Explanations for schizophrenia Flashcards

1
Q

What is the genetic basis of the biological explanation?

A

-Family studies have confirmed that the risk of schizophrenia increases in line with genetic similarity to a relative with the disorder.
-Although the families share the same environment, so the correlation provides evidence for both, family studies give support for the genetic importance in schizophrenia.

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2
Q

Gottesman and Sheild 1982?

A

A large scale family study, assessing the risk of developing schizophrenia.

Two parents= 46% compared to grandparents= 3.7%. Identical twin=48%.

In their twin study: MZ= 46% and DZ= 14%.

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3
Q

What are the candidate genes involved in?

A

Early research looked into a single gene variant however it now appears multiple genes are involved.

These genes would most likely be coding for dopamine production.

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4
Q

Candidate genes: Ripke et al?

A

Ripke et al (2014) combined all the data for previous genome wide studies and compared 37000 people with schizophrenia and 113000 controls. 108 separate genetic variations were associated with increased risk of schizophrenia.

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5
Q

What is the role of mutation in the biological explanation?

A

Schizophrenia can have genetic origin in the absence of a family history, due to mutation.
This can be caused by radiation, poison and viral infection.
Brown et al found a positive correlation between risk of schizophrenia and parental age (risk of sperm rotation).

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6
Q

Strengths of the genetic explanation: research support?

A

as well as family and twin studies, Tienari et al 2004 showed children with biological parents with schizophrenia were still at increased risk even when growing up with an adoptive family. A recent twin study Hilker et al 2018 found a 33% MZ rate and a 7% DZ rate.

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7
Q

Strengths of genetic explanations: twin studies?

A

The Concordance rate is 3 times as much for genetically identical twins. This suggests a genetic predisposition.

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8
Q

Strengths of the genetic explanation: application?

A

Genetic counselling- the process of investigating individuals and families affected by or at risk of genetic disorders to help them understand and adapt to the medical, psychological and familial implications of genetic contributions to disease.

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9
Q

Weaknesses of the genetic explanation?

A

There are small samples in the studies.

Higher MZ rates could be explained by environmental factors.

Environmental factors- There is clear evidence for environmental factors. These include smoking cannabis at an early age, complications in birth, childhood trauma. Morkved et al found that 67% of schizophrenia patients had experienced one childhood trauma, compared with 33% of non-psychotic patients.

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10
Q

What is the neural explanation?

A

-Scientists have found neural correlates for schizophrenia.
-The best known is the dopamine hypothesis:

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11
Q

What was the original dopamine hypothesis based on?

A

Based on the discovery that drugs used to treat schizophrenia (antipsychotics) produced side effects similar to symptoms of Parkinson’s disease. Parkinson’s is associated with low dopamine levels.

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12
Q

What is the dopamine hypothesis?

A

Therefore it was hypothesised that schizophrenia was caused by high levels of dopamine in subcortical areas of the brain.
Post mortem examinations showed excessive dopamine receptors , also shown in PET scans.

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13
Q

What is the updated 1991 dopamine hypothesis?

A

Davies et al proposed the addition of abnormally low dopamine levels, which can explain some schizophrenia symptoms (low DA in prefrontal cortex leads to cognitive problems).
It has also been suggested that hypodopaminergia leads to hyperdopaminergia.

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14
Q

What does the updated dopamine says about explaining dopamine levels?

A

The current dopamine hypothesis tries to explain the origin of these abnormal levels. It seems both genetic and psychosocial risk factors are linked to hypo/hyperdopaminergia.

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15
Q

Strengths of the neurochemical explanation?

A

Evidence- Curran et al 2014 showed amphetamine drugs increase dopamine levels and also worsen symptoms in people with schizophrenia and induce them in people without. Also antipsychotics that reduce dopamine reduce symptoms. Thirdly, some candidate genes are involved in dopamine production. This suggests dopamine is involved.

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16
Q

Weaknesses of the neurochemical explanation: glutamate?

A

post mortem and live scanning have consistently found increased glutamate neurotransmitter levels in schizophrenic brains and several of the candidate genes are involved in glutamate production. So there may be other neurotransmitters.

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17
Q

Weaknesses of the neurochemical explanation: oversimplistic?

A

it is over simplistic to assume just because antipsychotics block dopamine receptors and then reduce symptoms, that this is the cause. Neurotransmitters interact with each other so others may be involved.

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18
Q

Weaknesses of the neural chemical explanation: other drugs?

A

Apomorphine increases dopamine levels but does not induce schizophrenic symptoms.

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19
Q

Neural anatomical explanation: limbic system?

A

Located in the subcortex and includes the hippocampus and amygdala.

Post mortems have shown significant cell loss in the limbic system and unusual connections in the hippocampus.

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20
Q

Neural anatomical explanation: corpus callosum?

A

There are gender differences in normal brains and these are reversed in schizophrenic brains.

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21
Q

Neural anatomical explanation: abnormal early development?

A

Early brain development in the 3rd trimester leading to disordered organisation of synapses.

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22
Q

Neural anatomical explanation: brain imaging studies?

A

Showed reduced brain tissue, enlarged ventricles and under activity in the temporal frontal lobes compared to normal brains.

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23
Q

Strengths of the neural anatomical explanation?

A

Research is highly reliable due to high control with specialist high tech equipment.
Suddain et al 1990 used MRI scans to obtain the brian structures of MZ twins where one had schizophrenia and the other didn’t. The twin with schizophrenia generally had enlarged ventricles and a reduced anterior hypothalamus. Supports brian differences.

24
Q

Weaknesses of the neural anatomical explanation?

A

Biological determinism- the issue of causation, is a person doomed because of their brain structure and it is hard to identify cause and effect with brain scans.

25
Q

Who proposed the schizophrenogenic mother theory?

A

Fromm-Reichman 1948 proposed a psychodynamic explanation because many of her patients had similar parents and childhood experiences.

26
Q

What is the schizophrenogenic mother?

A

The schizophrenogenic mother is cold, rejecting, controlling and creates a family situation of tension and secrecy.
This leads to distrust that develops into paranoid delusions.

27
Q

Who proposed the double bind theory?

A

Bateson et al 1972 agreed that family climate is important and emphasised the importance of communication style in a family.

28
Q

What is the double bind theory?

A

It happens when a child is trapped in a situation where they want to avoid wrongdoing, but there are mixed messages about what this is, and they are unable to comment on the situation and receive clarity. When they behave wrongly, they are punished by the withdrawal of love.

29
Q

What is an example of double bind theory?

A

a mother tells a daughter/son they aren’t affectionate enough but when the child shows affection the mother pushes them away.

30
Q

Who is particularly affected by double bind theory?

A

Small children have particular difficulty as they cannot leave the relationship because they are so dependent on their parents.

31
Q

How does double bind theory lead to schizophrenia symptoms?

A

It creates a confused and dangerous outlook on the world and an internal state of conflict, prevents the development of a coherent construction of reality.

32
Q

What is expressed emotion?

A

=The level of negative emotion expressed towards the person with schizophrenia, often by carers and family members.

33
Q

What do high levels of EE cause?

A

can worsen the prognosis in patients and increase the likelihood of relapse.
-Has been suggested this is part of the diathesis stress model to trigger the onset of schizophrenia, not just relapse.

34
Q

What are the three elements of expressed emotion?

A

1) Hostility- includes anger, blaming problems in the family on the patient and rejection. 2) Critical comments- occasionally accompanied by violence. 3) Emotional overinvolvement- showing lots of concern and pity which makes the patient feel guilty.

35
Q

How is expressed emotion measured?

A

Measured using the Camberwell Family Interview which records the relatives’ speech and attitude towards the patient.

36
Q

Strengths of family dysfunctions?

A

Evidence supports the link between dysfunctional relations and schizophrenia-

Read et al 2005 suggested adults with schizophrenia were more likely to have an insecure attachment type (C or D). Also reported 69% of men and 59% had a history or physical/sexual abuse.
Morkved et al 2017 showed 67% of people with schizophrenia suffered at least one traumatic event. Strongly suggests family dysfunction is involved.

37
Q

Weaknesses of family dysfunctions?

A

-No evidence to support specific double bind theory and schizophrenogenic mother.

-The research is socially sensitive as we must ensure we don’t parent blame, as this adds insult to injury.

38
Q

What are cognitive explanations?

A

Schizophrenia is caused by faulty information processing and faulty thinking.

39
Q

What is dysfunctional thinking?

A

-Disruption to normal thought processes.

40
Q

What are specific associations of dysfunctional thinking?

A

-Thought to occur through reduced processing in the ventral striatum which is associated with negative symptoms.
-Hallucinations are associated with reduced processing in the temporal and cingulate gyri.
-Indicates that cognition is impaired.

41
Q

What is metarepresentation?

A

the ability to reflect on thoughts and feelings and allows insight into our own behaviours, also allowing us to interpret the behaviours of others.

42
Q

Meta representation dysfunction:

A

Frith et al 1992.

A dysfunction disrupts the ability to recognise our own action as carried out by ourselves rather than by ourselves.

This explains hallucinations and delusions by insertion (the experience of having thoughts placed there by someone else).

43
Q

What is central control dysfunction?

A

Frith et al 1992.
Cognitive ability to suppress automatic responses is also dysfunctional.
Speech poverty and thought disorder stems from being unable to suppress automatic thoughts and speech triggered by thoughts.
People with schizophrenia tend to experience the derailment of thoughts because each word triggers associations that they are unable to repress.

44
Q

Strengths of cognitive explanations?

A

Evidence- Stirling 2006 studied individuals with schizophrenia and their cognitive abilities using the stroop test. Participants had to suppress the tendency to say the word and not the colour or it. As Frith’s central control dysfunction theory predicted, the people with schizophrenia took longer to name the colours. So cognitive ability is impaired in those with schizophrenia.

45
Q

Weaknesses of cognitive explanations?

A

Proximal explanation- this explanation focuses on what symptoms are currently. They do not focus on the distal explanations, what caused the symptoms in the first place. Therefore is only a partial explanation. Distal explanations, like biological or dysfunctional families, do exist.

46
Q

What is the interactionalist approach?

A

A way to explain schizophrenia in terms of a combination of psychological and biological factors and these factors interact with each other.

47
Q

What is the diathesis stress model?

A

An interactionist approach linking biological vulnerability to environmental stressors.
Both are necessary to trigger the disorder.

48
Q

What was the original diathesis stress model so schizophrenia?

A

The original model (Meehl’s) diathesis was entirely genetic, one schizogeny. If the person experiences stressors such as schizophrenogenic mothers, this results in the development of the disorder. According to Meehl, if the person did not possess the gene, then no amount of stress will trigger the disorder.

49
Q

What is the modern understanding of diathesis?

A

It is now clear that many genes are associated with schizophrenia.
Modern diathesis factors also included psychological trauma (Ingram and Luxton 2005).
Read 2001 proposed a neurodevelopmental model, adding altered early brain development as a diathesis, caused by severe trauma.

50
Q

What is the modern understanding of stress?

A

In the original model stress was seen as psychological and mainly due to parenting.
The modern model includes any factors linked to risk of schizophrenia. (Houston et al 2008). Most recently, cannabis use has been identified as a risk factor, because it interferes with the dopamine system. It increases the risk of schizophrenia up to 7 times per dose.

51
Q

How is the diathesis stress model applied to treating schizophrenia?

A

Combining antipsychotic drugs with CBT.
Turkington et al 2006 pointed out it is possible to believe biological influences and still practise CBT.

52
Q

What are the differences between countries in terms of the interactionalist approach?

A

Combined treatment is quickly becoming the standard treatment in Britain. However in the US, they have been slower to adopt the interactionist approach and there is still a conflict between biological and psychological explanations.

53
Q

Strengths of interactionalist: research support?

A

Tienari et al 2004 carried out a study on 1900 Finnis children adopted away from biological mothers with schizophrenia. They also assessed the parenting style of the new families. In adulthood the genetic risk children were compared to a control group. It was found that high levels of criticism and conflict were strongly associated with development of schizophrenia, but only in the genetic risk group.

54
Q

Strengths of interactionalist: real world application?

A

combination of treatments. Tarrier et al showed combining treatments increases effectiveness. Participants in the combination group showed lower symptoms than the medication only and therapy only groups.

55
Q

Weaknesses of interactionalist approach: causation fallacy?

A

Jarvis and Okami 2009 criticised Tarrier et al and state there is a treatment causation fallacy. It is not always logical to suggest that just because something is successful in treating a disorder, it justifies a particular explanation. So we cannot automatically assume the interactionist approach is correct just because combination treatments are successful.W

56
Q

Weaknesses of interactionalist: over simplified?

A

The original diathesis stress model is too simplistic, as we know there are multiple biological associations, as well as multiple genes. We also have identified many more risk factors in the environment. This supports the modern understanding but this was based on the over simplified model.