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principles
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dopamine
hypothesis
people with schizophrenia have excess amounts of dopamine in the
limic
system
revised dopamine hypothesis
there is an excess amount of dopamine
receptors
in the post synaptic neurone which are more
sensitive
so dopamine is absorbed in various pathways
excess receptors can be due to
injury
, disease or
genetics
seeman evidence for dopamine hypothesis
drugs that increase dopamine increased
positive
symptoms such as
hallucinations
antipsychotic
drugs which block dopamine receptors
reduced
symptoms
post mortems of brains with schizophrenia show
higher
density of
D2
receptors than neurotypical brains
grey matter
enlarged ventricles of
schizophrenic
brains lead to less grey matter
temporal lobe =
verbal
and
acoustic
memory so auditory hallucinations
thalamus =
relay
station of
motor
movement which explains hallucinations (hearing, touch, sight, taste)
frontal lobe =
planning
coordination which explains
incoherent
speech and perceptual disturbances
brain size
reduced
overall size of the brain in
schizophrenic
brains with less grey matter than neurotypical brains
correlation between
less
grey matter and
length
of time with schizophrenia
reduction stops when patients taken
antipsychotics
which
reduces
symptoms
pol
et al
tested
159
brains with schizophrenia and
158
neurotypical brains
found an increase by
30
% of ventricle size and a reduction in
grey
matter
haijma
meta analysis on 317 studies using MRI scans using
8000
people with schizophrenia
found that patients with schizophrenia are
2.6
% smaller
brain areas like the thalamus which deal with
sensory
and
motor
integration were smaller in people who hadnt recieved treatment for schizophrenia
ventricle size
people with
schizophrenia
have
enlarged ventricles
could explain
cognitive
symptoms such as
disorganised speech
four ventricles hold cerebral spinal fluid which provide nutrients and protect the brain
positive
symptoms
hypofunction of
dopamine
in the
mesolimic
pathway
responsible for
motivation
,
emotion
and rewards
can explain
positive
symptoms of
schizophrenia
negative symptoms
erratic dopamine in the mesolimic pathway
can explain
cognitive deficits
and problems with affects during an
episode
responsible for executive
funtion
, mental control and
self regulation
adoption studies
Tienari
found that the lifetime risk of adopted children with
schizophrenic
biological mothers was 9.4%
strong
genetic
component
adpoted children with
unaffected
parents was
1.2
%
twin studies
concordance for DZ twins =
15%
concordance for MZ twins =
46%-53%
strongly implies a
genetic
component to
schizophrenia
family studies
Gottesman
and
Shields
- found that MZ twins had a higher concordance rate for both having schizophrenia than DZ twins
Gottesman
- increased risk of developing schizophrenia if parents have schizophrenia (7%)
Riley
and
Kendler
- the risk is ten times greater for first degree relatives of someone with schizophrenia
association studies
Ripke
- genome wide study with
36000
schizophrenia patients and 113000 non affected, found 108 separate genetic variations increasing risk
multifactional polygenic model
suggests many individual genes carry a small risk of schizophrenia
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