Treatments & Interactionist approach Flashcards
What is the interactionist approach to scz?
a broad approach to explain schizophrenia, acknowledging that a range of factors are involved in its development
What does the diathesis-stress model suggest?
underlying vulnerability (diathesis) and a trigger and both necessary for onset of scz
Outline Meehl’s model
diathesis was entirely genetic - schizogene + lead to development of biologically based schizotopic personality, a characteristic of which is sensitivity to stress
- no schizogene means can’t get scz no matter how much stress they’re exposed to but in carriers of gene chronic stress in childhood/adolescence, particularly presence of schizophrenogenic mother, could result in scz
Outline the modern understanding of the diathesis (interactionist)
as Ripke showed, many genes contribute to increase genetic vulnerability and there is not one schizogene - also a range of factors beyond genetic, rather than a stressor, psychological trauma - early trauma alter developing brain, also child abuse may make HPA system become overactive, making person more vulnerable to stress
Outline the modern understanding of stress (interactionist)
anything that risks triggering scz, e.g. cannabis use (increase risk 7x) as it interferes with dopamine system - may be one or two more factors influencing it
Treatment of scz according to interactionist model
model acknowledges importance of both biological and psychological factors so must be compatible with both biological and psychological treatments - combining antipsychotic medication & psychological therapies (CBT)
What did Turkington et al say
possible to believe in biological causes and use CBT to relieve symptoms
AO3 interactionist approach - evidence role of vulnerability and triggers
Tienari et al: adopted children away from scz mothers & adoptive parents’ parenting style assessed and compared with control group with no genetic risk
- child rearing with high criticism, conflict and low empathy - implicated in development of scz, only for children with high genetic risk - support
AO3 interactionist approach - original diathesis-stress model over-simplistic
NO schizogene and stress comes in many forms which can include biological factors e.g. childhood trauma was diathesis and cannabis = stressor
AO3 interactionist approach - effectiveness of combo of treatments
Tarrier et al: randomly allocated 315 patients to 1. medication and CBT, 2. medication and supportive counselling, 3. medication - patients in combo groups had lower symptom levels than control BUT no difference in hospital readmission
AO3 interactionist approach - don’t know how diathesis and stress actually work
don’t know mechanisms by which symptoms occur and how both vulnerability and does produce them
AO3 interactionist approach - treatment-causation fallacy
Turkington et al: fact both treatments effective together does not mean interactionist approach is correct - logical error
What are antipsychotics?
drugs used to reduce the intensity of symptoms, in particular the positive symptoms of psychotic conditions - taken as a tablet or syrup (injections for some)
What is an example of a typical antipsychotic? How do they work?
chlorpromazine - association between them and the dopamine system (dopamine hypothesis) act as antagonists - reduce the action of dopamine by blocking dopamine receptors in the synapses of the brain - initially, levels build up, but then are reduced - reduce hallucinations
- also as sedative to calm patients (affect on histamine receptors)
What is an example of atypical antipsychotics? How do they work?
clozapine - binds to dopamine receptors in the same way chlorpromazine does, also acts on serotonin and glutamate receptors - improve mood and reduce depression/anxiety and so improves cognitive functioning
Why were atypical antipsychotics formed after typical ones?
to improve effectiveness and reduce size effects
Why was risperidone developed?
another atypical drug - as effective as clozapine but safer as some clozapine patients died from blood condition - binds more effectively to dopamine receptors so is effective in smaller doses, with fewer side effects
AO3 drug therapy - evidence for effectiveness
Thornley et al: data from 13 trials and found chlorpromazine better associated with better functioning and reduced symptoms than placebo
- also then clozapine better than typical and 30-50% better in treatment resistant cases
AO3 drug therapy - serious side effects typical
typical: dizziness, agitation, sleepiness, weight gain - longterm use: lip smacking, grimacing due to dopamine sensitivity
NMS cause by blocking dopamine action in hypothalamus - can be fatal
AO3 drug therapy - serious side effects atypical
developed to reduce side effects, but still exist
AO3 drug therapy - depends on the dopamine hypothesis
idea of there being too much dopamine the subcortex of the brain - may not be correct and dopamine may be too low in some areas of the brain e.g. prefrontal cortex - if so, shouldn’t work which undermines the faith people have in the positive effects
AO3 drug therapy - problems with evidence of effectiveness
some successful trials published multiple times - exaggerating effectiveness and positive effects
most studies only look at short term effects
- effectiveness over estimated
AO3 drug therapy - benefit staff rather than patients
human rights abuse
Outline CBT for treat scz
5-25 sessions, in groups or individual, helps patients identify irrational thoughts and try to change them - help patients cope with symptoms, not get rid
