Revision. The most effective approach to evaluation was found in answers that focused on the findings of studies, and their relevance for explanations.

SCHIZOPHRENIAPSYA4

Revision

EXAMINER’S REPORT – SCHIZOPHRENIA IN GENERAL The most effective approach to

evaluation was found in answers that focused on the findings of studies, and their relevance for explanations and treatments. This is the most fundamental aspect of how science works.

Candidates should be dissuaded from presenting one line of evaluation: such statements are classed as basic or even rudimentary commentary and attract minimal credit.

PAST SCHIZOPHRENIA QUESTIONS

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Clinical characteristics

xClassification and diagnosis

x xBiological explanations xPsychological explanations

xTreatments

x x x

POSSIBLE PARTED QUESTIONS Outline clinical characteristics of

schizophrenia (4 marks) Outline one biological explanation of

schizophrenia (4 marks) Outline one psychological explanation of

schizophrenia (4 marks) Outline one biological therapy for

schizophrenia (4 marks) Outline one psychological therapy for

schizophrenia (4 marks)

POSSIBLE FULL ESSAY QUESTIONS Discuss issues surrounding the

classification and diagnosis of schizophrenia (8 +16 marks)

Outline and evaluate biological explanations for schizophrenia (8 +16 marks)

Outline and evaluate psychological explanations for schizophrenia (8 +16 marks)

Outline and evaluate one biological and one psychological treatment for schizophrenia (8 + 16 marks)

CLINICAL CHARACTERISTICS OF SCHIZOPHRENIAIncluding positive/negative symptoms and subtypes

SCHIZOPHRENIA FACTS AND FIGURES Approximately 1% of the population worldwide

are believed to suffer from schizophrenia It is equally common in men and women Average age of onset is 18 in men and 25 in

women It is rare to develop SZ before puberty After 30 years, of the people diagnosed with

schizophrenia: 25% Completely Recover 35% Much Improved, relatively independent 15% Improved, but require extensive support

network 10% Hospitalized, unimproved 15% Dead (Mostly Suicide)

DSM-IV-TR CRITERIA Two characteristic symptoms for at least one month.

Characteristic symptoms must include: delusions hallucinations disorganised speech grossly disorganised or catatonic behaviour negative symptoms (e.g. affective flattening)

OR one characteristic symptom if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behaviour or thoughts, or two or more voices conversing with each other

Social/occupational functioning below levels prior to onset Continuous signs of disturbance for at least six months, including

at least one month of characteristic symptoms Exclusion of mood disorders (e.g. schizoaffective disorder) No evidence of organic factors (e.g. drugs) or medical conditions If there is a history of developmental disorders (e.g. autism),

prominent delusions or hallucinations much be present for a month

POSITIVE AND NEGATIVE SYMPTOMS

+ POSITIVE

Excess or distortion of normal functioning

- NEGATIVE - Reduction or impairment of

normal functioning

Hallucinations Delusions Disorganised

speech Grossly

disorganised behaviour

Affective flattening Avolition Alogia Catatonic

behaviour

SUBTYPES OF SCHIZOPHRENIA

Paranoid The patient has false

beliefs (delusions) that somebody or some people

are plotting against them or members of their family. May also involve similar

hallucinations.

Disorganised Involves great disorganisation,

including delusions, hallucinations (not just

visual), incoherent speech, and large

mood swings.

ResidualPatient has suffered at least one

SZ attack but no positive symptoms in last 12 months.

UndifferentiatedA broad category that includes

patients who don’t clearly belong to any other category.

CatatonicMain characteristics are extreme immobility or involuntarily strange

movements.

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSISIncluding validity and reliability

EXAMINER’S REPORT – ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS Stronger students approached the question by

identifying an issue (such as the lack of reliability between ICD and DSM IV) then considering possible consequences of this and/or research evidence regarding reliability of diagnosis using the respective systems.

There was some useful discussion of the problems of co-morbidity, cultural differences and Szasz’s critique of the myth of mental illness in better answers.

Higher AO2/3 marks went to students who evaluated each issue as they went through the essay.

Those students who were able to consider a range of research evidence relating to reliability and validity were also rewarded.

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY) Lack of objective tests for SZ whilst physical

disorders use x-ray, scans, blood and urine tests. Means that diagnosis is a subjective process which relies on

the doctor’s opinion, therefore misdiagnosis is more likely than with physical disorders

Although some differences in brain structure and dopamine levels in SZs have been found, they are not yet definitive enough to be used as diagnostic measures

Difference in duration of symptoms - DSM requires symptoms to be present for 6 months, whereas ICD needs only one month. Means that same patient could be diagnosed differently

depending on which classification system is used May not receive correct diagnosis/treatment quickly enough

with DSM Using ICD, patients may be misdiagnosed with ICD when

psychotic symptoms are due to short term trauma (e.g. bereavement)

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY)

Subtypes may lack validity because the range of symptoms included is so wide. Means that two people with no symptoms in

common could both be diagnosed with SZ – e.g. paranoid and catatonic subtypes

Undifferentiated and residual may be especially problematic because criteria are vague e.g. undifferentiated is used when symptoms do not clearly fit any other subtype.

Raises the argument that subtypes may indicate different disorders rather than variations of SZ

DSM 5 will remove subtypes because they have not been found to aid effective treatment or offer predictive validity

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY)

Low predictive validity of diagnosis - If a disorder has high predictive validity then it should be clear how the disorder will develop and how people will respond to treatment. Around 20% of SZs recover completely, 10%

show significant improvement, 30% show some improvement and around 40% never really recover. This demonstrates low predictive validity.

However, Mason (1997) found that the use of newer classification systems has improved the predictive validity of diagnosis, particularly when the 6 month criteria for diagnosis was used (rather than 1 month).

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY) Poor inter-rater reliability - many studies have

demonstrated that clinicians find it difficult to use classification symptoms objectively. Beck et al (1962) found that agreement on diagnosis for 153

patients between two psychiatrists was only 54%. This was often due to vague criteria for diagnosis.

Cooper et al (1972) found New York psychiatrists were twice as likely to diagnose schizophrenia as London psychiatrists, who in turn were twice as likely to diagnose mania or depression when shown the same videotaped clinical interviews.

Mojtabi and Nicholson (1995) asked 50 psychiatrists to separate and label bizarre and non-bizarre delusions. A concordance rate of only 0.4 was found, suggesting that this central diagnostic criteria of delusions and hallucinations being 'bizarre' lacks reliability.

However, all these studies are quite old, meaning that classification systems have since been updated. Therefore, it is hoped that inter-rater reliability has been improved.

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY) Co-morbidity – Describes a person who suffers form

two or more mental disorders at the same time. It is estimated that 50% of those diagnosed with SZ also have depression. This makes it difficult for doctors to make an accurate

diagnosis because depression can be a negative symptom of SZ. If the correct diagnosis is not made, the patient may not receive the correct treatment.

Symptom overlap – This occurs because certain symptoms are common to multiple disorders. For example, delusions can be a symptom of bipolar disorder as well as SZ. Again, this means that patients can be misdiagnosed, at

least initially, which can delay appropriate treatment. For example, if misdiagnosed as SZ, antipsychotic medication will not help with the mania experienced by someone with bipolar disorder.

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY) Myth of mental illness – Thomas Szasz argued that there

is no such thing as mental illness, and that so called illnesses such as SZ are really just ‘sane responses to an insane world’. If Szasz is believed, then we should not aim to classify and

diagnose mental illness at all. However, Szasz’s view is quite extreme and most people would

agree that classification is needed to protect the individual and society.

Labelling – Diagnosing someone with a disorder means that we are labelling them and these labels can be extremely difficult to remove. This can be a particular problem with schizophrenia, as there are

many misconceptions around the condition (e.g. all schizophrenics are violent and potentially dangerous) which can lead to stigma and prejudice.

For example, the individual may have to declare their condition on job applications, etc. even when they no longer have active symptoms of SZ.

ISSUES SURROUNDING CLASSIFICATION AND DIAGNOSIS (INCLUDING RELIABILITY AND VALIDITY)

Social class bias – Certain social classes are more likely to be diagnoses with SZ than others. Keith et al (1991) found that 1.9% of lower class people,

0.9% of middle class people, and only 0.4% of upper class people were diagnosed with SZ.

This could be because doctors are biased towards certain social groups or do not understand their subcultures.

However, it could also be that lower classes suffer more stress so are more likely to develop SZ. A third explanation is that upper class people may be less likely to seek help.

Ethnic bias – Similarly, some ethnic groups have higher rates of SZ diagnosis. Blake (1973) asked clinicians to diagnose a patient from

their case records, and found that they were more likely to diagnose schizophrenia if told the person was African American than if they believed the patient to be white.

This appears to show a bias in diagnosis, possibly based on stereotypes and prejudice.

BIOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA

EXAMINER’S REPORT – BIOLOGICAL EXPLANATIONS Most candidates outlined the genetic explanation using

research and were able to achieve reasonable AO1 marks by doing so.

There were some impressive descriptions of the dopamine hypothesis, many including specific details relating to D2 receptors.

Some weaker candidates covered three or more explanations which limited AO2/AO3 and the development and elaboration of argument.

Higher AO2/AO3 marks went to candidates who evaluated each explanation as they went through the essay.

Those candidates who were able to consider the inter relationships between biological explanations (for example genetics and biochemistry) were also rewarded.

BIOLOGICAL EXPLANATIONS - GENETICS The gene for SZ is passed on in the

genetic code (DNA). Investigated using family, twin and

adoption studies. Family studies: Comparison of SZ

occurrence in family members. Twin studies: Comparison of concordance

rates between MZ or DZ twins raised together or apart.

Adoption studies: Comparison of children of SZ mothers adopted into non schizophrenic families and control groups of adopted children with non SZ mothers.

GENETICS – TWIN STUDIES Gottesman (1991) - Review of twin studies -

40 sets of twins - the concordance rate for MZ twins was about 48% and only about 17% for DZ twins.

Moldin (1998) reviewed twin studies published between 1920 and 1987 - concordance rates for MZ twins averaged 46%, even when reared in different families, whereas the concordance rates for DZ twins averaged only 14%.

The fact that MZ twins are more likely to share the disorder suggests that there is a genetic component as they have exactly the same DNA, whereas DZ twins share only 50%.

EVALUATION OF TWIN STUDIES The fact that the concordance rate between MZ twins is

not 100% suggests that genetics cannot be the only cause – could be diathesis stress explanation.

Greater concordance rate with MZ twins may be because they may be treated more similarly than DZ twins.

However, Gottesman found that concordance rates for MZ twins brought up together were similar to those reared apart, which suggests a nature (genetic) rather than nurture explanation.

Research is based on meta analyses which may have methodological flaws e.g. small sample sizes, differences in how concordance is calculated, early studies could not reliably differentiate between MZ and DZ twins – all affect validity of results.

However, all twin studies have shown significantly higher rates of SZ than found in the general population (1%), which strongly suggests that SZ has some genetic basis.

GENETICS – ADOPTION STUDIES Tienari et al (2000) studied 164

adopted children whose biological mothers had schizophrenia. He found that 8.1% of the children with a SZ mother developed the condition, but only 2.3% of the control group.

Similarly, Heston (1966) followed 47 children born to schizophrenic mothers who were adopted by non-schizophrenic families at 2 months old. It was found that 17% (5) of the sample developed SZ, compared to 0% of a control group.

EVALUATION OF ADOPTION STUDIES

Adoption studies may help to separate the effects of nature from nurture in the development of SZ. Higher occurrence in the children of SZ mothers suggests that genetics are important, even when the child is raised in a non SZ environment.

However, it could be argued that the children of SZ mothers may have experienced trauma before they were adopted which could explain the higher incidence of SZ. But, the children in Heston’s study were only 2 months old at adoption so any trauma is unlikely to have had a lasting effect.

Tienari found that the quality of communication in the adopted family had a significant effect on whether the child developed SZ. It seemed the higher genetic risk was only ‘activated’ in families with poor communication styles (e.g. high levels of expressed emotion).

Again, sample sizes are small, due to the nature of the study, making it difficult to generalise results.

GENERAL EVALUATION OF THE GENETIC EXPLANATION No specific gene has yet been identified as

responsible for the development of SZ, and scientists believe that up to a dozen different genes may be implicated. This means that a definitive genetic explanation has not yet been discovered.

Most research suggests that genetics offer only a partial explanation for the development of SZ. The most likely theory is that SZ is a result of an underlying genetic predisposition which is triggered by environmental factors such as stressful life experiences or recreational drugs (the diathesis-stress explanation).

BIOLOGICAL EXPLANATIONS – DOPAMINE HYPOTHESIS According to the dopamine hypothesis, SZ

results from an excess of dopamine activity at certain synaptic sites. This could be caused either by the release of excess dopamine by presynaptic neurons, an excess of dopamine receptors, or over sensitivity of dopamine receptors.

Dopamine is a neurotransmitter which plays a role in a variety of functions such as movement, memory and cognition, social functioning and mood.

It is believed that excess dopamine in SZs can explain some of the positive symptoms of the disorder, such as hallucinations and delusions.

EVIDENCE FOR THE DOPAMINE HYPOTHESIS Amphetamines work by causing the brain

to produce more dopamine and have been shown to produce psychotic-like symptoms.

L-Dopa – a drug for Parkinson’s disease - actually increases dopamine, and high doses have been found to produce symptoms of schizophrenia.

Post mortems of schizophrenics, show an increase of dopamine in parts of the brain. (Seeman, 1987)

Traditional anti-psychotic drugs, such as chlorpromazine, act by blocking dopamine receptors in the brain.

EVIDENCE AGAINST THE DOPAMINE HYPOTHESIS Amphetamines only mimic the positive

symptoms of SZ so don’t explain the negative symptoms.

Similarly, first generation (atypical) anti-psychotic drugs only reduce the positive symptoms of SZ – suggests dopamine is not the only cause.

It is unlikely that just one neurotransmitter can account for the broad range of SZ symptoms (serotonin has also been linked to SZ – atypical drugs).

It is impossible to be certain whether changes in biochemistry are the cause of SZ, or the result.

BIOLOGICAL EXPLANATIONS – BRAIN STRUCTURE There is growing evidence that people

with SZ may have abnormalities in the structure of the brain.

For example, Szesko et al (1995) found that the asymmetry found in normal brains is absent in people with SZ.

Similarly, Brown et al (1986) found enlarged ventricles (fluid filled cavities in the brain) and lower brain weight in SZ patients, especially in the temporal and frontal lobes (known to be important for coordination of thinking and judgment).

EVALUATION OF THE BRAIN STRUCTURE EXPLANATION SZ is known to be uncommon before

adolescence – this supports the brain structure explanation as it suggests that there may be progressive deterioration of brain structures.

There is currently no agreement on which areas of the brain are affected – Flaum et al (1995) and Buchsbaum (1990) found differences in hippocampus and basal ganglia (as well as the temporal and prefrontal lobes, as found by Brown et al).

EVALUATION OF THE BRAIN STRUCTURE EXPLANATION It has not yet been possible to establish

whether changes in brain structure in SZ patients are the cause of the disorder of the effect.

It is possible that drug treatment for SZ causes the changes in brain structure that have been found in sufferers, as many of those involved in research have been taking antipsychotic drugs for long periods.

Structural abnormalities are found more commonly in SZ’s with negative symptoms, which does not fully explain the positive symptoms of the disorder.

BIOLOGICAL EXPLANATIONS (GENERAL) It is likely that there is an interaction

between the three biological explanations discussed.

It is believed that brain structure and biochemistry (dopamine) may be the way in which the predisposition for SZ is passed on in the genetic code.

For example, if an individual inherits an oversensitivity to dopamine, this could make them more likely to develop SZ. Similarly, an abnormality in brain structure could be genetically predetermined.

EVALUATION OF BIOLOGICAL EXPLANATIONS (GENERAL) Reductionist – biological explanations can be

described as reductionist as they reduce complex human behaviour to the level of simple biology, without considering the role of psychological and social factors in the development of the disorder.

Deterministic – biological explanations suggest that a person does not have free will over the development of the disorder, as their tendency to develop SZ is biologically determined.

Inconclusive – no one biological explanation can explain all cases of SZ, which suggests that psychological and social factors are also important.

Variety of symptoms – it may be that certain biological explanations can explain some symptoms better than others because the disorder encompasses such as wide variety of possible symptoms.

PSYCHOLOGICAL EXPLANATIONS FOR SCHIZOPHRENIA

EXAMINER’S REPORT – PSYCHOLOGICAL TREATMENTS Better answers could, for example,

outline the double bind theory and provide a clear example of what this involves; or they could outline the cognitive model focusing on cognitive deficit theories.

Candidates could legitimately use biological explanations as AO2, but only if they were clearly used as evaluation of psychological explanations.

COGNITIVE EXPLANATIONS Many different cognitive explanations for the

development of SZ have been suggested. However, they all share the assumption that

the various cognitive impairments shown by people with SZ (e.g. poor attentional control, language deficits, disorganised thinking) play an important role in the development and maintenance of the disorder.

It is believed that symptoms such as disorganised speech, delusions and hallucinations may all depend at least in part on the poor ability of a person with SZ to concentrate.

HEMSLEY’S COGNITIVE THEORY Hemsley (1993) suggests there is a substantial

breakdown in the relationship between memory and perception in schizophrenics.

As a result, people with schizophrenia are often unable to activate schemas which would allow them to predict what will happen next, their concentration is poor, and they attend to unimportant or irrelevant aspects of the environment.

Their poor integration of memory and perception leads to disorganised thinking and behaviour.

Helmsley believes these deficits can be attributed to abnormalities in the hippocampus.

FRITH’S COGNITIVE THEORY Frith (1992) suggested that the positive symptoms

of SZ can be explained by an inability to filter out irrelevant information from the environment.

He claims that the positive symptoms of SZ might occur because individuals with SZ have problems with self monitoring, and so fail to keep track of their own intentions.

As a result, they mistakenly regard their own thoughts as having come from someone else (thus explaining auditory hallucinations). Similarly, they may attribute some of their thoughts or movements to others, explaining symptoms such as delusions of control.

He believes this ‘faulty filter’ is caused by abnormalities in the pathway connecting the hippocampus to the prefrontal cortex.

EVIDENCE FOR COGNITIVE EXPLANATIONS McGuigan (1966) found that the larynx of

patients with schizophrenia was often active during the time they claimed to be experiencing auditory hallucinations. This suggests that they mistook their own inner speech for that of someone else.

McGuire et al. (1996) found schizophrenics to have reduced activity in those parts of the brain involved in monitoring inner speech.

PET scans show under-activity in the frontal lobe of the brain, which is linked to self-monitoring and so provides biological support for this explanation.

EVALUATION OF COGNITIVE EXPLANATIONS Cognitive explanations appears to provide a

reasonable explanation for positive symptoms but do not explain negative symptoms.

It is not clear whether the cognitive dysfunction is a cause or effect of the disorder. Therefore, cognitive models may only be descriptive; explaining the symptoms of SZ rather than explaining them.

Many brain-damaged patients have problems with attention or with the relationship between memory and perception. Despite having these cognitive deficits, however, they fail to develop the symptoms of schizophrenia and so this challenges the cognitive explanations.

FAMILY INTERACTION EXPLANATIONS Family interaction explanations focus on

the role of dysfunctional patterns of family communication in explaining the symptoms of SZ.

The idea of the ‘schizophrenogenic mother’ – one whose patterns of behaviour can result in the development of SZ in her offspring – has largely been discounted, but it is suggested that understanding the effect of family communication patterns can still be useful in explaining the onset and maintenance of schizophrenic symptoms.

FAMILY INTERACTION -DOUBLE BIND THEORY According to the double bind theory (Bateson,

1956) a child has repeated experiences with one or more family members in which he/she receives contradictory messages. For example, telling the child ‘I love you’ whilst rejecting physical affection.

Repeated exposure to such messages causes the child to resort to self deception and to develop a false concept of reality to communicate effectively.

It is suggested that this could lead to some of the symptoms of SZ, such as hallucinations, delusions and disorganised thoughts and behaviour.

EVALUATION OF DOUBLE BIND THEORY There is little or no research evidence to

support the double bind theory. For example, Ringuette and Kennedy (1966) asked clinicians to analyse letters written by parents to their hospitalised children.

They found no difference in the amount of double-bind communication in the letters to children with schizophrenia than to those with other disorders. Therefore double bind can’t explain why some develop schizophrenia and others develop different disorders.

FAMILY INTERACTION -EXPRESSED EMOTION More recent research has centred on the concept of

expressed emotion (EE). This was originally based on the work of Brown (1972) which showed that patients with SZ were four times more likely to relapse if they returned to homes with high levels of EE.

EE is characterised by hostility, criticism and over involvement.

EE is assessed by taping an interview with a relative of someone with SZ and rating the following: Frequency of critical comments made by the relative Number of statements of dislike/resentment towards the

patient Number of statements reflecting emotional over

involvement with, or over protectiveness of, the patient

EVALUATION OF EXPRESSED EMOTION High expressed emotion has been well

supported as a factor in relapse (i.e. a factor in maintenance rather than cause) as individuals are four times more likely to relapse if expressed emotion is high (Kavanagh, 1992).

This is further supported by the success of family interaction therapies in preventing relapse.

The assessment of EE requires an interview or observation, so may not provide an objective and accurate assessment of levels of EE within the family environment.

EVALUATION OF FAMILY INTERACTION EXPLANATIONS Mischler and Waxler (1968) found significant

differences in the way mothers spoke to their schizophrenic daughters compared to their normal daughters, which suggests that dysfunctional communication may be a result of living with the schizophrenic rather than the cause of the disorder.

Many have argued that it is unhelpful and destructive to blame families for the development of SZ in their family member. Attributing blame may further damage family relationships, which could lead to further deterioration in the condition of the SZ patient.

Not all siblings develop schizophrenia, which challenges family interaction as a cause, although different family members will have their own micro-environment. But it is more likely that this can be explained by differences in genetic vulnerability, cognition, and unconscious motivations, so a multi-dimensional approach is needed.

BIOLOGICAL TREATMENTS FOR SCHIZOPHRENIA

EXAMINER’S REPORT - TREATMENTS The best route to good A01 and A02 marks was

to focus on treatments which are currently used for schizophrenia (anti-psychotic drugs and variations of CBT) and to include appropriate reference to outcomes studies.

In better answers, evaluation was clearly organised around three main areas, appropriateness, effectiveness and ethical issues.

Better answers shaped descriptions of CBT specifically to the symptoms of schizophrenia (e.g. logical disputing to challenge delusional beliefs).

ANTIPSYCHOTICS ‘Typical’ (first generation) antipsychotics

available since 1950s. Second generation or ‘atypical’ antipsychotics developed in 1990s.

Mode of action: Both relieve symptoms of SZ by blocking D2

dopamine receptors in the brain, thus preventing dopamine from attaching to them and reducing the affects of dopamine.

Atypical also affect serotonin activity and attach to dopamine receptors more transiently than atypical types (i.e. block them on a temporary basis).

EFFECTIVENESS OF TYPICAL ANTIPSYCHOTICS Research shows typical antipsychotics

are effective in reducing the symptoms of schizophrenia, particularly the positive symptoms, such as hallucinations and delusions.

However, they are less effective in reducing the negative symptoms, such as avolition and alogia, so do not seem to offer a complete treatment for all SZ patients.

APPROPRIATENESS OF TYPICAL ANTIPSYCHOTICS Side effects - More than 20% of patients

who take typical antipsychotic drugs for over a year develop tardive dyskinesia. Symptoms include involuntary sucking and chewing, jerky movements of the limbs, and writhing movements of the mouth or face; these effects can be permanent.

In addition, approximately 50% of patients report feeling groggy and tired, which can affect their ability to function normally whilst on the drugs, which may cause them to stop taking the medication, leading to relapse.

EFFECTIVENESS OF ATYPICAL ANTIPSYCHOTICS At least as effective as typical types at

reducing positive symptoms but also effective for negative symptoms.

Controlled clinical trials have found that clozapine produces significant clinical improvement in at least 30% of patients who fail to achieve an adequate response to or cannot tolerate conventional antipsychotic medications.

APPROPRIATENESS OF ATYPICAL ANTIPSYCHOTICS Fewer side effects than typical types =

higher chance of compliance/lower chance of hospitalisation.

Clozapine may cause a severe reduction in white blood cell count in approximately 1 in 100 patients who take it for at least one year, meaning that patients must be closely monitored with regular blood tests whilst taking the treatment.

Much more expensive than typical antipsychotics, which may mean that some doctors will at least try patients with typical treatments initially.

GENERAL EVALUATION OF ANTIPSYCHOTICS Drug therapy is fast acting in

comparison to psychological treatments - relieves distress quicker/more ethical.

Reduced risk of hospitalisation – prior to drug therapy most SZ patients were hospitalised so drugs can be seen as more ethical.

Can be combined with psychological treatments to improve effectiveness/reduce relapse. Drug therapy is shown to improve compliance with CBT.

GENERAL EVALUATION OF ANTIPSYCHOTICS Drug treatment is not effective for all

sufferers – success may be dependent on the type and severity of symptoms.

Not a ‘cure’ so relapse is likely when medication is stopped. Sampath et al (1992) found that 75% of those transferred to a placebo drug after a course of antipsychotics relapsed within one year (compared to 33% of a control group).

Side effects means that some patients stop taking the medication. This can be addressed using slow release injections, but leads to ethical concerns regarding informed consent.

ELECTROCONVULSIVE THERAPY (ECT) ECT was largely abandoned as a treatment for

schizophrenia after the discovery of antipsychotic drugs in the 1950s but has recently been re-introduced in the USA.

In the UK, the use of ECT is not recommended by NICE except in very particular cases (mainly for catatonic schizophrenia and/or drug resistant patients).

Patient is given anaesthetic and muscle relaxant. Brief electrical current applied to the brain, via

the temples, to produce a seizure. Mode of action is unclear but believed to work on

chemicals in the brain (probably dopamine), thus reducing positive symptoms of SZ.

EFFECTIVENESS OF ECT Champattana (2007) – Drug resistant

patients given ECT either on its own in combination with antipsychotics. Found a reduction in positive symptoms, especially when used with drug treatment. However, ECT produced no effect or worsening in regard to negative symptoms.

Tharyan (2002) meta analysis of 26 studies – effect of ECT on positive symptoms was short term only.

Has less effect on most of the negative symptoms of SZ.

APPROPRIATENESS OF ECT Side effects - Memory loss, other cognitive

impairments, and possible neurological damage do question the appropriateness of the treatment. However, this must be balanced against the fact that most side effects are relatively short lasting. The American Psychiatric Association and the British National Institute for Health and Clinical Excellence have both concluded that ECT does not cause permanent brain damage.

Ethical issues - Issues of protection and informed consent are raised because most patients dislike receiving ECT, and some might be put under excessive pressure to become involved in this form of therapy. Historically it was used as a form of punishment and to exert control over patients.

PSYCHOLOGICAL TREATMENTS

COGNITIVE BEHAVIOURAL THERAPY Various types of CBT Coping strategy enhancement aims to work with the

patient to improve the effectiveness of the coping strategies they already use to manage their SZ symptoms.

These may include distraction, self talk, or simply turning up the television or radio to drown out ‘voices’.

Firstly, the therapist will work with the patient to establish the content of the patient’s hallucinations and delusions, the triggers for these thoughts, and the coping strategies they use. Then, the patient will rate each of these strategies in terms of effectiveness for particular symptoms.

The aim is to identify two effective strategies for each symptom, which the patient will then put into action for ‘homework’.

COGNITIVE BEHAVIOURAL THERAPY Another form of CBT uses ‘reality testing’ to

challenge the patient’s hallucinations and delusions. Initially, the therapist questions the patients

irrational beliefs and ask the patient to think of alternative explanations.

Then the therapist and patient plan an activity that is designed to test the irrational belief.

For example, a patient called Nigel believed he had special powers which allowed him to make things happen through the power of thought. Nigel was shown videos, which were then paused, and he was asked to predict what would happen next.

In 50 trials, Nigel did not get one answer correct, leading him to conclude that he did not really possess special powers.

EFFECTIVENESS OF CBT Tarrier et al (2000) evaluated different kinds of

intervention following an acute schizophrenic episode. Participants were given drug therapy alone, drug therapy with CBT, or drug therapy with supportive counselling. At the end of the trial, 15% receiving drug therapy and CBT showed no Type 1 symptoms compared with 7% of those receiving drugs and supportive counselling, and 0% receiving drugs only.

One year after the study, Tarrier et al found that these differences remained, although two years later the CBT and counselling groups did not differ, although both were still better off than the drugs only group.

Other studies (e.g. Bradshaw, 1998) have shown that CBT can be effective in preventing relapse after a schizophrenic episode. Often, stressors can cause a relapse, and CBT can be effective in these cases because it helps a person (a) recognise the stressors and (b) recognise that their reaction to them is inappropriate.

APPROPRIATENESS OF CBT Costly - CBT costs approx £1,000 for a 16 week

course, which may make some doctors reluctant to prescribe it.

Recommended by NICE for all new SZ cases but estimated that only 46% receive it, due to lack of resources/therapists.

CBT is not a cure – it does not remove symptoms completely, but can lead to an improvement in coping/functioning which helps the patient to lead a more normal life.

No side effects, unlike drug treatment, so may be a more appropriate, more ethical treatment.

Has been shown to increase compliance with drug treatment, so may be used in conjunction with drugs for improved effectiveness.

FAMILY INTERVENTION THERAPY The aim of family intervention therapy is to

reduce the level of expressed emotion (EE) within the family, thus reducing the chance of relapse in SZ patients.

The main aim is to develop cooperative family relationships. This may be achieved in a number of ways: Family members will be provided with information about the

patient’s condition and educated on how it may affect them, so that they are better able to understand the SZ and do not have unrealistic expectations of the patient.

A therapist may teach family members coping strategies to deal with difficult behaviour from the patient

Family members will receive guidance on how to reduce negative behaviours toward the patient (hostility, criticism, over involvement)

Family members will be given advice on how to spot early signs of relapse so that help can be given more quickly

EFFECTIVENESS OF FAMILY INTERVENTION Falloon et al. (1985) found that the

relapse rate was markedly lower amongst patients receiving family therapy than those receiving individual therapy. 50% of those in the individual-therapy group returned to hospital compared with only 11% of those in the family-therapy group.

Birchwood and Jackson (2001) found that the relapse rate over 12 months was 60% for patients with schizophrenia receiving routine treatment, but was between 25% and 33% for those receiving family therapy.

APPROPRIATENESS OF FAMILY INTERVENTION Patients are more likely to be cared for at home.

This of course makes family therapy highly appropriate as a family being taught to better support their schizophrenic relative is highly positive.

Evidence for expressed emotion. There is much evidence that high expressed emotion can increase the relapse rate and so it is highly appropriate to focus on reducing expressed emotion.

Unlikely to work on its own. Family therapy would probably not be successful on its own, but needs to be used in conjunction with drug therapy, which means we cannot be sure how much any improvements are due to the family therapy as opposed to the drug therapy.

Not a cure. Family therapy does significantly improve functioning and some of the aspects it tackles, such as poor social skills, may well be the underlying causes of the disorder but it does not provide a cure for schizophrenia. Even when social functioning is the focus of therapy it is not possible to increase social functioning to the level of healthy controls.

SUMMARY You need to be able to:

Outline clinical characteristics of SZOutline and evaluate 8 issues surrounding the

classification and diagnosis of SZOutline and evaluate genetics, dopamine and

brain structure as biological explanations for SZOutline and evaluate cognitive factors and

family interaction as psychological explanations for SZ

Outline and evaluate drug therapy and ECT as biological treatments for SZ

Outline and evaluate CBT and Family Intervention Therapy as psychological treatments for SZ

ANY QUESTIONS?