Schizophrenia Flashcards
What do adoption studies demonstrate about genetic predisposition?
Teinari (2004) in Finland found that out of 164 adoptees who’s biological mothers had had schizophrenia, 6.7% developed schizophrenia. This was compared to a control group of 194 children - of which only 2% went on to develop schizophrenia. Therefore this study rules out the heightened presence of nurture over nature in the debate as to whether there is a stronger basis for genetic predisposition.
What are the 3 explanations for Schizophrenia?
- Genetic explanation
- The dopamine Hypothesis
- Neural correlations of schizophrenia
What are the family studies that demonstrate the genetic explanation?
Gottesman (1991) looked at the rate with which Schizophrenia occurs in families. When one biological parent had schizophrenia the concordance rate for their children was 13% while those who had both parents with schizophrenia developed it 46% of the time. Between siblings, the rate was 9%. Therefore there is a genetic predisposition to having schizophrenia. THsi can be added to by Ripke at al’s (2014) work looking at the genetic differences present in those with schizophrenia (108 gene sets within 37,000).
What is the issue of nurture in twin studies?
They still have nurture in common….but we have alternative information from Teinari’s study.
What is an issue with adoption?
People with a history of schizophrenia in their families are more likely to adopt a child with schizophrenic parents due to the selective adoption process.
What is an issue with adoption?
People with a history of schizophrenia in their families are more likely to adopt a child with schizophrenic parents due to the selective adoption process.
Criticism from Sorri et al (2004)? (Bio)
Comparatively, Sorri et al found that when looking at the effect of child-rearing on a long-term basis (over 21 years) the style they were raised in was key to the development of schizophrenia.
Criticism for it being a conspiracy? (Bio)
Hedgecoe (2001) states that the biological explanation given by adoption and twin studies is merely produced to make a profit from the prescriptions of antipsychotics that are given to all schizophrenia patients to treat positive symptoms.
How can mutation prove the biological explanation?
Brown et al (2002) found that mutation played a role in the development of schizophrenia. Therefore demonstrating that there s some genetic changes that occur to cause schizophrenia, supporting the idea it is rooted in biology.
Brown at al (2005) found that environmental exposures, including infections, nutritional deficits, and neurotoxins, are known causes of neuropsychiatric disorders, and are potent disruptors of brain development, which has been proposed to play a major role in the etiology of schizophrenia. Providing an alternative picture to biological explanations.
What are Candidate Genes?
They are individual genes that have a direct link to certain characteristics.
What does Polygenic mean?
A term that means the collaborative work of a group of genes to cause a specific condition.
But this is not incredibly effective as there are so many combinations of this that no gene code test can be produced, much like OCD.
(Tosato et al (2005) - gene mapping demonstrates it is due to more than one gene)
What are the specific genes and researchers that connect to susceptibility?
- Gurling et al (2006) - PCM1
- Benzel et al (2007) - NRG3
What is the outline of the dopamine hypothesis?
Dopamine aids the carrying of messages in the brain and aids its function. If there is too little or too much dopamine this causes issues within the system. In the case of schizophrenia the frequent firing of neurons in response to that dopamine causes schizophrenic-type symptoms.
What did Snyder (1974) and Comer (2003) find?
Schizophrenics seem to have a higher level of D2 reception neurons which have an effect on perception/attention.
What did Davis (1991) find?
Positive symptoms can be associated with high levels in the mesolimbic dopamine system.
Negative symptoms are associated with high levels in the mesocortical dopamine system.
What is hyperdopaminergia? (sub)
This is found in the subcortex where the highest levels of dopamine activity are present. For example, in this area, the Broca’s area would be affected leading to speech Avolition or auditory hallucinations.
How is there support from different forms of drugs? (DH)
There are many connections with drugs that can support the theory that dopamine deficiencies or increases affect the development of schizophrenia. For example, one dopamine agonist like amphetamines increases the symptoms of schizophrenia in non-sufferers (Curran et al 2004) and have even been shown to induce shizophrenia in rats (Randup and Munkvad). While antipsychotic drugs work by reducing the dopamine activity in the brain (Tauscher et al 2014). Davis et al (1980)’s research demonstrated their effectiveness by showing that those who took placebo’s relapsed 55% of the time while those with real treatment only 19%. Both of these suggest that dopamine plays a crucial role in the development of schizophrenia and is even further supported by Lindstroem et al (1999) who found that the rate of dopamine uptake in schizophrenic individuals was much faster, suggesting that they must therefore produce more dopamine.
There is also alternative evidence given by Grilly (2002) who found that patients with Parkinsons disease developed schizophrenic - like symptoms when given too much L-dopa. Demonstrating that again, these symptoms can be induced in connection with the effects of dopamine.
What is the counter-evidence for this support? (DH)
However, the dopamine explanation is not complete. Some genes identified by Ripke et al seem to produce other neurotransmitters as well as dopamine, meaning while it may play a role - it is not the only factor. Modern research has not shifted to look at the effects of glutamate (Moghaddam and Javitt 2012) further leading us to a less focused conclusion about dopamine being the sole inducer of schizophrenia than previously understood.
There has also been firmly contrasting research carried out by Haracz (1982) who found from post mortems that antipsychotics may in fact be harming them. There is also the additional fact that PET scans are yet to find evidence for the dopiamine hypothesis (Coplov and Crook (2000)).
What are Neural Correlates?
Structures in the brain that directly correlate with certain experiences.
How were these originally discovered?
Post mortems were originally what showed these triggers for schizophrenia, in the modern-day they can now be picked up by fMRIs by comparing the images of sufferers to non-sufferers.
What did Juckel at al (2006) find?
They found that the ventral striatum linked to the negative symptoms of schizophrenia, for this particular area the cause of avolition. If we anticipate rewards then we are likely to be more motivated to work towards something and so a lack of activity leads to a lack of motivation.
What did Allen et al (2007) find?
They found that schizophrenics who suffer from auditory hallucinations seem to have underactive superior temporal gyrus’ and anterior cingulate gyrus’ in comparison to the control group of neurotypical individuals.
What is the issue with causality? (NC)
The issue is that it is not possible to prove whether neural correlates cause schizophrenic symptoms or the symptoms are the cause of the neural correlates. Eg the ventral striatum may cause avolation or the avolation may cause the under stimulation of that area. When it comes to treating this makes it questionable whether you should be treating the cause of the correlates or change the state of these areas to affect the condition of the sufferer.
What is the diathesis-stress model by Gottesman and Reilly (2003)?
This model suggests that environmental factors act as triggers for the underlying biological predispositions of those suffering from schizophrenia.
How is Gottesman and Reily’s diathesis stress model a support and criticism? (NC)
- Therefore the biological and environmental sides of the argument are weak in isolation if it is more effective to use a mixed approach.
- Can be effective in a treatment when combining the biological concussions and providing medication alongside therapy and changing the possible triggers the environment around them.
What is the family dysfunction theory from the psychodynamic approach?
Fromm-Reichmann (1948) looked at schizophrenic patients using the psychodynamic approach and the DSM originally based of Freud’s definitions and treatments. She found that a particular patient was paid close attention to single parent - concluding that they must have a role in S’s development.
She suggested the presence of a schizophrenic mother or a family that was too protective, emotionally cold, rejecting, dominant and moralistic as the cause for the occurrence of schizophrenia. This set up leads to paranoia and delusions that they are being persecuted in some way or that everybody is always watching them.
Meta-analysis support….+attachment (P)
Read et al, although not considering the psychodynamic approach in their study, conducted a meta-analysis of 46 studies and found that child abuse was related to schizophrenia in 69% of the female in-patients. Therefore demonstrating a correlation between the events of childhood to the development of the condition. Berry et al (2008) also found that 59% male schizophrenics experienced insecure attachments to their primary caregivers, concluding the same as Read et al (2005).
