Biological Explanations Flashcards
What are the biological explanations for schizophrenia
All inter-related, as if schizophrenia is genetic, those genes lead to biological differences such as abnormal levels of dopamine and/or abnormal structures of the brain.
1 - Genentics
2 - Dopamine Hypothesis (Role of Neurotransmitters)
3 - Neural correlates
Genetics
Suggestion schizophrenia runs in families.
Gottseman - studied family members and occurrences of schizophrenia, found that if a person has schizophrenia, the following concordance rates apply:
Identical twins: 48%
Non-identical twins: 17%
Children: 13%
Siblings: 9%
Parents: 6%
Half-siblings: 6%
Grandchildren: 5%
Nephews/nieces: 4%
Uncles/aunts: 2%
First cousins: 2%
General population: 1%
The more genes the person shares with the sufferer, the more likely they are to have the disorder, suggesting there may be a genetic basis for schizophrenia.
Polygenic - lots of different genes contributing to an increased risk of developing it.
Aetiologically heterogeneous, meaning different combinations of genes are implicated in the disorder. Ripke et al (2014) found 108 genetic variations associated with schizophrenia.
Genetics Continued (Polygenic & Aetologically heterogenous)
Polygenic - lots of different genes contributing to an increased risk of developing it.
Aetiologically heterogeneous, meaning different combinations of genes are implicated in the disorder. Ripke et al (2014) found 108 genetic variations associated with schizophrenia.
Genetics EVALUATION
RESEARCH SUPPORT FOR GOTTSEMAN
Tienari - adopted children of biological mothers with schizophrenia more likely to develop the disorder themselves than adopted children of mothers without schizophrenia, supporting the genetic link
OTHER VARIABLES/LACK CONTROL
Increased concordance rates in Gottesman study were due to the increased chance of sharing the same environment
- Identical twins share the same environment (and may be treated similarly), whereas first cousins would not. This means that it can’t be concluded that genetics has caused schizophrenia.
LIMITED EXPLANATION
As identical twins share 100% of their genes, it would be expected that the concordance rate for schizophrenia would be 100% if it was purely genetic. As it is only around 50%, this suggests other influences are playing a part.
Dopamine Hypothesis
Dopamine is a neurotransmitter, levels associated with schizophrenia symptoms.
Hyperdopaminergia: higher than usual levels of dopamine in the subcortex (central) This is linked with positive symptoms such as hallucinations. There may be a higher number of dopamine receptors, causing over-activity of dopamine, causing sensory hallucinations.
Hypodopamineriga: lower than usual levels of dopamine in the cortex (outer) where less dopamine is being transmitted across synapses. This is linked with negative symptoms, as there is a reducing in normal functioning.
Dopamine Hypothesis EVALUATION
RESEARCH SUPPORT
Curran - found dopamine agonists (drugs which increase activity) produce schizophrenia-type symptoms in patients, supporting the hypodopaminergia aspect of the dopamine hypothesis.
Tauscher - found giving patients antipsychotic drugs which lower dopamine levels (antagonists- reducing activity) reduced the occurrence of positive symptoms, supporting the hyperdopaminergia aspect of the hypothesis.
There is likely to be other neurotransmitters involved in schizophrenia, some identified the Ripke’s genetic study, weakening the dopamine hypothesis as an incomplete explanation of schizophrenia.
Neural Correlates
Growing evidence that schizophrenia is down to abnormalities in the brain. The structure or functioning of the brain is correlatedwith positive and negative symptoms.
Negative symptoms: The ventral striatum is involved with reward anticipation. Schizophrenia patients have been found to have less activity in this region- the lower the activity, the more severe the negative symptoms. This could explain avolition (loss of motivation).
Positive symptoms: Allen scanned the brains of patients experiencing hallucinations whilst they completed an auditory processing task.
- Lower activation levels found in the superior temporal gyrus and anterior cingulate gyrus, and they made more errors, compared to a control group. Auditory hallucinations are therefore correlated with reduced activity in these areas.
Neural Correlates EVALUATION
The fact that there is a correlation between brain areas and symptoms does not mean that the neural mechanism has caused the symptoms. It may be that the difference in activity levels could be a consequence of the disorder.
Neural explanations have been criticised as reductionist, explaining schizophrenia at quite a simplistic level of explanation. The role of upbringing, learning and emotions is not considered, weakening this as a full explanation.
Drug Therapy
Antipsychotic drugs (drugs used to reduce the intensity of the symptoms) are the most common treatment for schizophrenia.
- They involve modifying/interfering with the action of neurotransmitters, in order to increase (agonists) or decrease (antagonists) their activity.
Typical antipsychotics
Atypical antipsychotics
Typical Antipsychotics
- 1950s
- Chlorpromazine.
- Dopamine antagonists - attempting to reduce dopamine activity.
- Block dopamine receptors on post-synaptic neurones, meaning that less dopamine is transmitted across the synapse reducing dopamine production, and reduces positive symptoms such as hallucinations.
Drugs such as Chlorpromazine also have a sedative effect, meaning that they calm patients down and reduce anxiety. As the drugs block dopamine activity, they tend to have (sometime severe) side-effects.
Atypical Antipsychotics
1970s, to find drugs with less severe side-effects than typical antipsychotics.
-Clozapine which is used when other drugs have failed, due to the risk of agranulocytosis (a potentially fatal blood condition).
- Clozapine acts in a similar way to Chlorpromazine, but also acts on serotonin and glutamate receptors.
- As well as reducing positive symptoms, the reduction of depression and anxiety, and the enhancement of mood. It is therefore prescribed when the patient is at risk of suicide.
Risperidone -designed to be as effective as Clozapine without the risky side-effects.
- Binds to dopamine receptors more strongly than Clozapine, and there is some evidence that it produces fewer side-effects.
Drug Therapy EVALUATION
SUPPORT
Thornley - meta-analysis that Chlorpromazine was associated with better functioning and reduced symptom severity than placebos
SUPPORY
Melzer - Clozapine is effective in 30-50% of cases where other drugs have failed, supporting its use in schizophrenia treatment.
Antipsychotic drugs are weakened by the fact that they have severe side-effects. For example, some patients on typical antipsychotics develop tardive dyskinesia- a condition where there are uncontrollable facial tics. Even after stopping the use of the drug, this condition can persist. Other side effects are potentially fatal, for example (NMS). Side effects are less severe where patients are taking a reduced dose, as many do today, but this can reduce the effectiveness of the drug as well. The severity of the side-effects is a weakness as patients will be reluctant to take them, or may even die as a result of the effect.
