Schizophrenia: explanations of Sz Flashcards

1
Q

Briefly outline family dysfunction

A

C/hood trauma in form of dysfunctional family
Probs with developing mind, foundations are at fault
Paranoia can develop
Disorganised thoughts can develop

Manifests in adulthood as signs of schiz

3 areas:
Schizophrenogenic mother / family – Fromm-Reichman 1948
Double bind communications- Bateson - 1956
High expressed emotion – Brown 1966

These explanations emphasize family-orientated theories of the disorder that emphasise the importance of upbringing and in particular trauma play a role in the development of schizophrenia.

Essentially these explanations stress the importance of how maladaptive family relationships and poor communication within the household contribute to the development of schizophrenia.
If a child is to experience TRAUMA in childhood (such as poor communication styles), this could be repressed or denied using DEFENSE MECHANISMS. In turn, this will create an unconscious ISSUE, which could reappear (MANIFEST) in adulthood in the form of schizophrenia symptoms.
The approach claims poor family relationships and deviant communication can drastically affect the way a growing child perceives reality and interacts with the world.
If these problems persist into adulthood, schizophrenia could result.

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2
Q

Outline the Schizophrenogenic mother as an explanation of schiz

A

Fromm-Reichmann (1948) - a mother who is domineering, insensitive, controlling, overprotective as well as rejecting.
This type of mother may micromanage her kids and refuse to acknowledge their independence which sets up lines of faulty communication between her and the child -contributing to symptoms of schiz in a/hood.
This can create excessive stress that could trigger psychotic thinking e.g. paranoia and develop into SCHIZ in adulthood.
In the 1970’s this theory was broadened to include how the father and entire family could have schizophrenogenic tendencies.

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3
Q

Outline Double bind hypothesis as an explanation of schiz

A

BATESON et al (1956) focused on contradictory communication coined ‘double-bind’
Families that communicate in this way make kids more susceptible to SCHIZ in adulthood. E.g. the mother tells her son she loves him, yet at the same time turns her head away in disgust. Hence, the child receives conflicting messages and becomes confused and suspicious and cannot develop an internally coherent construction of reality.
This may contribute to the development of schizophrenia in early adulthood, through paranoia and disorganised thinking

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4
Q

Outline High expressed Emotion as explanation of schiz

A

This revolves around how family interactions affect the development of schizophrenia rather than its onset. High EE families express considerable emotion – higher levels of concern for, and / or hostility towards the patient. Kuipers et al (1983) found that high EE relatives talk
more and listen less. Linszen et al (1997) found that patients returning to a high EE household is
four times more likely to relapse than those whose family has low EE. This finding has been replicated several times.

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5
Q

Outline Family schism as an explanation of schiz

A

this relates to severe and chronic disequilibrium (imbalance) in the household and persistent family discord (constant tension and arguing within the family).
These experiences may well be pushed to the back of a child’s mind - but may resurface in a/hood as symptoms of Schiz

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6
Q

Outline Family skew as an explanation of schiz

A

this is when one parent is dysfunctional and the other maintains a peacemaking stance. Sometimes this comes across as one domineering parent and one submissive parent, that refuses to criticise or recognise negative qualities in the other parent.
The child internalises this type of relationship as the norm, and may develop disorganised thoughts / speech as an adult - contributing to schiz

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7
Q

Evaluation for family dysfunction: Lidz

A

LIDZ 1965
Lidz et al (1965) looked at the cases of 50 schizophrenic patients and investigated their family backgrounds. Forty-five (90%) were found to have seriously disturbed
families. 60% of the patients had one or both parents with a serious personality disorder. Parental marriages were often skewed (characterised by one dominant and one submissive parent)

This implies Dysfunctional family backgrounds may well contribute to the develpment of Schiz

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8
Q

Evaluation for family dysfunction: cause and effect

A

There is a cause and effect argument with dysfunctional families.

Perhaps if you have a child that is particularly susceptible to mental health concerns - a normal parental response would show excessive concern, involvement and guidelines for their child. This may suggest that high expressed emotion may well be a response to kids with emotional distress, as opposed to a contributing factor to the condition

This suggests unusual family behavioural patterns may be a response to schizophrenia not a cause.

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9
Q

Evaluation for family dysfunction: alternative explanations

A

Alternative explanations of schizophrenia are more scientific and hence, more credible.

This approach explains the origins of schizophrenia as a consequence of a dysfunctional family, which is based on factors that are difficult to study objectively (e.g. childhood and the unconscious mind). These concepts are subjective and require a degree of interpretation which restricts the validity of the account.
A better more scientific alternatives include:
the dopamine hypothesis

Because
that can objectively identify abnormal levels of the neurotransmitter through sophisticated PET scans or cerebrospinal fluids

This could suggest…the family dysfunctional explanation of schiz is redundant as more trustworthy explanation are available

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10
Q

Evaluation for family dysfunction: high EE and relapse evidence

A

This is more compelling evidence to show how returning to a household with high EE effects relapse.

Butzlaff and Hooley (1998) completed a meta-analysis of 26 studies and found that when patients suffering from schizophrenia returned to families with high EE they experienced more than twice the rate of relapse of schizophrenia symptoms.

This provides further concurrent validity to Linszens et al (1997) findings that high EE clearly relates to schiz

Therefore, this shows how high levels of EE clearly impacts on the relapse of schizophrenia

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11
Q

Evaluation for family dysfunction: practical explanations

A

This explanation has been practically applied to help those suffering from schizophrenia.

Family therapy is a very effective treatment to come out of this explanation that aims to help the patient and the family come to terms with the schizophrenia diagnosis, how to readily spot early signs of relapse and how to cope without resorting to high levels of EE

This implies … the dysfunctional family explanation of schiz has been beneficial to the 1% of the population that struggle with this psychotic condition, and may help to restore family dynamics

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12
Q

Evaluation for family dysfunction: socially senstive

A

This explanation can be criticised for causing further problems for the sufferer and their families.

The explanation tends to blame the way parents have raised and interacted with their children as the sole cause of schiz. This is hardly protecting patients and their families from harm, and in some instances can be seen to make family dynamics even worse

This suggests …that in such a socially sensitive topic clinicians need to be mindful of how causal factors are discussed with patients and their families

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13
Q

What is the Central monitoring system (CMS)

A

Typically, this ‘process’ labels & recognises actions and thoughts as ‘being done by me’ or ‘mine’

With schiz, a malfunction within the CMS could explain positive symptoms
Hallucinations and delusions.

E.g. faults with misattributions our inner speech to external sources such as others voices

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14
Q

What is the Supervisory attentional system (SAS)

A

Typically this ‘process’ responsible for generating self-initiated actions

With Schiz, a malfunction can be seen to create negative symptoms
speech poverty, flat affect and avolition

E.g. Not responding to environmental stimuli with appropriate (or even any) emotions because of a faulty SAS (flat affect and speech poverty) Limiting interaction

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15
Q

What is Egocentric bias

A

Typically we can all see we are not central component to all events
Usually we grow out of this
With schiz, Egocentric bias – everything relates to them specifically, so jumps to false conclusions

E.g. muffled voices = peoples criticisms
E.g. flashes of light = signals from God

Delusions of…..

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16
Q

bentall

Evidence evaluation for cognitive dysfunction linked to schiz

A

There is evidence that supports the role of cognitive dysfunction being linked to Schiz:
BENTALL 1991
Asked participants to either generate category items themselves (e.g. animals beginning with the letter B) or read out category items.
One week later, participants were asked whether they had generated the words i) themselves,ii) read them, or iii) whether they were new.
Results showed schiz participants with hallucinations performed worse (i.e. were unable to identify the source of the words); than schiz patients without hallucinations and both groups performed worse that non- schiz controls
Hence, this research undelines the role of cognition in schiz.

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17
Q

Evaluate cognitive explanations of schiz: cause and effect issue

A

Like other explanations the cognitive account of schizophrenia suffers from a cause and effect issue.

Although cognitive deficits are rife with schizophrenia - these may well be the effect of schiz as opposed to a causal factor.

In fact both cognitive deficits and schiz could be caused by another factor completely e.g. high dopamine or urban living

This implies …dysfunctional thought processes may simply be a manifestation of schiz as opposed to an instigating factor

18
Q

Evaluation cogntive explanation of schiz: practical explanations

A

This explanation has been practically applied to help those suffering from schizophrenia

CBT aims to challenge and change the cognitive deficits of patients with schiz. and alter their behaviour simultaneously through developing more rational constructive ways of thinking and functioning.

This has been shown to be very effective with many patients with schiz

This implies …the cognitive dysfunctional explanation of schiz has been very useful to the 1% of the population that are suffering from schizophrenia

19
Q

Outline genetic inheritance as an explanation of schiz

A

Researchers have suggested that some people may have a genetic predisposition to schizophrenia, and hence the condition is at least partly inherited. This means the disorder runs in families through faulty genes.
Researchers believe that no one gene is likely to be responsible for all cases of schizophrenia, but several genes are involved (i.e. it’s polygenic). Ripke et al (2014) reported 108 genetic variants that could mediate a vulnerability to the disorder, including variations on chromosome 8 and 11, and the C4 gene. Similarly, Hong et al (2001) found that a variation on the gene TPH was far more common with Chinese patients with schizophrenia (interestingly this codes for serotonin production).
Having some of these genes ultimately increases a person’s vulnerability to developing schizophrenia, by inheriting biochemical imbalances or brain structure abnormalities.

20
Q

Outline The Function of the C4 Gene

A

Complement component 4 (C4) gene is found at synapses in the central nervous system and mediates the pruning of synapses that normally takes place during development.
A variant C4 is a clear risk factor for schizophrenia.
Research supports the hypothesis that excessive or hyper-pruning could lead to symptoms of schizophrenia.

The findings may help explain the longstanding mystery of why brains from people with schizophrenia tend to have a thinner cerebral cortex with fewer synapses than unaffected individuals do.

21
Q

Explain Gottesman & Shields (1991)

A

Children of two schizophrenic patients who share 100% genetic similarity, have a 46% chance of developing the disorder.
Similarly MZ (identical twins) who share 100% genetic similarity have a 48% chance of developing the disorder if one twin has been diagnosed.
First degree relatives, like children of a sufferer, share 50% genetic similarity have a 13% chance of developing the disorder if a parent has been diagnosed.
Likewise, second degree relatives, like grandchildren, share 25% genetic similarity and have a 5% chance of developing schizophrenia, if a grandparent had been diagnosed.

22
Q

Adoption Studies - Back ground

A

Adoption studies have some advantages over twin studies and family studies, such as…
If a child whose parent(s) have schizophrenia also develops schizophrenia when they’re older, we cannot say for certain whether there is a biological / genetic cause for the disorder, or an environmental one. For instance, we already know children often imitate their parents, so maybe schizophrenic behaviour is learnt from their parents.
With adoption studies, the child is not raised by their biological parent(s) with schizophrenia, so we can be more certain that it was not growing up in an environment with schizophrenic role models that influenced the development of the condition within the child.

23
Q

Adoption Studies: Tienari et al. (2000)

A

Tienari et al. (2000) completed an adoption study in Finland with over 164 adopted kids whose biological mothers had been diagnosed with schizophrenia. These were matched with kids whose biological mothers did not suffer from schizophrenia.
The study found 11 (7%) of the sample whose biological mothers had schizophrenia had also been diagnosed with the condition compared to just 4 (2%) from the control group.
This helps validate the idea that schizophrenia has a genetic component as the adopted children do not share environmental influences with their biological mothers and provides concurrent validity for the role of genes in schiz

24
Q

Evaluation biological explanation of schiz: evidence from Joseph

A

There is even further evidence to support the theoretical foundations of the biological explanation of schizophrenia.
Joseph et al. (2004) found a 40% concordance rate in schizophrenia for MZ twins (who share 100% genetic similarity) and a 7% concordance rate for DZ twins (who share 50% genetic similarity).
The higher concordance rate of schizophrenia for MZ twins (when the environmental influences on both groups can assumed to be no more similar than for DZs).
This implies… genes have some influence on the development of schizophrenia.

25
Q

Evaluation for genetic explanation of sz: incomplete

A

However, the genetic explanation is incomplete. Genetics cannot be the sole cause of schizophrenia, as if this was the case MZ twins would have a concordance rate of 100% as they share exactly the same genotype.
As this is not the case, nurturing (environmental) influences must play a role in the development of schizophrenia. Some environmental factors linked to schizophrenia could include… stress, drugs, alcohol and a difficult childhood (i.e., deprivation and/or abuse).
This would suggest that… the biological explanation of schizophrenia has limited explanatory power and a more holistic approach to understanding the development of schizophrenia is needed.

26
Q

family studies have methodolgical problems

A

Family studies into schizophrenia also have serious methodological problems. Although family studies show how schizophrenia may run in families, i.e., intergenerational, this is not necessarily genetic.
For instance,
Kids may pick up deviant ways of behaviour e.g. flat affect, through imitation of key role models - they may also adopt deviant parenting styles based on how they were raised (internal working model)
This suggests… that genetic evidence can actually be used to validate the role of the environment in Schiz

27
Q

Evaluation for biological explanation for sz; genetics practical applications

A

This knowledge concerning genetics and schizophrenia can have useful practical applications.
This type of knowledge could have significant impacts on family planning. Individuals with schizophrenia would be made aware of the risk of their biological children developing the disorder, so they can think about alternative options like adoption.
What’s more, vulnerable groups in society who have relatives suffering from schizophrenia are often advised by clinicians on their risk of developing the disorder.
This suggests… that the biological approach to understanding the cause of schizophrenia has had tangible effects in society.

28
Q

evaluation for genetic explanation of sz: biologically deterministic

A

The genetic explanation of schizophrenia can be accused of being biologically deterministic.
Although psychology is seeking general laws to explain all behaviours, this genetic theory into schizophrenia overlooks many aspects, including free will, and the role therapy could play in patients recovery. Clearly patients may choose to attend therapy and help themselves in the recovery process
This means that… the account neglects to consider the role of environmental factors (e.g., interactions in therapy) as well as free will in the development and potential recovery from Schiz

29
Q

evaluation for genetic explanation: promotes psychology as a science

A

The genetic explanation for schizophrenia promotes psychology as a scientific discipline.
This is because genetics can be studied in a controlled, objective and falsifiable manner. For instance, we can gather quantifiable data when studying genetic inheritance by looking at percentage similarity of genetic information between familial relations and then concordance rates for schizophrenia.
This is important as the more scientific the research, the more trusted the conclusions on the causes of schizophrenia are. This means more practical applications are likely to be put in place based on the conclusions. Furthermore, more funding is likely to be given for further research into schizophrenia.

30
Q

Outline dopamine hypothesis

A

What could be happening at a post synaptic level to account for elevated levels of dopamine in the surrounding brain cells?
Not enough dopamine could be being broken down after synaptic transmission, leaving too much dopamine in the surrounding cells.
Re-uptake processes may be impaired leaving to much D in the synapse
Hence, abnormalities in dopamine can manifest in odd behavioural patterns found in some schizophrenia patients, such as creating visual hallucinations.
This could be caused by a number of factors, including presynaptic neurons releasing too much dopamine.

31
Q

Summaries at least 2 observations that support the dopamine hypothesis of schizophrenia…

A

1-Drugs that increase dopamine production make symptoms of schizophrenia worse. Amphetamine based drugs (dopamine agonists) increase dopamine activity and can bring about symptoms of schizophrenia.

2 -Higher than normal concentrations of dopamine have been found in the post-mortems of patients that suffered from schizophrenia.

3 -Low levels of dopamine activity are found in people that suffer from Parkinson’s disease, a degenerative neurological disorder. It was found that some people taking the drug L-Dopa (a dopamine antagonist) to raise their dopamine levels were developing schizophrenic like symptoms (Grilly, 2002).

32
Q

Neural Correlates: Dopamine Hypothesis

Support for this argument comes from at least 2 areas…

A

THE REVISED DOPAMINE HYPOTHESIS
This modification is due to some inconsistencies in research findings.
Davis et al. (1991) pointed out that in the prefrontal cortex there are no D2 receptors and actually there appears to be a deficiency of dopamine in this region. Davis et al. suggest that low levels of dopamine in this region (i.e., the mesocortical pathway) are more responsible for negative symptoms of schizophrenia like avolition.
This is called HYPO-DOPAMINERGIA.

33
Q

Evaluation for dopamine hypothesis: evidence from randrup and munkvad

A

There is evidence to support the role of dopamine in schizophrenia.
Randrup and Munkvad (1966) created schizophrenia like behaviour in a sample of rats by giving them dopamine agonists (amphetamines).
The rats were given amphetamines to raise dopamine levels three times a day for six days. The rats then showed long lasting abnormalities including being unable to filter out irrelevant sounds (attentional issues, a key symptom with schizophrenia). This was then reversed using antipsychotic medication.
This suggests… that there is a link between high levels of dopamine and schizophrenia, supporting the dopamine hypothesis (hyperdopaminergia).

34
Q

Evaluation for dopamine hypothesis: incomplete

A

However, the dopamine hypothesis of schizophrenia is incomplete. For instance, most individuals with schizophrenia are prescribed antipsychotics, which work by reducing dopamine - hence correcting dopamine levels
Antipsychotics have been shown to be effective in up to 85% of patients with schizophrenia, which poses the question of why decreasing the dopamine activity for the remaining 15% of patients isn’t decreasing their symptoms
This implies… the neural explanation of schizophrenia is limited in explanatory power and there must be other factors beyond dopamine, involved in the development of the disorder.

35
Q

Evaluation for dopamine hypothesis: cannot establish cause and effect

A

There is clearly a relationship between high dopamine levels and schizophrenia, but we cannot infer cause and effect.
For instance, does high dopamine cause schiz or does schiz cause high dopamine (which comes first).

Perhaps a third factor unknown factor actually causes both, such as…..poor communications in the household

Hence, the dopamine hypothesis of schizophrenia is merely correlational and as such of limited use.

36
Q

Evaluation of dopamine hypothesis: practical applications

A

The dopamine hypothesis of schizophrenia has had important applications in society.
Understanding that schizophrenia is linked to elevated levels of dopamine in the mesolimbic pathway and limbic system has led clinicians to prescribe antipsychotics to patients.
Antipsychotics work by blocking the activity of dopamine and have shown to be effective in up to 85% of patients with schizophrenia.
This implies… that the neural explanation for understanding the cause of schizophrenia has had tangible effects in society.

37
Q

Evaluation of dopamine hypothesis: scientific

A

The neural explanation for schizophrenia is a scientific explanation.
This is because brain chemistry can be studied in a controlled, objective and falsifiable manner. For instance, we can study neurotransmitter levels, such as the dopamine levels of patients with schizophrenia, by analysing blood samples, cerebrospinal fluid and PET scans.
This implies the dopamine account of schizophrenia promotes psychology as rigorous scientific subject worthy of higher levels of Government funding

38
Q

Evaluation for dopamine hypothesis: can be used as part of diathesis- stress model

A

The dopamine hypothesis can be used as part of the diathesis + stress account of schizophrenia.

DIATHESIS - this biological vulnerability to schiz may be high levels
of dopamine
+
STRESS - (environmental factors) like urban living / raised in a household rife with poor communication could bring out this vulnerability
Hence,

39
Q

Neural Correlates: Enlarged Ventricles

A

Schizophrenics often have enlarged ventricles in the brain (fluid filled cavities that surround the brain).
The difference (about 15%) has been found in unmedicated patients, so is not the result of drugs.
These enlargements appear at the onset of illness, rather than being a result of deterioration over the course of the disorder.
Some studies have found links between ventricular enlargement and negative symptoms, such as avolition, flat affect and speech poverty.

40
Q

Evaluation for neural explanation for schiz: incomplete

McEwan

A

It could be argued that the neural explanation for schizophrenia is incomplete.
McEwan (2007) argues that nurturing influences could actually instigate these structural changes in the brains of schizophrenic patients, making the explanation incomplete. Children and adolescent brains are far more sensitive to chronic stressors (such as prenatal stressors or physical abuse) which can reshape the structure and organisation of cortical regions, contributing to schizophrenia.
This suggests that… …

41
Q

Evaluation of enlarged ventricles: not exclusive to schiz

A

Enlarged ventricles are not exclusive to schizophrenia, they may occur in the brains of those that suffer from Parkinson’s Disease and other disorders.
Plus, only some patients with schizophrenia have enlarged ventricles, not all. What’s more, some ‘normal’ individuals have enlarged ventricles and never experience schizophrenia.
This could suggest… …

42
Q

Evaluation of neural explanation: scientific

A

The neural explanation for schizophrenia is a scientific explanation.
This is because brain structure can be studied in a controlled, objective and falsifiable manner. For instance, we can study the brain structures of schizophrenic patients using MRI scans to be able to identify enlarged ventricles.
This could mean… psychology’s reputation as a science is upheld.
.