Schizophrenia Flashcards
Classification
The process of organising symptoms into categories based on which symptoms cluster together in people with mental disorders using the ICD-10 OR DSM-5 (statistical manuals)
DIagnosis
The process of identifying and determining the nature of a disease or disorder by its signs and symptoms, through the use of assessment techniques
Schizophrenia
A psychotic disorder marked by severely impaired thinking, emotions and behaviours, in which contact is lost with external reality
Positive symptoms
The changes or add-ons to normal behaviour
Negative symptoms
The symptoms that appear to reflect a reduction or loss of normal functions which often persist during periods of low positive symptoms
Hallucinations
hearing, seeing or feeling things that no one does
Delusions
Beliefs that seem strange to mose people and are often easy to prove wrong
Speech poverty
Lessening of speech fluency and productivity which reflects slowing or blocked thoughts
Avolition
Reduction of interests and desires as well as an inability to initiate and persist in goal-directed behaviour
Diagnosis “in remission”
A decrease or disappearance of symptoms
Symptom overlap
Many symptoms found in one disorder are also found in another
Co-morbidity
refers to the extent that 2 or more conditions can occur at the same time
Polygenic
Caused by multiple genes
Hyperdopaminergia
Processing involving high levels of dopamine
The dopamine hypothesis
Suggests that an excess of the neurotransmitter dopamine receptors in certain regions of the brain is associated with the symptoms of schizophrenia
Dopamine antagonist
Stimulates the nerve cells containing dopamine causing the synapse to be flooded with it
The revised dopamine hypothesis
Davis and Khan proposed the revised dopamine hypothesis which states that whilst the positive symptoms of SZ are caused by an excess of dopamine in subcortical areas of the brain including the mesolimbic pathway, the negative and cognitive symptoms arise from a deficit of dopamine in areas of the prefrontal cortex (hypodopaminergic) which is responsible for thinking and decision making.
Neural correlates
The difference in biostructure between schizophrenic sufferers and others
Antipsychotics
Drugs that are most effective in treating the most disturbing forms of psychotic illness
Typical Antipsychotics
Primarily combats the positive symptoms
Atypical Antipsychotics
Combats the positive and potentially the negative symptoms as well
Extrapyramidal side-effects
Long term side effect of taking Antipsychotics
Rapid dissociation
Temporal binding to the D2 receptors
Family dysfunction
Claims that schizophrenia is caused by abnormal patterns of communication within the family which may bias an individual toward developing negative schemas
Double-bind
The idea that children who frequently receive contradictory messages from their parents, especially on a verbal and non-verbal level are more likely to develop schizophrenia
High expressed emotion
when the members of a family talk about a patient in a critical or hostile manner or n a way that indicates over-involvement or over-concern
Meta representation
The Cognitive ability to reflect on thoughts and behaviour and have insights to our own intentions and goals
Central control
The ability to suppress automatic responses while we perform deliberate actions
Proximal cause
The immediate cause of a disorder
Distal cause
The underlying cause of a disorder
CBTp
A cognitive behavioural therapy which aims to provide treatment for residual symptoms that persist despite the use of antipsychotics
Engagement
The therapist empathise with the patients’ perspective and their feelings of distress, which may act as motivation to continue
Assessment
The patient expresses their thoughts about their experiences to the therapist
Normalisation
Teaching patients that many people have unusual experiences which can reduce anxiety and the sense of isolation
Critical collaborative analysis
The therapists use of gentle questioning to help the patient understand illogical deductions and conclusions
Developing alternative explanations
Helping the patient to d develop these for the previously unhealthy assumptions
Psychoeducation
Helping a person and their carers to understand and be better able to deal with the illness
Token economies
A form of behavioural therapy based on operant and classical conditioning where clinicians set target behaviours that they believe will improve the patients’ engagement in daily activities
Operant conditioning
Learning by reinforcement; that is rewarding good behaviour and removing stimuli to reduce bad behaviour
Classical conditioning
learning by association
Tokens
Items awarded that can be exchanged for a variety of different privileges and rewards
Primary reinforcer
The reinforcing stimulus which may take the form of food, priveleges and other incentives which can be gained through tokens after target behaviour is met
Secondary reinforcer
The neutral token which has been associated with the primary reinforcer
Interactionist approach
An approach that acknowledges that there are biological, societal and factors that lead to schizophrenia
Diathesis-Stress model
An explanation for schizophrenia that states that schizophrenia stems from genetic vulnerability and stress factors
Define classification, diagnosis and SZ
Classification is the process of organising symptoms into categories based on which symptoms cluster together in people with mental disorders. A diagnosis is the process of identifying and determining the nature of a disease by its signs and symptoms through the use of assessment and techniques. Schizophrenia is a psychotic disorder marked by severely impaired thinking, emotions and behaviours, in which contact is lost with external reality. It is characterised by an inability to filter sensory stimuli due to an enhanced perception of sensory information
How is SZ diagnosed
Schizophrenia is diagnosed using statistical manuals such as ICD-10 which requires two or more positive symptoms (in the EU) and DSM-V which requires one negative symptom(in America). Symptoms are compared to give an overall score.
Define and give examples of the positive and negative symptoms of SZ
Positive symptoms refer to changes which are ‘add-ons’ to normal behaviour, including hallucination (hearing, seeing, feeling or smelling things that are not there such as voices) and delusions (belief that seem strange to most people and are easy to prove wrong). Negative symptoms reflect a reduction or loss of normal behaviour including speech poverty (the lessening of speech fluency and productivity reflecting slowing or blocked thoughts characterised by fewer words, less complete syntax and a delay in verbal responses) and avolition (a reduction in interests and desires as well as an inability to initiate and persist in goal-directed behaviour).
What is the key study of classification and diagnosis of SZ?
Because the condition is so varied amongst sufferers and the symptoms are subjective experiences, it may be difficult to accurately identify and classify. Rosenhan aimed to investigate how situational factors affect a diagnosis of schizophrenia by having 8 sane confederates go into 12 different psychiatric hospitals as pseudo patients seeking a diagnosis. They claimed to hear voices but stopped pretending, wrote observations and behaved normally when they were in the ward. They were only discharged when they convinced staff that they were sane. On admission, staff diagnosed 11 pseudo patients with SZ and one with manic depression with an average hospital stay of 19 days. They were all discharged with diagnosis of SZ ‘in remission’. 35 real patients detected sanity. It was thus concluded that psychiatrists cannot really tell the difference between an insane and sane person, calling into question the reliability and validity of a schizophrenia diagnosis and suggesting the DSM was flawed
Evaluate diagnosis and Classification of SZ
Several studies have found low reliability in diagnosing and classifying DZ.
When trialling the DSM-V, Reiger found a kappa score (of agreement) of 0.46 between clinicians.
Cheniaux et al asked two psychiatrists to independently diagnose 100 patients using both DSM and ICD criteria. One psychiatrist diagnosed 26 with SZ using the DSM and 44 using the ICD while another diagnosed 13 with the DSM and 24 using the ICD.
Osozio found that the DSM V has produced some evidence of very high reliability of about 0.96 for Inter-rater and +0.92 for test-retest reliability.
These studies suggest that poor reliability is a weakness of classifying and diagnosing SZ. However, these are historical issues that are improving.
There are issues in diagnosing and classifying SZ.
Luhrman found Asian and African ppts had playful voices that offered advice, compared to negative and intrusive voices reported by US ppts. Negative voices may be seen as a western phenomenon.
SZ diagnoses for Africans and Indians are higher in predominantly white countries compared to countries of origin. Untrusting and judging white clinicians may explain this or cultural associations with having voices leading to higher self-reporting.
This could be due to the stress of fitting in and/or discrimination in a new country rather than doctors.
SZ experiences and diagnoses may depend on culture and interaction with clinicians, reducing the validity of the diagnosis and classification.
There is significant overlap between the symptoms of SZ and other conditions.
Both SZ and bipolar disorder involve positive symptoms like delusional dn negative symptoms like avolition.
Ellason and Ross have shown that individuals with dissociative identity disorder may have more symptoms of SZ than diagnosed schizophrenics. Indeed, most schizophrenics have met sufficient criteria to be diagnosed with a range of other conditions according to Read.
This is a weakness as the same patient with the same conditions may be given another diagnosis depending on how the criteria are applied or SZ and bipolar disorder are the same condition. Therefore, the diagnosis and classification are neither reliable nor valid
Outline the family study into the genetic explanation of SZ
Family studies by Gottesman and Shields found individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives. They have established that schizophrenia is more common among biological relatives of a sufferer and that the closer the degree of genetic relatedness, the greater the risk. For example, Gottesman et al found that children with two schizophrenic patients had a concordance rate of 46% while children with one schizophrenic patient had a rate of 13% and siblings a rate of 9%. There is a 17% chance of developing SZ in families in which the identical twin of one parent has SZ
Outline the twin study of the genetic explanation of SZ
In a twin study, Rikke Hilker calculates the pooled date for all SZ twin studies carried out prior to 2001 and found a concordance rate of 33% for MZ and 7% for DZ twins, supporting the genetic position as the concordance rate for MZ twins is many times higher than DZ twins. Gottesman also reported that the concordance rate for identical twins brought up apart was very similar to that for identical twins brought up together, suggesting that the high concordance rate for identical twins is not due to them being treated in a very similar way within the family.
Outline the adoption study into the genetic explanation of SZ
Because of the difficulties of disentangling genetic and environmental factors for individuals who share genes and environment, adoption studies are carried out using individuals who have been reared apart. Tienari et al did this in Finland using 164 adoptees whose biological mothers has been diagnosed with schizophrenia, 11 also received a diagnosis of SZ compared to just 4 of the 197 controls adoptees who were born to non-schizophrenic mothers. It was concluded that these findings showed that the genetic liability to SZ supported by empirical evidence.
Evaluate the genetic explanation for SZ
There is an issue with twin studies.
A critical assumption underlying twin studies is that the environment of MZ and DZ twins is equivalent. However, MZ twins are more likely to share a similar environment, experience more ‘identity confusion’ and be treated the same or more similarly than DZ twins according to Joseph.
Therefore, it is uncertain whether their behavioural similarity (known as concordance) in this case the experience of SZ is due to genetic similarity or shared environment.
This is a weakness as a shared environment is a confounding variable within the twin study that reduces the certainty that the concordance was the result of genetic factors alone.
It can be argued that genetics are not the only factor in the development of SZ.
As concordance rates are not 100% for MZ twins, environmental factors must explain why some who have the genetic predisposition don’t go on to develop SZ.
Some have argued that genes are only a risk factor which would require the presence of other risk factors in order to develop SZ. There is a wide body of evidence linking SZ with family experience, urban environments and ethnic minority.
This is therefore a weakness as the genetic explanation for SZ has not satisfactorily separated nature-nurture influences. It can also be described as reductionist as it fails to fully consider environmental explanations as causal factors.
Outline the dopamine hypothesis
The dopamine hypothesis suggests that an excess of the neurotransmitter dopamine receptors in certain regions of the brain is associated with the symptoms of SZ—Hyperdopaminergia. Schizophrenics are thought to have an abnormally large number of D2 receiving neurons that are over-sensitive and bind with dopamine too easily or too often, leading to more dopamine binding and positive symptoms such as hallucinations and delusions. This key role played by dopamine was highlighted in research into medication that reduces and increases dopaminergic activity.
Application of the dopamine hypothesis with examples
An example of a drug that increases dopaminergic activity is amphetamine, a dopamine antagonist which stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter. This would lead to hallucinations and delusions in ‘normal’ individuals that would disappear following abstinence from the drug. Likewise, some people who suffer from Parkinson’s disease, a neurodegenerative disease categorised by low levels of dopamine, who take the drug L-Dopa to raise their dopamine levels have been found to develop SZ type symptoms according to Grilly.
However, there are many different types of antipsychotic drugs which block the activity of dopamine in the brain. By reducing the activity in the neural pathways affected by this neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions. Thus, these drugs are referred to as dopamine antagonists.
Evaluate the dopamine hypothesis
There is evidence supporting the dopamine hypothesis from treatment.
Much of the evidence supporting the dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain.
The basic mechanism of antipsychotic drugs is to reduce the effects of dopamine imbalances and so reduce the symptoms of SZ. For example, Leucht et al carried out a meta-analysis of 212 studies that had analysed the effectiveness of different antipsychotic drugs compared with a placebo. They found that all drugs tested were significantly more effective than placebo in the treatment of positive and negative symptoms, achieved through the normalisation of dopamine.
This is a strength as it is reliable and empirical evidence supporting the Hyperdopaminergia hypothesis.
There is inconclusive supporting evidence.
Moncrieff claims that evidence for the dopamine hypothesis of SZ is far from conclusive, e.g although stimulant drugs such as cocaine and amphetamine have been shown to induce schizophrenic episodes, such stimulants are known to affect many neurotransmitters other then dopamine.
Likewise, evidence for dopamine concentrations in Post-mortem brain tissue has either been negative or inconclusive. Moncrieff also points out that other confounding sources of dopamine release, such as stress or smoking, have rarely been considered.
Therefore, she suggests the idea that the symptoms of SZ are caused by the overactivity of the dopaminergic system is not supported by current evidence.
There are some challenges to the dopamine hypothesis.
Noll claims that there is strong evidence against both the original dopamine hypothesis and the revised dopamine hypothesis. He argues that antipsychotic drugs do not alleviate hallucinations and delusions in about one-third of people experiencing these problems.
Noll also points out that, in some people, hallucinations and delusions are present even though dopamine levels are normal. Blocking D2 receptors of these people has little to no effect on their symptoms.
This suggests that, rather than dopamine being the sole cause of positive symptoms, other neurotransmitter systems may also produce the positive symptoms of SZ.
Outline neural correlates as an explanation for SZ
Neural correlates are measurements of the structure or function of the brain that correlates with an experience. By studying neural correlates, researchers aim to identify the differences in biostructure between SZ sufferers and others.
Juckel et al measured the activity levels in the ventral striatum (the centre region of the brain involved in motivation and believed to be involved in the development of avolition) and found lower levels of activity in SZ patients than in a control group. Also, there was a negative correlation linking lower activity levels to more severe SZ symptoms (e.g motivation decreased).
Allen et al scanned brains of patients experiencing auditory hallucinations and compared them to a control group. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group.
Evaluate neural correlates
There are issues with cause and effect when evaluating the role of neural systems in the onset of SZ symptoms.
For example, it is unclear whether lower levels of activity in the anterior cingulate gyrus is the cause of SZ symptoms or an effect of SZ symptoms, as it is equally logically plausible that these symptoms cause a lower level of activity in that particular neural network.
Equally, it is also possible that a 3rd factor variable, possible as yet unknown, causes both the symptoms and the lower level of neural activity.
This is a weakness as the underactivity in a particular neural network is only correlated with the SZ symptoms and as a result, it cannot be said with any certainty that the neural network is the cause of the SZ symptoms.
Briefly explain drug therapy and how it is used to help sufferers
Antipsychotics are the most effective in treating the most disturbing forms of psychotic illness such as SZ. They help the person function as well as possible while increasing their feelings of subjective well-being. They are usually recommended as the initial treatment for the symptoms after which a combination of medication and psychological therapies are suggested. All antipsychotics work by reducing dopaminergic transmission; i.e reducing the action of dopamine in areas of the brain associated with schizophrenic symptoms. Antipsychotics can be typical or atypical.
Explain typical Antipsychotics
Typical, also known as ‘conventional’, antipsychotics are used primarily to combat the positive symptoms such as thought disturbances by reducing the effects of dopamine. They are dopamine antagonists, such as chlorpromazine, in that they bind to but do not stimulate dopamine receptors (particularly the D2 receptors in the subcortical dopamine pathways), thus blocking their action. This links to research findings that correlates hyperdopaminergia in the subcortex with SZ symptoms. These antipsychotics also have a significant effect which aids the general treatment and management of the most behaviourally erratic and anxious SZ patients. Hallucination and delusion usually diminish a few days of beginning medication, although other symptoms may take several weeks before a significant improvement is noted. This has led to the development of the dopamine hypothesis.
What did Kapur et al state regarding drug therapy?
Kapur et al estimate that between 60% and 75% of D2 receptors in the mesolimbic Pathway must be blocked for these drugs to be effective. A similar number of D2 receptors in other areas of the brain must also be blocked, leading to undesirable side effects.
Explain atypical antipsychotics
Atypical antipsychotics, also known as ‘second-generation’ antipsychotics, combat these positive symptoms and have some beneficial effects on negative symptoms as well by also blocking D2 receptors. There are three main differences between atypical and typical antipsychotics including they carry a lower risk of Extrapyramidal side effects, they have a beneficial effect on negative symptoms and cognitive impairment and are suitable for treatment-resistant symptoms. They only temporarily occupy the D2 receptors and rapidly dissociate to allow normal dopamine transmission. It also acts on serotonin and glutamate receptors which helps to improve mood and reduce depression and may improve cognitive functioning. Clozapine is described when a patient is considered at high risk of suicide.
Evaluate drug therapy
There is a large body of evidence to support the idea that antipsychotics are moderately effective in reducing symptoms of SZ.
Thornley et al reviewed studies comparing the effects of chlorpromazine to patients receiving a placebo. A total of 1121 ppts has better overall functioning and the severity of symptoms was reduced for the antipsychotic drug group rather than the placebo group.
Furthermore, Meltzer supported the benefits of atypical antipsychotics. Clozapine was concluded to be more effective than typical Antipsychotics and found it was effective in 30 to 50% of treatment-resistant cases where typical antipsychotics had failed.
Therefore, empirical evidence suggests that antipsychotics are a reasonable treatment of SZ symptoms.
A serious issue with antipsychotic drugs is the likelihood of side effects.
Firstly, typical Antipsychotics are linked to side effects such as dizziness, stiff jaw, itchy skin , weight gain and sleeplessness. Long term use can result in Extrapyramidal side-effects such as tardive dyskinesia (involuntary facial movements such as lip smacking). Most serious side effects of typical Antipsychotics is neuroleptic malignant syndrome (NMS) which results in high temperature, delirium, coma and can be fatal. This is believed to be due to the effects interfering with dopamine transmission to the hypothalamus (which regulates various homeostatic systems).
Despite Atypical antipsychotics being developed to reduce the frequency of side effects, they do still have some side effects such as agranulocytosis (a lowered white blood cell count) which patients have to regularly take a test for.
These are significant weaknesses as they will cause significant distress to SZ sufferers which may cause further disruption to their daily lives and may also lead to cessation of drug therapy and an increased relapse rate.
Undergoing drug therapy for SZ may influence patients’ motivation to consider possible environmental triggers of their condition.
This is because the taking of medication suggests that there is something wrong with them and that it is a biological fact that the medication will target and resolve according to Reed. This, in turn, reduced their motivation to look for possible solutions that might alleviate these stressor and reduce their suffering.
In fact, a number of international surveys have shown that the public when asked what causes SZ cite social factors such as poverty and traumatic childhoods far more than biological factors according to Reed and Haslam, suggesting that environmental factors are the trigger and psychological therapies would need to be considered rather than a sole dependency on drug therapy as treatment.
This is a weakness as this may result in the causes of the symptoms remaining and therefore the symptoms themselves continue to have a disruptive effect on the sufferer’s life.
What do explanations based on family dysfunction claim?
Explanations based on family dysfunction claim that schizophrenia is caused by abnormal patterns of communication within the family which could lead to abnormalities in cognitive functions and can bias an individual towards developing cognitive schemas that can see the world in a more threatening manner.
Explain the double-bind theory
Gregory Bateson suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia. This is referred to as the double bind theory, which Bates on refers to as only a risk factor, and it suggests that when a child receives conflicting messages on a verbal and non-verbal level, they regularly find themselves trapped in situations where they fear doing the wrong thing and they feel unable to comment on the unfairness of the situation or seek clarification. When they make the wrong choice, which is often, they are punished by withdrawal of love which leaves them with an understanding that the world is confusing and dangerous and this is reflected in their emotions like disorganised things and paranoid delusions.
Explain expressed emotion
An explanation for relapse in patients with schizophrenia is expressed emotion which has been suggested to be a source of stress that can trigger the onset of schizophrenia in vulnerable people. Expressed emotion is a family communication style in which members of a family of a psychiatric patient talk about the patient in a critical or hostile manner or in a way that indicates emotional over-involvement with the patient or their behaviour. For example, research by Kuipers et al found that high EE relatives talk more and listen less. A patient returning to a family with high EE is about 4 times more likely to relapse than a patient whose family is low in EE according to Linszen. Furthermore, Noll states that sufferers have a lower tolerance for intense environmental stimuli so a negative emotional climate arouses the patient and leads to stress beyond their impaired coping mechanisms, triggering a schizophrenic episode. In contrast, a family environment that is relatively supportive and emotionally demanding may help the person to reduce their dependence on medication and reduce the likelihood of a relapseAn explanation for relapse in patients with schizophrenia is expressed emotion which has been suggested to be a source of stress that can trigger the onset of schizophrenia in vulnerable people. Expressed emotion is a family communication style in which members of a family of a psychiatric patient talk about the patient in a critical or hostile manner or in a way that indicates emotional over-involvement with the patient or their behaviour. For example, research by Kuipers et al found that high EE relatives talk more and listen less. A patient returning to a family with high EE is about 4 times more likely to relapse than a patient whose family is low in EE according to Linszen. Furthermore, Noll states that sufferers have a lower tolerance for intense environmental stimuli so a negative emotional climate arouses the patient and leads to stress beyond their impaired coping mechanisms, triggering a schizophrenic episode. In contrast, a family environment that is relatively supportive and emotionally demanding may help the person to reduce their dependence on medication and reduce the likelihood of a relapse
Evaluate family dysfunction
There is evidence to suggest difficult family relationships in childhoods associated with risk of SZ in adulthood.
Read et al reviewed 46 studies of child abuse and SZ and found that 69% of adult women and 59% of males had a history of physical abuse in childhood.
This shows that there is a link between childhood experiences and vulnerability to SZ.
However, there are issues with validity of this research as data is collected after the development of symptoms so SZ may have distorted the patients recall of childhood experiences.
This is reliable evidence suggesting that family dysfunction is a risk factor for the onset of SZ.
There is supporting evidence from adoption studies.
Tienari et al found during a study of 19,000 participants that adopted children with biological SZ parents were more likely to develop SZ symptoms if the adoptive family was rated as disturbed.
This supports the role of family dysfunction as a causal factor in the development of SZ.
At the same time, it supports the biological explanation as well, as genetic vulnerability was also required.
This is a strength because it is large scale empirical evidence from real-life situations over three decades that demonstrates a link between family dysfunction and SZ diagnoses and gives the explanation scientific credibility.
There is specific reluctance to pursue Double-blind as an explanation.
This theory was based on clinical observations of patients and assessing the personality of parents (typically/historically the mother) of SZ patients for crazy-making characteristics.
Historical blame of parents who, not least of all, are often responsible for the care of SZ sufferers, described as adding insult to injury, literally.
This is a weakness as these explanations are not tolerated by or accepted by parents and can be seen as inappropriate.
Explain cognitive explanations
Compared to normal controls, research has found evidence of dysfunctional thought processing in people with schizophrenia, i.e they process information differently to those without the disorder.
Cognitive Explanations of SZ emphasize the role of dysfunctional thought processing, particularly evident in those who display the characteristic positive symptoms of SZ such as delusions and hallucinations.
Who identidided the kinds of dysfunctional thought processing and what are they?
Frith et al identified 2 kinds of dysfunctional thought processing that could underlie some symptoms:
Meta-representation: the cognitive ability to reflect on thoughts and behaviour, giving insight to personal intentions and goals and interpreting the actions of others. A dysfunction in meta-representation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than by others. This would explain hallucination of voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others).
Central control: the cognitive ability to suppress automatic responses and to perform deliberate actions instead. This could result in symptoms such as disorganised speech and thought disorder. For example, 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.
Evaluate cognitive explanations
There is empirical evidence demonstrating cognitive deficits amongst SZ patients.
Stirling et al compared 30 patients with a diagnosis of SZ with 18 non-patient controls on a cognitive test called the Stroop task. SZ patients took twice the amount of time as the controls to name the link colour.
The suggestion is that they had more difficulty in suppressing the impulse to read the words which central control could enable them to do.
This is a strength as it is evidence for differences in information processing in the minds of SZ patients thereby supporting cognitive explanations.
Cognitive Explanations do not directly identify a possible cause for cognitive differences between sufferers and non-sufferers.
There are numerous studies that identify cognitive differences between SZ patients and non-SZ controls but there is no clear evidence as to why these differences exist (these can be described as proximal causes).
For example, lower ‘central control’ may have a genetic origin; or it may be due to imbalances in neurochemistry or even damage to a particular neural network. It is possible to argue that cognitive dysfunctions may be effects of another cause, as yet unspecified (known as the distal cause).
Cognitive Explanations can be seen as describing the behaviour of SZ patients but not explaining the causes and, for this reason, do not provide a clear and complete explanation for the onset of SZ.
How does CBTp help SZ
NICE (The National Institute for Health and Care Excellence) recommends that all people with schizophrenia are offered cognitive behavioural therapy. CBTp (Cognitive behavioural therapy for psychosis) in schizophrenia was originally developed to provide treatment for residual symptoms (such as hallucinations, negative symptoms, thought disturbances and delusions) that persist despite the use of antipsychotic medication. CBTp aims to make them easier to cope with rather than cure tham. It can be delivered in groups, but it is more usual to deliver on a one-to-one basis in at least 16 sessions.
The goal is to reduce distress caused by symptoms by changing the patients’ interpretations about the nature and consequences of the symptoms. CBTp is used to help people make sense of how their delusions and hallucinations impact their thoughts, actions and level of functioning by helping patients to consider alternative ways of explaining their feelings and behaviours. CBTp assumes that people often have irrational beliefs which influence their feelings and behaviours in maladaptive ways. These can lead to cognitive biases and faulty interpretations and even result in delusions. CBTp helps the patient to identify and correct these faulty interpretations. CBTp also reduces the distress caused by hallucinations by exploring the beliefs about the voices. Chadwick and Birchwood found that voices themselves do not cause distress, but they influence beliefs regarding the voices which in turn causes distress e.g beliefs that voices are in control.
How does CBTp work?
CBTp usually begins with an assessment where the patient expresses their experiences to the therapist, sets realistic goals and uses the current distress as motivation to change. Then, there is engagement where the therapist empathizes with the patient’s perspective and feelings of distress and stresses that explanations can develop together.
Finally, the ABC model is used where the patient gives their explanation of the activating events, especially any that trigger thoughts and beliefs to cause emotional and behavioural consequences. This belief can then be rationalised, disputed and changed through normalisation (the idea that many people have unusual experiences under different circumstances which reduces anxiety and isolation and possibility of recovery seems likely), critical collaborative analysis (using gentle questioning to help the patient understand illogical deductions and conclusions) and developing alternative explanations for their previously unhealthy assumptions by pointing out inconsistencies in the patient’s belief system and eliciting other interpretations. The patient may also be guided in reality-testing their beliefs where the therapist will encourage the patient to engage in specific behaviours for the purpose of testing the validity of their belief.
Evaluate CBTp
There are advantages of CBTp over standard care.
The NICE review of treatments for schizophrenia found consistent evidence that when compared with standard care (antipsychotics medication alone), CBTp was effective in reducing hospitalisation rates up to 18 months following the end of treatment.
CBTp was also shown to be effective in reducing symptom severity and, when compared to patients receiving standard care, there was some evidence for improvements in social functioning.
However, most of the studies in effectiveness of CBTp have been conducted with patients treated at the same time with antipsychotics medication. It’s difficult, therefore, to assess effectiveness of CBTp independent of antipsychotic medication.
This is a strength as it is empirical evidence for the effectiveness of CBTp to bring about improvements in patients’ quality of life.
Effectiveness of CBTp is dependent on the stage of the disorder.
CBTp appears to be more effective when it is made available at specific stages of the disorder and when the delivery of the treatment is adjusted to the stage that the individual is currently at. For example, Addington and Addington claim that, in the initial phase of schizophrenia, self-reflection is not particularly appropriate due to significant cognitive impairment.
Following stabilisation of the psychotic symptoms with antipsychotic medication, however, individuals can benefit more from group based CBTp. This can help normalise their experience by meeting other individuals with similar issues. Research has consistently shown that it is individuals with more experience of their schizophrenia and a greater realisation of their problems that benefit more than individual CBTp.
The effectiveness of CBTp may vary depending on the stage of the illness that the patient is in. This needs to be considered in order to fully evaluate the effectiveness and appropriateness of CBTp.
The benefits of CBTp may be overstated.
More recent and methodologically sound meta-analysis of the effectiveness of CBTp as a sole treatment for schizophrenia suggests that its effectiveness may actually be lower than originally thought. One recent large-scale meta-analysis by Jauhar revealed only a small therapeutic effect on the key symptoms of schizophrenia, such as hallucinations and delusions. However, even these small effects disappeared when symptoms were assessed ‘blind’; i.e when assessors were unaware of whether the patient was in the therapy or control condition.
Many studies of the effectiveness of CBTp appear to have similar design problems and, in their meta-analysis, this uncertainty over whether non-drug therapies such as CBTp really do offer superior outcomes to antipsychotic medications has led to conflicting recommendations even within the UK according to Taylor and Perera. In England and Wales, NICE emphasizes non-drug therapies such as CBTp, whereas in Scotland, SIGN places more emphasis on antipsychotic medications.
There are weaknesses in the scientific credibility of the evidence in support of CBTp and therefore uncertainty as to its effectiveness.
Why is family therapy recommended?
Family intervention in the treatment of schizophrenia has developed as a result of studies of the family environment and its possible role in affecting the course of the disorder. Research has found that the long term outcome of a sufferer could depend on their relationship with carers; e.g poor relationships could lead to consequences such as a relapse. Therefore, family therapy aims to make family life less stressful and so reduce.
Family therapy is the name given to a range of interventions aimed at the family of someone with schizophrenia and NICE recommends that it should be offered to all individuals diagnosed with schizophrenia who are in contact with or who live with family members, especially with frequent symptoms or high risk of relapse. It reduces this by encouraging the family members to listen to each other and discuss problems and potential solutions together
How is family therapy implemented and how does it aim to help the sufferer?
Family therapy is typically offered for a period of between 3 and 12 months and at least 10 sessions and it is aimed at reducing the level of expressed emotions within the family as high expressed emotion makes a patient 4 times more likely to relapse according Linszen et al. Family therapy typically provides the family with information about the disorder and ways to support the sufferer. It should also involve the person with psychosis as they are often suspicious about their treatment and an involvement overcomes this problem.
Family therapy treatments
Family therapy includes a range of strategies such as: psychoeducation (helping the person and their carers to understand and be better able to deal with the illness), forming an alliance with relatives who care for the person with schizophrenia, reducing the emotional climate with the family and the burden of care for family members, enhancing relatives’ ability to anticipate and solve problems, reducing expressions of anger and guilt by family members, maintaining reasonable expectations among family members for patient performance and encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed.
key study of family therapy
Pharoah et al investigated the effectiveness of family therapy by reviewing 53 studies between 2002 and 2010 conducted in Europe, Asia and North America which compared outcomes from family therapy to standard care alone. They found that evidence of mental state was mixed as some found improvement while others didn’t, compliance with medication increased, there wasn’t much effect on social functioning and there was a reduction in relapse and readmission.
Evaluate family therapy
There is doubt as to the cause of the effectiveness of family therapy.
Pharoah et al’s meta-analysis established that family therapy can be effective in improving clinical outcomes such as mental state and social functioning.
However, the authors suggest that the main reason for its effectiveness may have less to do with any improvements in these clinical markers and more to do with the fact that it increases medication compliance so patients are more likely to reap the benefits of medication because they are more likely to comply with their medication.
This is a weakness as the possibility of medication compliance being an intervening variable questions the effectiveness of family therapy.
There is evidence of the positive effect of family therapy on family members.
Family therapy has been shown to improve outcomes for the individual with schizophrenia but there may be an additional advantage in that they have a positive impact on the family members as well.
Lobban et al analysed the results of 50 family therapy studies that had included an intervention to support relatives. 60% of these studies reported a significant positive impact of the intervention on at least one outcome for category for relatives e.g coping and problem-solving skills, family functioning and relationship quality (including expressed emotion)
However, the researchers also concluded that the methodological quality of the studies was generally poor, making it difficult to distinguish effective from ineffective interventions.
This is a strength as it improves the quality of life of carers and sufferers likely benefit from more effective care.
There are doubts as to the effectiveness of family therapy.
A study by Garetu et al failed to show any better outcomes for patients given sessions of family therapy compared to those who simply had carers but not fairly therapy. Individuals in both groups were found to have unexpectedly low rates of relapse, contrasting markedly with the rates found in the ‘No carer’ group. The researchers found that most of the carers in this study displayed relatively low rates of expressed emotion, which may reflect widespread cultural changes in carers’ knowledge and attitudes of schizophrenia.
Garety et al suggests that, for many people, family intervention may not improve outcomes further than a good standard of treatment (antipsychotics drugs) as usual.
This is a weakness as evidence challenged the effectiveness of family therapy, suggesting that it might not be useful or necessary for sufferers and families, providing they are provided with good quality care.
Evaluate token economy
There is supporting research for token economy
Dickerson et al have provided research support for the effectiveness of token economies in psychiatric settings. The reviews 13 studies of the use of token economy systems in the treatment of schizophrenia. 11 of these studies had reported beneficial effects that were directly attributable to the use of token economies
Dickerson et al concluded that, overall, these studies provide evidence of the token economy’s effectiveness in increasing the adaptive behaviours of patients with schizophrenia.
However, they did caution that many of the studies reviewed had significant methodological shortcomings that limited their impact in the overall assessment of token economies in this context
There is reliable empirical evidence for the effectiveness of token economies as it improves their ability to cope with everyday life and therefore the quality of life.
There are difficulties assessing the success of token economies.
Comer suggests that a major problem in assessing the effectiveness of token economies is that studies of their use tend to be uncontrolled. When a token economy system is introduced into a psychiatric ward, typically all patients are brought into the programme rather than having an experimental group that goes through token economy and a control group that does not.
As a result, patients’ improvement can only be compared with their past behaviours rather than a control group. Comer claims that this comparison may be misleading as other factors (e.g increase in staff attention) could be caused by the patients’ improvements rather than the token economy.
There may be confounding variables with the research into token economies that reduces the internal validity of studies.
Token economies are less useful for people living in the community.
Token economies may be effective in reducing negative symptoms for people when in hospital settings. However, outpatient schizophrenics living in the community are only seen a few hours a day and so a token economy can only be used for part of the day. In comparison, schizophrenics in institutions receive 24hr care, monitored and rewarded appropriately with the use of token economy.
This given need for reinforcement has to be immediate and is unlikely to be effective for outpatient schizophrenics, therefore suggesting that Token economy may not be maintained beyond clinical setting.
This is a weakness as token economy may not be the most appropriate treatment for outpatients.
explain token economy
A token economy is a form of behavioural therapy based on operant and classical conditioning, where clinicians set target behaviours, such as brushing their hair or helping other patients that they believe will improve the patients engagement in daily activities. Tokens are awarded whenever the patient engages in one of the target behaviours and they can be later exchanged for various rewards and privileges. Therefore, the patient will engage in these desirable behaviours as they become associated with rewards.
Outline the key study of SZ
Ayllon and Azrin used a token economy on a ward of female schizophrenics patients, many of whom had been hospitalized for many years. They were given plastic tokens, each embossed with the word ‘one gift’ for behaviours such as making their bed, which could be exchanged for privileges such as watching a movie. Researchers found that the use of token economy with these patients increased dramatically the number of desirable behaviours that the patients performed each day.
How does token economy work?
To give the neutral token some value, it needs to be presented alongside a reinforcing stimulus such as watching a movie. By pairing the neutral tokens with the reinforcing stimulus, the neural token eventually acquires the same reinforcing properties. As a result, these neural tokens become secondary reinforcers which can be used to modify behaviour through operant conditioning.
When the patient targets behaviours, the clinician awards them tokens which can be exchanged for different privileges or rewards, referred to as a generalised reinforcer. The more rewards the token can be exchanged for, the more powerful the token becomes. Sran and Borrero compared behaviours reinforced by tokens that could be exchanged for one single highly preferred edible item with those that could be exchanged for a variety and they found that all ppts had higher responding rates in those sessions where tokens could be exchanged for a variety of items.
An important part of the token economy is the exchange of tokens for backup rewards chosen by the clinician. During the early stages of the token economy, frequent exchange periods mean that patients can be quickly reinforced and target behaviours can then increase in frequency. The effectiveness of the token economy may decrease if more time passes between presentation of the token and exchange for the backup reinforcers (Kazdin)
Evaluate token economy
There is supporting research for token economy
Dickerson et al have provided research support for the effectiveness of token economies in psychiatric settings. The reviews 13 studies of the use of token economy systems in the treatment of schizophrenia. 11 of these studies had reported beneficial effects that were directly attributable to the use of token economies
Dickerson et al concluded that, overall, these studies provide evidence of the token economy’s effectiveness in increasing the adaptive behaviours of patients with schizophrenia.
However, they did caution that many of the studies reviewed had significant methodological shortcomings that limited their impact in the overall assessment of token economies in this context
There is reliable empirical evidence for the effectiveness of token economies as it improves their ability to cope with everyday life and therefore the quality of life.
There are difficulties assessing the success of token economies.
Comer suggests that a major problem in assessing the effectiveness of token economies is that studies of their use tend to be uncontrolled. When a token economy system is introduced into a psychiatric ward, typically all patients are brought into the programme rather than having an experimental group that goes through token economy and a control group that does not.
As a result, patients’ improvement can only be compared with their past behaviours rather than a control group. Comer claims that this comparison may be misleading as other factors (e.g increase in staff attention) could be caused by the patients’ improvements rather than the token economy.
There may be confounding variables with the research into token economies that reduces the internal validity of studies.
Token economies are less useful for people living in the community.
Token economies may be effective in reducing negative symptoms for people when in hospital settings. However, outpatient schizophrenics living in the community are only seen a few hours a day and so a token economy can only be used for part of the day. In comparison, schizophrenics in institutions receive 24hr care, monitored and rewarded appropriately with the use of token economy.
This given need for reinforcement has to be immediate and is unlikely to be effective for outpatient schizophrenics, therefore suggesting that Token economy may not be maintained beyond clinical setting.
This is a weakness as token economy may not be the most appropriate treatment for outpatients.
Evaluate the Interactionist approach
The diathesis may not be exclusively genetic.
Most Diathesis-Stress models emphasize ‘vulnerability’ in terms of genetic influences alone, which are assumed to cause neurochemical abnormalities that, in turn, result in an increased risk of schizophrenia. However, this increased risk can also result from brain damage caused by environmental factors.
Verdoux et al estimated the risk of developing SZ later in life for individuals who have experienced obstetric complications at birth e.g prolonged labour which can cause oxygen deprivation, is four times greater than those who experience no complications.
Furthermore, Read et al proposed a neuro developmental model of SZ in which the effects of early childhood trauma on the developing brain result in a vulnerability. They proposed that the stress from early child abuse leads to overactivity of the hypothalamic-pituita-adrenal (HPA) axis and increased vulnerability to schizophrenia.
A more accurate understanding of the diathesis model should recognise that environmental experiences can create a physiological vulnerability which acts as a diathesis.
There is support for the usefulness of adopting an interactionist approach from studies comparing the effectiveness of combinations of biological and psychological treatments vs biological treatments alone
As Turkington et al points out, it is not really possible to use combination treatments without adopting an interactionist approach. Tarrier et al studies 315 patients who were randomly allocated to a medication and CBT group, medication and supportive counselling or a control group.
Patients in the two combination groups showed lower symptom levels than those in the control group (medication only) although there was no difference in rates of hospital readmission. Studies like this show that there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes and therefore highlight the importance of an interactionist approach.
Treatment resulting from the Interactionist approach is more effective, suggesting that SZ causes are both biological and environmental as proposed by the Diathesis-Stress Model.
Adoption studies provide evidence for the role of vulnerability and triggers.
Tienari et al investigated children adopted from Finnish mothers with SZ. Their adoptive parents were also assessed for child-rearing style. The rates of SZ were compared to control group adoptees who were without genetic risks. The child-rearing characteristics of criticism, conflict and low empathy impacted on the children with high genetic risk but not in the control group.
This suggests that both genetic vulnerability and family-related stress are important in the development of SZ with genetically vulnerable children being more sensitive to parenting behaviour.
This is large-scale, real-life empirical evidence for the influence of both genetic and environmental factors in the onset of SZ as predicted by the Interactionist approach.
Explain the Interactionist approach
The Diathesis-Stress Model proposes that schizophrenia is the result of a combination of psychological/environmental and biological/genetic influences. According to this model, the symptoms of schizophrenia are triggered or made worse when significant stressor in a person’s life are combined with a biological vulnerability to the disorder. Thus, this model might explain why not all people who have a genetic predisposition to schizophrenia go on to develop the disorder.
Explain the diathesis part of the Interactionist approach
The diathesis part of the Interactionist approach states that it has a genetic component in terms of vulnerability. This is supported by twin studies (Joseph) which have found that monozygotic twins with the disorder are at a greater risk of developing it than a dizygotic twin and that adoptive relatives don’t share the increased risk of biological relatives. However, this concordance rate does not reach 100% - in about 50% of identical twin pairs in which one twin is diagnosed, the other never meets the diagnostic criteria. This discordance indicates that environmental factors must also play a role in determining whether a biological vulnerability for schizophrenia actually develops into the disorder
Explain the stress part of the Interactionist approach
Stressful events, such as childhood trauma or the stresses of living in a highly urbanised environment, can also trigger schizophrenia. For example, Varese et al found that children who experienced severe trauma before the age of 16 were 3 times as likely to develop schizophrenia in later life compared to the general population. Additionally, Vassos et al found through a meta analysis that the risk of schizophrenia in the most urban environments was estimated to be 2.37 times higher than in the most rural environments, possibly due to the more adverse living conditions of densely populated urban environments. However, of the many people living in such areas, only a minority will develop schizophrenia. The relationship between urban stress and schizophrenia is conditional on some other factor, such as pre-existing genetic risk for the disorder.
Additive stress
Several combinations of stress and diathesis could lead to the onset of schizophrenia such as relatively minor stressor and high vulnerability or vice versa. Nonetheless, this idea proposes additivity i.e that diathesis and stress add together in some way to produce the disorder.
