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Schizophrenia Flashcards

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1
Q

define schizophrenia

A

a psychotic disorder characterised by severe symptoms in areas of judgement, emotions, perception and behaviour

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2
Q

what 3 things are needed for a schizophrenia diagnosis (DSM-4)

A

characteristic schizophrenia symptoms, social/occupational dysfunction and duration

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3
Q

what are the conditions of characteristic schizophrenia symptoms (DSM-4)

A

2 or more symptoms, present for a significant time in a 1-month period

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4
Q

what are the conditions of social/occupational dysfunction (DSM-4)

A

below prior level in one or more major areas of functioning such as work, interpersonal relations or self care

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5
Q

what are the conditions of duration (DSM-4)

A

at least 6 months, in which symptoms must persist for at least 1 month

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6
Q

define delusions

A

incorrect beliefs due to distortions or exaggerations of reasoning and/or misinterpretation of experiences

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7
Q

define hallucinations

A

distortions or exaggerations of perception in the senses

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8
Q

what types of delusions are there

A

paranoid delusions (delusions of persecution), delusions of grandeur, delusions of reference- believing things in the environment are related to you, somatic delusions- false beliefs about the body

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9
Q

name the positive symptoms of schizophrenia

A

delusions, hallucinations, disorganised speech/thinking

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10
Q

name the negative symptoms of schizophrenia

A

alogia, affective flattening, avolition

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11
Q

explain validity in schizophrenia diagnosis

A

predictive validity- if diagnosis leads to successful treatment the diagnosis is valid
descriptive validity- patients with schizophrenia should differ in symptoms from patients with other disorders

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12
Q

explain reliability in schizophrenia diagnosis

A

test retest reliability- same clinician makes same diagnosis from same information on separate occasions
inter rater reliability- different clinicians make identical, independent diagnoses of the same patient

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13
Q

what did rosenhan study

A

reliability and validity in diagnosis of schizophrenia

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14
Q

describe rosenhan’s study

A

8 pseudo patients called a hospital with symptoms of hearing a same-sex voice saying ‘empty’, ‘hollow’ and ‘thud, once admitted patients acted and spoke normally and didn’t mention the voices, pseudo patients did everything they were told but didn’t take medication, they made notes

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15
Q

what did rosenhan’s study find

A

7 out of 8 pseudo patients were admitted with a diagnosis of schizophrenia and discharged with schizophrenia in remission, they stayed an average of 19 days (range of 7-52 days), they were never detected as being fake

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16
Q

describe rosenhan’s second experiment

A

staff at a hospital were told to detect any pseudo patients that rosenhan’s had sent, rating them on a scale of 10 of how likely they were to be a fake (1/2- high confidence), however none were sent

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17
Q

what did rosenhan’s second experiment find

A

after 3 months one staff member highly confidently rated 41 patients as pseudo patients, 23 patients were rated highly confident by at least 1 psychiatrist, 19 by a psychiatrist and another member of staff

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18
Q

classification of schizophrenia peel 1

A

p- criticism of reliability, cultural variations
ev- luhmann et al, 60 adults with sz (20 each- Ghana, India, US), African/Indian ppts reported positive experiences with playful voices, not one US ppt did- more likely to report violent/hateful voices
ex- classification of sz is changeable dependent on culture, more socially acceptable in Africa/India where hallucinations are viewed as positive, so diagnosis rates are lower, less socially acceptable in US so diagnosis rates are higher, low reliability- no cultural agreement of what sz is
l- socially sensitive research, diagnosing other cultures by western standards, are they really experiencing sz, is it more of a spiritual experience in those cultures, do they need a diagnosis

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19
Q

classification of schizophrenia peel 2

A

p- criticism of reliability, poor inter-rater reliability
ev- chenioux et al, 2 psychiatrists diagnosed 100 patients using DSM and ICD, one diagnosed 26 by DSM and 44 by ICD, the other diagnosed 13 by DSM and 24 by ICD
ex- no consistency in how to diagnose sz, poor reliability between psychologists and classification systems, a clear diagnosis is difficult
l- is sz a true disorder if its so difficult to diagnose, hard to distinguish between symptoms of other disorders, definition is constantly changing, more of a spectrum

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20
Q

classification of schizophrenia peel 3

A

p- criticism of validity, gender bias
ev- loring and powell, 290 randomly selected male and female psychiatrists, 56% gave diagnosis of sz when case was described as ‘male’, 20% for ‘female’, women more likely to receive depression diagnosis
ex- women underdiagnosed, ability to mask emotions and cope in work/relationships so don’t hit criteria for sz, low validity in diagnosis
l- biased diagnosis in male psychiatrists, gender bias not as prominent in female psychiatrists, can see through masking in female patients

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21
Q

classification of schizophrenia peel 4

A

p- criticism of validity, co-morbidity, symptom overlap
ev- most people with sz tend to be diagnosed with another: 50% with depression, 47% lifetime substance abuse, 12% fulfil OCD criteria
ex- symptom overlap could lead to misdiagnosis, low validity, when co-morbidity can be difficult to treat disorders appropriately when different treatments are needed, are conditions seperate or interactionist
l- real life implications, if not receiving correct treatment, will not get better, implications for the economy, more individualistic approach needed looking at specific individuals’ symptoms

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22
Q

what explanations are included in the biological explanation of sz

A

genetic, dopamine hypothesis, neurophysiological (neural correlates)

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23
Q

what 3 key terms are needed in the genetic explanation about sz

A

polygenic- not caused by one gene but several interacting
aetiologically heterogeneous- the disorder has different causes
candidate gene- any genes thought to cause a disease or disorder

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24
Q

what did ripke find

A

meta-analysis of 37,000 patients and 113,000 controls, 108 separate genetic variations associated with increased risk of sz, genes coded for function of neurotransmitters like dopamine

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25
Q

what did gottesman research

A

family study, secondary data (danish civil registration, danish psychiatric central register), of approx 3 million danish people, diagnosis of sz by ICD, 4 groups: 1- both parents with sz, 2- one parent with sz, 3-neither parent, 4- no data (3/4 controls)

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26
Q

what did gottesman find

A

risk of sz increases with % of DNA shared, risk is highest in mz twins (48%) followed by dz twins (17%), parents 6%

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27
Q

genetic explanation of sz peel 1

A

p- research support from family study
ev- gottesman, meta analysis, denmark, 3 million people, 48% concordance mz twins, 17% dz, 6% parents
ex- increased risk of sz with more genes shared, must be genetic component
l- not 100% concordance in mz twins who share 100% DNA, must be other causes, environment, SLT, sharing similar env to parents

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28
Q

genetic explanation of sz peel 2

A

p- research support from adoption study
ev- heston, 30 sz mothers and 33 non sz mothers, children put immediately into foster care, 16.67% concordance sz in biological, 0% in adopted
ex- rates of sz higher in mothers with sz, 50% DNA shared, rates lower in mothers without sz, must be some genetic component
l- better than gottesman, no env influence (adopted from birth), but would expect higher concordance if genetics was cause, 50% DNA is shared but concordance is only 16.67%

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29
Q

genetic explanation of sz pee (3)

A

p- diathesis stress may best explain sz
ev- tienari,145 children in genetic risk group with at least one bio parent with sz, control group had no genetic risk, family dysfunction only triggered sz if the child had a genetic risk
ex- genetic vulnerability combined with an env trigger = sz, interactionism, high risk of developing sz genetically + stress from high criticism and conflict

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30
Q

what are the 4 dopamine explanations for sz

A

hyperdopaminergia in broca’s, mesolimbic area, hypodopaminergia in mesocortical area, prefrontal cortex

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31
Q

explain the influence of hyperdopaminergia in broca’s area on sz

A

responsible for speech production, excess in dopamine -> auditory hallucinations

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32
Q

explain the influence of hyperdopaminergia in mesolimbic area on sz

A

associated with positive symptoms, limbic system associated with controlling emotions like fear -> implications in delusions of persecution, responding to sensory info -> sensory hallucinations

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33
Q

explain the influence of hypodopaminergia in mesocortical area on sz

A

responsible for motivation, decision making, goal oriented behaviour -> symptoms like avolition

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34
Q

explain the influence of hypodopaminergia in prefrontal cortex on sz

A

responsible for decision making, motivation -> negative symptoms like avolition

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35
Q

dopamine hypothesis peeleel

A

p- research support
ev- antipsychotic drugs which reduce activity of dopamine reduce psychotic symptoms
ex- reduction in dopamine leads to reduction in psychotic symptoms, dopamine must have implications in positive symptoms (hallucinations/delusions)
l- not only dopamine causes positive symptoms, only 1/3 of psychotic drugs alleviate hallucinations, some people have symptoms when dopamine levels are normal, must be another factor too
ev- likely dopamine is involved but other neurotransmitters too, glutamate may be more influential, current research focus
ex- dopamine hypothesis alone is reductionist, dopamine not only cause, likely multiple neurotransmitters
l- may not even be purely biological, diathesis stress, epigenetics, childhood trauma may switch on/off genes, in this case diathesis is trauma which causes the biological stressor of high or low levels of dopamine

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36
Q

define neural correlates

A

measurements of the structure/function of the brain that correlate with an experience (schizophrenia)

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37
Q

neural explanation- mesolimbic system

A

amygdala, responsible for emotion -> affective flattening
hippocampus, fear and stress response -> delusions

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38
Q

neural explanation- mesocortical system

A

deficits in nerve connections between ml + mc (prefrontal cortex), reasoning, speech production -> alogia, delusions
dopamine released in basal ganglia indirectly affects processing of info in pfc

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39
Q

neural explanation- ventricles

A

enlarged ventricles associated with damage to pfc
reduction in grey matter + enlarged ventricles -> negative symptoms
less myelin sheath on axons in white matter -> decrease in info processing

40
Q

neural explanation peel 1

A

p- theory on neural correlates, supported by meta analysis
ev- analysed 19 results, higher reduction in cortical grey matter than healthy controls, specific to frontal, temporal, parietal
ex- sz is a biological disorder, due to degeneration of neurons, particularly evident in early stages of sz
l- meta analysis uses secondary sources with different methodological approaches, unique sz symptoms, can’t say reduction in grey matter causes sz or whether responsible for only positive/negative symptoms

41
Q

neural explanation peel 2

A

p- important implications, treatment of sz
ev- early intervention, prevent later stages, north american longitudinal study, different assessments including neuroimaging, predict who will develop psychosis
ex- neuroimaging means that early treatments can be used (antipsychotics) with at risk patients before psychosis develops, preventing sz
l- ethical concerns, right to assess people through neuroimaging, informing people that they might develop sz without 100% certainty, can lead to type 1 error and treating patients incorrectly, potentially labelling- stigma

42
Q

which drugs to treat sz are typical/atypical

A

typical- chlorpromazine
atypical- clozapine, risperidone

43
Q

how does chlorpromazine work

A

reduces effect by binding to but not activating receptor, blocks dopamine from being uptaken

44
Q

how does clozapine work

A

binds to dopamine receptors, but also acts on serotonin and glutamate receptors, blocks d2 receptors

45
Q

how does risperidone work

A

binds to dopamine and serotonin receptors more strongly than clozapine

46
Q

what symptoms does chlorpromazine help

A

positive symptoms- hallucinations and delusions

47
Q

what symptoms does clozapine help

A

positive and negative symptoms
improves mood, reduces depression, anxiety and suicidal thoughts, may improve cognitive functioning

48
Q

what symptoms does risperidone help

A

deals with positive symptoms, though more negative symptoms

49
Q

biological therapies peel 1

A

p- effectiveness/symptoms
ev/ex typical- binds to receptors and blocks dopamine, reduces dopamine in mesolimbic pathway, helps positive symptoms like hallucinations and delusions caused by hyperdopaminergia (70% had better functioning), acts as a sedative
ev/ex atypical- binds to receptors but activates serotonin and glutamate, helps with negative symptoms like avolition (caused by low serotonin in mesocortical area), effective in 81% with negative symptoms, improves mood, decreases depression, decreases depression and anxiety, less delusions and hallucinations, 30-50% treatment resistant
l- drugs show improvement, dopamine hypothesis proved, could start with typical and move to atypical, atypical better and more effective, treating positive and negative symptoms, dependent on individual and their choice

50
Q

biological therapies peel 2

A

p- side effects
ev/ex typical- parkinson related symptoms (tardive dyskinesia- involuntary muscle contraction), can be permanent and severe, cost benefit analysis, creates more stigma
ev/ex atypical- less severe, headache, dizziness, weight gain, agranulocytosis (blood condition), reduced effects compared to typical
l- atypical has less side effects so better, however still present, all drug therapy has a risk, up to the individual to make choice with informed consent

51
Q

biological therapies peel 3

A

p- how long to work and risk of relapse
ev/ex typical- few days-weeks, takes time to build up in system, 55% risk of relapse after 2 years
ev/ex atypical- generally 3-6 weeks to work, 41% risk of relapse depending on the individual
l- typical usually takes less time to work, higher chance patients will continue with treatment, effective more quickly, typical has greater risk of relapse, however both have high relapse rates

52
Q

what 3 components come under family dysfunction

A

double bind theory, expressed emotion, schizophrenogenic mother

53
Q

explain the concept of double bind

A

suggests schizophrenia develops due to abnormal and inadequate patterns of communication by the family- paralanguage and verbal language may not match
the sz will receive contradicting messages in which they can’t win either way
this creates distorted understanding which can lead to delusions/hallucinations

54
Q

explain the concept of high ee (explanation for relapse)

A

hostility- negative attitude directed at patient because the family feel that sz is controllable and the patient’s fault, family problems are blamed on the patient
emotional over involvement- family members blame themselves for the mental illness, show high concern for the patient, pity and guilt can cause stress
critical comments- an openness that the disorder is not entirely the patient’s fault but still negative criticism

55
Q

what are the conditions of low ee

A

warmth- kindness, concern and empathy expressed by the caregiver while talking about the patient, vocal qualities and smiling
positive regard- statements that express appreciation or support for patient’s behaviour, verbal/non-verbal reinforcement from caregiver

56
Q

family dysfunction peel 1

A

p- research support
ev- sz interviewed, higher recall of double bind statements than non-sz controls
ex- higher occurrence of double bind statements than non-sz controls, double bind may have impact upon development of sz, inadequate and confusing communication can lead to symptoms of sz such as hallucinations
l- methodological issues, self report, biased recall, requires someone already suffering a mental disorder to recall possibly traumatic experiences which they may not have tried to accurately remember, also retrospective, cannot guarantee accurate recall

57
Q

family dysfunction peel 2

A

p- biological explanation may better account for development of sz
ev- correlation between parents and child with sz could be genetic, liem found no difference between sz and non-sz families in parental communication, may be more bio than environmental
ex- family dysfunction does not have implication in sz, bio explanation may be better, 108 separate genetic variations, could even be explained by dopamine hypothesis, high levels of dopamine in mesolithic -> positive symptoms, low dopamine in mesocortical -> negative symptoms
l- sz could be explained by diathesis stress, has a biological basis, such as too low/high dopamine or genetics as the origin, environmental exploitation (stressor) leads to the development of sz

58
Q

family dysfunction peel 3

A

p- research suggests ee has implications in relapse rates of sz patients
ev- kavanagh, families with high ee, sz 4x more likely to relapse, compared to those in low ee families
ex- high ee creates a stressful environment which causes stress in sz patients and increases the risk of relapse, family dysfunction can explain why sz can relapse when returning to families with damaging and inadequate communication
l- individual differences in stress response to high ee, 25% of patient’s studied showed no physiological responses to stressful comments from family members, ee alone cannot account for relapse rates, family dysfunction may not be able to explain relapse in all cases

59
Q

what are the 4 types of cognitive distortion

A

egocentrism, meta-representation, central control, hypervigilance

60
Q

how can an egocentric bias explain sz

A

delusions result from events being wrongly interpreted due to the egocentric bias, meaning the sz jumps to conclusions, relating outside events back to themselves

61
Q

how can a meta representation explain sz

A

hallucinations due to own thoughts being misinterpreted as coming from an external source, confuse sound of own thoughts as a voice, belief of actions carried out by someone else rather than self

62
Q

how can central control explain sz

A

disorganised speech and thought could result from poor central control, inability to suppress thoughts and speech triggered by thoughts

63
Q

how can hypervigilance explain sz

A

hallucinations are due to neutral stimuli being perceived as threatening, therefore there is heightened anxiety and the expectation that something negative will happen

64
Q

define egocentrism

A

believing that everything is centred around you

65
Q

define meta representation

A

the cognitive ability to reflect on thoughts, experiences and behaviour, insight into our own and other’s actions

66
Q

define central control

A

the ability to suppress automatic responses while we perform deliberate actions

67
Q

define hypervigilance

A

heightened awareness of surroundings

68
Q

what explanations come under the psychological explanation of schizophrenia

A

family dysfunction, cognitive distortions

69
Q

cognitive explanation peel 1

A

p- research support
ev- stirling et al, 30 sz patients vs 18 controls, range of cognitive tasks like stroop test, name ink colour not word, sz patients took over twice as as long to do this
ex- task requires suppress impulse to read word, sz can’t suppress thoughts due to impaired central control, explains symptoms like disorganised speech/thoughts
l- cognitive approach and this study relies heavily on inferencing, assumptions about results from stroop test, cannot directly observe thought processes, unlike biological approach, we can measure dopamine levels, rely less on inferencing, reliable cause of sz

70
Q

cognitive explanation peel 2

A

p- cause may be biological
ev- biochemical research, cognitive problems are caused by increased dopamine
ex- faulty thought processes are a symptom of the biological cause of sz
l- cognitive neuroscience may provide the best explanation for sz, biological basis which affects thoughts, diathesis stress

71
Q

what are the 6 steps of family therapy

A
  1. in people’s homes (natural environment), two family therapists
  2. lasts 3-12 months, sessions every 2-4 weeks, minimum of 10
  3. family made more aware of sz, addresses hostility and reduces patient blaming
  4. whole family gains coping skills, addressing emotional over involvement
  5. family learns more constructive ways to communicate, addresses double bind, and concentrate on good things that happen (low ee)
  6. family and patient trained to look for early signs of relapse
72
Q

family therapy peel 1

A

p- effective
ev- nccmh, meta analysis, 32 studies, 2500 ppts, family therapy vs drug therapy, relapse in family therapy- 26%, drug therapy- 50%
ex- family therapy more effective than drug therapy alone, halved relapse rates
l- issues with meta analysis, secondary data, all studies may not have same level of control

73
Q

family therapy peel 2

A

p- issues comparing family therapy to drug therapy
ev- most patients undergoing family therapy will also be on antipsychotics
ex- difficult to establish causation, which therapy is working
l- can’t assess effectiveness of family therapy alone in a study because would be unethical to deny antipsychotics to someone suffering from psychosis

74
Q

family therapy peel 3

A

p- family therapy may be a management of sz not a treatment
ev- hogarty et al, 103 sz patients in high ee household, compare relapse rates with family therapy compared to medication only, 25% relapse with family therapy, 62% medication only
ex- helps to reduce relapse rates, however is not treating the cause of sz
l- family therapy is more expensive than drug treatment, implications for the economy, not treating sz, but helps to reduce amount of people re hospitalised and out of work

75
Q

name the six stages of CBT

A
  1. assessment
  2. engagement
  3. ABC model
  4. normalisation
  5. critical collaborative analysis
  6. developing alternative explanations
76
Q

detail step 1 of cbt

A

assessment- patient expresses thoughts about experience with sz, realistic therapy goals created using patient’s distress as motivation for change

77
Q

detail step 2 of cbt

A

engagement- therapist empathises with patient and feelings of distress, tells that explanations for distress can be developed together

78
Q

detail step 3 of cbt

A

ABC model- patient explains activating event (a) and their beliefs (b) that cause the emotional and behavioural consequences (c), beliefs can then be rationalised, disputed (d) and with effect (e) being the beliefs changed, creating more positive feelings (f)

79
Q

detail step 4 of cbt

A

normalisation- told that many people have unusual experiences, reducing anxiety and sense of isolation, placing psychotic experiences on a continuum with normal ones, less stigma, recovery seems more likely

80
Q

detail step 5 of cbt

A

critical collaborative analysis- therapist uses gentle questioning to help patient understand illogical deductions, trust between therapist and patient, empathy and non-judgement required to minimise distress

81
Q

detail step 6 of cbt

A

developing alternative explanations- patient develops own alternative explanation for previously unhealthy assumptions, if patient can’t, new ideas can be constructed with therapist

82
Q

cbt peel 1

A

p- research support
ev- NICE review, compared to antipsychotics alone, cbt was effective in reducing re hospitalisation rates up to 18 months following end of treatment, also reduces symptom severity
ex- difficult to reflect in acute stages of sz, best used after psychosis stage for most effectiveness, when stabilised (maybe via antipsychotics)
l- difficult to establish causation, antipsychotics or cbt working

83
Q

cbt peel 2

A

p- cbt not as effective as first thought
ev- jauhar et al, meta analysis, only small therapeutic effect on key symptoms of sz, small effects disappeared when symptoms were assessed blind
ex- little evidence to support widespread improvement due to cbt, led to conflicting recommendations in UK for treatment of sz
l- meta analysis, unreliable conclusions due to biased findings, no random allocation, studies don’t report cbt effectiveness reliably

84
Q

cbt peel 3

A

p- lack of availability and accessibility of cbt
ev- haddock et al, 187 randomly selected sz patients, only 13 had been offered cbt
ex- implications for economy, allocation of money, if cbt effective more money needs to be put into funding it to treat more people, in turn increasing amount of people who can go back to work
l- cbt has high drop out rate and in attendance, cannot guarantee that if offered patient will want it, can waste money, however patient is assessed in step 1 to see if they are ready to undertake cbt

85
Q

token economy AO1

A
86
Q

token economy peeleel

A

p- research support
ev- dickerson et al, meta analysis, 13 studies, 11 found beneficial effects directly attributable to token economy
ex- effective in increasing adaptive behaviours of sz patients in majority of cases
l- methodological issues in many of studies used, limits extent of effectiveness of token economies in improving symptoms of sz, difficulty assessing effectiveness
ev- comer, studies used to evaluate token economies are uncontrolled, when implemented on psychiatric wards all patients are brought onto programme, cannot compare a control group against the experimental group in the token economy system
ex- patient improvements can only be compared to past behaviours, issues with causation, cannot be sure improvement is due to token economy or another factor like staff attention
l- evidence for effectiveness of token economies is inconclusive

87
Q

interactionist approach to sz (AO1)

A
  1. biological- original schizogene belief and polygenic
  2. environment- stress in the environment
  3. original diathesis stress model- genetic vulnerability with environmental stress causes sz
  4. modern diathesis stress model- environment can affect genetics which can affect the environment
  5. treatments- cbt, biological, neuroscience, but works on a cognitive aspect which helps environmentally
  6. treatment should be a combination- drugs, cbt and family therapy, drug reduces symptoms so patient can engage in therapy with family and become self aware of own thoughts
88
Q

detail what the original diathesis stress model thought about sz

A

a single schizogene, develops a schizotypic personality, particularly sensitive to stress, without the schizogene, sz cannot develop, unless a carrier of the gene and exposed to chronic stress in childhood

89
Q

detail what the modern diathesis stress model thinks about sz

A

early trauma (diathesis) can alter the brain and make the hypothalamic-pituitary-adrenal system become overactive, making a person more vulnerable to stress, cannabis can also be stressor

90
Q

interactionist explanation peel 1

A

p- support for original diathesis stress model
ev- tienari, 145 children in genetic risk group with at least one bio parent with sz, control group had no genetic risk, family dysfunction only triggered sz if the child had a genetic risk
ex- interaction between genetic vulnerability and stress in the family
l- however, the original method is oversimplified, suggested one schizogene, however sz is polygenic, ripke found 108 genetic variations implicated in sz

91
Q

interactionist explanation peel 2

A

p- original diathesis stress model was not a complete explanation and so has been modernised
ev- verdoux, oxygen deprivation during labour leads to a 4x greater risk of developing sz, cannabis can increase the likelihood of developing sz by 7x
ex- this shows that the environment can affect our biology which can then interact with the environment, sz can develop without an initial genetic vulnerability
l- environment may be more important than our biology in determining sz, can environment and biology ever really be separated, must be an interaction between nature and nurture

92
Q

interactionist explanation peel 3

A

p- research support for interactionist treatments being effective
ev- tarrier, compared treatment of sz with meds, cbt + meds, cbt + meds + family therapy, found that when all treatments were had, lower symptom levels and re admissions to hospital were seen
ex- the medication works on dopamine, cbt works on cognitive distortions, family therapy works on family dysfunction, works on all causes of sz, if interactionist treatments have more success, then there is a greater chance that sz is interactionist
l- however, there could be a treatment fallacy, causation not established, treatment may treat symptoms, not the cause, sz may not be interactionist

93
Q

interactionist treatments peel 1

A

p- research support
ev- tarrier, compared treatment of sz with meds, cbt + meds, cbt + meds + family therapy, found that when all treatments were had, lower symptom levels and re admissions to hospital were seen
ex- the medication works on dopamine, cbt works on cognitive distortions, family therapy works on family dysfunction, works on all causes of sz, better long term, provides patient with coping strategies
l- if adopting the interactionist explanation of sz, as modern psychologists are, then interactionist treatment is needed, economic implications, more expensive treatment, but most successful and successful long term, means people can return to work

94
Q

interactionist treatments peel 2

A

p- interactionist treatments lowers relapse rates
ev- hogarty, combination of medication, family therapy and cbt is most effective, 0% relapse after 1 year
ex- medication helps to enter therapy, cbt helps to provide coping mechanisms to challenge thoughts themselves and reduce risk of relapse, family therapy reduces ee at home and so reduces risk of relapse also, no point trying to distinguish one cause/explanation/treatment, accept interactionist approach, treat people idiographically, unique treatment plan
l- relapse rates for drug therapy alone is 50% (NCCMH, meta analysis)

95
Q

interactionsit treatments peel 3

A

p- practical issues with implementing interactionist treatments
ev- USA tends to use drug treatments, pharmaceutical power, UK has long waiting lists for non-drug therapies, tend to be on drugs long before able to access family therapy or cbt
ex- both USA and UK are not interactionist, since lockdown wait list for mental health services has increased, less access to psychological therapies, annual cost of £2.6billion for sz in UK,
l- cost benefit analysis, economic implications, short term interactionism has high cost, but long term is worth it as people can go back to work and don’t relapse or offend

Psychology (9 decks)

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