 1986).
(Link) This is weakness because it often leads to sufferers stopping the medication and suggests that drug therapy is not the most effective treatment for some sufferers of schizophrenia. However, one strength of atypical antipsychotic drugs is that rates of tardive dyskinesia have been found to be much lower for atypical antipsychotics at just 5% (Jeste et al, 1999). This suggests atypical antipsychotics may ultimately be more appropriate than conventional antipsychotics as they have fewer side effects, which in turn means patients are more likely to continue their medication and therefore see more benefits.

  • Drop out rates:
    A problem with all drug treatments for Sz is that the side effects can lead to problems with patient compliance. It has been argued that, on average, 50% of schizophrenia patients stop taking their medication after a year, and 75% after two years. This causes what is known as the “Revolving Door Syndrome”- where the patient is reluctant to take their medication and regularly relapses before being admitted for care, treated successfully with drugs again, only to then avoid taking them when released. This is a problem as it raises doubt over how appropriate antipsychotic treatments are if they rarely lead to a long-term and stable recovery. This also suggests that at least for some patients, they may benefit from psychological treatments in addition to drug therapy to prevent relapse.
44
Q

What are the psychological explanations of SZ?

A

Family dysfunction, Double-bind hypothesis, high expressed emotion and schizophrenogenic mother

45
Q

What is family dysfunction?

A

Many of the psychological explanations of schizophrenia (Sz) have focused on the role of the family. ‘Family dysfunction’ explanations claim that the risk of SZ is increased when there are abnormal patterns of communication within the family. Parents of sufferers often display three types of dysfunctional characteristics:
1. High levels of interpersonal conflict (arguments).
2. Difficulty communicating with each other.
3. Being excessively critical and controlling of their children.

46
Q

What is the double-bind hypothesis?

A

Bateson (1956) suggested children can find themselves ‘trapped’ in situations where they fear doing the wrong thing, but are not given clear guidance on what ‘the wrong thing’ is. When they do ‘get it wrong’ the parent withdraws affection/love as a punishment. The child frequently receive contradictory messages from parents I.e. where a verbal message is given but opposite behaviour is exhibited. For example, if a mother tells her son that she loves him, yet at the same time turns her head away in disgust, the child receives two conflicting messages about their relationship. Bateson argued this was reflected in symptoms such as disorganised thinking and paranoid delusions. The double-bind behaviour from parent/caregiver can lead to a negative reaction from the child of social withdrawal and flat affect (a lack of emotional expression) in order to escape double bind situations. Bateson was also clear he viewed these double-binds as a risk factor rather than the sole cause of schizophrenia.

47
Q

What is high expressed emotion?

A

High expressed emotion (EE) refers to the level of negative emotion expressed towards a patient by their carers. EE contains several elements:

  • Verbal criticism of the patient
  • Hostility towards the patient (anger and rejection)
  • Emotional over-involvement in the life of the patient.
    These high levels of EE towards the patient are a serious source of stress for the patient. It is argued that this stress can trigger the onset of schizophrenia in a person who is already genetically vulnerable to the disorder (diathesis-stress disorder). EE has been primarily linked to the course of the disorder rather than being seen as the cause. High levels of EE in carers have been found to lead to poorer outcomes and an increased likelihood of relapse and a return to psychotic experiences for the patient.
48
Q

What is a schizophrenogenic mother?

A

According to Fromm-Reichmann (1948) a schizophrenogenic mother (schizophrenia causing) is cold, rejecting, controlling and tends to cause a family environment characterised by tension and secrecy. This leads to distrust which may manifest itself into paranoid delusions in the child. There is often a family schism or skew with a dominant mother and passive father.

49
Q

What are the positive evaluation points of family dysfunction as an explanation?

A

There is evidence to support double-bind theory of family dysfunction as a risk factor for SZ. Berger (1965) found that sufferers of Sz reported higher recall of double-blind statements from their mothers than non-sufferers. This seems to suggest contradictory messages during upbringing may increase the risk of SZ in later life. However, most professionals now agree that while there is evidence that poor childhood experiences within the family are associated with adult schizophrenia there is very little support for the double bind and schizophrenogenic mother explanations. These theories have been based on clinical observations and personality assessments of the mother of someone with Sz and are not viewed as valid in comparison with other objectively supported theories.

There is support for the role of EE in the course of Schizophrenia. Tienari et al (2004) assessed adopted children whose biological mother had SZ compared to a control group of adoptees without any genetic risk. He found that when the parenting style of the adoptive family was characterised as highly critical with low levels of empathy, this greatly increased the risk of SZ but that being reared in a ‘healthy’ adoptive family had a protective effect on those at a high genetic risk This suggests that EE in families can increase the risk of SZ but also that being a low EE family can help prevent SZ. However, there is difficulty in establishing cause and effect with this theory. For example, having a child suffering with schizophrenia within a family can be problematic and stressful on family relationships. Therefore, rather than dysfunctional families causing schizophrenia, it could be that having an ill child within a family leads to dysfunction.

One advantage of family dysfunction theories is that they have led to practical applications. This means the focus on the role of the family in SZ has led researchers to develop family therapy to increase the patient’s chance of recovery and decrease chances of relapse. Evidence for this comes from NICE (2009) who found that the relapse rate in a family therapy condition was 26% compared to 50% relapse in a control group receiving ‘standard’ care. This is positive as it suggests family dysfunction theories have led to psychological therapies that have benefitted real people’s lives. By supporting the family it allows the sufferer of schizophrenia a reduced chance of relapse.

50
Q

What are the cognitive explanations of SZ?

A

Metarepresentation and central control. The cognitive approach is based on mental processes and explains symptoms of schizophrenia as being a result of a disruption of normal thought processing. Compared to controls, research has found evidence of dysfunctional thought processing in people with schizophrenia i.e., they process information differently to those without the disorder.

51
Q

What is metarepresentation?

A

Is the cognitive ability to reflect on our own thoughts and behaviour. It is believed that a dysfunction in metarepresentation contributes to the onset of hallucinations. For example, a person may start to believe that their actions and thoughts are being carried out by others. A dysfunction in metarepresentation may also cause the patient to believe that their own inner voices are actually the thoughts of others being projected into their heads. (Frith, 1992)

52
Q

What is central control?

A

Is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts. For example, sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient has difficulty supressing an automatic response to these. (Frith 1992).

53
Q

What are the positive evaluation points for cognitive explanations of sz?

A
  • There is research evidence for dysfunctional thought processing. (Evidence) O’Carroll (2000) reviewed available evidence and found that cognitive impairments existed in 75% of people with schizophrenia, mainly affecting attention, memory, and verbal learning. They also found that cognitive impairments often pre-dated the illness.
    (Additionally) Further support for the evidence of dysfunctional thought processing in sufferers of schizophrenia comes from Stirling (2006) who compared performance on a range of cognitive tasks in 30 people with schizophrenia and a control group of 30 people without schizophrenia. Tasks included the Stroop test where participants have to name the font-colours of colour words, so have to suppress the tendency to read the words aloud. As predicted by Frith’s central control theory, people with schizophrenia took over twice as long on average than the control group to name the font colours.
    (Link) Both studies show clear support for the cognitive explanation of schizophrenia because it demonstrates the impairment in cognitive processes in sufferers compared to those without Sz.
  • Real world applications
    (Point) Furthermore, a major strength is that the cognitive explanation of schizophrenia has led to practical applications. This is because cognitive explanations have helped in the development of Cognitive Behavioural Therapy for psychosis (CBTp) which has been extremely effective in treating SZ. Evidence for this comes from NICE (2014) who reviewed a range of treatments for SZ and found that, compared with antipsychotic drug therapy, CBTp was far more effective in reducing symptom severity and improving social functioning.
    This is positive as the theory leading to treatment has benefitted real people’s lives in helping them to develop strategies to improve cope with and improve their dysfunctional thought processes.
54
Q

What are the negative evaluation points of cognitive explanations of SZ?

A

It has been suggested that the cognitive impairments found in schizophrenia may be due to antipsychotic medication.
(Example) This medication has serious side effects that may account for some of the deficits found in patients with schizophrenia. It has also been suggested that the cognitive differences are a result of neural correlates and abnormal neurotransmitter levels rather than the cause of Sz.
(Link) Therefore casting doubt on the belief that the cognitions are to blame for the schizophrenia.

Lacks explanation
Cognitive theories have been criticised for only identifying the reason for current symptoms.
The theories identify faulty cognition as the cause of some of the symptoms such as disordered thinking and deficits in processing but does not explain what led to the cognitive impairments in the first place. Therefore, faulty cognition explains symptoms, but not causes. This is a weakness because it suggests that we cannot fully explain the cause of schizophrenia using a cognitive theory alone.
(Additionally) (you could develop this by explaining about the wealth of evidence we have suggesting that Sz has a genetic/biological cause. You could also talk about the diathesis-stress/interactionist explanation too as this would offer a more complete and valid explanation of the cause of Sz

55
Q

What is CBT in the treatment of SZ?

A

It usually takes place for between five and twenty sessions, either in groups or individually. A CBT therapist begins by developing a trusting relationship with the schizophrenic patient, helping them to see that many of their symptoms, such as having paranoid thoughts, are more common than they think (normalisation), thus helping to reduce anxiety levels.

The basic assumption is that it is not events themselves that cause the person problems (Activating events or ‘A’) but the beliefs (B) they have about events. If a person has distorted beliefs this will, in turn, have a negative effect on their feelings and behaviours (consequences or ‘C’). For example, someone with SZ may believe their behaviour is being controlled by something else. CBTp is used to help the patient identify and correct these faulty interpretations or beliefs.

The therapist will discuss with the patient how likely these irrational beliefs are to be true (reality testing) and consider other more rational beliefs instead (known as ‘dispute’ or ‘D’). By doing this, CBTp allows the patient to make sense of how their delusions and hallucinations impact on their feelings and behaviour. For example, if a patient hears voices and believes the voices are demons, they will naturally be very afraid. By thinking about these more rational, disputing beliefs (e.g. considering how likely are they to be true), the client should feel the ‘Effect’ (E) of challenging irrational thoughts and become less anxious which will have a positive effect on their behaviour. This process is sometimes called the ‘ABCDE’ model.

Patients are also encouraged to develop coping strategies. A common coping strategy employed to deal with auditory hallucinations is to limit the time they actively listen to voices, e.g. 30 minutes per day. The rest of the time the patient is encouraged to ignore the voices.

56
Q

What are the positive evaluation points of CBT in the treatment of SZ?

A

There is some support showing the benefits of CBTp when treating Sz.
(Evidence)Tarrier (2005) - reviewed 20 studies using CBTp and found persistent evidence of reduced positive symptoms, lower relapse rates and a faster recovery rate in ill patients in the short term. Jauhar et al (2014) reviewed 34 studies and concluded that CBTp has a significant but fairly small effect on both positive and negative symptoms.
(Link) These findings suggest that CBTp is an effective therapy for helping people with schizophrenia control their symptoms.

(Additionally) Unlike drug therapy, CBTp produces no side effects and therefore, could be considered a more suitable treatment for many people with schizophrenia, making the condition more manageable and improve patient’s quality of life. For example, CBTp helps to raise the patient’s self-esteem by helping them realise that healthy people also sometimes experience delusions and hallucinations (normalisation).

57
Q

What are the negative evaluation points of CBT as a treatment for SZ?

A

many patients with severe symptoms of schizophrenia drop out of CBTp.
(Evidence) Tarrier (1993) found 45% of the sample refused to cooperate or dropped out during the trial. Patients need to be highly motivated and have the ability to put in the time and effort for the therapy to be a success. Some patients with Sz suffer with avolition so engaging in a lengthy therapeutic process will be problematic for those patients in particular.
(Link) Therefore, this suggests CBT may not be a suitable treatment for all patients suffering with Sz and alternative treatments such as drug therapy may be more appropriate.

Combination therapy may be the best approach
(Point) The effectiveness of CBT is increased when mixed with combination of treatments and may depend on the stage of the disorder.
(Evidence) Addington and Addington (2005) claim that in the initial phase of SZ, self-reflection on symptoms is not particularly appropriate. However, following stabilisation of the symptoms with antipsychotic medication, individuals can benefit from group-based CBT which can help normalise their experience by meeting other individuals with similar issues. This suggests that CBT may only be useful for specific stages of treatment and may need to be constantly adapted.
(Additionally) However, despite it’s success for many patients, CBT is not suitable for all patients, especially those too disorientated, agitated or paranoid to form trusting alliances with practitioners.
(Link) Therefore CBT may not be an effective for all patients with Schizophrenia and alternative treatments may be necessary.

58
Q

What is family therapy in the treatment of SZ?

A

a form of psychotherapy which is based on the idea that communications and interactions amongst the family of patients with schizophrenia are dysfunctional. The therapy involves the patient’s whole family and aims to improve the quality of communication and interaction between family members and to reduce the levels of expressed emotion (EE) and stress. Family therapy is usually offered for a period of between 3 and 12 months and at least 10 sessions.

Family therapists such as Pharoah (2010) aim to improve the functioning of a family with a member suffering schizophrenia by employing a number of strategies:

  • Forming a therapeutic alliance with all family members.
  • Reducing the stress of caring for a relative with schizophrenia.
  • Problem solving
  • Reduction of anger and guilt
  • Helping family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives
  • Improving believes and behaviour towards schizophrenia
    NICE recommends that family therapy should be offered to all individuals diagnosed with schizophrenia who are in contact with or live with family members. They also stress that such interventions should be seen as a priority where there are persistent symptoms or high risk of relapse.
59
Q

What are the positive evaluation points for family therapy as a treatment for SZ?

A

Family therapy has been found to be effective.
(Evidence) Pharoah et al (2010) carried out a meta-analysis on 53 studies to compare the effectiveness of family therapy for the treatment of schizophrenia with antipsychotic medication. They found a reduction in the risk of relapse and a reduction in hospital admission during treatment and in 24 months after. The use of family therapy also increased patient’s compliance with medication.
(Link) This suggests that family therapy is an effective treatment, which could hint that better family relationships are the key element in helping a patient to recover.

(Additionally) There are economic benefits of family therapy. The NICE review of family therapy studies show that family therapy is associated with significant cost savings when offered to patients with schizophrenia. The extra cost of family therapy is offset by a reduction in costs of hospitalisation because of lower relapse rates.

Provides insight into the schizophrenia
(Point) A further strength of family therapy as a treatment for schizophrenia is that it is useful for patients who lack insight into their schizophrenia.
(Explanation) This is because family members are able to assist with providing lots of useful information about the patient’s schizophrenia in a coherent way, whereas the patient may be unable to do so. They have insight into the patient’s moods and are able to speak for them when the patient cannot speak for themselves.
(Link) This can help them start to receive therapy immediately and is a clear strength of family therapy in helping to treat schizophrenia effectively.
(Additionally) Studies have suggested that family therapy is also highly beneficial for family members and not just the sufferer of schizophrenia. Lobban et al (2013) analysed the results of 50 family therapy studies that had included an intervention to support relatives. 60% of these studies showed a positive impact of the intervention on at least one outcome for relatives e.g. coping and problem solving skills. This therefore shows that investment in family therapy can have positive consequences for many family members which in the long term should be cost effective in reducing the relapse and re-hospitalisation of the person with schizophrenia and the mental health of carers.

60
Q

What are the negative evaluation points of family therapy as a treatment for SZ?

A

not all evidence suggests that family therapy is effective in treating schizophrenia
(Evidence) Garety et al (2008), found little difference in the improvement of symptoms of schizophrenia in patients that received family therapy compared to patients that received no family therapy but had carers. Patients in both groups had low incidences of relapse. Researchers found that the carers had low levels of EE (expressed emotion) and this could explain why there was little difference between the two groups.
(Link) This clearly shows that low levels of EE are important for improving symptoms of schizophrenia, but it also shows that family therapy may not necessarily be any more effective than a high quality standard of care provided by emotional responsive carers.

61
Q

How are token economies used in the management of SZ?

A

a form of behavioural therapy used primarily in hospitals. This is based on the principles of operant conditioning. The aim of token economy is to change maladaptive behaviours (negative symptoms such as social withdrawal and poor motivation) shown by individuals with schizophrenia into more desirable behaviours through the use of tokens. The tokens reinforce desirable behaviour. This helps in the management of schizophrenia. The idea is that the token (a coloured disk) is given immediately on completion of a desired behaviour e.g. getting dressed in a morning, making a bed, engaging in conversation. The tokens can be later swapped for material treats such as sweets, magazines or for services such as having a room cleaned, breakfast in bed or privileges such as walk outside the hospital.
These modified behaviours DO NOT cure schizophrenia, but rather improve the patient’s quality of life and increase the likelihood of living outside a hospital/care setting.

During the early stages of the token economy, frequent exchange periods mean that patients can be quickly reinforced and target behaviours can then increase in frequency. Over time, to encourage further improvements, more may be expected of patients to achieve token rewards. For example, they may only be rewarded for helping others or completing ‘chores’. In this way, their behaviour can be developed and ‘shaped’ over time, working towards being more and more able to function and look after themselves and become less reliant on staff, carers and medication too.

62
Q

What are the positive evaluation points of token economy in the management of SZ?

A

there is evidence for token economies being effective in managing the symptoms of schizophrenia
(Evidence) Glowacki (2016) identified 7 studies published between 1999 and 2013 and reported that all studies had shown a reduction in negative symptoms and a decline in the frequency of unwanted behaviours
(Link) The findings demonstrate support for the view that token economies are effective in managing schizophrenia in hospitalised patients. This is because it is possible to control the environment and ensure that patients are rewarded consistently for desirable behaviours. The tokens can be tailored to the individual patients’ requirements and used to target different behaviours.
(Additionally) However, critics argue that using only 7 studies to support the effectiveness is limited and may not accurately represent the effectiveness of token economies to manage symptoms of schizophrenia.

63
Q

What are the negative evaluation points for token economies in the management of SZ?

A

One problem with token economies is that they are not effective in managing all symptoms of schizophrenia.
(Explanation) Token economy is only really effective in treating the negative symptoms which involve social withdrawal yet not effective in treating the positive symptoms such as hallucinations and delusions. It has also been argued that token economies produce only token (minimal) learning. For example, it is possible that what patients learn in token economies is merely to imitate normal behaviour without any deeper changes in their thoughts and beliefs.
(Link) This suggests the therapy may be limited in terms of its effectiveness in that it may be very superficial and temporary. Additionally, it may only be useful within an institution and may not provide the patient with skills for living in the outside world.

Could be viewed as manipulative and unethical
(Point) There are ETHICAL ISSUES surrounding the use of token economies.
(Explanation) Most significantly, that privileges and services become more accessible for patients with milder symptoms, and less available for patients with severe symptoms. In addition, it has the potential for abuse. Corrigan (1995) claimed that token economy can be abusive and humiliating. It has the potential for taking away the power from the patient and allowing others to have power over the patient.
(Link) This suggests token economy therapies may not always be appropriate when they are used for reasons other than the treatment of patients.

64
Q

What is the importance if an interactionist approach for explaining SZ?

A

The interactionist approach (sometimes called a biosocial approach) is an approach that acknowledges that there are biological and psychological/societal factors that contribute to the development of schizophrenia.
Biological factors include: Genetic Vulnerability, Neurochemical Abnormality and Neurological Abnormality. Psychological/Societal factors include: Stress and poor quality family interactions.

65
Q

What is the diathesis-stress model?

A

. The diathesis-stress model suggests that an individual must have the genetic vulnerability and a stress-trigger present in order to develop the condition. An individual may have more than one underlying biological factor which would make them vulnerable to developing schizophrenia but the onset of schizophrenia is triggered by stress. Psychological triggers for schizophrenia can be things such as family dysfunction, substance abuse, stressful life events.

In Meehls (1962) original model, Diathesis was also Biological and stress was always Psychological/Societal.
However, research has lead to a modern understanding of Diathesis-stress in which explains;

  • Diathesis can be biological (e.g. genes) or psychological (e.g. early or severe trauma, child abuse etc). We know that many genes have been linked to causing schizophrenia ‘polygenic’. We also know that early and severe trauma can affect the developing brain For example, the HPA (hypothalamic-pituitary-adrenal) system becomes more over-active, this makes the person more vulnerable to later stress and so can also be a diathesis as well as genes.
  • Stress can be caused by psychological, societal or BIOLOGICAL factors. For example, much recent research has looked at cannabis as a triggering ‘stress’ factor, due mainly to the fact that cannabis appears to increase schizophrenia rates by seven times. This is probably because cannabis interferes with the dopamine system.
66
Q

What are the positive evaluation points of using an interactionist approach for explaining SZ?

A

) There is evidence to support the dual role of vulnerability and stress in the development of schizophrenia
(Evidence) Tienari et al (2004): They assessed adopted children whose biological mother was a sufferer of schizophrenia compared to a control group of adoptees without any genetic risk. He found that parenting style characterised as high levels of criticism and conflict with low levels of empathy was implicated in the development of the disorder but only for the children with high genetic risk and not in the control group.
This suggests that both genetic vulnerability and family-related stress are important in the development of schizophrenia and that poor parenting could be a possible source of stress.

(Additionally)
(Evidence) Furthermore, Varese (2012) found that children who experienced severe trauma before the age of 16 were three times as likely to develop schizophrenia in later life compared to the general population. There was a relationship between the level of trauma and the likelihood of developing schizophrenia, with those severely traumatised as children being at greater risk.
(Link) This suggests that the early trauma is a diathesis meaning the person was vulnerable to developing Sz later due to their early experience. The fact that they developed Sz was due to the presence of a stress trigger later in life. This evidence supports the modern understanding of a diathesis in the diathesis stress explanation of Sz.

Twin studies offer further support that an interactionist approach is important to explain the cause of Sz
(Point) Although there is much evidence to suggest Sz is caused by genetic inheritance.
(Evidence) MZ twin concordance rates for schizophrenia seldom rise above 50%, supporting the view that environmental factors must also play a role in determining whether a biological vulnerability actually develops into the disorder.
(Link) This supports an interactionist view when explaining the development of Sz because it clearly demonstrates that a genetic vulnerability alone does not automatically lead to the disorder developing. If genes alone were the cause we would be expecting 100% concordance for MZ twins when one of the twins has schizophrenia

67
Q

What is the importance of an interactionist approach for treating SZ?

A

As the interactionist model of SZ acknowledges both biological and psychological factors in schizophrenia it is therefore compatible with both biological and psychological treatments. The model would recommend to combine antipsychotic medication and psychological therapies (most commonly CBT). Turkington (2006) believes it is possible to believe in biological causes for schizophrenia and still practise CBT to relieve psychological symptoms. For many patients, they will be treated with a number of treatments such as CBT and family therapy alongside antipsychotic medication.

68
Q

What is the positive evaluation point for taking an interactive approach for treating SZ?

A

There is lots of evidence that combining treatments for schizophrenia is highly effective.
(Evidence) Tarrier (2004) studied 315 patients who were randomly allocated to either; 1. Medication & CBT, 2. Medication & Counselling, or 3. Control group (Medication only). Tarrier found symptom levels were lower in both combination groups compared to the control group although there was no difference in rates of hospital readmission.
(Link) This clearly demonstrates the benefits of adopting an interactionist approach (holistic) when treating schizophrenia.

(Additionally) However, a problem with using a combination of treatments for schizophrenia is that it is difficult to assess which treatment is the most successful. As the evidence above suggests, a combination of antipsychotics and CBT is the most effective treatment for schizophrenia but it is uncertain which of these therapies is having the greatest effect. In addition, just because a treatment is effective does not mean that the cause was biological or psychological (depending on the treatment you are considering). (A* you could talk about the treatment-causation fallacy here)