Biological Explanations of schizophrenia Flashcards
what does l-dopa increase? what did this create?
L-Dopa increases dopamine in brain and reduced symptoms for Parkinson’s. Created side effects like hallucinations and unusual beliefs
What’s the cause of schizophrenia?
What did drugs reduce?
What are the subtypes?
What’s the main focus?
Schizophrenia = too much dopamine
Drugs to reduce dopamine only stopped positive symptoms.
Subtypes (D1-D5) = dopamine has a different effect on the brain dependent on the type of dopamine.
Limbic system = main focus.
what do nerve pathways leave to?
what are the 2 main pathways?
Nerve pathways leave to subcortical structures to cerebral cortex – 2 main pathways include the Mesolimbic and Mesocortical.
Mesolimbic = positive symptoms. Pathway carries signals from VTA to nucleus accumbens. Too much dopamine causes overstimulation and positive symptoms.
Mesocortical = negative symptoms. Signals carried from VTA to frontal lobe.
what supporting research is there for the dopamine hypothesis?
The supporting evidence for the link between high levels of dopamine and schizophrenia came from Griffeth et al who induced psychosis in non-schizophrenic volunteers by administering a drug to increase dopamine. They experienced paranoid delusions and a cold, detached emotional response.
This shows that the dopamine hypothesis is high in external validity and so results may generalise to other schizophrenics.
what an alternative explanation for the dopamine hypothesis?
The dopamine hypothesis does not explain what causes the dopamine imbalances. Although this theory does not state this, one explanation could be an inherited genetic abnormality. Gottesman et al looked at the incidence of schizophrenia in cousins, grandchildren, half-siblings, parents, non-identical twins and identical twins. It was found that as genetic similarity increased so did the probability of both individuals having schizophrenia.
Gottesman’s findings support the dopamine hypothesis by offering a reason for the abnormalities, but the theory does not state this, showing the dopamine hypothesis as only a partial explanation lowering the validity.
What methodological issues are there with the dopamine hypothesis?
It’s difficult to measure the actual levels of neurotransmitters like dopamine in the brain. To measure, we need to measure the metabolite levels in cerebrospinal fluid through a lumbar procedure. This is an unpleasant experience. An individual’s diet and drug use may also influence their metabolite levels.
This suggests low ecological validity and that causation may need to be taken when drawing conclusions from research that use these methods.
Why is the dopamine hypothesis only a partial explanation?
Serotonin also plays a role. Typical antipsychotics block D2 receptor sites but not everyone benefits from these drugs. Atypical antipsychotics block D2 receptors and the serotonin receptor 5 – HT2A.
The dopamine hypothesis can only be a partial explanation as another neurotransmitter is involved. There is a superior effectiveness of atypical antipsychotics.
what are ventricles? what does it help? research? (How are changes to brain ventricles associated with schizophrenia?)
ventricles are cavities that produce and transport cerebrospinal fluid. It helps to protect the brain from damage and keeps the chemicals in the brain stable. Larger in schizophrenics. Enlarged ventricles linked to negative symptoms. Gaser et al – shrinkage in the thalamus lead to enlarged. Smaller ventricles with positive symptoms (Andreason et al).
How is cortical atrophy linked to schizophrenia?
the loss of neurons in the cerebral cortex. Makes the brain look like it shrunk. it results in the widening of the grooves (sulci) covering the cortex. Characterises 20-35% of people with schizophrenia.
How is reversed cerebral asymmetry linked to schizophrenia?
temporal, parietal and occipital lobes usually larger on left side of the brain. Frontal larger on the right. More folds on left hemisphere. More folds mean more surface area and more cortical space. The right hemisphere is larger in schizophrenics. E.g. - alogia caused by less folds and therefore less surface area in the frontal cortex where the language function is associated.
What supporting research is there for the structural abnormality hypothesis?
McCarley et al claims that the presence of enlarged ventricles in people with schizophrenia is the most reliable finding in research that uses brains scans. The link between cortical atrophy and schizophrenia has been confirmed using brain scans.
The confirmation of the link between cortical atrophy and schizophrenia through brain scans further reinforces the theory. The use of imaging techniques to validate such associations provides a concrete and measurable basis for understanding the physiological aspects of schizophrenia.
What methodological issues are there with the structural abnormalities hypothesis?
Many schizophrenics will be on anti-psychotics. Therefore, the structural abnormalities found may be the result of the medication and not the illness itself. Particularly, taking antipsychotics for long periods of time may account for the changes to the size of the Cortex.
Anti-psychotics acts as a confounding variable making it difficult to isolate the cause and effect of schizophrenia.
Why is the structural abnormalities hypothesis only a partial explanation?
Structural abnormalities are present in all schizophrenics. Also, factors such as age, gender and severity of symptoms can have an affect on the prevalence and pattern of these structural differences.
Therefore we need to acknowledge that there be other factors that may account for the illness like a genetic pre disposition or environmental factors.
