SZ Flashcards
Classification - positive symptoms
Hallucinations
These are unusual sensory experiences. Some are related to events in the environment whereas others bear no relationship to what the senses are picking up from the environment. For example, voices heard either talking to or commenting on
the sufferer, often criticising them.
They can be experienced in relation to any sense. The sufferer may see distorted faces or occasionally people or animals that are not there.
Delusions Also known as paranoia, delusions are irrational beliefs. These can take a range of forms. Common delusions involve being an important historical, political or religious figure, such as Jesus or Napoleon. Delusions also commonly involve being persecuted, perhaps by government or aliens or of having superpowers. Another class of delusions concerns the body. Sufferers may believe that they or part of them is under external control.
Classification - negative symptoms
Avolition This can be defined as losing the will to perform the behaviours necessary to accomplish purposeful acts, such as activities of daily life, goals, and desires. Can also be described as finding it difficult to begin or keep up with goaldirected activity i.e. actions performed in order to achieve a result. Sufferers of schizophrenia often have very reduced motivation to carry out a range of tasks and results in lowered activity levels, sometimes called ‘apathy’. Andreason (1982) identified 3 identifying signs of avolition; • Poor hygiene and grooming • Lack of persistence in work/education • Lack of energy
Speech poverty Schizophrenia is characterised by changes in patterns of speech. Speech poverty can be defined as minimal verbal communication that lacks the additional unprompted content characteristic of normal speech. The ICD-10 recognises speech poverty as a negative symptom. This is because the emphasis is on reduction in the amount and quality of speech. This is sometimes accompanied by a delay in the sufferer’s verbal responses during conversation. Characteristic of the symptom is the tendency only to speak when prompted, and to provide very limited answers. For example, a person might respond to the question, “How did you feel when your mother yelled at you?” with “bad.” When prompted to provide more
validity
Validity is the extent to which we are
measuring what we are intending to measure;
in the case of schizophrenia it concerns how
accurate the diagnosis is.
One standard way to assess validity of
diagnosis is concurrent validity (amount of
agreement between two different assessments)
Evidence investigating validity:
Cheniaux et al. (2009)
Psychiatrist 1 Psychiatrist 2
DSM 26 13
ICD 44 24
Looking at the results from the Cheniaux et al. study above we can see that
schizophrenia is much more likely to be diagnosed using ICD than DSM. This suggests
that schizophrenia is either over-diagnosed in ICD or under diagnosed in DSM. Either
way, this highlights an issue with concurrent validity. Different assessment systems
do not arrive at the same diagnosis.
Reliability
Reliability means consistency of symptom
measurement - an important measure
being inter-rater reliability; this is the
extent to which different clinicians agree
on their assessments.
In the case of diagnosis inter-rater
reliability means the extent to which two
or more mental health professionals arrive
at the same diagnosis for the same
patients.
Evidence investigating reliability:
Cheniaux et al. (2009) had two psychiatrists independently diagnose 100 patients
using both DSM and ICD criteria.
Psychiatrist 1 Psychiatrist 2
DSM 26 13
Psychiatrist 1 Psychiatrist 2
ICD 44 24
Inter-rater reliability was poor, with one psychiatrist diagnosing 26 with
schizophrenia according to DSM and 44 according to ICD, and the other diagnosing 13
according to DSM and 24 according to ICD. This evidence highlights weaknesses in
the use of classification systems to diagnose schizophrenia. This is an issue as the
external reliability is low as the psychiatrists failed to diagnose the patients
consistently. This poor reliability is an issue for the diagnosis of schizophrenia.
HOWEVER, It is important to note that Cheniaux research was carried out using the
DSM-IV and not DSM-5 and evidence generally suggests that the reliability and
validity of diagnoses has improved as classification systems have been updated.
Jakobson et al (2005) tested the reliability of the ICD-10 classification system
during the diagnosis of schizophrenia. 100 Danish patients with a history of psychosis
were assessed using operational criteria, finding a concordance between clinicians of
98 per cent, demonstrating the high inter-rater reliability of clinical diagnosis of
schizophrenia using up-to-date classifications.
Even if reliability and validity of diagnosis based on classification systems is
not perfect, they do provide clinicians with a common language, permitting
communication of research ideas and findings, which may ultimately lead to
a better understanding of the disorder. They can then predict the outcome of
the disorder and aid in the development of effective treatments.
symptom overlap
Symptom overlap is the perception that symptoms of schizophrenia are also
symptoms of other mental disorders.
Despite the claim that the classification of positive and negative symptoms would
make for more valid diagnosis of schizophrenia, many of the symptoms of the
disorder are often found with other disorders, which makes it difficult for clinicians to
decide which particular disorder someone is suffering from.
Read (2004) argued people diagnosed with schizophrenia have sufficient symptoms
of other disorders that they could also receive at least one other diagnosis.
For example, Symptom overlap especially occurs with bipolar disorder, where
negative symptoms e.g. depression and avolition are common symptoms, as well as
positive symptoms e.g. hallucinations.
This highlights issues with the validity of trying to classify schizophrenia because a
patient might be diagnosed as schizophrenic with the ICD, however, many of the
same patients would receive a diagnosis of bipolar disorder according to DSM criteria.
A consequence of this issue could mean that individuals are misdiagnosed which can
lead to years of delay in receiving relevant treatment, during which time suffering and
further degeneration of symptoms can occur for the individual.
comorbidity
Co-morbidity is the phenomenon that 2 or more
conditions occur together.
One issue which impacts the reliability and validity of a
diagnosis is comorbidity. This is when two or more
conditions occur together (e.g. Depression and Bipolar).
For example, Schizophrenia is commonly diagnosed with
other conditions. Buckley et al. (2009) concluded that
around half of patients with a diagnosis of schizophrenia
also have a diagnosis of depression (50%) or substance abuse (47%). Posttraumatic stress disorder also occurred in 29% of cases and OCD in 23%.
Therefore, comorbidity is an issue for the diagnosis and classification of
schizophrenia. Different diagnoses could be given for the same person; in one
instance they could be diagnosed with schizophrenia, diagnosed with bipolar in
another instance or they could be diagnosed with both conditions. This issue could
lead to inconsistencies in diagnoses between clinicians in relation to which disorder is
diagnosed e.g. Schizophrenia or Depression, creating problems for the reliability of
diagnosis.
Furthermore, comorbidity is also an issue for the classification of schizophrenia.
Having simultaneous disorders suggests that schizophrenia may not actually be a
separate disorder. A consequence is that it lowers the (descriptive) validity of
schizophrenia, which can make effective treatment for schizophrenia difficult to
achieve.
Cultural bias
Culture bias concerns the tendency to over-diagnose
members of other cultures as suffering from
schizophrenia.
Culture bias is another problem which affects the validity
of diagnosis. Although cross-cultural research of
schizophrenia suggest a similar prevalence across races,
research has shown that Schizophrenia, despite culturally
formulated updates to diagnostic manuals, is repeatedly
diagnosed at a higher rate in the African American population.
Research by Cochrane (1977) reported the incidence of schizophrenia in the West
Indies and Britain to be similar, at around 1%, but that people of Afro-Caribbean
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origin are 7 times more likely to be diagnosed with schizophrenia when living in
Britain. Considering the incidence in both cultures is very similar this suggests that
higher diagnosis rates are not due to a genetic vulnerability, but instead may be
due to a cultural bias
Although there is not one explanation determining why African Americans are
overrepresented. Two possible speculations are:
• Clinician bias - unconscious process stemming from stereotypes and biases
which results in misdiagnosis (Schwartz, 2014).
• Under diagnosis of other disorders (Depression/Bipolar) in African Americans
could contribute to the over-diagnosis of Schizophrenia.
Gara et al (2019) found that African American men with severe depression tend to
be misdiagnosed with schizophrenia in comparison to other racial groups. The findings
suggest that clinicians put more emphasis on psychotic than depressive symptoms in
African-Americans, which skews diagnoses toward schizophrenia even when these
patients show similar depressive and manic symptoms as white patients.
This is an issue as it suggests a lack of validity in diagnosing schizophrenia in people
of African-American origin as differences in symptom expression are overlooked or
misinterpreted by clinicians. The consequence of the misdiagnosis is that it prevents
them receiving the optimal treatment for their disorder and puts them at risk of the
side effects of medication taken for schizophrenia, such as diabetes and weight gain.
Gender bias
The tendency for diagnostic criteria to be applied differently to male and
females and for there to be differences in
the classification of the disorder.
There is some disagreement between
psychologists over the gender prevalence rate
of schizophrenia. The accepted belief was that
males and females were equally vulnerable to
the disorder. However, some argue that
clinicians (the majority of whom are men)
have misapplied diagnostic criteria to women.
Long and Powell (1988) randomly
selected 290 male and female psychiatrists to read
cases studies of patients’ behaviour and make a
judgement on these people using standardised
diagnostic criteria (e.g. DSM). When the patients were described as ‘male’ or no info about
gender was given, 56% of psychiatrists have a schizophrenia diagnosis. When patients were
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described as ‘female’, only 20% were given a diagnosis of schizophrenia. Interestingly, the
gender bias was not as evident among the female psychiatrists, suggesting that diagnosis is
influenced not only by gender of the patient but also the gender of the clinician.
There is also gender bias in the fact that when making diagnoses, clinicians often fail
to consider that males tend to suffer more negative symptoms than women
(Galderisi et al., 2012) and women typically function better than men, being more
likely to go to work and have good family relationships (Cotton et al. 2009).
This high functioning may explain why some women have not been diagnosed with
schizophrenia when men with similar symptoms might have been; their better
interpersonal functioning may bias clinicians to under-diagnose the disorder, either
because symptoms are masked altogether by good interpersonal functioning, or
because the quality of interpersonal functioning makes the case seem too mild to
warrant a diagnosis.
These misconceptions could be affecting the validity of a diagnosis as clinicians are
not considering all symptoms. This can be an issue and can lead to men and women
who experience similar symptoms being diagnosed differently
Clinicians also have tended to ignore the fact that there are different predisposing
factors between males and females, which give them different vulnerability levels at
different points of life, which may impact the validity of diagnosis. The first onset
occurs in males between 18-25 years whereas, females between 25-35 years. This
difference may be related to differences in the types of stressors both sexes
experience at different ages and to age-related variations in female menstrual cycle,
which tends to be overlooked during diagnosis.
Biological explanations
There are several biological explanations for schizophrenia, which
see the disorder as determined by physiological means. The
biological factors focused on here are genetics, abnormal
dopamine functioning and neural correlates. Although causes of
schizophrenia are not fully understood, research does indicate that
biological factors play a role in the development of the disorder.
General Genetic Link Theory
The genetic explanation sees schizophrenia as transmitted
through genes passed on to individuals from their families.
We share a different % of genetics with our relatives
depending on how genetically similar we are to them.
For example, we share 50% of our genetics with 1st degree
relatives e.g. parents, siblings (purple on graph). We share
25% with 2nd degree relatives e.g. grandparents,
aunts/uncles (pink on graph) We share 12.5% with 3rd
degree relatives e.g. cousins, great grandparents (green).
Investigations that look at the genetic similarity between family members and how it
is associated with the likelihood of developing schizophrenia are good evidence for
understanding the influence that genes play. However, we have to be careful when
using this evidence as showing a genetic link because family members tend to share
aspects of their environment as well as many of their genes (see evaluation).
Gottesman (1991) conducted a large-scale family study and found a strong
relationship between the degree of genetic similarity and shared risk of schizophrenia.
For example, 48% concordance rate in MZ twins in comparison to 17% in DZ twins.
More specific genetic explanation
It is not believed that there is a single ‘schizophrenic gene’,
but that several genes are involved, which increase an
individual’s overall vulnerability to developing schizophreniathis is a polygenic approach to schizophrenia i.e. it requires
a number of factors to work in combination. Because different
studies have identified different candidate genes it also
appears that schizophrenia is aetiologically heterogenous,
i.e. different combinations of factors can lead to the condition.
Ripke et al. (2014) carried out a huge study combining all previous data from
genome-wide studies (i.e. those looking at the whole genome as opposed to
particular genes) of schizophrenia. The genetic make-up of 37,000 patients was
compared to that of 113,000 controls; 108 separate genetic variations were
associated with increased risk of schizophrenia.
Genes associated with increased risk included those in the brain and in tissues with
an important role in immunity, as well as those coding for functioning of a number of
neurotransmitters including dopamine. This supports the overall idea of a biological
causation in the disorder
Evaluation of genetic explanations
There is overwhelming evidence for the idea that genetic factors
make some people more vulnerable to developing schizophrenia
than others.
Kety and Ingraham (1992) found that prevalence rates of
schizophrenia were 10 x higher among genetic than adoptive
relatives of schizophrenics, suggesting that genetics play a greater
role than environmental factors.
This is because the role of environment has been eliminated by
looking at individuals who grew up away from their biological
parents.
So if the individual still develops schizophrenia this must be due to
genes and not due to living with parents whose behaviour may
have had an impact on development of the disorder.
The research conducted to assess the relative contribution of
genetics to the development of schizophrenia could be criticised for
a number of reasons. For example, a crucial assumption underlying
all twin studies is that the environment of MZ twins and DZ twins is
equivalent. It’s assumed, therefore, that the greater concordance
for schizophrenia between MZ twins is a product of greater genetic
similarity rather than greater environmental similarity.
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However, as Joseph (2004) points out, it’s widely accepted that MZ
twins are treated more similarly than DZ twins, encounter more
similar environments (more likely to do things together) and
experience more ‘identity confusion’ (frequently being treated as
twins rather than 2 separate identities). As a result, Joseph argues
there is reason to believe that the differences in concordance rates
between MZ and DZ twins reflect nothing more than the
environmental differences that distinguish the two types of twin.
The issues we encounter in this research means the contribution of
genes to schizophrenia can never truly be established.
P - The nature nurture debate is highly relevant in the discussion of
the causes of schizophrenia.
E - Genetic explanations would fall under the nature side of the
debate, implying that schizophrenia is solely caused by genes
inherited from the parents and therefore fails to consider the
involvement or contribution from environmental factors e.g. family
dysfunction or abnormal cognitive processes.
E - However, this argument may be faulty as schizophrenia
development cannot be entirely genetic in basis. Demonstrated by
the evidence that concordance rates between MZ twins would be
100% if it was entirely genetic, which they are not.
L - The diathesis-stress model may be a better way to explain
the development of schizophrenia, where individuals inherit
different levels of genetic predisposition, but ultimately it is
environmental triggers that determine whether individuals go on to
develop schizophrenia.
Dopamine hypothesis
Original hypothesis High levels of the neurotransmitter dopamine (hyperdopaminergic activity) Found…. mesolimbic pathway and subcortex (central areas of the brain e.g. Broca’s area) May be associated with the…. Positive symptoms of schizophrenia e.g. auditory hallucinations as well as poverty of speech May be associated with the…. Negative symptoms. e.g. decision making Why? This could be because a person has an increased number of D2 receptors in the brain (especially in subcortical areas such as the limbic system) or it is thought that messages from neurons that transmit dopamine either fire to readily or too often leading to the change
New hypothesis Low levels of the neurotransmitter dopamine (hypodopaminergic activity) Found…. Mesocortical pathway particularly the frontal lobes (pre-frontal cortex) May be associated with the…. Negative symptoms. e.g. decision making
Dopamine evaluation
There is support from a number of sources for abnormal dopamine
functioning in schizophrenia.
Curren et al. (2004) found that when amphetamines, which
activate dopamine production (agonists), are given to non-sufferers
it can produce schizophrenia-like symptoms and make symptoms
worse in those already suffering from schizophrenia.
Equally, Kessler et al. (2003) used PET and MRI scans to
compare people with schizophrenia with non-sufferers, finding that
schizophrenics had elevated dopamine receptor levels in certain
brain areas and differences in levels of dopamine in the cortex were
also found.
Both types of experimental research suggest an important role for
dopamine in the onset in schizophrenia.
However, evidence for the dopamine hypothesis is still inconclusive
and there are issues with establishing causation.
The differences in the biochemistry of schizophrenics could just as
easily be an effect rather than a cause of the disorder.
Lloyd et al. (1984) believe that if dopamine is a causative factor,
it may be an indirect factor mediated through environmental
factors, because abnormal family circumstances can lead to high
levels of dopamine, which in turn trigger schizophrenic symptoms.
This research illustrates that we should be cautious in drawing firm
conclusions about the direct role of dopamine in the development of
schizophrenia.
P - This theory can be criticised for being biologically reductionist.
This is because it simplifies the complex development of
schizophrenia to a single biological component, in this case the
neurotransmitter dopamine.
E - It could be the case that many other neurotransmitters are also
involved in the development of the disorder. For example, much of
the attention in current research has shifted to the role of a
neurotransmitter called glutamate (Moghaddam and Javitt,
2012), as well as newer anti-psychotic drugs that also implicate
serotonin’s involvement too.
E - This reductionist approach can be problematic because a variety
of factors that may be involved in the development of the
schizophrenia are being overlooked by isolating a single biological
cause.
Neural correlates
The neural correlates explanation suggests that abnormalities within specific brain
areas may be associated with the development of schizophrenia. Research uses noninvasive scanning techniques, such as fMRI, to compare the brain functioning of
sufferers of schizophrenics and non-sufferers, to identify brain areas that may be
linked to the disorder.
Negative symptoms
Early research (Johnstone et al., 1976)
focused on schizophrenics having enlarged
ventricles (fluid-filled gaps between brain areas).
Enlarged ventricles are especially associated with
damage to central brain areas and the prefrontal cortex, which more recent scanning
studies have also linked to the disorder
Positive symptoms
Allen et al. (2007) found that positive symptoms also have neural correlates. They
scanned the brains of patients experiencing auditory hallucinations and compared
them to a control group whilst they identified pre-recorded speech as theirs or others.
Lower activation levels in the superior temporal gyrus and anterior cingulate
gyrus were found in the hallucination group, who also made more errors than the
control group. We can thus say that reduced activity in these two areas of the brain is
a neural correlate of auditory hallucination.
Evaluation of neural correlates
There are a number of neural correlates of schizophrenia symptoms,
including both positive and negative symptoms. The research helps
to identify particular brain systems that might not be working
normally.
For example, Tilo et al. (2001) used fMRI scans to investigate the
level of activity in the Wernicke brain area (an area associated with
coherent speech) when schizophrenic and non-schizophrenic patients
were asked to talk about a Rorschach ink-blot.
They found that in schizophrenic patients the severity of their though
disorder was negatively correlated with the level of activity in
Wernicke’s area.
This supports the idea of abnormal functioning in specific brain areas
being related to schizophrenic symptoms e.g. speech disorganisation.
A major limitation of the correlational research in this area of study
is that we cannot establish causation; does the unusual activity in
that region cause the symptoms of schizophrenia or does the
disorder itself cause these brain differences?
For example, it appears to be that people who have severe
symptoms of schizophrenia and who do not respond to medication
are the individuals who mainly exhibit enlarged ventricles (not all
sufferers’ do).
This could mean that the physical brain damage (enlarged ventricles)
is an effect of suffering from schizophrenia over a long period rather
than brain damage leading to schizophrenia in the first place.
The existence of neural correlates in schizophrenia therefore tell us
relatively little in itself.
Furthermore, there is scientific evidence to support this issue with
causation conducted by Ho et al. (2003)
They performed MRI scans on recent-onset schizophrenics and rescanned them 3 years later. They found evidence of brain damage in
the recent-onset patients, which worsened over time, especially in
the frontal lobes, which correlated with an increase in the severity of
their symptoms.
This suggests brain damage does increase in schizophrenics
over time and may not be the initial cause of the disorder.
Consideration also needs to be given to the possible role of a third
variable impacting on the relationships we see between brain
abnormalities and the development of schizophrenia. For example,
environmental factors such as substance abuse and stress levels may
also be having a damaging influence upon brain tissue.
More longitudinal research that assesses whether damage
progressively worsens as the disorder continues is needed.
Biological treatments - antipsychotic drugs
Typical antipsychotics- around since the
1950s
Typical antipsychotics e.g. Chlopromazine work
by acting as antagonists in the dopamine system,
in other words they reduce the action of a
neurotransmitter.
Dopamine antagonists work by blocking D2
receptors in the synapses of the brain that absorb dopamine, thus reducing positive
symptoms of the disorder, such as hallucinations and delusions.
Chlorpromazine is also an effective sedative and is often used to calm patients
when they are very anxious, this may be because it affects histamine receptors
(but it is not fully understood why it has this effect).
Typical antipsychotics tend to block all types of dopamine activity, (in other parts of
the brain as well) and this causes side effects and may be harmful.
Atypical antipsychotics-used since the 1970s
The aim of developing new antipsychotics was to improve upon the effectiveness of
drugs in suppressing symptoms and also to minimise extrapyramidal side
effects (EPSE) (drug-induced movement disorders). There are a range of atypical
antipsychotics and they work in different ways.
Atypical antipsychotics, such as Clozapine also acts on dopamine receptors
reducing positive symptoms. In addition it acts as an antagonist for serotonin
and an agonist (increasing the release of) for glutamate receptors and it is believed
that this action helps improve mood and reduce negative symptoms in patients
e.g avolition this may also improve cognitive functioning by reducing
disorganized thinking. These benefits mean that it is sometimes prescribed when a
patient is considered at high risk of suicide.