biological explanations for sz Flashcards
(14 cards)
there is evidence that sz runs in families and so appears to have a genetic basis , gottesman demonstrated a
positive correlation between the increasing genetic similarity of family members and their increasing risk of developing sz
Mz twins = 48% Dz = 17%
siblings = 9% parents = 6%
gottesmans results strongly suggests a genetic basis and the existence of candidate genes for sz however it is important to note that
there are no 100% concordance rates , therefore demonstrating that there are environmental influences acting on the development of sz
ie the sz mother and dysfunctional thought processing
candidate genes have been identified for sz for example Ripke et al conducted a genome wide study of 5001 cases of sweidah nationals with sz and compared them to 6243 healthy controls . the researcher found that
loci associated at genome wide significant ; 13 od these are new and 1 was previously implicated in bipolar disorder , alongside 8300 serrate candidate genes. each candidate gene represents a genetic variation which marginally increases the risk of developing sz.
therefore sz is a polygenetic disorder
the original dopamine hypothesis suggest that hyperdopaminergia in the sub cortex is responsible for sz whereas the revives dopamine hypothesis suggest that
hypodoperminergia in the cortex is more likely to be responsible for sz.
the modern understanding is that both hyper and hypodopaminergia in different ares of the brain contribute
to the development of sz
for example hyperdopaminergia in the frontal lobe and specifically brocas area which may have an excess of D2 receptors may be responsible for
the positive sz symptoms of auditory hallucinations , due to the overactivity of neurotransmission in the auditory ares of the brain
in addition Rakic et al suggested that hypodopaminergia in the prefrontal cortex may be responsible for
negative symptoms of sz such as speech poverty and avolition.
this is because the prefrontal cortex is associated with logical thinking , so abnormally low dopamine levels in this are may impair an indviduals ability to construct grammatical sentences that are focused upon one topic or the ability to make decisions about how to function in day to day living.
the dopamine hypothesis has particularly important implications for the development of
drug treatments for sz
such as antipsychotics/dopamine antagonists
neural correlates are specific patterns of cortical acidity or neural structures which
coincide with specific psychological symptoms and so are assumed to contribute towards those symptoms
juckel et al suggested that abnormally low levels of activation in the ventral striatum when compared to healthy neurotypical controls may be associated with the negative symptoms of avolition. this is because the
ventral striatum is associated with evaluating reward values , predictably and risks .
therefore low levels of activation and neurotransmission may mean that indviduals cannot accurately assess the reward of having enough motivation to carry out normal day to day tasks , and so are therefore unable to cope with normal life
allen et al concluded that “ the mis identification of self generated speech in patients with auditory verbal hallucinations is associated with functional abnormalities in the anterior cingulate and left temporal cortex “ as sz patients brain activity was recorded using
Fmri during auditory hallucinations and compared to a control group who identified pre recorded words as their own or not
therefore this suggests that speech poverty may be associated with this neural correlate , as shown by the sz group also making more mistakes compared to the control group
+ there is evidence supporting the biological and genetic basis of sz
for example brown er al found that the risk of having offspring with sz increased by over 1.3% if the father was over 50 years old , compared to if the father was under the age of 25 . therefore this suggests that mutatiations in the sections of DNA containing the candidate genes such as those
coding for serotonin and dopamine production specifically , means that sz is likely to have a strong heritability coefficient and biological basis . this supports the use of family studies and neural correlates as ways of studying and explaining incidence rates of sz
- the evidence for the dopamine hypothesis can be best described as ‘ mixed ‘
on the other hand supports comes from Tauscher et al who found antipsychotics which act as dopamine antagonists and so reduce dopamine activity by binding to complementary receptors on the post synaptic membrane , alleviated the symptoms of the sz suggesting that dopamine has a key role in development in line with the predictions of the dopamine hypothesis. on the other hand , some researchers such as
moghaddam and javitt have criticised the dopamine hypothesis and biological explanations of sz as emphasising the role of dopamine too far . for example the neurotransmitters glutamate and serotonin may also play a key role , as evidenced by the antipsychotic clozapine acting upon both of these substances and being more effective than other atypical antipsychotics in reducing sz symptoms as suggested by Meltzer
- the main issue associated with the use of neural correlates as a means of explaining sz is that such evidence is correlational
and so does not take into account the third variable problem whereby a third unstudied factor could be affecting both outcomes . taking the example of the line between lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus and the experience of auditory hallucinations , one explanation would be the
lowered activation levels causing the hallucinations or the hallucinations causing the lowered activation levels .
a third possible explanation would be the third variable problem.
therefore thus demonstrates that correlational research cannot be used to reliably demonstrate a ‘ cause and effect ‘ relationship between two variables.
