The idea that dopamine transmitted from neurons for sending messages
are being fired too regularly and easily, causing scz symptoms to develop.
Dopamine can't be used for treatment as it's said to play a part in the cause of scz, but it can be used
in the sense that the understanding of its actions allows for treatments to be delivered to reduce the
amount of dopamine binding with neurons or the no. of dopamine receptors.
Comer 2003- interfering the actions of dopamine could lead to
problems with perception and attention as it plays a big part in guiding
attention
Drugs used as treatment can increase dopamine rather than reduce it as the
sudden deficiency can lead to neurons struggling to compensate
Haracz 1982 looked at post mortem studies and dfound that those with
high dopamine levels had recieved anti-psychotic drugs before death
neuroimaging studies have not provided sufficient evidence to
support the idea that dopamine activity is altered in those who
have scz.
Genetics
Diathesis stress model
There is a genetic disposition (diathesis part)
From a biological imbalance(too much dopamine)
Symptoms are triggered --> Cognitive dysfunction= which leads to SCZ
Upbringing triggers
Environmental factors
Family relationships= Nature vs Nurture
Determinist
Reductionist
Problems with twin studies
Family studies established that scz is more
common among biological relatives of a person
with scz and that the closer the degree of genetics
relatedness the greater the rish
Children with 2 scz parents have a concordance rate (chance
of) 46%. A child of 1 scz parent the concordance rate was
13% and siblings only 9%.
SUPPORTING EVIDENCE
Joseph 2004, found that MZ twins (identical)
had a concordance rate of 40.4% and DZ
twins (fraternal) 7.4%. This supports the
genetic position of MZ concordance rate is
many times higher than DZ.
Tienari et al 2000 found of the 164 adoptees
whose biological mothers have been diagnosed
with scz, 11 (6.7%) also received a diagnosis of scz
compared to just 4 (2%) of the 197 control
adoptees (born to non-scz mothers) This
concluded that these findings showed that the
genetic liability to scz had been "decisively
confirmed".
CRITICISMS- Referring to studies of family Findings
SCZ appears to run in families
which supports the argument for a
genetic basis for the disorder.
However the fact that SCZ appears
to run in families may be more to
do with common rearing patterns
or other factors that have nothing
to do with heredity
MZ twins are treated more similarly, encounter
more similar environments e.g. more likely to do
things together and experience more "identity
confusion" than DZ twins. The differences in
concordance rates between DZ and MZ twins
reflects nothing more than the environmental
differences that distinguish the 2types of twins
IDA- most adoption studies would not have found statistically
significant differences between the adoptees born to scz and
non-scz parents without boarding the definition of scz to
include non-zygotic "scz spectrum disorders".
Psychological Explanations
Cognitive explanation
Acknowledges the role of biological factor initial sensory
experience and claim further features of the disorder come
when individuals try to understand those experiences.
Faulty thought processing causes SCZ.
e.g. experiencing sense that aren't real and when told they aren't
real they feel conspired against and faulty thinking is the
problem of mistaking unreal for real leading to paranoia
Research: Meyer and Lindenberg found a link between excess dopamine in
the prefrontal cortex and the state of working memory. Suggesting that
there's a scientifically proven link between faulty processing and high
dopamine levels. Supporting the connection between the biological and
cognitive explanations.
Socio-Cultural explanation
Double Bind Theory
Bateson et al 1956 suggests children who frequently receive contradictory messages from their
parents are more likely to develop scz. for example when a mother tells her son she loves him and
turns away at the same time he is receiving 2 mixed messages from the mother which invalidate
each other. These interaction prevent the development of internally coherent constructions of reality
and in the long run will manifest symptoms of scz (flattened affect and withdrawal
Berger 1965 found that sczs reported a higher recall of double
bind statements by their mother than non-sczs. However, this
evidence may not be reliable, as patients recall may be
affected by their scz
Hall and Levin 1980 analysed data from various previous studies and
found no difference between families with and without a scz member in
the degree to which verbal and non verbal communication were in
agreement
Tienari et al 1994 found that adopted children with scz biological parents were more likely to become
ill themselves than those children with non scz biological parents. However this difference only
emerged in situations when adopted families were rated as distured, thus meaning the illness only
manifested itself under appropriate environment conditions. Genetic vulnerability alones wasn't
sufficient
Expressed emotions: this is family
communication which involves critisicim:
hostility and emotional over- involvement.
high levels of EE most likely influence
relapse rates
Linszen et al 1997 found that a pp who comes home to a family
with high EE levels will be 4 times more likely to encounter
relapses than a pp returning to a family with low EE
Kalafi and Torabi 1996 in Iran found high prevalence in Iranian
culture, which is full of over protective mothers and rejective fathers
were the ones to cause scz relapses
Negative emotion climates would arouse patients leading to a place of
stress beyond capability mechanisms causing scz episodes. The effects of EE
are more universal empirical support than the double bind theory, however
the issue with EE is a cause or effect of SCZ and what the conditions for high
EE levels are.