the biological explanation of schizophrenia Flashcards
(30 cards)
which family study is a good example?
Gottesman and Shields (1991)
what was Gottesman and Shield’s study?
•conducted a twin study
•looked at twins of which one had developed schizophrenia
•used 56 pairs of twins
•concordance rates
DZ twins: 17%
MZ twins: 48%
•shows that there must be a strong genetic basis, due to the general incidence rates being 1%
•the closer the genetic relatedness, the higher the risk
what role do candidate genes play in schizophrenia?
•schizophrenia is believed to be polygenic (the result of a number of different genes)
•the most likely genes would be those coding for neurotransmitters including dopamine
•schizophrenia is aetiologically heterogenous (combinations of different factors can lead to the condition)
three limitations of Gottesman and Shields study
- because the concordance rate is not 100%, it implies it is not entirely down to genes and that environmental factors are involved
- cannot be sure if they were DZ or MZ twins, as genetic testing was not advanced enough so there was no scientific way of seeing what type of twins they were
- the original study was in 1972, this predates the DSM and the ICD, therefore how to we know the twins actually had schizophrenia? they may have been misdiagnosed as the schizophrenia is co-morbid with other illnesses (depression 50%). therefore the validity is questioned
who conducted an adoption study?
The Copenhagen high-risk study (Kety 1962)
what was the Copenhagen high-risk study (Kety 1962)
•Kety identified 207 offspring of mothers diagnosed with schizophrenia (high-risk) along with a matched control of 104 children with ‘healthy’ mothers (low-risk) in 1962
•the children were aged between 10-18 years at the start of the study
•used a matched pairs design. they were matched on:
- age, socioeconomic status, gender of babies, urban/ rural
•schizophrenia was diagnosed in 16.2% of the high-risk group compared to 1.9% of the low-risk group
limitations of Kety’s study
- pre-dates the diagnostic tools, so it’s unsure whether the kids/ moth had schizophrenia as it was assessed using different criteria, none of which was standardised
- no control over the age of adoptees (so they could have been adopted at 1 or 9 years old), so their risk would have increased with the longer they were in a high risk environment
what percentage of people have depression / substance abuse and schizophrenia?
50% depression
49% substance abuse
what percentage of caring responsibilities still fall down to women?
84%
results of the twin study:
DZ: 17%
MZ: 48%
what is one of the hypothesis’ in the biological explanation?
the dopamine hypothesis
what is dopamine related to?
reward, motivation and movement
what type of neurotransmitter is dopamine?
excitatory
what are the two things in the dopamine hypothesis that could relate to schizophrenia?
•too much dopamine will lead to perception without sensation (hallucinations)
•hyper sensitive receptor sites
what does a lack of dopamine cause?
parkinson’s disease. L-dopa is a synthetic dopamine, given to people to restore dopamine levels. taking too much can lead to schizophrenic like symptoms.
3 drugs related to proving the dopamine hypothesis:
- LSD/ Amphetamines
- Anti-psychotics
- L-Dopa
LSD/ Amphetamines showing dopamine association
•LSD and Amphetamines work by flooding the synapse with dopamine and making the dopamine receptors hyper-sensitive, resulting in schizophrenia-like positive symptoms . Therefore dopamine is associated with schizophrenia.
Anti-psychotics showing association between dopamine and schizophrenia
Antipsychotics work by blocking the dopamine receptors by binding to the receptor site, reducing the symptoms of schizophrenia. therefore dopamine is associated with schizophrenia.
L-Dopa showing dopamine association
L-Dopa was a drug manufactured in the 1950s to control parkinson’s disease. it is an artificial dopamine and functions like dopamine. if you take too high a dose it can produce schizophrenia-like symptoms. therefore dopamine is associated with schizophrenia.
two limitations of the dopamine hypothesis
- it is reductionist, reducing behaviour down to a single neurotransmitter. schizophrenia is complex and cannot be explained by one component.
- correlation does not equal causation, we cannot establish cause and effect.
what are neural correlates?
structural brain abnormalities correlated with symptoms
what are the three parts of the brain associated with schizophrenia?
• ventral striatum
• gyrus
•enlarged ventricles
what is the ventral striatum and how does it effect schizophrenia?
•an abnormality in this area may be involved in the development of avolition (the loss of effect)
•they observed a negative correlation between activity levels in this area and the severity of overall negative symptoms
•the area is involved in motivation and reward, as well as anticipation
what is the gyrus and how is it related to schizophrenia?
•lower activation levels in the gyrus were found in participants with hallucinations (specifically auditory hallucinations)
•associated with the auditory areas of the brain
•Allen did an fMRI scan and found the lower activity levels
•recorded conversations with them and found that the more serious the auditory hallucinations the more mistakes they made identifying their own voice in a recording