Issues with diagnosis of SZ: Reliability AO1+AO3
An issue with the diagnosis of schizophrenia (SZ) is low reliability- specifically low inter rater reliabiliry. Inter rater reliability refers to the consistency of diagnosis between different clinicians. Diagnosing schizophrenia relies heavily on patients self reports of symptoms, which must be interpreted by psychiatrists- this process is subjective- meaning clinicians may interpret the same information differently, with one psychiatrist identifying a symptom while another may not. In addition patients may describe their experiences differently further reducing the consistency of diagnosis.
Loring and Powell also found that reliability in diagnosing schizophrenia may be reduced due to gender bias. Psychiatrists in this study were more likely to diagnose schizophrenia in male patients than female patients, despite symptoms between the two being identical. This gender bias was less evident if the psychiatrist diagnosing the patient was female. This suggests that both psychiatrist gender and patient gender can influence the diagnosis of SZ- further reducing inter rater reliability.
However one weakness of suggesting the diagnosis of schizophrenia lacks reliability is that symptoms are clearly operationalised in the diagnostic manuals. Operationalisation means the symptoms are clearly defined and psychiatrists are trained to recognise and apply these defenitions and how they are measured consistently. This can reduce subjetivity when interpreting self reports of patients and increase inter rater reliability. Therefore although diagnosis of schizophrenia involves judgement, the use of standardised criteria can improve the consistency of diagnosis.
One strength of Loring and Powell’s study is that it is extremely controlled, as symptoms between male and female patients were identical, while the only thing that was changed was the gender of the patient- meaning differences in diagnosis can be attributed to gender bias- increasing internal validity of the study.
Issues with diagnosis of SZ: Validity
The diagnosis of schizophrenia is determined through using either the DSM 5 or the ICD 11. The idea that these two diagnostic manuals have 2 conflicting ideas on how to diagnose SZ is problematic (The DSM 5 states you need to show 2 or more positive symptoms/ one positive and one negative symptom for at least a month as well as 6 months of extreme social withdrawl in order to be diagnosed with SZ- meanwhile the ICD 11 suggests that you need to show one positive and one negative symptom or 2 negative symptoms for a period of 1 month in order to be diagnosed with SZ) The reason for this is because this suggests the diagnosis of SZ has low construct validity. this is because SZ is one disorder yet defined differently by two diagnostic manuals (which were made by proffessionals in the field)- Because there is no single agreed defenition of SZ. it questions the construct validity of us diagnosing it.
In addition to this, Rosenhan’s study which investigated the validity of diagnosing SZ- in this study Rosenhan found that psychioatrists were unable to accurately distinguish between mentally healthy individuals and individuals with SZ. Confederates were admitted into the hospital after reported hearing voices, after admission they behaved normally- these confederates tried convinving staff they were normal and wanted to leave the hospital. None of the mentally healthy confederates were reported misdiagnosed. If they were discharged they were said to be discharged with SZ in reminission. This shows that psychiatrists could not distinguish between those with and those with not schizophrenia reducing the validity of diagnosing people with SZ.
One strength of rosenhans study is that it is a natural study making it a realistic study, making people less likely to experience social desireability bias.
However one weakness of this study is that it is quite old (1970s), diagnostic systems have since improved. and thus this study may not be representative of the validity of diagnostic systems we have today.
Diagnosis of schizophrenia
Schizophrenia is a mental psychotic disorder severely disrupting ones cognition and emotion.
Two classification systems are used: DSM 5 (used in america) and ICD 11 (used in Europe and other parts of the world)
In order to be diagnosed with schizophrenia:
According to the DCM-5 you need to show two or more positive symptoms such as hallucinations or delusions for a period of one month as well as extreme social withdrawl for at least six months to be diagnosed with schizophrenia.
According to the ICD 11 you need to show 1 positive and 1 negative symptom or 2 negative symptoms for at least 1 month to be diagnosed with schizophrenia.
Crow made a distinction between 2 types of schizophrenia, type 1 and type 2
Type 1= more positive symptoms
Type 2= more negative symptoms
Positive symptoms refer to a symptom which is in excess of normal functions (something which is ADDED)
-Hallucinations
-Delusions
-Disorganised speech
-Disorganised behaviour / catatonic behaviour
Negative symptoms refer to a symptom which is in a reduction of normal functions (something which is LESS)
-Alogia
-Avoliation
-Affective flattening
-Anhedonia
Alogia
Reduction is characterised by a reduction in the amount and quality of speech.
Avoliation
Apathy, finding it difficult to keep up with goal related activities
Affective flattening
A reduction in the range and intensity of emotional expression
Anhedonia
Loss of pleasure in all or most activities
Co morbidity
two or more mental disorders occur together at the same time with the same person. SZ is commonly diagnosed with other conditions and thus this can cause us to question the validity of SZ.
The high level of comorbidity associated with schizophrenia does suggest reduced construct validity, as it raises doubts about whether schizophrenia is a distinct disorder with unique symptoms. However, since comorbidity is common across many psychiatric diagnoses and may reflect limitations of classification systems rather than the disorder itself, schizophrenia cannot be dismissed as an invalid construct.
symptom overlap
Means there is a considerable overlap between the symptoms of SZ and other disorders. Making it harder to distinguish and diagnose SZ from other disorders. Thus lowers construct validity of diagnosing schizophrenia
Gender bias.
Men tend to be diagnosed more with schizophrenia than women.
Loring and Powell also found that reliability in diagnosing schizophrenia may be reduced due to gender bias. Psychiatrists in this study were more likely to diagnose schizophrenia in male patients than female patients, despite symptoms between the two being identical. This gender bias was less evident if the psychiatrist diagnosing the patient was female. This suggests that both psychiatrist gender and patient gender can influence the diagnosis of SZ- further reducing inter rater reliability.
Cultural Bias
Is SZ diagnosed more/less in one culture compared to another?
There is evidence of cultural bias in the diagnosis of schizophrenia. In some African cultures, hallucinations may be viewed as positive spiritual experiences, such as communication with ancestors, and therefore are not considered symptoms of mental illness. As a result, schizophrenia is less likely to be diagnosed in these cultures. In contrast, Western cultures interpret hallucinations as a positive symptom of schizophrenia, leading to higher diagnosis rates. This suggests that schizophrenia may be over-diagnosed in Western societies and under-diagnosed in African cultures, reducing the validity of the diagnosis
ADVANTAGES OF CLASSIFICATION AND DIAGNOSIS OF SZ
+Another advantage of the classification of schizophrenia is that it allows psychologists and psychiatrists to develop appropriate and specific treatments. Once a patient is diagnosed with schizophrenia, clinicians can select treatments that are known to be effective for this disorder, such as antipsychotic medication and psychological therapies. This means treatment can be more targeted and effective than if symptoms were treated in isolation.
+One advantage of the classification of schizophrenia is that it improves communication between professionals. It would be difficult and time-consuming to describe a wide range of symptoms to another psychologist. However, if a patient is diagnosed with schizophrenia, other psychologists have a clear and shared understanding of the type of symptoms and difficulties the patient is likely to experience. This allows professionals to communicate more quickly and effectively.
Biological explanations for SZ (intro)
biological explanations for SZ are based on two factors: the genetic basis and neural correlates (neural links to behaviour.)
Genetic basis of SZ
Genetic explanations for any behaviour (including SZ) is normally tested through family, twin and adoption studies.
FAMILY STUDIES
They compare how often a behaviour or disorder occurs in relatives of an affected person with how often it occurs in the general population.
If close relatives are more likely to show the behaviour
→ this suggests a genetic contribution
How they work (step by step)
1)Identify a person with a behaviour or disorder (the index case)
2)Study their biological relatives (parents, siblings, children)
3)Measure how common the behaviour is in those relatives
4)Compare it to people not related
One example of a family study into SZ is done by Gottesman. He found if both parents of a child were schizophrenic, the likely hood of a child having SZ was 46%. if one parent of a child was schizophrenic, the likely hood of a child having SZ was 13%. If a sibling only had SZ the likelyhood of the other sibling having SZ was 9%. This study shows the more closer (genetically) / related you are to a person the more likely you are to get SZ.
TWIN STUDIES.
measures concordance rates of a behaviour in identical and non identical twins. if concordance rates are significantly higher in identical twins it suggests a genertic basis. If concordance rates are simillar in identical twins and non identical twins- the behaviour may not be caused through a genetic basis.
Gottesman found a 48% concordance rate for identical twins and a 17% concordance rate in SZ for non identical twins. This study shows the more genetically simillar you are- the more likely you are to get SZ
CONCORDANCE RATES ARENT 100%
That being said. Because families share the same environment as well as genes, similar behaviour may be caused by factors such as parenting, social learning, or socioeconomic status rather than genetics alone.
This is were adoption studies help, because they are better able to help seperate the effects of nature vs nurture.
This is where family is seperated from others due to being adopted by new families, and the environment of the adopted child is different to its original family environment.
Tienari et al carried a adoption study where it was found that adoptees whose biological mothers had been diagnosed with SZ (6.7%) was also diagnosed with SZ compared to a control group of adoptees who’s mother did not have SZ where only 2% were diagnosed with SZ. showing a small link between genes and SZ in children whos biological mothers were schizophrenic.
Higher concordance rates are found when genetic similarity is high, but this effect is reduced when the environment changes. This shows that schizophrenia is influenced by both genetic and environmental factors.
Candidate genes which affect SZ
Candidate genes are genes that increase an individual’s risk of developing a particular disorder.
It is now agreed that SZ is polygenic- meaning that there are multiple different genes which have been found to be associated with SZ
Candidate genes such as COMT and PCM1 have been linked to schizophrenia. The COMT gene is involved in dopamine regulation in the brain, and different mutations of this gene can lead to either high or low levels of dopamine. Both dopamine imbalances have been associated with schizophrenia, with excessive dopamine activity linked to positive symptoms and reduced dopamine activity linked to negative symptoms. In addition, the PCM1 gene is involved in brain development, and mutations in this gene may result in abnormal brain structure, such as enlarged ventricles, which have been linked to schizophrenia.
Ripke et al found 108 seperate genetic variations were associated with an increased risk of SZ- in particular genes variations associated with neurotransmitter (particularly dopamine) imbalances in the brain
The genetic basis of SZ AO3
+one strength of this approach is that there is a plethora of research to support the idea that SZ has a genetic basis such as Ripke, Tienari + Gottesman. This shows there is validity in the genetic basis for SZ.
– one weakness of this approach is that it is biologically reductionist → suggesting SZ is only caused due to faulty genes is unable to explain why other factors e.g. a schizophrenogenic mother can contribute to SZ.
-A limitation of the genetic explanation is that adoption studies tend to show lower concordance rates for schizophrenia than twin studies. Concordance rates for SZ in identical twins are also have never been found to be 100% in a study. This suggests that genes alone are insufficient to cause schizophrenia, as individuals who share genes but are raised in different environments are less likely to both develop the disorder. Therefore, environmental factors must also play a role, reducing the explanatory power of a purely genetic account.
+ Furthermore, genetic studies use objective, quantitative measurements such as concordance rates, which improves reliability and scientific credibility.
neural correlates for sz
neural correlates
→ Neural structures and their links to behaviour.
Enlarged ventricles
These are fluid-filled spaces in the brain. Research has shown that enlarged ventricles are associated with schizophrenia. This may be because enlarged ventricles are linked to negative symptoms of schizophrenia and cognitive impairments.
Dopamine activity in subcortical brain regions
Research has shown that high dopamine activity in subcortical areas is linked to the positive symptoms of schizophrenia.
Dopamine activity in the prefrontal cortex
Research has shown that low dopamine activity in the prefrontal cortex is linked to the negative symptoms of schizophrenia.
Superior temporal gyrus
The superior temporal gyrus is an area involved in auditory processing. Research has shown increased neural activation in the superior temporal gyrus during auditory hallucinations. It is suggested that internally generated voices may be misinterpreted as external sounds.
The hippocampus is involved in memory formation and learning. Research has shown that people with schizophrenia often have a reduced hippocampal volume, which is associated with memory impairments and difficulties forming new memories, commonly seen in schizophrenia.
Grey matter contains neuronal cell bodies and is important for information processing. Research has shown that people with schizophrenia have lower levels of grey matter, particularly in areas such as the prefrontal cortex and temporal lobes, which is associated with cognitive deficits and negative symptoms of schizophrenia.
neural correlates for sz ao3
+One strength of neural correlates is that they are objective, as they are based on brain scanning techniques such as fMRI and PET scans rather than self-report. This means that researchers can directly observe structural and functional differences in the brains of people with schizophrenia, giving the research high face validity. Additionally, identifying specific neural correlates may help inform and tailor drug treatments that target particular brain areas or neurotransmitter systems, which could help to reduce symptoms of schizophrenia.
+Another strength of neural correlates is the extensive research support. A large number of brain imaging studies have reliably shown differences in brain structure and function between individuals with schizophrenia and mentally healthy controls. The consistency of these findings across different samples and scanning techniques increases the reliability of the evidence and supports the view that neural correlates are strongly associated with schizophrenia, making this a convincing explanation for the disorder.
-A major weakness of neural correlates is that the evidence is correlational, meaning that cause and effect cannot be established. It is unclear whether brain abnormalities cause schizophrenia or whether schizophrenia leads to changes in brain structure and function. Furthermore, the association between neural correlates and schizophrenia may be explained by a third variable, such as medication use or environmental factors, which could independently affect brain structure. This limits the extent to which neural correlates can be considered a causal explanation for schizophrenia.
-Another weakness of neural correlates is that brain abnormalities are not present in all individuals with schizophrenia. There is considerable individual differences in neural correlates, meaning that one person with schizophrenia may show enlarged ventricles, while another may instead show reduced grey matter or altered activity in different brain regions. This lack of universality suggests that neural correlates cannot fully explain schizophrenia for all patients, limiting their explanatory power.
the dopamine hypothesis
dopamine is a neurotransmitter which has alot of roles it is associated with- some examples include its role associates with movement, attention, learning and emotional responses- it also enables us not only to see rewards, but to take action to achieve them.
the dopamine hypothesis claims that an excess of the neurotransmitter dopamine in certain areas of the brain are associated with positive symptoms of sz, such as hallucinations and delusions.
Dopamine activity in subcortical brain regions
Research has shown that high dopamine activity (hyperdopaminergia) in subcortical areas is linked to the positive symptoms of schizophrenia.
Dopamine activity in the prefrontal cortex
Research has shown that low dopamine activity (hypodopaminiger) in the prefrontal cortex is linked to the negative symptoms of schizophrenia.
the dopamine hypothesis ao3
+A strength of the dopamine hypothesis is that it has led to effective drug treatments for schizophrenia. Antipsychotic drugs such as Clozapine reduce dopamine activity in the brain by blocking dopamine receptors, which helps to reduce positive symptoms like hallucinations. The success of these treatments supports the dopamine hypothesis and shows it has practical applications, increasing its validity.
-A major weakness of the dopamine hypothesis is that the evidence is correlational, meaning that cause and effect cannot be established. It is unclear whether dopamine imbalance cause schizophrenia or whether schizophrenia leads to dopamine imbalance. Furthermore, the association between dopamine imbalance and schizophrenia may be explained by a third variable, such as medication use or environmental factors, which could independently affect brain structure. This limits the extent to which the dopamine hypothesis can be considered a causal explanation for schizophrenia.
-one weakness of this hypothesis is that it is biologically reductionist → suggesting SZ is only caused due to dopamine imbalance is unable to explain why other factors e.g. a schizophrenogenic mother can contribute to SZ.
psychological explanations for sz (intro)
2 main psychological explanationd: family disfunction and cognitive explanations
family disfunction as an explanation for sz
psychologists have attempted to link sz to childhood and adult experiences of living in a dysfunctional family
family dysfunction can be explained in 3 ways:
1)schizophrenogenic mother
2)double bind theory
3)expressed emotion
the schizophrenogenic mother
Fromm-Reichmann proposed this explanatipn for sz based of what was heared from many patients. They spoke about a particular type of mother known as the schizophrenogenic (schizophrenia causing) mother. Characteristics of this type of mother is rejecting and cold and controlling. The mother also creates a family atmosphere full of secrecy and tension. this results in the child having a lack of trust in relationships which then further develops into delusions which ultimately develops into sz. in these scenarios the father tends to be passive and doesnt really get involved in the childs upbringing.
double bind theory
focuses on how family communication affects a patient with sz . suggested that the child recieves lots of contadictory messages from their parents, eg mother says come give me a hug and when child gives a hug she stiffens and pushes child off. the child is unable to seek clarification for these contradictory messages or confront the unfairness of it. the child may also be punished for responding to an already ambigous situation wrongly by parents withdrawl from love. the child will feel confused and see the world as a dangerous place and gain paranoid delusions which can contribute to the development of sz.
