Paper 3: Schizophrenia Flashcards
Explain the family dysfunction model and list the 3 explanations.
The family dysfunction model sees maladaptive relationships and poor patterns of communication within families as a source of stress which can potentially cause or influence the development of schizophrenia.
3 explanations that look at family dysfunctions:
- The schizophrenic mother
- Difficulty communicating – double bind theory
- Expressed emotion
FDM - 1) Freida Fromm-Reichmann -The schizophrenic mother
Freida Fromm-Reichmann proposed a psychodynamic explanation for schizophrenia based on accounts she heard from her patients about their childhoods.
Fromm-Reichmann noted that many of her patients spoke of a particular type of parent, which she called the schizophrenic mother.
According to Fromm-Reichmann the schizophrenic mother is cold, rejecting and controlling and tends to create a family climate that is often tense and has an element of secrecy.
This leads to distrust that later develops into paranoid delusions and ultimately schizophrenia.
1❌Evaluate the schizophrenic mother
❌Little / bias evidence - As most of the schizophrenia mother theory was based on clinical observations of patients, there is very little evidence to support this theory.
Also, the idea that mothers should be assessed for ‘crazy-making characteristics’ was too awkward & harsh to investigate.
FDM - 2) Bateson - Difficulty communication in a family (ie double bind theory)
Bateson emphasised the importance of communication styles within a family.
He suggested that issues arise when a developing child regularly finds themselves in fear of doing the wrong thing, but received mixed messages from parents.
They often feel unable to comment on the unfairness they feel or even to seek clarification.
When they get it wrong such children tend to be punished by withdrawal of love.
This leaves the child understanding the world as a confusing and dangerous and this is reflected in symptoms like disorganised thinking and paranoid delusions.
Bateson created the term double bind theory to explain the contradictory situations children could be placed in by such parents, where a verbal message is given but opposite behaviour is exhibited.
For example, if a mother tells her son that she loves him, while at the same time turning her head away in disgust, the child receives two conflicting messages about their relationship on different communicative levels, one of affection on the verbal level, and one of animosity (hostility) on the nonverbal level.
It is argued that this contradiction makes a child’s unable to respond to the mother because one message invalidates the other – making it difficult to communicate.
1✅1❌ - Evaluation of difficulty of communication.
✅Bateson reported on a case where a recovering schizophrenic was visited in hospital by his mother.
He embraced her warmly (hugged) but she stiffened, and when he withdrew his arms she said ‘Don’t you love me anymore?’ to which he blushed.
Then she commented, ‘Dear, you must not be so easily embarrassed and afraid of your feelings’.
She then left, and he went onto assault a worker and had to be restrained. This gives support to the double bind theory.
❌However, t is possible that Bateson was bias in his observations and the only support for double bind theories have come from clinical cases, which would question the overall validity of his theory.
FDM - 3) Expressed emotion
This refers to the level of negative emotion that is expressed towards a patient by their carers.
Expressed emotion contains several elements:
- Verbal criticism of the patient, (accompanied by violence)
- Hostility towards the patient, including anger and rejection.
- Emotional over-involvement in the life of the patient, including needless self-sacrifice.
These high levels of expressed emotions in carers directed towards the patient are a serious source of stress for the patient. This is primarily an explanation for relapse in patients with schizophrenia.
However, it is also been suggested that it may be a source of stress that can trigger the onset of schizophrenia in a person who is already vulnerable, for example, due to their genetic make-up.
✅❌Evaluation of expressed emotion in schizophrenia
✅❌Kavanagh reviewed 26 studies of expressed emotion; he found that the mean relapse rate for schizophrenics who returned to live with high expressed emotion families was 48% compared with 21% for those who went to live with families that were rated low on expressed emotions.
This supports that idea that expressed emotions can increase the risk of relapse in recovering patients.
✅❌Butzlaff who carried out a Meta analysis of 26 studies and found that patients returning to family environments of high expressed emotions were twice as likely to relapse as the average relapse rates.
1✅2❌Evaluation of family dysfunction
✅There is support for the claim that dysfunctional family relationships might be linked to schizophrenia.
For example Read et al reviewed 46 studies of child abuse and schizophrenia, and found that 69% of the female patients that had been diagnosed with schizophrenia had a history of physical, sexual abuse or both in childhood. For men the figure was 59%.
Also adults with insecure attachments during childhood with their primary caregiver were more likely to have schizophrenia.
❌Validity issue
However most of the studies that have linked dysfunctional families to schizophrenia have a weakness. This is regarding the fact that most of the information collected about childhood experiences was gathered after the development of symptoms, and the schizophrenia may have distorted the patient’s recall of their childhood.
This creates a serious problem of validity. A small number of studies have been carried out prospectively (i.e. they followed a sample of children to see if their childhood experiences could predict adult behaviours). There is still evidence that links family dysfunction to schizophrenia but not a huge amount and results have been inconsistent.
✅❌Parent blaming
Another major issue with the dysfunctional family explanations for schizophrenia is that they have led historically to parent-blaming.
Parents, who have already suffered at seeing their children, develop schizophrenia and who are likely to bear a lifelong responsibility for their care – now have to deal with further trauma by receiving the blame for the condition.
This is literally adding insult to injury. In fact the shift in the 1980s from hospital to community care, often involving parental care, may be one of the factors leading to the decline of schizophrenic mother and double bind theories – parents no longer tolerated them.
cognitive explantions of schizophrenia
The cognitive explanation focuses on the role of mental processes. Schizophrenia is associated with several types of ‘abnormal information processing’ and as a result it can be presented as an explanation of schizophrenia.
Beck proposed that a cognitive model combines a complex interaction of neurological, environmental, behavioural and cognitive factors to explain the disorder.
It is thought that abnormalities within brain functioning increase the vulnerability to stressful life experiences, which in turn can lead to dysfunctional beliefs and behaviours.
Schizophrenia is characterized by disruptions to normal though processing and this is reflected in the symptoms of schizophrenia.
For instance, reduced processing in the ventral striatum is associated with negative symptoms of schizophrenia.
List the two dysfunctional thoughts found by Frith.
Frith identified two types of dysfunctional thought-processing that could underlie some symptoms:
- Meta-cognition
- Central control
Explain the meta cognition and how it’s a DYSFUNCTION in schizophrenics?
Meta-cognition is the cognitive ability to reflect on thoughts (cognitive monitoring) and behaviour (reactions triggered by thoughts and feelings).
It allows individuals to ‘view’ their own mental states and the wishes and intentions of others, allowing them to make sense of their lives and deal with their ever-changing environments.
However, schizophrenics experience meta-cognitive dysfunction. This disrupts our ability to recognise our own thoughts and actions, and sufferers may believe these reflect the views and action of someone else. This would explain hallucinations of voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others).
Explain the central control and how it’s a DYSFUNCTION in schizophrenics?
Central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead.
However, schizophrenics are unable to supress their
automatic thoughts which in turns triggers their disoranised speech and though disorder.
Sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these.
4✅1❌ Evaluation for the cognitive explantions of schizpohrenia
✅Support of meta-cognition - Brunet reviewed 20 years of evidence to report that many symptoms of schizophrenia and the consequent impairments in social functioning result from poor meta-cognition, especially the ability to self-reflect and empathise with others, supporting the idea that meta-cognition dysfunction is an important part of schizophrenia.
✅Support for central control - There is strong support for the idea that information is processed differently in the mind of the schizophrenia sufferer.
In one study Stirling compared 30 patients with a diagnosis of schizophrenia with 18 non-patient controls on a range of cognitive tasks including the Stroop test, in which participants have to state the colour of the ink a set of words are written in and not the colour stated in written form; thus the task requires participants to suppress the impulse to read the words.
It was found that Schizophrenic patients took over twice as long to name the ink colours than the control group. This is therefore in line with Frith’s theory of ‘Central control dysfunction’.
✅ Another key strength of the cognitive explanation is that it can account for both positive and negative symptoms. Also the fact that the cognitive explanation can be combined with other explanations, such as biological ones gives a fuller understanding of the causes and maintenance of the disorder.
✅Also there are practical applications associated with the meta-cognition factor in the development of schizophrenia, as it indicates that therapies for the disorder will need to concentrate on improving meta-cognitive abilities in sufferers in order to be effective.
Indeed therapies could be targeted at specific areas of meta-cognitive impairment. Woodward (2007) conducted a pilot study offering meta-cognition therapy for schizophrenic patients and it offered promising results and patients stated that they enjoyed their sessions (also reflected by high attendance rates) more than their usual therapy sessions.
❌Although there is a mass of evidence that suggests that information processing is different in the mind of schizophrenic patients, there is a problem with the cognitive explanations.
Links between symptoms and faulty cognitive are clear; however, this link does not tell us anything about the origins of those cognitions or of schizophrenia.
Cognitive theories can explain the proximal (closet) causes of schizophrenia i.e. what causes current symptoms but not the origins of the condition.
Also as these are only links we cannot determine whether cognitive factors are a cause or a result of neural correlates and abnormal neurotransmitter levels seen in schizophrenia.
What is the biological treatment for schizophenia?
Drug therapy: typical and atypical antipsychotics.
What are the psychological treatments of schizophrenia?
1) Cognitive behaviour therapy
2) Family therapy
3) Token economies
What are antipsychotic drugs? Describe its effects between a few days to 6 months.
Antipsychotic drugs can be taken in tablet form, as syrup or by injection (intravenous – through the veins by injection).
After a few days – Tends to reduce symptoms such as hallucinations and feelings of anxiety.
After a few weeks - Delusions start to reduce.
After 6 weeks – Patients see a lot of improvement, but there are wide individual differences in the types of responses to taking antipsychotic drugs
Patients often have to take several types of antipsychotic drugs before they find the best one for them.
Some patients’ may require a short term course of antipsychotics then stop their use without the return of symptoms.
Other patients may require antipsychotics for life or face the likelihood of a recurrence of schizophrenia.
What are the two types of antipsychotics?
Antipsychotic drugs are divided into:
Typical antipsychotics - original neuroleptic drugs created in the 1950s to treat schizophrenia).
Atypical antipsychotics - Atypical drugs were introduced as they were supposedly more effective than typical ones and incurred fewer side effects, although the validity of this claim has been questioned. Also found to be more effective with negative symptoms of schizophrenia.
Discuss chloropromazine - Typical antipsychotics (First-generation – original neuroleptic drugs created in the 1950s to treat schizophrenia).
The first antipsychotic drug was Chlorpromazine this can be taken as tablets, syrup or by injection.
If taken orally, doses often start small e.g. 400-800mg, with a maximum of 1000mg daily.
There is a strong association between the use of typical antipsychotics drugs like Chlorpromazine and the dopamine hypothesis.
Antipsychotic drugs are likely to lead to movement side effects (similar to Parkinson’s disease).
How does chlopromazine work?
Typical antipsychotics like Chlorpromazine work by acting as antagonists in the dopamine system.
Antagonists are chemical which reduce the action of a neurotransmitter.
Therefore Dopamine antagonists work by blocking dopamine receptors in the synapse of the brain, reducing the action of dopamine.
This has been found to reduce positive symptoms of the disorder e.g. auditory hallucinations and delusions
Chlorpromazine is also an effective sedative. This is believed to be related to its effect on histamine receptors (to do with allergies) but it is not fully understood how this leads to sedation.
Chlorpromazine is often used to calm patients not only with schizophrenia but with other conditions.
Discuss clozapine
Clozapine was developed in the1960s and trialled in 1970s.
However Clozapine was withdrawn for a while in the 70s following the deaths of some patients from a blood condition called Agranulocytosis.
Resold in the 1980s.
It is still used today, and people taking it have regular blood tests to ensure they are not developing agranulocytosis. Because of its potentially fatal side effects Clozapine is not available as an injection and daily dosages are less than Chlorpromazine, typically 300-450mg a day.
how does clozapine work
How the Atypical antipsychotic drug ‘Clozapine’ works
Clozapine binds to dopamine receptors in the same way that Chlorpromazine does, but in addition it acts on serotonin and glutamate receptors.
It is believed that this action helps improve mood and reduce depression and anxiety in patients, and that it may improve cognitive functioning.
The mood-enhancing effects of Clozapine mean that it is sometimes prescribed when a patient is considered at high risk of suicide.
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How does Risperidone work?
It binds to dopamine and serotonin receptors, but binds more strongly to dopamine receptors than Clozapine and is therefore effective in much smaller doses than most antipsychotic drugs.
There is also evidence that this drug also leads to fewer side effects than is typical for antipsychotics.
What is Risperidone?
Risperidone is a more recently developed atypical antipsychotic, since the 1990s. It was developed in an attempt to produce a drug as effective as Clozapine but without its serious side effects.
Risperidone can be taken in the form of tablets, syrup or an injection (like Chlorpromazine).
A small dose is initially given and this is built up to a typical daily dose of 4-8mg and a maximum of 12mg.
strengths on drug treatment
Strengths
There is a large body of evidence to support the idea that antipsychotic drugs are effective in tackling the symptoms of schizophrenia. For instance Davis carried out a meta-analysis of more than 100 studies that compared antipsychotics with placebos. Davis found that the antipsychotic drugs were more effective at treating the symptoms of schizophrenia, 70% of sufferers started to show improvements in condition after 6 weeks. This is important as it shows that antipsychotics have a beneficial medical effect. Further support comes from Marder, he reported that the atypical antipsychotic drug Clozapine is as effective as typical antipsychotics in relieving the positive symptoms of schizophrenia, and is effective in approximately 30-61% of patients who are resistant to typical antipsychotics. This suggests that atypical drugs might be a superior form of treatment.
There is some evidence that suggests that atypical antipsychotics are more effective than typical antipsychotics for treating schizophrenia. For instance Schooler compared both types of drugs and although he found 75% of patients experienced at least a 20% reduction in symptoms. He found that 55% of those receiving typical antipsychotic suffered relapses (that is when you suffer from the same condition again), compared to only 42% of the atypical treatment. This could be due to the fact that atypical drugs have fewer side effects. However Kahn found no major difference in the effects of typical and atypical antipsychotic drugs, which casts doubts on the claim that atypical drugs are superior.
weaknesses of drug therapy
A major problem with antipsychotic drugs is the likelihood of side effects, ranging from the mild to the serious and even fatal.
Typical antipsychotics are associated with a range of side effects including dizziness, agitation (anxiety), sleepiness, stiff jaw and weight gain.
Long term use can result in tardive dyskinesia which leads to involuntary facial movements such as grimacing (e.g. facial expression for pain/disapproval) or blinking. https://www.youtube.com/watch?v=FUr8ltXh1Pc. The most serious side effect of typical antipsychotics is neuroleptic malignant syndrome (NMS). This results in high temperature and coma which can be fatal, however as doses of typical drugs have declined, NMS cases have become rarer.
Atypical drugs were developed to reduce the frequency of side effects and generally this has succeeded. However, side effects still exist and patients taking Clozapine have to have regular blood tests to help doctors detect early signs of agranulocytosis. This is important as it shows that side effects are still a significant weakness of antipsychotic drugs.
There is a theoretical issue with the use of antipsychotic drugs. Antipsychotic drugs work by reducing the activity of dopamine by blocking dopamine receptors which is concordance with the dopamine hypothesis .
However it has been found that there are very low levels of dopamine (rather than high) in other parts of the sub cortex in schizophrenic patients.
This then raises doubts about how useful it would be to reduce levels of dopamine in sufferers. In fact some psychologist’s modern views suggest that antipsychotic drugs should not work.
