4.3.5 Schizophrenia Flashcards

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1
Q

schizophrenia

A
  • a psychological disorder characterised by a loss of contact with reality
  • affects around 1% of the world’s population
  • affects thought processes and the ability to determine reality
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2
Q

classification of schizophrenia

A
  • schizophrenia doesn’t have a single defining characteristic as it’s a cluster of symptoms, some of which appear to be unrelated
  • these symptoms may be positive or negative
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3
Q

positive symptoms of schizophrenia

A
  • atypical experiences in addition to normal experiences
  • hallucinations; distorted perceptions of reality or perceptions that aren’t even based in reality
  • e.g. a sufferer may see distorted faces, or occasionally, people that aren’t even there
  • delusions; irrational beliefs with no basis in reality
  • e.g. a sufferer may have a delusion that they’re an important figure, such as Jesus
  • different types of delusions include that of persecution, grandeur (they’re someone of a high-status) , jealousy, erotonomia (someone’s in love with them), or somatic (something’s wrong with them)
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4
Q

negative symptoms of schizophrenia

A
  • a lack of normal experiences
  • speech poverty; a reduction in the quality and amount (frequency) of speech
  • e.g. a sufferer may give one-word answers to questions without elaborating any further detail
  • avolition; a lack of interest, desire and motivation for anything
  • i.e. the inability to cope with the normal pressures and motivations associated with everyday tasks
  • e.g. a sufferer may sit around without engaging in daily tasks such as work, socialising, or maintaining personal hygiene
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5
Q

diagnosis of schizophrenia

A
  • the 2 types of classification systems for diagnosing mental disorders are the DSM-5 (the american psychiatric association’s diagnostic and statistical manual) and the ICD-10 (WHO’s international classification of disease)
  • these 2 systems have different requirements for the diagnosis of schizophrenia; DSM-5 requires at least one positive symptom to be present, whereas the ICD-10 can base a diagnosis on negative symptoms alone
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6
Q

reliability of diagnosis

A
  • refers to how consistently schizophrenia is diagnosed
  • inter-rater reliability; the extent to which multiple doctors arrive at the same diagnosis for the same patients
  • if it’s diagnosed inconsistently it can be problematic as it may be over / under-diagnosed by psychiatrists, so patients will be incorrectly labelled as schizophrenic or not diagnosed at all, meaning they won’t receive the treatment they need
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7
Q

reliability of diagnosis - strengths

A
  • there have been improvements in inter-observer reliability as more recent studies of schizophrenia diagnosis generally find higher concordance rates among psychiatrists, suggesting it’s become more reliable over time
  • Soderberg et al. (2005) found a concordance rate of 81% among psychiatrists using the DSM classification to diagnose schizophrenia
  • the reliability of diagnosis for schizophrenia is higher than other disorders, e.g. 81% concordance for this, vs 63% for anxiety disorders
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8
Q

reliability of diagnosis - limitations

A
  • low inter-rater reliability and poor reliability between the DSM and ICD; Cheniaux et al. (2009) had 2 psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. psychiatrist 1 found 26 patients according to DSM and 44 with ICD. psychiatrist 2 found 13 patients according to DSM and 24 with ICD
  • co-morbidity or symptom overlap can reduce the reliability of diagnosis as different doctors may diagnose patients with different diseases
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9
Q

validity of diagnosis

A
  • the extent to which the classification of schizophrenia is a true reflection of the illness the patient is suffering from, i.e. does it measure what it’s intended to measure
  • i.e. refers to how genuine the diagnosis is
  • Rosenhan (1973) questioned the validity of schizophrenia diagnosis in his study;
  • 8 healthy volunteers presented themselves to various psychiatric hospitals claiming to hear voices
  • all 8 ppts were successfully admitted to the hospitals and diagnosed with schizophrenia
  • depending on the ‘patient’, doctors took between 8-52 days to release them
  • in a later experiment, doctors were falsely told that healthy patients would attempt to admit themselves, which led to doctors turning away genuine schizophrenic patients as they thought they were actors
  • the results of these experiments suggest the doctors didn’t have valid methods for diagnosing schizophrenia
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10
Q

validity of diagnosis - strengths

A
  • improvements in validity; more recent studies, after Rosenhan’s, suggest schizophrenia diagnosis has become more accurate
  • e.g. Mason et al. (1997) found that improvements to diagnostic manuals (DSM and ICD) over time led to more accurate diagnosis of schizophrenia
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11
Q

validity of diagnosis- limitations

A
  • Rosenhan’s (1973) study
  • co-morbidity
  • symptom overlap
  • gender bias
  • culture bias
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12
Q

limitations of validity - co-morbidity

A
  • refers to the presence of 2 or more disorders occurring simultaneously in a patient
  • e.g. schizophrenia and depression - Buckley et al. (2009) found that around 50% of schizophrenia patients also have depression, or substance abuse (47%). PTSD also occurred in 29% of cases and OCD in 23%
  • it can lead to inconsistent diagnoses between clinicians in relation to which disorder is diagnosed, i.e. schizophrenia, or depression, or both, which also causes issues with reliability
  • Jeste et al. (1996) also stated that schizophrenics with co-morbid conditions are excluded from research, but they form the majority of patients, suggesting that research findings into the causes of schizophrenia can’t be generalised to most sufferers
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13
Q

limitations of validity - symptom overlap

A
  • when different mental illnesses have similar symptoms so making an accurate diagnosis is difficult
  • e.g. schizophrenia and bipolar disorder, where negative symptoms such as depression and avolition are similar, as well as positive symptoms like hallucinations
  • it can lead to inconsistencies in diagnosis as different clinicians may diagnose different disorders, also reducing the reliability of diagnosis
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14
Q

limitations of validity - gender bias

A
  • the tendency for diagnostic criteria to be applied differently to males and females
  • men seem to be far more likely to be diagnosed, perhaps because women are able to cope better with the symptoms
  • Long and Powell (1988) randomly selected 290 male and female psychiatrists to read descriptions of patients’ behaviour and then diagnose them. when patients were described as males, 56% gave a diagnosis, compared to 20% when described as female
  • this disparity may be due to gender bias in diagnosis, as no gender bias was found when the psychiatrist was female
  • or, it may be due to valid differences in the incidence of schizophrenia between men and women, e.g. Cotton et al. (2009) suggests the better interpersonal functioning of women may cause doctors to miss schizophrenia diagnosis in women
  • however, Kulkarni et al. (2001) found that administration of oestrogen reduces schizophrenia symptoms, suggesting biological differences may partly explain gender differences in schizophrenia
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15
Q

limitations of validity - culture bias

A
  • the tendency to over-diagnose members of other cultures as suffering from schizophrenia
  • several studies have found that people of Afro-Caribbean descent living in Britain are much more likely than white people to be diagnosed as schizophrenic, and are also more likely to be confined in secure hospitals than white schizophrenics
  • e.g. Cochrane (1977) found that rates of schizophrenia among Afro-Caribbeans living in the Caribbean are roughly the same as white people in Britain, suggesting either;
  • an invalid diagnosis; Afro-Caribbean people in Britain are being over-diagnosed or the people in the Caribbean are being under-diagnosed
  • a valid diagnosis; the diagnosis reflects a valid difference in schizophrenia rates and so environmental stressors in Britain, e.g. poverty and racism, are contributing to higher levels of schizophrenia in such cultural groups
  • this suggests higher diagnosis rates are due to a cultural bias, rather than a genetic vulnerability
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16
Q

biological explanations for schizophrenia

A
  • sees schizophrenia as determined by biological factors, including genetics, abnormal dopamine functioning, and neural correlates
  • although causes of schizophrenia aren’t fully understood, research indicates that biological factors do play a role in the development of the disorder
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17
Q

genetics

A
  • sees schizophrenia as transmitted through genes passed onto individuals from their families
  • Gottesman (1991) conducted a large-scale family study and found a strong relationship between the degree of genetic similarity and shared risk of schizophrenia - e.g. 48% concordance rate in MZ twins compared to 17% in DZ twins
  • it’s believed that several genes are involved in increasing an vulnerability to developing schizophrenia, rather than one single gene - Ripke et al. (2014) found 108 genetic variations correlated with schizophrenia in a study of over 37,000 patients
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18
Q

genetics - strengths

A
  • Kety and Ingraham (1992) found that prevalence rates of schizophrenia were 10x higher among genetic than adoptive relatives of schizophrenics, suggesting genetics play a greater role than environmental factors
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19
Q

genetics limitations

A
  • methodological issues; family studies fail to consider the contribution of shared environmental influences on the development of the disorder, i.e. by living in the same house, and it may also be argued that MZ twins are treated more similarly than DZ twins, causing their concordance rate to be higher in Gottesman’s study
  • concordance rates in MZ twins would be 100% if it was entirely genetic, but it’s not, suggesting environmental factors do play a role
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20
Q

neural correlates

A
  • suggests that abnormalities within specific brain areas may be associated with development of schizophrenia
  • by using scanning techniques such as fMRI, researchers can compare the brains of schizophrenics and non-schizophrenics to identify differences in brain structures that may be linked to the disorder
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21
Q

neural correlates - strengths

A
  • several studies demonstrate correlations between neural structures and schizophrenia, e.g;
  • Johnstone et al. (1976) found that enlarged ventricles are particularly linked with negative symptoms of the disorder, such as avolition and speech poverty
  • Allen et al. (2007) found that reduced activity in the superior temporal gyrus and anterior cingulate gyrus is linked to positive symptoms of schizophrenia, such as auditory hallucinations
  • Boos et al. (2012) found that schizophrenics had reduced grey matter and cortical thinning compared to their non-schizophrenic relatives
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22
Q

neural correlates - limitations

A
  • conflicting evidence; there are many people with enlarged ventricles who don’t have the disorder, and also many people with the disorder that don’t have enlarged ventricles
  • it can be difficult to determine whether abnormal brain structures are a cause of schizophrenia, or an effect of it, i.e. correlation vs causation
  • Ho et al. (2003) found evidence of brain damage worsening over time in patients as the severity of their symptoms also increased, suggesting brain damage increases in schizophrenics over time and may not be the initial cause of the disorder
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23
Q

the dopamine hypothesis

A
  • explains schizophrenia as a result of abnormal activity of the neurotransmitter dopamine
  • it’s probable that genetic factors are linked to faulty dopaminergic systems;
  • the original dopamine hypothesis focused on the role of high levels / activity of dopamine in the subcortex, e.g. an excess of dopamine receptors in Broca’s area may be associated with speech poverty
  • more recent versions of the dopamine hypothesis instead focus on low levels of dopamine in the prefrontal cortex, e.g. in the negative symptoms of schizophrenia
  • so, both high and low levels of dopamine in different brain regions may be involved in schizophrenia
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24
Q

the dopamine hypothesis - strengths

A
  • original hypothesis; many studies, e.g. Creese et al. (1976), reported that several drugs that reduce schizophrenia symptoms are dopamine receptor antagonists (reduce dopamine activity), implying that schizophrenia is caused by increased dopamine
  • Kessler et al. (2003) used PET and MRI scans and found that schizophrenics had elevated dopamine receptor levels in certain brain areas and differences in levels of dopamine in the cortex
25
Q

the dopamine hypothesis - limitations

A
  • issues with establishing causation; the differences in dopamine levels may be an effect rather than a cause of the disorder
  • conflicting evidence; Farde et al. (1990) compared brain scans of 18 schizophrenics with 20 controls and found no difference in dopamine activity between the 2 groups
  • allegations of bias; psychiatrist David Healy (2002) argues that pharmaceutical companies exaggerated the dopamine hypothesis of schizophrenia to sell more drugs
  • can be seen as biologically reductionist, as it simplifies the complex development of schizophrenia to a single biological component of dopamine - other neurotransmitters may also be involved, e.g. newer anti-psychotic drugs indicate the involvement of serotonin too
26
Q

drug therapy for schizophrenia

A
  • antipsychotic drugs are the primary biological treatment for schizophrenia
  • they can be taken as tablets, as syrup, or by injection
  • some patients may require a short course where symptoms don’t return, but others may be required to take them for life
  • they’re divided into typical and atypical antipsychotics
27
Q

typical antipsychotics

A
  • been around since the 1950s; ‘first-generation’
  • they’re dopamine antagonists, i.e. work by reducing dopamine activity, so are strongly associated with the dopamine hypothesis
  • e.g. chlorpromazine; the first antipsychotic drug, which blocks dopamine receptors in the brain to try and reduce positive symptoms of the disorder, such as hallucinations and delusions
  • they have a sedative effect, which relaxes patients and calms anxiety
  • however, they block all dopamine activity and in other parts of the brain as well, causing side effects which may be harmful
  • the most serious effect is extrapyramidal symptoms (EPSE) - drug-induced movement disorders
28
Q

atypical antipsychotics

A
  • been used since the 1970s; ‘second-generation’
  • the aim of these was to improve upon the effectiveness of typical antipsychotics while reducing side effects such as EPSE
  • these drugs target several neurotransmitters, not just dopamine
  • e.g. clozapine; acts on dopamine receptors to reduce positive symptoms, and acts as an agonist (increasing release) for serotonin and glutamate, to improve mood and reduce negative symptoms such as avolition. these benefits mean it can be prescribed when a patient is at high risk of suicide
  • risperidone is believed to bind to dopamine receptors more strongly than clozapine, so is more effective in smaller doses which can lead to fewer side effects
  • however, they also carry a risk of side effects such as weight gain, increased risk of a heart attack, increased risk of diabetes, and extrapyramidal symptoms
29
Q

drug therapy - strengths

A
  • several studies, e.g. Thornley et al. (2003), have found both typical and atypical drugs to be more effective than placebo in reducing schizophrenia symptoms
  • support for atypical antipsychotics; Herbert Meltzer (2012) concluded that clozapine is more effective than an typical antipsychotics and other atypical ones, and that it’s effective in 30-50% of cases where typical drugs have failed
  • drug therapies can have positive economic implications - if anti-psychotics lead to symptom reduction, they could enable individuals to return to work / prevent them from being admitted to hospital, therefore reducing the negative impacts these have on the economy
30
Q

drug therapy - limitations

A
  • criticism of the distinction between typical and atypical antipsychotics; atypical ones were designed to be more effective with less side effects, but some studies question whether this is actually the case
  • all antipsychotics carry a risk of side effects which can range from mild ones, e.g. weight gain or dizziness, to potentially fatal, e.g. heart attack, stroke, EPSE)
  • Lieberman et al. (2005) found that 74% of 1342 schizophrenic patients discontinued antipsychotic drug treatment within 18 months due to side effects
31
Q

psychological explanations for schizophrenia

A
  • explains schizophrenia through;
  • family dysfunction, i.e. high levels of conflict or difficulties communicating, including double bind and expressed emotion
  • cognitive explanations, such as dysfunctional thought processing
32
Q

family dysfunction - double bind

A
  • proposed by Bateson et al. (1956)
  • it suggests that children who often get conflicting messages from their parents are more likely to develop schizophrenia
  • 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 seek clarification - ‘no win’ situation
  • the words spoken can present different meanings, or the message (words spoken) and the meta-message (the way in which the message is transmitted through tone of voice and body language) can have different meanings
  • e.g. a mother hugging her child but being critical with her words
  • constant exposure to such interactions means the child is unable to form a coherent picture of reality, which leads to disorganised thinking, which in extreme cases can manifest as symptoms of schizophrenia such as delusions and hallucinations
33
Q

family dysfunction - expressed emotion

A
  • an environment with a high degree of expressed emotion, (particularly negative, e.g. criticism, hostility, exaggerated involvement / control), causes stress which increases the risk of schizophrenia
  • it’s primarily associated with relapse in schizophrenic patients
  • e.g. an unhealthy level of involvement / control can affect how an individual responds to future stress and interprets new, challenging experiences, resulting in paranoia
34
Q

family dysfunction - strengths

A
  • Vaughn and Leff (1976) showed that relapse rates were higher amongst patients who had been discharged into home environments higher in expressed emotion - this was 51%, compared to 13% for low EE families - however, it doesn’t support it as a cause as it just suggests it contributes to maintaining schizophrenia
  • Tienari et al. (2004) found that adoptees raised in dysfunctional families had much higher rates of schizophrenia (36.8%) compared to adoptees raised in healthy families (5.8%)
  • considers how social and environmental factors may contribute to the onset of the condition, which has contributed to an interactionist approach in explaining the cause of the disorder more holistically
  • practical applications as informed methods of family therapy have been successful in preventing relapse
35
Q

family dysfunction - limitations

A
  • there are exceptions; not everyone raised in a dysfunctional family develops schizophrenia, and not everyone with schizophrenia was raised in a dysfunctional family, suggesting other factors also contribute to explaining it, e.g. biology
  • even if family dysfunction is correlated with schizophrenia, it doesn’t prove that it actually causes it, so it may just be an effect of the disorder
  • lots of evidence to suggest that there’s a genetic / neural cause to the disorder, and family dysfunction may simply act as a trigger for the condition, rather than the root cause
  • may be interpreted as blaming parents for their child’s development of the disorder
  • methodological concerns; Bateson et al’s double bind theory is based on a handful of case studies and interviews, and some critics have suggested researchers focus on examples that support their theory, while ignoring examples that conflict with it (selection bias)
36
Q

cognitive explanations of schizophrenia

A
  • looks at how schizophrenics think and process information
  • their cognition may differ in several ways;
  • cognitive biases
  • cognitive deficits
  • dysfunctional thought processing
37
Q

cognitive biases

A
  • an unusual attentional bias to stimuli of a threatening nature
  • can explain positive symptoms of schizophrenia, e.g. delusions
  • bias may mean a schizophrenic interprets the ordinary actions of other people as sinister, supporting their delusion that they’re a victim of a conspiracy or that people are trying to harm them
38
Q

cognitive deficits

A
  • Bowie and Harvey (2006) describe various cognitive deficits associated with schizophrenia, such as;
  • attention deficits; schizophrenics often have difficulty concentrating and paying attention
  • speech deficits; schizophrenics often have low verbal fluency and difficulty finding words
  • memory deficits; schizophrenics often have impaired working memory, particularly verbal working memory
39
Q

dysfunctional thought processing

A
  • Frith et al. (1992) identified two kinds of dysfunctional thought processing, including metacognition and central control, that contribute to the development of schizophrenia;
  • metacognition; the ability to think about and reflect on one’s own thoughts, emotions and behaviours - schizophrenics are seen to suffer from metacognitive dysfunction, which may explain some symptoms of schizophrenia such as hallucinations as an inability to recognise their thoughts as their own may explain symptoms like hearing voices; the person attributes their own thoughts to some external sources outside their mind
  • central control; the cognitive ability to suppress an automatic response while carrying out a deliberate action - it’s often measured using the Stroop test which involves identifying the colour of words where there’s often discrepancies in the colour of the font, so the automatic response of reading the word must be suppressed to allow for identification of the font colour - schizophrenics often dysfunctional central control abilities, so often suffer from derailment and begin to talk off-topic
40
Q

cognitive explanations - strengths

A
  • Stirling et al. (2006) compared 30 schizophrenics with 18 non-patients on cognitive tasks such as the Stroop test, and found that sufferers took over 2x as long as the control group to name the font colour, suggesting they have central control dysfunction
  • practical applications as it’s been used to develop effective therapies for treating schizophrenia
  • therapies like CBT which reduce cognitive impairment often improve schizophrenia symptom, supporting cognitive explanations
  • complements other explanations as they can be combined to give a more holistic account of schizophrenia
41
Q

cognitive explanations - limitations

A
  • many people have cognitive biases and deficits, e.g. as a result of brain damage, but don’t develop schizophrenia, suggesting cognitive explanations alone are too reductionist and there’s more to explaining schizophrenia
  • it doesn’t explain the cause of the disorder, as it simply just describes the thought processes that occur, but not why people have these in the first place
  • it may be that biological factors, such as structural brain abnormalities, lead to the differences in thought processes, suggesting an interactionist approach would be more effective in explaining schizophrenia
42
Q

psychological treatments of schizophrenia

A
  • cognitive behavioural therapy (CBT)
  • family therapy
  • token economies
43
Q

cognitive behavioural therapy (CBT)

A
  • a structured talking therapy which looks at the way people interpret, make sense of, and react to their experiences
  • the main aim is to help patients identify and challenge the maladaptive thoughts underlying schizophrenia
  • e.g. a patient may have delusional thoughts that there’s a conspiracy to kill them, which causes negative emotions like fear and anxiety, and irrational behaviours like hiding from or attacking people
  • process;
  • therapist works with patient to create a formulation showing how events / experiences lead to thinking patterns and specific behavioural responses
  • the patient is encouraged to describe their thoughts to the therapist, who then helps them identify and challenge the reality of these thoughts, i.e. by asking them how likely these thoughts are to be true, and consider alternative explanations
  • the therapist may then help tackle symptoms from the behavioural (e.g. teaching behavioural coping skills) and emotional angle (e.g. teaching relaxation techniques)
  • CBT is primarily used to treat positive symptoms of schizophrenia and is commonly used in combination with antipsychotic drug therapy
  • a typical course may consist of 12 sessions, spaced 10 days apart
44
Q

CBT - strengths

A
  • many studies have shown that CBT effectively reduces schizophrenia symptoms, e.g. Zimmermann et al. (2005) conducted a meta-analysis of 14 studies involving around 1500 schizophrenics, and found that CBT significantly reduced positive symptoms of the disorder
  • complements other treatments as it’s commonly used in combination with other treatments, like antipsychotic drugs
  • less side effects than antipsychotic drugs which carry a risk of serious side effects
45
Q

CBT - limitations

A
  • conflicting evidence, as Jauhar et al. (2014) found CBT only had minor effects on schizophrenia symptoms
  • a potential reason for the small effect found could be due to CBT being investigated as a lone treatment; Tarrier et al. (2000) suggests CBT and antipsychotics are more effective in treating schizophrenia than either treatment alone
  • it isn’t suitable for all patients as it relies on patients to engage with the therapist, but some schizophrenics may be too paranoid or anxious to do this
46
Q

family therapy

A
  • a treatment for schizophrenia based on the family dysfunction explanation
  • the aim is to address the dysfunction in families, rather than focusing on the patient in isolation, to reduce the stress levels in families to aid recovery for patients
  • this involves talking openly about the patient’s illness and how it affects them with an aim to;
  • improve communication patterns; increase positive communication and decrease negative communication among the family, i.e. reducing levels of expressed emotion
  • increase tolerance and understanding; educating the family about schizophrenia and how to deal with it
  • reduce feelings of guilt and anger; family members may feel guilt and responsibility or anger towards the patient
  • a typical course may consist of weekly sessions for a year, after which the family members will have developed skills they can use after the therapy has ended
47
Q

family therapy - strengths

A
  • evidence supporting the efficacy of family therapy, e.g. Pilling et al. (2002) conduced a meta-analysis, looking at 18 studies of family therapy for schizophrenia and found that it had a clear effect on reducing relapse rates
  • complements other treatments as evidence suggests when it’s used with antipsychotic drugs, it’s more effective at reducing relapse rates than the drugs alone, as suggested by Xiong et al. (1994)
  • family therapy has very few side effects compared to treatments like antipsychotics
  • cost effective, as the schizophrenia commission (2012) estimate that it results in cost savings of around £1000 per patient over a 3-year period - it reduces costs by preventing the need and costs for further treatment
48
Q

family therapy - limitations

A
  • it may be counterproductive, as family therapy emphasises being open and honest, but in some families this may reveal difficult truths or reignite old arguments, which could increase negative communication and potentially make the problem worse
  • not suitable for all patients, as severity of symptoms may prevent some sufferers from participating, and causes high dropout rates, and not all patients have dysfunctional families, so it’s not a suitable treatment for them
49
Q

token economies

A
  • a behaviourist approach to schizophrenia based on operant conditioning
  • schizophrenics are awarded tokens, which can be exchanged for rewards, in return for desirable behaviour
  • primarily used for long-term patients in psychiatric institutions
  • i.e. the staff identify target, desirable behaviours and reward patients with a token every time they display one of these (secondary reinforcer) which can then be exchanged for a reward (primary reinforcer)
  • so patients are positively reinforced to carry out the desirable behaviours
  • mainly used to treat negative symptoms, such as avolition, as it provides an incentive for the patient to undertake tasks, which changes their behaviour
50
Q

token economies - strengths

A
  • evidence supporting the efficacy of token economies, e.g. McMonagle and Sultana (2000) found token economies reduces the negative symptoms of schizophrenia
  • complements other treatments as they can be used in conjunction with antipsychotic drugs, for example
51
Q

token economies - limitations

A
  • however, in McMonagle and Sultana’s study, the researchers note that the evidence isn’t conclusive, with questions about the replicability of the findings and uncertainty about whether behavioural changes can be maintained after the treatment ends
  • ethical concerns as the use of token economies can be seen as dehumanising as they take away the patient’s rights to make their own choices, and they can be discriminatory as severely ill patients will have greater difficulty complying with behavioural demands, thus getting fewer privileges than patients who are less severe
  • if behaviour improvements are dependent on receiving tokens, the patient may relapse once token economy therapy is withdrawn
52
Q

interactionist approach to schizophrenia

A
  • explains schizophrenia as a combination of various factors, rather than trying to reduce it down to either a psychological or biological phenomena
  • e.g. the diathesis-stress model
53
Q

the diathesis-stress model

A
  • says that both a vulnerability to schizophrenia and an stress-trigger are necessary to develop the condition
  • diathesis; vulnerability and stress; a negative psychological experience
  • i.e. a person with a high genetic predisposition may never develop it, e.g. if they live in a supportive low-stress environment, but someone with a lower genetic predisposition may develop it if exposed to enough environmental stress such as a dysfunctional family, drug abuse, etc.
  • the model originated with Meehl (1962) who proposed that vulnerability was entirely genetic, as a result of a single ‘schizogene’
  • more recent research, e.g. from Ripke et al. (2014), has made it clear that multiple genes contribute to increasing genetic vulnerability
  • it’s now recognised that vulnerability can be genetic or environmental (e.g. a traumatic event in early childhood), and the stress-trigger may be environmental or biological (e.g. drug use, illness, physical trauma)
54
Q

diathesis-stress model strengths

A
  • many studies support the idea of there being both a genetic and environmental influence on schizophrenia, e.g. Gottesman’s family studies supported the role of genetics, but concordance rates among identical twins were much less than 100%, suggesting that environmental influences play a role too
  • many studies suggest stress is a key environmental component, e.g. a review by Walker et al. (2008) found schizophrenia is associated with elevated baseline stress hormones, e.g. cortisol, and drugs which increase stress hormones worsen schizophrenia symptoms
  • more holistic which provides a more complete picture of schizophrenia, rather than reducing it to a single cause
55
Q

diathesis-stress model limitations

A
  • incomplete, as although it emphasises the role of vulnerability and stress in the development of schizophrenia, it hasn’t clearly explained why they cause it
56
Q

interactionist treatment of schizophrenia

A
  • tackles the disorder from multiple angles by providing combination treatments
  • e.g. a patient may be given antipsychotic drug therapy in combination with cognitive behavioural therapy
  • research generally suggests such interactionist approaches are more effective than either treatment in isolation
57
Q

interactionist treatment - strengths

A
  • several studies suggest combination therapy is more effective than treatments alone, e.g. Hogarty et al. (1986) reported relapse rates of 19% among patients with treated with drug therapy and family therapy, compared to 41% for patients treated with drug therapy alone
  • Sudak (2011) also describes how CBT makes patients more likely to adhere to drug therapy as it helps them understand the benefits of doing so
  • a more holistic, complete approach to treatment, which addresses both the biological and psychological components to schizophrenia
58
Q

interactionist treatment - limitations

A
  • more expensive, as you have to pay for multiple treatments, however if it leads to lower relapse rates, this may save money in the long-run anyway as it prevents further costs down the line