Schizophrenia-explanations- psychological Flashcards
most current theories of psychological factors of sz can be seen within either of which two models
diathesis stress model the stressor
something that influences the presynaptic dopamine dysfunction
stressful life events
seen as a stressor in the DS model- those at the genetic risk will be affected by stressor others will not.
stressful life events can also been seen as a possible contributor to the dopamine dysfunction in the final common pathway version of the dopamine hypothesis
name stressors
bereavement
losing your job
a divorce/relationship breakdown
physical/sexual/emotional/racial abuse
for younger people things like exams, first jobs, starting or ending relationships
measurement of stress
Holmes and Rahe social readjustment rating scale
questionnaire aimed to investigate changes or adjustments (events) to rate level of concern or relevance in life (measured in life change units)
mechanisms of how SLE impact SZ
via the HPA (hypothalamic pituitary adrenal axis)
disregulation in the hormone cortisol (stress hormone) has been associated with psychosis and higher levels of cortisol predicts severity of symptoms
or
conbrituor to the DD within the final common pathway version of the DH- stressful events are one of the facts that lead to dopamine dysfunction, which leads to psychosis
evaluation of SLE
norman and mall’s review found that sevrity of symptoms over time was correlated with SLE
suggesting that those already predisposed to SZ are susceptible to the affect of such events.
it is notable there is no evidence that those at risk have a higher number of stressful life events than the general population, in fact they have less (according to Horon et al), but it is the ability to cope with them that means they are adversely affected.
the main finding has been replicated by Day’s cross-national study: which found higher rates of SLE in the 2-3 weeks preceding the onset of SZ.
methodological evaluation of SLE
research into the effects of SLE has been sufficient in testing both western and cross-cultural samples for there have been a number of meta analyses and there is consistency in findings: so can be confident there is a relationship of some sort between SLE and SZ
but major prob: is it a casual one?!? fraught with methodologigcally probs
since many of these studies were retrospectively conducted:
it could be that patients inaccurately report more SLE preceding full onset - either because their precise recall is poor in the first place or that because they are already experiencing build up of symptoms which alters this ability as well. the development of the illness could also mean that events are fabricated- many this assumptions about the link between SLE and SZ a little more tenuous- due to inaccuracy of LE recorded.
however a prospective study is able to address this problem fairly well, even as a small study. Ventural et al and horon et al found that SLE preceded illness as recorded at the time (rather than retrospectively),
brown’s 3 elements of expressed emotion
hostility - negative attitude toward patient because family believe it can be controlled but patient choosing not to get better
criticism- relative feels that the patient is partly or fully responsible for their disorder
over emotional involvement- relative takes blame for the disorder, so shows over concern, this pity is stressful for the sz- so relapse to cope with the pity
measurement of expressed emotion
typically determined though a taped interview known as the camberwell family interview
- conducted with carers of the patient
- interviewer tries to create a picture of how thing have been in the household the months leading up to the onset
- interview is taped and transcript is rated.
- obtain objective info- about events and circumstances in the home months before onset
- obtain subjective info- about relatives feelings and attitudes towards the patient when talking about the disorder
RATE:
- the frequency of critical comments made by the relative
- the number of statements of resent towards the patient
- a rating of statements reflecting emotional over involvemnet/ over protectiveness of patient
expressed emotion
a qualitative measure of the ‘amount’ of emotion displayed typically in a family setting by caregivers or relatives.
it is thought that high level EE can worsen prognosis or act as a potential risk factor for the development of SZ
EE can be seen as a stressor in the diathesis stress model
or a contributor to the final common pathway model of the dopamine hypothesis that leads to psychosis
difficulties of camberwell family interview
fluctuations in behaviour
interview is open to interpretation (emotions of patient)
people lie
social desirability effects- with family members
inside the patient may feel angry /sad but cannot articulate these feelings due to hold of the illness
may be showing psychosis during interview causing more difficulty in interpretation.
emotion could be heightened
why EE makes relapse more likely
each type of EE makes the SZ feel more isolated and alien the stress of feeling blamed increases cortisol levels
evaluation of EE (evidence)
Brown initially identified that patients returning to home with EE (criticism, hostility and over involvement) was high were at greater risk of relapse than those returning to a home of low EE.
then replicated by Vaughn and Leff relapse rate: 53% in high EE homes and 13% in low EE homes
& amount of face to face time spent with relative correlated with risk of relapse
A MA also drew these same conclusion (butzlaff) 27 studies 65% relapse rate with high EE and 35% low EE (a moderate effect size)
evaluation of EE (explain/methodology)
such research is plentiful but only correlational
EE- could be response to symptom severity (not cause of relapse?)
if this is the case then this support for the theory is weaker
King, in a prospective- tracking EE and symptoms over time- study found that some elements of EE were a response to rather than a cause of worsening symptoms which contracts the theory that EE causes relapse.
however this had only 28 ptts and there was PPT attrition due to it’s prospective nature (mothers and Szs had to be interviewed 3 times at 9 month intervals)
On the other hand treatment studies (e.g pharaoh’s cochrance review) have shown, in line with the retrospective studies by brown, bustle and vaughn and leff- that reducing levels of EE through therapy (family intervention) have reduced levels of EE and therefore relapse (as well as increased medication compliance and reduced hospital admission)
but there are doubts about random allocation in these studies
but the direction of causality is still difficult to judge
it is possible to have a bidirectional causality between EE and relapse
evidence is overall mixed likely that causality goes int both directions i.e from EE to relapse and from symptom severity to high EE
more better quality, prospective and intervention studies are needed
