explanations of schizophrenia Flashcards

(109 cards)

1
Q

what are the three biological explanations of schizophrenia?

A

-genetic factors
-dopamine hypothesis (usually neurotransmitters)
-neural correlates

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2
Q

what is the genetic explanation of schizophrenia?

A

according to the genetic explanation, schizophrenia runs in families, and people with schizophrenia have inherited mutated genes that cause, or make them more vulnerable to, SZ

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3
Q

how much of a part do genetics play in schizophrenia?

A

it’s difficult to be certain how much of a part genetics do play as many family members are also exposed to the same environments

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4
Q

studies that provide evidence for the genetic basis of schizophrenia:

A

family study → Gottesman (1991)
twin studies → Joseph (2004)
adoption studies → Tienari et al
(2000) in Finland

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5
Q

Gottesman (1991) study:

A

found that the risk of developing schizophrenia increased as the genes shared with a relative increases

e.g:
relationship to person with
schizophrenia / risk of developing SZ

siblings → 9%
identical twins → 48%

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6
Q

Joseph (2004) study:

A

found a concordance rate of 40.4% for monozygotic twins and 7.4% for dizygotic twins, the occurrence rate in the general public is 1%
↳ this suggests there is a genetic element to schizophrenia

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7
Q

Tienari et al (2000) in Finland study:

A

of 164 adoptees whose biological mothers had been diagnosed with schizophrenia…
-11 (7%) also received a diagnosis of schizophrenia
-just 4 (1.5%) of the 197 controls adoptees
(those born to non-schizophrenic mothers)

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8
Q

what are candidate genes?

A

genes which, through research, have been implicated in the development of schizophrenia

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9
Q

schizophrenia is…

A

polygenic → multiple genes are linked to SZ / different studies have found lots of different candidate genes (SZ is aetiologically heterogeneous)

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10
Q

define aetiologically heterogeneous:

A

different combinations of factors can lead to SZ

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11
Q

evidence for candidate genes:

A

Ripke et al. (2014)
-compared the genetic make up of 37,000 people with schizophrenia to
113,000 people who did not (control group)
-they found 108 separate genetic variations that were associated with schizophrenia

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12
Q

strength of genetic explanation of schizophrenia:

A

-one strength of the genetic explanation is the strong evidence
base

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13
Q

ao3 / strength of genetic explanation of schizophrenia - strong evidence base

A

P - one strength of the genetic explanation is the strong evidence
base

E - family studies like Gottesman show that risk increases with genetic
similarity to a family member with schizophrenia
↳ joseph (2004) showed concordance rate of 40.4% MZ and 7.4% for DZ

L - this supports that some people are more vulnerable to schizophrenia as a result of their genetic make up

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14
Q

criticisms of genetic explanation of schizophrenia:

A

-there is clear evidence to show that
environmental factors also increase the risk of developing schizophrenia

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15
Q

ao3 / criticism of genetic explanation of schizophrenia - there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia

A

P - there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia

E - environmental factors include both biological (birth complications and smoking THC-rich cannabis in teenage years) and psychological (childhood trauma) influences which leaves people more vulnerable to schizophrenia
↳ morkved (2017) found 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues

L - this means that genetic factors alone cannot provide a complete explanation for schizophrenia

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16
Q

what is dopamine?

A

a neurotransmitter that generally has an excitatory effect and is associated with regulating attention, perception & thought

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17
Q

what does the original dopamine hypothesis state?

A

schizophrenia was caused by excessive activity of dopamine → neurons that respond to dopamine to fire too often and transmit too many messages

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18
Q

what does the transmission of too many messages do?

A

the message overload produces many symptoms of schizophrenia (hallucinations and delusions)

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19
Q

schizophrenics are thought to have…

A

abnormally high numbers of dopamine receptors on receiving neurons (high sensitivity) resulting in messages from neurons that fire dopamine to fire too easily

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20
Q

term for the original dopamine hypothesis:

A

hyperdopaminergia in the subcortex

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21
Q

what is hyperdopaminergia in the subcortex?

A

it focuses on the possible role of high levels or activity of dopamine in the subcortex (the central areas of the brain)

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22
Q

term for the new dopamine hypothesis:

A

hypodopaminergia in the cortex

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23
Q

what is hypodopaminergia in the cortex?

A

-more recent version of the hypothesis
-abnormal dopamine levels in the brain’s cortex, particularly low levels of dopamine in the pre-frontal cortex

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24
Q

what is the PFC responsible for?

A

thinking and decision making - this could explain negative symptoms

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25
overall explanation of schizophrenia:
-it is more probable that both hyper- and hypodopaminergia are correct explanations -high and low levels of dopamine in different regions are implicated in schizophrenia
26
strength of the dopamine hypothesis:
-the idea that dopamine (DA) is involved in schizophrenia
27
ao3 / strength of the DA hypothesis - the idea that dopamine is involved in schizophrenia
P - one strength of thw dopamine hypothesis is the idea that dopamine is involved in schizophrenia E - research has found that amphetamines increase DA and worsen symptoms in people with schizophrenia, they induce symptoms in people without / second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms L - this strongly supports that dopamine is involved in the symptoms of schizophrenia
28
criticism of the dopamine hypothesis:
dopamine abnormalities are not present in all schizophrenics, especially those with negative symptoms
29
ao3 / strength of the DA hypothesis - dopamine abnormalities are not present in all schizophrenics
P - dopamine abnormalities are not present in all schizophrenics, especially those with negative symptoms E - problems with dopamine seem to be associated more with positive symptoms, so it may only explain certain aspects or types of the illness L - the diversity of types and symptoms in schizophrenia implies that there are several neurotransmitters involved and not just dopamine
30
what are neural correlates?
measurements of the structure or function of the brain that occur in conjunction with schizophrenia
31
what does the neural correlate approach believe?
that schizophrenia has developed due to structural and functional brain abnormalities
32
which neural correlates of schizophrenia have been found?
enlarged ventricles → schizophrenia lower levels of activity in the ventral striatum → negative symptoms lower activation levels in the superior temporal & anterior cingulate gyrus → positive symptoms
33
neural correlates of schizophrenia:
-brain scans have found that schizophrenia is caused by enlarged ventricles (fluid-filled gaps between brain areas) -these are associated with damage to central brain areas, such damage is often associated with negative symptoms
34
evidence of enlarged ventricles being linked to schizophrenia:
Johnstone (1976) found that schizophrenia had enlarged ventricles while non-sufferers did not, which suggests schizophrenia is related to a loss of brain tissue.
35
neural correlates of negative symptoms of schizophrenia:
-one negative symptom, avolition involves the loss of motivation -motivation involves the anticipation of a reward, and the ventral striatum, is believed to be involved in this anticipation -abnormality of the ventral striatum may be involved in avolition
36
evidence of the ventral striatum being involved in the negative symptoms of schizophrenia:
Juckel (2006) -found lower levels of activity in the ventral striatum than in controls -they observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms
37
evidence of neural correlates of positive symptoms of schizophrenia:
Allen (2007) -scanned the brains of patients experiencing auditory hallucinations and compared them to a control group -brain scans occurred whilst they identified pre-recorded speech as theirs or others
38
results & conclusion of allen (2007)
-lower activation levels in the superior temporal and anterior cingulate gyrus were found in the hallucination group, they also made more errors than the control group ↳ we can therefore say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination
39
ao3 / criticism of neural correlates as an explanation of schizophrenia
-one criticism of the role of enlarged ventricles is that the research evidence is inconclusive -one limitation of neural correlates explanation is that the research evidence is correlational
40
ao3 / criticism - one criticism of the role of enlarged ventricles is that the research evidence is inconclusive
P - one criticism of the role of enlarged ventricles is that the research evidence is inconclusive E - some non-schizophrenics have enlarged ventricles, while not all schizophrenics do / this goes against the ideas of schizophrenia being linked to a loss of brain tissue L - if it were the sole cause every person with enlarged ventricles would suffer from the illness
41
ao3 / criticism - one limitation of neural correlates explanation is that the research evidence is correlational
P - one limitation of neural correlates explanation is that the research evidence is correlational E - correlational research looks at the relationship between two co- variables, in this case the role of the ventral striatum and negative symptoms of schizophrenia / it may be that something wrong in the striatum is causing the negative symptoms ↳ however, it is possible that another factor influences both the negative symptoms and the ventral striatum activity L - the existence of neural correlates in schizophrenia tells us very little and hard to be certain of a cause and effect relationship
42
what are drugs that treat psychotic illnesses called?
anti psychotics
43
what are antipsychotics based on?
the dopamine hypothesis, which assumes that dopamine activity is linked to schizophrenia
44
what is the purpose of antipsychotics?
-to helps the individual improve their functioning and well-being -they do not cure the illness, they can only reduce the symptoms so that a degree of normal functioning can occur
45
how can antipsychotics be taken?
as tablets, in the form of syrup or sometimes injections (every 2-4 weeks if at risk of failing to remember to take their medication)
46
what are the types of antipsychotics?
-typical drugs (came around in the 1950s) -atypical drugs (appeared in the 1970s)
47
what is the purpose of typical antipsychotics?
to reduce the effects of dopamine and combat the positive symptoms (hallucinations, delusions)
48
examples of typical antipsychotics:
chlorpromazine, pimozide
49
basic function of antipsychotics:
to reduce or block the effects/actions of dopamine (antagonists)
50
steps of dopamine antagonists:
1) they bind to dopamine receptors (particularly the D2 receptors), 2) binding blocks the stimulation of these receptors so they cannot absorb the dopamine 3) this normalises neurotransmission as the postsynaptic neurons receive less dopamine
51
effects of dopamine antagonists:
by reducing stimulation of the dopamine system in the limbic system in the brain, antipsychotic drugs can eliminate the hallucinations and delusions experienced by sufferers
52
what is the aim of atypical antipsychotics?
they combat the positive symptoms of schizophrenia, but there are claims that they also have beneficial effects on negative symptoms as well
53
examples of antipsychotics drugs:
Clozapine, Risperidone
54
how do atypical antipsychotics differ from typical antipsychotic?
these drugs also work on the dopamine system but also block serotonin and glutamate receptors
55
steps of how atypical antipsychotics work:
1) they temporarily occupy the D2 receptors 2) they dissociate the dopamine, to allow normal dopamine distribution, 3) the receptors still receive dopamine but just in smaller levels
56
what is the benefit of atypical antipsychotics compared to typical antipsychotics?
these drugs are thought to be responsible for lower levels of side effects (such as tardive dyskinesia) compared with typical antipsychotics
57
ao3 / strengths of anti-psychotics:
-a benefit of antipsychotics is evidence to support their effectiveness
58
ao3 / benefit of antipsychotics - a benefit of antipsychotics is evidence to support their effectiveness
P - a benefit of antipsychotics is evidence to support their effectiveness E - a researcher reviewed studies comparing the effectiveness of chlorpromazine (typical antipsychotics) to control conditions / data from 13 trials with a total of 1121 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity compared to placebo ↳ researchers also studied atypical antipsychotics & concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics / it is effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed L - this shows that antipsychotics are successful in treating sz
59
ao3 / criticisms of anti-psychotics:
-one limitation of antipsychotic drugs is side effect -drugs are only palliative,
60
ao3 / criticism of antipsychotic drugs - one limitation of antipsychotic drugs is side effect
P - one limitation of antipsychotic drugs is side effect E - typical antipsychotics are associated with dizziness, agitation, sleepiness and tardive dyskinesia ↳ atypical antipsychotics were then developed to reduce side effects but some still exist, for example, a fatal drop in white blood cell count L - these side effects are a serious limitation to the use of antipsychotics as they mean that people can die or stop medication due to them
61
ao3 / criticism of antipsychotic drugs - drugs are only palliative
P - drugs are only palliative, meaning that they only treat the symptoms of schizophrenia and do not offer a cure E - if a patient stops taking their medication, their schizophrenia symptoms will return / people argue that drugs treat the symptoms of the illness but not the cause L - this leads to the ‘revolving door phenomenon’, where patients are constantly being discharged and re-admitted to the hospital. ↳ they take their medication and therefore feel better; then they wrongly assume that they are cured and stop taking their drugs, only to get ill again and need to be hospitalised L - this means that antipsychotics are only a surface level drug
62
what are the psychological explanations for schizophrenia?
-family dysfunction -cognitive explanations
63
what is family dysfunction?
theories that believe that the problems within family contribute to onset and relapse of schizophrenia
64
what are the types of family dysfunction?
-schizophrenogenic mother -double-bind theory -expressed emotion
65
what is a schizophrenogenic mother?
early theorists, influenced by freudian ideas, proposed that schizophrenia comes from being reared by a **cold and dominant mother who is both overprotective and rejecting**
66
what is the effect of a schizophrenogenic mother on a family?
she tends to create a family climate cause characterised by secrecy and tension
67
what does schizophrenogenic mean?
schizophrenia causing
68
why do children with schizophrenogenic mothers develop schizophrenia?
they are confused by their mothers overprotective but rejecting nature → this leads to distrust that later develops to paranoid delusions (as the child begins to doubt their own emotions and utimately schizophrenia
69
what does double bind mean?
no-win
70
what does the double-bind hypothesis suggest?
-that schizophrenia is a reaction to a parent presenting the child with a no win situation -non verbal communication (body language, tone) conflicts with verbal communication
71
example of double bind communication:
a mother may say, ‘Come and give mummy a cuddle’, but then freezes when the child approaches, and then tells the child off for not being affectionate
72
what does double-bind communication lead to?
the child get confused on whether to trust their thoughts & won’t be able to develop an accurate perception of their reality ↳ the child develops schizophrenia
73
what is expressed emotion?
a measure of the amount of emotion displayed within the family setting
74
what does the expressed emotion theory suggest?
high levels of EE are implicated in SZ, they worsen the prognosis in patients with SZ & can Increase the likelihood of relapse into hospital for the patient
75
a household with high expressed emotion is made up of…
three dimensions -hostility -emotional over-involvement -critical comments
76
what is hostility?
a negative attitude directed at the patient because the family feels that the disorder is controllable and that the patient is choosing not to get better
77
what is emotional over-involvement?
-when the family members blame themselves for the mental illness -this is the opposite of a hostile attitude, but still has the same negative effect on the patient as it makes the patient feel guilty
78
what are critical comments?
critical attitudes are combinations of hostile and emotional over-involvement
79
why does expressed emotion lead to relapse?
-people with schizophrenia have a lower tolerance for intense emotional situations -this high level of EE becomes too much for the patient to handle as they have to deal with criticism from those they would need support from in their time of recovery
80
evaluation of expressed emotion:
-there is evidence for the association of expressed emotion to schizophrenia
81
ao3 / strength of EE - there is evidence for the association of expressed emotion to schizophrenia
P - there is evidence for the association of expressed emotion to schizophrenia E - a researcher conducted a meta-analysis of 26 studies and found that schizophrenics returning to a family environment of high EE experienced more than twice the average rate of relapse L - these studies support the claim that EE could be responsible for a patient’s relapse
82
evaluation of double-bind theory:
there is inconsistent evidence of double-bind communication in families associated with schizophrenia
83
ao3 / drawback of DB - there is inconsistent evidence of double-bind communication in families associated with schizophrenia
P - there is inconsistent evidence of double-bind communication in families associated with SZ E - in support, berger (1965) found that schizophrenics reported higher recall of double bind statements by their mothers than non-schizophrenics ↳ in contrast, analysed data from previous studies and found no difference between families with and without a schizophrenic mother L - this contradictory evidence casts doubt on double bind as a cause of SZ
84
strengths of family dysfunction theory:
-one strength of Family dysfunction explanations of SZ is that they have practical application
85
ao3 / strengths of family dysfunction - one strength of Family dysfunction explanations of SZ is that they have practical application
P - one strength of Family dysfunction explanations of SZ is that they have practical application E - family therapy was developed to help make family interactions more constructive and less problematic L - this therapy is successful and so despite conflicting evidence, this explanation of SZ has some value
86
criticisms of family dysfunction theory:
-all of the theories involving the family fail to explain why some children in such dysfunctional families often do not go on to develop schizophrenia -having a schizophrenic within a family can be extremely stressful
87
ao3 / criticism of family dys - all of the theories involving the family fail to explain why some children in such dysfunctional families often do not go on to develop schizophrenia
P - all of the theories involving the family fail to explain why some children in such dysfunctional families often do not go on to develop schizophrenia E - if family dynamics were the sole cause of schizophrenia, then all children raised in similar environments should be schizophrenic / this is not the case family dysfunctions cannot be the sole cause of the illness L - it is more likely that the SZ has a biological predisposition to the disorder and that the unhealthy family environment combines with the biological vulnerability to cause the illness, like the diathesis-stress model proposes
88
ao3 / criticism of family dys - having a schizophrenic within a family can be extremely stressful
P - having a schizophrenic within a family can be problematic and extremely stressful E - therefore, it is possible that rather than dysfunctions within families causing schizophrenia, it could be that having a schizophrenic within a family leads to these dysfunctions ↳ it’s possible that rather than dysfunctions within families causing schizophrenia, it could be that having a schizophrenic within a family leads to these dysfunctions L - there is a general lack of support for family dysfunction as a causal factor, if anything it is more likely to be a maintenance factor
89
Maha and Jessica are talking about their different upbringings in a group therapy session with other schizophrenics. Maha described a time when she was given compliments by her mother and how this helped to develop her self-esteem. Jessica also recalls a time that she was given compliments from her parent, but she also remembers negative criticism immediately before and after the compliment. Explain what is meant by 'double bind communication' and refer to the scenario above in your answer. (4 marks)
Double bind is a style of communication that has been found to be implicated in schizophrenia. This is where the individual receives mixed messages from the parent, for example where their non-verbal communication does not match their verbal communication. It is clear that Maha is not experiencing double bind communication as the non-verbal message she received from her mother is the same as the compliment. However, Jessica is receiving a double bind statement as the compliment is mixed with criticism making is confusing for Jessica to know which reality to trust.
90
**cognitive explanations: including dysfunctional thought processing**
91
what is the cognitive explanation of schizophrenia is based around?
the idea of faulty information processing and faulty thinking
92
what is the difference between schizophrenic and non-schizophrenic brains?
non-schizophrenic brains are able to filter irrelevant stimuli, these filtering mechanisms and processing stimuli systems are thought to be different in the brains of schizophrenics → there is sensory overload & SZ brains let in too much irrelevant information
93
when do cognitive deficits occur?
when sufferers experience problems with attention, communication and information overload
94
what are the positive symptoms of schizophrenia caused by?
faulty attention system → this accounts for the positive symptoms of schizophrenia ( hallucinations, delusions) -reduced processing of information in the temporal and cingulate gyri is associated with hallucinations
95
what are the negative symptoms of schizophrenia caused by?
-reduced thought processing in the ventral striatum is associated with negative symptoms → this lower-than-usual level of information processing suggests that cognition is likely to be impaired
96
how is schizophrenia diagnosed and why?
using the stroop test ↳ it is an indicator of whether irrelevant stimuli can be filtered out
97
what are the two kinds of dysfunctional thought processing:
Frith (1992) identified -meta representation -central control
98
what is meta representation?
our ability to reflect on thoughts and behaviour & interpret the actions of other people
99
what does meta representation dysfunction lead to?
-it would disturb our ability to recognise our own actions and thoughts as being ours, rather than being carried out by someone else
100
which symptom can meta-representation dysfunction explain?
hallucinations as the inner voice is experienced as coming from an external source
101
evidence for meta representation as an explanation of schizophrenia:
there is supporting evidence for faulty information processing
102
ao3 / strength of meta representation - there is supporting evidence for faulty information processing
P - there is supporting evidence for faulty information processing E - McGuigan found that the vocal cords of patients with schizophrenia were tense during the time they experienced auditory hallucinations ↳ this suggests that instead of hallucinating, they were mistaking their own inner speech for someone else's voice L - this could mean that hallucinations are not biological but a result of a dysfunctional thought process, which adds support to the cognitive explanations such as metarepresentation ↳ much of the research into cognitive explanations is scientific and replicable
103
what is central control?
our ability to suppress automatic responses while we perform deliberate actions instead
104
which symptom can central control dysfunction explain?
disorganised speech → it could be due to an inability to suppress automatic thoughts
105
further explanation for dysfunctional speech:
-many schizophrenics experience derailment of thoughts and words/sentences -each word triggers an association and the schizophrenic cannot stop the automatic responses to these associations
106
evidence for central control dysfunction:
P - there is evidence that suggests that information is processed differently in the mind of a schizophrenic E - stirling at al. (2006) compared 30 patients with schizophrenia with 18 controls on a range of cognitive tasks including the Stroop Test ↳ in the stroop tests participants have to name the ink colours of coloured words and suppress the impulse to read the word L - schizophrenic patients took twice as long to name the ink colours as the control group, indicating that they were struggling to have central control and suppress the automatic associations
107
strengths of cognitive explanations of schizophrenia:
-a strength of the cognitive explanations is that it provides practical applications -[evidence from stroop test]
108
ao3 / strength of cognitive explanation - it provides practical applications
P - a strength of the cognitive explanations is that it provides practical applications E - the claim that the symptoms of SZ have their origin in faulty cognition is reinforced by the success of cognitive therapies for SZ ↳ in CBTp, patients are encouraged to evaluate the content of their delusions and to test the validity of their faulty beliefs ↳ research has shown that when compared with antipsychotic medication, CBT was more effective in reducing symptoms and improving levels of social functioning L - the fact that a treatment based on the explanation is effective provides support for the role of cognitions as a cause of schizophrenia
109
ao3 / strength of cognitive explanation - Stroop Test
P - there is evidence that suggests that information is processed differently in the mind of a schizophrenic E - stirling at al. (2006) compared 30 patients with schizophrenia with 18 controls on a range of cognitive tasks including the Stroop Test ↳ in the stroop tests participants have to name the ink colours of coloured words and suppress the impulse to read the word L - schizophrenic patients took twice as long to name the ink colours as the control group, indicating that they were struggling to have central control and suppress the automatic associations