biological explanations and therapies Flashcards
(20 cards)
genetic explanation
schizophrenia runs in families, inherited as genes from parents
Gottesman
twin studies
- conducted a large scale family study
- MZ twins have 48% concordance rate than DZ twins, only 17%
- support bc MZ share 100% of genes and DZ only 50%
candidate genes
believed to be associated with risk of inheritance of SZ
- believed to be polygenic (Ripke found 108 gene variations associated w SZ)
Dopamine hypothesis
high dopamine activity leads to acute episodes and positive symptoms
amphetamines
increase the amount of dopamine, so if small dose given to a SZC, symptoms worsen
the role of dopamine
important in the functioning of several brain systems that may be implicated in the symptoms of SZ
hyperdopaminergia (subcortex)
high levels/ activity of dopamine in the subcortex may be associated w positive symptoms such as auditory hallucinations
- bc Broca’s area (regulates speech)
- original version of dopamine hypothesis
hypodopaminergia (cortex)
low levels of dopamine in prefrontal cortex may be associated w negative symptoms
neural correlates
structure/ activity in the brain that occur along with an experience
- associated w positive & negative symptoms
neural correlates of negative symptoms
avolition = loss of motivation
- motivation involves anticipation of reward
- ventral striatum involved w anticipation
- Juckel et al found lower levels of activity in VS in SZC’s than control
- pos correlation between Vs activity and negative symptoms
neural correlates of positive symptoms
Allen et al found lower activation in superior temporal gyrus and anterior cingulate gyrus in SZ group
- they all experienced auditory hallucinations
- reduced activity in these 2 areas = neural correlate of auditory hallucinations
supporting evaluation for biological explanations
research support for genetics
- Gottesman twin study
> CA, MZ twins usually treated as ‘twins’ rather than individuals and treated similar
- Tienari et al adoption study
- genetic factors make some ppl more vulnerable to developing SZ than others
Tienari et al
long term study in Finland
- 124 adoptees w SZC biological mothers
- 147 socia-demographically matched control
- 9/124 became psychotic
- 2/147 became psychotic
limiting evaluation for biological explanations
mixed evidence for dopamine hypothesis
- dopamine agonists (amphetamines) increase symptoms in SZC’s and can create SZ like symptoms in normal ppl
- antipsychotics reduce dopamine activity, used to treat SZ
- chemicals needed to produce dopamine are taken up faster in SZC’s brains, shows they create more dopamine
- but also evidence that dopamine is not the only hormone to be associated w SZ
- Ripke found genes that call for the production of other neurotransmitters
- shows dopamine is important but others exist too (eg. glutamate)
drug therapy
most common treatment for SZ
- uses antipsychotics
antipsychotics
- may be required in LR or SR
- some can take for a short time and stop w/o return of symptoms
- others need them for life or face recurrence
typical antipsychotics
work as dopamine antagonists (chlorpromazine)
- block dopamine receptors in the synapses of the brain, reducing action of dopamine
- normalises neurotransmission in key areas, reducing symptoms like hallucinations
- initially dopamine levels increase but then production reduces
atypical antipsychotics
minimise side effects, also addresses neg symptoms
- clozapine, can cause a blood condition so ppl who take it have regular blood tests
- binds to dopamine receptors like typical, but also serotonin and glutamate receptors
- helps improve mood, reduce depression and anxiety
- prescribed to suicidal ppl, 30-50% of SZC’s
supporting evaluation for biological therapies
evidence for effectiveness
- Thornley et al, ppl on chlorpromazine had better overall functioning and reduced symptom severity
- Leucht et al, meta-analysis of 65 studies, 6000 ppt, all on antipsychotics, some taken off and given placebo
- withing 12m, 64% of placebo relapsed, only 27% of antipsychotics
limiting evaluation for biological therapies
likelihood of side effects
- typical = dizziness, agitation, sleepiness…
- long-term use can = tardive dyskinesia
- most serious = neuroleptic malignant syndrome = high temp, delirium, coma
- atypical have fewer but still some like agranulocytosis