Schizophrenia

Question 1

What is schizophrenia?

Answer 1

• It is a serious mental psychotic disorder characterised by a profound disruption of cognition and emotion.
• It is so severe, that it affects a person’s language, thought and perception, emotions and even their sense of self.

Question 2

Where is schizophrenia more commonly diagnosed?

Answer 2

• Men more than women
• Cities rather than the countryside
• Working class than middle class people

Question 3

Is schizophrenia psychotic or neurotic?

Answer 3

• It is psychotic

Question 4

What does the term psychotic refer to?

Answer 4

refers to serious mental issues causing abnormal thinking and perceptions and also the fact that people lose touch with reality.

Question 5

What two classification systems are used to diagnose schizophrenia?

Answer 5

• The DSM 5

- The ICD 10

Question 6

What is DSM 5?

Answer 6

• The Diagnostic and Statistical Manual of Psychiatric Disorders
  – devised by the American Psychological Association (APA)
  – the DSM is currently now in its 5th edition.

Question 7

What is ICD 10?

Answer 7

• The International Classification of Diseases
  – devised by the World Health Organisation (WHO)
• the ICD is currently in its 10th edition (ICD 11 will be used in 2022)

Question 8

How does the DSM 5 diagnose schizophrenia?

Answer 8

• DSM states that you need to show at least two or more positive symptoms (or one positive and negative) such as hallucinations or delusions for a period of one month (as well as extreme social withdrawal for at least six months) to be diagnosed with schizophrenia

Question 9

How does ICD 10 diagnose schizophrenia?

Answer 9

• The ICD states you need to show one positive and one negative (or two negative) symptoms for at least one month to be diagnosed with schizophrenia.
• Also the ICD recognises that there are subtypes of schizophrenia (such as Catatonic Schizophrenia, Paranoid Schizophrenia) whereas the DSM has now deleted the subtypes of schizophrenia

Question 10

Who made a distinction between two types of schizophrenia?

Answer 10

Crow (1980)

Question 11

What are the types of schizophrenia?

Answer 11

• Type 1

- Type 2

Question 12

What is Type 1 Schizophrenia?

Answer 12

• characterised more by positive symptoms (those which are an addition to an individual’s behaviour)
• e.g. visual or auditory hallucinations or delusions of grandeur.
• Generally better prospects for recovery.

Question 13

What is Type 2 schizophrenia?

Answer 13

• characterised more by negative symptoms
• e.g. loss of appropriate emotion of poverty of speech.
• Generally poorer prospects for recovery.

Question 14

What are the two types of symptoms in patients with schizophrenia?

Answer 14

• Positive symptoms

- Negative symptoms

Question 15

Positive symptoms of schizophrenia

Answer 15

• Hallucinations
• Delusions
• Disorganised Speech

Question 16

What are the different types of hallucinations as positive symptoms of schizophrenia

Answer 16

• these are sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that are there
• Can include:
  Auditory (hearing)
  Visual (seeing)
  Olfactory (smelling)
  Tactile (touching and feeling)

Question 17

Auditory (hearing) hallucinations

Answer 17

• this is when the person will experience hearing voices making comments or talking to them in their head normally criticising them.

Question 18

Visual (seeing) hallucinations

Answer 18

seeing things which are not real

e.g. distorted facial expressions on animals or people

Question 19

Olfactory (Smelling) hallucinations

Answer 19

• smelling things which are not real

- e.g. a person could be smelling disinfectant which is not real

Question 20

Tactile (touching and feeling) hallucinations

Answer 20

• touching things which are not there

- for example, bugs are crawling on your skin

Question 21

Delusions as a positive symptom of schizophrenia

Answer 21

• Also known as paranoia
• these are irrational, bizzare beliefs that seem real to the person with SZ.
• Believing you are a important political figure, aliens are coming.
• May lead to aggression sometimes

Question 22

Disorganised speech as a positive symptom of schizophrenia

Answer 22

• this is the result of abnormal thought processes, where the individual has problems organising his or her thoughts and this shows up in their speech.
• They may slip from one topic to another (derailment), even in mid-sentence, and in extreme cases their speech may be so incoherent that it sounds like complete gibberish

Question 23

Negative symptoms of schizophrenia

Answer 23

• Speech Poverty (Alogia)
• Avolition
• Affective flattening
• Anhedonia

Question 24

Speech Poverty (Alogia) as a negative symptom of schizophrenia

Answer 24

• SZ is characterised by changes in patterns of speech
  – meaning the emphasis is on the reduction in the amount and quality of speech.
  -This is sometimes accompanied by a delay in the sufferer’s verbal responses during conversation

Question 25

Avolition as a negative symptom of schizophrenia

Answer 25

• this can sometimes be called apathy
  – and can be described as finding it difficult to begin or keep up with goal-directed activity,
• i.e. actions performed in order to achieve a result.
• Sufferers of SZ often have sharply reduced motivation to carry out a range of activities.
• Andreason (1982) identified these signs of avolition; poor hygiene and grooming, lack of persistence in work or education and lack of energy

Question 26

Affective flattening as a negative symptom of schizophrenia

Answer 26

• a reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language.
• Individuals who are schizophrenic have fewer body and facial movements and smiles, and less co-verbal behaviour.
• When speaking, patients may also show a deficit in prosody (e.g. intonation, tempo, loudness and pausing) which gives cues to the emotional content of the conversation

Question 27

Anhedonia as a negative symptom of schizophrenia

Answer 27

• a loss of interest or pleasure in all or most activities, or a lack of reactivity to normally pleasurable stimuli.
• Physical anhedonia is the inability to experience physical pleasures such as pleasure from food, bodily contact etc.
• Social anhedonia is the inability to experience pleasure from interpersonal situations such as interacting with other people

Question 28

Advantages of classification and diagnosis

Answer 28

• Communication shorthand: a patient with a mental disorder often has numerous symptoms. It is simpler to incorporate these symptoms into a single diagnosis and this makes communication between mental health professionals much easier
• Treatment: treatments are often specific to certain disorders e.g. symptoms of schizophrenia respond well to certain anti-psychotic drugs but not anti-anxiety. A reliable diagnosis can point to a therapy that will alleviate symptoms.
• Although there is variation, there are many underlying biological abnormalities seen in people with schizophrenia. It is hoped that a greater understanding of these abnormalities will lead to even more effective treatment.

Question 29

Disadvantages of classification and diagnosis

Answer 29

• Reliability- Psychologist found inter-rater reliability between diagnosticians as low as +0.11 (using DSM). Inter-rater reliability between ICD and DCM was also very low in a more recent study.
• Validity- Criterion validity shows that SZ is more likely to be diagnosed using ICD than DSM, suggesting that SZ is either overused in ICD or under used in DSM.
• Co-morbidity- the idea that two or more mental disorders occur together. We can therefore question the validity of diagnosis of SZ as it is commonly diagnosed with other conditions. We are unable to distinguish between two disorders.
• this means that there is considerable overlap between the symptoms of SZ and other conditions such as depression and bipolar disorders. For example, people with DID (Dissociative Identity Disorder) actually have more SZ symptoms than people diagnosed with SZ. In fact, most people diagnosed with SZ have sufficient symptoms of other disorders that they could also receive at least one other diagnosis.
• Gender Bias in diagnosis- Males are more likely to be diagnosed than women. Could be due to the fact that women seem to have better interpersonal function.
• Cultural Bias- African American and English people of Afro Caribbean origin are nine times more likely to be diagnosed with SZ. Auditory hallucinations may be acceptable in Africa and not warranted of diagnosis. Or racism in diagnosing.

Question 30

What factors are the biological explanations of SZ based on?

Answer 30

• Genetic basis

- Neural correlates including the dopamine hypothesis

Question 31

How are genetic basis factors usually tested?

Answer 31

• Family studies
• Twin Studies
• Adoption Studies

Question 32

Family studies to test the genetic basis of SZ

Answer 32

• They find individuals who have SZ and determine whether their biological relatives are similarly affected more often than non-biological relatives.
• Family studies have shown that the closer the genetic relatedness, the greater the risk.

Question 33

Example of family study to test the genetic basis of SZ

Answer 33

• Gottesman (1991) found that if both parents were schizophrenic, then the likelihood of the offspring also having SZ was 46%, if one parent was schizophrenic, then the likelihood dropped to 13% and if a sibling (brother or sister) had SZ, the likelihood was 9%
• this study shows that the more closer you are genetically related the more likely you are to get SZ.

Question 34

Twin studies to test the genetic basis of SZ

Answer 34

• They are an opportunity for researchers to investigate the nature/nurture debate in terms of the contribution of heredity and environmental influences in having SZ.
• As Monozygotic twins (MZ) (identical twins) share 100% of their genes whereas as Dizygotic twins (DZ) (non-identical) twins share 50% of their genes, if SZ is genetic, then the concordance rates should be much higher for MZ rather than DZ twins!

Question 35

Example of Twin study to test the genetic basis of SZ

Answer 35

• Gottesman (1991) found a 48% concordance rate for MZ twins and 17% concordance rate for DZ twins
• this study shows that the more genetically similar you are then the more likely you are to get SZ.

Question 36

Adoption studies to test the genetic basis of SZ

Answer 36

• Because it is difficult to separate genetic from environmental influences in twin and family studies, adoption studies are often carried out to understand the influence of nature and nurture.
• For example, adoption studies are researched to see the nature/nurture influences when MZ twins may be reared apart or offspring of SZ parents are adopted.

Question 37

Example of adoption study to test the genetic basis of SZ

Answer 37

• Tienari et al (2001) carried out a study in Finland. 164 adoptees whose biological mothers had been diagnosed with SZ, 11 (6.7%) were also diagnosed with SZ compared to a control group of 197 adoptees where only 4 (2%) were diagnosed with SZ.
• This study shows that although the overall percentage of children (who have been adopted by non- schizophrenic parents) having SZ was very low, as there was a small link between genes and SZ with children whose biological mothers were schizophrenic.

Question 38

How are candidate genes associated with SZ?

Answer 38

• There are specific genes that seemed to be associated with SZ although it is now agreed that SZ is polygenic
  – this means that there is a combination of different genes that have been implicated in SZ.

Question 39

Study into association of candidate genes with SZ

Answer 39

• Ripke et al (2014) compared the genetic makeup of 37000 SZ patients worldwide with 113000 controls.
• They found that 108 separate genetic variations were associated with an increased risk of SZ.
• The genes that were particularly vulnerable were the ones that had some connection to the functioning of certain neurotransmitters such as dopamine

Question 40

Strengths of genetic basis of SZ

Answer 40

There is a wealth of research evidence to support the genetic basis for SZ as can be seen from the findings of Gottesman, Joseph’s and Tienari’s study, thus there is a link between genes and SZ.
This is a strength because it shows that if a child grows up in a family where both their biological parents has SZ, then the chances of them getting it is heightened compared to if only one parent or none of the parents have it suggesting that genetics is an important factor

Question 41

Weaknesses of the genetic basis of SZ

Answer 41

• Problem with twin and family studies is separating nature from nurture. For example, MZ twins are normally reared together and sent to the same school, where the same clothes (in childhood), this then makes it difficult to separate upbringing from genes. Even if we look at adoption studies that attempt to separate genes from the environment, children tend to be adopted by relatives who may still rear the child similarly to its biological parents – thus adoption studies may not always be a good comparison for the effects of nature and nurture.
• SZ can take place in the absence of a family history. One explanation is that there may be a mutation in parental DNA, for example in paternal sperm cells. Evidence for role of mutation showed a positive correlation between paternal age and increased risk of SZ increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. This suggests that although no direct genes are involved, a person can still get SZ if their father was older at the time of fertilisation. This suggests that the role of nature and nurture may both play a part rather than just genes.
• Similarly, the diathesis stress model states that there is a genetic vulnerability in schizophrenia but this vulnerability is only likely to be triggered if there is a stress-trigger in the individual’s life. In other words, you may be born with a gene which makes you particularly vulnerable to SZ but if your life is relatively stress free, then you may not end up having the disorder at all. Thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ.

Question 42

What are Neural correlates of SZ

Answer 42

Neural correlates refers to how different neurotransmitters such as dopamine and serotonin (either excessive levels or low levels) in different parts of the brain can also play a part in SZ.

Question 43

What is Dopamine?

Answer 43

• Dopamine is one of the brain’s neurotransmitters
• a chemical that ferries information between neurons.
• It also enables us not only to see rewards, but to take action to move toward them.
• Since dopamine contributes to feelings of pleasures and satisfaction as part of the reward system, the neurotransmitter also plays a part in addiction.

Question 44

What is the dopamine hypothesis?

Answer 44

• It claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of SZ.
• Thus messages from neurons that transmit dopamine fire too easily and often, leading to hallucinations and delusions.
• Schizophrenics are thought to have particularly high levels of D2 receptors on receiving neurons resulting in more dopamine binding and therefore more neurons firing

Question 45

What are the Two consequences of the dopamine hypothesis?

Answer 45

• Hyperdopaminergia in the subcortex

- Hypodopaminergia in the cortex

Question 46

What is Hyperdopaminergia in the subcortex?

Answer 46

• It is based on the original version of the dopamine hypothesis in explaining SZ
  – this states that there are high levels of activity of dopamine in an area of the brain known as the subcortex (i.e. the central areas of the brain).
• For example an excess of dopamine receptors in the Broca’s area (which is responsible for speech production) may be associated with problems in speech and/or the experience of auditory hallucinations

Question 47

What is Hypodopaminergia in the cortex?

Answer 47

• The recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex.
• Psychologists have focused on the role of low levels of dopamine in the prefontal cortex (responsible for decision making and thinking) on negative symptoms of SZ.
• It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia

Question 48

Strengths of the neural correlates explanations of SZ

Answer 48

• With regards to the dopamine hypothesis, this neural correlates explanation is supported through drug research since dopamine agonists like amphetamines tend to increase dopamine levels and make the schizophrenic symptoms worse in sufferers and can produce schizophrenic-like symptoms in non-sufferers thus supporting this idea of Hyperdopaminergia.
• Antipsychotic drugs act like antagonists – which act to reduce the levels of dopamine in schizophrenic patients (which thus help control the symptoms of SZ) supporting the idea that dopamine levels are high in SZ and can be reduced through drugs (e.g. Tauscher et al, 2014).
• Psychologists have found that that chemicals needed to produce dopamine are taken up faster in the brains of schizophrenics compared to controls again suggesting that schizophrenics produce more dopamine.

Question 49

Weaknesses of the neural correlations explanation of SZ

Answer 49

• Problems with the dopamine hypothesis -the dopamine hypothesis alone cannot be seen as the sole cause of SZ since there are other biological and psychological factors that contribute such as upbringing in terms of family dysfunction or cognitive explanations which focus on impaired thinking which could definitely explain the hallucinations and delusions.
  Also much more recent research has also focused on the attention of glutamate – another neurotransmitter that has been implicated in SZ (Moghadamm and Javitt, 2012) suggesting that dopamine might not be the only neurotransmitter responsible for SZ and other neurotransmitters may also be involved.
• The Correlation-causation problem – as there are a number of neural correlates of SZ such as brain structure and neurotransmitters and although studies support neural correlates, cause and effect not known.
  For example, there is a correlation between high levels of dopamine and experiencing symptoms of SZ. However, did the individual start having excess levels of dopamine in that brain region and start experiencing symptoms of SZ or did the individual first experience symptoms of SZ and consequently have high levels of dopamine? This point poses a serious problem to the neural correlates explanation as it does not really explain the cause and effect

Question 50

Psychological explanations for SZ?

Answer 50

• Family dysfunctions

- Cognitive explanations

Question 51

In what three ways can family dysfunction be explained as an explanation of SZ?

Answer 51

• The schizophrenogenic mother
• Double-bind Theory
• Expressed emotion

Question 52

The schizophrenogenic mother as a family dysfunction explanation for SZ

Answer 52

• The term ‘schizophrenogenic’ means ‘schizophrenia’ causing.
• Characteristics of this type of mother are: cold, rejecting and controlling as well as creating a family climate full of secrecy and tension.
• This leads the child to having a lack of trust in relationships that later develop into paranoid delusions thus ultimately developing SZ.
• A point to be noted about the schizophrenogenic mother is that in those type of families, the father is often passive and doesn’t really get involved in child upbringing.

Question 53

Double bind theory as a family dysfunction explanation for SZ

Answer 53

• Bateson et al. (1972) agreed that family climate is important in the development of SZ but focused more on the actual family communication style.
• The child finds themselves trapped in situations which they fear doing the wrong thing but receive mixed messages about what this is.
• (An example of a mixed message could be when a mother tells her child she loves him but is actually showing disgust when she tells him.)
• As a result the child is unable to comment about the unfairness of the situation or seek clarification.
• Thus when the child may get it wrong , the child is punished by withdrawal of love.
• The child then feels confused about the world and sees it thus as a dangerous place
  – this may be reflected in SZ symptoms such as paranoid delusions.
• However, Bateson did clarify that this family communication style was a risk factor in the development of SZ but not the only cause!

Question 54

Expressed Emotion as a family dysfunction explanation for SZ

Answer 54

• It is the level of emotion, in particular negative emotion, expressed towards a patient by their carers.
  EE has several parts:
  • Verbal criticism of the patient, occasionally shown with violence
  • Hostility towards the patient, including anger and rejection
  • Emotional over-involvement in the life of the patient, including self sacrifice
• High levels of EE by the carers of the patients creates a serious source of stress
  – this may be a reason for the SZ patient to relapse
  – although EE can also be a trigger for the onset of SZ as well especially if the person has a genetic vulnerability to the disorder (diathesis-stress model)

Question 55

Strengths of family dysfunction as explanations for SZ

Answer 55

• There is research support for family dysfunction as a risk factor. Study where those adopted children who had schizophrenic biological parents were more likely to have SZ themselves than those children with non-schizophrenic biological parents. However, this difference only emerged in situations where the adopted family was rated as disturbed or ‘dysfunctional’. In other words, the illness only manifested itself under appropriate environmental conditions. Genetic vulnerability alone was not sufficient. This shows that family dysfunction is a contributing factor to SZ.
• Psychologist reviewed 46 studies of child abuse and SZ and concluded that 69% of adult women in-patients with a diagnosis of SZ had a history of physical abuse, sexual abuse or both in childhood. For men the figure was 59%. This study shows that family dysfunction contributes to an individual developing SZ.
• Adults with insecure attachments to their primary carer are also more likely to develop SZ thus strengthening the family dysfunction explanation.
• There is some evidence to support the Double-bind theory and psychologist found that schizophrenics reported a higher recall of double-bind statements by their mothers than non-schizophrenics.

Question 56

Weaknesses of family dysfunction as explanations for SZ

Answer 56

• The evidence for family dysfunction as a contributing factor to developing SZ is not very strong. For example, with regards to Double-bind theory, Liem (1974) measured patterns of parental communication in families with a schizophrenic child and found no difference when compared to normal families.
• Also not all patients who live in high EE families relapse, and not all patients who live in low EE homes avoid relapse. Altorfer et al (1998) found that one-quarter of patients that they studied showed no physiological responses to stressful comments from their relatives. This shows that the evidence for EE as a contributing factor towards relapse and SZ is very mixed.
• One problem with dysfunctional family explanations for SZ is that they have led historically to parent blaming – parents who have already suffered seeing their son/daughter developing SZ and having to bear life-long responsibility for their care will also suffer further trauma by being blamed for their son/daughter’s condition.

Question 57

What are the cognitive explanations for SZ?

Answer 57

• Cognitive explanations for schizophrenia focus on the role of mental processes.
• SZ is associated with several types of dysfunctional thought processing and thus provide explanations for SZ as a whole.

Question 58

Two kinds of dysfunctional thought processing linked to SZ

Answer 58

• Metarepresentation

- Central control

Question 59

Metarepresentation as a dysfunctional thought process for SZ

Answer 59

• It is the cognitive ability to reflect on thoughts and behaviour which enables us an insight into our own intentions and goals as well as allowing us to interpret the actions of others.
• Thus dysfunction in metarepresentation would disrupt this ability to recognise our own actions and thoughts as being our own rather than someone else.
• This could explain auditory hallucinations and delusions

Question 60

Central control as a dysfunctional thought process for SZ

Answer 60

• It is the cognitive ability to suppress automatic responses while we perform other actions instead (e.g. a voice in you might say: ‘don’t do this’ – but then you choose to do it)
• Disorganised speech and thought disorder could result from the inability to ignore your own automatic thoughts as well as what other could be saying to you (in your head) (e.g. so and so would tell me not to do this)
• Sufferers with SZ tend to experience derailment (a confusion and breakdown) of their thoughts and what they say because there is too much going on in their thought processes thus they lose control of their own thoughts.

Question 61

Strengths of the cognitive explanations of SZ

Answer 61

There is strong evidence for dysfunctional thought processing in SZ. Psychologist compared 30 patients with a diagnosis of SZ with 18 non-patient controls on a range of cognitive tasks such as the stroop effect (this is when the colour word is written in a different colour and you have to actually say the colour of the word rather than just reading the word). In his study Stirling found that patients with SZ took twice as long to say the colour of the word than controls – this study shows dysfunctional thought processing in schizophrenics since they were struggling with separating the colour word from the actual colour that it was (e.g. saying the colour blue but the actual colour word written is red) because the Schizophrenics were not able to separate the actual colour from the written word.

Question 62

Weaknesses of cognitive explanations of SZ

Answer 62

• It is difficult to establish whether this is a cause or consequence of SZ for example did the dysfunctional thought processing begin and then then person had symptoms of SZ or is the dysfunctional thought processing a consequence of SZ?
• The cognitive explanation in explaining SZ is problematic in that it fails to take into account biological factors and does not acknowledge the fact that dysfunctional thought processing could also be due to abnormal dopamine levels in the brain. This explanation is therefore reductionist because it is simplifying SZ to very basic elements e.g. dysfunctional thoughts rather than considering other factors such as genes, neurotransmitters and stress.

Question 63

What are the biological therapies for SZ?

Answer 63

• Drugs

- Specifically antipsychotic drugs

Question 64

How can the SZ drugs be administered?

Answer 64

• Can be taken in the form of tablets, syrups or even injections.

Question 65

Two types of antipsychotic drugs?

Answer 65

• Typical (traditional or first generation) antipsychotics

- Atypical (second generation) antipsychotics

Question 66

How do typical antipsychotics work?

Answer 66

• They are antagonists and work by reducing the effects of dopamine and thus reduce symptoms of SZ. (Linked to dopamine hypothesis)
• Drugs bind to but do not stimulate dopamine receptors, (D2 receptors in mesolimbic dopampine pathway) blocking dopamine actions.
• This reduces positive symptoms of SZ.

Question 67

Example of a typical antipsychotic

Answer 67

Chlorpromazine

Question 68

Chlorpromazine as a typical antipsychotic

Answer 68

• Can be taken as a tablet, syrup or injection
• It is also an effective sedative and was used to calm patients with other conditions too.
• Maximum dosage is 1000mg

Question 69

How do atypical antipsychotics work?

Answer 69

• Work like typical antipsychotics by blocking D2 receptors.
• They only temporarily occupy the D2 receptors and then rapidly dissociate to allow normal dopamine transmission.
• This rapid dissociation is thought to be responsible for the lower level of side effects.

Question 70

Example of atypical antipsychotics

Answer 70

• Chlozapine

- Risperidone

Question 71

Chlozapine as an atypical antipsychotic

Answer 71

• Used in the 1980s
• More effective treatment for SZ than typical antipsychotics
• Only available as syrup or tablet
• Binds to dopamine receptors but also works on serotonin and glutamate receptors.
• Improves mood and is therefore is given to high suicide risk patients.

Question 72

Risperidone as an atypical antipsychotic

Answer 72

• Emerged in the 1990s
• Attempt to reduce serious side effects of chlozapine but still be as effective.
• Can be taken as syrup, tablets or injection.
• Binds to dopamine receptors but binds better than chlozapine leading to less side effects.
• Therefore smaller doses are needed.

Question 73

Strengths of Drug therapy

Answer 73

• There is research evidence to support the moderate effectiveness of typical antipsychotic drugs in treating SZ. For example: Thornley et al (2003) compared the use of chlorpromazine (typical antipsychotics) with a placebo. Data from 13 trials with a total of 1121 pps showed that chlorpromazine was associated with reduced symptoms and better overall functioning. Furthermore, data from three trials with a total of 512 pps showed that relapse rate was also lower when chlorpromazine was taken. This study this shows that typical antipsychotics were effective in reducing the symptoms of SZ compared to a placebo showing that drug therapy is appropriate in treating SZ.
• There is also research evidence to support the appropriateness of atypical antipsychotics. In a review by Meltzer (2012), he concluded that Clozapine (atypical antipsychotics) is more effective than typical antipsychotics and other atypical antipsychotics in treating SZ. In fact Clozapine was seen as effective in 30-50% of cases where typical antipsychotics had failed. This study shows that use of clozapine as a treatment for SZ is a very appropriate drug as Meltzer clearly showed especially when other drugs failed!
  Interestingly, a number of studies have compared the effectiveness of clozapine and risperidone but results have been inconclusive suggesting that some patients responded better to one drug than the other and also supporting the idea that SZ is a complex psychotic disorder.
• There is also research evidence to support the fact that relapse rates are much lower when patients take antipsychotic drugs (both typical and atypical) as opposed to placebos.
  Leucht et al. (2012) carried out a meta-analysis of 65 studies, published between 1959 and 2011, and involving nearly 6000 patients. Some patients were taken off their antipsychotic medication and given placebos instead. Within 12 months, 64% of those patients who had been given the placebo relapsed whereas only 27% relapsed when on antipsychotic medication. The results of this study clearly show that antipsychotic medication is both effective and appropriate in preventing a schizophrenic patient from relapsing.

Question 74

Weaknesses of drug therapy

Answer 74

• The biggest weakness of drug therapy in treating SZ is the serious side effects ranging from mild ones to the fatal one.
  For typical antipsychotics, the side effects include: dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. A more profound side effect can result in ‘tardive dyskinesia’ which is caused by dopamine supersensitivity and manifests as involuntary facial movements such as grimacing, blinking and lip smacking.
  The most serious side effect of typical antipsychotics is NMS (neuro malignant syndrome – area of the brain associated with the regulation of a number of body systems) – which could lead to high temperature, delirium and coma and can cause death – this may occur in between 0.1% - 2% of schizophrenics.
  Whereas atypical antipsychotics were developed to overcome these side effects. However, side effects do exist for atypical antipsychotics such as Clozapine thus regular blood tests need to be taken of the patients to test for early signs of agranulocytosis (a rare blood condition where the production of white blood cells is prevented – leads to problems with immunity)
• There are problems with the evidence for the effectiveness of drugs and this has been challenged by Healy (2012) has suggested that some successful drug trials have had their data published on multiple occasions thus exaggerating the effectiveness. Also because antipsychotics have powerful calming effects, it seems as though the drugs are successful. However, this does not really show how much the drugs actually reduce the symptoms. Furthermore, most published studies only assess the short-term benefits of drug therapy rather than the long term benefits especially for those patients who have stopped taking the drugs.
• There is of course ethical issues related to using drug therapy for SZ. The most profound ethical issue would be consent – e.g. due to the fact that schizophrenia is a psychotic disorder, patients may not be in the right frame of mind to give fully informed consent in taking the drugs and because the drugs do have such severe side effects, one would question the extent of the harm (both physical and mental) and whether the effects of the drugs were reversible especially with side effects such as NMS and tardive dyskinesia

Question 75

What are the three main psychological therapies for schizophrenia?

Answer 75

Cognitive Behaviour therapy
Family therapy
Token economies

Question 76

What is CBT for schizophrenia?

Answer 76

• It is a cognitive behavioural therapy for psychosis
• It was originally developed to provide treatment for residual symptoms that persist despite the use of antipsychotic medication.
• Can be delivered in groups, at least 16 sessions
• The therapist lets the patient develop their own alternatives to these previous maladaptive beliefs, ideally by looking for alternative explanations and coping strategies that are already present in the patients mind.

Question 77

Phases of CBTp

Answer 77

Assessment 
Engagement 
The ABC model
Normalisation 
Critical collaborative analysis 
Developing alternative explanations

Question 78

Assessment as a phase of CBTp

Answer 78

• The patient expresses his thoughts to the therapist. - Realistic goals for therapy are discussed – using the patient’s current distress as motivation for change.

Question 79

Engagement as a phase of CBTp

Answer 79

the therapist emphasises with the patient’s perspective and their feelings of distress, and stresses that explanations for their distress can be developed together.

Question 80

The ABC model as a phase of CBTp

Answer 80

• the patient gives their explanation of the activiating events (A) that appear to cause their emotional and behavioural (B) consequences (C).
• The patient’s own beliefs, which are actually the cause of C, can then be rationalised, disputed and changed.
• E.g. the belief that ‘people won’t like me if I tell them about my voices’ might be changed to a more healthy belief, e.g. ‘some may, some may not, friends may find it interesting’

Question 81

Normalisation as a phase of CBTp

Answer 81

• conveying to patients that many people have unusual experiences such as hallucinations and delusions under many circumstances reduces anxiety and the sense of isolation.
• By doing this the patient feels less alienated and stigmatised, and the possibility of recovery seems more likely.

Question 82

Critical collaborative analysis as a phase of CBTp

Answer 82

• the therapist uses gentle questioning to help the patient understand illogical deductions and conclusions.
• For example, ‘if your voices are real, why can’t other people hear them?’
• Questioning can be carried out without causing distress, provided there is an atmosphere of trust between the patient and the therapist, who remains empathetic and non-judgemental.

Question 83

Developing alternative explanations as a phase of CBTp

Answer 83

• the patient develops their own alternative explanations for their previously unhealthy assumptions.
• If the patient is not forthcoming with healthy alternative explanations – new ideas can be constructed in cooperation with the therapist.

Question 84

Strengths of CBT

Answer 84

CBTp seems to be more effective in treating SZ compared to standard care - antipsychotic medication alone – The NICE (2014) review of treatments for SZ found consistent evidence that when compared with standard care (antipsychotic medication alone), CBTp was effective in reducing rehospitalisation rates up to 18 months following the end of treatment. CBTp was also shown to be effective in reducing the severity of symptoms as well as improvements in social functioning. Although it is difficult to assess the effectiveness of CBTp alone as patients were being treated with both medication and CBTp.

The effectiveness of CBTp is dependent on the stage of the disorder – CBTp appears to be more effective when it is made available at certain stages of the disorder and when the delivery of CBTp is adjusted to the stage the individual is currently at. Addington and Addington (2005) claim that, in the initial acute phased of SZ, self reflection is not particularly appropriate. However following stabilisation of the psychotic symptoms with medication, patients can benefit from group based CBTp –which can normalise their experience by meeting similar individuals. Thus research has shown that it is individuals with more experience of the SZ and a greater realisation of their problems are most likely to benefit from CBTp.

Question 85

Weaknesses of CBT

Answer 85

Lack of availability of CBTp and patients refusal to attend sessions– Despite being recommended by NICE as treatment for SZ, it is estimated that in the UK only one in ten individuals with SZ actually have access to CBTp. This figure is even lower in some areas of the UK. In a survey by Haddock et al (2013), they found that in the North West of England out of 187 SZ patients, only 13 (7%) had been offered CBTp. However, of those who are offered CBTp as a treatment for SZ, a significant number either refuse or fail to attend the therapy sessions (Freeman et al., 2013) thus limiting its effectiveness even more.

Problems with meta-analysis of CBTp as treatment for SZ – The problems with meta-analysis in this area which can reach unreliable conclusions about CBTp is the failure to take into account the quality of the studies. For example, some studies fail to randomly allocate participants to CBTp or a control condition; other studies fail to assess the patients subsequent assessment of symptoms and general functioning after they have been treated with CBTp. Juni et al. (2001) concluded that there was clear evidence that the problems associated with methodologically weak trials translated into biased findings about the effectiveness of CBTp. Infact, Wykes et al. (2008) actually found that the more rigorous the study, the weaker the effect of CBTp.

Question 86

What is family therapy in schizophrenia?

Answer 86

• Provides support for carers to make family life less stressful and reduce rehospitalisation.
• NICE recommend that family therapy should be offered to ‘all individuals diagnosed with SZ who are in contact with or live with family members’.

Question 87

What is the aim of schizophrenia?

Answer 87

• Aimed at reducing the level of expressed emotion within the family.
• It typically involves providing family members with information about SZ, finding ways of supporting an individual with SZ and resolving any practical problems.

Question 88

How does family therapy work?

Answer 88

By reducing levels of expressed emotion and stress, and by increasing the capacity of relatives to solve related problems, family therapy attempts to reduce the incidence of relapse for the person with SZ.

Question 89

What strategies are used in family therapy?

Answer 89

• Psychoeducation – helping the person and their carers to understand and be better able to deal with the illness.
• Forming an alliance with relatives with care for the person with SZ
• Reducing the emotional climate within the family and the burden of care for family members
• Enhancing relatives’ ability to anticipate and solve problems
• Reducing expressions of anger and guilt by family members
• Maintaining reasonable expectations among family members for patient performance
• Encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed

Question 90

Research on family therapy and schizophrenia by Pharoah (2010): AO1

Answer 90

• Reviewed 53 studies between 2002-2010 from Europe, Asia and North America
• Investigated outcomes for family therapy versus standard drug care for schizophrenia patients
• The results found similar outcomes for both therapies
• Patients who used family therapy increased their compliance to take medication successfully
• Family therapy did not have much effect on improving schizophrenic patients employability skills or for them to live more independently
• Family therapy does reduce relapse rates and reduces the chances of the schizophrenic patients being hospitalized in the next two years.

Question 91

Evaluation of family therapy

Answer 91

1. Is family therapy effective? According to Pharoah’s study, it increases patient compliance with medication which can then lead to improvements in their mental state and social functioning – this then suggests that family therapy is effective in the sense that it teaches family members about the importance of taking medication rather than other factors. Does this mean that it is the medication or the family therapy that improves patients symptoms? Overall the evidence for family therapy according to Pharoah’s study is mixed.
2. There is an overall problems with a lack of blinding in family therapy studies. For example, in Pharoah’s study 10 of the 53 studies reported in this meta-analysis did not use any form of blinding – this means that the raters were not blinded to the condition to which participants has been allocated – which meant that they knew whether participants were attached to the experimental or control conditions – this would then create rater bias – as the raters would know which conditions participants would be allocated to so they may rate the participants allocated to the family therapy conditions as showing an improvement in their symptoms rather than the participants allocated to the control conditions. This is a problem because it does not really tell us whether family therapy is really effective.
3. There are economical benefits to family therapy. For example the NICE review of family therapy studies (NCCMH, 2009) demonstrated that family therapy is associated with significant cost savings when offered to people with SZ in addition to standard care. The extra cost of family therapy is offset by a reduction in costs of hospitalisation because of the lower relapse rates associated with this form of intervention. There is also evidence that family therapy reduces relapse rates for a significant period after completion of the intervention. This means that the cost savings associated with family therapy would be even higher (due to less chances of rehospitalisation)
4. The impact of family therapy on family members is also advantageous. For example, Lobban et al. (2013) analysed the results of 50 family therapy studies that had included an intervention to support relatives. 60% of these studies reported a significant positive impact of the intervention on at least one outcome category for relatives, e.g. coping and problem-solving skills, family functioning and relationship quality (including expressed emotion) – although the methodological quality of most of these 50 studies was poor, making it difficult to distinguish effective from ineffective interventions.

Question 92

Token economies in schizophrenia?

Answer 92

Token economies are reward systems used to manage the behaviour of patients with schizophrenia in hospital settings, in particular to those who have developed maladaptive behaviours through spending too long in hospital with other patients who may have showed catatonia.

Question 93

Principle of token economies

Answer 93

The principle of token economies are based on the principles of operant conditioning when the patient is given a token (reward) for carrying out a good behaviour (positive reinforcement) – this should then encourage them to repeat that behaviour in hope for another token. These tokens are then accumulated and swapped for a tangible reward e.g. sweets, cigarettes or even a walk outside the hospital.

Question 94

Evaluation of token economies

Answer 94

There is research support for token economies for example Dickerson et al. (2005) reviewed 13 studies in the use of token economies in the treating SZ. 11 of these studies had reported beneficial effects that were directly attributable to the use of token economies. Dickerson et al. concluded that, overall, these studies provide evidence of the token economy’s effectiveness in increasing the adaptive behaviours of patients with SZ. However, Dickerson et al. did caution that many of these studies had methodological issues which could have then effected the overall impact of token economies i.e. whether they were indeed successful.

There are ethical concerns concerning the use of token economy programmes in psychiatric settings. For example, in order to make reinforcement effective, clinicians may exercise control over important primary reinforcers such as food, privacy or access to activities that stop patients from being bored. Patients may then exchange tokens if they display the target behaviours (e.g. domestic duties or personal hygiene). However, it is generally accepted that all human beings have certain basic rights that should not be violated regardless of the positive consequences that might be achieved through the token economy programme.

Token Economy programmes lack ecological validity. Although the token economy programme has been shown to be effective in reducing negative symptoms for people with SZ, it has only been shown to work in a hospital setting. For example, Corrigan (1991) argues that there are problems administrating the token economy method with outpatients who live in the community. In a hospital, patients receive 24 hour care and can be given tokens straight away. In the real world, when people with SZ are living in the community, who will give them the tokens straightaway and how will they exchange them for a tangible item? Thus token economies lack ecological validity because they cannot be used in the real world community.

Do token economy programmes really work? As yet there is no real conclusive evidence. For example, there are very few randomised trials that have been carried out in token economy research studies. In an era where everything requires research support, token economy programmes are not really used in the developed world but would be very prominent if randomised trials were used so there may be hope for this programme in treating SZ in the future especially in a hospital setting. However, critics would argue that token economies are only used in hospitals to manage and control schizophrenic patients rather than ‘treat’ their symptoms.

Question 95

What is the interactionist approach?

Answer 95

The interactionist approach (also referred as the biosocial approach) is an approach that acknowledges that there are biological, psychological and societal factors in the development of SZ.

Question 96

What is the diathesis stress model explaining onset SZ

Answer 96

• Diathesis means vulnerability – we have seen that SZ has a genetic component in terms of vulnerability. In this context, stress simply means a negative psychological experience.
• This model states that both a vulnerability to SZ and a stress-trigger are necessary in order to develop the condition.
• One or more underlying factors make a person particularly vulnerable to developing SZ but the onset of the condition is triggered by stress.

Question 97

What are the two research studies based on the diathesis stress model and schizophrenia?

Answer 97

• Murray (1996)

- Barlow and Durand (2009)

Question 98

Murray research study on schizophrenia and the dithesis stress model

Answer 98

• He investigated children born after a flu epidemic.
• Their biological mothers had flu when they were 4-6 months pregnant.
• These children had an 88% increased chance of developing schizophrenia than children whose mothers did
not have flu when pregnant.
• Flu (stress) causes defects in neural development in the brain (diathesis) which can lead to brain damage and
problems in dopamine functioning (diathesis).
• Schizophrenia is caused by an interaction of many factors (diathesis stress).

Question 99

Barlow and Durand research study on schizophrenia and the dithesis stress model

Answer 99

Studied patients who had a family history of schizophrenia.
• The genetic link to the illness was a very important factor when looking at the cause of the illness, but a
stressor (family dysfunction) was also needed.
• This evidence supports the idea of the diathesis stress model and how an interactionist approach is needed
when examining the causes of schizophrenia e.g. genes and stress.

Question 100

Treatment according to the interactionist model

Answer 100

• The interactionist model of SZ acknowledges both biological and psychological factors in SZ and is therefore compatible with both biological and psychological treatments
• – in particular the model is associated with combining antipsychotic medication and psychological therapies such as CBT.
• In Britain it is increasingly standard practice to treat patients with a combination of drugs and CBT.
• It is unusual to treat SZ using psychological therapies alone.
• CBT, family therapy and the use of token economies with sufferers of SZ are usually carried out with patients taking antipsychotics

Question 101

Strengths of the interactionist approach

Answer 101

Evidence for the role of vulnerability and triggers – there is research support for the dual role for genetic vulnerability to SZ and stress triggers. For example, Tienari et al. (2004) studied children adopted away from schizophrenic mothers. The adoptive parents’ parenting styles were assessed and compared with a control group of adoptees with no genetic risk. A child-rearing style with high levels of criticism and conflict and low levels of empathy was implicated in the development of schizophrenia but only for children with a high genetic risk. This is very strong direct support for the interactionist approach – genetic vulnerability and family-related stress combine in the development of SZ.

Support for the effectiveness of combination of treatments - Another strength is the usefulness of the interactionist approach in treatment of SZ – Tarrier et al. (2004) randomly allocated 315 patients to (1) medication and CBT group or (2) a medication and supportive counselling group, or (3) a control group. Patients in the two combination groups (groups 1 and 2) showed lower symptom levels than those in the control group (medication only) – but no difference in hospital readmission. Studies like this show that there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.

Question 102

Weaknesses of the interactionst approach

Answer 102

One limitation is that the original diathesis-stress model is too simplistic – multiple genes increase vulnerability, each with a small effect on its own –there is no schizogene. Stress comes in many forms, including dysfunctional parenting. Researchers now believe stress can also include biological factors. For example, Houston et al. (2008) found childhood sexual trauma was a diathesis and cannabis use a trigger. This shows that the old idea of diathesis as biological and stress as psychological has turned out to be overly simple

Another limitation is we don’t know exactly how diathesis stress work –There is strong evidence to suggest that some sort of underlying vulnerability coupled with stress can lead to schizophrenia. But we don’t understand the mechanisms by which symptoms of schizophrenia appear and how both vulnerability and stress produce them. This does not undermine support for the approach, but it does mean we have an incomplete understanding of the actual medication.

A further limitation is the treatment-causation fallacy - Turkington et al. (2006) argue the fact that combined biological and psychological therapies are more effective than either on their own does not necessarily mean the interactionist approach to schizophrenia is correct. Similarly the fact that drugs help does not mean that schizophrenia is biological in origin. This error of logic is called the treatment-causation fallacy. It means that the superior outcomes of combined therapies should not be over-interpreted in terms of evidence in support of the interactionist approach.