Schizophrenia Flashcards
(40 cards)
Osorio support reliability of diagnosis
DSM-5 inter rater .97, test re test .92
H - doesn’t support ICD
Read limitation reliability of diagnosis
37% test re test reliability
Cheniaux limitation validity diagnosis
two psychiatrists, 100 patients 1) DSM 39 diagnosed
2) ICD 68 diagnosed
Low criterion validity
H - Osorio found exzcellent agreement between clinicians of DSM > good criterion validity if diagnosis takes place in one system
Co-morbidity limitation of diagnosis
more than one condition at once
around 1/2 SZ have depression or substance abuse
exist as one condition together, SZ not distinct
Lowers descriptive validity
Gender bias in diagnosis of SZ
since 1980 more men diagnosed > women closer relationships lead to better functioning but may not receive necessary treatment
Loring and powell: male or no gender 56% diag, female 20% diag - beta bias
Culture bias in diagnosis of SZ
symptoms have diff meanings - afro caribbean hearing voices common from ancesteror (hallucinations) > in UK 10x more likely to be diagnosed than white british > over interpretation
Copeland: 69% US psychiatrists diagnosed patient and 2% british diagnosed
Symptom overlap limitation of diagnosis of SZ
Symptoms of one disorder present in another
SZ and bipolar disorder involve +ve and -ve symptoms > variations of one condition ? > hard to distinguish as seperate disorders
Biological explanations of SZ
Genetic basis : risk inc w relative genetic similarity
- family studies > gottesman 9% share w sibling, 48% MZ twins
- Twin studies > Joseph 40% MZ , 7% DZ - H also share env
- Candidate genes > SZ polygenic :** Ripke 108 genes > diff studies diff genes, SZ aetiologically heterogeneous (diff combinations)
- Mutation : correlation between paternal age (more chance sperm mutate) and risk of SZ
- Neural correlates > patterns of activity in brain relate to SZ e.g dopamine
- Enlarged Ventricles**
Original dopamine hypthesis (neural correlates)
Hyperdopaminergia in subcortex (D2 receptors)
Antipsychotics for SZ caused symptoms similar to Parkinson’s, associated w low DA
suggests SZ due to high levels
Excess DA receptors
Updated dopamine hypothesis (neural correlates)
Hypodopaminergia in PFC (D1 receptors)
Leads to hyperdopaminergia in subcortex
Evidence support for genetic explanation
Gottesman, Joseph and Adopt studies
risk increases with genetic similarity 9% sibling 48% MZ
adopt studies show child w bio parents w SZ at heightened risk (tienari)
Joseph twin studies 40% MZ, 7% DZ > similar to Hilker: 33%MZ 7%DZ
Env risk factors limitation genetic explanation
genetic bio reductionist ignore env
env increase risk e.g THC as teenager is risk factor, trauma> vulnerable mental health problems
Genetic counselling support bio explanation (RWA)
Identify risk of developing SZ, avoid risk factors
H - figures only avg.
Evidence support dopamine hypothesis involved w SZ
Amphetamines increase DA and worsen symptoms
Antipsychotics lower DA and reduce symptoms
Candidate genes act on production of DA or receptors
Limitation of DA hypothesis role of glutamate
post mortem and scanning found raised glutamate in SZ ppl
candidate genes are associated w glutamate production
not just DA neurotransmitter
Tenn support neural correlates
induced symptoms in rats w amphetamines which increase DA, H - other drugs that increase DA didnt work
H - only tested on rats
2 Parts to dysfunctional thinking cognitive explanation and who
Developed by frith - disruption to normal though processing
1) meta representation dysfunction : can’t recognise thoughts and actions as their own > explains hallucinations and delusions
2) central control dysfunction : issues w ability to suppress automatic responses > explains disorganised speech
Research support for dysfunctional thought processing, Stirling
Stirling compared ability on cog tasks 30 SZ 30 control, SZ 2x longer to name font colours (stroop task) > cog processes impaired
Cog explanation only proximal explanation (limitation)
explains what is happening now
distal ( e.g genetics) focus on on initial cause > cog theory only partial explanation
Antipsychotics drug therapy aim and types
reduces psychosis symptoms, short course or rest of life
1) **Typical 1st ** > e.g chlorpromazine - dopamine antagonists reduce DA action reduce symptoms. Have sedation effects to calm pp
2) Atypical 2nd > less side effects, updated version e.g clozapine (agranulocytosis)
bind to DA, serotonin and glutamate receptors, reduce depression + suicide
e.g Risperidone - binds more strongly to DA receptors means smaller dose needed > less side effects
syrup absorbed faster than tablets
Evidence effectiveness drug therapy Thornley +Meltzer
> Counterpoint
thornley : chlorpromazine (typical) reduce symptoms compared to placebo
Meltzer : clozapine (atypical) more effective than typical antipsychotics, works in 30-50% cases where typical don’t.
COUNTER - Healy: evidence flawed, only have short term effects + same data published many times exaggerates effects - improved symptoms not mean reduced psychosis
Side effects of typical and atypical
dizziness and agitation - typical long term use causes tardive dyskinesia (involuntary face movement), atypical long term risk agranulocytosis (affect immune system)
What are enlarged ventricles which symptoms they effect and who limitation
ventricle=Fluid filled cavities between brain areas: PFC and central areas, associated w -ve symptoms
Weyandt - enlarged ventricles only associated w -ve symptoms so can’t explain all of SZ
- problems w cause effect: SZ cause brain damage or brain damage SZ
- problems w extent of brain abnormality, not all SZ have ventricles
What was Rosenhan’s study
7/8 pseudopatients admitted to psychiatric hospital w diagnosis of SZ
2nd part, told hospitals pseudopatients would try to get in but didn’t actually send any - 10% w SZ suspected of being fakes
invalid and unreliable (inter-rater)
