Schizophrenia Flashcards
Mr Quemby’s friend
Was pregnant and didn’t quit smoking - have to slowly wean off drugs, can’t go cold turkey if heavily addicted
schizophrenia
def
A severe mental illness where contact with reality and insight are impaired – an example of psychosis
schizophrenia misconsepti0on
Schizophrenia is not, as many people think, a split
personality
The term comes from two Greek words: ‘schizo’, meaning
‘split’, and ‘phrena’ meaning ‘mind’
The ‘split’ in schizophrenia occurs between a person’s
thought processes and reality.
Who does it affect?
- It affects 1% of the population
Men are more likely to be diagnosed than women
The onset is typically in late adolescence and early
adulthood
Commonly diagnosed in cities and the working class
The disorder severely affects daily life, which can
lead to homelessness and hospitalisation
Classification of a mental disorder
the process of organising symptoms into
categories based on which symptoms cluster together in sufferers
Classification of
schizophrenia
Schizophrenia doesn’t have a single defining
characteristic – it is a cluster of symptoms that seem to
be unrelated
We group them as positive symptoms and negative
symptoms
two main systems used to classify mental
disorders:
International Classification of Disease edition 10 – (ICD-10)
Diagnostic and Statistical Manual edition 5 – (DSM-5)
classification systems
Differences in classification
- E.g. the DSM-5 system says that at least one ‘positive’ symptom must be present for diagnosis
- Whereas the ICD-10 says that two or more ‘negative’ symptoms are sufficient for a diagnosis
The ICD-10 used to recognise subtypes of schizophrenia
- E.g. Paranoid schizophrenia (more positive symptoms)
- Old versions of the DSM recognised subtypes but these were dropped in DSM-5 due to inconsistent symptoms
postive syptoms
Atypical symptoms experienced in addition to normal experiences
Postive symptom 1
Hallucinations – sensory experiences of stimuli that either have no basis in reality or are distorted perceptions of things that are there
E.g. hearing voices, seeing animals/people that aren’t there
Postive sysmptom 2
Delusions – involve beliefs that have no basis in reality
Also known as paranoia or irrational beliefs
- Can involve conspiracy (government, politics, religion)
- Can involve being an important political or religious figure
- Can involve the body – beliefs of being controlled externally
Negative sysmpoms
Atypical experiences that represent the loss of a usual experience and
abilities
Negative symptom example 1
Avolition – involves the loss of motivation to carry out tasks and results in lowered activity levels
Sometimes called apathy, sufferers have difficulty starting or keeping at a goal-orientated task
Andreason (1982) identified 3 signs of avolition – poor
hygiene and grooming, lack of persistence at work/school,
lack of energy
Negative symptoms example 2
Speech poverty – involves reduced frequency and quality of speech – often accompanied with delay in responding to conversation
Speech disorganisation (more of a focus these days) is classified differently (as a positive symptom)
Reliability of classification and diagnosis
Diagnosis of schizophrenia for an individual needs to be consistent among clinicians (inter-rater reliability) and consistent over time (test-retest reliability)
Before the DSM-5, diagnosis had low reliability
Osório et al. (2019) found that when diagnosing a group of 180 individuals, inter-rater reliability was +.97 and test-retest reliability was +.92 between two clinicians
This shows that there is now high reliability in diagnosis
- schitzophenic symptoms might be interpreted differently based on cultural norms leading to variability in diagnoses across different populations
cognitive explanation def
Explanations that focus on mental processes (thinking, language, attention)
to explain behaviour
cognitive explanation
dysfunctional thought processing
Information processing that doesn’t accurately represent reality and produces undesirable consequences
cognitive explanation
impared cognition
Impaired cognition can explain symptoms of schizophrenia
E.g. reduced thought processing in the ventral striatum is associated with negative symptoms. Reduced processing in the temporal gyri (crease that separates the temporal lobe) is
associated with positive symptoms.
cognitive explanations
There are two main types of dysfunctional thought processing
Metarepresentation dysfunction
Central control dysfunction
Metarepresentation dysfunction
Metarepresentation is one’s cognitive ability to reflect on thoughts and behaviours allowing us to :
have insight on our personal goals and intentions
interpret other people’s actions
Schizophrenic patients are likely to have dysfunctional meta representation which disrupts their ability to recognise that their thoughts and actions are their own rather than someone else’s.
— This is used to explain delusions and hearing voices as schizophrenic patients fail to recognise that these processes are projected in their mind by themselves and NOT by someone else.
cognitive explanation
centeral control dysfunction
- The ability to suppress automatic responses whilst doing a deliberate task.
- Schizophrenics have trouble with dysfunctional central control which can explain speech poverty and disorganised thoughts.
- Eg: delay in speech may be caused by interfering thoughts and automatic thoughts which are triggered by other parts of the conversation.
def
CBT
A method for treating mental disorders based on both cognitive and
behavioural techniques
CBT
- Aims to identify and correct irrational and maladaptive thoughts (e.g. delusions are due to faulty interpretations)
- Patients can be seen alone or in groups – and between 5-20 sessions – NICE recommend at least 16
-CBT helps patients make links between their thoughts, feelings, behaviours and symptoms
- Enables alternative thought processing, distress reduction
and improved functioning - It does not necessary reduce symptoms, it reduces distress if
patients understand them better (normalisation)
Evaluation – research support CBT
CBT
Jauhar et al. (2014) did a review of 34 studies that used CBT to
treat schizophrenic patients – they concluded that CBT has
significant effects on both positive and negative symptoms
Furthermore, Pontillo et al. (2016) found CBT to reduce both
frequency and severity of symptoms in patients
This validates the effectiveness of CBT
It is also recommended by NICE – – all patients with schizophrenia
should be offered CBT
However, the research has been criticised as many patients
treated with CBT are usually treated with antipsychotics at the
same time - which one is actually helping
whats NICE
The National Institute of Health and Care Excellence
cognitive treatment
Effectiveness is stage dependent
Research has shown that CBT is only effective when made
available at certain stages of the treatment
Addington and Addington (2005) – claim that
self-reflection isn’t appropriate during the initial phase of schizophrenia - after theyv’e been stabalised
Only once symptoms are stabilized with antipsychotic medication can patients benefit from normalising their experience with CBT
Furthermore, research has consistently shown that CBT is more effective on patients that have had longer
experience with their symptoms
weakess?
cognotive treatment
Lack of avalibility
Despite being recommended by NICE, only around 1 in 10 patients in the UK get access to CBT for schizophrenia – the average is found to be even lower in some parts of the country
Haddock et al. (2013) found that out of 187 randomly selected patients form North West England, only 6.9% had been offered CBT for schizophrenia
Colling et al. (2017) found that 34.6% of patients received at least one session and 26.4% at least two sessions of CBT
Issue?
However, Freeman et al. (2013) found that from those who are offered CBT, a significant number refuse or fail to turn up
def
Family therapy
psychological therapy carried out on some/all family members to improve communication and reduce stress in the family environment
Family therapy
Prioritised when there are persistent symptoms or a high risk of relapse
Offered for between 3-12 months with at least 10 sessions
Sessions aim to reduce EE, educate family members about schizophrenia and provide ways to support the patient
Family members are to listen to one another and discuss solutions together
Burbach’s model of practice: Phase 1: sharing info, 2: identifying resources, 3: create a safe space for expression, 4: identify unhealthy communication, 5: stress management skills, 6: relapse prevention planning, 7: future maintenance
family therapy
research support
McFarlane (2016) carried out a review on family therapy
and concluded that it is one of the most consistent
treatments for schizophrenia
For example, relapse rates typically reduce by 50-60%
He also concluded that family therapy is highly effective
when mental health is initially declining (early stages)
Furthermore, NICE also recommends family therapy –
they advise that all patients should be offered it once
diagnosed with schizophrenia
family therapy
Economic benefits
The NICE review of family therapy studies found that there
is significant reduction in costs for standard care of
patients
This is because of lower relapse rates 🡪 less hospitalisation
The cost of taking additional care of relapsed patients is
much more expensive than family therapy
Additionally, family therapy reduces relapse rates even
after the intervention is completed – meaning even more
money is being saved
family therapies
Positive impact on family members
Family therapy is seen to have a positive impact on family
members, as well as the patients themselves
It can reduce negative impact schizophrenia has on family
members and strengthens ability to support the patient
Lobban et al. (2013)
meta analysis on 50 family therapy studies that included
intervention to support relatives
60% of studies reported a significant positive impact on relatives
for at least one outcome category (problem-solving skills,
relationship quality)
Long term, keep using the resourses and not relasping
However, methodological quality of those studies was generally
poor, making it difficult to distinguish between
effective/ineffective interventions
Token economies def
A form of behaviour modification where desirable behaviours are
encouraged via reinforcement
token economy
A management technique based on operant conditioning
Patients are given tokens whenever they engage in a target behaviour 🡪 tokens exchanged 🡪 rewards and privileges
Ayllon and Azrin (1968) – female hospitalised patients
1. Neutral tokens given after functional tasks are completed (making bed, finishing meals)
2. tokens are then exchanged for a variety of rewards (e.g. TV, visits from family, etc.)
3. frequent exchange = frequent desirable behaviours
No longer used as ‘treatment’ for ethical reasons
Rationale
To correct bad habits developed due to prolonged
hospitalisation
Helps modify personal care (hygiene), condition-related
behaviours (e.g. avolition) and social behaviour
(interaction)
Such modifications:
Improve quality of life in hospital settings
Normalise behaviours that will help patients adapt to
demands in the outside world
How and why does token ecoony work
- Based on operant conditioning – tokens are secondary reinforcers that allow for access to primary reinforcers (TV, snacks, visits, etc.)
- Tokens that can be exchanged for a range of rewards are also known as generalised reinforcers (like money)
- Tokens are awarded for target behaviours decided on a case by case basis
- They work best when the reward is given directly after the token is received – immediate reward is more effective than delayed reward
rresearch support
Token economy
- Glowacki et al. (2016) identified and reviewed 7 high quality studies published between 1999 and 2013 that tested the effectiveness of token economies on patients hospitalised with chronic mental disorders
- All studies showed a reduction in negative symptoms and a reduction in unwanted behaviours
- Counter - is this research as strong as it looks?
- Reviews containing fairly small numbers of studies indicate that there is a file drawer problem
This means that studies that show insignificant or mixed (unreliable) results are ‘filed away’
This reduces the number of studies available for review, leaving a bias selection of ‘high quality’ studies to draw conclusions from
Although there is research that demonstrates the effectiveness of token economies, it may not be as credible as it seems
token economy
Ethical issues
- Despite token economies no longer being in use as a ‘treatment’ for schizophrenia, ‘behaviour management’ in this way still raises ethical concerns (ristricts individual free will, failire to protect psychological harm)
Token economies give the professionals with authority the power to control their patients’ behaviour
This can become problematic when target behaviours are not decided sensibly – e.g. staff can modify behaviours to fit their norms instead of their patients’ norms
Problem?
It can become easy to restrict patients of their rights to choose their norms and behaviours, as well as restricting pleasure altogether
E.g. a patient may enjoy to appear scruffy or sleep in late but staff can ‘modify’ those behaviours with reward
Patients may lose out on basic pleasures like watching tv or speaking to family if they do not comply to the chosen system
The benefits of token economies may be outweighed by the ethical concerns
The interactionist approach def
A way of explaining behaviour using a range of factors, such as biological and psychological factors
interactionalist approach
Most importantly, an interactionist approach focuses on
how different factors combine to explain behaviour, rather
than simply adding/including various factors together
(the ways in which factors combine cannot be predicted by
each factor separately)
The interactionist approach to explaining schizophrenia
acknowledges the role of biological, psychological and
social factors to explain its development
(e.g. genetic vulnerability, stress and poor familial
communication respectively)
The diathesis-stress model def
An interactionist approach to explain behaviour that suggests that a
vulnerability and a stress-trigger are needed to develop a condition
The diathesis-stress model
For schizophrenia, diathesis can include one or more factors
that make someone vulnerable to developing it
(historically this just included genetics, but now we understand
trauma to be a diathesis)
But the onset of symptoms of schizophrenia is triggered by
stress
The diathesis-stress model explanation can be split into two –
the original model (Meehl’s model) and the modern model
Meehl’s model (original) 1962
The original diathesis-stress model suggested that the
diathesis for schizophrenia is purely genetic (schizogene)
This led to the development of a biologically based
‘schizotypic’ personality – characterised by sensitivity to
stress
Furthermore, an individual without the schizogene would
never develop schizophrenia, regardless of any stressful
events
But an individual that possesses the schizogene could
develop schizophrenia if they experience chronic stress
during childhood – in particular, if they have a
schizophrenogenic mother
Modern understanding of the
diathesis-stress model
Diathesis – we now know there is no one ‘schizogene’
Different variations of candidate genes only increase vulnerability to schizophrenia by a fraction
Early psychological trauma is also considered a diathesis now (rather than an environmental stressor)
Read et al.’s neurodevelopmental model (2001) suggests
that severe early trauma (e.g. child abuse) can alter many
aspects of brain development
For example, it can cause overactivity in the
hypothalamic-pituitary-adrenal (HPA) (too much adrenaline) system, making the
individual more vulnerable to later stress
Modern understanding of stress
In Meehl’s original model, stress was mainly psychological
and related to parenting
Although still important, ‘stress’ in this model is now
considered to include anything that risks triggering
schizophrenia
Example: Cannabis
Cannabis has been found to increase risk of developing
schizophrenia by up to 7 times (particularly THC-rich doses)
Research indicates that cannabis interferes with the dopamine
system
Many people that smoke cannabis do not develop
schizophrenia, suggesting that most do not have the
vulnerability for triggering it in the first place
interactionalist
Research support - Tienari
Hospital records were reviewed from 19,000 Finnish adoptees
with biological mothers that had a diagnosis of schizophrenia
(high genetic risk)
They were compared with a control group of adoptees with no
family history of schizophrenia (low genetic risk)
They also assessed the parenting style of the adoptive parents
They found that a parenting style involving high levels of
criticism and hostility and low levels of empathy were strongly
associated with the development of schizophrenia in the
children
But this relationship was only found to be the case for children in the
high genetic risk group – so?
This suggests that a combination of genetic vulnerability and
family stress may cause schizophrenia – validating the
interactionist approach
iteractionalist
simplistic models
The original model has been criticised for being too simplistic –
there is no one schizogene or stressor that causes schizophrenia
There are multiple genes found to increase vulnerability to
schizophrenia (they have very little effect on their own)
Stress can also come in many forms – stress can be biological as
well as psychological
Houston et al. (2008) – found that childhood sexual trauma was a
major vulnerability factor, whereas cannabis use was a major
trigger for developing schizophrenia
Shows that diathesis is not strictly biological and stressors are not
strictly psychological
Problem?
This invalidates the original model and supports newer versions
But still suggests more research and understanding is needed to
effectively apply the diathesis-stress model to schizophrenia
interactionalist approach
effective treatment
There has been support for the effectiveness of combined
treatment
Biological and psychological treatments combined are more
effective than biological treatment alone
Tarrier et al. (2004) – randomly allocated 315 patients to
either medication+CBT, medication+counselling or
medication only (control)
They found that both combined groups showed lower
symptom levels than the control group
Strength?
However, they found no differences in hospital readmissions
interactionalist
however… treatment -causation fallacy
Researchers have critiqued the popular assumption that
‘effective treatment = valid explanation’
This is known as the ‘treatment-causation fallacy’
Successful treatment does not justify it’s matching explanation
E.g. drinking alcohol reduces shyness – does this make lack of
alcohol the cause of shyness?
No. But the same logic is applied explanations and treatments
for disorders like schizophrenia
Just because combined treatment is the most effective
doesn’t necessarily mean combined (interactionist)
explanation is the most valid
of classification
Validity
Just because clinicians are consistent in diagnosis (while using
the same system) doesn’t mean they are accurately
diagnosing schizophrenia
As the ICD-10 and DSM-5 use different criteria to diagnose,
the same patient may not get a consistent diagnosis across
clinicians
Cheniaux et al. (2009) had two psychiatrists diagnose 100
patients independently using DSM-5 and ICD-10 criteria
They found that one psychiatrist diagnosed 70/100 patients (26
using DSM and 44 using ICD) and the other diagnosed only
37/100 patients (13 using DSM and 24 using ICD)
This also means 68 were diagnosed using the ICD and only 39 were
diagnosed using the DSM in total
There is low criterion validity – at least one of the systems is wrong when diagnosing schizophrenia – this means patients may be misdiagnosed depending on the system their clinician uses.
Co-morbidity
‘morbidity’ refers to how common a medical condition is
Co-morbidity refers to the idea that two or more conditions occur together - Schizophrenia is often diagnosed with other conditions
A review by Buckley et al. (2009) found that half of patients diagnosed with schizophrenia are also diagnosed with depression (50%) or substance abuse (47%)
PTSD also occurred in 29% and OCD in 23%
- Validity issues with diagnosis – there may be issues telling the difference between different conditions – misdiagnosis
Validity issues with classification – if the symptoms overlap with other conditions, schizophrenia may not be a distinct condition
People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
Similarly, symptom overlap
Even if an individual does not have two conditions (co-morbidity), the symptoms of schizophrenia still overlap with symptoms of other disorders
For example, symptoms of bipolar disorder also include delusions (a positive symptom) and avolition (a negative symptom)
This again means we may be classifying and diagnosing schizophrenia incorrectly for patients – validity issue
Not only may we misdiagnose patients, it also implies that schizophrenia may not be a distinct disorder
e.g. an individual may just have a rare variation of bipolar disorder
People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
Symptom overlap (extra/alternative research)
Ellason and Ross (1995)
found that people with dissociative identity disorder (DID) have more symptoms of schizophrenia that people diagnosed with schizophrenia
Symptom overlap (extra/alternative research)
Read (2004)
most people diagnosed with schizophrenia have enough sufficient symptoms to be diagnosed with at least one other disorder
Gender bias in diagnosis
Men are diagnosed with schizophrenia more often than women
This could be due to genetic factors, but it is more likely due to social factors
Women are more likely to have close relationships and social support – leading to better functioning in society
Cotton et al. (2009) – women generally function better and at a higher level than men (better interpersonal skills, etc.)
Higher functioning may be why women’s symptoms are easily overlooked, leading to under-diagnosis
Schizophrenia is not properly understood in women – samples are more likely to be men – treatments will therefore be tailored for men – leading to more bias in the medical field
Biological explanations
Genetics
Neural correlates
Genetics
genes consisting of DNA that contain instructions for physical features of an organism, which can also influence psychological features (e.g. disorders)
the genetic basis
Family studies – Gottesman (1991)
- He found that someone with an aunt with schizophrenia had a 2% chance of developing it
- A 9% chance if their sibling had it
- And a 48% chance if they had a MZ twin that had it
- This clearly shows a relationship between genes and schizophrenia
Candidate genes
- Schizophrenia is suggested to be polygenic – no one specific gene has been found to explain schizophrenia
- The genes involved are most likely to be related to dopamine
- Ripke et al. (2014) did a review of genome-wide studies on schizophrenia (studies that look at one’s full genetic makeup)
- After comparing 37,000 people with schizophrenia to 113,000 controls, he found 108 different genetic variations that are associated with increased risk of schizophrenia
- This suggests that schizophrenia is aetiologically heterogeneous –
Different combinations of genes (and other factors) can lead to schizophrenia
genetic explanation
Research support
Twin studies – Hilker et al. (2018) found a concordance rate of 33% for MZ twins that shared schizophrenia compared to 7% of DZ twins that shared it
The difference is best explained by the amount of genes shared (100% vs 50%)
Adoption studies – Tienari et al. (2004) studied adopted children from Finland and found that of those that had schizophrenia, many of them had a biological mother that also had schizophrenia
This shows that even without being raised by a schizophrenic parent, you can still develop the disorder (best explained by genes)
Genetic explanation
Environmental factors
- Although research shows that genetics have a role in the development of schizophrenia, there is also a lot of evidence for environmental factors being involved
- Examples include birth complications, childhood trauma and smoking cannabis during adolescence
- Morkved et al. (2017) found that 67% of people with schizophrenia and other related psychotic disorders reported at least one experience of childhood trauma compared to 38% of a control group with non-psychotic disorders
- incomplete explanation, as ignores enviromental factors,
Neural correlates def
Patterns of structure or activity in the brain that occurs in conjunction with (correlates with) an experience
neural correlates
Dopamine
a neurotransmitter found to be important in several brain systems related to schizophrenia
It is excitatory and linked to pleasure
Very low levels are associated with Parkinson’s disease
Because there is no hard evidence to pinpoint exactly what the role of dopamine is in the development of the disorder, hypotheses have been generated to explain the link
The dopamine hypothesis (the original)
Research showed that drugs used to treat schizophrenia
(antipsychotics which reduce dopamine levels) also cause
symptoms similar to those that people with Parkinson’s
disease experience – PD is also associated with low dopamine
levels…
Therefore, from this it was hypothesised that schizophrenia
may be caused by high levels of dopamine in subcortical areas
of the brain (hyperdopaminergia – hyper=high)
For example, speech poverty and auditory hallucinations may be
caused by an excess of dopamine receptors between the
subcortex and Broca’s area
The updated dopamine hypothesis
Davis et al. (1991) hypothesised that low levels of dopamine
in the cortex may cause schizophrenia (cortical
hypodopaminergia – hypo=low)
Low levels of dopamine in the pre-frontal cortex can explain
negative symptoms associated with cognitive functioning
(However, this does not oppose the original hypothesis)
It is suggested the low levels of dopamine in the cortex may
cause high levels in the subcortex
Howes et al. (2017) suggests that this caused by genetic
variations and early experiences of stress
These factors may make people more sensitive to cortical
hypodopaminergia and eventually 🡪 subcortical
hyperdopaminergia
biological explanation
research support
Curran et al. (2004) found that when amphetamines are given
to patients with schizophrenia, they increase dopamine levels
and worsen symptoms of the disorder
Amphetamines also induce similar symptoms in people without
schizophrenia!
Tauscher et al. (2014) also found that antipsychotics decrease
dopamine levels and symptoms of schizophrenia
Both studies suggest that dopamine levels (in particular high
levels) are associated with schizophrenia
Furthermore, some candidate genes identified also affect
dopamine production and dopamine receptors
Amphetamines are stimulant drugs. They make the messages between your brain and body move faster. As a result, you are more alert and physically active. Some people use amphetamines to help them stay awake on the job or to study for a test. Others use them to boost their performance in sports
Role of other transmitters?
Research has also found glutamate (another excitatory neurotransmitter) to be associated with schizophrenia
McCutcheon et al. (2020) found increased levels of glutamate in several brain regions of schizophrenic patients across brain-imaging and post-mortem studies
Furthermore, some of the candidate genes identified affect the production of glutamate as well
- neural explanation, brain activity can be investigated to find schitzophernia, practical value as can make it easier to diagnose
Two psychological explanations
Family dysfunction
Cognitive explanations
Family dysfunction
Abnormal patterns of communication within the family, such as cold parenting, poor communication and high expressed emotion
Such aspects of the family dynamic are suggested to be risk factors for both the development and maintenance of schizophrenia
3 key factors to family dysfunction
- Schizophrenogenic mother (cold parenting)
- Double-bind theory (poor communication)
- Expressed emotion
The schizophenogenic mother
Fromm-Reichmann (1948)
Noted that many of her patients spoke about a particular type of parent – she named the ‘schizophenogenic’ mother
This means ‘schizophrenia-causing’
This is a mother that is cold, rejecting and controlling
She creates a family dynamic characterised by tension and secrecy
This is suggested to cause distrust which later develops into paranoid delusions, and eventually, schizophrenia
This is a psychodynamic explanation – how childhood experiences can affect you psychologically
family dysfunction
Double-bind theory
Bateson et al. (1972)
Children receive contradictory messages from parents
E.g. verbal and non-verbal contrasts
Children then fear doing the wrong thing, even when they don’t understand what the wrong thing is (due to mixed messages)
They feel unable to protest about the unfairness of a situation, nor do they feel able to seek clarity on it
They learn that doing the wrong thing leads to a withdrawal of love, causing them to understand the world to be confusing and dangerous
Bateson argues that this is what leads to paranoid delusions and disorganised thinking patterns
Bateson et al. clarified that this was not a generalisable sole cause for schizophrenia, just a risk factor
EE includes elements of verbal criticism, sometimes accompanied by violence, hostility including anger and rejection and over-involvement
Expressed emotion (EE)
EE refers to the level of emotion expressed towards the schizophrenic patient by family members/carers
A high level of negative expressed emotion is suggested to be a significant source of stress and can trigger the onset of the disorder (in those already vulnerable), as well as relapse
EE contains the following elements
- Verbal criticism and sometimes violence towards the patient
- Hostility, anger and rejection
- Emotional over-involvement in the patient’s life
family dysfunction
Research support
There is a range of research to suggest that issues within the family dynamic play a role in schizophrenia
Insecure attachment – Read et al. (2005) found that adults with schizophrenia are disproportionately likely to have had insecure resistant or disorganised attachment as a child
Abuse – Read also found that 69% of women and 59% of men have a history of physical and/or sexual abuse
Trauma – Morkved et al. (2017) found that 67% of patients with a psychotic disorder reported at least one childhood trauma
All of the research suggests that family dysfunction can make you more vulnerable to developing schizophrenia
family dysfunction
Weak explanations
Although research shows a link between childhood family-based stress and schizophrenia (generally) there is little evidence to support specific explanations such as schizophrenogenic mother and double-bind theory
Research on these explanations come from clinical observation of individual patients and informal assessments of the mother’s personalities
Furthermore, research that does exist contradicts the explanations
Liem (1974) found no differences in parental communications between schizophrenic and non-schizophrenic patients
Hall and Levin’s (1980) meta analysis found no differences in contradictory statements made in families with and without a schizophrenic patient
Low explanatory power – FD may not be good enough to explain the link between childhood experiences and schizophrenia
Low validity – contradictory suggests FD is an incorrect explanation
Cognitive explanations def
Explanations that focus on mental processes (thinking, language, attention) to explain behaviour
Psychological explanation
Research support
cognitive
Stirling et al. (2006) gave the stroop test to 30 schizophrenic patients and 30 controls
(the task was to say the colour of the font of the word rather than reading the word)
The schizophrenic patients took twice as long as the control group to complete the task correctly – so?
This suggests that those with schizophrenia struggled to supress the tendency to read the words instead of the colours, showing dysfunctional central control
This validates the role of central control dysfunction in schizophrenia
Psychological explanati0on
Only a proximal explanation
cognitive
A proximal explanation only goes as far to explain present circumstances as opposed to explaining how the circumstances developed in the first place (distal explanations)
Biological and family dysfunction explanations can explain how symptoms of schizophrenia develop initially
But cognitive explanations offer no insight on how dysfunctional thought processing develop initially
Furthermore, cognitive explanations are difficult to link with the others – genetic variations nor childhood trauma can explain how dysfunctional thought processing develops
Low explanatory power- only a partial explanation
drug treatments spec
Drug therapy – antipsychotics
Typical antipsychotics
Atypical antipsychotics
Drug therapy - antipsychotics def
Drugs used to reduce the intensity of symptoms of a psychotic disorder (usually
positive ones)
when was drug therapy introduced
Introduced in the 1950s – no treatment before this
antipsychotics use
- ecommended for initial treatment
- then used in combination with psychological therapies later on
-some use them in the short term without symptoms returning
- but most need to take them for life
Two types of antipsychotics:
typical antipsychotics
aytpical antipsychotics
typical antipsychotics
used primarily for positive symptoms
Atypical antipsychotics
also combat positive symptoms, but has
some beneficial effects on negative symptoms as well
Typical antipsychotics history
The first generation of antipsychotic drugs, having been used since the 1950s. They
work as dopamine antagonists. E.g. Chlorpromazine
Typical atypsychotics
Antagonists are blockers – they block the activity of neurotransmitters
Typical antipsychotics are dopamine antagonists which bind to D2 receptors on neurons, blocking their action (blocking transmission of dopamine)
At first dopamine levels build up (because transmission is blocked) but over time, less and less dopamine is produced
elimination of hallucinations and delusions happens after a few days
Other positive symptoms may take longer (several weeks)
The effectiveness eventually led to the original dopamine hypothesis
Can be taken via tablet , syrup or injection – up to 1000mg a day (avg 400-800mg for most patients)
typical antipsycotics
Sedation effects
Typical antipsychotics like chlorpromazine also work as a sedative (although not properly understood why)
They can be given to patients with other conditions to calm them
E.g. patients that are very anxious may be given them when they are first admitted to hospital
They are most likely given as syrup for these purposes as they are absorbed faster than tablets
Kapur et al. (2000) – estimated 60-75% of D2 receptors must be blocked in the mesolimbic pathway
But this means D2 receptors in other areas are blocked too
This can lead to undesirable/possibly harmful side effects
harmful effects of typical antipsychotics
Kapur et al. (2000) – estimated 60-75% of D2 receptors must be blocked in the mesolimbic pathway
But this means D2 receptors in other areas are blocked too
This can lead to undesirable/possibly harmful side effects
drug therapy
Clozapine
atypical
First trialled in the 1970s – despite some patients later dying from a blood condition after taking them (agranulocytosis), they were remarketed in the 80s as the treatment to use if other treatments failed – and were found to be more effective than typical antipsychotics
(today regular blood tests are taken and dosages are kept low)
- Clozapine binds to D2 receptors, as well as serotonin and glutamate receptors
- This consequently improves mood and reduces anxiety and depression
- As well as suicidal thoughts (which can occur in 30-50% of patients)
No injections as side effects can be fatal
Risperidone
atypical
Developed in the 90s – develop to reduce side effects that come with Clozapine
It binds to more dopamine receptors than Clozapine so smaller doses are needed – and it can be taken in any form
Some evidence suggests it has fewer side effects than the other antipsychotics
difference between typical and atypical
typical proved effect on positive sysmptoms
atypiclal claimed effect on cognitive imparmnet and negative symptoms
Atypical antipsychotics context
Drugs that developed after typical antipsychotics (1970s). They typically target both dopamine and serotonin. E.g. Clozapine and Risperidone
AKA second-generation antipsychotics
Three main differences between typical and atypical
atypical :
less extrapyramidal side effects, more beneficial for negative symptoms, better for treatment-resistant patients
atypical antipsycotics examples
Clozapine and Risperidone
drug therapy a03
Research support
Lots of research compares relapse rates for antipsychotics and placebos
Leucht et al. (2012)
did a meta-analysis of 65 studies from 1959-2011, involving ~6000 stabilised patients
They were stabilised with either typical/atypical drugs
Some were taken off their medication and given a placebo instead
Within 12 months, 64% given the placebo relapsed, compared to 27% who stayed on the antipsychotic drug
- suggests the drug is effective, high practical use
drug therapy AO3
Side effects
Typical antipsychotics are more likely to produce side effects than atypical ones
- Including dizziness, sleeplessness, weight gain, stiff jaw and itchy skin
More long-term effects include tardive dyskinesia which Involves involuntary facial movements (blinking, grimacing)
This is caused by dopamine supersensitivity
The most serious side effect is neuroleptic malignant syndrome (NMS) which causes delirium, coma and sometimes death (up to 2% risk), suggested to be caused by the blocking of dopamine to the hypothalamus
- may not be worth the risk,
Typical antipsychotics have been criticised for its overall cost-benefit analysis
This is because the drugs have led to many harmful side-effects, deaths and psychosocial consequences
E.g. Chari et al. 2002 – covered a large out-of-court settlement for a patient suffering from tardive dyskinesia in the US
Based on the Human Rights Act 1988, the patient was compensated for the side effects experienced – as it states ‘no one shall be subjected to inhuman or degrading treatment or punishment’
Further suggesting that drug therapy may do more harm than good in real life (for patients, professionals and economy)
Drug therapy A03
Poor clarity
- It is not fully understood why antipsychotic drugs work to reduce symptoms
- The use of drugs is heavily tied with the original dopamine hypothesis (that schizophrenia is caused by subcortical hyperdopamineria) but we now know that the original dopamine hypothesis is not the full explanation – the updated hypothesis suggests that low levels of dopamine in the cortex may also cause the condition
- Therefore, drugs that ultimately decrease dopamine levels overall should not work – so why do they?
- low explanatroy power
Token economy used to go together with the other
therapies but due to much critique…
it is now considered a
method of management as opposed to treatment
Discuss issues associated with the classification and /
or diagnosis of schizophrenia. (16)
AO1 – identify the issues
Introduce the classification
systems (ICD-10 and DSM-5)
Explain how diagnosis differs
depending on the system used
Start introducing the issues
(it makes sense to start with reliability
and validity issues if none are
specifically named in the question)
AO3 – discuss the issues
(what implications do they have for
patients, the economy and the
medical field?)
Discuss why having low
reliability/validity is a problem
when diagnosing/classifying
schizophrenia
Discuss the issues of co-morbidity,
symptom overlap, gender bias and
culture bias
The issues with classification/ diagnosis
Reliability
Validity
Symptom overlap
Co-morbidity
Gender bias
Culture bias
The reliability and validity of diagnosis and classification AO3
validity
Just because clinicians are consistent in diagnosis (while using the same system) doesn’t mean they are accurately diagnosing schizophrenia
As the ICD-10 and DSM-5 use different criteria to diagnose, the same patient may not get a consistent diagnosis across clinicians
Cheniaux et al. (2009) had two psychiatrists diagnose 100 patients independently using DSM-5 and ICD-10 criteria
They found that one psychiatrist diagnosed 70/100 patients (26 using DSM and 44 using ICD) and the other diagnosed only 37/100 patients (13 using DSM and 24 using ICD)
This also means 68 were diagnosed using the ICD and only 39 were diagnosed using the DSM in total
There is low criterion validity – at least one of the systems is wrong when diagnosing schizophrenia – this means patients may be misdiagnosed depending on the system their clinician uses.
The reliability and validity of diagnosis and classification AO3
Co-morbidity
‘morbidity’ refers to how common a medical condition is
Co-morbidity refers to the idea that two or more conditions occur together - Schizophrenia is often diagnosed with other conditions
A review by Buckley et al. (2009) found that half of patients diagnosed with schizophrenia are also diagnosed with depression (50%) or substance abuse (47%)
PTSD also occurred in 29% and OCD in 23%
Why is this a problem?
Validity issues with diagnosis – there may be issues telling the difference between different conditions – misdiagnosis
Validity issues with classification – if the symptoms overlap with other conditions, schizophrenia may not be a distinct condition
People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
The reliability and validity of diagnosis and classification
symptoms overlap
Even if an individual does not have two conditions (co-morbidity), the symptoms of schizophrenia still overlap with symptoms of other disorders
For example, symptoms of bipolar disorder also include delusions (a positive symptom) and avolition (a negative symptom)
This again means we may be classifying and diagnosing schizophrenia incorrectly for patients – validity issue
Not only may we misdiagnose patients, it also implies that schizophrenia may not be a distinct disorder
e.g. an individual may just have a rare variation of bipolar disorder
People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
Ellason and Ross (1995) found that people with dissociative identity disorder (DID) have more symptoms of schizophrenia that people diagnosed with schizophrenia
Read (2004) – most people diagnosed with schizophrenia have enough sufficient symptoms to be diagnosed with at least one other disorder
The reliability and validity of diagnosis and classification
Cultural bias in diagnosis
hearing voices is a symptom that may be interpreted differently in different countries
Black British people are up to 10 times more likely to be diagnosed with Schizophrenia than white British people, even though rates of schizophrenia in African and Caribbean countries are not particularly high
Escobar (2012) suggested that (overwhelmingly white) psychiatrists may tend to over-interpret symptoms and distrust the honesty of ethnic minorities during diagnosis
Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient
69% of the US psychiatrists diagnosed the patient, but only 2% of the British ones did!
This suggests that there are huge cultural differences in how doctors diagnose patients
The reliability and validity of diagnosis and classification AO3
Gender bias in diagnosis
Men are diagnosed with schizophrenia more often than women
This could be due to genetic factors, but it is more likely due to social factors
Women are more likely to have close relationships and social support – leading to better functioning in society
Cotton et al. (2009) – women generally function better and at a higher level than men (better interpersonal skills, etc.)
Higher functioning may be why women’s symptoms are easily overlooked, leading to under-diagnosis
Schizophrenia is not properly understood in women – samples are more likely to be men – treatments will therefore be tailored for men – leading to more bias in the medical field
aetiologically heterogeneous
Different combinations of genes (and other factors) can lead to schizophrenia
token economies def
A form of behaviour modification where desirable behaviours are encouraged via reinforcement
A management technique based on operant conditioning
Patients are given tokens whenever they engage in a target behaviour 🡪 tokens exchanged 🡪 rewards and privileges
token economy
Ayllon and Azrin (1968) – female hospitalised patients
- Neutral tokens given after functional tasks are completed (making bed, finishing meals)
- tokens are then exchanged for a variety of rewards (e.g. TV, visits from family, etc.)
- frequent exchange = frequent desirable behaviours
No longer used as ‘treatment’ for ethical reasons
why do token economies exist
To correct bad habits developed due to prolonged hospitalisation
Helps modify personal care (hygiene), condition-related behaviours (e.g. avolition) and social behaviour (interaction)
token economies
examples of modicfation
- Improve quality of life in hospital settings
-Normalise behaviours that will help patients adapt to demands in the outside world
token economies
How and why does it work?
- Based on operant conditioning – tokens are secondary reinforcers that allow for access to primary reinforcers (TV, snacks, visits, etc.)
- Tokens that can be exchanged for a range of rewards are also known as generalised reinforcers (like money)
- Tokens are awarded for target behaviours decided on a case by case basis
- They work best when the reward is given directly after the token is received – immediate reward is more effective than delayed reward
token economies
research support
