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Biological Explanation of Schizophrenia - Coggle Diagram
Biological Explanation of Schizophrenia
Genetic:
Assumes that the disorder can be passed on to individuals from their families, meaning it is hereditary. Although it isn't thought that there is a single gene, genetics could make some people more vulnerable than others
The concept
- if you inherit a gene related to schizophrenia this does not mean that you will definitely inherit the disorder, but you are more likely to (you are more vulnerable to it)
Candidate genes:
Individual genes are thought to be associated with a risk of inheriting schizophrenia
A number of genes each appear to show a small risk, so it may be that schizophrenia is polygenic
Recent research also shows that these genes can be mutations rather than directly inherited
Ripke et al (2014)
Procedure
- Meta- analysis of all previous data from a genome wide studies, genetic make up of 37,000 patients was compared with 113,000 control participants
Findings
- 108 (polygenic) separate candidate gene variations; genes indicating an increased risk were often associated with the production of dopamine
Evaluation
-
S - Huge sample size, easy to collect, cross cultural
W - Comparing data that my be incomparable (data may have been collected in different ways) - affects reliability and validity
Genetic susceptibility:
Gottesman (1991):
As the genetic relations increases so does the prevalence of schizophrenia - environment must play a role if identical twins are only 48%
Meta-analysis - secondary data lacks reliability
MZ twins 100% DNA, 48% risk
Tienari (1969):
Tienari (1990):
Follow up study found that environment may be more important than genetics
W - BIas, subjectivity in rating, high drop out rate
Identified adopted offspring of Finnish biological mothers who had been diagnosed (112) and compared with a group that had not been diagnosed (135)
7% with schizophrenic mothers developed the disorder, 1.5% control
7% is not 50% (shared DNA) therefore environment must play a role
The role of mutation:
Sometimes schizophrenia can take place without a family member having a diagnosis. This can suggest that genetic influence is not as strong as indicated by other evidence
Brown et al (2002):
Demonstrates it could be possible for sperm DNA mutation to be related to schizophrenia
Found a positive correlation between paternal age and the risk of schizophrenia - risk being 0.7% with fathers who were under 25 and over 2% with fathers over 50
Biological treatments:
When the cause of schizophrenia is deemed to be biological, Anti-Psychotic drugs are used to treat the disorder - they focus on neurotransmitters in the brain and aim to equal out their balance
Typical:
Work by blocking dopamine receptors within the brain, minimising its effects
Chlorpromazine - can be taken as either tablets, syrup or injection (orally - dosage begins at low and can go up to 800/1000mg)
Strong link between chlorpromazine and the dopamine hypothesis
Work as an antagonist in the dopamine system - block the dopamine receptor sites so the dopamine can't get through into the brain
Hallucinations are reduced and the drug has a sedating effect
Can cause negative side effects eg. stiff jaw, dizziness
Atypical:
Clozapine, Risperidone help to reduce the negative side effects caused by the typical antipsychotic drugs
Unsure as to how they work exactly within the brain
Clozapine -
Binds to the receptors in the same way as chlorpromazine but also acts on serotonin and glutamate receptors
Helps improve mood and reduce anxiety and depression - thus helping with their cognitive functioning
Lower doses - 300-450mg a day
Severe side effect - Agranulocytosis which can be fatal
Risperidone -
Aim to reduce the severe side effects that clozapine has
Taken as a tablet, syrup or injection - daily dosage of 4-8mg up to 12mg
Binds to the dopamine and serotonin receptors in the same way as clozapine
Fewer side effects than other anti-psychotics
Evaluation:
W (ethical) - There are potentially serious side effects such as Tardive dsykinesia
Suffer side effects particularly with typical - dsykinesia due to the reduction of dopamine in the hypothalamus
However, A Typical anti-psychotics were produced to reduce side effects
S - (effectiveness) - Thornley et al (2003) found that chlorpromazine was effective
Associated with overall better functioning and reduced symptom severity
However, Meltzer (2012) found that A Typical anti-psychotics were more effective
W - (appropriateness) - Much of the original research into antipsychotics was completed using animals
Low generalisability, cannot see how humans react to drugs
We are unable to test them on humans
S - (appropriate) - Patients often welcome drug therapy as it is quicker, easier and less threatening than 'talking therapies'
Some may respond to therapy better than others - also may find it more accessible
Drugs may only be used as a 'chemical cosh'
Bagnall (2003):
Aim
- To compare effectiveness, safety and cost of typical and a typical anti-psychotics
Procedure
- Data (171 randomly controlled trials, 52 non-randomised trials, 31 economic evaluations of treatments) analysed by two independent researchers
Findings
- Atypical more effective in reducing symptoms with the exception of two, also caused fewer movement side effects
Conclusions
- Atypical are more effective overall, however all have their issues and must be suited to the patient
Evaluation
-
Main issue - need to take into consideration side effects that may occur (side effects may mean medication is no longer taken)
Individual differences - some may experience worse side effects in comparison to their symptoms
Anti-psychotics treat symptoms not the cause
Therapies can be evaluated in 3 different ways - effectiveness, appropriateness, ethics
Effective and cheap
Kapur et al (2000)
- estimate that between 60% and 75% of D2 receptors in the mesolimbic pathway need to be blocked in order for drugs to be effective
Neural correlates:
The biochemical explanation:
This explanation links to the idea that the neurotransmitter dopamine is responsible for the disorder
Hyperdopaminergia:
Too much dopamine in the Broca's area where there are too many receptors in dopamine pathways - positive symptoms
Hypodopaminergia:
Too little dopamine within the prefrontal cortex - could be an explanation for symptoms such as avolition (negative symptoms)
Randrup + Munkvad (1966):
Evaluation:
W - Study is anthropomorphic therefore low generalisability as rats cannot report whether they have the disorder or not
Findings:
All known symptoms of schizophrenia were reported including stereotyped activity
As the dosage increased the rats lost their ability to perform basic tasks/functions
Conclusion:
Experiments with a number of different animals show that stereotyped schizophrenic activity can be produced by amphetamines. This supports the idea that dopamine contributes to schizophrenia
Procedure:
Amphetamines (dopamine agonists) which worsen schizophrenic symptoms were injected into rats with doses of 1-20mg/kg
Lindstroem et al (1999):
Used a radioactive tracker in the blood and found that chemicals needed to produce dopamine are taken up faster in those who suffer from schizophrenia
Found that more dopamine is used by people with schizophrenia - hyperdopiminergia explanation
Ripke et al (2014):
Research indicates that other neurotransmitters are involved in schizophrenia
Found that genetic markers were linked with other neurotransmitters such as glutamate
In many parts of the brain, glutamate has the effect of regulating dopamine activity - eg. when glutamate activity increases, dopamine activity decreases
Brain areas:
Measurements of the structure or function of the brain that correlate with an experience - means that schizophrenics may have specific brain abnormalities (may be correlated with +/- symptoms)
MRI and Post mortem are scanning techniques used to discover neural correlates
Evaluation:
Older research: focused on ventricles of the brain
Enlarged ventricles are particularly correlated with negative symptoms
However new research,
Eom et al (2020):
Found that when part of chromosome 22 (a gene related to schizophrenia) was deleted in mice, it was related to enlarged ventricles - gives evidence for the genetic mechanism which may create enlargement
Newer research: focused on other areas
Ventral Striatum to explain negative symptoms:
Juckel et al (2006)
Found that levels of activity in the ventral striatum were lower in schizophrenic patients than controls - this area is believed to be involved in the symptoms of avolition
Superior Temporal Gyrus and Anterior Cingulate Gyrus to explain positive symptoms:
Allen et al (2007)
Found that lower activity levels in the superior temporal gyrus and anterior cingulate gyrus in schizophrenia patients when they were identifying pre-recorded speech as their own or others
This area is linked with the anticipation of a reward which is a feature of motivation
Reduced activity in this area is correlated with auditory hallucinations
W - Not all schizophrenics have enlarged ventricles or brain abnormalities - therefore this cannot be the only explanation
W - We are unsure whether the brain area causes the symptoms or if the brain area has changed because of the symptom