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Schizophrenia - Coggle Diagram
Schizophrenia
Classification of Schizophrenia
Two classification tools: ICD-10 and DSM-5
DSM-5 - one positive symptom must be present for diagnosis
ICD-10 - two or more negative symptoms are sufficient.
positive symptoms
hallucinations
sensory experiences of stimuli that have either no basis in reality or are distored perceptions
can be experienced in relation to any sense
Add something to the person not usually there
delusions
irrational beliefs that have either no basis in reality or are distorted perceptions
delusions of grandeur = belief that one is somebody who is/was important or powerful
delusions of persecution = belief that one is being plotted against or being interfered with by certain organised groups
delusions of control = an over inflated sense of control over events
disorganised or catatonic behaviour
disorganised speech
negative symptoms
weaken the person’s ability to cope with everyday activities, affecting their quality of life and their ability to manage without significant outside help
speech poverty (alogia) – characterised by changes in patterns of speech
emphasis is on reduction in the amount and quality of speech in people with SZ
delay in verbal responses during communication
may produce fewer words in a given time on a task of verbal fluency
difficulty is in spontaneously producing the words
avolition – a reduction in interests or desires as well as an inability to initiate and persist in goal-directed behaviour/experiences that are available to the individual different to poor social function or disinterest examples include ‘sitting in the house and doing nothing all day’.
reliability and validity in diagnosis and classification of schizophrenia - AO1
reliability
Reliability: in relation to diagnosis and classification
level of agreement on the diagnosis by different psychiatrists across time and cultures
stability of diagnosis over time given no change in symptoms
issues
Cultural differences in diagnosis - culture bias - issues in consistency of diagnosis across cultures
Copeland
gave 134 US and 194 British psychiatrists a description of the patient
69% of US psychiatrists diagnosed SZ whereas only 2% of British ones gave the diagnoses
Highlighting poor consistency in diagnosis across cultures
Luhrmann et al
interviews 60 adults diagnosed with SZ: 20 in Ghana, India and the US
The African and Indian reported positive emotions associated with the voices they heard (playful or offering advice) but no American sufferers gave the same account
Luhrman suggests that the ‘harsh, violent voices common in the West may not be an inevitable feature of SZ’
validity
Validity: the extent to which schizophrenia is a unique syndrome with characteristics, signs and symptoms
issues
Co-morbidity due to symptom overlap – extent to which two or more conditions co-occur.
Buckley et al estimate that co-morbid depression occurs in 50% of patients with SZ
Boverman et al found that clinicians in the US equated mentally ‘healthy’ adult behaviour as mentally healthy ‘male’ behaviour. Resulting in a tendency to see women as less mentally healthy.
Symptom Overlap – Many of the symptoms of schizophrenia are found in other disorders and so it is difficult to determine whether the symptom is part of their schizophrenia or another disorder.
e.g. social withdrawal may be a symptom of depression or schizophrenia.
Ellason and Ross point out that people with dissociative identity disorder actually have more SZ symptoms that those diagnosed with SZ.
Reed said that most people who are diagnosed with SZ have sufficient symptoms of other disorders that could also receive at least one other diagnosis.
Gender bias – the accuracy of diagnostic judgements can vary across genders
Reasons include gender - biased diagnostic criteria or clinicians basing their judgements on stereotypical beliefs held about gender.
E.g. critics of the DSM criteria argue that some diagnosis categories are biased toward pathologising one gender rather than the other
reliability and validity in diagnosis and classification of schizophrenia - AO3
validity
co-morbidity
Co-morbidity is an issue in diagnosis of SZ
e.g. 1% of population develop SZ and 2-3% develop OCD
both fairly uncommon and we would expect that only a few people with SZ go onto develop OCD
:green_cross: BUT Swets et al
found that at least 12% of patients with SZ also fulfilled the diagnostic criteria for OCD and about 25% displayed significant OCD symptoms
creates an issue for diagnosis of both disorders
reduces validity
:check: Stringent criteria of DSM (high descriptive validity)
reduce the issue of misdiagnosis
e.g. needing rule out substance-abuse etc
anxiety, substance abuse, post-traumatic stress disorder and OCD all have symptoms which are shared with schizophrenia which can result in validity issues when trying to determine which disorder they belong to
Evidence - None of the symptoms of schizophrenia are exclusive to the disorder
For example, 13% of the population hear voices but only 1% have schizophrenia
This makes diagnosis difficult and potentially invalid
reliability
culture bias
Schizophrenia is more commonly diagnosed amongst African-American and African-Caribbean populations in the US and UK than other groups (Harrison et al.)
It is unclear whether this reflects greater genetic vulnerability, psychosocial factors associated with being part of a minority group or misdiagnosis due to expectation
:green_cross: However, cultural differences in behaviour and expression could be misdiagnosed as schizophrenia, therefore cultural variations should be an important consideration made by clinicians
For example, in the upper Amazon people take hallucinogenic drugs in order to have hallucinations, which are seen as having spiritual advantages (connecting with the dead)
This shows that certain cultures regard such symptoms in a positive light and so the negative connotations imposed by western culture may lack validity
Prevention > indigenous psychologies > each culture should have their own diagnosistic manual
gender bias
Powell (1988) clinicians were given the same description of a patient; when p’s described as female 20% were diagnosed, when described as male or non-gender specific the diagnosis of SZ was 56%
This shows that clinicians may have a certain expectation of gender and their diagnosis is affected by such schemas
Perhaps this is because women have a label of being less mentally stable as a baseline so many clinicans overlook such behaviour
For example, Boverman et al found that clinicians in the US equated mentally ‘healthy’ adult behaviour as mentally healthy ‘male’ behaviour. Resulting in a tendency to see women as less mentally healthy.
Rosenhan (1973) conducted a study to see if healthy sane people could be mistakenly diagnosed as having a mental illness
7 of the 8 people were diagnosed with schizophrenia and were admitted to hospitals in the US
Once admitted, all patients stopped pretending to have symptoms and asked to be released
Despite having no symptoms, they were confined to the hospital for an average of 19days
The longest stay was 52 days!
Later, hospital staff were told that a number of pseudo-patients would try to enter the hospital
This never happening, 10% of admissions were suspected to be “fakes” by at least one staff member
This study shows that clinicians and other staff may be unable to detect the presence or absence of mental illness – highlighting issues with consistent diagnosis
biological explanations - AO1
genetics
Twin studies: Gottesman - MZ twins have a 48% concordance and DZ twins have a 17% concordance rate.
Family studies: Gottesman- 2 SZ parents = concordance rate of 46%, one SZ parent = 13%
No single gene has been identified – polygenic
Weinberger found a gene variant which doubles risk of SZ
neural correlates
There is a correlation between brain structure and function and symptoms of schizophrenia
Neural correlates are measurements of the structure or function of the brain that correlate with an experience
Both positive and negative symptoms of schizophrenia have neural correlates
People with schizophrenia have abnormally large ventricles in the brain
Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste
This means that the brains of schizophrenics are lighter than normal
Torrey (2002)
The ventricles of a person with schizophrenia are on average about 15% bigger than normal
Neuroanatomy – differences in brain structure (including ventricle size, brain weight and symmetry) have been identified in people with schizophrenia. Increase in negative symptoms.
Neural correlates of positive symptoms:
Auditory hallucinations are a neural correlate with low activity in the superior temporal gyrus and anterior cingulate gyrus
Neural correlates of negative symptoms:
Avolition (lack of motivation) is a neural correlate with low activity in the ventral striatum as this area of the brain is involved in anticipation of rewards (something which motivates us)
Reduced processing in the temporal and cingulate gyri are associated with positive symptoms such as hallucinations.
dopamine hypothesis
Increase in dopamine leads to SZ
Messages from neurons that transmit dopamine fire too easily and often leading to positive symptoms.
SZ sufferers have higher number of D2 receptors on receiving neurons = more dopamine binding = more neurons firing = higher rate of communication between neurons
Davis et al - suggested that the hypothesis relates more on higher levels of dopamine in the mesolimbic pathway as the correlation with positive symptoms whilst higher levels of dopamine in the mesocortal pathway are associated with negative symptoms
biological explanation - AO3
genetics
:green_cross: inability to separate environment from genetics
e.g. if SZ purely genetic, MZ concordance would be 100% but it isn’t
must be some environmental explanation for the disorder
hard to establish cause and effect
:check: focusing on adoption studies we are able to separate the environmental effect as researchers can control studies to only focus on either upbringing or genetics
e.g. Tienari
found a higher concordance rate of SZ in adoptees with biological mothers who have been diagnosed with SZ compared to adoptees whose biological mothers have not had SZ.
:green_cross: Although, such genetic research does not consider individual differences such as gender
e.g. Gottessman and Shields
found a higher concordance rate in females than in males thus demonstrating inconsistencies in genetic research
dopamine hypothesis
:check: effectiveness of antipsychotic drugs
Carlsson and Lindqvist
found that antipsychotic drugs were reducing the effectiveness of dopamine in the brain
research into the use of recreational drugs such as amphetamine, pointed to dopamine being a candidate for SZ
Amphetamines produce psychotic symptoms and a drug called reserpine which reduced these symptoms, decreased dopamine levels
supports the idea that positive symptoms are caused by excess dopamine
:green_cross: However, it is clear that dopamine isn’t the only neurotransmitter involved in SZ
It has been found that disruptions to serotonin and glutamate play an important role in regulating levels of dopamine and in producing some of the symptoms directly
thus doesnt give a complete explanation of the cause of SZ
:green_cross: issues with cause and effect
Davis et al
pointed out that in the prefrontal cortex there are only D1 receptors so it cannot only be D2 receptors that are involved in SZ
Davis also found that dopamine activity in this area was low instead of high
He argued that reduced dopamine in the frontal parts of the brain may cause the negative symptoms (apathy and lack of emotion) which explains cognitive deficits associated with the disorder
whilst increased dopamine in other regions such as the limbic system were causing positive symptoms
aetiological treatment fallacy
neural correlates
psychological explanations - AO1
family dysfunction
schizophrenogenic mother
Fromm-Reichmann (1948)
based on patients accounts of their childhood
Psychodynamic theorists recognised a schizophrenogenic mother - typically cold, controlling and rejecting
which leads to excessive stress which triggers psychotic thinking (because of distrust
father in such families is often passive
creates a family climate characterised by tension and secrecy
Schizophrenia is due to family experiences of conflict, communication problems, criticism and control
double-blind communication
Bateson (1972)
focus on communication style within the family
Child receives mixed messages and cannot do the right thing – results in disorganised thinking and paranoia
When they do ‘get it wrong’ child is punished by withdrawal of love
Leads to an understanding of the world as confusing and dangerous
expressed emotion
Where family shows exaggerated involvement, control, criticism and hostility which increases likelihood of relapse
e.g. micro-managing
Kavanagh (1992)
causes SZ through high levels of stress
genetic vulnerability triggered by stressful events
high levels of stress triggers psychotic thinking due to disorganised thoughts
Also used as a trigger for SZ when considering the diathesis-stress model
psychological explanations - AO3
family dysfunction
:check: Tienari et al. (1994)
compared adopted individuals whose biological mothers were schizophrenic with those whose mothers were not
found that when raised in a disturbed family environment, both groups of adoptees showed greater psychopathology
this demonstrates the strength of family dysfunction as an explanation of SZ
furthermore, the use of adoptive studies helps to disentangle genetic causes from psychological ones
:green_cross: lack of evidence to support the role of the schizophrenogenic mother or double-bind explanation
both theories are based on observations of patients
Harrington argued this to be a significant limitation due to subjectivity and poor operationalisation such as ‘crazy making characteristics’
such psychodynamic theories lack scientific support and must be used to explain SZ with caution
:green_cross: social sensitivity
parent-blaming - parents have already suffered as their child has a mental illness and such explanations of SZ force the parent to bear lifelong responsibility for their care
such theories are ethically insulting to parents of those suffering SZ and are now seen as destructive rather than productive
:green_cross: methodology
unreliability of recall leading to data that may lack validity – patients report childhood experiences retrospectively
Recall may be inaccurate and distorted by the need to explain Prospective evidence is rare
:green_cross: poor cause and effect
family dysfunction may be the result of the child’s disturbing behaviour rather than the cause
impossible to show cause and effect
drug therapy - typical and atypical psychotics - AO1
typical
Dopamine antagonists work by binding to dopamine receptors in the brain and thus preventing dopamine itself from binding to the receptors
By blocking dopamine, the positive symptoms (hallucinations and delusions) of schizophrenia are contained and there is a marked cognitive and behavioural improvement
Chlorpromazine - Chlorpromazine has recently been termed the “dirty drug” owing to its widespread action in the body
In addition to targeting dopamine receptors, chlorpromazine also targets serotonin, histamine, adrenergic and acetylcholine receptors, which results in problematic side effects
Haloperidol - is another antipsychotic drug and is 50 times more potent than chlorpromazine (high potency)
This means that it can have the same effectiveness of chlorpromazine, but in smaller doses
atypical
More recent drug therapies have been developed from 1970 onwards which were developed in an attempt to maintain potency of traditional drugs but to reduce side effects
Clozapine - greater effectiveness in patients than traditional antipsychotics
It binds to serotonin and dopamine receptors, acting as a partial agonist for serotonin (increasing levels to improve depression and cognitive deficits)
Clozapine also blocks dopamine receptors in order to reduce psychotic symptoms
Risperidone – recently developed
Act on both serotonin and dopamine
As effective as Clozapine will fewer side effects
Binds to dopamine receptors more strongly than Clozapine and is effective in smaller doses
This is what causes fewer side effects
Helps with negative symptoms such as avolition