1decreased levels of dopamine in the mesocortical pathway is
shown to cause negative symptoms of sz such as apathy and lethargy
2what is PCP and what does it do
PCP is an NDMA antagonist, that blocks the receptors of glutamate, lowering glutamate levels therefore causing negative symptoms such as withdrawing from friends
3what does increased 5HT receptors in PFC do
increases serotonin levels impacting cognitive functions such as disorganised thinking
4what does increased dopamine in mesolimbic pathway do
shown to cause positive symptoms of sz such as hallucinations and delusions
5weakness of nt explanation - reductionist
only considers increased levels of dopamine to be linked to positive symptoms of sz ignoring other potential causes. some individuals can have increased levels of dopamine but not develop sz. therefore the explanation is limited, and other factors are likely involved such as social stressors
6questionnaire - weakness
self report
social desirability bias
inaccurate - invalid
7brain Structure intro
- substantial amount of research suggests brain structure in ppl with sz is different from those who do not have sz. Crow (1985) suggests this is related to the distinctions between positive and negative symptoms - concluding that positive symptoms are better explained by neurotransmission and negative symptoms are better explained by brain structure, providing explanation for why dopamine antagonist drugs were ineffective for neg symptoms.
8enlarged ventricles
-sz patients have smaller brains and enlarged ventricles in comparison to ppl without sz
- ventricles are fluid filled cavities that supply oxygen and blood to the densely packed neurons and remove waste products - enlarged ventricles are caused by the death of brain tissue surrounding the ventricles and the fluid expanding to fill the space
- the neurodevelopmental hypothesis suggests that sz is due to abnormal brain development which is latent in the individual and triggered by brain maturation of adulthood.
- research using CAT scans has shown that approximately 25% of sz patients have enlarged ventricles in the brain
9damage to the frontal lobes
- the most popular theory for the cause of negative sz symptoms is that they're the result of structural damage in the brain
- this is because while the positive symptoms are unique to sz, the negative symptoms are like other neurological disorders that result from brain damage - for example symptoms such as catatonia or the absence of a blink reflex
- brain imaging techniques indicate that sz patients show a low level of activity like those with frontal lobe damage and perform very similarly on the card sorting task
- the pfc controls behaviours such as logical thinking and decision making linking to sz symptoms such as disorganised thoughts
/ difficulty communicating and inability to make decisions
10loss of grey matter in the brain
- individuals with sz have a reduced volume of grey matter in the brain, especially in frontal and temporal lobes
- patients with the worst brain tissue loss also tend to have the worst symptoms including hallucinations, delusions, depression and psychotic thoughts
-?? need more
11foetal development
- in 1957 in Helsinki there was an epidemic of influenza virus and researchers examined sz rates in adults who were exposed to this during pregnancy - people exposed during 2nd trimester had much higher rates due to cortical development being in a critical stage of growth
- sz doesn't develop until much later due to how the brain injury interacts with normal brain development and dopamine activity peaks in adolescence
- another cause of sz is a difficult birth - Murray 1997 reviewed studies of birth difficulties and found that 7/8 studies found an association
12eval points
- supporting research
- use of brain scanning
- deterministic
- reductionist
- opposing research
- correlations data