Schizophrenia Flashcards
Outline the diagnosis and classification of schizophrenia
Diagnosis and classification:
- schizophrenia is a type of psychosis, a severe mental disorder characterised by profound disruption of cognition and emotion so that contact with external reality and insights are impaired
- this affects a person’s language, thought, perception, emotions, and even their sense of self
- the peak of onset is between ages 25-30
- classification is organising symptoms into categories based on which symptoms cluster together in sufferers
- diagnosis is deciding whether someone has a particular mental disorder using the classifications
- the 2 major systems for the classification of mental disorder are the ICD-11 and the DSM-5
Positive symptoms:
- positive symptoms are atypical symptoms experienced in addition to normal functioning, so in excess or distortion of normal functioning
- these include hallucinations and distortions
Hallucinations-
- hallucinations are disturbances of perception in any of the senses
- they are false perceptions that either have no basis in reality, or distorted perceptions of things that are
- these perceptions can be auditory, visual, olfactory, or tactile
Delusions -
- delusions are firmly held irrational beliefs that have no basis in reality
- common types of delusions include:
-> delusions of persecution, which is the belief that others want to harm, threaten, or manipulate you, such as the government or aliens
-> delusions of grandeur, which is the belief that they are an important individuals, even godlike and have extraordinary powers, such as the belief that they are Jesus
-> delusions of control, which is the belief that their body is under external control, such as being controlled by aliens or the government
-> delusions of reference, which is the belief that events in the environment appeared to be directly related to them, such as special personal messages that are being communicated through the TV
Catatonic or disorganised behaviour -
- where an individual behaves in ways that seem inappropriate or strange to the norms of society
- might include a lack of motivation or inability to complete daily tasks
Disorganised speech -
- often known as ‘word-salad’, where an individual speaks in ways that are completely incomprehensible, for instance, sentences might not make sense, or the topic of conversation changes with little to no connection between sentences
Negative symptoms:
- atypical experiences that represent the loss or subtraction of a usual experience
Avolition -
- a lack of purposeful, willed behaviour, sometimes called ‘apathy’
- it is the reduction, difficulty, or inability to start and continue with goal directed behaviour
- people with schizophrenia often have sharply reduced motivation to carry out a range of activities
- the three signs of avolition are poor hygiene and grooming, a lack of persistence in work or education, and lack of energy
Speech poverty -
- limited speech output with limited, often repetitive content
- it involves reduced frequency and quality of speech
- this is sometimes accompanied by a delay in the sufferers further responses during the conversation
- it’s not they don’t know the words, but that they have a difficulty in spontaneously producing them
Affective flattening -
- a lack, or ‘flattening’ of emotions, where a person’s voice becomes dull and monotonous, and their face takes on a constant blank appearance
Alogia -
- speech poverty, where speech becomes lessened, and it may become difficult to produce words or coherent sentences
Anhedonia -
- an inability to enjoy things that they used to enjoy, such as food, which is physical anhedonia, or social withdrawal, where they find it hard or become reluctant to speak, which is social anhedonia
Outline issues in the diagnosis and classification of schizophrenia
- there are four issues with the reliability and validity in the diagnosis and classification of schizophrenia:
-> gender bias
-> cultural differences/cultural bias
-> symptom overlap
-> co-morbidity
Reliability:
- reliability is the level of agreement on the diagnosis by different psychiatrists (inter-rater reliability) across time (test-retest reliability) and cultures
- the stability of diagnosis over time given no change in symptoms
Prior to the DSM-V, reliability for diagnosis was low, but this has now improved. Osorio et al report excellent reliability for the diagnosis of schizophrenia in 180 individuals using the DSM-V. Pairs of interviewers achieved inter-rater reliability of .97 and test-retest reliability of .92. This means we can be reasonably sure that the diagnosis of schizophrenia is constantly applied.
There is a lack of inter-rater reliability in the diagnosis of schizophrenia. Despite the claims for increased reliability in the DSM III and later revisions, over 30 years later, there is still little evidence that the DSM is routinely used with high reliability by mental health clinicians. For example, Whaley found inter-rater reliability correlations in the diagnosis of schizophrenia as low 0.11. Low inter-rater reliability was also demonstrated in Rosenhan’s study. Although the majority of his Confederates were diagnosed with schizophrenia upon presentation to hospital, throughout their stay in a mental institution, none of the staff recognised that they were not actually displaying symptoms of schizophrenia. This suggests that, because psychiatric diagnosis lack some of the more objective measures enjoyed by other branches of medicine, it inevitably faces additional challenges with inter-rater reliability.
Validity:
- validity is the extent to which schizophrenia is a unique syndrome with characteristics, signs, and symptoms
- reliability and validity are inextricably linked, as the diagnosis cannot be valid if it is not reliable
A limitation of the diagnosis of schizophrenia is validity. In general, validity concerns whether we assess what we are trying to assess. One way to assess validity of a psychiatric diagnosis is with criterion validity. A psychologist had two psychiatrists independently assess the same 100 clients using ICD 10 and DSM IV criteria and found that 68 were diagnosed with schizophrenia under the ICD system and 39 under DSM. This suggests that schizophrenia is either over or under diagnosed according to the diagnostic system. Either way, this suggests that criterion validity is low. However, in the Osorio study, there was excellent agreement between clinicians when they used two measures to diagnose schizophrenia, both derived from the DSM system. This means that the criterion validity for diagnosing schizophrenia is actually good provided it takes place within a single diagnostic system.
Co-morbidity:
- comorbidity is the extent to which two or more conditions occur at the same time in a patient
- some common comorbidities in schizophrenia patients include substance abuse, anxiety, and depression
A limitation of schizophrenia diagnosis is its comorbidity with other conditions. If conditions occur together a lot of the time then this calls into question the validity of the diagnosis and classification, because they might actually be a single condition. Schizophrenia is commonly diagnosed with other conditions, for example, one review found that about half of those diagnosed with schizophrenia also had a diagnosis of depression or substance abuse. This is a problem for classification because it means schizophrenia may not exist as a distinct condition, and there is a problem with the diagnosis, as at least some people diagnosed with schizophrenia may have unusual cases of conditions like depression.
A wider implication of receiving a diagnosis of schizophrenia is revealed when considering comorbidity rates. A study of nearly 6 million US hospital discharge records reported many incidents of comorbid non-psychiatric diagnosis. Many of the patients labelled schizophrenic were also diagnosed with conditions such as hypothyroidism, hypertension, asthma, and type two diabetes. The authors of the study concluded that because of the schizophrenic diagnosis, these individuals then tended to receive a lower standard of medical care, leading to the development of further conditions, which then had an adverse effect on the likelihood of recovery.
Symptom overlap:
A limitation of schizophrenia diagnosis is symptom overlap with other conditions. There is considerable overlap between the symptoms of schizophrenia and symptoms of other conditions. For example, schizophrenia and bipolar disorder involve both positive symptoms, such as delusions, and negative symptoms, such as avolition. In terms of classification, this suggests that schizophrenia and bipolar disorder may not be two different conditions but variations of a single condition. In terms of diagnosis, it means that schizophrenia is hard to distinguish from bipolar disorder. As with co-morbidity, symptom overlap means that schizophrenia may not exist as a distinct condition, and that even if it does, it is hard to diagnose. This means both schizophrenia’s classification and diagnosis are flawed.
A number of factors can affect the accuracy of diagnostic judgements. One such factor is the problem of symptom overlap. For example, people with dissociative identity disorder were found to have more schizophrenic symptoms then people who had just been diagnosed with schizophrenia. The suggestion that most people diagnosed as schizophrenic have enough symptoms of other disorders that they could receive another diagnosis casts doubt on the validity of schizophrenia diagnoses.
Gender bias in diagnosis:
A limitation of schizophrenia diagnosis is the existence of gender bias. Since the 1980s, men have been diagnosed with schizophrenia more commonly than women, at a ratio of 1.4:1. One possible explanation for this is that women are less vulnerable than men, perhaps because of genetic factors. However, it seems more likely that women are underdiagnosed because they have closer relationships and hence get support. This leads to women with schizophrenia often functioning better than men. This underdiagnosis is a gender bias, and means that women may not therefore be receiving treatment and services that might benefit them.
Loring and Powell found evidence of gender bias among psychiatrists in the diagnosis of schizophrenia. They randomly selected 290 male and female psychiatrists to read 2 case files of patient’s behaviour. These psychiatrists were asked to offer their judgement using standard diagnostic criteria. When the patients were described as males, or no information was given about their gender, 56% of the psychiatrists gave a diagnosis of schizophrenia. However, when the patients were described as female, only 20% were given a diagnosis of schizophrenia. This gender bias was not as evident among the female psychiatrists, suggesting that diagnosis is influenced not only by the gender of the patient, but also the gender of the clinician.
Culture bias in diagnosis:
A limitation of schizophrenia diagnosis is the existence of culture bias. Some symptoms of schizophrenia, particularly hearing voices, have different meanings in different cultures. For example, in Haiti, some people believe that voices actually are communications from ancestors. British people of African-Caribbean origin are up to 9 times as likely to receive a diagnosis as white British people, although people living in African-Caribbean countries are not, ruling out a genetic vulnerability. The most likely explanation for this is culture bias in diagnosis of clients by psychiatrists from different cultural backgrounds. This appears to lead to an overinterpretation of symptoms in black British people. This means that British African-Caribbean people may be discriminated against by a culturally biased diagnostic system.
Research has established cultural and racial differences in the diagnosis of schizophrenia. However, the prognosis for members of ethnic minority groups may be more positive than the majority group members. The ethnic culture hypothesis predicts that ethnic minority groups experience less distress associated with mental disorders because of the protective characteristics and social structures that exist in these cultures. Psychologists found evidence to support this hypothesis in a study of 184 individuals diagnosed with schizophrenia or a schizophrenia spectrum disorder. This sample was drawn from 2 non-white minority groups, African-Americans and Latinos, and a majority group which were white Americans. Consistent with the predictions of the ethnic culture hypothesis, they found that non-minority group members were consistently more symptomatic than members of the two ethnic minority groups.
Outline biological explanations for schizophrenia
The genetic basis of schizophrenia:
Family studies -
- family studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder
- this relationship is shown by got Gottesman’s large-scale family study:
-> 9% concordance siblings
-> 13% concordance in children with one schizophrenic parent
-> 17% concordance for DZ twins
-> 48% concordance MZ twins
- of course, family members tend to share aspects of their environment as well as many of their genes, so the correlation represents both, but family studies still give good support for the importance of genes in schizophrenia
- due to the difficulties of disentangling genetic and environmental influences, studies of genetically related individuals who have been reared apart are used
- Tienari et al conducted an adoption study in Finland, and found that of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 also received a diagnosis of schizophrenia
- only 4 of the 197 control adoptees developed schizophrenia
- they concluded that these findings show there is a genetic component to the onset of schizophrenia
Candidate genes -
- schizophrenia is thought to be polygenic, and so different combinations of genes can lead to the condition
- the most likely genes would be those coding for neurotransmitters including dopamine
- Ripke et al combined all previous data from genome-wide studies of schizophrenia and found 108 separate genetic variations were associated with slightly increased risk of schizophrenia
- because different studies have identified different candidate genes, it also appears that schizophrenia is aetiologically heterogeneous, i.e. different combinations of factors, including genetic variation, can lead to the condition
The role of mutation -
- schizophrenia can also have a genetic origin in the absence of a family history of the disorder
- one explanation for this is mutation in parental DNA, which can be caused by radiation, poisoning, or viral infection
- evidence for mutation comes from positive correlations between paternal age, associated with increased risk of sperm mutation, and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al)
Neural correlates of schizophrenia:
The original dopamine hypothesis -
- the original hypothesis was based on the discovery that drugs used to treat schizophrenia, antipsychotics, cause symptoms similar to those in people with Parkinson’s disease, a condition associated with low dopamine levels
- therefore, schizophrenia might be the result of high levels of dopamine, hyperdopaminergia, in subcortical areas of the brain
- for example, and excess of dopamine receptors in pathways from the subcortex to Broca’s area may explain specific symptoms of schizophrenia, such as disorganised speech and/or auditory hallucinations
- this theory claims that hyperdopaminergia in subcortical areas of the brain, or an oversensitivity of the brain to dopamine, is the cause of schizophrenia
- dopamine is a substance that is known to be active in the limbic system, an area of the brain governing emotion
- dopamine neurons are instrumental in regulating attention, therefore if this process is disturbed, it may lead to problems with attention, perception, and thought, which are all characteristics of schizophrenia
The revised dopamine hypothesis -
- Davis and Khan proposed a revised dopamine hypothesis, where they added cortical hypodopaminergia -> abnormally low levels of dopamine in the brain’s cortex
- this can explain the negative symptoms, as low levels in the prefrontal cortex, which is responsible for thinking, explain cognitive problems, i.e. negative symptoms of schizophrenia
- it has been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia, so it may be that both high and low levels of dopamine in different brain regions are involved in schizophrenia
Evaluate biological explanations for schizophrenia
One strength of the genetic explanation of schizophrenia is the strong evidence base. Gottesman’s family study showed that risk increased with genetic similarity to a family member with schizophrenia, finding a 48% concordance rate between MZ twins and 17% concordance rate with DZ twins. Furthermore, a study by Hilker showed a concordance rate of 33% with MZ twins and 7% with DZ twins. These studies suggest a strong genetic basis in schizophrenia. However, a crucial assumption underlying all twin studies is that the environments of MZ twins and DZ twins are mutually similar. Contrary to this, Joseph pointed out that MZ twins are treated more similarly, encounter more similar environments, and experience more identity confusion rather than DZ twins, suggesting that differences in concordance rates between MZ and DZ twins reflect nothing more than environmental differences, rather than genetic.
One limitation of the genetic explanation is there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia. These environmental factors include both biological and psychological influences. Biological risk factors include birth complications and smoking THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma, which leaves people more vulnerable to adult mental health problems in general, but there is now evidence for particular link with schizophrenia. In one study by Morkved et al, 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma, as opposed to 38% of a matched group with non-psychotic mental health issues. This means that genetic factors alone cannot provide a complete explanation for schizophrenia.
A strength of the dopamine hypothesis as an explanation for schizophrenia is research evidence. 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. A psychologist carried out a meta analysis of 212 studies and concluded that all the antipsychotic drugs tested in the studies were significantly more effective than placebos in the treatment of positive and negative symptoms, achieved by reducing the effects of dopamine. These findings also challenged the classification of antipsychotics into typical and atypical groupings because differences in their effectiveness were only small. However, Noll claims there is strong evidence against both the original and revised dopamine hypothesis. He argues that the antipsychotic drugs do not alleviate hallucinations and delusions in about one third of people experiencing these symptoms. Noll also points out that in some people, hallucinations and delusions are present despite levels of dopamine being normal. This suggests that rather than dopamine being a sole cause of positive symptoms, other neurotransmitter systems, acting independently of the dopaminergic system, may also produce the positive symptoms associated with schizophrenia.
One limitation of the dopamine hypothesis is evidence for a central role of glutamate. Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia. In addition, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing. This means that an equally strong case can be made for a role of other neurotransmitters.
What are the two psychological explanations for schizophrenia?
- Family dysfunction
- Cognitive explanations
Outline the family dysfunction explanation for schizophrenia
The schizophrenogenic mother:
- Fromm-Reichmann proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from her patients about their childhoods
- the schizophrenogenic mother is cold, rejecting, and controlling, and tends to create a family climate characterised by tension and secrecy
- this leads to distrust that later develops into paranoid delusions, i.e. beliefs of being persecuted by another person, and ultimately schizophrenia
Double-bind theory:
- Bateson et al agreed that family climate is important in the development of schizophrenia, but emphasised the role of communication style within a family
- 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 unable to comment on the unfairness of the situation or seek clarification
- when they get it ‘wrong’, which is often, the child is punished by withdrawal of love
- this leaves them with an understanding of the world as confusing and dangerous, and this is reflected in symptoms like disorganised thinking and paranoid delusions
- Bateson was clear that this was neither the main type of communication in the in the family of someone with schizophrenia, nor the only factor in developing schizophrenia, just a risk factor
Expressed emotion:
- expressed emotion is the level of emotion, in particular negative emotion, expressed towards a person with schizophrenia by their carers, who are often family members
- expressed emotion contain several elements:
-> verbal criticism of the person, occasionally accompanied by violence
-> hostility towards the person, including anger and rejection
-> emotional overinvolvement in the life of the person, including needless self-sacrifice
- these high levels of expressed emotion directed towards the individual are serious source of stress for them
- this is primarily an explanation for relapse in people 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
Evaluate the family dysfunction explanation for schizophrenia
A limitation of family dysfunction explanations of schizophrenia is they have limited applications. It is very difficult to change the family dynamic unless the family is very willing to try, which is often not the case. Therefore, the value of this research to the field of psychology is debatable.
The importance of family relationships in the development of schizophrenia was demonstrated in an adoption study by Tienari et al. In this study, adopted children who had a schizophrenic biological parent were more likely to become ill themselves than children with non-schizophrenic biological parents. However, this difference emerged only in situations where the adopted family itself was rated as disturbed. This suggests that the illness only manifests itself under appropriate environmental conditions. Therefore, genetic vulnerability alone is not sufficient as an explanation for schizophrenia.
The expressed emotion explanation for schizophrenia has research support. Brown found that in families that had high levels of expressed emotion, 58% of people with schizophrenia returned to hospital for further treatment, compared to only 10% of those from low expressed emotion families. However, this study shows the effect of expressed emotion on relapse rates of schizophrenia but not necessarily in the development of the disorder. Furthermore, it is unclear whether expressed emotion is a causal agent in the relapse rates, or just a reaction to the patients schizophrenic behaviour. Therefore, the significance of this explanation is unclear.
Research into family explanations for schizophrenia is highly socially sensitive. Although early explanations for the family-schizophrenia link have little research support, research in this area may be useful in showing that insecure attachment and experience of childhood trauma affect individual vulnerability to schizophrenia. However, research linking family dysfunction to schizophrenia is highly socially sensitive because it can lead to parent blaming, and mothers seem to be particularly blamed. The parents are already having to watch their child experience the symptoms of schizophrenia and take responsibility for their care, and to be blamed adds insult to injury and may add to the stigma of the disease and mistreatment of people with schizophrenia.
Outline cognitive explanations for schizophrenia
Dysfunctional thinking:
- a cognitive explanation of schizophrenia suggest that it is due to abnormal information-processing
- dysfunctional thought processing is cognitive habits or beliefs that cause the individual to evaluate information inappropriately and produce undesirable consequences
- schizophrenia is characterised by disruption to normal thought processing
- reduced thought processing in the ventral striatum is associated with negative symptoms, whilst reduced processing of information in the temporal and cingulate gyri is associated with hallucinations
- the slower than usual level of information processing suggest that cognition is likely to be impaired
Metarepresentation dysfunction:
- meta representation is the cognitive ability to reflect on thoughts and behaviour, which allows us insight into our own intentions and goals
- it also allows us to interpret the actions of others
- dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else
- this would explain hallucinations of hearing voices and delusions like thought insertion
Central control dysfunction:
- central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead
- dysfunction in this would lead to disorganised speech and thought disorder, as we are unable to suppress automatic thoughts and speech triggered by other thoughts
- for example, schizophrenics tend to experience derailment of thoughts and spoken sentences, because each word triggers associations, and the patient can’t suppress automatic responses to them
Evaluate cognitive explanations for schizophrenia
A strength of cognitive explanations for schizophrenia is evidence for dysfunctional thought processing. Stirling et al compared performance on a range of cognitive tasks in 30 people with schizophrenia and a control group of 30 people without. Tasks included the stroop task, in which patients have to name the font colours of colour words, so have to suppress the tendency to read the words aloud. As predicted by Frith et al’s central control theory, people with schizophrenia took over twice as long on average to name the font colours. This means that the cognitive processes of people with schizophrenia are impaired.
A limitation of cognitive explanations is that they only explain the proximal origins of symptoms. Cognitive explanations for schizophrenia are proximal explanations because they explain what is happening now to produce symptoms, in contrast to distal explanations, which focus on what initially caused the condition. Possible distal explanations are genetic and family dysfunction explanations. What is currently unclear, and not well addressed, is how genetic variation or childhood trauma might lead to problems with metarepresentation or central control. This means that cognitive theories on their own only provide partial explanations for schizophrenia.
The claim that the symptoms of schizophrenia have their origin in faulty cognition is reinforced by the success of cognitive based therapies for schizophrenia. The effectiveness of cognitive behavioural therapy for psychosis was demonstrated in the NICE review of treatments for schizophrenia. This review found consistent evidence that, when compared with treatment by antipsychotic medication, cognitive behavioural therapy was more effective in reducing symptom severity and improving levels of social functioning. This supports the view that faulty cognitions have an important causal influence in the development of schizophrenia.
Outline biological therapy for schizophrenia
- the most common treatment for schizophrenia involves the use of antipsychotic drugs
- the term ‘antipsychotic’ refers to psychosis
- a person with psychosis experiences some loss of contact with reality, for example through hallucinations or delusions
- psychosis as a defining characteristic of schizophrenia and related disorders
Typical antipsychotics:
- they were discovered in the 1950s
- they block the activity of the neurotransmitter dopamine within 48 hours, but it can take weeks to show substantial improvement in symptoms
- the most frequently used typical antipsychotic is chlorpromazine
- typical antipsychotics like chlorpromazine work by acting as antagonists in the dopamine system; antagonists are chemicals which reduce the action of a neurotransmitter
- they work by binding to dopamine receptors, particularly D2 receptors, and thus reducing the action of dopamine
- initially when an individual begins taking chlorpromazine dopamine levels build up, but then its production is reduced
- by reducing the stimulation of the dopamine system in the brain, antipsychotic drugs can eliminate the hallucinations and delusions experienced by people with schizophrenia
- the effectiveness of these dopamine antagonists in reducing the symptoms of schizophrenia is what led to the development of the dopamine hypothesis
- as well as having antipsychotic properties, chlorpromazine is also an effective sedative
- this is believed to be related to its effect on histamine receptors, but it is not fully understood how this leads to sedation
Atypical antipsychotics:
- atypical antipsychotics have been used since the 1970s
- the aim in developing newer antipsychotics was to maintain or improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and also minimise the side-effects of the drug used
- atypical antipsychotics act on the dopamine system as well as blocking serotonin receptors
- in the same way as typical antipsychotics, they bind to D2 receptors but rather than permanently block the dopamine action, they temporarily bind to the receptors and then rapidly disassociate to allow normal dopamine transmission
- only temporarily binds to receptors then releases, which reduces side-effects
Clozapine -> clozapine was first trialled in the early 1970s. 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 an individual is considered a high risk of suicide. This is important as 30 to 50% of people with schizophrenia attempt suicide at some point.
Risperidone -> risperidone is a more recently developed atypical antipsychotic, having been around since the 1990s. It was developed in an attempt to produce a drug as effective as clozapine but without it serious side-effects. Like clozapine, risperidone is believed to bind to dopamine and serotonin receptors. Risperidone binds more strongly to dopamine receptors than clozapine, and is therefore effective in much smaller doses the most antipsychotics. There is some evidence to suggest that this leads to fewer side-effects than other antipsychotics.
Evaluate drug therapy as a biological treatment for schizophrenia
A limitation of drug therapy as a treatment for schizophrenia is antipsychotic drugs have a high likelihood of side-effects. Typical antipsychotics are associated with a range of side-effects, including dizziness, agitation, sleepiness, stiff jaw, weight gain, and itchy skin. Hill’s research suggests that approximately 30% of people taking typical antipsychotic drugs develop tardive dyskinesia, which is involuntary movements of the tongue, face, and jaw, and in most cases it is irreversible. Furthermore, the most serious side-effect of antipsychotics, and particularly typical antipsychotics, is neuroleptic malignant syndrome. This is believed to be caused when the drug blocks dopamine action in the hypothalamus, an area of the brain associated with the regulation of a number of body systems. NMS can be fatal. This means that antipsychotics can do lots of harm as well as good, and that many patients may stop taking their antipsychotics due to these severe side-effects.
One strength of antipsychotics is evidence to support their effectiveness. There is lots of evidence to support the idea that both typical and atypical antipsychotics are at least moderately effective in tackling the symptoms of schizophrenia. Thornley et al reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with a total of over 1100 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity when compared to placebo. There is also evidence of the benefits of atypical antipsychotics, as Meltzer concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics, effective in 30 to 50% of treatment resistant cases where typical antipsychotics have failed, suggesting that antipsychotics work in the treatment of schizophrenia. However, Healy has suggested serious flaws with evidence for effectiveness. For example, most studies are of short-term effects only, and some successful trials have had their data published multiple times, exaggerating the size of the evidence base for positive effects. Also, because antipsychotics have powerful calming effects, it is easy to demonstrate that they have some positive effect on people experiencing symptoms of schizophrenia. This is not the same as saying they really reduce the severity of psychosis. This means the evidence base for antipsychotic effectiveness is less impressive then it first appears.
Furthermore, ethical problems have arisen with the use of antipsychotics. It is widely believed that antipsychotics have been used in hospital situations to calm people with schizophrenia and make them easier for staff to work with, rather than for the benefits to the people themselves. On the other hand, calming people distressed by hallucinations and delusions almost certainly makes them feel better, and allows them to engage with other treatments, such as CBTp and services, such as meeting with a social worker to organise accommodation. While the use of medication to treat possibly disruptive patients may be an ethical grey area, as long as it as it is done for the patient’s best interests, the positives outweigh the negatives.
More support for the effectiveness of antipsychotics comes from studies that have compared relapse rates for antipsychotics and placebos. Leucht et al carried out a meta analysis of 65 studies published between 1959 and 2011, involving nearly 6000 patients. Some of these patients were taken of their antipsychotic medication and given a placebo instead. The remaining patients remained on their regular antipsychotic. Within 12 months, 64% of those patients who had been given the placebo had relapsed compared to 27% of those who stayed on the antipsychotic drug. The study clearly demonstrates the superiority of antipsychotic drugs compared to placebo in preventing relapse, though as rate relapse rates weren’t 0%, it suggests that other non-biological treatments are also needed for schizophrenia.
Outline CBT as a psychological therapy for schizophrenia
- CBT usually takes place over a period of 5 - 20 sessions, either in groups or an individual basis
- CBT aims to deal with both cognitions and behaviour
- CBTp aims to help patients to identify irrational thoughts and challenge them, and reality testing them to reduce distress
- CBTp uses the ABCDE model, which involves identifying activating events (A) and the resulting beliefs from the events (B) that appear to cause their emotional and behavioural consequences (C), and these beliefs can then be rationalised, disputed (D) and changed through a critical collaborative analysis, leading to the effect (E) of restructured beliefs
- critical collaborative analysis is where the therapist uses gentle questioning to help the patient to understand and challenge illogical deductions and conclusions, e.g. ‘if your voices are real, why can no one else hear them?’
- rather than ‘getting rid’ of schizophrenia, CBTp helps patients to cope better with their symptoms because it reduces distress
- CBTp also uses normalisation, which is where the therapist shares with the patient that many people have unusual experiences such as hallucinations and delusions in many different circumstances, which reduces anxiety and the sense of isolation by making the patient feel less alienated and stigmatised, which makes the possibility of recovery seem more likely
- patient may also be set behavioural assignments to improve their general level of functioning, such as to shower every day or to go out and socialise with friends between now and the next session
The procedure of CBTp:
1. Assessment -> to understand the person’s condition/situation, and discuss what they want to achieve from the sessions/their goals
2. Engagement -> to build up a relationship/trust, and to reiterate working together to establish ways of managing the condition
3. ABC model -> the patient applies the ABC model to their own life
4. Normalisation -> the therapist helps them realise they aren’t alone and that others suffer as well, which helps reduce the stigma
5. Critical collaborative analysis -> ways of questioning illogical thoughts and delusions
6. Developing alternative explanations -> the patient develops their own alternative explanations for their previously unhealthy assumptions
Evaluate CBT as a treatment for schizophrenia
One strength of CBTp for schizophrenia is evidence for its effectiveness. Jauhar et al reviewed 34 studies of using CBT to treat schizophrenia, concluding that there is clear evidence for significant effects on both positive and negative symptoms. Other studies have focused on symptoms, for example, Pontillo et al found reductions in frequency and severity of auditory hallucinations. Clinical advice from NICE recommends CBT for schizophrenia. This means that both research and clinical experience supports the benefits of CBT for schizophrenia.
CBTp only aims to make schizophrenia more manageable and improve the patient’s quality of life. It allows patients to make sense of and challenge some of the symptoms through critical collaborative analysis. While this is worth doing, it should not be confused with curing schizophrenia. Therefore, whilst CBTp may provide patients with strategies that they can use to manage their current and future symptoms, it does not effectively cure schizophrenia.
The 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. Addington and Addington claimed that in the initial acute phase of schizophrenia, self reflection is not particularly appropriate. Following stabilisation of the psychotic symptoms with antipsychotic medication, however, individuals can benefit more from group based CBT. 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 from CBT, but it means that CBT alone is not a comprehensive treatment that it is not appropriate for everyone with schizophrenia.
CBTp is difficult to access. Despite being recommended by NICE as a treatment for schizophrenia, it is estimated that only 1 in 10 people in the UK who could benefit from CBTp can get access to it. Haddock et al found that in Northwest England, only 6.9% of patients have been offered CBTp. This limits the effectiveness of CBTp, as patients are unable to participate in the therapy. Of those who are offered CBTp, a significant number either refuse or fail to attend the therapy sessions, thus limiting its effectiveness even more.
Outline family therapy as a psychological therapy for schizophrenia
- family therapy is a range of interventions aimed at the family, such as parents siblings and partners, of someone who has schizophrenia, and should also involve the person with schizophrenia if practical
- it aims to improve the quality of communication and interaction between family members and reduce the stress of living as a family and so reduce rehospitalization
- it is commonly used in conjunction with drug therapy and outpatient clinical care
How it works:
- usually takes place within the people’s homes with two family therapists
- lasts between 3-12 months with sessions every 2 to 4 weeks
- a minimum of 10 sessions are recommended by NICE
- family therapists make sure family members have all the information they need about the diagnosis
- everyone is encouraged to ask questions
- the views of every member of the family can be listened to, including those of the person who has schizophrenia
- often the individual who is unwell will be asked to talk about their own symptoms and to discuss them with the family
- the goal is to provide the whole family with practical coping skills which enables them to manage the everyday difficulties arising from having schizophrenia in the family
How family therapy helps:
- Pharoah et al identified a range of strategies that family therapists used to try to improve the functioning of a family that has a member with schizophrenia
- during sessions the individual with schizophrenia is encouraged to talk to the family and explain what sort of support they do and do not find helpful, which improves relationships within the household because the therapist encourages family members to listen to each other, discuss problems, and negotiate potential solutions together
- these strategies reduce stress and expressed emotion while increasing the chances of patients complying with medication, which tends to result in a reduced likelihood of relapse and readmission to hospital
Reduces negative emotions -> family therapy aims to reduce levels of expressed emotion, i.e. reduce the level of emotion generally, but especially negative emotions such as anger and guilt, which creates stress. Reducing stress is important to reduce the likelihood of relapse.
Improves the families’ ability to help -> the therapist encourages family members to form a therapeutic alliance whereby they all agree on the aims of therapy. The therapist also tries to improve the families’ beliefs about, and behaviour towards, schizophrenia. A further aim is to ensure that family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.
A model of practice:
- Burbach has proposed a model for working with families dealing with schizophrenia:
Phase 1 -> sharing basic information and providing emotional and practical support
Phase 2 -> identifying resources, including what different family members can and cannot offer
Phase 3 -> encourages mutual understanding, creating a safe space for all family members to express their feelings
Phase 4 -> identifying unhelpful patterns of interaction
Phase 5 -> skills training, such as learning stress management techniques
Phase 6 -> relapse prevention planning
Phase 7 -> maintenance for the future
Evaluate family therapy as a treatment for schizophrenia
A strength of family therapy for schizophrenia is it has supporting research evidence. Pharoah et al reviewed the evidence for the effectiveness of family therapy compared to antipsychotics alone. They found that there was a reduction in the risk of relapse and a reduction in hospital admission during treatment, and then 24 months after. Some studies also reported an improvement in the overall mental state of the patient, but others did not. There was an increased compliance with medication, although family therapy did not appear to have much of an effect on more concrete outcomes, such as living independently or employment. This suggests that family therapy significantly reduces rehospitalisation and somewhat improves the quality of life for patients and their families, but the findings are inconsistent. Therefore, the evidence to support the effectiveness of family therapy as a treatment for schizophrenia is fairly weak.
Furthermore, Pharoah et al suggest that the main reason for family therapy effectiveness may have less to do with any improvements in functioning and more to do with the fact that it increases medication compliance. Patients are more likely to reap the benefits of medication because they are more likely to comply with their medication regime. Therefore, it may be that it is antipsychotics that are the more effective treatment for schizophrenia and that family therapy may only be necessary to the extent that it encourages patients to take antipsychotics.
A further strength of family therapy for schizophrenia is the benefits for all family members. Therapy is not just for the benefit of the identified patient but also for their families. A review of evidence by psychologists concluded that these effects are important because families provide the bulk of care for people with schizophrenia. By strengthening the functioning of a whole family, family therapy lessens the negative impact of schizophrenia on other family members and strengthens the ability of the family to support the person with schizophrenia. This means that family therapy has wider benefits beyond the obvious positive impact on the identified patient.
