revision flashcards
(11 cards)
Introduction
-Sz is a HIGHLY COMPLEX DISEASE
-the causes are largely misunderstood.
- a range of biological and social factors can be attributed to causing the disorder such as genetics, brain disorders, childhood trauma and family environment.
-It is also likely that the role of epigenetics is highly influencial on the development of the disease.
-this combines biological and social causes, for example, biological factors such as genetic dispositions are triggered by a social stimulus, leading to the development of the disorder.
Para 2- genetics
Firstly, looking at schizophrenia from a biological perspective, there is evidence to support the role of genetics.
-** De Lisi et al 2002- ** conducted a twin study which showed that the concordence rate for sz between MZ twins is approximatley 30-40%, HOWEVER, for DZ twins it is only 10-15%.
-This highlights the strong role of genetics on the development of this disorder due to the weaker concordence rate between non-identical twins.
-However, the fact that there is still a 10-15% concordence between non identical twins suggests that external factors such as the home environment also have a part to play.
-This claim is supported by KRINGLEN 2000- who found that 60-70% of the offspring of 2 patients with SZ did not develop the disorder.
-This shows that SZ can not be solely attributed to genetics and other social factors also have a part to play.
references from para 2
DE LISI ET AL 2002- Twin studies, 30-40% concordence for MZ twins.
10-15% concordence for DZ twins.
KRINGLEN 2000- 60-70% of offspring of 2 SZ patients do not develop the disorder.
Para 3- Social, childhood trauma
There is significant evidence to support childhood trauma as having significant influence on the development of SZ.
-MORGAN AND FISHER 2007- found a significant link between early childhood trauama such as sexual, physical and emotional abuse and the later development of SZ.
-** JANSSEN ET AL 1998** This study supports the claims by morgan and fisher (2007)- a study of 4045 adults, aged between 18 and 64, found that those who had experienced any form of abuse (sexual, physical or emotional) before the age of 16, were more likely to report psychotic symptoms after a 3 year follow up compared to a control group.
-These findings follow the dose-response pattern, which in this context means the more severe the trauma, the more severe the psychotic symptoms.
-The adjusted odds ratio of these findings are 7:3, meaning the childhood trauma group are 2.33 times more likely to develop SZ than the control group, highlighting the significance of the link between childhood abuse and the development of SZ.
-However, despite the significance of these findings, one limitation of both of these studies is they are both diagnostically heterogeneous.
-For example, in the study by Jannsen et al (1998), only 7 out of 4045 patients suffered the most severe symptoms of SZ.
-therefore, the data from this study has wide confidence intervals, meaning the estimates drawn from this data may not be very precise.
-Therefore, this provides limitations of assuming the etiological importance of social factors solely from this data as the conclusions may lack external validity.
References from para 3
Morgan and Fisher 2007- significant link between those that suffered childhood trauama and the development of SZ later in life.
Jannsen et al 1998- study of 4045 adults from 18-65.
-found that those who had experienced any form of abuse by the age of 16 were more likely to report symptoms of psychosis after a 3 year follow up.
-follow dose response pattern- more severe abuse- more severe psychosis.
-ADJOR of 7.3- 2.33x more likely to develop SZ than control patients.
-limitation= diagnostically heterogenerous= wide confidence intervals= data lacks precision= may lack external validity- difficult to assume etiological importance.
Para 4- biological, brain function and structure
LAWRIE ET AL 2002- Research that could provide more empirically sound data providing support for brain structure influencing the development of SZ.
-this study involved FMRI imaging to investigate brain structure and found a link between reduced frontal-temporal functional connectivity and schizophrenia. (RFTFC)
-has been found that sz patients have significantly lower correlation coefficients between the LEFT TEMPORAL CORTEX (LTC) and the LEFT DORSOLATERAL PRE FRONTAL CORTEX (LDPFC).
-This can be linked to positive symptoms of SZ such as auditory hallucinations due to the pre-frontal cortex failing to regulate activity in the temporal cortex.
-Thus, inner thoughts can be misinterpreted as outside voices.
-this research provides clear experimental data that highlights a potential biological cause for the development of sz.
-however, these findings are still preliminary as only 3 out of 8 patients in this study were actively experiencing hallucinations during the scan.
Therefore, further research is needed on a wider population to increase the generalisability of this explanation.
references from PARA 4-
LAWRIE ET AL 2002- conducted FMRI imaging.
found a link between REDUCED FRONTAL TEMPORAL FUNCTIONAL CONNECTIVITY AND SZ.
-found that sz patients have significantly lower correlation coefficients between their left temporal cortex and the left dorsolateral prefrontal cortex
-due to the prefrontal cortex failing to regulate activity in the temporal cortex, this can influence positive symptoms of SZ such as auditory hallucinations because inner voices may get mistaken as outside noise.
-findings preliminary, only 3 out of 8 patients were actively experiencing hallucinations during scan.
PARA 5- Social, high EE
Further evidence to support social explanations for SZ come from findings about the impact of high expressed emotion family members on SZ patients.
High EE family members are described as those that are either highly critical or over involved in the patients life.
Vaughn and Leff 1976= found that patients usually respond to high EE relatives by socially withdrawing or completley isolating, which is a common negative symptom of SZ.
-Vaughn and Leff (1976) also found a link betwene high EE environments and a higher relapse rate from SZ patients.
-Although this research is significant, it is also important to consider the impact of individual differences.
-For example, in this research, over half of the patients did not relapse under the same conditions, which suggests while this research is useful, it is important to consider other factors in order to get a more complete explanation.
References from 5
VAUGH AND LEFF 1976-
-sz patients usually respond to high EE families by socially isolating or withdrawing from family members= negative symptom of SZ.
-also found a significant link between high EE environments and higher relapse rate from SZ patients.
-however, individual differences, over half of these patients didnt relapse under same conditions.
PARA 6- Epigenetic
Despite the evidence to support seperate biological and social factors, it is critical to note the importance of epigenetic factors in explaining SZ.
- A key example of the epigenetic argument is the affect of premorbid cannabis use on SZ patients.
-CASPI ET AL 2005 conducted research that showed the use of cannabis can lead to SZ due to the COMT gene.
-individuals with the VAL ALLELE of this gene are more vulnerable to developing sz compared to individuals with the MET ALLELE.
-the use of cannabis increases dopamine release in the mesolimbic pathway, which could explain positive symptoms of the disorder.
-furthermore, childhood trauma studies by Morgan and Fisher 2007 highlights the impact of the diathesis stress model on increasing the impact of genetic predispositions on sz patients.
-this study highlights how biological mechanisms can explain how environmental factors like childhood trauma can impact brain development.
-for example, trauma victims may develop dopamine sensitisation, which occurs when the brain overreacts to normal situations as a trauma-response and release more dopamine than needed- which in turn contributes to positive sz symotoms such as hallucinations.
-linking this to genetic predispositions, if an individual possesses the VAL allele of the comt gene, they may be more vulnerable to dopamine sensitisation.
-This claim is supported by Meyer and Lindenberg’s 2005 research, finding that ppts with the VAL allele show greater dopamine response to stress in imaging studies.
-thus, the interaction between genetic vulnerability and environmental triggers suggests the complexity of sz etiology. These findings support the diathesis-stress model, which illustrates how environmental stressors can activate underlying genetic risks through neurobiological mechanisms such as dopamine sensitisation.
-Acknowledging the interplay between genes and the environment is crucial for a deeper and more nuanced understanding of the disorder.
references for 6
CASPI ET AL 2005- the use of cannabis can lead to the development of sz due to the COMT gene- people with the val allele of the gene are more vulnerable to developing sz than people with the met allele.
MORGAN and FISHER 2007- childhood trauma studies show the influence that abuse can have on brain development.
-affects such as dopamine sensitisation could be a potential cause for Sz because the brain over reacts to normal situations as a trauma-response, and over releases dopamine, which contributes to positive symptoms of sz.
MEYER AND LINDENBERG 2005- ppts with the VAL allele show greater dopamine response to stress in imaging studies.
-highlights role of genetic predispositions as people with VAL allele are more vulnerable to dopamine sensitisation, therefore, more vulnerable to developing SZ in highly stressful environments.
