biological explanations for schizophrenia Flashcards

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1
Q

what is dopamine?

A

a neurotransmitter level associated with the experience of pleasure which has an excitatory effect on neighbouring neurons

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2
Q

what are neural correlates?

A

patterns or structures in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience

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3
Q

gottesman (1991)

A

great genetic similarity is associated with a higher likelihood of developing sz
reviewed over 40 other studies and found similar results to gottesman and shields
-they found that the average concordance rate of sz in Mz to be 48% and in DZ 17%

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4
Q

gottesman and shields (1972)

A
  • examined medical records of 57 twins with schizophrenia
  • approximately 23 were MZ and 34 DZ
    -found MZ had a concordance rate of 42% compared to DZ who had 9% concordance rate
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5
Q

Joseph (2004)

A
  • found concordance rates amongst monozygotic twins to be 40.4% for schizophrenia development and for dizygotic twins to be 7.4%
  • more recent evidence reports an even lower concordance rate for monozygotic twins in relation to schizophrenia development
    -states that Mz are raised more similarly than DZ and suffer from identity confusion due to encountering similar environments
    -therefore, such assumptions mean concordance rates are not a genetic outcome but that of the environment.
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6
Q

family studies?

A
  • studies have found that schizophrenia is more prevalent in individuals who are closely related genetically with someone who already has schizophrenia
  • children with 2 schizophrenic parents have a 46% chance to develop sz
  • those with one parent have 13% and siblings 9%
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7
Q

adoption studies?

A
  • Tienari conducted a study in Finland of 164 adoptees who has schizophrenic mothers, of which 11 (6.7%) were also diagnosed with sz, compared with 4 cases in 197 control adoptees with no schizophrenic parents.
  • they concluded this evidence confirmed the genetic position within sz development.
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8
Q

kety (1988)

A
  • studied over 5000 danish children between 1923 and 1947 compared to a control group of 18%,
    -sz was developed in 32% of adoptees separated from biological parents who had the disorder.
    -furthermore, children born with no biological relatives with sz yet raised by sz parent were no more likely than the general population to develop sz.
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9
Q

condradictory point of kety?

A

however, in the study the concordance rate of 32% included related disorders, not purely schizophrenia
-therefore, this reduces the validity of the findings for a genetic basis of sz

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10
Q

what are candidate genes?

A

these are genes which create vulnerability.

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11
Q

candidate genes contributing to schizophrenia?

A

a number of genes appear to contribute a small increased risk of sz making it polygenic - a combination of different factors is needed.

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12
Q

why could schizophrenia be considered aetiologically heterogeneous?

A

as many different genetic DNA combinations or multiple factors can lead to the condition.

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13
Q

Ripke et al (2014)

A
  • compared the genetic makeup of 37,000 sz with 113,000 controls
  • found that 108 separate genetic variations were associated with increased risk of sz
    -genes associated with increased risk were those that code for neurotransmitter function, including dopamine.
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14
Q

what are the strengths and issues with studies such as gottesman, tiernari, kety and ripke?

A

a wealth of strong evidence from studies supports this explanation. however, many of these are correlations so causality cannot be inferred.

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15
Q

one limitation of the genetic explanation?

A

environmental factors may play a role such as smoking cannabis in teenage years and psychological childhood trauma.
this means that genetic explanations alone cannot provide a complete explanation of schizophrenia.

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16
Q

what is the dopamine hypothesis?

A

suggests that over-production of the neurotransmitter (dopamine) is responsible for the symptoms of schizophrenia.

17
Q

why was the dopamine hypothesis developed?

A
  • after observations of LSD and amphetamine; both of which enhance the activity of dopamine in the brain.
  • sometimes an overdose in these drugs can cause symptoms indistinguishable from schizophrenia such as schizophrenic-like hallucinations.
18
Q

where are dopamine neurons concentrated?

A

in the basal ganglia and frontal cortex which are concerned with the initiation and control of movements.

19
Q

what was the early version of the dopamine hypothesis?

A

that too much hypodopaminergia in the subcortex or that an excess of dopamine receptors in brocas area may be responsible for poverty of speech and/or auditory hallucinations.

20
Q

what is suggested if there is not enough hypodopamingeria in the cortex?

A

Goldman-rakic et al (2004) identified a role for low levels of dopamine in the prefrontal cortex, which is an areas associated with thinking and decision making, in the negative symptoms of schizophrenia.

21
Q

why could both of these explanations be correct?

A

high and low levels of dopamine in different parts of the brain are involved in schizophrenia.

22
Q

amphetamines evaluation?

A
  • amphetamines are dopamine antagonists which mean that they stimulate nerve cells that contain dopamine which causes the synapse to be flooded with this neurotransmitter (dopamine)
  • large doses of amphetamines can initiate the characteristic delusions and hallucinations of a schizophrenic episode in non-sufferers, which strongly suggests that dopamine plays a very important role in the behaviours of schizophrenics (Curran et al 2004)
23
Q

antipsychotic drugs evaluation?

A

there are many types of antipsychotic drugs which all block the activity of dopamine by reducing the stimulation of the dopamine system.
-therefore, symptoms such as hallucinations and delusions are reduced, this again shows the link between dopamine and schizophrenic symptoms.

24
Q

parkinsons disease evaluation? grilly (2002)

A

found that some people with parkinsons who were taking the ‘L-dopa’ to raise their levels of dopamine started to develop schizophrenic-like symptoms, which supports the idea that schizophrenics have abnormally high levels of dopamine.

25
Q

the role of glutamate as an evaluation point?

A

post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia.

26
Q

Haracz

A
  • reviewed post mortem studies finding that schizophrenics who had been taking antipsychotic drugs before death, had high dopamine levels. whereas those who did not take drugs showed normal levels of dopamine.
  • suggests that drugs that are given to lower dopamine levels, may actually have the opposite effect.
27
Q

what are neural correlates?

A

neuroanatomy is the study of anatomy and stereotypes organisation of the nervous systems.

28
Q

what are ventricles in the brain and what did Torrey suggest?

A
  • ventricles are spaces in the brain filled with cerebrospinal fluid.
  • found that ventricles of suffers of schizophrenia are 25% larger than non-sufferers, and this is more apparent in the case of type 2 schizophrenics.
    -suggested that the ventricles themselves were not the cause of schizophrenia itself but the decrease in the brain tissue that would have occupied the space.
29
Q

Ho et al (2004)

A
  • researched the relationship between the size of ventricles and development of schizophrenia
  • compared non-schizophrenic ventricle size with schizophrenic ventricles
  • found that they had much larger ventricles which contained cerebrospinal fluid
  • longitudinal study up to several years and found that the larger the ventricles became, the less easy it was for patients to cope with their symptoms.
30
Q

what is one issue with all the research evidence on the ventricles in the brain?

A

although there is much evidence supporting this explanation, a problem is that it doesn’t suggest whether the differences in neuroanatomical structures of sufferers of schizophrenia caused the condition or whether having schizophrenia causes the changes in the brain.

31
Q

individual differences in the ventricles of the brain evaluation?

A

brains also vary in size and weight therefore it is not easy to measure ventricle enlargement accurately as there is not a set criteria for what constitutes as enlargement

32
Q

nature nurture evaluation?

A

there is an overwhelming amount of evidence supporting biological factors in the development of sz, however, the effect of the environment cannot be ignored.