SZ developmental factors Flashcards
SZ Developmental
Genes DISC 1
Genetic mutations can arise causing developmental changes
one such Gene involving this is the disc1 Gene
It seems to regulate neuro development and neurotransmition
Therefore a mutation of this Gene impairs the functioning of neurodevelopment leading to name the positive skits for symptoms such as hallucinations
In the CNS it’s develops gabber expression and dopamine and serotonin receptors
It is linked with grey matter levels and the PFC and working memory and cognitive aging
It has an impact on dopamine levels and with dopamine D2 receptor binding potential
The presence of this Gene allows for D2 dopamine receptors to develop if this Gene is mutated there may be more or sensitive D2 receptors which has been linked with the cause of hyperdopaminergia (And + symptoms of SZ if in messolimbic pathway)
Haploinsufficiency is when there is half the normal levels of disc1 protein from conception
this could have a negative effect on neurodevelopment as it may affect the creation of dopamine receptors
which may lead to schizophrenic symptoms later on once the area has fully developed possibly in adollecence
The these genetic deficiencies or mutations occur in the pre-birth and could lead to irregular development of dopamine receptors leading to schizophrenia
If simply it is not a case of a mutation but a the Gene causes this to occur in itself then it will likely be inherited from parents
SZ Developmental
brain abnormalities
Virus damage or malnutrition in the brain in fetal development from the pre-birth may lead to brain abnormalities that could lead to the development of schizophrenia
Loss of Grey brain matter and the replacement with ventricles especially in the PFC and amygdala which become fully developed in late Adolescents which cohenlines with the onset of schizophrenia symptoms may also be a cause
This is in line with the malnutrition of the PFC as it seems the damaged to the brain isn’t apparent until the PFC matures in Adolescents
SZ Developmental
NT
Hyperdopaminergia in the messolimbic pathway
and hypodopaminegia in the mesocortical pathway
Responsible for the positive and negative symptoms of schizophrenia respectively
High levels of glutamate results in Low levels of dopamine and vice versa
Glutamate failure in the cerebral cortex results in the negative symptoms of schizophrenia
whereas glutamate failure in the basal ganglia results in the positive symptoms of schizophrenia
Considering dopamine activity Peaks in adolescence which coincides with the onset of schizophrenia symptoms it can be assumed that abnormally high levels of dopamine caused by development become even higher in adolescence which is what causes the initial onset of schizophrenia
SZ Developmental
NT and Brain structure
1 potential explanation of how these two phenomenon may work together
relies on the concept of super sensitivity
there’s a pathway rich in glutamate neurons that run from the prefrontal cortex to the area that regulates the release of dopamine in the messolimbic pathway
in the structural explanation these areas of the brain are said to be smaller in volume due to the increase of the ventricles
and therefore this part of the brain is underdeveloped this would affect how it deals with neurotransmission
The low levels of glutamate activity in the frontal lobe would presumably lead to lower basal release of dopamine in the messolimbic pathway
Basal release is the spontaneous release of neurotransmitters which is constantly occurring in a nervous system independently in any environmental stimuli
this low level of Base release would in turn cause dopamine receptors in the messolimbic pathway to become super sensitive
so that they would overreact to the environmental stimuli giving them the positive symptoms which are well explained in the neurotransmission explanation
SZ Developmental
Wright et al 1999 + grey brain matter
Wright et al 1999
Fines that schizophrenic patients can significantly less grey matter than a control group
this may be due to localize neurodevelopment analysis
which may be linked to a disorder of cortical lamination during neurodevelopment
Therefore this provides evidence linking grey matter to the neurodevelopmental hypothesis of schizophrenia
SZ Developmental
Susser et al 1996 + famine
susser et al 1996 +
Schizophrenic prevalence and three famine in the west Netherlands
Participants were born between 1944-6 and they were either exposed or not exposed to the Dutch hunger winter in 1944-5 in early gestation
Find an increase risk of schizophrenia in both men and women who exposed to the famine in early gestation
This is evidence for support for malnutrition as a cause of brain damage during neuro development that can lead to schizophrenia
SZ Developmental
Walker savoie and Davis 1994
Results support the assumption that childhood neuromotor dysfunction proceeds the onset of schizophrenia
It’s agrees the findings of fish at al 1992 that dysfunction is most apparent in the developmental period in the first two months since birth
This therefore supports the idea that’s neuromotor dysfunction eventually becomes schizophrenia
and neuromotive dysfunction originates from developmental period in the first two years from birth
therefore supporting the developmental hypothesis of schizophrenia
SZ Developmental
alt social
Research explanation suggests that actually schizophrenia’s caused by the environment of their four main ways to increase the risk of schizophrenia:
social adversity such as living standards and the economy,
urbanicity such as light and the pace of life
social isolation which may worse and prognosis which is the symptom intensity
and immigration / minority status which makes you self perceive yourself as the out group and further enhance the social isolation
Therefore by not allowing for this in the hypothesis of developmental issues in schizophrenia it becomes reductionist
as it doesn’t allow for the explanation to consider all possible that could be affecting the development of schizophrenia
Therefore the diathesis stress model should be used to consider both social and biological developmental Factors in schizophrenia development
SZ Developmental
+
O’Callaghan et al (1991)
O’Callaghan et al (1991)
• suggested that the influence of an influence outbreak in 1957
found that amongst children who were in The 4-6 months of gestation during the Outbreak there was a high incidence of SZ
Supports the developmental explanation of schizophrenia as the virus impact on the development which led to the development of schizophrenia
SZ Developmental
O’Callaghan SL 1991 weakness
It cannot be certain that the mother had influencer back in 1957 during the gestation of the child
as they rely on self-report data which may have memory inaccuracies and therefore could be another factor that’s causing the high instance of schizophrenia during this outbreak
which makes O’Callaghan poor evidence to support the developmental hypothesis of schizophrenia
SZ Developmental
Strauss 1982 supports social
Strauss 1982
Finds that when studying countries such as the USA there’s a high instance of SZ among low socioeconomic groups compared to the middle +upper class
which supports the idea that socioeconomic class in this case being lower part of the social adversity factor
affects the prevalence of schizophrenia and thus its risk
therefore this link supports the social explanation of schizophrenia and is therefore criticism of the developmental one
