SZ Flashcards

1
Q

Classification - positive symptoms

A

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.
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2
Q

Classification - negative symptoms

A
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
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3
Q

validity

A

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.

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4
Q

Reliability

A

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.

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5
Q

symptom overlap

A

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.

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6
Q

comorbidity

A

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.

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7
Q

Cultural bias

A

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
10
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.

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8
Q

Gender bias

A

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
11
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.

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9
Q

Biological explanations

A

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

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10
Q

Evaluation of genetic explanations

A

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.
14
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.

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11
Q

Dopamine hypothesis

A
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
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12
Q

Dopamine evaluation

A

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.

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13
Q

Neural correlates

A

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.

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14
Q

Evaluation of neural correlates

A

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.

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15
Q

Biological treatments - antipsychotic drugs

A

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.

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16
Q

Evaluation of drug therapy

A

Thornley et al. (2003) reviewed studies comparing the effects
of chlorpromazine to control conditions in which patients
received a placebo, so their experiences were identical except
for the presence of chlorpromazine in their medication. Data
from 13 trials with a total of 1121 participants showed that
chlorpromazine was associated with better overall functioning
and reduced symptom severity. There was also evidence from
three trials that relapse rates were also lower when
chlorpromazine was taken. Thus supporting the use of typical
antipsychotics.

In addition, there is support for the benefits of atypical
antipsychotics, particularly clozapine. Herbert Meltzer (2012)
concluded that clozapine is more effective than typical
antipsychotics and other atypical anti-psychotics, and that it is
effective in 30-50% of treatment-resistant cases where typical
antipsychotics have failed. This suggests atypical antipsychotics
could be seen as a more effective drug therapy in comparison to
typical antipsychotics as well as being a more appropriate drug
treatment for certain individuals who do not respond well to
other types of anti-psychotics.

Drug therapies can also have positive economic implications.
People who suffer from schizophrenia are often prevented from
going to work and sometimes have to be hospitalised which has
significant implications on the economy.
Therefore, if anti-psychotics lead to symptom reduction they
could enable individuals to return to work and/or could prevent
them from having to be admitted to hospital which reduces the
negative impact these factors have on the economy.

Drug therapies can also have positive economic implications.
People who suffer from schizophrenia are often prevented from
going to work and sometimes have to be hospitalised which has
significant implications on the economy.
Therefore, if anti-psychotics lead to symptom reduction they
could enable individuals to return to work and/or could prevent
them from having to be admitted to hospital which reduces the
negative impact these factors have on the economy.

17
Q

Psychological explanations of SZ

A

Family Dysfunction
Much evidence has now accumulated to suggest that like other
mental health problems schizophrenia can be a reaction to stressful
events and life circumstances. The family dysfunction explanation
identifies sources of stress within families, which can cause or
influence the development of schizophrenia.
These include:
• Maladaptive patterns of communication
• Experience of conflict
• High levels of criticism
• Controlling behaviours

Double Bind theory
This theory was proposed by Bateson et al. (1972), who believes that family
climate is important in the development of schizophrenia and emphasises the role of
communication style within a family. The developing child regularly finds
themselves trapped in situations where they fear doing the wrong thing, but receive
mixed messages about what this is, and feel unable to comment on the unfairness
of this situation or seek clarification. The words spoken can present different
meanings but also the message (words spoken) and the meta-message (way in
which the message is transmitted through tone of voice and body language) can have
different meanings. This double bind situation is also referred to a ’no-win’ situation.
When they ‘get it wrong’ (which is often) the child is punished by withdrawal of love.
Prolonged exposure to such interactions may leave an individual with an
understanding of the world as confusing and dangerous. The individual loses touch
with reality and this is reflected in schizophrenic symptoms like disorganised
thinking and speech and paranoid delusions.

High Expressed emotion
Another feature of family dysfunction considers the role of Expressed
Emotion (EE) where families may exhibit criticism, hostility
exaggerated involvement and/or control and exert a negative
influence on the sufferer. This is primarily an explanation for relapse
in recovering schizophrenics. However, it has also been suggested that
it may be a source of stress that can trigger the onset of
schizophrenia in a person who is already vulnerable due to their
genetic make-up (diathesis-stress model). Where families show high
expressed emotion including exaggerated involvement, control or criticism this has
been found to increase the likelihood of relapse.

18
Q

Family dysfunction evaluation

A

P- There is research evidence to support the role of family dysfunction in
childhood and an increased risk of developing schizophrenia in adulthood.
E Tienari et al. (2004) found that the level of schizophrenia diagnosed in
adopted children of schizophrenic mothers was 5.8% for those adopted into
healthy family environments. This increased to 36.8% for those children raised
in dysfunctional families. This supports not only the family dysfunction
explanation but also the idea that individuals with high genetic vulnerability to
schizophrenia are more affected by environmental stressors.
E Butzlaff & Hooley (1998) performed a meta-analysis of 26 studies to find
that schizophrenics returning to a family environment of high expressed
emotion experienced more than twice the average relapse rate of symptoms.
L This research provides valuable support for the role of family dysfunction in
the onset and relapse of those suffering with schizophrenia

The family dysfunction explanation highlights the importance of considering how social
and environmental factors may contribute to the onset of the condition.
The theory emphasises the role families can play in the onset and in relapse of
Schizophrenia, which other explanations fail to consider.
As a result, the theory has contributed to an interactionist approach to explaining
the cause of the disorder which adopts a more holistic approach highlighting the
complexity of the onset of symptoms and providing an explanation for high relapse
rates.
The theory and research also has useful application as it confirms that people’s
friends and families can be very important in helping their loved ones recover and has
informed methods of family therapy which has been found to be successful in
preventing relapse. People whose home atmosphere is supportive, calm and tolerant
tend to do better.
This demonstrates the theories value and the useful contributions the explanation
has made to our understanding and explanation of schizophrenia.

The support for the role of family dysfunction can be criticised due to its
correlational nature and its inability to establish the true cause of
schizophrenia.
It is very difficult to establish the direction of the relationship between
environment and behaviour. Family dysfunction including maladaptive
communication may be the result of the child’s symptomatic behaviour
rather than the cause of the illness.
Furthermore there is ample theory and evidence to suggest there is a genetic
and or neural cause to the disorder and that family dysfunction might act as a
contributing factor or trigger for the condition; not be at the root cause of
the condition.
This challenges the support for the theory of family dysfunction and its ability
to explain the cause of schizophrenia.

Adopting the family dysfunction explanation may have negative implications as
it can be interpreted as blaming the parents of sufferer’s for their child’s
development of the disorder.
The theory suggests the cause of schizophrenia is the families’ maladaptive
communication and the home environment. As a result of this explanation
parents of sufferers may then feel responsible for their child’s illness.
Furthermore, responsibility being placed on parents for their child’s illness can
cause even greater levels of stress and anxiety in the family which may in turn
then trigger off or exacerbate the illness.

19
Q

Family therapy

A

Family dysfunction is known to play a role in the relapse rates of individuals with
schizophrenia and potentially contribute to the development of the disorder as well.
Family therapy is a form of psychotherapy that involves the whole family, including
the family member with schizophrenia (if it is practical). A characteristic of
schizophrenia is that individuals are often suspicious about their treatment and thus
the benefit of involving the individual more actively in their treatment helps to
overcome this problem and reduce symptoms of paranoia.
Family therapy’s main aim is to reduce the stress levels in families to aid
recovery for schizophrenia sufferers. Therapists meet regularly with the patient and
family members, for usually between 9 months and a year.

20
Q

Evaluation of family therapy

A

There is reliable support from research into the effectiveness of using
family therapy to help reduce symptoms and prevent relapse in
sufferers of Schizophrenia.
McFarlane et al. (2003) reviewed available evidence to find that
family therapy improved family relationships resulting in symptom
reduction and reduced relapse rates, among family members, which
leads to increased well-being for patients. This suggests that family
therapy is an effective treatment, with an indication that better
family relationships play a role in symptom reduction.
Furthermore Pharoah et al. (2010) concluded that there is moderate
evidence to show that family therapy significantly reduces hospital
readmission over the course of a year and improves quality of life for
patients and their families. This further demonstrates the therapies
effectiveness in not only symptom reduction but reducing the
likelihood of relapse and improving the quality of life for individuals
suffering from the disorder.

Family therapy may be a more appropriate treatment for some
sufferers than for others. Family interventions in early psychosis have
been found to significantly reduced relapse and readmission rates. This
treatment is particularly useful for younger patients who still live at
home with their families who are also undergoing medical treatment
and require support and for patients who lack insight into their illness or
cannot speak coherently about it, as family members may be able to
assist here and act as an advocate. Family therapy however may not
always be an appropriate form of treatment for all sufferers and
families. First, attending a family program conveys a series of demands
to the sufferer and caregivers, such as transportation (which also
implies money), time, motivation, and energy. Stigma can sometimes
cause relatives to quit. Severity of symptoms may also prevent some
sufferers from participating in family therapy and lead to high dropout
rates. Therefore family therapy should be carefully considered in
relation to the appropriateness for each individual and their family.

An advantage of this therapy is the considerable economic benefits.
Family therapy is often not widely available due to its time consuming
and costly nature however the NICE review of family studies
demonstrated that when implemented it was associated with
significant cost savings when offered to service users in
combination with other treatments such as drug therapy.
The extra cost of the resource required for family therapy is offset by a
reduction in cost through preventing the need for further and long
lasting treatment.
Family therapy has been found to reduce relapse rates and therefore
prevent the cost for further care which may require e.g family
therapy may prevent the individual requiring medication or in extreme
cases hospitalisation.

21
Q

cognitive explanations

A

Attentional Bias
Bentall (1994) proposed that people with schizophrenia have deficits and biases in the
way they process information. This means there is an unusual attentional bias to stimuli
of a threatening and/or emotional nature. For example, the content of hallucinations and
the delusions regarding their origin may be understood in terms of biased information
processing. Paranoid delusions may be a result of an individual misinterpreting an
event as threatening due to an exaggerated amount of processing surrounding that
experience or specific stimuli. For example if a person was cutting a cake with a knife… the
knife is given too much focus and the individual becomes paranoid that the knife will be used
as a weapon to harm them.

Dysfunctional thought processing
Frith et al. (1992) identified two kinds of dysfunctional thought processing that could
underlie some symptoms of Schizophrenia

Metarepresentation is the cognitive ability to identify and reflect on our own
thoughts, behaviours, emotions and experiences. A lack of or dysfunction in this selfmonitoring tool would disrupt our ability to recognise our own thoughts and actions and
distinguish them from the thoughts actions being carried out by others and therefore our
own thoughts and ideas may be attributed to external sources. Frith suggested that this can
explain the experience of auditory hallucinations. Also commonly experienced delusions such
as of being controlled or persecuted can be explained by failures in metarepresentation and
inability to make judgements about peoples intentions. Thought insertion (the experience of
having thoughts projected into the mind by others) is a common delusion experienced by
suffers which can also be explained through faulty meta-representation.

Central control is the cognitive ability to suppress undesired automatic
responses while we perform deliberate actions that reflect our wishes and intentions. To
be able to fit in to society’s norms and expectations around public behaviour, central control
enables us to suppress stimulus driven behaviour and activate willed behaviour and a
dysfunction in central control may result in the display of behaviour seen as abnormal. If an
individual has impaired central control then they are unable to control their automatic
response to any stimuli. Specific language communicated to sufferers through conversation
can trigger associations and memories that they would be unable to suppress their automatic
responses to and disorganised speech and derailment of thought could present as a
result. The inability to suppress automatic thoughts and speech can even be triggered by
other thoughts explaining the experience of paranoia and delusions.
27
For example, if you lived with the symptoms of schizophrenia and you were having
a conversation about what you did at the weekend but then you suddenly had a
thought about forgetting to buy sausages, you would
say that out loud because you cannot suppress the
thought. For example, ‘I had a really nice time with
Harry last night. I must remember to buy sausages. He
came over with some beers. There is a fly on the wall by
the TV…’ etc. The inability to suppress those thoughts
leads to disorganised speech.

22
Q

Evaluation of cognitive explanations

A

There is strong support for the
idea that information is processed
differently in the mind of a
sufferer of schizophrenia.
Accounting for both positive and
negative symptoms.
E- Stirling et al. (2006)
compared 30 patients with schizophrenia with 18 non-patients on a
range of cognitive tasks including the Stroop Test, in which
participants had to name the ink colours of colour words,
suppressing the impulse to read the words in order to do this task.
Sufferers took over twice as long as the control group to name the
ink colour which would suggest that that the sufferers are therefore
presenting with central control dysfunction.
This research supports Frith’s theory that dysfunctional thought
processes including central control have a role in the cause of
schizophrenia supporting cognitive explanation for the disorder.

Despite a large body of research supporting the link between
symptoms and faulty cognition (proximal causes), the cognitive
theories do not tell us anything about the origins of those faulty
cognitions (distal causes).
It may be the case that structural brain abnormalities lead to the
differences in thought processes seen in symptoms of the disorder.
For example research has found that some schizophrenics have
enlarged ventricles in the prefrontal cortex and also that sufferers
experiencing hallucinations have lower activation levels in the
superior temporal gyrus. This would suggest that there is a neural
basis to cognitive symptoms such as derailment of thought and
language. The cognitive approach to schizophrenia therefore may be
criticised as it does provide us with understanding about the
underlying causes of dysfunctional cognitive processing and the
symptoms experienced by sufferers. This would suggest
Interactionist explanations using theories of cognitive neuroscience
that consider biological and cognitive contributions to the disorder
would be more effective in explaining onset.
The cognitive explanation alone therefore can be found to be
limited in its ability to provide a complete explanation of
schizophrenia.

Cognitive treatments have been found to be effective which would further
support the validity of the explanation.
Research findings demonstrate that Cognitive Behaviour Therapy has a
significant effect in reducing both positive and negative symptoms
of schizophrenia through brief intervention programmes (Tarrier et al.,
2005). For example CBT can help develop the functioning of meta
representation through the sufferer challenging the origin of delusions and
recognise the source of hallucinations. As such strategies adopted in the
therapy have been found to improve symptoms this suggests the
cognitive dysfunction is the cause of such symptoms
The effectiveness of Cognitive treatments demonstrates the predictive
validity of the cognitive explanation for schizophrenia

23
Q

CBT

A

CBTp (Cognitive behavioural therapy for psychosis) is a structured talking therapy
for schizophrenia. The National Institute for Health and Care excellence (NICE)
currently recommends CBTp for everyone with Psychosis. It usually takes place for
between 5-20 sessions, either in groups or an individual basis.
The basic assumption of CBTp is that people often have distorted beliefs, which
influence the feelings and behaviours in maladaptive ways, for example, someone
with schizophrenia may believe that their behaviours is being controlled by someone
or someone else. Delusions are thought to result from faulty interpretations of
events, and CBTp is used to help the patient identify and correct these faulty
interpretations.
The aim of CBTp is to help the patient make links between their cognition, emotions
and behaviours and their symptoms. By monitoring this, they are better able to
consider alternative ways of explaining why they feel and behave the way they do
which reduces distress and improves functioning (e.g. how a particularly
traumatic event has contributed to their paranoid delusions)
CBTp strategies include challenging beliefs (including origin of ‘voices’) and reality
testing (to reduce distress) via the ABCDE framework.
Cognitive restructuring via ABCDE framework.
• Initial Assessment of patient’s experiences.
• Engagement from the therapist
• ABC model
o the patient gives their explanation of the activating events (A) that
appear to cause their emotions, behaviours and beliefs (B).
o Their beliefs which are actually the cause of the consequences (C) can
then be rationalised, disputed (D) and changed.
Predictive
validiy
Positive
contribution
to effective
treatment
Cognitive treatments have been found to be effective which would further
support the validity of the explanation.
Research findings demonstrate that Cognitive Behaviour Therapy has a
significant effect in reducing both positive and negative symptoms
of schizophrenia through brief intervention programmes (Tarrier et al.,
2005). For example CBT can help develop the functioning of meta
representation through the sufferer challenging the origin of delusions and
recognise the source of hallucinations. As such strategies adopted in the
therapy have been found to improve symptoms this suggests the
cognitive dysfunction is the cause of such symptoms
The effectiveness of Cognitive treatments demonstrates the predictive
validity of the cognitive explanation for schizophrenia
29
For example through reality testing, the patient is encouraged to evaluate
the content of their delusions and voices and consider ways to test their
validity. The therapist will challenge the patient’s delusions so that they can
come to learn their beliefs are not based on reality. For example if they
believe that they are being watched or followed the individual can identify
that this is their internal belief, there is no evidence of this and control the
way they respond to this future. This can also reduce negative symptoms
like avolition as the sufferer is less like to demonstrate avoidant
behaviour.
The therapist can also use strategies such as normalisation (placing psychotic
experiences on a continuum with normal experiences (many people have
unusual experiences such as hallucinations/delusions under different
circumstances) to reduce alienation and stigma) and critical collaborative
analysis (gentle questioning to help patient understand illogical deductions and
conclusions) with the goal of helping the patient develop alternative
explanations for their previously unhealthy assumptions.

24
Q

CBT evaluation

A

There is evidence for the effectiveness of using CBT to treat
schizophrenia
For example, Tarrier (2005) reviewed 20 controlled trials of
CBT using 739 patients, showing consistent evidence that CBT
reduces persistent positive symptoms in chronic patients and
may have modest effects in speeding recovery in acutely ill
patients.
This suggest CBT is viable treatment for schizophrenia,
particularly for reducing positive symptoms such as delusions
and hallucinations.

However, Jauhar et al. (2014) performed a meta-analysis of
34 studies of CBT for schizophrenia. They concluded that CBT
has a significant but fairly small effect on positive and negative
symptoms.
A potential reason for the small effect found could be due to
CBT being investigated as a lone treatment. Tarrier et al,
(2000) suggests that CBT plus antipsychotics is effective in
treating schizophrenia and more effective than drugs or CBT
alone.
With this in mind, it may be more beneficial for CBT to be used
as part of a combination treatment for schizophrenia.

CBT may not be an appropriate therapy for all sufferers of
schizophrenia.
This is because it relies on the individual to engage with the
therapy and therapist, which may be especially difficult for
those who are experiencing paranoia, or who are too
disorientated or agitated to form trusting alliances with
practitioners.
Therefore, it is important to consider the individual sufferer
when suggesting CBT as a treatment option as it may only be
appropriate when the sufferer is in a position to engage in the
process of CBT.

25
Q

Token economy

A
Token economies are a behaviourist approach to the
management of schizophrenia, where
tokens are rewarded for demonstrations
of desired behavioural change.
The technique is mainly used with longterm hospitalised patients to enable
them to leave hospital and live relatively
independently within the community.
Similar programs have also been used in
outpatient facilities.
Token economies are particularly aimed
at changing negative symptoms,
such as low motivation, poor attention
and social withdrawal.
The technique uses operant
conditioning principles, where patients
receive reinforcements in the form of
tokens immediately after producing a
desired behaviour e.g. getting dressed in
the morning, making the bed. The
tokens can then later be exchanged for
goods or privileges e.g. sweets,
cigarettes, or a walk outside the hospital.
The reward acts as the primary
reinforcer and the token acts as the
secondary reinforcer.
26
Q

Ealuation of token economies

A

There is some evidence to support the effectiveness of token
economy within a care setting.
For example, one small study looking at token economy being used
in a psychiatric hospital favoured the token economy approach with
improvement in negative symptoms at three months.
Therefore, this partially supports token economy as a way of
managing schizophrenia and its ability to reduce symptoms.
However, overall there is limited evidence to support the
effectiveness of token economy at treating symptoms long term

A problem with token economy is that the effects may not be
maintained beyond the care setting.
This is because desirable behaviour becomes dependent on being
reinforced which means these rewards stop when individuals with
schizophrenia are no longer under the care of the provision.
This could lead to a relapse of symptoms for example, the sufferer
may lose motivation which could lead to avolition reoccurring and
may lead to high re-admittance rates.