biological explanations for schizophrenia Flashcards
(32 cards)
what is dopamine?
a neurotransmitter level associated with the experience of pleasure which has an excitatory effect on neighbouring neurons
what are neural correlates?
patterns or structures in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience
gottesman (1991)
great genetic similarity is associated with a higher likelihood of developing sz
reviewed over 40 other studies and found similar results to gottesman and shields
-they found that the average concordance rate of sz in Mz to be 48% and in DZ 17%
gottesman and shields (1972)
- examined medical records of 57 twins with schizophrenia
- approximately 23 were MZ and 34 DZ
-found MZ had a concordance rate of 42% compared to DZ who had 9% concordance rate
Joseph (2004)
- found concordance rates amongst monozygotic twins to be 40.4% for schizophrenia development and for dizygotic twins to be 7.4%
- more recent evidence reports an even lower concordance rate for monozygotic twins in relation to schizophrenia development
-states that Mz are raised more similarly than DZ and suffer from identity confusion due to encountering similar environments
-therefore, such assumptions mean concordance rates are not a genetic outcome but that of the environment.
family studies?
- studies have found that schizophrenia is more prevalent in individuals who are closely related genetically with someone who already has schizophrenia
- children with 2 schizophrenic parents have a 46% chance to develop sz
- those with one parent have 13% and siblings 9%
adoption studies?
- Tienari conducted a study in Finland of 164 adoptees who has schizophrenic mothers, of which 11 (6.7%) were also diagnosed with sz, compared with 4 cases in 197 control adoptees with no schizophrenic parents.
- they concluded this evidence confirmed the genetic position within sz development.
kety (1988)
- studied over 5000 danish children between 1923 and 1947 compared to a control group of 18%,
-sz was developed in 32% of adoptees separated from biological parents who had the disorder.
-furthermore, children born with no biological relatives with sz yet raised by sz parent were no more likely than the general population to develop sz.
condradictory point of kety?
however, in the study the concordance rate of 32% included related disorders, not purely schizophrenia
-therefore, this reduces the validity of the findings for a genetic basis of sz
what are candidate genes?
these are genes which create vulnerability.
candidate genes contributing to schizophrenia?
a number of genes appear to contribute a small increased risk of sz making it polygenic - a combination of different factors is needed.
why could schizophrenia be considered aetiologically heterogeneous?
as many different genetic DNA combinations or multiple factors can lead to the condition.
Ripke et al (2014)
- compared the genetic makeup of 37,000 sz with 113,000 controls
- found that 108 separate genetic variations were associated with increased risk of sz
-genes associated with increased risk were those that code for neurotransmitter function, including dopamine.
what are the strengths and issues with studies such as gottesman, tiernari, kety and ripke?
a wealth of strong evidence from studies supports this explanation. however, many of these are correlations so causality cannot be inferred.
one limitation of the genetic explanation?
environmental factors may play a role such as smoking cannabis in teenage years and psychological childhood trauma.
this means that genetic explanations alone cannot provide a complete explanation of schizophrenia.
what is the dopamine hypothesis?
suggests that over-production of the neurotransmitter (dopamine) is responsible for the symptoms of schizophrenia.
why was the dopamine hypothesis developed?
- after observations of LSD and amphetamine; both of which enhance the activity of dopamine in the brain.
- sometimes an overdose in these drugs can cause symptoms indistinguishable from schizophrenia such as schizophrenic-like hallucinations.
where are dopamine neurons concentrated?
in the basal ganglia and frontal cortex which are concerned with the initiation and control of movements.
what was the early version of the dopamine hypothesis?
that too much hypodopaminergia in the subcortex or that an excess of dopamine receptors in brocas area may be responsible for poverty of speech and/or auditory hallucinations.
what is suggested if there is not enough hypodopamingeria in the cortex?
Goldman-rakic et al (2004) identified a role for low levels of dopamine in the prefrontal cortex, which is an areas associated with thinking and decision making, in the negative symptoms of schizophrenia.
why could both of these explanations be correct?
high and low levels of dopamine in different parts of the brain are involved in schizophrenia.
amphetamines evaluation?
- amphetamines are dopamine antagonists which mean that they stimulate nerve cells that contain dopamine which causes the synapse to be flooded with this neurotransmitter (dopamine)
- large doses of amphetamines can initiate the characteristic delusions and hallucinations of a schizophrenic episode in non-sufferers, which strongly suggests that dopamine plays a very important role in the behaviours of schizophrenics (Curran et al 2004)
antipsychotic drugs evaluation?
there are many types of antipsychotic drugs which all block the activity of dopamine by reducing the stimulation of the dopamine system.
-therefore, symptoms such as hallucinations and delusions are reduced, this again shows the link between dopamine and schizophrenic symptoms.
parkinsons disease evaluation? grilly (2002)
found that some people with parkinsons who were taking the ‘L-dopa’ to raise their levels of dopamine started to develop schizophrenic-like symptoms, which supports the idea that schizophrenics have abnormally high levels of dopamine.
