schizophrenia P3 Flashcards
definition of schizophrenia
severe mental disorder where contact with reality and insight are impaired
definitions of positive symptoms
atypical symptoms experienced in addition to normal experiences
e.g. Hallucinations
definition of negative symptoms
atypical experiences that represent a loss of usual experience
e.g. loss of clear thinking
prevalence of schizophrenia
serious mental disorder affecting 1% of population
more common in males, city-dwellers and lower socio-economic groups
diagnosis
diagnosis & classification = interlinked
to diagnose we must be able to distinguish one disorder from another
classification = identify symptoms that go together to form a disorder
diagnosis == identify symptoms and use classification systems to identify the disorder
DSM-5 & ICD-10 differences
- DMS-5 = one positive symptom must be present
- ICD-10 = two or more negative symptoms are sufficient for diagnosis
Hallucinations - positive symptoms
unusual sensory experiences that have no basis in reality or distorted perceptions of real things
experienced in relation to any sense
e.g. hearing voices
Delusions - positive symptoms
beliefs that have no basis in reality
make person behave in ways which make sense to them but unusual to others
e.g. believing that they are napoleon
Speech poverty - negative symptoms
a reduction in the amount & quality of speech
can be a delay in verbal responses during conversation
but speech disorganisation = positive symptom
Avolition - negative symptoms
a severe loss of motivation to carry out everyday tasks e.g. personal care
Resulting in lowered activity levels & unwillingness to carry out goal-directed behaviours
S of diagnosis of schizophrenia is good reliability
a reliable diagnosis between clinicians and between occasions.
-> Osorio 2019, reported excellent reliability for schizophrenia diagnosis as the inter-rater agreement was +0.97 and test retest reliability of +0.92
This means that diagnosis of schizophrenia is consistently applied
A limit of diagnosis is low validity
criterion validity involves seeing whether different procedures used to assess the same individuals arrive at the same diagnosis
->Cheniaux 2009, 2 psychiatrists independently assess the same 100 clients, 68 were diagnosed with ICD & 39 with DSM
This means that schizophrenia is either over or under diagnosed, suggesting that criterion validity is low.
Another Limit of diagnosis is co-morbidity with other conditions
if conditions co-occur then they might be a single condition -> Sz diagnosed w other conditions.
Buckley 2009 concluded that Sz is co-morbid with depression (50%), substance abuse (47%) & OCD (23%)
This suggests that Sz may not exist as a distinct condition
a limit of diagnosis is culture bias
some symptoms e.g. hearing voices are accepted in some cultures like Afro-Caribbean societies ‘ hear voices from ancestors’ -> Afro-Caribbean British men are 10X more likely to receive a diagnosis as white men -> due to overinterpretation of symptoms by UK psychiatrists.
This means that Afro-Caribbean men living in the UK appear to be discriminated against by a culturally-biased diagnostic system .
Family studies -genetic basis of Sz
a strong relationship between the degree of genetic similarity and shared risk of schizophrenia.
Gottesman 1991
Gottesman 1991
large scale study
for fraternal twins there is a 17% likelihood that if one is diagnosed, the other may develop it
but, identical twins it is 48% & for siblings it is 9%
-can share environment but indicates support for genetic view
Candidate genes - genetic b
Schizophrenia is polygenic - requires several genes to develop
aetiologically heterogeneous - the risk of developing Sz is affected by a combination of genes
Ripke 2014
combined previous data from genome-wide studies
found 108 separate genes associated with slightly ^ risk of schizophrenia
Mutation - genetic basis
Sz can have a genetic origin in absence of family history due to mutation in parental DNA
-evidence comes from correlation between paternal age & risk of schizophrenia
Brown 2002
evidence for sperm mutation being correlated with the risk of sz
increasing from 0.7% under 25 fathers to over 2% fathers over 50
A strength for the genetic basis is the strong evidence base
family studies e.g. Gottesman show risk increases with genetic similarity. Hilker 2018 Twin study found 33% in MZ twins & 7% for DZ twins.
Tienari 2014, adoption studies show that biological children of parents w SZ are at greater risk even if they in adoptive family.
-> This shows that some people are more vulnerable to sz because of their genes
A limitation for the genetic basis is evidence for environmental risk factors
Biological risk factors include both complications and smoking THC rich cannabis in teenage years ->Psychological risk factors include childhood trauma e.g. 67% w Sz reported at least one childhood trauma.
->this means genes alone can’t provide a complete explanation for schizophrenia
Neural correlates
measurements of the structure or function of the brain that occur in conjunction with an experience
Dopamine- neural correlates
believed to be involved
it’s featured in the functioning of brain systems related to symptoms of schizophrenia
Original Dopamine hypothesis
high dopamine activity in subcortex -> hallucinations & speech poverty
can explain positive symptoms
‘Hyperdopaminergic’
Hyperdopaminergia
excessive levels of dopamine in the subcortex and broca’s area
Hypodopaminergia
low levels of dopamine in prefrontal cortex
Updated dopamine hypothesis
low levels of Dopamine in the prefrontal cortex can explain negative symptoms
explains origin of abnormal dopamine - genetic variations & experiences of stress can ppl more sensitive to cortical hyperdopaminergia -> subcortical hypodopaminergia
Strength for neural correlates is the support for dopamine in the symptoms of schizophrenia
Amphetamines mimic symptoms (Curran 2004) Antipsychotic drugs reduce intensity of symptoms (Tauscher 2014)
Candidate genes act on the production of Dopamine or dopamine receptors
-> this strongly suggests that dopamine is involved in the symptoms of schizophrenia
A limitation for neural correlates is evidence for a central role for glutamate
Post-mortem and scanning studies found raised glutamate in people with schizophrenia (McCutcheon 2020)
several candidate genes for Sz are believed to be involved in glutamate production or processing
-> this means that a strong case can be made for a role for other neurotransmitters in schizophrenia.
What is family dysfunction?
A psychological explanation for Sz composed of: Schizophrenogenic Double bind theory Expressed emotion
Schizophrenogenic mothers
-Fromm- Reichmann 1948
-psychodynamic approach
‘Schizophrenia causing’
mothers are cold, rejecting and controlling -> family climate of tension & secrecy -> child is distrusting -> develop paranoid delusions -> Schizophrenia
Double bind theory
conflicting family communication
Bateson 1972
a child who feels trapped in situations where they fear doing the wrong thing -> receive conflicting messages about what counts as wrong -> can’t express their feelings of unfairness -> if get it wrong parents withdraw love -> learn world is confusing & dangerous ->disorganised thinking & delusions
Expressed emotion
criticism and hostility -> relapse
the high level of emotion expressed including; Verbal criticism, Hostility, Emotional over-involvement in their life
-> stress in Sz sufferer -> relapse
A strength for family dysfunction is the evidence links to schizophrenia
Read 2005, reported that adults with schizophrenia are disproportionately likely to have insecure-attachment. Also 69% of women and 59% of men with Sz have experienced physical or sexual abuse.
-> This strongly suggests that family dysfunction does make people more vulnerable to Sz.
A limit for family dysfunction is the poor evidence base for any explanation.
there is almost no evidence to support the importance of traditional family-based theories e.g. Double bind, Schizophrenogenic mother.
Both theories are based on clinical observation of patients and informal assessment of the personality of the mothers.
-> This means that family explanation have not been able to explain the link between childhood trauma and Sz
Cognitive explanations
dysfunctional thought processing
Metarepresentation
Dysfunction in the central control
What is dysfunctional thought processing?
lower levels of information processing in some areas suggest that cognition is impaired.
E.g. Reduced processing in the ventral stratum is associated with negative symptoms
what is Metarepresentation?
the cognitive ability to reflect on thoughts and behaviour (Frith 1992)
disruption can lead to auditory hallucinations and though insertion delusions
What does central control dysfunction cause?
-speech poverty
ppl w Sz experience derailment of thoughts as each word triggers automatic associations that they can’t suppress
What is the role of central control?
to suppress automatic responses while performing deliberate actions
A strength to cognitive explanations - evidence for dysfunctional thought processing
Stirling 2006, compared performance on a range of cognitive tasks in ppl w & w/o Sz
- > found that ppl with Sz took over twice as long to name the font-colours
- > this supports the view that the cognitive processes of ppl w Sz are impaired
A Limitation to cog is only proximal origins of symptoms are explained
proximal explanations explain what is happening now to produce symptoms -> cog exp are weaker as distal explanations (what causes cognitive problems), possible distal exp are genetic and family dysfunction.
-» this means that cognitive theories alone only provide partial explanations
Evaluation extra for cog exp - is it psychological or biological?
The cog approach provides excellent explanation for symptoms of Sz suggesting that Sz is a psychological condition
- > abnormal cognition is partly genetic in origin & the result of abnormal brain development
- > > this means that although it has psychological symptoms, Sz is best seen as a biological condition.
Biological therapy for Sz includes:
- Typical antipsychotics
- Atypical antipsychotics
What are typical antipsychotics?
dopamine antagonists reduce positive symptoms Chlorpromazine 1950s aim to reduce the action of dopamine Associate with the dopamine hypothesis
How do typical antipsychotics work?
block dopamine receptors in synapses
reduce action of dopamine
initially dopamine levels rise then fall as production is decreased
normalises neurotransmission in key areas of the brain -> reduces the symptoms of hallucinations
what are the side effects of chlorpromazine?
-affects histamine receptors -> sedation effect
used to calm anxious patients when they are first admitted to hospital
What are Atypical antipsychotics?
1970s
suited for treatment-resistant patients
based on revised dopamine hypothesis
aim of AA was to be more effective in supressing the symptoms of psychosis & to minimise the side effects of the drugs used
Name two Atypical antipsychotics:
clozapine
Risperidone
how do atypical antipsychotics work?
bind to dopamine (D2), serotonin receptors but also dissociates
to reduce action of dopamine
reduce positive symptoms and some negative symptoms
How does Clozapine work?
binds of dopamine & serotonin receptors
reduces depression & anxiety, improves cognitive functioning
-improves mood, up to 50% of ppl w Sz attempt suicide
How does risperidone work?
developed due to fatalities of clozapine
1990s
binds to dopamine & serotonin receptors
binds strongly to dopamine receptors but also dissociates -> fewer side effects & effective in smaller doses
What is a negative side effect of clozapine?
it can cause a blood condition -> ‘’ Agranulocytosis’’
A strength of biological therapy - evidence for the effectiveness
Thornley 2003 -> reviewed data from 13 trials and found that chlorpromazine was associated with better functioning and reduced symptoms severity compared with a placebo
- > support for benefits of atypical antipsychotics -> Meltzer 2012, concluded that clozapine is more effective than typical antipsychotics, it is effective in 30-50% of treatment-resistant cases.
- > this means that as far as we can tell, antipsychotics work
A counterpoint to strength of biological therapy
most studies are of short-term effects only and some data sets have been published several times, exaggerating the size of the evidence base. Benefits may be due to calming effects of drugs rather than real effects on symptoms.
-> the evidence of effectiveness is less impressive than it seems
A limit to biological therapy is the likelihood of side effects
Typical Ap’s are associated with dizziness, agitation, sleepiness and weight gain. Long term use -> lip-smacking & grimacing due to dopamine super sensitivity.
- > most serious is neuroleptic malignant syndrome -> caused by blocking dopamine action in the hypothalamus which disrupts body systems
- > > this means that antipsychotics can do harm as well as good & individuals may avoid them therefore reducing the effectiveness
EVAL extra for biological therapy, the chemical cosh.
believed that Antipsychotics are used in hospitals to calm people w Sz & make it easier for staff to deal with
- > However, calming ppl distressed by hallucinations & delusions probably makes them feel better and allows them to engage with other treatments like CBT
- > > on balance then there are clear benefits to using antipsychotics to calm ppl w Sz and in the absence of a better alternative they should be prescribed.
What are the two psychological therapies?
Cognitive behaviour therapy
Family therapy
What are the aims of CBT?
to help clients identify irrational thoughts (hallucinations & delusions) and try to change them
-occurs in 5-20 sessions, individually or in a group
How does CBT help patients w Sz?
make sense of how their delusions and hallucinations impact on their feelings and behaviour
what is ‘normalisation’?
where people who hear voices can be taught that voice-hearing is an extension of an experience of thinking in words
what is reality testing?
delusions testing, in which the person w schizophrenia and their jointly examine the likelihood that beliefs are true
what happens in a CBT session?
therapist teaches client to identify distorted cognitions through evaluation
- set homework -‘reality testing’
- idea is for client to identify their irrational beliefs and go against it to prove wrong
Turkington 2004, case study for CBT
treated a paranoid client who believed the Mafia were plotting against to kill him (Delusions of persecution)
therapist acknowledged the client’s anxiety & explained that there were other less frightening possibilities
-> explained the clients evidence for his beleif in the mafia explanation
A strength for CBT is evidence for it’s effectiveness?
Jauhar 2014 -> reviewed 34 studies of CBT for Sz & concluded that there is evidence for significant effects on symptoms
- > Pontillo 2016, found reductions in auditory hallucinations, clinical advice from NICE recommends CBT for schizophrenia.
- > > this means that both research & clinical experience support CBT for schizophrenia
A limit for CBT is the quality of evidence
Thomas 2015, points out that different studies have focused on CBT techniques and people with different symptoms
- > overall modest benefits of CBT for Sz may conceal a range of effects of different symptoms.
- > > this means that it is hard to say how effective CBT will be treating a particular person with Sz
what is the aim of family therapy?
reduce levels of expressed emotion, especially negative like guilt & anger -> stress
reducing stress to reduce the likelihood of response
improve communication within family
How does family therapy help?
Fiona pharaoh, identified a range of strategies that family therapies improve the functioning of family members w Sz
- form a therapeutic alliance whereby all family members agree on aims
- improve families beliefs about and behaviour towards Sz
- achieve a balance between caring for person w Sz & maintaining their own lives
Family therapy, model of practice 2018
Burbach 2018
- Phase 1 &2: share info, identify resources family can offer
- Phases 3&4: learn mutual understanding and look at unhelpful patterns of interaction
- Phase 5,6&7: skills training, relapse prevention and maintenance
A strength of family therapy is the evidence of it’s effectiveness
McFarlane 2016, concluded that family therapy is effective for Sz, relapse rates were reduced by 50-60%. -> particularly promising during time when mental health initially starts to decline, NICE recommends
-» this means that family therapy is good for people with both early and ‘full-blown’ schizophrenia.
Another strength is the benefits for the whole family
therapy is not just for benefit of identified patient but also for the families that provide bulk of care for people w SZ
- > Family therapy lessens the negative impact of schizophrenia on the family and strengthens the ability of the family to give support
- > > this means that family therapy has wider benefits beyond the obvious positive impact on the identified patient
Who developed token economies?
Ayllon & Azrin 1968 used a token economy in a SZ ward
extensively used in 1960s & 70s but declined due to shift of care in community rather than hospitals & of ethical concerns
What is a token economy?
A gift token is given for a desirable behaviour
target behaviours decided individually based on knowledge of person
tokens are swapped for rewards like a walk outside or watch a film
given immediately following target behaviour
The rationale for token economies
institutionalism occurs in long-term hospital treatment
Matson 2016 identified 3 categories of institutional behaviour that can be tackled using token economies: personal care, condition-related behaviours and social behaviours
What do token economies benefit?
Quality of life - improve within hospital settings e.g. more sociable with other residents
Normalises behaviour - encourages the return back to more normal behaviour, easier to adapt into the community e.g. Making your bed.
What is the theory based behind token economies?
Operant conditioning - behaviour modification
-secondary reinforces which are exchanged for rewards
Tokens that can be exchanged for a range of different primary reinforces are ‘generalised reinforcers’ - more powerful
A strength for token economies is the evidence of effectiveness
Glowacki 2016
identified 7 high quality studies published between 1999 - 2013 on the effectiveness of token economies in a hospital setting
-> all studies showed a reduction in negative symptoms and a decline in frequency of unwanted behaviours
-» This supports the value of token economies
Counterpoint for strength of token economies - file drawer problem
seven studies is quite a small evidence base.
a issue with such a small number of studies is the file drawer problem - a bias towards publishing positive findings.
This means that there is a serious question over the effectiveness of token economies
A limit for token economies is the ethical issues raised
professionals have the power to control people’s behaviour and this means imposing one persons norms on to others e.g. a patient may like to look scruffy
- > also restricting the availibility of pleasures to people who don’t behave as desired means that very ill people experiencing distressing symptoms, have an even worse time
- > > this means that benefits of token economies may be outweighed by the impact on freedom and short-term reduction in quality of life
A limit for token economies is the existence of more pleasant and ethical alternatives
Other approaches do not raise ethical issues e.g. Art-therapy is a high gain low risk approach to managing Sz (Chaing 2019)
- > even if the benefits of art therapy are modest, this is true for all approaches to treatment and management of schizophrenia and art therapy is a pleasant experience
- > > this means that art therapy might be a good alternative to token economies as there are no side effects or ethical abuses
The interactionist approach consists of:
the diathesis-stress model
treatment according to the interactionist model
What does the diathesis-stress model suggests about schizophrenia?
A Vulnerability +trigger = Sz
Trigger is a negative experience which stresses
both vulnerability and trigger are needed to develop Sz
-The interaction of both is which causes Sz
What is Meehl’s model for the interactionist approach?
in the original, the diathesis was entirely the result of one ‘schizogene’
-Meehl argued that someone w/o this gene should never develop Sz no matter how much stress they were exposed too
A person who does have the gene is vulnerable to the effects of chronic stress
-schizogene is neccesary but not sufficient for development of Sz
What is the modern understanding of the diathesis model?
the diathesis is not down to a single ‘schizogene’, many genes cause the diathesis
-> also, doesn’t have to be genetic -> early psychological trauma affecting brain development-> e.g. child abuse affects the HPA axis -> more vulnerable to stress
What is the modern understanding of stress?
a modern definition includes anything that risks triggering schizophrenia
Psychological e.g. parenting or Biological e.g. Cannabis use
What is the risk of cannabis use?
7x more likely to develop schizophrenia
as it interferes the dopamine system (increases)
Antipsychotics and CBT according to the interactionist model
Antipsychotic drugs taken in combination with CBT
-interactionist model
Turkington 2006
not possible to adopt biological approach, telling the patients their condition is purely biological and then treat them with CBT
what is the difference between the UK and USA when adopting the interactionist approach?
UK- treat with drug therapy & CBT
USA - conflict between biological and psychological models led to slower adoption of interactionist approach, more likely to be treated with just drug therapy
What is a strength of the interactionist approach, referring to the support for the dual role of vulnerability and stress?
Tienari 2004 studied children adopted away from mothers diagnosed with SZ.
the adoptive parents parenting style was assessed and compared with a control group of adoptees with no genetic risk
-> a child rearing style with high levels of criticism & conflict and low levels of empathy was implicated in the development of Sz but only in the adoptees with a high genetic risk. -» this shows that a combination of genetic vulnerability & family stress leads to increase risk of Sz
What is a strength of the interactionist approach referring to the real world application of interaction?
Tarrier 2004
randomly allocated 315 ppts to medication & CBT group, Medication &supportive counselling group and control group of only medication
-> ppts in the two combination groups showed lower symptom levels than those in the control group, but no difference in hospital readmission
-» this means that there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.
What is a limitation to the interactionist approach, referring to the original diathesis stress model it is too over simplistic?
multiple genes increase vulnerability each with a small effect on it’s own - no schizogene
Stress comes in many form, including dysfunctional parenting
-> researchers now believe stress can also include biological factors, Houston 2008 found that childhood sexual trauma was a diathesis & cannabis use a trigger
-» this means that there are multiple factors, biological and psychological affecting both diathesis and stress.
