Schizophrenia

Question 1

Schizophrenia

Answer 1

Schizophrenia 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. It is suffered by approximately 1% of the population.

Question 2

What kind of disorder is SZ

Answer 2

Schizophrenia is a psychotic rather than neurotic disorder – the term psychotic refers to serious mental issues causing abnormal thinking and perceptions and also the fact that people lose touch with reality and even their sense of self. Many people who suffer from schizophrenia end up homeless or hospitalised. It is not uncommon for a person suffering with SZ to commit or attempt suicide.

Question 3

Classification systems used to diagnose SZ

Answer 3

Two classification systems are used to diagnose schizophrenia.
1. The DSM 5(The Diagnostic and Statistical Manual of Psychiatric Disorders) – devised by the American Psychological Association (APA) – the DSM is currently now in its 5th edition.

2. The ICD 11 (The International Classification of Diseases) – devised by the World Health Organisation (WHO) - the ICD is currently in its 11 th edition

The DSM is thus used in America and the ICD is used in Europe and the other parts of the world too.

Question 4

How do the classification systems diagnose SZ

Answer 4

DSM 5 states that you need to show at least two or more positive symptoms such as hallucinations or delusions (or one positive and one negative) for a period of one month (as well as extreme social withdrawal for at least six months) to be diagnosed with schizophrenia

The ICD 11 states you need to show one positive and one negative symptom (or two negative symptoms) for at least one month to be diagnosed with schizophrenia.

Also both the ICD and DSM recognises that there are subtypes of schizophrenia (such as Catatonic Schizophrenia, Paranoid Schizophrenia) but both manuals have deleted these subtypes of schizophrenia as it made diagnosis more complex and had little effect on the treatments.

Question 5

Positive symptoms of SZ (hallucinations)

Answer 5

Positive symptoms are those that appear to reflect an excess or distortion of normal functions and can be seen below:

1. Hallucinations – these are sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that are there

Auditory (hearing) hallucinations: this is when the person will experience hearing voices making comments or talking to them in their head normally criticising them.

Visual (seeing) hallucinations: seeing things which are not real e.g. distorted facial expressions on animals or people

Olfactory (Smelling) hallucinations: smelling things which are not real e.g. a person could be smelling disinfectant which is not real

Tactile (touching and feeling) hallucinations: touching things which are not there for example, bugs are crawling on your skin

Question 6

Positive symptoms of SZ (delusions)

Answer 6

2. Delusions – also known as paranoia – these are irrational, bizzare beliefs that seem real to the person with SZ. These can take a range of forms. Common delusions involve being an important historical, religious or political figure such as Jesus or Napoleon. Delusions also may involve being persecuted perhaps by government, aliens or even superpowers. Delusions may involve the body – sufferers may believe that they or part of them is under external control. Some delusions can lead to aggression but this is not often.

Question 7

Positive symptoms of SZ (disorganised speech and catatonic behaviour)

Answer 7

3. Disorganised speech – 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 – this is often referred to as ‘word salad’. (this symptom is diagnosed in the DSM but not ICD – extra symptom)
4. Grossly disorganised or catatonic behaviour – includes the inability or motivation to initiate or even complete a task – this can lead to problems of personal hygiene or the person could be over active and doing loads of different activities simultaneously. The person may dress in a bizarre way such as wearing warm clothes on a hot summer’s day. Catatonia refers to adopting rigid postures or aimless repetition of the same behaviour. (this symptom is diagnosed in the DSM but not ICD – extra symptom)

Question 8

Negative symptoms of SZ (speech poverty and avolition)

Answer 8

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

1. Speech Poverty (Alogia): 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. Speech poverty may also be reflected in less complex syntax, e.g. fewer clauses, shorter utterances, etc. This type of speech appears to be associated with long illness and earlier onset of the illness.
2. Avolition: 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 9

Negative symptoms of SZ (affective flattening and anhedonia)

Answer 9

3. Affective flattening: 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

Anhedonia – 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 (extra symptom)

Question 10

Problems associated with the classification and diagnosis of SZ (reliability)

Answer 10

1. Reliability – consistency of a measuring instrument (e.g. the DSM or ICD). An example of reliability is inter-rater reliability – this is when two or more diagnosticians agree with the same diagnosis for the same individual – diagnosis would be done separately. Whaley (2001) found the interrater reliability between diagnosticians as low as +0.11 (using the DSM). Another more recent study that also showed low inter rater reliability amongst diagnosticians was carried out by Cheniaux et al (2009). In this study, they had two psychiatrists independently diagnose 100 schizophrenic patients using both ICD and DSM criteria. Inter-rater reliability was poor with one psychiatrist diagnosing 26 with SZ according to DSM and 44 according to ICD and the other psychiatrist diagnosing 13 according to DSM and 24 according to ICD. This poor reliability is a weakness of diagnosis of SZ

Question 11

Problems with classification and diagnosis of SZ (validity)

Answer 11

2. Validity – the extent to which we are measuring what we intend to measure. In other words, are we diagnosing schizophrenia correctly based on the symptoms used in the manuals. This can be assessed using criterion validity which is when different assessment systems arrive at the same diagnosis for the same patient – (e.g. both using ICD and DSM – the patient is seen as schizophrenic). According to Cheniaux’s study we can see the SZ is much more likely to be diagnosed using ICD than DSM suggesting that SZ is either over diagnosed in ICD and under diagnosed in DSM. Either way, this problem is a sign of poor validity

Question 12

Problems with classification and diagnosis of SZ (co-morbidity)

Answer 12

3. Co-morbidity – the idea that two or more mental disorders (or conditions) occur together at the same time with the same person. If this is the case, then we can question the validity of diagnosis for schizophrenia. Infact, schizophrenia is commonly diagnosed with other conditions.

In one review Buckley et al. (2009) concluded that around half of the patients with SZ also have a diagnosis of depression (50%) or substance abuse (47%). Post- traumatic stress disorder also occurred in 29% of cases and OCD in 23% of cases.

This poses a challenge for both classification and diagnosis of SZ. In terms of diagnosis, if half the patients are diagnosed with both SZ and depression, this suggests that we are not able to distinguish between both disorders very well.

Question 13

Problems with classification and diagnosis of SZ (symptom overlap)

Answer 13

4. Symptom overlap – this means that there is considerable overlap between the symptoms of SZ and other conditions such as depression and bipolar disorders. For example, a person can show a symptom of SZ and this symptom will also be in another disorder. For example, Ellason and Ross (1995) point out that people with DID (Dissociative Identity Disorder) actually having more schizophrenic 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 (Read, 2004)
   This overlap would question the validity of the classification and diagnosis of SZ. For example, under the ICD, a patient may be diagnosed with SZ but under the DSM the same person will be diagnosed with bipolar disorder – because of this overlap, this suggests that SZ and bipolar may not be two disorders but one

Question 14

Problems with classification and diagnosis of SZ (gender bias in diagnosis)

Answer 14

Longenecker et al (2010) reviewed SZ studies since the 1980s and found men more likely to be diagnosed than women. Is it because men more genetically vulnerable than women? There could be a gender bias in diagnosis as women seem to function better than men having good family relationships and more likely to work (Cotton 2009). Therefore it is less likely to be diagnosed with SZ because women showing better interpersonal function than men. Thus, there seems to be a gender bias in diagnosis of SZ with more males getting diagnosed than females

Question 15

Problems with classification and diagnosis of SZ (cultural bias in diagnosis)

Answer 15

African American and English people of Afro Caribbean origin are nine times more likely to be diagnosed with SZ. (Pinto and Jones, 2008)Why?
It may be because positive symptoms of SZ such as auditory hallucinations may be acceptable in Africa because of cultural beliefs in communication with ancestors (e.g. hearing their dead ancestors talking to them) which are acceptable and not warranted to a diagnosis in Africa (as SZ rates low in Africa).
However in the UK, this is more likely to be seen as a positive symptom of SZ.
Or, could it be that in Western cultures, we doubt the honesty of black people (Escobar, 2012)

Question 16

Advantages of classification and diagnosis of SZ (3p)

Answer 16

• 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 17

Biological explanations consist of what

Answer 17

Biological explanations of schizophrenia are based on two factors: the genetic basis and neural correlates including the dopamine hypothesis.

Question 18

Genetic basis - family studies

Answer 18

Family studies 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. 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 19

Genetic basis twin studies

Answer 19

Twin Studies 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!
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.

Furthermore in a more recent study, Joseph (2004) did a review of twin studies that were carried out up to 2001, and found an overall concordance rate for MZ twins as 40% but DZ twins as 7.4%. As the concordance rate is still relatively high for the MZ twins, his study supports the idea of genes playing a big part in SZ

Question 20

Genetic basis - adoption studies

Answer 20

Adoption Studies - 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. 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 21

Genetic basis - candidate genes

Answer 21

There are specific candidate genes that seemed to be associated with SZ (such the the PCM1) 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.

Gurling et al (2006) used evidence from family studies indicating that SZ was associated with chromosome 8p21-22 to identify a high-risk sample. Using gene mapping, the PCM1 gene was implicated in susceptibility to SZ, providing more evidence for genetics. Also Benzel et al. (2007) used gene mapping to find evidence suggesting that NRG3 gene variants interact with both NRG1 and ERBB4 gene variants to create susceptibility to developing SZ, suggesting an interaction of genetic factors.

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 22

Evaluation of genetic basis of SZ (1p,3n)

Answer 22

+ 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.

• the problem with twin and family studies is separating nature (genes) from nurture (the environment). 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. This can be caused by radiation, poison or infection. Evidence for role of mutation comes from Brown et al’s. (2002) study which 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. Shows how nature and nurture may both play a part rather than just genes
• Genetic explanation of SZ is also biologically reductionist as it is stating that one cause of SZ is simply your genes. In other words it is insinuating that if you possess the PCM1 gene then you will have SZ. This means that this explanation is ignoring other factors such as psychological factors and family upbringing which could be more important in explaining SZ – for example it has been found that certain parenting styles (e.g. the schizophrenogenic mother) in an individuals childhood could trigger symptoms of SZ in adulthood.

Question 23

Neural correlates of SZ

Answer 23

Neural correlates are measurements of the structure or function of the brain that have a relationship with SZ especially different regions of the brain. Neural correlates also 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 24

Neural correlates AO3 (2p,2n)

Answer 24

+ There is research evidence to support the structural changes in the brain between SZ and non SZ such as Torrey’s study with reference to enlarged brain ventricles and Conrad’s study with regards to the hippocampus.

+ Furthermore, this research evidence can be validated through brain scanning which is an objective method suggesting that there is face validity to the neural correlates explanation because one can actually observe the structural brain changes that occur with schizophrenic patients – this can then help to tailor make treatments that will reduce the symptoms of SZ.

• The problem with looking at different brain regions is the fact that there are individual differences in sufferers of schizophrenia and not all patients have deficits in the functioning of different brain regions.
• Also as there are different brain regions involved in SZ, it may be difficult to pinpoint which brain region is causing the symptoms.
  Furthermore, it may be difficult to establish cause and effect in terms of neuroanatomy as evidence is correlational in other words, did the sufferer have abnormalities in a particular brain region and then contract schizophrenia or did the individual contract schizophrenia and then show brain abnormalities?

Question 25

Neural correlates - the dopamine hypothesis

Answer 25

One of the best known and researched example of neural correlates is the neurotransmitter dopamine – known as the Dopamine Hypothesis

Neurotransmitters are the brains chemical messengers. These appear to work differently in the brains of schizophrenics. In particular, dopamine (DA) seems to have an important role since DA is necessary in the functioning of several brain systems. DA has also been implicated in SZ.

Thus the dopamine hypothesis 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 26

Consequences of dopamine hypothesis

Answer 26

Hyperdopaminergia in the subcortex – this 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

Hypodopaminergia in the cortex – recent versions of the dopamine hypothesis have focused on lower levels of dopamine in the cortex. Goldman-Rakic et al, (2004) 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 27

Evaluation of dopamine hypothesis (2p,2n)

Answer 27

+ There is evidence from drug research to support the Dopamine Hypothesis
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.

+ Also, 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).
Furthermore, Lindstroem et al. (1999) 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.

• the dopamine hypothesis could be criticised to being biological determinist which means an individual has no control over this whatsoever. However, 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
• as there are a number of neural correlates of SZ such as brain structure and neurotransmitters and although studies support neural correlates, there are some important questions that are left unanswered with such evidence. Most importantly, does high or low levels of dopamine cause SZ? There could be other explanations for the correlation. This point poses a serious problem to the neural correlates explanation as it does not really explain the cause and effect

Question 28

What is family dysfunction

Answer 28

Psychologists have attempted to link SZ to childhood and adult experiences of living in a dysfunctional family (i.e. a family that is not functioning properly e.g. where there may be abuse, messy divorces, criminal activities, high poverty etc)
The family dysfunction explanation can be explained in three ways:
1.The schizophrenogenic mother
2.Double-bind Theory
3.Expressed Emotion

Question 29

Schizophrenogenic mother

Answer 29

Fromm-Reichmann (1948) proposed a psychodynamic explanation for SZ based on the accounts she heard from her patients about their childhoods. She noted that many of her patients spoke about a particular type of parent which she called the schizophrenogenic mother. 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 (the belief that one is being persecuted by another person) 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 30

Double bind theory

Answer 30

Bateson et al. (1972) agreed that family climate is important in the development of SZ but focused more on the actual family communication style. He suggested that children who frequently receive contradictory messages from their parents. In this case, the child finds themselves trapped in situations which they fear doing the wrong thing but receive mixed messages about what this is. 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 (which they often do), 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.

Question 31

Expressed emotion

Answer 31

Expresssed Emotion (EE) 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 needless 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 32

Family dysfunction AO3 positives

Answer 32

1.There is research support for family dysfunction as a risk factor. For example in an adoption study by Tienari et al (1994). In this study, 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.

2. Read et al. (2005) 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.
3. evidence to support the Double-bind theory and SZ. Berger (1965) found that schizophrenics reported a higher recall of double-bind statements by their mothers than non-schizophrenics. However, this evidence may not be reliable as patient’s recall may be affected by their SZ in other words because they have suffered from hallucinations and delusions – they may just be assuming that their mothers used more double bind statements and we don’t know if their memory may have been affected by their symptoms.

Question 33

Family dysfunction AO3 negatives

Answer 33

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. This shows that this theory may not be specifically related to SZ.

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. This means that family dysfunction explanations may not be entirely ethical and may cause more harm than help to both the sufferer and their parents.

Finally the family dysfunction explanation of SZ can be criticised as being environmentally reductionist as it is simplifying the cause of SZ to family upbringing and ignoring other factors which could be more important for example, it has been suggested that individuals who possess the PCM1 gene are more likely to become schizophrenic. Therefore we should be cautious when stating that family dysfunction could be a cause of SZ as other factors may be important. It is therefore important to look at a more holistic explanation of SZ rather than just focusing on family upbringing.

Question 34

Cognitive explanations of SZ

Answer 34

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 35

Dysfunctional thought processing

Answer 35

Frith et al (1992) identified two kinds of dysfunctional thought processing that could underlie some symptoms:

1. Metarepresentation – this 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 a 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 (like thought insertions – where you believe that someone is putting thoughts into your head)
2. Central control – this 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’ – then you choose whether you do it or not)
   Speech poverty 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 36

Cognitive explanations for SZ AO3 (2p, 2n)

Answer 36

+ There is strong evidence for dysfunctional thought processing in SZ. In one study Stirling et al (2006) 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

+ Another strength of cognitive explanations of schizophrenia is the success of cognitive behaviour therapy (CBT) used alongside drugs to treat schizophrenia. As schizophrenia is a thought disorder, clearly drugs cannot completely treat the disorder thus cognitive behavioural therapy will aim to question and challenge the hallucinations and delusions - as well as using behavioural techniques (such as positive reinforcement). CBT has been proven to be effective thus further supporting the cognitive explanations of SZ.

• Although there is a wealth of evidence to support the idea that schizophrenics have dysfunctional thought processing, 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 which have all been shown to contribute to schizophrenia.

Question 37

How does drug therapy work for SZ

Answer 37

These drugs can be taken in the form of tablets or syrup or even injections. Injections tend to be given to those patients who are at risk of not taking their medication or don’t take it properly. Injections would be given every 2 – 4 weeks.
To control the symptoms of SZ, nearly all patients are first given antipsychotic drugs either for a short or long period depending on the control of their symptoms.
Some patients may have the drugs for a short period and be completely cured whereas others may need to take these drugs for a long period or even forever.
Sometimes, once the patient is stable, they may be given psychological therapies as well such as family therapy or CBT.

Question 38

Typical antipsychotics

Answer 38

These drugs are dopamine antagonists and work by reducing the effects of dopamine and thus reduce the symptoms of SZ. These drugs therefore bind to but do not stimulate dopamine receptors (particularly the D2 receptors in the mesolimbic dopamine pathway), thus blocking their action. This in turn will reduce the positive symptoms of SZ. Typical antipsychotics have been around since the 1950s and include Chlorpromazine. This drugs can be taken as a tablet, syrup or injection.

Typical antipsychotics are dopamine antagonists in that they bind to but do not stimulate dopamine receptors. In other words, they block the dopamine receptors in the synapses of the brain, reducing the actions of dopamine.

Question 39

Atypical antipsychotics

Answer 39

These drugs emerged in the 1970s and were used to improve upon the effectiveness of typical antipsychotics and also minimize the side effects that were occurring when patients were given typical antipsychotics. They also have a beneficial effect on negative symptoms and cognitive impairment are suitable for treatment-resistant patients

These drugs work like typical antipsychotics by blocking D2 receptors. However, they only temporarily occupy the D2 receptors and then rapidly dissociate to allow normal dopamine transmission – it is this rapid dissociation that is thought to be responsible for the lower levels of side effects.

Question 40

Clozapine

Answer 40

Clozapine then came back in the 1980s as it was seen as a more effective treatment for SZ rather than typical antipsychotics. Clozapine was used as an alternative treatment for SZ if the typical antipsychotic drugs failed to work.
Even today, clozapine is still used as an alternative. However, patients are given regular blood tests to make sure that they don’t have agranulocytosis. Because of its fatal side effects, clozapine is not available as an injection but only in syrup or tablet. The dosage given to patients is between 300 – 450 mg per day – much lower than chlorpromazine.
Clozapine works by binding to dopamine receptors but in addition, acts on serotonin and glutamate receptors. By the drug working on other neurotransmitters, this helps to reduce depression and anxiety and improve cognitive functioning. Because clozapine does improve mood, it is generally given to patients who are at high risk of suicide

Question 41

Risperidone

Answer 41

This drug emerged in the 1990s as an attempt to reduce the serious side effects of clozapine but still be as effective as clozapine.
Risperidone can be taken as syrup, tablets or injection. Patients are given a dose of about 4-8mg and up to a maximum of 12mg.
Risperidone like clozapine works by binding to dopamine receptors but works better in binding to dopamine receptors than clozapine leading to less side effects. As a result, much smaller doses are required of risperidone.

Question 42

Drug therapy AO3 positives (3)

Answer 42

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!

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 43

Drug therapy AO3 (3n)

Answer 43

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)

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.

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

Question 44

Three main psychological therapies for SZ

Answer 44

1. Cognitive Behaviour Therapy (CBT)
2. Family Therapy
3. Token Economies

Question 45

CBTp

Answer 45

Cognitive behavioural therapy for psychosis has 6 stages

a) Assessment – the patient expresses his thoughts to the therapist. Realistic goals for therapy are discussed – using the patient’s current distress as motivation for change.
b) Engagement – the therapist emphasises with the patient’s perspective and their feelings of distress, and stresses that explanations for their distress can be developed together.
c) The ABC model – the patient gives their explanation of the activating 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.

d) Normalisation – 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.
e) Critical collaborative analysis – the therapist uses gentle questioning to help the patient understand illogical deductions and conclusions. 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.
f) Developing alternative explanations – 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. E.g. Positive self talk – where the therapist encourages the client to repeat things such as ‘I can do this, I don’t need to think like this’

Question 46

CBT AO3 (2p,2n)

Answer 46

+ 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

+ 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. 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.

• 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
• 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 47

Aim of family therapy

Answer 47

The main aim of family therapy, therefore, is to provide support for carers in an attempt to make family life less stressful and so reduce rehospitalisation.

Question 48

How does family therapy work

Answer 48

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. Family therapy makes use of a number of strategies including:
a)Psychoeducation – helping the person and their carers to understand and be better able to deal with the illness.
b)Forming an alliance with relatives with care for the person with SZ
c)Reducing the emotional climate within the family and the burden of care for family members
d)Enhancing relatives’ ability to anticipate and solve problems
e)Reducing expressions of anger and guilt by family members
f)Maintaining reasonable expectations among family members for patient performance
g)Encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed

Question 49

Family therapy AO3 (2p,2n) Lexi notes

Answer 49

+ Procedure: Pharoah reviewed 53 studies published between 2002 and 2010 to investigate the effectiveness of family intervention. Studies chosen were conducted in Europe, Asia and Noeth America. The studies compared outcomes from family therapy to ‘standard’ care (antipsychotic medication alone). The researchers concentrated on studies that were randomised controlled trials (RCTs).
Findings: the main results (individuals receiving family therapy compared to those receiving standard care) were:
• Mental state – the overall impression was mixed, some studies reported an improvement in the overall mental state of patients compared to those receiving standard care, whereas others did not
• Compliance with medication - the use of family therapy increased patients compliance with medication
• Social functioning – although appearing to show some improvement on general functioning, family intervention did not appear to have much of an effect on more concrete outcomes such as living independently or employment
• Reduction in relapse and readmission – there was a reduction in the risk of relapse and a reduction in hospital admission during treatment and in the 24 months after.

+ 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.

+ 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)

• 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.
• 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

Question 50

Token Economy

Answer 50

Token economies are reward systems used to manage (rather than treat) 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. Under these circumstances, it is common for patients who are institutionalised (spent too long in hospital) to develop bad hygiene or perhaps remain in pyjamas all day.
Changing these bad habits does not cure SZ but it improves the patient’s quality of life and makes it more likely that they can live outside a hospital setting.

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.

Although the tokens have no value in themselves they can be swapped later for more tangible rewards. Token are secondary reinforcers because they only have value once the patient has learned that they can be used to obtain rewards.

Question 51

Token economy AO3 (1p,3n)

Answer 51

+ 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.

• 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
• 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?
• critics argue that token economies are only used in hospitals to manage and control schizophrenic patients rather than ‘treat’ their symptoms.

Question 52

Interactionist approach

Answer 52

Approach that acknowledges that there are biological, psychological and societal factors in the development of SZ. Biological factors include genetic vulnerability and neurochemical (e.g. dopamine) and neurological (brain) abnormality. Psychological factors include stress resulting from life events and daily hassles, including poor quality interactions in the family.

Question 53

Diathesis stress model - explaining onset of SZ

Answer 53

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.

Meehl (1962) stated that the diathesis (vulnerability) was a schizogene and that anyone with this would be susceptible to stress and develop schizophrenia (especially if they have a schizophregenic mother).

Now we understand that many genes could contribute to vulnerability and even childhood trauma could be the diathesis, such as child abuse. Stressors can also extend beyond the ided of parenting, for instance the use of cannabis could act as a stressor.

The modern understanding of stress as opposed to the original understanding of it (which was that stress was psychological in nature and due to parenting), is that it is anything that risks triggering schizophrenia e.g. cannabis use which makes it 7 times more likely for a person to develop schizophrenic symptoms. This is because cannabis interferes with the dopamine system – although most people do not develop SZ through cannabis use as most people do not take cannabis but will develop SZ – this suggests that there are clearly other stressors which contribute to the development of SZ.

Question 54

Treatment of SZ according to the interactionist approach

Answer 54

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

It is unusual to treat SZ using psychological therapies alone this is because SZ is a complex psychotic disorder, drug therapy will be first given to control the symptoms of SZ, the drug therapy will be used in a hospital setting perhaps with token economy to manage the behaviour of patients with SZ. Then CBT and family therapy will precede this.

Question 55

Interactionist approach AO3 (2p,3n)

Answer 55

+ 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.

+ 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.

• 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
• 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. Incomplete understanding
• 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.