SCHIZOPHRENIA-biological explanations Flashcards Preview

Psychology Unit 3 > SCHIZOPHRENIA-biological explanations > Flashcards

Flashcards in SCHIZOPHRENIA-biological explanations Deck (48):
1

what does evidence derive from for biological explanations?

family studies-genetics exp
twin studies -genetics exp
adoption studies -genetics exp
biochemical explanations
neuroanatomical explanations

2

studies supporting family studies?

kendler et al
main study KETY ET AL

3

studies supporting twin studies?

gottesman and shields
fischer
cardno et al

4

studies supporting adoption studies?

tienari et al x 2
wahlberg et al *
kety et al

5

studies supporting biochemical explanations?

falkai et al
wong et al

6

studies supporting neuroanatomical explanations?

wood et al
weinberger
buchsbaum
flaum et al
woodfruff et al
castner et al

7

what are the bullet point for evidence from family studies? (3)

1.1st degree rels share 50% of genes and 2nd degree 25%
2.family studies involve comparison of rates of schiz of relatives of diagnosed cases compared with relatives of controls
3. evidence the closer bio relationship the greater risk of schiz developing

8

support for family studies kendler et al?

first degree rels of schiz = 18x more at risk compared to general population

9

opposition to kendler et al?

family studies conducted retrospectively when comparing cross section of people already diagnosed

10

what is bad about retrospective data?

unreliable as problems in memory and records= likely whereas prospective = more reliable as follow people over time b.f and after conditions

11

support for family studies main study?

kety et al

12

what happened in kety et al?

-high risk group= 207 offspring schizo mothers
-low risk=104 control children with healthy mothers
-children ages 10-18 matched age-gender-socio eco status-follow up testing on children conducted
-schizo diagnosed in 16.2% of high risk and only 1.9% of low risk group

13

positive of kety et al?

prospective study which follow development of schizo
matching of risk factors in children

14

negative & opposition of kety et al?

cant differentiate btw genetic and environmental influences as there is shared environment

15

another opposition of family studies?

many began before effective diagnostic symptoms so possible that there was variation of symptoms for original diagnosis of schiz

16

bullet point for evidence for twin studies? (4)

1.compare difference in concordance rates of both twins mz and dz
2.only mz have identical genes
3.higher concordance rate in mz than dz
4.mz twins reared apart can be used to distinguish effects of genetics and environ

17

what is concordance rates?

likelihood of both twins being affected with the disorder

18

what happened in support for twin studies gottesman and shields?

58% of twins who reared apart were concordant for schizophrenia

19

opposition of gottesman & shields?

even mz that rear apart share same womb envi b4 birth. The contrib of environ factors cant be entirely discounted

20

what happened in support for twin studies for fischer?

9.4% of offspring from non affected mz twin developed schiz comapred to 1% of general pop

21

opposition of fischer?

where twins reared apart,such sep could be from fam problems which could influence mental health

22

what happened in support for twin studies for cardno et al?

40% of concordance rate in mz twind compard with 5.3% in dz twins

23

bullet point for evidence for adoption studies?

1.adopted children who develop can be compared to biological and adoptive parents
2. if schiz has genetic comp,the development of disorder should be maintained even if change in environ
3.adoption studies attempt to highlight such genetic influence

24

what happened in support for adoption studies for tienari et al?

risk of developing was 4 x greater in adopted with schiz biological mothers compared to mother w/ schiz

25

opposition for tienari et al study?

wahlberg et al

26

opposition of wahlberg et al?

re examined tin data and found strong effect of environmental factors where those at risk of developing schiz were adopted into families with poor communication

27

what happened in support for adoption studies for kety et al?

study of national sample from denmark. high rates of schiz were found in adopted children whose biolo parents schiz

28

opposition of kety et al?

longitudinal research:diagnostic criteria of schiz continually changing

30

overall evaluation of genetic explanation-support?

1. there is strong evidence that genetics are a risk factor for schiz

31

overall evaluation of genetic explanation-oppositional?

1. even if a mz twin has disorder the risk for the other twin is less than 50 % suggesting that genetic influences dont offer a complete explanation
2. 89% of ppl w schiz dont have relative who been diag with disorder
3. research into location of specific genes has not produced definitive results. it is impossible to understand the underlying mechanism that leads form genetic risk to disorder

32

what is the biochemical explanation of schizophrenia?

the dopamine hypothesis

33

what happens in the dopamine hypothesis 4 bullet points?

1.dopamine is a neurotransmitter that is found in the limbic system
2.over activity in the dopamine controlled parts of brain can result in schiz
3. phenothiazines which inhibit dopamine activity can reduce the symptoms of schiz
4.-l dopa (dopamine releasing drug) can caus schiz symptoms in non psychotic people
5. lsd/amphetamines increase dopamine activity and induce schiz symptoms

34

what is a neurotransmitter?

chemical that acts as messenger to transmit impulses from one nerve cell to another that is found in limbic system

35

what happened in support for dopamine in falkai et al?

examinations of brain from dead schizophrenic patients show that there is an excess of dopamine in the left amygdala

36

opposition for falki et al?

difficult to determine if increases in dopamine found in brain regions are result of schiz or cause of it

37

what happened in support for dopamine in wong et al?

PET scans show great dopamine receptor density in the caudate nuclei in those with schizophrenia

38

opposition for wong et al?

drugs tend to be effective at alleviating positive symptoms of schiz,but not negative symptoms,suggesting that all of the symptoms of schiz may not be directly related to dopamine

39

opposition for dopamine hypothesis? (3)

1. clozapine =effective in treating however it changes levels in serotonin not dopamine
2. dopamine unlikely to be only factor in schiz
3.biochemical exp = reductionist where stress and irrational thought processes not taken into consideration

40

what is neuroanatomical explanation for schiz?

magnetic resonance imaging

41

what is magnetic resonance imaging in bullet points (3)

1.non invasive technique where radio waves recorded in brain
2. recordings are computerised and assembled into 3d image of brain structures
3.studies= definite structural abnormalities in the brains of patients with schiz

42

what happened in support for magnetic resonance imaging?

earlier research depended on post morterm studies where difficult to determine whether structural damage/causal factor or result of drug therapy or natural progression of disorder.examination of living patients provides clearer understanding of causal relationship

43

opposition for magnetic resonance imaging?

brain imaging in relation to schiz has been restricted mainly to those who have already been diagnosed so the direction of causality is difficult to determine

44

what happened in support for magnetic resonance imaging for wood et al ?

79 males considere high risk for schiz were compard to 49 healthy for their hippocampus size. High risk individ has smaller h than control. Brain abnormality excisted b4 condition

45

opposition for magnetic resonance imaging in weinberger?

there is inconclusive evidence concerning whther brain changes are b4 the onset of schiz or whether following clinical symptoms

46

what happened in support for magnetic resonance imaging for buchsbaum ?

abnormalities in the frontal and pre-frontal cortex,the basal ganglia,the hippocampus and the amygdala for patients

47

opposition for magnetic resonance imaging in flaum et al?

found no abnormalities in the temporal lobe regions of those with schiz

48

what happened in support for magnetic in woodruff et al?

significant reductions in temporal lobe compared to controls

49

what happened in support for magnetic in castner et al?

exposed monkeys to brain damaging x rays during foetal development. no ill effects found during childhood but adolescence developed symptoms of schiz