Schizophrenia Flashcards
Describe and evaluate the classification and diagnosis of schizophrenia.
A01
Classification of schizophrenia:
Doesn’t have a single defining feature; cluster of symptoms.
There are 2 systems for classification: ICD-10 and DSM-5.
In the DSM-5 system one of the positive symptoms - delusions, hallucinations or speech disorganisation - must be present for diagnosis whereas 2 or more negative symptoms are sufficient for the ICD-10.
ICD-10 recognises a range of subtypes of Sz.
Paranoid Sz - characterised by powerful delusions and hallucinations but relatively few other symptoms.
Catatonic Sz - disturbance to movement, leaving the sufferer immobile or overactive.
Positive symptoms:
These are additional experiences beyond those of ordinary experience.
Hallucinations:
Unusual sensory experiences.
Some are related to events in the environment whereas some have no relation to what the senses pick up.
Can be experienced in relation to any sense.
Delusions:
Irrational beliefs.
Common delusions involve being an important historical or political figure.
Commonly involve being persecuted or having superpowers.
Delusions can also be bodily; sufferers may believe that they or part of them is under external control.
Negative symptoms:
Involve the loss of usual abilities and experiences.
Avolition:
Finding it difficult to keep up with goal-orientated activities.
Sufferers of Sz often have sharply reduced motivation to carry out a range of activities.
3 signs of avolition: poor hygiene, lack of persistence in work and lack of energy.
Speech poverty:
Changes in pattern of speech.
Emphasis is on the reduction in the amount and quality of speech.
Often accompanied by a delay in verbal responses during conversations.
However, the DSM places its emphasis on speech-disorganisation in which speech becomes incoherent or the speaker changes topic mid-sentence.
This is classified as a positive symptom in the DSM-5.
A03
Reliability of diagnosis:
An important measure of reliability is inter-rater reliability.
In the case of diagnosis this means the extent to which 2 or more mental health professionals arrive at the same diagnosis for the same patients.
Cheniaux et al - had 2 psychiatrists independently diagnose 100 patients using both the DSM-5 and the ICD-10 criteria.
Inter rate reliability was poor, one psychiatrist diagnosed 26 with Sz with the DSM-5 and 44 according to the ICD-10.
The other diagnosed 13 according to the DSM-5 and 24 according to the ICD-10.
Shows that the process of diagnosing Sz is poor as the reliability is very low.
This has consequences such as mis-diagnosis.
Co-morbidity:
Co-morbidity is the phenomenon that 2 or more conditions occur together.
If conditions occur together a lot of the time then this calls into question the validity of their diagnosis and classification because they might actually be a single condition.
Buckley - concluded that 1/2 of patients with a diagnosis of Sz also have a diagnosis of depression or substance abuse.
PTSD also occurred in 29% of the cases and OCD in 23%.
This is a limitation of both classification and diagnosis of Sz.
It may be the case that psychiatrists are just quite bad at telling the difference between Sz and depression or Sz and substance abuse. (DIagnosis)
In terms of classification, it may be that, if severe depression and Sz look very similar, then we might be better classifying them as one condition.
This confusion is a weakness of diagnosis and classification of Sz.
Gender bias in diagnosis:
Longenecker - reviewed studies of the prevalence of Sz and concluded that since the 1980s men have been diagnosed with Sz more than women.
May simply be because men are more genetically vulnerable to the disorder.
Another possible explanation is gender bias; female patients typically function a lot better than men, being more likely to do work and have better family relations.
This high functioning may explain why some women have not been diagnosed with Sz and women with similar symptoms have.
Their better interpersonal functioning may bias diagnosis as their symptoms are masked or because the quality of interpersonal functioning makes the case seem too mild to warrant a diagnosis.
Describe and evaluate biological explanations for schizophrenia.
A01
The genetic basis of Sz:
Sz runs in families - this is quite weak evidence to suggest a genetic basis as family members tend to share very similar environments as well as their genes.
There have been many investigations to show the relationship between genes and developing Sz; e.g. twin studies and family studies.
Candidate genes:
Individual genes are believed to be associated with risk of inheritance.
Sz is polygenic - it requires a number of factors to work in combination.
Because different studies have identified different candidate genes, Sz is also aetiologically heterogeneous - different combinations.
Ripke - the genetic make-up of 37,000 patients was compared to that of 113,000 controls; 108 separate genetic variables were associated with increased riskof Sz.
These include those associated with dopamine.
The Dopamine hypothesis:
Neurotransmitters:
Chemical messengers appear to work differently in the brains of patients with Sz.
Dopamine is widely believed to be involved.
Dopamine is important in the functioning of several brain systems that may be implicated in symptoms of Sz.
Hyperdopaminergia in subcortex:
High levels or activity of dopamine in the subcortex.
E.g. an excess of dopamine receptors in Broca’s area may be associated with poverty of speech or auditory hallucinations.
Hypodopaminergia in the cortex:
Abnormal dopamine systems in the brain’s cortex.
Goldman-Rakic et al - identified a role for low levels of dopamine in the prefrontal cortex in the negative symptoms of Sz.
It may be that both hyper and hypo are correct explanations.
A03
Multiple sources of evidence for genetic susceptibility:
Gottesman - large family study. Results show that as genetic similarity increases so does the probability of sharing Sz. Identical twins had a 48% risk compared to siblings who only had 9% risk.
Tienari - Adoption studies. Shows that children of Sz sufferers are still at hightened risk of developing Sz if adopted into families with no history of Sz.
Molecular studies also show that particular genetic variations significantly increase the risk of Sz.
There is thus overwhelming evidence for the idea that genetic factors make some people much more vulnerable.
This doesn’t mean Sz is entirely geneticbut the available evidence suggests that genetic susceptibility is very important.
Mixed evidence for the dopamine hypothesis:
There is support for the abnormal functioning of dopamine in Sz; dopamine agonists that increase the levels of dopamine make Sz worse and can produce Sz-like symptoms in non-sufferers.
Antipsychotic drugs reduce dopamine levels and both kinds of drug study suggest an important role for dopamine in Sz.
Lindstroem- Found that chemicals needed to produce dopamine are taken up faster in the brains of Sz sufferers, suggesting they produce more dopamine.
There is also evidence to suggest that sopamine does not provide a complete explanation for Sz.
Some of the genes identified in Ripke’s study also code for other neurotransmitters and so it seems that although dopamine is likely to be an important factor, so are other neurotransmitters.
Research is now focused on the neurotransmitter glutamate.
The role of mutation:
Sz can take place in the absence of family history.
One explanation is DNA mutation in the parental DNA.
This can be caused by radiation, poison or viral infection.
Evidence for the role of mutation comes from a study showing a positive correlation between paternal age (increased risk of sperm mutation) and risk of Sz.
0.7% with fathers under 25 to over 2% in fathers over 50.
Shows that there are alternate explanations to the biological explanations.
Describe neural correlates of Schizophrenia, include 1 or more studies. (Biological explanations)(8 marks)
Measurements of the structure or function of the brain that correlate with and experience.
Neural correlates of negative symptoms:
Avolition, involves the loss of motivation. Motivation involves the anticipation of a reward, and the ventral striatum is believed to be involved in this anticipation.
Abnormality in the ventral striatum may be involved in the development of Sz.
Juckel - measured activity levels in the VS in Sz and found lower levels of activity than those in the controls.
Observed a negative correlation between activity levels in the VS and the severity of overall negative symptoms.
Thus activity in the VS is a neural correlate of the negative symptoms of Sz.
Neural correlates of positive symptoms:
Allen - scanned the brains of patients experiencing auditory hallucinations whilst they identified pre recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus were found in the hallucination group.
We can thus say that reduced activity in these 2 areas of the brain is a neural correlate of auditory hallucinations.
Describe and evaluate psychological theories of schizophrenia.
A01
Family dysfunction:
The schizophrenogenic mother:
Fromm-Reichm noted that many of her patients spoke pf a particular type of parent, which she called the Sz mother.
Schizophrenogenic = Schizophrenia causing.
The Sz mother is cold and rejecting and controlling, and tends to create a tense family climate.
This leads to distrust that later leads to paranoid delusions and ultimately Sz.
Double-blind theory:
The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed messages about what this is, and feel uncomfortable to comment on the unfairness of the situation.
When they get it wrong, the child is punished with withdrawal of love.
Their confusion of the world s reflected in symptoms like disorganised thinking and paranoid delusions.
This is just a risk factor and not the only causing factor.
Cognitive explanations:
Sz is associated with several types of abnormal info processing, and these can provide possible explanations for Sz as a whole.
This lower than usual level of info processing suggests that cognition is likely to be impaired.
Frith identified 2 types of dysfunctional thought processing that could underline some symptoms.
Metarepresentation:
The cognitive ability to reflect on thoughts and behaviour.
Allows us insight into our own goals and intentions.
We can interpret the actions of others.
Dysfunction would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves.
This would explain hallucinations and delusions.
Central control:
Cognitive ability to suppress automatic responses while we perform deliberate actions instead.
Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts.
E.g. sufferers tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these.
A03
Support for family dysfunction as a risk factor:
Read et al - reviewed 46 studies of child abuse and Sz and concluded that 69% of adult women in-patients with a diagnosis of Sz had a history of abuse in childhood.
For men the figure was 59%.
Berry et al - Adults with insecure attachments to their primary carers are also more likely to have Sz.
There is a large body of evidence linking family dysfunction to Sz.
Most of this evidence shares a weakness; info about childhood experiences was collected after the development of symptoms and the Sz may have distorted the patient’s experience. This creates a validity problem.
However, there is prospective evidence linking family dysfunction to Sz but not a huge amount and results have been inconsistent.
Strong evidence for dysfunctional info processing:
Stirling et al - compared 30 patients with a diagnosis of Sz with 18 non-patient controls on a range of cognitive tasks, including the stroop test.
Ppts have to name the ink colours of colour words, suppressing the impulse to read the words when doing this.
Sz patients took over twice as long to name ink colours compared to controls.
Although there is a mass of evidence similar to this to suggest that info processing is different in Sz patients, there is a problem.
Links between symptoms and faulty cognition are clear; however, this doesn’t tell us anything about the origins of those cognitions or of Sz.
Cognitive theories can explain the proximal causes of Sz but not the distal causes.
Evidence for biological factors is not adequately considered:
Psychological explanations of Sz can be difficult to reconcile with the biological explanations.
It could be that both biological and psychological factors can separately produce the same symptoms, which raises the question of whether both outcomes are really Sz.
Alternatively, we can view this in terms of the diathesis-stress model where the diathesis may be biological or psychological.
Describe Expressed emotion and schizophrenia in family dysfunction as a causing factor of schizophrenia.
Is the level of emotion, in particular negative emotion, expressed towards a patient by their carers.
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.
Serious source of stress for the patient.
This is primarily and explanation for relapse in patients with Sz.
It has also been suggested that it may be a source of stress that can trigger the onset of Sz in a person who is already vulnerable (diathesis-stress model).
Describe and evaluate antipsychotics as a treatment for schizophrenia.
A01
Typical antipsychotics:
There is a strong association between antipsychotics like chlorpromazine and the dopamine hypothesis.
Typical antisychotics work as antagonists in the dopamine system; reduce action of dopamine.
They block dopamine receptors in the synapses of the brain.
Initially when a patient begins taking chlorpromazine, the dopamine builds up, but then it’s production is reduced.
The dopamine-antagonist effect normalises neurotransmissions in key areas of the brain, reducing symptoms like hallucinations.
Chlorpromazine is also a sedative.
It is often used to calm patients down not only with sz but other disorders.
Atypical antipsychotics:
Clozapine:
Discovered to be more effective than typical antipsychotics.
Clozapine has potential serious side effects such as blood clotting and so it is only used when all else fails in treatment for Sz.
Clozapine binds to dopamine receptors but it also acts on serotonin and glutamate receptors.
It is believed that this helps improve mood and reduce depression and anxiety in patients.
May improve cognitive functioning.
It is sometimes prescribed when a patient is considered at a high risk of suicide; 30-50% of sz patients are suicidal at some point.
Risperidone:
Developed in an attempt to have a drug as effective as clozapine but without the side-effects.
Risperidone binds to dopamine and serotonin receptors.
It binds more strongly to dopamine receptors than clozapine and so is more effective in smaller doses.
A03
Evidence for effectiveness:
Thornley - reviewed studies comparing the effects of Chlorpromazine to controls in which patients received a placebo.
Data from 13 trials with a total of 1121 ppts showed that chlorpromazine was associated with better overall functioning and reduced symptom severity.
Data from 3 trials also showed that relapse rates were lower with chlorpromazine.
There is support for the benefits of atypical drugs.
Meltzer - concluded that clozapine is more effective than typical drugs and that it is effective in 30-50% of treatment-resistant cases where typical drugs have failed.
Evidence shows that antipsychotics are reasonably effective and this is a strength.
Problems with the evidence for effectiveness:
Although there is a mass of evidence to support the effectiveness of antipsychotics, there have been challenges to their effectiveness.
Healy - suggested that some successful trials have had their results published multiple times, exaggerating the evidence for positive effects.
Because antipsychotics have powerful calming effects, it easy to demonstrate that they have some positive effect on patients.
Not the same as saying they reduce symptoms.
Most published studies assess short term benefits rather than long-term benefits and compare patients who keep taking the drugs with those suffering withdrawal having just stopped taking them.
Use of antipsychotics depends on the dopamine hypothesis:
Theoretical issue.
There is a lot of evidence to suggest that the original dopamine hypothesis is not a complete explanation for Sz, and that in fact dopamine levels in parts of the brain other than the subcortex are too low rather than too high.
If this is true, it is not clear how antipsychotics which are antagonists can help with Sz when they reduce dopamine levels.
Our modern understanding of the relationship between dopamine and psychosis suggests that antipsychotics shouldn’t work.
This has undermined the faith in some people that antipsychotics do indeed work.
‘Cognitive behaviour therapy, family therapy and token economies are all used in the treatment and management of schizophrenia’. Discuss the use of these methods.
A01
CBT:
Takes place between 5-20 sessions.
Involves helping patients identify irrational thoughts and trying to change them.
This will not get rid of the symptoms of Sz but it can make patients better able to cope with them.
Patients can be helped to make sense of how their delusions and hallucinations impact on their feelings and behaviour.
Just understanding where symptoms come from can be hugely helpful.
Delusions can also be challenged so that a patient can come to learn that their beliefs are not real.
Family therapy:
Takes place with families rather than individual patients, aiming to improve the quality of communication and interaction between family members.
Some therapists see the family as the root cause of Sz (double blind and Sz mother).
Most family therapists are more concerned with reducing stress within the family that may contribute to risk of relapse.
Strategies that improve family functioning:
- Forming a therapeutic alliance with all family members.
- Reducing the stress of caring for patient.
- Reduction of anger and guilt in family members.
Pharoah - suggests that these strategies work by reducing stress and expressed emotion, whilst increasing the chances of patients’ complying with medication.
Token economies:
Reward systems used to manage the behaviour of patients.
In particular those who have developed a pattern of maladaptive behaviour.
Modifying bad habits does nor sure Sz but it improves the patient’s quality of life and makes it more likely that they can live outside a hospital setting.
The idea of tokens has been targeted as reinforcement.
The immediacy of the token is important because it prevents ‘delay discounting’; the reduced effect of a delayed reward.
Token economies are behavioural therapies based on operant conditioning.
Tokens are secondary reinforcers because they only have value once the patient has learned that they can be used to obtain rewards.
A03
Evidence for effectiveness:
Jauhar - Reviewed results of 34 studies of CBT for Sz.
They concluded that CBT has a significant but fairly small effect on the symptoms of Sz.
Pharoah - reviewed the evidence for the effectiveness of family therapy. Concluded that there is moderate evidence to show that family therapy significantly reduces hospital readmission over the course of a year and improves quality of life.
However, results of different studies were inconsistent.
Overall, the evidence base for family therapy is fairly weak.
A review of the evidence for token economies found only 3 studies where patients had been randomly allocated to conditions.
Only 1 of the 3 showed improvement in symptoms and none yielded useful info about behaviour change.
Overall there is only modest support for the effectiveness of psychological treatments and Sz remains one of the harder mental problems to treat.
Limitation.
Treatments improve quality of life but do not cure:
CBT helps by allowing patients to make sense of their symptoms; family therapy helps by reducing the stress on the family and the patient; token economies help by making patients’ behaviour more socially acceptable so that they can re-integrate into society.
These are all good things but they do not cure Sz.
Biological treatments don’t cure Sz but they reduce symptom severity and so can be seen as helping patients more as it gives them a sense of a better life without their symptoms.
The failure to cure Sz is a weakness of psychological treatments.
Ethical issues:
Token economy systems have proven controversial.
The major issue is that privileges and services become more available to patients with mild symptoms and less for those with more severe symptoms that prevent them from complying with desirable behaviours.
Means that the most severely ill suffer from discrimination.
This has in turn reduced the use of token economy systems.
CBT may involve challenging an individual’s paranoia, but to what point does this interfere with an individual’s freedom of thought?
Describe and evaluate the interactionist approach to both explaining and treating schizophrenia.
A01
This approach acknowledges that there are biological, psychological and societal factors in the development of Sz.
Explaining the interactionist approach: the diathesis-stress model:
The diathesis-stress model says that both a vulnerability to Sz and a stress-trigger are necessary in order to develop Sz.
Meehl’s model:
The original diathesis-stress model (DSM) was entirely genetic; the result of a single ‘schizogene’.
This led to the development of a biologically based schizotypic personality.
If a person does not have the schizogene then no amount of stress can lead to Sz, but if they do and they have childhood trauma, this could result inSz.
The modern understanding of diathesis:
Many genes now each appear to increase genetic vulnerability slightly.
Modern views also include a range of other factors beyond genetic, including psychological trauma.
Read proposed a neurodevelopmental model in which early trauma alters the developing brain, e.g. the HPA system can become over-active, making the person more vulnerable to later stress.
The modern understanding of stress:
Stress was seen as psychological in nature in original model.
A modern definition of stress includes anything that risks triggering an episode of Sz.
Treatment according to the interactionist model:
Compatible with both biological and psychological treatments.
The model is associated with combining antipsychotic drugs with psychological therapies.
It is possible to believe in biological causes of Sz and still practise CBT to relieve psychological symptoms.
In Britain, it is increasingly common to treat patients with a combination of the 2.
It is unusual to treat Sz using psychological therapies only because patients need their symptoms to be reduced so that they can be coherent and understand the processes of therapy.
A03
Evidence for the role of vulnerability and triggers:
Tienari et al - investigated the combination of genetic vulnerability and parenting style. Children adopted from 19,000 Finnish mothers with Sz were followed up.
A child-rearing style characterised by high levels of criticism and conflict was implicated in the development of Sz but only for children with a high genetic vulnerability.
This suggests that both genetic vulnerability and family stress are important in the development of Sz.
This is very strong support for the importance of adopting an interactionist approach to Sz, including hanging onto the idea that poor parenting is a possible source of stress.
Support for the effectiveness of combination of treatments:
Studies show an advantage to using combinations of treatments for Sz.
Tarrier - 315 patients were randomly allocated to a medication + CBT group, medication + supportive counselling or just medication.
Patients in the 2 combination groups showed lower symptom levels than those in control group.
Studies like this show that there is a clear practical advantage of adopting an intersactionist approach in the form of superior treatment outcomes, and therefore highlight the importance of taking the interactionist approach.
The treatment-causation fallacy:
Turkington argues that there is a good fit between the interactionist approach and using combination treatments.
However, the fact that combined biological and psychological treatments are more effective than either on their own doesn’t mean the interactionist approach is correct.
