Schizophrenia- Paper 3

What is Schizophrenia?

Schizophrenia= a type of psychosis, a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality 

• Most common psychotic disorder

• Affects about 1% of the population 

• Men are more likely to have schizophrenia than women 

• Hallucinations and delusions are most commonly reported by people with the disorder

Diagnosis of Schizophrenia

Diagnosis of any mental health condition are made using the Diagnostic and Statistical manual of Psychiatric Disorders (DSM) 

Classifying Schizophrenia from DSM-V: 

A: Two (or more) of the following each present for a significant portion of time during a 1 month period (or less is successfully treated). At least one of these must be 1, 2 or 3;

1. Delusions

2. Hallucinations 

3. Disorganised speech (e.g. frequent derailment or incoherence)

4. Grossly disorganised or catatonic behaviour 

5. Negative symptoms (i.e. diminished emotional expressions) 

Symptoms of Schizophrenia

• Delusions (false beliefs) – bizarre beliefs that seem real to the person with schizophrenia, but they are not real. Sometimes these delusions can be paranoid (i.e. persecutory) in nature. Delusions may also involve inflated beliefs about the person’s power and importance. There may also be delusions of reference where it is believed that events in the environment are directly related to them e.g. special messages being relayed via TV.

• Speech poverty – lessening of speech fluency and productivity, reflecting slow or blocked thoughts. May produce fewer words in a test of verbal fluency (e.g. name as many animals as you can in one minute) due to a difficulty in spontaneously producing the words. May also be reflected in less complex syntax e.g. fewer clauses, shorter utterances (associated with long illness and early onset of illness).

• Hallucinations (false perceptions) – bizarre, unreal perceptions of the environment that are usually auditory (hearing voices) but may also be visual (seeing lights, objects or faces), olfactory (smelling things) or tactile (e.g. feeling that bugs are crawling on or under the skin). Many schizophrenics report hearing a voice or voices telling them to do something (ie hurt themselves or others) or commenting on their behaviour. 

• Avolition – the reduction of, or inability to initiate and persist in, goal-directed behaviour (e.g. sitting in the house for hours every day, doing nothing). Avolition is distinct from poor social function or disinterest, but is often confused with this.

Positive vs Negative Symptoms of Schizophrenia

Positive  Reflecting an excess or distortion of ‘normal functioning’ Not usually present in a neurotypical individual	Negative  Reflecting a reduction or loss of ‘normal’ functioning  Causes a decline in functioning
Speech Poverty	Hallucinations
Avolition	Delusions

DSM-V: One positive symptom must be present 

ICD-11: Two or more negative symptoms are sufficient for diagnosis 

Reliability in Schizohrenia diagnosis

Reliability= The consistency of a measuring tool (e.g. The DSM) or other tests used in diagnosis. A test/tool must be valid for it to be reliable 

Test-Retest Reliability

Doctors must be able to reach the same conclusions about a patient at two different points in time. The DSM and other tests must enable this to occur, so a patient isn’t ‘labelled’ with a diagnosis which then changes or is re-diagnosed as another condition later on. 

Inter-Rater Reliability

• The extent to which different assessors agree on their assessments. 

• Doctors must reach the same conclusions about a patient’s diagnosis. The DSM and other tools must enable inter-rater reliability. Eg. Doctors should be able to consult the DSM about a patient, independently from each other and achieve the same diagnosis. 

Cheniaux et al (2009) study

Two psychiatrists asked to independently diagnose 100 patients using both DSM and ICD criteria. One psychiatrist diagnosed 26 with schizophrenia according to the DSM and 44 according to the ICD. The other diagnosed 13 with schizophrenia according to DSM and 24 according to ICD. This research suggests the inter-rater reliability of classification systems is poor because we would expect the same number of diagnoses made irrespective of criteria used

AO3 EVALUATION: Reliability in Schizophrenia

• Cultural differences in diagnosis- Research suggests there is a significant variation between countries when it comes to diagnosing schizophrenia i.e. culture has an influence on the diagnostic process. Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed schizophrenia but only 2% of the British ones did. 

• Research support- Roseham (1973) investigated how situational factors affect a diagnosis of Schizophrenia. 8 pseudo-patients went to 12 different hospitals in the US and reported hearing voices. Once admitted, they stopped simulating symptoms. All pseudo-patients admitted with a diagnosis of Sz, one admitted with manic-depression. Normal behaviour was interpreted as symptoms of the disorder. Pseudo-patients were kept in for periods ranging from 7-52 days, the average stay was 19 days. All pseudo-patients discharged as “in remission”. 35 real patients detected sanity. This demonstrated the unreliability of diagnostic tools

Validity in Schizophrenia Diagnosis

Validity= The correctness, accuracy and meaningfulness of a diagnosis- do different classification systems arrive at the same diagnosis of the same patient?

• This means it must represent something real and be distinct from other disorders. 

• The DSM must enable a valid diagnosis to be made, by ensuring it measures what it claims to measure (symptoms of a disorder, schizophrenia) which is different to other mental health conditions and enables psychiatrists to recognise symptoms & provide treatment.

AO3 EVALUATION: Validity in Schizophrenia Diagnosis

• Gender Bias- Occurs when accuracy of a diagnosis is dependent on the gender of an individual.  This may occur due to gender-biased diagnostic criteria, or clinicians basing their judgements on stereotypical beliefs held about gender. Broverman et al. (1970) found the clinicians in the US equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour therefore women tended to be seen as less mentally healthy.

• Symptom Overlap- Many of the symptoms of schizophrenia are also found in other disorders such as depression and bipolar disorder. Read (2004) states that most people with schizophrenia have sufficient symptoms of other disorders that they could also receive at least one other diagnosis.

• Comorbidity- Refers to the extent that two or more conditions co-occur.  Schizophrenia often occurs alongside substance abuse, anxiety and depression.  If conditions occur together a lot of the time, then this calls into question the validity of their diagnosis and classification (may actually be a single condition). Buckley et al. (2009) estimated that co-morbid depression occurs in 50% of patients, and 47% also have a lifetime diagnosis of co-morbid substance abuse. Swets et al. (2014)carried out a meta-analysis and found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant OCD obsessive-compulsive symptoms.

Biological explanations of Schizophrenia

Biological explanations of schizophrenia suggest that individuals are biologically determined to develop schizophrenia based on genes and neurotransmitters

What are the biological explanations of Schizophrenia?

1. Genetics

2. The Dopamine Hypothesis

3. Neural Correlates

Biological explanations of Schizophrenia: Genetics

Heredity (genetics) is one possible cause of schizophrenia. Schizophrenia tends to run in families and the risk of an individual developing schizophrenia is higher for those with biological relatives with schizophrenia than those without. It is thought that different combinations of genes make a person more vulnerable to schizophrenia. 

• Schizophrenia is thought to be polygenic – this means that its development is not determined by a single gene but a few (maybe as many as 108 genes).

• Each individual gene confers a small increased risk of SZ (it is polygenic).

• Other research has identified different candidate genes implicated in the development of Sz. This suggests the disorder is aetiologically heterogeneous - different combinations of genes can lead to the condition. 

• Genes associated with the increased risk included those coding for the functioning of a number of neurotransmitters including dopamine

Family Studies

• Family Studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder. In Gottesman’s (1991) large-scale family study. He concluded that Sz is more common in the biological relatives of a Schizophrenic individual and the closer the degree of genetic relatedness, the greater the risk. For example, someone with an aunty with schizophrenia has a 2% chance of developing it, increasing to 9% if the individual is a sibling and 48% if they are an identical twin. 

• This shows that genes do play an important factor, however if genes were the only cause of schizophrenia then the percentages surely should be 100%, 

• The theory could be seen as deterministic; just because we are ‘predisposed’ by our genes cannot mean we necessarily get the disorder schizophrenia. 

Twin Studies

• If Monozygotic (MZ) twins are more concordant than Dizygotic (DZ) twins, then this suggests that the greater similarity is due to genetics. 

• Joseph (2004) points out that MZ twins are treated much more similarly, encounter more similar environments and experience more ‘identity confusion’ (frequently being treated as ‘the twins’ rather than as individuals) than DZ twins. 

Adoption Studies

• Are a way of truly separating the influence of genetics and environment, by investigating individuals who are genetically related by reared apart.

• Tienari et al. (2000) found that of 164 adoptees whose biological mothers had been diagnosed with Schizophrenia, 6.7% also received a diagnosis, compared to just 2% of the 197 control adoptees (born to non-schizophrenic mothers).

• Adoption Study (Heston, 1966)- Followed up on 47 children whose mothers were hospitalised with schizophrenia in Oregon, USA. The children were placed with family or into foster homes within 72 hours of their birth. Heston found that 16.6% of the children were diagnosed with schizophrenia.  Heston also looked at 50 control children, none of whom developed schizophrenia.  The children of schizophrenic mothers were also more likely to be diagnosed as mentally retarded or psychopathic. They were also involved more frequently in criminal activities. 

AO3 EVALUATION: Genetics as an explanation of schizophrenia

• Environmental factors- One limitation of the genetic explanation is that there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia. These factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years. Psychological risk factors can include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia. In one study by Nina Markved at al (2017), 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues. This means that genetic factors alone cannot provide a complete explanation for schizophrenia

• Twin Studies

  • Twin studies seem to indicate that there is a strong genetic component to the disorder

  • Twin studies demonstrate that there may be a predisposition to develop schizophrenia, however, the fact that both twins do not always develop schizophrenia means that environmental factors must also play a part

  • The fact that the concordance rate for twins is not 100% means that schizophrenia cannot be accounted for by genetics alone

  • Sample sizes of such twin studies is always going to be very small so therefore it is difficult to generalise to the general population

Biological explanations of Schizophrenia: The Dopamine Hypothesis

The Dopamine Hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia. 

The Role of Dopamine

•  Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure 

• Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions. 

• Schizophrenics are said to have too many D2 receptors on receiving neurons, resulting in more dopamine binding and, therefore, more neurons firing.

• Drugs that increase dopaminergic activity: amphetamine is a dopamine agonist (it stimulates nerve cells containing dopamine, causing the synapse to be flooded with dopamine).

• Drugs that decrease dopaminergic activity: there are many different antipsychotic drugs but what they all have in common is that they block the activity of dopamine, thus eliminating symptoms such as hallucinations and delusions

Hyperdopaminergia

• The original dopamine hypothesis focused on the role of high levels of dopamine (hyperdopaminergia) in the subcortex (central areas of the brain). 

• For example, an excess of dopamine receptors in Broca’s area may be associated with speech poverty and/or auditory hallucinations. 

Hypodopaminergia

• More recent versions of the dopamine hypothesis focus on abnormal dopamine systems (hypodopaminergic) in the cortex. 

• Goldman-Rakic et al. (2004) concluded that low levels of dopamine in the prefrontal cortex are implicated in the negative symptoms of Sz. 

  • It may be that both hyper and hypo dopaminergia are correct. It could be that high levels in some parts of the brain are linked to  positive symptoms and low levels in other parts of the brain are linked to negative symptoms. 

  • The dopamine hypothesis has been revised by Davis and Kahn (1991), who proposed that the positive symptoms are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway. 

AO3 EVALUATION: The Dopamine Hypothesis

• Research support- Research support comes from the development of drug therapies that specifically target dopamine. The effectiveness of these drugs demonstrate that dopamine is implicated in schizophrenia. Curran et al. (2004) - dopamine agonists (e.g. amphetamines) increased levels of DA and can induce Sz-like symptoms in non-sufferers

• Individual differences- This explanation does not consider individual differences  It can be considered biologically reductionist as it only explains schizophrenia by focusing on the role of one neurotransmitter. 

Biological explanations of Schizophrenia: Neural Correlates

Neural correlates changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour or mental disorder.

• Neural correlates are measurements of the structure or function of the brain that occur in conjunction with an experience, in this case schizophrenia.

• There is growing evidence that schizophrenia is down to structural abnormalities in the brain.

• Brain scanning techniques have made it possible to investigate living brain images.

• Both positive and negative symptoms have correlates. 

Neural Correlates- Ventricular Space

• Weinberger and Wyatt (1982) found that the ventricles in the brains of schizophrenic patients were, on average, twice as large as those of normal subjects.

• Suddath et al. (1990) found that in 15 pairs of twins, the schizophrenic twin was easily identified by visual inspection of the ventricles in 12 of the pairs. 

• Keshavan et al. (2008) found evidence for alterations in the brain’s structure and suggested that these alterations could be related to the genetic predisposition to the disorder. The alterations include a loss of grey matter in certain areas of the brain.

Neural Correlates- Avolition and Ventral Staritum

• Neural correlates are patterns of structure or function in the brain that occur alongside specific experiences, e.g. Sz. 

• These patterns of structure or function may be implicated in origins of positive and negative symptoms.

• Motivation involves anticipation of a reward. The ventral striatum is believed to be involved in this anticipation. Juckel at al. (2006) measured activity levels in the ventral striatum and a control group. They found lower levels of activity in this area in the brains of schizophrenic individuals.

Neural Correlates- Hallucinations and superior temporal gyrus

• Allen et al (2007) using brain scanning techniques for schizophrenic patients suffering from auditory hallucinations and compared them to a control group.

• During this procedure, the participants identified pre recorded speech as theirs or others.

• The research found lower activation levels in the superior temporal gyrus and anterior cingulate gyrus in the hallucination group. They also made more errors.

• We can conclude that reduced activity in these two areas is a neural correlate of auditory hallucination.

Neural Correlates- active flattening and Amygdala

• The amygdala is responsible for our basic feelings such as lust, fear and hunger.

• Research suggests that a small amygdala in schizophrenic individuals can be linked to affective flattening (a loss of emotion)

Neural Correlates- Disorganised thoughts/Delusions and the Prefrontal Cortex

• The prefrontal cortex enables us to think logically and organise our thoughts

• Research suggests that in schizophrenic individuals, there is a lower level of activity in the prefrontal cortex. This can help to explain positive symptoms such as delusions and disorganised thoughts

AO3 EVALUATION: Neural Correlates

• Empirical Evidence-  There is objective, scientific evidence to support the theory that neural correlates are implicated in the development of schizophrenia. MRIs have made it possible to investigate living brain images which is an advance on merely having to rely on post mortems. 

• Correlational Evidence- Findings of the research are inconsistent and it is biologically reductionist. There are also issues of causality. Cause and effect can not be established with brain abnormalities, it is still uncertain whether structural abnormalities/reduced functioning predispose to schizophrenia, or whether the onset of the clinical symptoms causes these changes. 

• An alternative hypothesis: the diathesis-stress model - this suggests that there may be a disposition to schizophrenia but it only develops if there is an environmental stressor

Drug therapy treatments for Schizophrenia

• The most common treatment for Sz is drug therapy which seeks to target the biological causes of Sz - dopamine.

• Antipsychotics can be taken as a short-term or long-term solution for Schizophrenic individuals. 

• Antipsychotics can also be taken alongside other forms of therapy.

• They can be divided into typical (traditional) or atypical (second-generation drugs)

• These drugs are not cures but only aim to minimise the symptoms of the disorder

Typical Antipsychotic drugs

Dopamine antagonist:

• Typical drugs work by reducing the effects of dopamine and therefore reducing the positive symptoms of schizophrenia (hallucinations and delusions). 

• They are dopamine antagonists (they bind to, but do not stimulate, dopamine receptors; especially the D2 receptors).

• For example, Chlorpromazine is a dopamine antagonist 

Block of Dopamine receptors:

• In order to be effective, Kapur et al. (2000) estimate that between 60% and 75% of D2 receptors in the mesolimbic pathway must be blocked.

• Block dopamine receptors in the synapses, and can also have a sedation effect.

• Unfortunately, however, for this to happen a similar number of D2 receptors in other areas of the brain must also be blocked, leading to undesirable side-effects. 

Atypical Anitpsychotic drugs

Target Dopamine and Serotonin:

• Second generation e.g. clozapine.

• Compared to typical antipsychotics, atypical antipsychotics have a lower risk of side effects, have a beneficial effect on negative symptoms and cognitive impairment, and are suitable for treatment-resistant patients. 

• Target dopamine and serotonin.

• Reduces depression and anxiety as well as improving cognitive functioning.

• Atypical antipsychotics work by blocking D2 receptors, but unlike typical antipsychotics, they rapidly dissociate to allow normal dopamine transmission; this is what leads to less side effects. 

• Furthermore, whereas typical antipsychotics bind only to D2 receptors, atypical antipsychotics have a stronger affinity for serotonin receptors and a lower affinity for D2 receptors. 

• Atypical receptors have proven to reduce the symptoms of schizophrenia and have only claimed to reduce the effects of negative symptoms, but there is not clear evidence for this yet

Side effects of the drug Chlorpromazine

Tiredness

Feeling Woozy

Dry mouth

Stuffy nose

Constipation

Difficulty peeing

Blurred eyesight

Side effects of Clozapine

Confusion

High Cholesterol

Irregular heartbeat or pulse

Sweating

Trembling

Faintness

Weight gain (which can lead to diabetic conditions)

AO3 EVALUATION: Drug therapies for treating Schizophrenia

• Research support- Thornley et al. (2003) - compared Chlorpromazine to a placebo group. Results showed that Chlorpromazine was associated with better functioning and reduction of symptom severity (1121 ppts analysed). Relapse rate was also lower when Chlorpromazine was taken (512 ppts analysed). Gilbert et al. (1995) - 53% of patients relapsed within 10 months of stopping medication, compared to 16% who continued taking it. 

• Positive implications for the economy- Drug therapies are relatively cheap to manufacture and work more quickly than psychological therapies. This enables individuals to manage their symptoms more quickly and live “normal” lives. This means they can hold down a job, pay their taxes and contribute to the economy.

• Over-reliance on the dopamine hypothesis- Antipsychotics work on the assumption that dopamine levels are too high (they block dopamine receptors). However, in parts of the brain, dopamine levels are too low.

• Side effects can range from mild to fatal- Neuroleptic malignant syndrome (NMS) is a side effect of typical drugs.  NMS can cause fever, muscular rigidity and an altered mental state. Agranulocytosis is a side effect of atypical drugs. This symptom affects the white blood cells in the body which are needed to fight infection 

• Chemical cosh argument- It is widely believed that antipsychotic drugs are used in hospital situations to calm and control the patient, rather than to benefit them. Short-term use is recommended to calm patients by the National Institute for Health and Clinical Excellence (NICE). Some researchers argue that this is human rights abuse (Moncrieff, 2013). As a result of the calming effects antipsychotics can have on patients, some researchers question the validity of research demonstrating them to be effective. Healy (2012) suggests it is easy to show “positive effects” in patients who have been calmed as a result of these drugs

• Nature vs Nurture debate- Drug therapies only target dopamine as a cause of schizophrenia. Drug therapies only focus on the nature side of this debate and ignores the role of nurture in the development of schizophrenia. Research also suggests that schizophrenia can occur due to family dysfunction, childhood trauma, migration, etc. Arguably, an interactionist approach is best when considering forms of treatment for schizophrenia

Psychological explanations for schizophrenia

• Family Dysfunction

• Cognitive explanations

Family Dysfunction

Consist of 3 main theories:

1. Schizophrenogenic mother

2. Double blind theory

3. Expressed emotion

Schizophrenogenic mother

• Fromm-Reichmann (1948) put forward the theory that the development of Sz stems from experiences in childhood.

• Many patients spoke of a particular type of parent - the schizophrenogenic mother.

• Characteristics of a schizophrenogenic mother include being cold, rejecting their child, controlling their child and creating a family climate that has tension and secrecy. 

• This can explain symptoms of T of paranoid delusions (false beliefs) because the hostility received from the mother may cause a schizophrenic individual to have beliefs that others are out to get them, or that others have more power over them. Another symptom caused by a schizophrenogenic mother is hallucinations, specifically auditory hallucinations that are critical or abusive towards the individual, this may mirror the critical words said by the mother.

Double Blind Theory

• Bateson et al. (1972) also theorised that family climate is an important factor within the development of Sz.

• It is suggested that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia.

• For example, if a mother tells her son that she loves him but at the same time turns her head away in disgust, the child receives two conflicting messages about their relationship.

• These messages invalidate each other so the child is unable to respond, which in turn prevents the development of an internally coherent construction of reality. In the long run this manifests itself as schizophrenic symptoms e.g. flattened affect and withdrawal.

• This is argued to be a risk factor in the development of Sz, not the only factor.

Expressed Emotion

• Expressed emotion focuses on the quality of social interaction between an individual with Sz and their carers and/or family. 

• There are three key elements present:

  • Criticism – dislike or disapproval of the patient

  • Hostility – dislike or rejection of the patient as a person (more extreme than criticism)

  • Emotional over involvement – a dramatic or over-concerned attitude toward the patient’s illness.

• It suggests that people with schizophrenia have a lower tolerance for these intense interactions with family members; and that the negative emotional climate in these families arouses the patient and leads to stress beyond their impaired coping mechanisms, thus triggering a schizophrenic episode.

AO3 Evaluation: Family Dysfunction

• Inconclusive Support- One limitation of family explanations is the poor evidence base for any of the explanations. Although there is plenty of evidence supporting the idea that childhood family-based stress is associated with adult schizophrenia, there is almost none to support the importance of traditional family-based theories such as the schizophrenogenic mother and double blind. Both these theories are based on clinical observation of people with Sz and also informal assessment of their mother’s personalities, but noy systematic evidence. This means that family explanations have not been able to account for the link between childhood trauma and schizophrenia. 

• Social Sensitivity- Research in this area may be useful in showing that insecure attachment and experience of childhood trauma affect individual vulnerability to schizophrenia. On the other hand, research linking family dysfunction to schizophrenia is highly socially sensitive because it can lead to parent blaming. Mothers seem to be particularly balamed. For parents already having to watch their child experience the symptoms of schizophrenia and take responsibility for their care, to be blamed only adds insult to injury. 

• Nature vs Nurture- This explanation focuses on the family as a sole explanation for the development of schizophrenia. It does not consider any biological (nature) factors which might contribute. The effectiveness of drug therapies suggests that biological factors (dopamine) do play a role in schizophrenia. Similarly, not all children raised in dysfunctional families go on to develop schizophrenia. Therefore it can be argued that only focusing on one element of nurture is not sufficient enough to explain the development of this complex disorder and an interactionist approach (diathesis-stress model) would be most appropriate for explaining schizophrenia.

Cognitive Explanations

Consists of 3 main theories:

1. Lack of central control

2. Meta represenation

3. Dysfunctional thought processing

Lack of central control

• Issues have also been identified with the cognitive ability to suppress automatic responses while we perform deliberate actions.

• Speech poverty and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.

• For example people with schizophrenia tend to experience derailment of thoughts because each word triggers associations, and the person cannot suppress automatic responses to these.

Meta represenation

• Metarepresentation is the ability to reflect on thoughts and behaviours.

• This allows us insight into our own intentions and goals. It also allows us to interpret the actions of others.

• Dysfunction disrupts our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else.

• This would explain hallucinations of hearing voices and delusions like thought insertion.

• Hallucinations: People with hallucinations focus excessive attention on auditory stimuli (hypervigilance) so they have a higher ‘expectancy’ to hear a voice.  Aleman (2001) suggests that people prone to hallucinations find it difficult to distinguish between imagery and sensory-based perception ie the inner representation of an idea (what other people think of me) can override the actual sensory stimulus and produce an auditory image (he is not a good person). Those who hallucinate are significantly more likely to misattribute the source of self-generated auditory experience to an external source than are those who do not hallucinate. These hallucinations are difficult to correct because patients with schizophrenia do not go through the same processes of reality testing that others would do

Dysfunctional thought processing

When delusions are formed the patient’s interpretations of their experiences are controlled by inadequate information processing. A critical characteristic of delusional thinking is egocentric bias i.e. the extent to which the individual sees himself as a central component to events.  This leads to the individual jumping to false conclusions about external events; irrelevant stimuli are related to themselves. Very difficult to prove these as delusions as the individual has ‘impaired insight’ meaning they are unable to recognise cognitive distortions and substitute more realistic explanations.

AO3 Evaluation: Cognitive explanations

• Research Support- One strength of cognitive explanations is evidence for dysfunctional thought processing. John Stirling et al (2006) compared performance on a range of cognitive tasks in 30 people with Sz and a control group of 30 people without Sz. Tasks included the Stroop tasks in which participants have to name the font colours of colour-words, so have to suppress the tendency to read the words aloud. As predicted, people with Sz took longer- over twice as long on average- to name the font colours. This means that cognitive processes of people with Sz are impaired. 

• Proximal Explanation- One limitation of cognitive explanations is that they explain the proximal origins of symptoms. Cognitive explanations for Sz are proximal explanations because they explain what is happening now to produce symptoms- as distinct from distal explanations which focus on what initially caused the condition. Possible distal explanations are genetic and family dysfunction explanations. What is currently unclear and not well addressed is how genetic variation or childhood trauma might lead to problems with metarepresentation or central control. This means that cognitive theories on their own only provide partial explanations for schizophrenia. 

Cognitive behaviour therapy treatments

• NICE (National Institute for Health & Care Excellence) recommends that all patients with schizophrenia should be offered cognitive behaviour therapy for psychosis (CBTp).

• CBTp is used to help the patient identify and correct faulty interpretations of events and to help establish links between their thoughts, feelings or actions and their symptoms in order to consider alternative ways of explaining why they think and behave the way they do. This reduces distress and therefore improves functioning.

What is the process of cognitive behaviour therapy?

• Patients are encouraged to trace back the origins of their symptoms to try to understand how they might have developed.

• They are also encouraged to study the content of their delusions/hallucinations and to consider ways of testing the validity of their faulty beliefs (discussion of how likely the beliefs are to be true)

• The patient is encouraged to develop their own alternatives to these maladaptive beliefs and to look for coping strategies.

• Use of positive self-talk  or distraction as examples of coping strategies

• This will not get rid of the symptoms of Sz but it can make patients better able to cope with them

AO3 Evaluation: Cognitive behaviour therapy

• Effectiveness vs Appropriateness- Limited availability as only around 1 in 10 who could benefit get access to this form of therapy. Also, the length of therapy can be a practical issue (drop out rates). A significant number refuse or fail to attend – limiting effectiveness. The therapy requires self-awareness and willingness to engage with the process (positive symptoms lead to lack of awareness; negative symptoms lead to reluctance / inability to engage)

• Research Support- Kingdon and Kirschen (2006) found that CBT is not suitable for all patients, especially those who are too paranoid to form trusting alliances with practitioners or those who may be experiencing delusions of persecution and believe that people are trying to control their thoughts. This would mean that CBT may be a threatening experience for these patients and would hinder their progress and recovery, rather than help it, challenging the appropriateness of treatment. Allows patient to take some responsibility for their own treatment and can have long-term effectiveness

• Idiographic vs Nomothetic- Takes a nomothetic approach as it applies general rules to all of schizophrenia patients (i.e. there is a cognitive basis for all the patients). However, treatment can be carried out at an idiographic approach; patient by patient basis to make a treatment plan.

Family therapy treatments

• The main aim of family therapy is to provide support for carers in an attempt to make family life less stressful and so reduce re-hospitalisation. 

• NICE recommends that family therapy should be offered to all individuals with schizophrenia who are in contact with, or live with, family members. This should be a priority for those with persistent symptoms or high risk of relapse. 

• Research shows that schizophrenics from families with high levels of criticism, hostility or over-involvement (expressed emotion) had more frequent relapses than those with comparable problems from families that were less expressive in their emotions; therefore, the aim of family therapy is to reduce levels of expressed emotion. 

• Garety et al. (2008) estimate the relapse rate for individuals who receive family therapy as 25%, compared to 50% for those who receive antipsychotic treatment only.

What is the process of family therapy treatments?

• Involves weekly meetings with a therapist and multiple interviews in order to establish the cause of the family dysfunction that could be contributing to Sz.

• During family therapy, family members are provided with information about schizophrenia, shown ways of supporting the individual with schizophrenia, and resolving any practical problems. 

• Relationships are improved by family therapy as family members are encouraged to listen to each other and openly discuss/negotiate potential solutions together.

• The individual with schizophrenia is also encouraged to talk to their family and explain what sort of support they find helpful – and what makes things worse for them.

AO3 Evaluation: Family Therapy

• Effectiveness of Family Therapy- A review of studies by McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments available for Sz. In particular relapse rates were found to be reduced, typically by 50-60%. McFarlane also concluded that using family therapy as mental health initially starts to decline is particularly promising. Clinical advice from NICE recommends family therapy for everyone with a diagnosis of schizophrenia. This means that family therapy is likely to be of benefit to people with both early and ‘full blown’ Sz. 

• Benefits to the whole family- Therapy is not just for the benefit of the identified patient but also for the families that provide the bulk of care. A review of evidence by Lobban and Barrowclough (2016) concluded that these effects are important because families provide the bulk of care for people with Sz. By strengthening the functioning of a whole family, family therapy lessens the negative impact of Sz on other family members and strengthens the ability of the family to support the person with Sz. This means that family therapy has wider benefits beyond the obvious positive impact on the identified patient. 

• Economic Benefits- The NICE review of family therapy studies 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.

Token economy in the management of Schizophrenia

• Token economy is a form of behavioural therapy, based on the principles of operant conditioning. It was widely used in the 1960s and 1970s but nowadays this has been replaced by other forms of intervention such as social and life skills training. 

• Token economies are reward systems used to manage the behaviour of schizophrenic patients, particularly those who have developed patterns of maladaptive behaviour. 

• TE has been used to manage the negative symptoms of schizophrenia. Negative symptoms, such as apathy and social withdrawal, can result in the individual’s lack of interest in aspects of normal healthy living such as washing, eating and maintaining physical appearance. 

• This does not aim to cure Sz but aims to improve the patient’s quality of life, giving them the skills needed to live outside of a hospital setting.
  

Ayllon & Azrin (1968) trialled a token economy system in a ward of female patients diagnosed with Sz. Every time they carried out a task seen as a desirable behaviour (e.g. making their bed or cleaning up), they were given a plastic token. These tokens could then be swapped for ward privileges such as being able to watch a film. The number of tasks carried out increased significantly.

Rationale of Token Economies

Matson et al. (2016) identify three categories of institutional behaviour commonly tackled by token economies: personal care; condition-related behaviours (e.g. apathy); and social behaviour.

There are two major benefits to modifying these behaviours:

• Improves the person’s quality of life within the hospital setting, for example make-up for someone who usually takes a lot of pride in their appearance or social interaction for a usually sociable person

• ‘Normalises’ behaviour and this makes it easier for people who have spent a time in hospital to adapt back into life in the community, for example getting dressed in the morning or making their bed

Primary Reinforcers

anything that give pleasure (ie food or comfort) or remove unpleasant states (ie a film to alleviate boredom).

Secondary Reinforcers

Secondary reinforcers initially have no value to the individual, but acquire their reinforcing properties after being paired with primary reinforcers. In token economy the tokens given as a result of target behaviours are secondary reinforcers (they only have value due to the learned association with innate primary reinforcers).

AO3 Evaluation: Token economies

• Research Support- Glowacki et al (2016) identified 7 high quality studies published between 1999 and 2013 that examined the effectiveness of token economies for people with chronic mental health issues, such as schizophrenia and involved patients living in a hospital setting. All the studies showed a reduction in negative symptoms and a decline in the frequency of unwanted behaviours, This supports the value of token economies. However, 7 studies is very small evidence to support the effectiveness of a technique. One issue with this is the file drawer problem- this is a bias towards positive published findings because undesirable results have been ‘filed away’. 

• Appropriateness- One problem with token economies is that they are very difficult to continue once a person is outside a hospital setting, This is because target behaviours cannot be monitored closely and tokens cannot be administered immediately. On the other hand, some people with Sz may only get the chance to live outside a hospital if their personal care and social interaction can be improved. And perhaps the best way to achieve this is using a token economy during hospital care. 

• Social Sensitivity- The use of token economies raises ethical issues because it gives professionals considerable power to control the behaviour of people in the role of patient. This inevitably involves imposing one person’s (or institutions) norms on others, which is especially problematic if target behaviours are not identified sensitively. Perhaps restricting the availability of pleasures to people who don’t behave as desired means that seriously ill people, who are already experiencing distressing symptoms, have an even worse time. This means that the benefits of token economies may be outweighed by their impact on personal freedom and short-term reduction in quality of life. 

Interactionist Approach to Schizophrenia: The Diathesis stress model

The diathesis-stress model sees schizophrenia as a result of a combination of psychological/environmental and biological/genetic influences. The symptoms of schizophrenia are triggered when significant stressors (the ‘stress’) in a person’s life are combined with a biological vulnerability (the ‘diathesis’) to the disorder. 

• The environmental risks in themselves do not cause schizophrenia but, combined with a pre-existing genetic risk, this may become a trigger. 

• The additive nature of diathesis and stress

• Biological Vulnerability + Stressor = Schizophrenia

Diathesis

• Research into twins has shown us that schizophrenia has a genetic component in that MZ twins have a higher concordance rate than DZ twins. However, in about 50% of cases where one identical twin has schizophrenia the other does not develop it. 

• This discordance between MZ twins shows us that environmental factors must also play a role in determining the development of schizophrenia.

Stress

• Stresses that may trigger schizophrenia come in various forms eg childhood trauma or the stresses of urbanised living. 

• Varese et al. (2012) found that children who experienced severe trauma before the age of 16 were three times more likely to develop schizophrenia than the general population. The more severe the trauma, the greater the risk. 

• Vassos et al. (2012) estimated that the risk of schizophrenia in the most urban settings was 2.37 times higher than in rural areas. The link between urbanisation and schizophrenia isn’t clear but it is suggested that adverse living conditions in densely populated areas may be a contributory factor. 

AO3 Evaluation: The Diathesis Stress model in schizophrenia

• Research Support- Tienari et al (2004) investigated the link between genetic vulnerability and parenting style. 19,000 children adopted from schizophrenic mothers studied and adoptive parents studied for their parenting style. Parenting style characterised by high levels of criticism and low levels of empathy was implicated in the development of Sz for children with high genetic vulnerability compared to the control group (no genetic vulnerability)

• Interactionist treatment (Practical Application)- Tarrier et al. (2004) randomly allocated 315 patients to one of three groups: medication & CBT, medication & supportive counselling, or a control group (medication only). Ppts in the two combination groups showed lower symptom levels compared to the control group This suggests that adopting an interactionist approach for treatment has a practical advantage. However, just because an interactionist treatment is seemingly more effective, it does not mean that the interactionist approach is correct.

• Issue and Debate- Interactionism is a more effective explanation as it considers the role of both nature and nurture in the development of a complex mental health disorder. Consequently, it avoids the issues of a reductionist approach and can be considered a holistic view.

• Reductionism (vulnerability)- In the original diathesis-stress model (Meehl, 1962) put forward the idea of a single ‘schizogene’ and considered stress to be psychological in nature, in particular related to parenting. As shown by Ripke et al. (2004), there are up to 108 genes implicated in the development of schizophrenia, contradicting Meehl’s original model. Similarly, modern research highlights that stress can take many forms and is not solely determined by parenting (although this is still important). Houston et al. (2008) defines stress as anything that risks triggering Sz. Cannabis is considered to be a stressor and increases risk of Sz by up to 7 times (dependent on dose). This may be because cannabis interferes with the dopamine system. However, many people do not develop Sz after smoking cannabis presumably because they lack the vulnerability factors.