Schizophrenia Cue Cards Flashcards
Paper 3, Option 2: Schizophrenia. As outlined in the aqa specification.
demonstrate knowledge and understanding of psychological concepts, theories, research studies, research methods and ethical issues in relation to the specified Paper 3 content
apply psychological knowledge and understanding of the specified Paper 3 content in a range of contexts
analyse, interpret and evaluate psychological concepts, theories, research studies and research methods in relation to the specified Paper 3 content
evaluate therapies and treatments including in terms of their appropriateness and effectiveness.
Knowledge and understanding of research methods, practical research skills and mathematical skills (see Annex:Mathematical requirements and exemplification) will be assessed in Paper 3. These skills should be developed through study of the specification content and through ethical practical research activities, involving:
designing research
conducting research
analysing and interpreting data.
In answering questions on Issues and Debates in Psychology students will be expected to illustrate their answers with knowledge and understanding of topics studied elsewhere in the specification as appropriate.
Schizophrenia
Classification of schizophrenia. Positive symptoms of schizophrenia, includinghallucinations and delusions. Negative symptoms of schizophrenia, including speechpoverty and avolition. Reliability and validity in diagnosis and classification ofschizophrenia, including reference to co-morbidity, culture and gender bias andsymptom overlap.
Biological explanations for schizophrenia: genetics and neural correlates, including the dopamine hypothesis.
Psychological explanations for schizophrenia: family dysfunction and cognitiveexplanations, including dysfunctional thought processing.
Drug therapy: typical and atypical antipsychotics.
Cognitive behaviour therapy and family therapy as used in the treatment ofschizophrenia. Token economies as used in the management of schizophrenia.
The importance of an interactionist approach in explaining and treatingschizophrenia; the diathesis-stress model.
SZ: T1. Classification and diagnosis. Firstly explain what is meant by the term ‘schizophrenia’.
Schizophrenia is a severe mental illness where contact with reality and insight are impaired, an example of psychosis.
Exam Tip:
With these particular questions there is a sizeable risk that people don’t understand the difference between the questions, and then write about the wrong thing. Make sure you know which is which, for example do you understand the difference between “genetic explanation” and “neural correlates explanation”, and do you have a model essay for each?
SZ: T1. Classification and diagnosis: Outline the process of classification.
Classification is the process of organising symptoms into categories based on which symptoms cluster together in sufferers. Psychologists use the DSM and ICD to diagnose a patient with schizophrenia.
Diagnosis refers to the assigning of a label of a disorder to a patient. The ICD-10 (only negative symptoms need to be present) is used worldwide and the DSM-5 (only positive symptoms need to be present) is used in America.
In order to diagnose Schizophrenia the Mental Health Profession developed the DSM (Diagnostic and Statistical Manual) still used today as a method of classifying mental disorders (particularly in the USA).
It is also used as a basis for the ICD (International Classification of Diseases) used by the World Health Organisation in classifying all disorders (mental and physical).
Note: you may come across the terms DSM-IV and ICD-10. These refer to the latest editions of the two classification systems.
SZ: T1. Classification and diagnosis: Outline and differences between positive and negative symptoms.
Positive and negative symptoms can also be termed to be characterized by Type 1 and Type 2 symptoms. The difference between the two types of schizophrenia:
InType I schizophrenia, the symptoms appear quite suddenly – perhaps after a stressful event. Within a few days the individual may show quite disturbed behaviour.
InType II schizophrenia, the changes take place over time and the more obvious signs of schizophrenia such as hallucinations or other disturbed behaviour may not be evident for a few months or years.
- There has been an attempt to divide the symptoms of schizophrenia into ‘positive’ and negative’ ones. This does not indicate a judgement, i.e. ‘good‘ or ‘bad‘ symptoms.Positive symptomsare what a person has;negative symptomsare what the person lacks.
The most common positive symptom is the hearing of ‘voices’ or auditory hallucinations. One common negative symptom is the inability to control motor movements; the person might adopt a frozen posture like a statue or exhibit repetitive movements such as pacing.
Type I is characterised by mostly positive symptoms and has better prospects for treatment. Type II is characterised by negative symptoms and has a poorer prognosis.
- To be diagnosed with schizophrenia, two or more symptoms must be apparent for more than one month, as well as reduced social. Others differentiation are chronic onset schizophrenia, where individuals become increasingly disturbed through gradual withdrawal and motivational loss overcapacity provided period, and acute onset schizophrenia, where symptoms appear suddenly, after a stressful incident.
SZ: T1. Classification and diagnosis: Explain the positive symptoms of schizophrenia.
Positive Symptoms:
= an excess or distortion of normal functions: including hallucinations and delusions.
Positive symptoms are an excess or distortion of normal functions, for example hallucinations,delusionsand thought disturbances such as thought insertion.
AO1:
• Hallucinations are usually auditory or visual perceptions of things that are not present. Imagined stimuli could involve any of the senses. Voices are usually heard coming from outside the person’s head giving instructions on how to behave.
• Delusions are false beliefs. Usually the person has convinced him/herself that he/she is someone powerful or important, such as Jesus Christ, the Queen (e.g. Delusions of Grandeur). There are also delusions of being paranoid, worrying that people are out to get them.
• Psychomotor Disturbances: Stereotypyical - Rocking backwards and forwards, twitches, & repetitive behaviors. Catatonia- staying in position for hours/days on end, cut off from the world.
Positive symptoms – involve the displaying of behaviours concerning loss of touch with reality, such as hallucinations and delusions. These generally occur in acute, short episodes, with more normal periods on between, and respond well/ better to medication.
SZ: T1. Classification and diagnosis: Explain the negative symptoms of schizophrenia.
Negative Symptoms:
= where normal functions are limited: including speech poverty and avolition.
Negative symptoms are a diminution or loss of normal functions such as psychomotor disturbances, avolition (the reduction of goal-directed behavior), disturbances of mood and thought disorders.
AO1:
• Thought disorder in which there are breaks in the train of thought and the person appears to make illogical jumps from one topic to another (loose association). Words may become confused and sentences incoherent (so called ‘word salad). Broadcasting is a thought disorder whereby a person believes their thoughts are being broadcast to others, for example over the radio or through TV. Alogia - aka speech poverty – is a thought disorder were correct words are used but with little meaning.
• Avolition: Lack of volition (i.e. desire): in which a person becomes totally apathetic and sits around waiting for things to happen. They engage in no self motivated behavior. Their get up and go has got up and gone!
Negative symptoms – involve the displaying of behaviours concerning disruption of normal emotions and actions. These occur in chronic, longer-lasting episodes, and are resistant to medication. Negative symptoms contribute most to people with schizophrenia not being able to function effectively in society, such as in relationships or at work.
SZ: T1. Classification and diagnosis: Outline the research evidence behind these symptoms and their classifications.
Classification AO3:
- Slater & Roth (1969) say that hallucinations are the least important of all the symptoms, as they are not exclusive to schizophrenic people.
- Scheff (1966) points out that diagnosis classification labels the individual, and this can have many adverse effects, such as aself-fulfilling prophecy(patients may begin to act how they are expected to act), and lower self-esteem.
- Ethics – do the benefits of classification (care, treatment, safety) outweigh the costs (possible misdiagnosis, mistreatment, loss of rights and responsibility, prejudice due to labelling).
SZ: T1. Classification and diagnosis: Outline the importance/ difference between reliability and validity in research.
The importance/ difference between reliability and validity in research studies:
- Reliability:
Reliability refers to the extent to which a test produces consistent results. In other words, if we repeat a study keeping every variable the same, do we get the same results each time? If we do, the test is a reliable one.
Make sure that you understand the difference between internal and external reliability:
Internal reliability –is about consistency within a test (the textbook gives the example of a pair of scales), whereasexternal reliability –is about reliability over time, as a test is repeated.
Reliability refers to consistency. As said above, if a study is repeated using the same method, design and measurements, and the same results are obtained, the results then said to be reliable. – Reliability can be improved by developing, or consistent forms of measurement, using clearly defined operational definitions and by improving inter-observer reliability.
(Observer reliability has been briefly covered in previous topics: for revsion reference).
· Internal reliability – concerns the extent to which something is consistent within itself, for example a set of scales should measure the same weight between 50 and 100 grams as between 160 and 200 grams.
· External reliability – concerns the extent to which a test measures consistently over time.
There are three main ways of assessing reliability:
Thesplit-half methodsplits a test into two and asks the same participant to do both halves. If the two halves give similar results, the test is internally reliable.
Thetest–retest methodinvolves giving the same test to the same participants on two occasions. If the two tests give similar results, the test is externally reliable.
Inter-observer reliability(also known asinter-rater reliability) measures whether different observers are applying the test in the same way. If there is a high correlation between the scores of two independent observers, inter-observer reliability is good. Inter-observer reliability is improved by developing clearly defined and separate categories of observational criteria.
If results are unreliable, they can not be trusted. However, results can be reliable but not valid (accurate). For example, if you add up 1 + 1 several times and each time calculate the answer as 3, then your result is reliable (consistent), but not valid (accurate).
Reliability isn‘t the end of the story, though.
Imagine that a number of observers have been taught to measure a particular variable by someone who has misunderstood the methodology. These observers might get consistent results – so the test is reliable, but it isn‘t accurate. This is where validity comes in.
- Validity:
Validity is about appropriateness and accuracy – whether a particular test measures what it is supposed to measure in terms both of the methodology of the study itself (internal validity) and the extent to which its results can be generalised (external validity).
Can it be generalised to other settings (ecological validity), to other people (population validity) and over time (temporal validity)?
We can improve the validity of a test by:
improving its reliability
improving its internal validity
improving its external validity.
ØStudy hint: Remember, a study can be reliable (consistent) but not valid (accurate). That‘s because it‘s possible to be reliably inaccurate. Reliability is part of validity. A study cannot be valid if it‘s not reliable.
Validity refers to how accurately a study investigates what it claims to and the extent to which findings can be generalised beyond research settings as a consequence of a study’s internal and external reliability (see above ) and by improving internal and external validity (see below).
· Internal validity – concerns whether results are due to the manipulation of the IV and have not been affected by confounding variables. Internal validity can be improved by reducing investigator effects, minimising demand characteristics and by the use of standardised instructions and a random sample. - These factors ensure a study is highly controlled is highly controlled, leaving less doubt that observed effects are due to poor methodology.
· External validity – refers to the extent to which an experimental effect (the results) can be generalised to other settings (ecological validity), other people (population validity and over time (temporal validity).
– Milgram’s electric shock study lacked external validity, as it is not usual to shock people for getting questions wrong, the study only used make participants and was a product of it’s time. External validity can be improved by setting experiments in more naturalistic settings. (See Hofling’s study page 25 in textbook).
We can assess validity by asking some key questions:
Face validity– does the test measure what it claims to measure?
Concurrent validity– is there a good correlation between the scores on this test and those from a test we know to be valid?
Predictive validity– does the test accurately predict future behaviour?
Temporal validity– do the research findings remain true over time?
A valid test will produce the answer ‘Yes‘ to all of these.
The next activity will give you the opportunity to check your understanding of reliability and validity.
Example in psychological research:
Melhuish (1993) suggests, the Strange Situation is the most widely used method for assessing infant attachment to a caregiver, Lamb et al. (1985) have criticized it for being highly artificial and therefore lacking ecological validity.
The child is placed in a strange and artificial environment, and the procedure of the mother and stranger entering and leaving the room follows a predetermined script.
Mary Ainsworth concluded that the strange situation could be used to identify the child’s type of attachment has been criticized on the grounds that it identifies only the type of attachment to the mother. The child may have a different type of attachment to the father or grandmother, for example (Lamb, 1977). This means that it lacks validity, as it does not measure a general attachment style, but instead an attachment style specific to the mother.
Key points:
You should have stated that reliability is to do with consistency of a measurement, i.e. the extent to which it produces consistent results. Validity is the ‘truth’ of the measurement, i.e. the extent to which the results accurately measure what they are supposed to measure.
If a non-standardised procedure is used in an investigation then there will be a number ofvariables; these could change each time the procedure is used, resulting in inconsistent – unreliable – outcomes.
The strange situation is a well-prescribed procedure and so does not suffer from inconsistency (i.e. it is reliable). However if it is only carried out on a smallrangeof cultures it lackspopulation validity, i.e. the findings cannot be generalised to cultures other than those used in the investigations. Also the procedure is very ‘controlled’ and as such does not reflect real-life experiences of children; there is doubt that the child is behaving naturally. In other words, ecological validity is an issue.
SZ: T1. Classification and diagnosis: Outline the importance/ difference between reliability and validity in research on schizophrenia.
- Reliability -AO1
For the classification system to be reliable, differfent clinicians using the same system (e.g. DSM) should arrive at the same diagnosis for the same individual.
Reliability is the level of agreement on the diagnosis by different psychiatrists across time and cultures; stability of diagnosis over time given no change in symptoms.
Reliability concerns the consistency of symptom measurement and affects diagnosis in two ways:
- Test-reset reliability – occurs when a clinician makes the same diagnosis on separate occasions from the same information. E.g. measures test consistency — the reliability of a test measured over time. In other words, give the same test twice to the same people at different times to see if the scores are the same.
- Inter-rater reliability – occurs when a different clinicians make identical, independent diagnoses of the sane patient. E.g. refers to the reproducibility or consistency of decisions between two reviewersand is a necessary component of validity [16, 17]. Inter-consensus reliability (ICR) refers to the comparison of consensus assessments across pairs of reviewers in the participating centers.
In the diagnosis of schizophrenia (or any other condition), reliability refers to the consistency of diagnoses. If two independent clinicians were to diagnose the same person they should come up with the same diagnosis. Similarly, if one clinician saw a patient on two separate occasions they should give the same diagnosis both times. However, just because the diagnosis is consistent does notmeanthat it is an accurate one, i.e. that it has validity. After all, a person can be reliably wrong!
Research (in depth) taken on reliability of schizophrenia diagnosis:
- Beck et al. (1962) – reported a 54 per cent concordance (similarity) rate between experienced practitioners diagnosed when assessing 153 patients. - While Sőderberg et al. (2005) – reported a concordance rate of 81 per cent using the DSM classification system. This suggests that classification systems have become more reliable over time. - Interestingly, as briefly mentioned above, Nilsson et al. (2000) – found only a 60 per cent concordance rate between practitioners using the ICD classification system, implying the DSM system is more reliable.
AO3:
Diagnosis of schizophrenia is difficult as the practitioner has no physical signs but only symptoms (what the patient reports) to make a decision on.
Jakobsen et al. (2005) tested the reliability of the ICD-10 classification system in diagnosing schizophrenia. A hundred Danish patients with a history of psychosis were assessed using operational criteria, and a concordance rate of 98% was obtained. This demonstrates the high reliability of the clinical diagnosis of schizophrenia using up-to-date classification.
Comorbidity describes people who suffer from two or more mental disorders. For example, schizophrenia and depression are often found together. This makes it more difficult to confidently diagnose schizophrenia. Comorbidity occurs because the symptoms of different disorders overlap. For example, major depression and schizophrenia both involve very low levels of motivation. This creates problems of reliability. Does the low motivation reflect depression or schizophrenia, or both?
Evaluation (important for revision) :
· The DSM classification system is more reliable than the ICD because the symptoms outlined for each category are more specific.
· The reliability of schizophrenia diagnosis, assessed at 81 per cent, is superior to that for anxiety disorders, at 63 per cent. The reliability of schizophrenia diagnosis is also generally considered superior to the validity of schizophrenia diagnosis.
· Even if reliability of diagnosis based on classification systems is not perfect, they do not provide practitioners with a common language, permitting communication of research ideas and findings, which may ultimately lead to a better understanding of the disorder and the development of effective treatments.
- Validity -AO1
Validity - the extent to which schizophrenia is a unique syndrome with characteristics, signs and symptoms.
For the classification system to be valid it should be meaningful and classify a real pattern of symptoms, which result from a real underlying cause.
AO3
The validity of schizophrenia as a single disorder is questioned by many. This is a useful point to emphasise in any essay on the disorder. There is no such thing as a ‘normal’ schizophrenic exhibiting the usual symptoms.
Since their are problems with the validity of diagnois classification, unsuitable treatment may be administered, sometimes on an involuntary basis. This raises practical and ethical issues when selecting different types of tretment.
Problems of validity: Are we really testing what we think we are testing? In the USA only 20% of psychiatric patients were classed as having schizophrenia in the 1930s but this rose to 80% in the 1950s . In London the rate remained at 20%, suggesting neither group had a valid definition of schizophrenia.
Types of validity in Schizophrenia:
Predictive validity. If diagnosis leads to successful treatment, the diagnosis can be seen as valid. But in fact some Schizophrenics are successfully treated whereas others are not. Heather (1976) there is only a 50% chance of predicting what treatment a patient will receive based on diagnosis, suggesting that diagnosis is not valid.
Aetiological validity – for a diagnosis to be valid, all patients diagnosed as schizophrenic should have the same cause for their disorder. This is not the case with schizophrenia: The causes may be one of biological or psychological or both.
Culture - One of the biggest controversies in relation to classification and diagnosis is to do withcultural relativismand variations in diagnosis. Cochrane (1977) reported that the incidence of schizophrenia in the West Indies and the UK is 1 %, but that people of Afro-Caribbean origin are seven times more likely to be diagnosed as schizophrenic when living in the UK.
Cultural bias – African Americans and those of Afro-carribean descent are more likely to be diagnosed than their white counterparts but diagnostic rates in Africa and the West Indies is low - Western over diagnosis is a result of cultural norms and the diagnosis lacks validity.
SZ: T1. Classification and diagnosis: Outline and explain the significance of co-morbidity, culture and gender bias and symptom overlap in the diagnosis and treatment of schizophrenia.
The significance of co-morbidity, culture and gender bias and symptom overlap in the diagnosis and treatment of schizophrenia:
There are a number of specific problems in the diagnosis of schizophrenia. These are:
co-morbidity.
culture bias.
gender bias.
symptom overlap.
- The significance of co-morbidty in the diagnosis and treatment of schizophrenia:
Co-morbidityrefers to the presence of one or more additional disorders (e.g.depression) occurring simultaneously with schizophrenia. This makes it difficult to know which disorder is being investigated and difficult to give a valid diagnosis. It highlights the point of view that schizophrenia is not a discrete disorder (descriptive validity).
Co-morbidity will also affect the reliability of the diagnosis, which may vary depending upon which symptoms are most prominent at any one time. Treatment for schizophrenia may also be compromised if other disorders are present.
Co-morbidity in research:
People which schizophrenia often suffer from forms of depression, as well as schizophrenia, at the same time. Co-morbidty also raises issues of descriptive validity, as having simultaneous disorders suggests, as stated above, that schizophrenia may not actually be a separate disorder.
Research:
- Sim et al. (2006) – reported that 32 per cent of 142 hospitalised people with schizophrenia had an addiction mental disorder, illustrating the problem that co-morbidty can create in achieving reliable and valid diagnosis of schizophrenia.
- Goldman. (1999) – reported that 50 per cent of people with schizophrenia had a co-morbid medical condition, such as substance abuse or polydipsia (excessive thirst), making reliable and valid diagnosis of schizophrenia a problem.
- Buckley et al. (2009) – reported that an estimated 50 per cent of people with schizophrenia had co-morbid depression, 15 per cent co-morbid panic disorder, 29 per cent post-traumatic stress disorder and 23 per cent obsessive-compulsive disorder, with an additional 47 percent of patients diagnosed with co-morbid substance abuse.
This again illustrates the difficulties in reliability and validity diagnosing schizophrenia.
Evaluation into the scale of the problem:
· Jeste et al. (1996) stated that people with schizophrenia with co-morbid conditions are excluded from research and yet form the majority of patients of patients, which suggests that research findings into the causes of schizophrenia cannot be generalised to most patients. This also has a knock-on effect as to what treatments such patients should receive.
• The high levels of certain co-morbid disorders found in people with schizophrenia have led to some arguing that such co-morbidities are actually separate sub-types of the disorder.
· The biggest problem in reliability diagnosing schizophrenia is differentiating it from bipolar disorders (manic depression). Schizophrenia-related changes in mood often include mania and depression, but such changes often do not meet classification system criteria for diagnosis of separate bipolar conditions.
· Alcohol, cannabis and cocaine are substances frequently abused by patients with schizophrenia and not only does such co-morbid substance abuse make reliable and valid diagnosis of schizophrenia difficult to achieve, it also leads to lower levels of functioning, increased hospitalizations and lower compliance with medication, which makes effective treatment more difficult to achieve.
If many sufferers of schizophrenia are displaying additional disorders there is a problem in generalising research findings. Studies of schizophrenia patients who do not demonstrate co-morbidity may not be relevant to most people with schizophrenia who do.
The high incidence of co-morbidity suggests that some co-morbidity states are actually other sub-types of schizophrenia rather than separate conditions.
- The significance of culture bias in the diagnosis and treatment of schizophrenia:
Culture bias:
Culture Bias in Psychology is whena piece or pieces of research are conducted in one culture and the findings are generalised and said to apply to lots of different cultures.
In Britain, people of Afro-Caribbean descent are much more likely to be diagnosed with schizophrenia than white people. One study showed the same incidence (1%) of schizophrenia in the West Indies and in Britain, yet when people of Afro-Caribbean origin live in Britain they are seven times more likely to be diagnosed with schizophrenia. More worryingly, they are also more likely to be compulsorily confined in secure hospitals.
Several suggestions have been made for this bias:
Most psychiatrists are white and so perhaps view black schizophrenics as more ‘dangerous’.
Heightened stress levels in ethnic minorities may contribute to the symptom presentation. If ethnic groups are subjected to higher levels of racism, poverty, etc. then it is not unreasonable to suggest that there might be a higher level of mental disorders such as schizophrenia. However, in Britain it only appears to be Afro-Caribbean ethnic groups that suffer in this way.
Another explanation might be of a biological origin in that there is evidence that Afro-Caribbean groups have lowered immunity to flu. Children born to mothers who had flu during their pregnancy have an 88 per cent increased chance of developing the disorder (see Topic 4).
There may be cultural differences in terms of expectation of behaviour. In some cultures it is not considered abnormal to hear the voices of dead people; in fact this is considered to be part of the grieving process, whereas elsewhere this would be a clear sign of mental disorder.
Research into culture bias:
- McGovern & Cope. (1977) – reported that two thirds of patients detained in Birmingham hospitals were first- and second-generation Afro-Caribbeans, the other third being white and Asian, suggesting a cultural bias to over-diagnose schizophrenia in the black population.
- Whaley. (2004) – believes the main reason for the incidence of schizophrenia among black Americans (2.1 per cent) being greater than among white Americans (1.4 per cent) is cultural bias, where ethnic differences in symptom expression are overlooked or misinterpreted by practitioners. This shows a lack of validity in diagnosing schizophrenia cross-culturally.
Evaluation into the scale of the problem:
· Rack (1982) points out that in many cultures it is normal to see and hear recently deceased loved ones (it is part of the grieving process and how loss it often dealt with) but people exhibiting such behaviour in Western culture are liable to be diagnosed as schizophrenic.
· Other psychologists argue that the racism and social deprivation immigrants suffer is bound to negatively affect mental health, but that clinicians wrongly attribute their behaviour to their ethnicity.
- Explain the significance of Gender bias in the diagnosis and treatment of schizophrenia:
Gender bias in research could be defined asa systematically erroneous gender dependent approach related to social construct, which incorrectly regards women and men as similar/different.
Gender bias is not as clear-cut an issue as culture bias. It has been accepted for a long while that both genders were equally vulnerable. However, recently there have been some who argue that in fact males are up to 50% more vulnerable and that women have been over-diagnosed, maybe because most psychiatrists are male and have misread female symptoms.
Some differences that are now being considered are as follows:
Males display more negative symptoms than females.
Men have higher levels of substance abuse, which could relate to schizophrenia-type symptoms.
Different predisposing factors occur at different stages of life for men and women, resulting in different vulnerabilities at different times in their lives. First onset schizophrenia occurs at around 18–25 years for men but at 25–35 for women. There are two peaks for men at age 21 and 39, while there are three peaks for women at 22, 37 and 62 years of age.
- Research into gender bias:
- Lewin et al. (1984) – found that if clearer diagnosis criteria were applied, the number of female individuals with schizophrenia became much lower, suggesting a gender bias in original diagnosis.
This was supported by Castle et al. (1993) – who found using more restrictive diagnostic criteria that the male incidence of the disorder was more than twice that of females.
- Kulkarni et al. (2001) – found that the female sex hormone estradiol was effective in treating schizophrenia in women when added to antipsychotic therapy, which suggests there may be different protective and predisposing factors in make and female vulnerability to schizophrenia which clinicians are not considering at diagnosis.
Evaluation into the scale of the problem:
· The fact that females also tend to first develop schizophrenia on average between four to ten years later than males and that women can develop a much later form of post-menopausal schizophrenia suggests there are different types of schizophrenia to which males and females are vulnerable, calling into question the validity of diagnosis.
· Research findings indicate that there is a case to be made for different diagnostic considerations when diagnosing males and females. However, this would cast doubts on the validity of schizophrenia as a separate disorder.
· Differences in the ages at which males and females experience schizophrenia may be related to differences in the types of stressors both sexes experience at different ages to age-related variations in female menstrual cycles.
The fact that women seem to develop schizophrenia up to 10 years later in life than men, and that they can develop a form of post-menopausal schizophrenia, casts doubt on the validity of diagnosis.
This leads some to suggest that different diagnostic criteria are needed for women and men.
As with culture bias it might be that the different stressors experienced at different times of life are factors in explaining the variation between men and women in the frequency of schizophrenia diagnosis.
Ø Study hint: The specification states that you must know about culture and gender bias and so you could get a direct question on either of them. However, these topics are also extremely important in discussing the validity of diagnosis and so all this information would be useful in answers to questions about the validity of the diagnosis of schizophrenia.
Ø The same is true for co-morbidity and symptom overlap.
- Explain the significance of symptom overlap in the diagnosis and treatment of schizophrenia:
Another serious validity issue with the diagnosis of schizophrenia is that the symptoms used in identifying the disorder occur in other disorders, therefore making it difficult for clinicians to decide which particular disorder is being presented by the patient.
The most concerning is bipolar disorder, which is commonly characterised bydepressionand hallucinations. There have also been suggestions of overlap between schizophrenia symptoms and autism as well as with cocaine intoxication.
Misdiagnosis of schizophrenia as bipolar disorder and vice versa can have disastrous consequences, not least because that person will receive inappropriate treatment and not receive the therapy they need.
Note: Symptom overlap especially occurs with bipolar disorder, where depression is a common symptom, as well as with cocaine intoxication.
Research into symptom overlap:
- Serper et al. (1999) – assessed patients with co-morbid schizophrenia and cocaine abuse, cocaine intoxication on it’s own and schizophrenia on it’s own. They found that although there was considerable symptom overlap in patients with schizophrenia and cocaine abuse, it was possible to make accurate diagnosis.
Evaluation into the scale of the problem:
· The fact that there is genetic overlap between mental disorders suggests that gene therapies might be developed which simultaneously treat different disorders.
· One recently developed method of ascertaining which particular disorder someone is suffering with is to examine the grey matter content of the brain, as people with schizophrenia can experience a decrease of grey matter, while people with bipolar disorder do not.
· Ketter. (2005) reported that misdiagnosis due to symptom overlap can lead to years of delay in receiving relevant treatment, during which time suffering and further degeneration can occur, as well as high levels of suicide.
There are improvements being made in diagnosis based on developments in biological techniques and new evidence for biological changes in the brain in people with schizophrenia (Topic 2). For instance, the quantity of grey matter in the brain is decreased in schizophrenic sufferers but not in bipolar disorder.
The evidence that some genes are associated with both schizophrenia and bipolar disorder, whereas others are only implicated in schizophrenia, is leading to the development of specific gene therapies.
Key points:
Co-morbidity is when more than one disorder occurs together.
Co-morbidity creates problems with reliability because it causes confusion over which disorder is being diagnosed.
Culture bias involves the tendency to over-diagnose schizophrenia in certain ethnic groups.
People of Afro-Caribbean descent are more likely to be diagnosed with schizophrenia than white people in the UK.
Culture bias matters because there is not a valid application of the diagnosis. Some people might receive treatment who don’t need it, while others in need might not receive treatment.
Clinicians may ignore the fact that males and females have different predisposing factors and so have different vulnerability levels at different points in life.
If the same symptoms occur in different disorders then the validity of the diagnosis is going to be affected and consequent treatment will be a problem.
SZ: T2. Explanations for schizophrenia: Outline the genetic explanation of schizophrenia.
The genetic explanation of schizophrenia:
Schizophrenia tends to run in families, but nosingle gene is thought to be responsible.
It’s more likelythat different combinations of genes make people more vulnerable to the condition. However, having these genes does not necessarily mean you’ll develop schizophrenia.
Three kinds of studies are used in explaining the genetic link with schizophrenia:
- family studies.
- twin studies.
- adoption studies.
- Family studies:
The idea behind family studies is to look at the concordance values between different types of relatives. If concordance is 100% between two people and one person has schizophrenia, then so does the other. If identical or monozygotic (MZ) twins have a high concordance but other siblings show lower concordance, then genetics is suspected to play an important role.
In general terms, if the concordance values go up as the relationship gets closer genetically, then it is more probable that the behaviour is inherited.
Early family studies tended to use unclear diagnostic criteria for schizophrenia and were flawed in other ways. However, despite these problems, family studies still showed that the risk of getting schizophrenia is about 10 per cent if an individual has a sibling or parent with schizophrenia, as compared to a 1 per cent risk in the general population (Gottesman and Shields, 1982).
More recent family studies have used standardised diagnostic criteria (such as the DSM) and have also assessed individuals without knowing whether they had any relatives with schizophrenia.
For example, Kendler and Gruenberg (1984) found a risk of 3.7 per cent in first-degree relatives of people with schizophrenia, as compared to a lifetime risk in a normal control group of only 0.2 per cent. First-degree relatives include parents, siblings and children.
Research studies:
- Varma & Sharma. (1993) – found a concordance rate of 35 per cent for first-degree relatives of individuals with schizophrenia, compared with 9 per cent in first-degree relatives of people without schizophrenia, indicating a role for genetic factors.
- Additionally, Parmas et al. (1993) – conducted a longitudinal family study of schizophrenia, finding that 16 per cent of children whose mothers had schizophrenia developed the disorder, compared with the 2 per cent of children whose mothers did not have schizophrenia, again suggesting a genetic link.
Such family studies have shown that schizophrenia does tend to run in families. However, as we have already noted, families tend to have similar environments as well as having genetics in common, and it is hard to disentangle these two factors. That said, both twin and adoption studies have tried to separate the effects of the environment and of genetics in schizophrenia. We will look at these next.
Summary of evaluative points about family studies.
Family studies are often conducted retrospectively and study a group of people who have already been diagnosed, which may affect the reliability of the study.
The individuals being studied tend to share environments as well as genetics, and it is hard to separate out the effects of these.
Early studies used flawed and unstandardized diagnostic criteria.
We might conclude that there is a familial link to schizophrenia and schizotypal personality disorder, but we must interpret the results with caution due to the limitations of the studies. In particular, these studies cannot tell us anything definite about the role of genetics in schizophrenia, as it is impossible to disentangle the roles of the environment and of genetics.
- Twin studies.
Twin studies examine the likelihood of both twins having schizophrenia. As you know, this likelihood is called a concordance rate.
If there is a genetic component to schizophrenia, we would assume that the concordance rates in identical or monozygotic (MZ) twins would be higher than in non-identical or dizygotic (DZ) twins. This is because the two types of twins differ in their genetic make-up, although they are quite likely to share environmental factors that affect them.
MZ twins are genetically identical, but DZ twins have approximately 50 per cent of their genes in common.
It is difficult to study concordance rates in twins. You would expect only 1 per cent of all twins – as members of the general population – to be affected by schizophrenia, so very large-scale (usually national) studies have to be done to be able to study statistically significant numbers of twins.
MZ twins who have been reared apart are the most interesting to study as this enables researchers to separate out the effects of genetics and of the environment. However, it is even harder to find twins in this situation, and even if researchers do find sets of MZ twins who have been reared apart, they must carefully note the reasons for the twins being separated – it could be due to problems in the family, which may affect the results of the study.
Despite these problems, most twin studies have shown that concordance rates in MZ twins are higher than those in DZ twins. Gottesman (1991) reported on 40 European studies conducted over a period of 30 years and found that the average concordance rate for MZ twins was 48 per cent and for DZ was 17 per cent.
Gottesman and Shields (1982) found that 7 (58 per cent) of their study group of 12 pairs of MZ twins reared apart were concordant for schizophrenia.
Research studies:
- Gottesman & Shields. (1976) – reviewed five twin studies and reported a concordance rate of between 75 per cent and 91 per cent for MZ (identical) twins with severe forms of schizophrenia, suggesting that genetics plays a larger role with chronic forms of the disorder.
- Torrey et al. (1994) – reviewing evidence from twin studies, found that if one MZ twin develops schizophrenia, there is a 28 per cent chance that the other twin will do so too, supporting the idea schizophrenia is inherited.
Summary of evaluative points about twin studies.
Twin studies tend to be small scale because of the difficulties in finding participants. In addition, it is not always known whether twins are MZ or DZ. In the twenty-first century, doctors and researchers are usually certain as to whether twins are MZ or DZ, but until relatively recently twins who looked identical would have been assessed as MZ; some of these sets of twins would in fact have been DZ.
This error may have affected the results of some studies.
It is hard to compare the results of different twin studies as they may use different criteria for diagnosis (e.g. some studies use DSM and others use ICD). Similarly, there are a number of different methods for calculating concordance rates. Before comparing rates between studies it is important to check that the same methods of calculation and diagnosis have been used.
In some studies the researchers were not ‘blind’. In other words, they knew the diagnoses of the individuals they were studying. It is important to do blind studies so that the results are more reliable.
If schizophrenia was totally governed by genes then concordance for MZ twins should be 100%. This figure has never been obtained, showing that there must be some environmental factors as well.
In addition, the values for MZ twinsrangefrom 58% down to as low as 11%. This lack of reliability hints at problems with the validity of the conclusions.
- Adoption studies.
In adoption studies, researchers look at individuals who were born to schizophrenic parents but then adopted and brought up by parents with no history of schizophrenia. The individuals being studied do not have any genes in common with the adoptive family. For research purposes it is best if the adoption happened in the first few weeks after birth, as then the effects of the birth family will be minimal.
Researchers compare children who later develop schizophrenia with both their birth parents and their adoptive parents.
One of the largest adoption studies is the Danish study reported by Ketyet al(1994). The researchers found a higher rate of schizophrenia (and related disorders such as schizotypal personality disorder) in the biological relatives of children with schizophrenia (20.3 per cent), compared to that of the adoptive relatives (5.3 per cent).
This would suggest a genetic component in these disorders. Other studies have found similar trends. Kety and Ingraham (1992) also showed a ten times factor between genetic rather than adoptive relatives of schizophrenics.
Summary of Evaluatative points of adoption studies.
• In adoption studies, researchers do not always look for interactions between factors. For example, Wahlberg et al (2000) found a significant interaction between high genetic risk for schizophrenia and deviant communication patterns in the adoptive parents.
• Individuals at high risk of developing schizophrenia (because of their genetic inheritance) showed greater evidence of thought disorder if their adoptive parents showed deviant communication patterns (for example, communicating in an incoherent way).
• There was no such evidence of deviant communication in the control group. One explanation for these findings is that an individual’s inherited genetic make-up may give them an increased sensitivity to factors in the environment such as communication strategies. It is therefore important to be aware of the possibility of the interaction between genetics and the environment in adoption studies.
• Similar methodological problems occur with adoption studies as with twin studies. For example, not all research uses the same diagnostic criteria. This may affect the results of such studies.
Research studies:
- Sorri et al. (2004) – performed a longitudinal study over 21 years on Finnish adoptees with biological mothers with schizophrenia, comparing them with adoptees whose biological did not have schizophrenia, but also considered family rearing styles among adoptive families. Adoptees with a high genetic risk of developing schizophrenia were more sensitive to non-healthy rearing patterns, suggesting that environmental factors are important, too.
- Leo. (2006) – argues that Kety’s (see above) adoption study evidence is not convincing as sample sizes were small, making generalisation difficult, and many of the biological relatives with schizophrenia were distant relatives, such as half-siblings, with low biological similarity.
- Additional findings from genetic studies provide evidence for the diathesis-stress model, where individuals inherit different levels of genetic predisposition to developing schizophrenia, but ultimately it is environmental triggers that determine whether individuals go on to develop a schizophrenia.
Evaluation of genetic explanations of schizophrenia:
The research evidence seems to be very convincing that genetics is a risk factor for schizophrenia. However, it is not the case that an individual will definitely have schizophrenia if a close relative is diagnosed with the disorder, even if the close relative is an MZ twin. This tells us that other factors must be involved too. Most people with schizophrenia do not have a relative who also has the disorder so there must be another factor or factors involved.
There is still no confirmed gene that is implicated in schizophrenia. There is a lot of research going on in this area but as yet there are no consistent findings from these studies. One of the problems is that there is still no single accepted definition of schizophrenia and also that individuals with schizophrenia may all be very different – and behave very differently.
It seems likely that there is more than one gene involved in schizophrenia. Research searching for multiple genetic factors is the hardest kind of research to do successfully, so it may be many years before more conclusive findings are reported.
SZ: T2. Explanations for schizophrenia: Biochemical explanations - Explain the dopaminehypothesis.
Biochemical explanations - The dopamine hypothesis:
Biochemical explanations for schizophrenia focus on the chemicals that transmit messages from one nerve cell to another. These chemicals are called neurotransmitters. It may be that any genetic influence comes about via these biochemical systems.
There are three main biochemical systems that may be involved in schizophrenia:
· The dopamine system.
· The serotonin system.
· The noradrenaline system.
Dopamine is the neurotransmitter that has been most widely researched in schizophrenia and the one that we will focus on here.
Thedopaminehypothesisis that schizophrenia is a result of increased dopamine activity in the brain. Thehypothesisarose from the finding that some drugs such as amphetamines and L-dopa work by increasing the level of dopamine in the brain.
- Such drugs also produce a state that is very similar to paranoid schizophrenia in normal individuals. They also affect the severity of schizophrenia in individuals who have already been diagnosed with the disorder. Rats treated with these drugs have been shown to develop schizophrenic-like symptoms.
There is a class of drugs called the phenothiazines, which act by blocking dopamine activity. These drugs are effective in relieving some of the major symptoms of schizophrenia.
Post mortems on people known to have had schizophrenia have shown an increase in dopamine in the limbic system.
However, studies have not always shown consistent support for thishypothesis. The dopaminehypothesishas therefore been modified to suggest that, rather than there being increased levels of dopamine in schizophrenic individuals, the receptors on the nerve cells may be extra-sensitive to dopamine.
Seemanet al(1993) used PET scans (a type of brain scan) to show that individuals with schizophrenia have a much denser network of certain dopamine receptors than healthy individuals. Kessleret al(2003) used both PET and MRI scans and showed elevated dopamine receptors in the basal forebrain and sustantia nigra/ventral tegmental areas.
Dopamine: further information:
Snyder (1976) argued that if too much dopamine is released during synapse it can lead to the onset of schizophrenia. As stated above – the theory developed after it was discovered that phenothiazines: antipsychotic drugs that lessen the symptoms schizophrenia, seem to work by decreasing dopamine activity.
Other drugs influencing the dopaminergic system, such as LSD: a hallucinogenic, Aldo create schizophrenic-like behaviour in people without schizophrenia and heighten symptoms in people with schizophrenia. It is probable that genetic factors are linked to faulty dopaminergic systems in those with schizophrenia.
Research studies:
The neurotransmitter glutamate may be involved, too, as there is reduced function of the NMDA glutamate receptor in people with schizophrenia, with dopamine involved, as dopamine receptors restrict the release of glutamate.
- Javitt et al. (2000) – found that glycine: a glutamate receptor agonist, reversed phenylalanine hydrochloride-induced psychosis (which closely resembles schizophrenia) in rats and brought about improvements in people with schizophrenia, lending support to the glutamate theory.
Evaluation of the dopaminehypothesis.
In terms of evaluating the dopaminehypothesis, your textbook makes reference to several points which you should consider carefully, namely:
A possible vested interest on the part of pharmaceutical companies
The time lag between the recovery of sufferers and the effect of drugs on dopamine levels
The environmental effect on dopamine levels
The problem of cause and effect on dopamine levels
Dopamine and positive symptoms.
There are a number of strengths and limitations of the dopaminehypothesis. However, there is no way of knowing whether these differences from the brains of healthy individuals are the cause of schizophrenia or if the schizophrenia causes the changes in the brains of people with the disorder.
The fact that drugs which act on the brain’s dopamine system relieve many of the symptoms of schizophrenia appears to be further evidence for the dopaminehypothesis. However, not everyone with schizophrenia responds to such drugs, so this maymeanthat other systems are involved, too.
In general it would seem reasonable to conclude that dopamine has a role to play in schizophrenia – although it is not clear what that role is – but that other factors are involved too.
Additional evaluation points from the textbook (studies):
· Lloyd et al. (1984) believe that even if dopamine is a causative factor, it may be an indirect factor mediated through environmental factors, because abnormal family circumstances can lead to high levels of dopamine which in turn trigger schizophrenic symptoms.
· Differences in the biochemistry of people with schizophrenia could just as easily be an effect rather than a cause of the disorder.
· Dopamine seems to be associated more with positive symptoms, do it may contribute only to certain aspects of the disorder. Alternatively, this could also suggest that there are several types of schizophrenia, with dopamine lined to certain types only.
Overall the evidence is inconclusive, as there I’d no consistent difference in dopamine levels between drug-free schizophrenic patients and people without schizophrenia.
AO3:
One of the biggest criticisms of the dopamine hypothesis came when Farde et al found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.
Noll (2009) also argues around one third of patients do not respond to drugs which block dopamine so otherneurotransmittersmay be involved.
A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is because if the individual does have excessive amounts of dopamine then does it really mean that thy ey will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
SZ: T2. Explanations for schizophrenia: Neural explanations - Explain what is meant by neural correlates.
Neural correlates:
The term‘neural correlates’refers to the idea that specific abnormalities of the brain could be associated with certain behaviours, such as schizophrenic symptoms.
With the recent development of scanning techniques it is now possible to see the functioning of the brain in real time rather than using post mortem findings. Sufferers of schizophrenia can be compared to non-sufferers in an effort to identify brain areas that are functioning differently, for example by giving people tasks relevant to schizophrenia to do and then monitoring brain function.
This approach has led to various neural correlates being identified.
Abnormalitywithin the ventral striatum has been shown to be involved in the development of avolition (the loss of motivation), which is one of the negative symptoms in schizophrenia. Motivation is associated with the anticipation of a reward, and the ventral striatum appears to be particularly involved in this anticipation.
- Lower levels of activity have been found within the ventral striatum in schizophrenics compared to control participants (Juckelet al, 2006).
Lower activation in the superior temporal gyrus and anterior cingulate gyrus has been identified as being involved in auditory hallucinations, a positive symptom of schizophrenia (Allenet al,2007). - An important question to be addressed is whether these brain abnormalities precede the condition or are a consequence of it. Improvements in brain scanning techniques offer the possibility of following people at high risk longitudinally to see which comes first.
Research studies:
- Tilo et al. (2001) – gave fMRI scans to six patients with schizophrenia and six people without schizophrenia while they looked at and spoke about Rorschach ink-blots. In the schizophrenic patients it was found that the severity of thought disorder, a core symptom of schizophrenia, was negatively correlated with the level of activity in the Wernicke’s brain area; a region associated with the production of coherent speech, supporting the idea of abnormal functioning in specific brain areas being related to schizophrenia.
- Li et al. (2010) – performed a meta-analysis of fMRI studies investigating the difficulties patients with schizophrenia often have in processing facial emotions, to find that although both people with and without schizophrenia activate bilateral amygdala and right fusiform when processing facial emotion (lateral hemispheric functioning) the activation was severely limited in patients with schizophrenia. This suggests that abnormal brain functioning in patients with schizophrenia may explain their difficulties in processing facial emotions.
Structural brain damage is often evident at first onset of schizophrenia, but only by performing longitudinal studies would it be possible to assess whether damage progressively worsens as the disorder continues.
Evaluation of neural correlates.
There are some problems with trying to establish neural correlates. For example, some studies (e.g. Johnstone et al (1976)) have demonstrated that people with schizophrenia have enlarged ventricles. However, not all schizophrenics demonstrate the presence of enlarged ventricles, and some non-schizophrenics do.
There seems to be an association between enlarged ventricles and non-response to medication. This may point to enlarged ventricles being a result of prolonged damage caused by the disorder, rather than being a cause of schizophrenia.
Summary of biological factors.
Research strongly suggests that schizophrenia is a brain disorder that is partly genetic, and also that biochemicals, particularly the neurotransmitter dopamine, may be involved in the disorder. Some definite abnormalities of the brain have been linked to specific characteristics of schizophrenia.
However, the fact that many people with schizophrenia have no family history of the disorder, and that some people do not respond to drugs that act on the dopamine system of the brain, suggests that there are likely to be other factors, possibly psychological and psychosocial, involved. In the next part of the topic we will study some psychological explanations of schizophrenia.
A second weakness of the neuroanatomical explanations is that it is biologically deterministic. The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
SZ: T2. Explanations for schizophrenia: Psychological explanations for schizophrenia - Identify the possible role of family dysfunction in schizophrenia.
Family Dysfunction
Family Dysfunction refers to any forms of abnormal processes within a family such as conflict, communication problems, cold parenting, criticism, control and high levels of expressed emotions.
These may be risk factors for the development and maintenance of schizophrenia.
AO1:
• Laing and others rejected the medical / biological explanation of mental disorders. They did not believe that schizophrenia was a disease. They believed that schizophrenia was a result of social pressures from life. Laing believed that schizophrenia was a result of the interactions between people, especially in families.
As mentioned earlier, there is strong evidence that biological factors contribute to schizophrenia. However, it is also clear that they do not provide a complete explanation, so psychologists have looked for other factors that may explain or help to explain schizophrenia. In this topic we will look at the dysfunctional family explanation and at the cognitive approach to explaining schizophrenia.
Family dysfunction:
Family dysfunction is about patterns of communication and maladaptive relationships within the family.
The family dysfunction explanation sees maladaptive relationships and patterns of communications within families as sources of stress, which can cause of influence the development of schizophrenia. (As dysfunctional families are associated with high levels of schizophrenia.
Parents of people (children or once children) with schizophrenia often display three types of dysfunctional characteristics:
- High levels of interpersonal conflict (arguments).
- Difficulty communicating with each other.
- Being excessively critical and controlling of their children.
Research studies:
- Patino et al. (2005) – established seven problems associated with family dysfunction:
- Poor relationship between adults in the household.
- Lack of warmth between parents and child.
- Visible disturbance of the mother-child.
- Father-child relationship.
- Sibling-child relationship.
- Parental overprotection.
- Child abuse.
- They found that migrants who had experienced at least three of these seven problems had four times the normal level of vulnerability to developing schizophrenia, compared with the double level of risk for migrants not experiencing family dysfunction.
This suggests that family dysfunction increases the likelihood of life stressors triggering the onset of schizophrenia.
For example, a parent may tell a child to be ‘more spontaneous’, but if the child is then spontaneous, it becomes confused and uncertain, as by doing what the parent said it is clearly not being spontaneous. This leads to a negative reaction of social withdrawal and flat effect (a lack of emotional expression) in order to escape double bind situations.
- Another feature of the theory is that of expressed emotion, where families who persistently exhibit criticism and hostility exert a negative influence, especially upon people recovering from schizophrenia, who when returning to their families react to expressed emotion by relapsing to an active phase of the disorder and experience severe positive symptoms of hallucinations and delusions of persecution.
A concept known asExpressed emotion(EE) has been proposed to explain the relapse of sufferers and the maintenance of the disorder within families. Expressed emotion refers to high levels of critical comments, hostility and emotional over-involvement.
It is usually assessed by a standardisedsemi-structured interviewwith a relative of the patient; it is not just the content of what is said that is assessed, but also the tone.
In the 1970s it was found that schizophrenic patients who were discharged from hospital to homes high in EE were more likely to relapse than other patients (Brownet al, 1972).
The research shows that it is not usually the occurrence of the first episode of schizophrenia that is related to the levels of family EE, but rather the maintenance of schizophrenia.
Kavanagh (1992) found a 48%meanrelapse rate for sufferers who were returned to high EE families compared to 21% if the family possessed low EE.
Evaluation of the role of EE in the maintenance of schizophrenia:
First, it is important to note that many of the studies of EE are correlational; they show an association between the levels of EE and relapse rates, but this does not necessarilymeanthat the high levels of EE caused the relapse. In fact, it could be that living with an individual who has a diagnosis of schizophrenia is a cause of EE, rather than the other way round.
High levels of EE are also found in the homes of individuals with other disorders, such asdepression, so it is not a defining characteristic of families where one individual has schizophrenia, nor is it limited to such families. Also, many individuals with schizophrenia become isolated or estranged from their families for a variety of reasons.
This suggests that the high levels of EE in the family home cannot be a cause of the maintenance of schizophrenia in these cases.
The model is well established in the field of schizophrenia and has resulted in the development of training programmes for the families of individuals with schizophrenia. This means that the concept of EE has a practical use, as well as being of theoretical benefit in explaining the maintenance of schizophrenia.
Key points:
Parents in dysfunctional families show (amongst other characteristics) high levels of interpersonal conflict and excessive control of their children. You might also have noted down difficulty in communicating with each other.
‘Expressed emotion’ refers to high levels of critical comments, hostility and emotional over-involvement in the family of the schizophrenic individual. It may affect the maintenance of schizophrenia in that patients discharged into homes with high levels of EE have a higher relapse rate than those discharged into homes with lower levels of EE.
There are practical advantages in that programmes have been designed to help the families of schizophrenics, based on what psychologists know about EE and schizophrenia.
The link with relapse and EE is correlational – it is an association, and it is not possible to infer that the EE causes the relapse, nor to say with any authority whether it is the disorder that is causing the EE. Also, many individuals with schizophrenia do not live with their families, so EE cannot explain relapse in these cases. (There are other limitations too that you may have mentioned).
SZ: T2. Explanations for schizophrenia: Describe cognitive theories of schizophrenia.
Cognitive theories of schizophrenia:
+ The main assumptions of the cognitive approach:
· That it is the mind which influences our behaviour.
· Methods like introspection should be prioritised when explaining behaviour.
· Humans are information processors, with stimuli, input and output processing.
· Psychology should be seen as an actual science.
The cognitive approach centres on the idea that thoughts are the primary determinants of our behaviour.
Two symptoms of schizophrenia that could be termed cognitive:
· Thought disorder and intrusive thoughts.
· Auditory hallucinations (hearing voices, extra interpretations, etc).
An important assumption of the cognitive approach is that our brains behave as a computer, receiving input from the senses, where it is processed, and an output is created, such as language. Such processes can and should be studied scientifically.
Another assumption is that maladaptive behaviour can be created by maladapted thought processes.
In this context a symptom of schizophrenia is the inability to produce coherent language. Another is the hearing of ‘voices’, which are not stimuli from the auditory system but internally created within the brain.
We have already seen that in patients with schizophrenia there is often thought disturbance, and so the cognitive approach may have some useful insights that may help to explain schizophrenia. These models concentrate on the impaired thought processes in schizophrenia.
Cognitive theories:
Cognitive explanations focus upon maladaptive thought processes as a central feature of schizophrenia, with Beck & Rector (2005) – proposing a cognitive model that combines a complex interaction of neurological, environmental, behavioural and cognitive factors to explain the disorder.
Abnormalities within brain functioning are seen as increasing vulnerability to stressful life experiences, which in turn lead to dysfunctional beliefs and behaviours.
Cognitive deficits occur, where individuals with schizophrenia experience problems with attention, communication and information overload.
Individuals are also seen as being unable to deal with inappropriate ideas, such as misperceiving voices in their head as people actually trying to speak to them, rather than perceiving them more sensibly as ‘inner speech’, which most people experience.
- With positive symptoms, (positive presence of problematic behaviours) delusions are seen as occurring because of active cognitive biases (thinking in irrational ways), such as external attribution like individuals believing that they are being persecuted. Hallucinations, meanwhile, are understood in terms of biased information processing, while the cognitive deficits experienced by people with schizophrenia to as alien control symptoms, where they believe that external people and forces are exerting influence over their thoughts and behaviours.
- With negative symptoms, (negative absence of healthy behaviours) are seen as occurring due to the use of cognitive strategies to control the high levels of mental stimulation being experienced. Patients with schizophrenia may actually experience a greater level of emotion than they physically display, as not expressing emotions is one strategy that can be used to try to control the levels of emotion being experienced internally.
+ If you have had time to watch the filmA Beautiful Mindyou will have a clear idea of how John Nash believed things that were not true and created an imaginary world. This might be rather bizarre, but we all do this to a certain extent.
We make attributions every day of our lives and many of them are not very accurate.
For instance if a car driver ‘cuts you up’ by overtaking and pushing in in front of you in queued traffic, do you say to yourself that there is an emergency and the car driver needs to get to the destination urgently, or do you say the driver is selfish and behaving inappropriately by forcing their car ahead of the queue? We don’t know which is correct, but we feel justified in judging others, usually on the basis of schemas.
If you observe young children you can see how easy it is to imagine a world within which we can act out our desires. We are socialised into ceasing to do this as adults, but we never lose the ability completely – as our dreams show us, as does our love and engagement with ‘soaps’ on television.
Delusions can be explained by people making the incorrect attribution that people are persecuting them. Have you ever misread other people’s behaviour as being negative towards you?
Similarly, hallucinations can be seen as biased information-processing. Most of us have had the experience of seeing things that aren’t there. We are actually quite easy to fool and many special effects used in modern films rely on this.
People with schizophrenia may demonstrate negative symptoms in an attempt to reduce the high level mental stimulation they are experiencing.
- On this reading, their inability to show emotion is not because they don’t feel it but instead the exact opposite. They feel so much emotion internally that they have to exercise huge willpower to control it.
Research studies:
- Bowie et al. (2006) – reviewed evidence to find that cognitive impairments are the core feature of schizophrenia mainly affecting attention, working memory, verbal learning and executive functions. – These impairments pre-date the onset of the disorder and are found throughout the course of the illness. This again gives support to Beck & Rector’s cognitive model, with additional support coming from the fact that effective therapies seem to reduce cognitive deficits.
Cognitive deficits have been suggested as possible explanations for a range of behaviors associated with schizophrenia. These include reduced levels of emotional expression, disorganised speech and delusions.
Cognitive Biases:
•Cognitive biasesrefer to selective attention. The idea of cognitive biases has been used to explain some of the behaviors which have been traditionally regarded as ‘symptoms’ of ‘schizophrenia’.
• - Delusions: The most common delusion that people diagnosed with schizophrenia report is that others are trying to harm or kill them – delusions of persecution. Research suggests that these delusions are associated with specific biases in reasoning about and explaining social situations. Many people who experience feelings of persecution have a general tendency to assume that other people cause the things that go wrong with their lives.
AO3:
A strength is that it takes on board the nurture approach to the development of schizophrenia. For example, it suggests that schizophrenic behavior is the cause of environmental factors such as cognitive factors.
One weakness of the cognitive explanation is that there are problems with cause and effect. Cognitive approaches do not explain the causes of cognitive deficits – where they come from in the first place. Is it the cognitive deficits which causes the schizophrenic behavior or is the schizophrenia that causes the cognitive deficits? This suggests that there are problems with the chicken and egg problem.
A second weakness of the cognitive model is that it is reductionist. The reason for this is because the approach does not consider other factors such as genes. It could be that the problems caused by low neurotransmitters creates the cognitive deficits. This suggests that the cognitive approach is oversimplistic when consider the explanation of schizophrenia.
