Biological Explanations of SZ Flashcards
1
Q
What are the two biological explanations for SZ?
A
- Genetic Inheritance
- Neural Correlates: Hyperdopaminergia
2
Q
How does genetic vulnerability explain SZ?
A
- It has been proposed that there is a genetic component to schizophrenia which predisposes some individuals to the illness.
- The genetic explanation suggests that whether a person develops schizophrenia is at least partly due to their genes.
- This may explain why patients often have other family members with schizophrenia which could be inherited through FAULTY genes.
- Candidate genes are ones which, through research, have been implicated in the development of schizophrenia… e.g. C4 gene variations in chromosome 8 & 11
- Schizophrenia is thought to be polygenic – this means that its development is not determined by a single gene but a few (maybe as many as 108 genetic variants - Ripke et al 2014 )
– This means that there is little predictive power from this explanation.
Genes associated with the increased risk of SZ include those coded for the functioning of a number of neurotransmitters including dopamine.
- Having some of these faulty genes ultimately increases a person’s vulnerability to developing schizophrenia by inheriting biochemical imbalances or brain structure abnormalities.
3
Q
What is the link between the C4 gene and SZ?
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.
- Some researchers have shown that individuals with increased C4 activity have a higher chance of developing SZ.
- Increased C4 activity is a genetic mutation ( it has survival value as it helps the brain to adapt and learn and prune synapses that are no longer needed) - but too much of this synaptic pruning can ‘backfire’.
- A faulty variant of C4 is a clear risk factor for schizophrenia as this faulty variant can lead to hyper-pruning. Research supports the hypothesis that excessive or hyper-pruning could lead to symptoms of schizophrenia.
- This explains which SZ emerges after adolescence/early adulthood and not before.
- This also explains why the brains of SZ patients have a thinner cerebral cortex with fewer synapses compared to health brains and could explain the cognitive symptoms seen in schizophrenia.
4
Q
What are some family studies of SZ?
A
- Family studies find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives.
- One very large-scale family study was carried out by Gottesman (1991)-there is more than 1 study!
He concluded that if both parents suffer from schizophrenia, then there is a 46% chance of also developing the disorder (compared to a 1% chance for the general population). - Findings have shown that the greater the degree of genetic relatedness, the greater the risk of developing schizophrenia.
5
Q
What are some twin studies of SZ?
A
- MacDonald and Schultz (2009) have suggested that among MZ twins, if one twin is diagnosed with schizophrenia then the other twin is 99 times more likely to suffer from the condition.
- This is further convincing research to imply that genetics are involved in the development of schizophrenia.
- Joseph (2004) found some convincing support to show how genetic similarity can increase risks of developing the condition.
- Joseph 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 for MZ twins (when the environmental influences on both groups can assumed to be no more similar than for DZs) suggests genes have some influence on the development of the disorder.
6
Q
What are some adoption studies of SZ?
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 SZ has a genetic component as the adopted children do not share environmental influences with their biological mothers.
- They are better at separating nature from nurture as the children are not raised by the biological parents.
7
Q
What are the positive evaluations of genetic explanations of SZ?
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) suggests genes have some influence of the development of schizophrenia.
(In your workbook there is an extra bit on MacDonald and Schultz)
This implies… schizophrenia may in part be caused by genetic inheritance, possibly through inheriting the fault variant C4 gene. - This knowledge concerning genetics and schizophrenia can have useful practical applications.
Vulnerable groups in society who have relatives suffering from schizophrenia are often advised by clinicians on their risk of developing the disorder.
What’s more, 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 or using surrogates.
This suggests… that the biological approach to understanding the cause of schizophrenia can have positive tangible effects in society. - 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.
8
Q
What are the negative evaluations of genetic explanations of SZ?
A
- However, the genetic explanation is incomplete. Faulty 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 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). The psychological explanations of schizophrenia also puts forward explanations such as: the schizophrenogenic mother by Fromm-Reichmann and the role of dysfunctional thought processing such as dysfunction in the central monitoring system.
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. - Family studies into schizophrenia also have serious methodological problems. Although family studies show how schizophrenia may run in families, i.e., intergenerational, this still might not necessarily mean that faulty genes are the cause.
For instance, children 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 due to how this shapes their internal working model. Therefore, instead of inheriting schizophrenia from their parents, children may be learning schizophrenic ways of behaving from them instead.
This suggests… that genetic evidence of schizophrenia running in families can actually be used to validate the role of the environment in its development. - The genetic explanation of schizophrenia can be accused of being biologically deterministic.
Although psychology is seeking general (nomothetic) laws to explain all behaviours, this genetic theory into schizophrenia overlooks many aspects.
What is bad about this theory being biologically deterministic?
This implies that… the account neglects to consider the role of environmental factors a well as free will in the development and potential recovery from schizophrenia.
9
Q
What are Neural Correlates?
A
- Neural correlates are instances where brain structure differences correlate with certain psychological disorders or symptoms.
- Neural correlates in schizophrenia suggest that structures in the brain are associated with the positive and negative symptoms of schizophrenia, such as in the enlarged ventricles found in schizophrenic patients.
10
Q
What is the Dopamine hypothesis?
A
- SZ is caused by elevated levels of dopamine (DA) at key synaptic sites within the subcortical (central) regions of the brain e.g. the mesolimbic pathway and limbic system (the areas of the brain governing emotion)
- An excess of the neurotransmitter dopamine has been implicated in the symptoms of schizophrenia.
Dopamine neurons are instrumental in regulating attention, therefore if this process is disturbed it may lead to problems with attention, perception and thought – these are all characteristic symptoms of schizophrenia. - This theory claims that excessive amounts of dopamine or an oversensitivity of the brain to dopamine is the cause of schizophrenia. (HYPERDOPAMINERGIA)
- The dopamine hypothesis states that messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic positive symptoms of schizophrenia.
- Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.
11
Q
What is the revised Dopamine hypothesis?
A
Davis et al (1991):
Suggests that actually negative symptoms of schizophrenia ( e.g. Avolition) can also be explained by lower levels of dopamine in the prefrontal cortex where there are no D2 receptors.
This is called HYPODOPAMINERGIA.
12
Q
What is the evidence for the Dopamine Hypothesis?
A
- An agonist is a chemical that binds to a receptor of a cell and triggers a response by that cell.
- An antagonist blocks or reduces the effect of a neurotransmitter.
- Amphetamines; (e.g speed- methamphetamine) this is a dopamine agonist, this stimulates nerve cells containing dopamine causing the synapse to be ‘flooded’ – large doses of the drug can cause hallucinations and delusions of a schizophrenic episode.
- Cocaine also increases the levels of dopamine in the brain. Can cause the positive symptoms of schizophrenia and exaggerate them in people who already have the disorder.
- Antipsychotic drugs (dopamine antagonists) which block the activity of dopamine in the brain, by reducing the stimulation of the dopamine system, eliminates hallucinations and delusions.
- Higher than normal concentrations of dopamine have been found in the post-mortems of patients that suffered from schizophrenia.
- 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).
13
Q
What are the positive evaluations of Dopamine Hypothesis explanation for SZ?
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). - 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 by helping patients reduce their symptoms and maintain a better quality of life. - 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.
14
Q
What are the negative evaluations for the Dopamine Hypothesis for SZ?
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. - There is clearly a relationship between high dopamine levels and schizophrenia, but we cannot infer cause and effect.
For instance, does high dopamine cause schizophrenia or does schizophrenia cause high dopamine (which comes first)?
Perhaps there is a third unknown factor that actually causes both, such as a variant TPH gene as found by Hong et al (2001) to be associated with schizophrenia in Chinese patients. As the TPH gene plays a role in serotonin production, faults here could impact dopamine activity as serotonin can have an inhibitory effect on dopamine.
Hence, the dopamine hypothesis of schizophrenia is merely correlational and as such of limited use.
15
Q
What is the neuroanatomy/ chemistry explanation for SZ?
A
- There is growing evidence that schizophrenia is linked to structural abnormalities in the brain and/or biochemistry.
- Brain scanning techniques have made it possible to investigate living brain images.
- Both positive and negative symptoms have correlates (brain structure changes correlate with symptoms of SCH).
16
Q
How are enlarged ventricles responsible for SZ?
A
- People with schizophrenia have abnormally large ventricles. (Ventricles= cerebrospinal fluid filled cavities)
- This means brains of schizophrenics are lighter than normal and hence the grey matter volume shrinks in SZ patients as ventricles enlarge.
- This could be a consequence of nearby parts of the brain not developing properly or being damaged.
- This loss of grey matter leads to cognitive decline linked to NEGATIVE SYMPTOMS.
17
Q
How is Hypofrontality responsible for SZ?
A
- Hypofrontality is a state of decreased cerebral blood flow (CBF) in the prefrontal cortex of the brain.
- This means an underactivation of the dorsolateral prefrontal cortex, particularly on cognitive activation linked to negative symptoms- tested by using the WISCONSIN CARD SORT .
- Those with SZ have difficulty in tasks
requiring executive memory functions.
18
Q
How is the Hippocampus- Amygdala Region responsible for SZ?
A
- Schizophrenia patients have smaller volume in bilateral amygdala and hippocampus compared with healthy controls (especially in early onset SZ).
- Significant negative correlations between volumes and symptoms were found between:
(i) Lower volume of left amygdala & thought disorder
(ii) Lower volume of left hippocampus & negative symptoms
(iii) Lower left anterior & posterior hippocampus volumes with positive & negative symptoms. - When researchers scan the frontal lobes of those with schizophrenia, they discover that there is a large decrease in neural waves in this brain area.
- Which means there is less synchronized neural firing or communication.
- The disruption of neural network communication is a contributor to symptoms of schizophrenia.
19
Q
What are the positive evaluations for the neuroanatomy/ chemistry explanation for SZ?
A
- There is evidence to support the theoretical foundations of dysfunctional thinking and schizophrenia.
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 for themselves, read them, or whether they were new.
Results showed schizophrenic participants with hallucinations performed worse (i.e., were unable to identify the source of the words); than schizophrenic patients without hallucinations and both groups performed worse that non-schizophrenic controls.
This highlights the idea that schizophrenics have a deficit when it comes to monitoring ‘own’ behaviour and therefore supports the idea that the positive symptoms of schizophrenia are linked to a faulty CMS. - This explanation has been practically applied to help those suffering from schizophrenia.
For example, Cognitive Behavioural Therapy aims to challenge and change the cognitive deficits of patients with schizophrenia 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 schizophrenic patients.
This implies… the cognitive dysfunctional explanation of schiz has been very useful to the 1% of the population that are suffering from schizophrenia. - The cognitive explanation is praised for being able to link both physiological and psychological aspects together to explain cases of schizophrenia.
Cognitive neuroscience links areas of the brain and information processing together to explain behaviour and with schizophrenia this can be readily appreciated.
For instance, by looking at damage to the hippocampus and regions linked to working memory we can see how they contribute to cognitive and memory deficits.
This means the explanation should be praised for taking a more comprehensive account of schizophrenia.
20
Q
What are the negative evaluations for the neuroanatomy/ chemistry explanations for SZ?
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 schizophrenia as opposed to a causal factor.
In fact both cognitive deficits and schizophrenia could be caused by another factor completely, e.g., high levels of dopamine activity in the mesocortical pathway.
This implies… dysfunctional thought processes may simply be a manifestation of schizophrenia as opposed to an instigating factor, reducing the usefulness of this theory when considering treatment options.
