Schizophrenia Flashcards
(85 cards)
1
Q
Diagnosis and classification of schizophrenia
- How do we diagnose a specific disorder?
- What are the two major systems of classification?
- How are they different to each other?
A
- Diagnosis and classification interlinked
- In order to diagnose a specific disorder, need to distinguish disorders from each other
- Done by identifying cluster of symptoms that occur together, classifying this as one disorder
- Two major systems for the classification of mental disorder
- World Health Organisation’s International Classification of Disease (ICD-10)
- American Psychiatric Association’s Diagnostic and Statistical Manual edition 5 (DSM-5)
- Differ slightly, DSM-5 positive symptoms must be present for diagnosis
- ICD-10, 2+ negative symptoms are sufficient for diagnosis of schizophrenia
2
Q
Positive Symptoms
- What are positive symptoms?
- Give two examples of positive symptoms
- What is example (1), give an example
- What is example (2), give an example
- What are the three types of (2), describe each briefly with an example
A
- Experiences beyond ordinary existence, this includes hallucinations and delusions
- Hallucinations are a disturbance in perception, false perceptions that have no basis in reality
- This includes hearing voices, seeing distorted facial expressions or seeing people/things that are not there
- Delusions are false/irrational beliefs that are firmly held despite being illogical as well as having no evidence
- Delusions of Persecution, belief others want to harm, threaten or manipulate you (People want to kill you)
- Delusions of Grandeur, belief they are an important individual (They are God, have powers)
- Delusions of Control, belief they are under the control of an alien force that has invaded their mind/body (possessed by spirits, implanted radio transmitters)
3
Q
Negative Symptoms
- What are negative symptoms?
- Give two examples of negative symptoms
- What is example (1), give an example
- What is example (2), give an example
- What are the signs of (2)?
A
- Loss of normal functioning, this includes speech poverty and avolition
- Speech poverty, changes in speech patterns, reduction in amount and quality of speech
- Sometimes accompanied by delay in verbal responses
- In the present more emphasis placed on speech disorganisation
- This is when speech is incoherent and the speaker changes topic mid-sentence
- Classified as positive symptom in DSM-5, speech poverty negative symptom
- Avolition (Apathy), reduction difficulty or inability to start or continue goal-directed behaviour
- Sharply reduced motivation, poor hygiene and grooming, lack of persistence in work, lack of energy
- Anderson (1982) identified three signs of avolition as shown above (everything except motivation)
4
Q
Issues in diagnosis and classification
A
- Good reliability
- Low Validity
- Counterpoint (Good validity, Osorio et al)
- Co-morbidity
- Gender bias
- Culture bias in diagnosis
- Symptom overlap
5
Q
Good reliability (Osorio et al 2019)
A
- Osorio et al (2019) reported excellent reliability for diagnosis in 180 individuals using DSM-5
- Pairs of interviewers achieved inter-rater reliability of +0.97 and test-retest reliability of 0.92
- Can be reasonably sure that diagnosis of schizophrenia is consistently applied
6
Q
Low Validity (Cheniaux et al 2009)
A
- Cheniaux et al (2009), two psychiatrists independently asses 100 clients using ICD-10 and DSM-4 criteria
- 68 diagnosed with Schizophrenia under ICD-10. 39 under DSM-4
- Suggests schizophrenia is under or over diagnosed, criterion validity therefore low
7
Q
Counterpoint (Good validity, Osorio et al)
A
- Osorio et al, excellent agreement between clinicians, used two measures derived from DSM system
- Suggests criterion validity good provided it takes place within a single diagnostic system
8
Q
Co-morbidity (Buckley et al)
A
- When two or more condition occur together (for example schizophrenia and depression)
- Questions validity, might be single condition
- Buckley et al, 50% individuals diagnosed with schizophrenia also have depression, 47% have co-morbidity with substance abuse, 23% with OCD
- Suggests schizophrenia may not be a distinct disorder, some individuals may have been wrongly diagnosed when they just have unusual cases of depression for example
9
Q
Gender bias (Cotton et al 2009)
A
- Men more commonly diagnosed with schizophrenia
- Could mean women less vulnerable
- Cotton et al (2009), women underdiagnosed due to closer relationships hence getting support
- Leads to women functioning better than men
- Underdiagnosis is gender bias, women may not be receiving treatment and services that might benefit them
10
Q
Culture bias in diagnosis (Pinto and Jones 2008)
A
- Hearing voices for example, different cultures different meanings
- Pinto and Jones (2008), British people of African-Caribbean origin 9x more likely to get diagnosed with schizophrenia than White British people
- Caused when psychiatrists are of a different culture to the client they are diagnosing
- Suggests people could be discriminated against by a culturally biased diagnostic system
11
Q
Symptom overlap
A
- Considerable overlap between symptoms of schizophrenia and symptoms of bipolar disorder
- Share positive symptom (delusions) and negative symptom (avolition)
- Suggests they may not be two different disorders, variation of single condition
- Schizophrenia is hard to distinguish from bipolar disorder
- Classification and diagnosis are flawed
12
Q
Biological explanations for schizophrenia
- What are the two biological explanations for schizophrenia?
A
The two biological explanations for schizophrenia are genetics and neural correlates.
13
Q
Genetic Basis-Family studies
- What was Gottesman’s study, what did it demonstrate?
- How does this link to issues and debates?
A
- People with schizophrenia often have relatives with disorder
- Gottesman’s (1991) large scale family study
- MZ twins higher concordance rate (48%) than DZ twins (17%)
- Family members share aspects of their environment
- Correlation represents both nature and nurture
14
Q
Genetic Basis-Candidate genes
- What was the original belief with genes and Sz?
- What do we now know?
A
- Originally believed that one gene could explain schizophrenia
- We now know that several different genes are involved (polygenic)
- For example, genes that code for functioning of neurotransmitters including dopamine
15
Q
Genetic Basis-Mutation
- What mutation causes schizophrenia?
- What did Brown et al demonstrate?
A
- Schizophrenia can have a genetic origin even if previous family members did not have the disorder
- One explanation is mutated parental DNA caused by radiation, poison or viral infection
- Brown et al (2002) positive correlations between paternal age (age of father when child conceived) and risk of schizophrenia
- 0.7% father under 25, 2+% father over 50
16
Q
Neural correlates of schizophrenia
- What does neural corelate mean?
- What is the best-known neural correlate for Sz?
- How does it link to schizophrenia?
A
Neural correlate means the brain structure or function. The best known neural corelate for schizophrenia is dopamine, due to its importance in the functioning of several brain systems related to symptoms of schizophrenia
17
Q
Neural correlates-Original dopamine hypothesis
- What discovery did Seeman 1987 make?
- What is schizophrenia the result of according to this hypothesis?
- Give an example of this, what could this example explain?
- What is Hyperdopaminergia?
- What is Hypodopaminergia?
A
- Based on discovery that drugs (antipsychotics, reduce dopamine) used to treat schizophrenia caused symptoms similar to people with Parkinson’s (associated with low dopamine levels)- Seeman 1987
- Schizophrenia result of high levels of dopamine in subcortical areas of the brain
- Example- excess dopamine receptors in pathways from subcortex to Broca’s area
- May explain poverty of speech, auditory hallucinations
- Hyperdopaminergia means high levels of dopamine
- Hypodopaminergia means low levels of dopamine
18
Q
Neural correlates-Updated versions of dopamine hypothesis
- What did Davis et al propose?
- What could explain cognitive problems?
- What two things does the updated hypothesis attempt to explain?
A
- Davis et al (1991) proposed abnormally low levels of dopamine in the brains cortex to be an explanation
- Low dopamine in prefrontal cortex (responsible for thinking) could explain cognitive problems
- Both high and low levels of dopamine are in the updated version
- Attempts to explain link between abnormal dopamine levels and symptoms
- Also attempts to explain the origins of the abnormal dopamine function
19
Q
Evaluation for Genetic and Neural correlates of Schizophrenia
A
- Research support (Gottesman, Tienari)
- Environmental factors (Not just genetic)
- Evaluation for dopamine hypothesis
- Glutamate
20
Q
Research support for Genetic (Gottesman, Tienari)
A
- Genetic explanation of schizophrenia has strong evidence
- Gottesman showed risk increases with genetic similarity to a family member with schizophrenia
- Tienari et al (2004) showed bio children of schizophrenic still at risk even when growing up in an adoptive family
- Suggests some people more vulnerable to schizophrenia due to their genetic make up
21
Q
Environmental factors (Morgan et al 2017, Morkved et al 2017)
A
- Environmental factors also increase the risk of schizophrenia
- Include both biological and psychological influences
- Birth complications (Morgan et al 2017), Smoking cannabis in teen years (Di Forti et al 2015)
- Childhood trauma, more vulnerable to mental problems in adulthood
- Nina Morkved et al (2017), 67% people with schizophrenia or related psychotic disorders at least one childhood trauma
- 38% matched group with non-psychotic mental health issues
- Suggests genetic factors alone cannot provide a complete explanation for schizophrenia
22
Q
Evaluation for dopamine hypothesis (Curran et al 2004, Tauscher et al 2014)
A
- Evidence for dopamine being involved
- Curran et al (2004), amphetamines increase dopamine, worsen symptoms in people with schizophrenia
- Induces (Brings about) symptoms in people without the disorder
- Tauscher et al (2014) antipsychotic drugs reduce dopamine, reduce intensity of symptoms
- Some candidate genes act on production of dopamine and dopamine receptors
- Suggests dopamine is involved in symptoms of schizophrenia
23
Q
Limitation of Dopamine Hypothesis-Glutamate
A
- Post-mortem and live scanning studies found raised levels glutamate in several brain regions of schizophrenics
- Several candidate genes believed to be involved in glutamate production or processing
- Suggests equally strong case for other neurotransmitters
24
Q
Psychological explanations for schizophrenia
- What are the two psychological explanations for schizophrenia?
A
The two psychological explanations for schizophrenia are family dysfunction and cognitive explanations
25
Family dysfunction
* What is family dysfunction?
This is childhood and adult experiences of living in a dysfunctional family
26
Family dysfunction-Schizophrenogenic mother
* What did Reichmann (1948) propose?
* What is a Schizophrenogenic mother?
* Describe the characteristics of a SM
* What does an SM create?
* What does this lead to?
* Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on patients accounts about their childhood
* Patients spoke of type of parent (labelled schizophrenogenic mother)
* Schizophrenogenic mother means “schizophrenia causing mother”
* Mother is cold, rejecting and controlling
* Creates family climate characterised by tension and secrecy
* Leads to distrust which later develops into paranoid delusions and ultimately schizophrenia
27
Family dysfunction-Double bind theory
* What did Bateson et al (1972) emphasis?
* What is double bind theory?
* What does the child receive when they “get it wrong”?
* How does this leave their understanding of the world?
* How does this relate to symptoms of schizophrenia?
* What does Batson make clear?
* Give an example of a situation using double bind theory
* Bateson et al (1972) emphasised role of communication style within a family
* Developing child trapped in situations where they fear doing the wrong thing
* Receive mixed messages about what this is
* Feel unable to comment on unfairness of situation, cannot seek clarification
* When they “get it wrong” (which is often), punished with withdrawal of love
* Leaves their understanding of the world as confusing and dangerous
* Reflected in symptoms such as disorganised thinking, paranoid delusions
* Bateson makes it clear this is just a risk factor, nothing more than that
* Example, mother saying “I love you” to child, same time turning away in disgust
28
Family dysfunction-Expressed emotion (EE)
* What is expressed emotion?
* What elements are in EE?
* How does EE affect a schizophrenic?
* What is EE primarily an explanation for?
* What can it trigger?
* This is the level of emotion (in particular negative emotion) expressed towards schizophrenic by their carers (usually family members)
* EE contains several elements as shown in the following
* Verbal criticism (occasionally accompanied by violence)
* Hostility towards person (includes anger and rejection)
* Emotional overinvolvement in the life of the person (needless self-sacrifice)
* High levels of EE, serious source of stress for individual
* Primarily explanation for relapse
* Can trigger onset of schizophrenia in vulnerable people due to their genetic make up for example
29
Cognitive Explanations
* What do these explanations focus on?
* Give examples
Explanations that focus on mental processes such as thinking, language and attention.
30
Cognitive Explanations-Dysfunctional thinking
* What is schizophrenia associated with?
* How is schizophrenia characterised?
* Give examples of this, how does this link to symptoms?
* What does a lower level suggest?
* What are the two types of dysfunctional thought processing?
* Schizophrenia associated with several types of dysfunctional thought processing (info processing that does not represent reality accurately, produces undesirable consequences)
* Schizophrenia is characterised by disruption to normal thought processing
* Reduced thought processing in ventral striatum associated with negative symptoms
* Reduced processing of information in temporal and cingulate gyri associated with hallucinations
* Lower level of info processing suggests cognition likely to be impaired (damaged)
* Two types of dysfunctional thought processing, Meta representation dysfunction and Central control dysfunction
31
Cognitive Explanations-Meta representation dysfunction
* What did Frith et al 1992 identify?
* What is meta representation, what does this allow?
* What would dysfunction to this do?
* What could this explain?
* Frith et al (1992) identified two kinds of dysfunctional thought processing
* Meta representation is the ability to reflect on thoughts and behaviour
* Allows insight to our own intentions and goals, interpret action of others
* Dysfunction would disrupt our ability to recognise our own actions, thoughts as our own
* Explains hallucinations of hearing voices and delusions of control
32
Cognitive Explanations-Central control dysfunction
* What us central control?
* How does this relate to schizophrenia?
* How could derailment of thoughts be explained with this?
* Frith et al also identified issues with ability to supress automatic responses while performing deliberate actions
* Speech poverty, thought disorder could result from inability to supress automatic thoughts and speech triggered by other thoughts
* People with schizophrenia tend to experience derailment of thoughts
* Could be because each word triggers associations, person cannot suppress automatic responses to these
33
Evaluation for psychological explanations
* Research support (Read et al, Morkved et al)
* Explanations lack support
* Socially sensitive research
34
Research support (Read et al, Morkved et al)
* Evidence linking family dysfunction to schizophrenia
* Read et al (2005), adults with schizophrenia disproportionally likely to have insecure attachment (Type C and D particularly)
* Also reported 69% women, 59% men with schizophrenia have history of abuse
* Morkved et al (2017) showed adults with schizophrenia reported at least one childhood trauma
* Suggest family dysfunction makes people more vulnerable to schizophrenia
35
Explanations lack support
* Plenty of evidence supporting idea that childhood family-based stress associated with adult schizophrenia
* No support of importance of traditional family-based theories (Schizophrenogenic mother, double bind)
* Both based on clinical observation, informal assessment of mother’s personalities, not systematic evidence
* Family explanations not been able to account for link between childhood trauma and schizophrenia
36
Socially sensitive research
* Research linking family dysfunction to schizophrenia highly socially sensitive
* Can lead to parent blaming, mothers particularly
* Research is therefore controversial
37
Evaluation for cognitive explanations
* Research support (Stirling et al)
* Proximal explanation
38
Research support (Stirling et al 2006)
* Evidence for dysfunctional thought processing
* Stirling et al (2006) compared performance cognitive tasks in 30 people with schizophrenia with a control group without schizophrenia
* Task to name font colours of colour words (Stroop task)
* Required to suppress the tendency to read words aloud
* Schizophrenics took over twice as long to complete the task
* Suggests cognitive processes of people with schizophrenia is impaired
39
Proximal explanation
* Only explains the proximal origins of symptoms (explain what is happening now to produce symptoms)
* Distal explanations focus on what initially caused the condition (Genetics and Family dysfunction)
* Unclear how genetic variation or childhood trauma might lead to problems with meta representation or central control
* Means cognitive theories on their own only provide partial explanations for schizophrenia.
40
Drug Therapy
* What are antipsychotics and what are they used for?
* Describe the two courses of antipsychotics
* What are the two types of antipsychotics?
* What is the difference between the two?
* Antipsychotics are drugs prescribed to individual
* They are used to reduce the intensity of symptoms in particular positive symptoms of psychotic disorders
* Antipsychotic refers to psychosis (loss of contact with reality)
* Short course of antipsychotics, after symptoms do not return in some people’s cases
* Others may need antipsychotics for life or face the likelihood of recurrence of schizophrenia
* Typical (Traditional, First Gen) Antipsychotics or Atypical (New, Second Gen) Antipsychotics
41
Typical Antipsychotics
* Give one example of a typical antipsychotic drug
* How and when is it administered, what is the typical dosage?
* What properties does the drug mentioned contain?
* What are Antagonists and how are these used in the dopamine system?
* What effect does this have?
* What is sedation effect?
* What method should be used when attempting to use a drug for sedative properties?
* Around since 1950s, includes chlorpromazine
* Taken as tablets, syrup or injection, if taken orally, administered daily max 1000mg
* Initially smaller doses gradually increase to max 400 to 800mg
* Strong association between use of typical antipsychotics and dopamine hypothesis
* Antagonists are chemicals, reduce action of neurotransmitter
* Dopamine antagonists such as chlorpromazine work by acting as antagonists in the dopamine system
* Dopamine antagonists block dopamine receptors in synapses of brain, reduces action of dopamine
* When taking chlorpromazine, initially dopamine levels build up, production is reduced
* Normalises (Back to normal levels) neurotransmission in key areas of the brain, reduces symptoms such as hallucinations
* Chlorpromazine is an effective sedative (promotes calmness, induces sleep)
* Not fully understood how but it is used to calm individuals, for example when they are first administered to hospital
* When using chlorpromazine for sedative properties syrup used, absorbed faster than other methods
42
Atypical Antipsychotics
* When has it been used since?
* What is the aim for atypical antipsychotics?
* Which two will we cover?
* Used since 1970s
* Aimed to maintain or improve the effectiveness of drugs in suppressing symptoms of psychosis
* Also attempts to minimise side effects
* Two to focus on, clozapine and risperidone
43
Clozapine
* When was it developed, trialled?
* Why was it withdrawn, what was the name of this condition?
* When is clozapine used?
* How and when is it administered, what dosage?
* What does it do?
* What effect does this have on individuals?
* How is this important?
* Clozapine, developed in 1960s first trialled in 1970s
* Withdrawn same year due to deaths of some from blood condition (agranulocytosis)
* 1980s discovered to be more effective than typical antipsychotics, remarketed as treatment for schizophrenia
* Used only when other treatments failed
* Regular blood tests performed on people to ensure blood condition not developing blood condition not developing
* Cannot be injected due to potential of fatal side effects
* Daily dosage of 300 to 450mg administered
* It binds to dopamine receptors, also acts on serotonin and glutamate receptors
* Improves mood, reduces depression and anxiety, may improve cognitive functioning
* May be prescribed to individual who are high risk of suicide (important, 30-50% people with Sz attempt suicide)
44
Risperidone
* How long has it been around for what does it aim to be?
* How is it administered, what is the dosage and how often is it administered?
* How does it work, what is the difference between this and clozapine?
* What benefits does this have?
* Around since 1990s, developed as attempt to make drug as effective as clozapine without serious side effects
* Taken as tablets, syrup or injection, lasts around two weeks
* Small doses initially built up to daily dose (4-8mg) max 12mg
* Binds to dopamine and serotonin receptors, binds more strongly, effective in smaller doses
* Some evidence suggests this leads to fewer side effects compared to other antipsychotics
45
Evaluation for Drug Therapy
* Evidence for effectiveness (Thornley et al 2003, Meltzer 2012)
* Counterpoint (Healy 2012)
* Serious side effects
* Mechanism unclear
46
Evidence for effectiveness (Thornley et al 2003, Meltzer 2012)
* Evidence to support the effectiveness of antipsychotics
* Thornley et al (2003) reviewed studies comparing effects of chlorpromazine to control conditions
* Showed chlorpromazine associated with better overall functioning, reduced symptom severity compared to placebo
* Meltzer (2012), clozapine more effective than typical antipsychotics, effective 30-50% of cases where typical antipsychotics failed
* Suggests that both typical and atypical antipsychotics work
47
Counterpoint (Healy 2012)
* Healy (2012) suggested flaws with evidence for effectiveness
* Most studies are of short-term effects only, successful trails published multiple times (exaggeration of size of evidence of positive effects)
* Calming effects means it’s easy to demonstrate some positive effect
* Not the same as saying they really reduce severity of psychosis
* Suggests evidence is less impressive than it first appears
48
Serious side effects
* Typical antipsychotics associated with range of side effects
* Dizziness, agitation, sleepiness, stiff jaw, weight gain and itch skin
* Long term use result in tardive dyskinesia, caused by dopamine super sensitivity
* Causes involuntary facial movements (grimacing, blinking, lip smacking)
* Most serious, neuroleptic malignant syndrome (NMS)
* Caused when the drug blocks dopamine action in the hypothalamus (associated with regulation of body systems)
* Results in high temperatures, delirium and coma, can be fatal
* Frequency range from less than 0.1% to just over 2%
* Suggests antipsychotics do harm as well as good, individuals may avoid this treatment (ineffective)
49
Mechanism unclear
* We do not know why antipsychotics work
* Our understanding of its functionality is strongly linked to the original dopamine hypothesis
* We know this is incomplete, schizophrenia can be caused by too low levels of dopamine as well
* If this is the case most antipsychotics should not work
* This as well as the questioning of its effectiveness is an argument that they may be ineffective
* Suggests antipsychotics may not be the best treatment since some other factor may be involved in its apparent success
50
Psychological Therapy for Schizophrenia
* What are the two psychological therapies for Schizophrenia?
The two psychological therapies for Schizophrenia are CBT and Family Therapy.
51
Cognitive Behaviour Therapy (CBT)
* How many sessions?
* What does it aim to do?
* How does it help the client?
* Give two ways CBT can help the client.
* 5-20 Sessions in groups or individually
* Aim to deal with thoughts (cognitions) and behaviour
* Help client make sense of how irrational cognitions (Hallucinations and Delusions) impact on their feelings and behaviour
* Understanding is helpful, reduces distress and improves ability to function adequately
* For example, individual hearing voices think there demonic scared, convince it’s just a malfunction in their brain speech centre, less scared
* Delusions challenged with reality testing, examine likelihood of beliefs with therapist
* Some delusions resistant to reality testing, still can reduce anxiety and depression with CBT
* Turkington et al (2004) described an example of CBT used to challenge where paranoid client’s delusions come from
52
Family Therapy
* What is the aim?
* What are strategies identified by Pharoah et al (2010)?
* How do these strategies help the family as well as the patient?
* What is the further aim of the therapy?
* Aims to improve the quality of communication and interaction between family members
* Pharoah et al (2010) identified strategies to use to try improve functioning of family with schizophrenic
* Reduce negative emotions, reduce levels of EE (reduce emotion generally, especially negative emotion such as anger and guilt)
* Negative emotion creates stress so reducing this shall reduce stress and reduce likelihood of relapse
* Improve family’s ability to help, encourages a therapeutic alliance, agree on aims of therapy
* Improves family’s beliefs about behaviour towards schizophrenia
* Further aims to create balance between caring for individual and maintaining their own lives
53
Burbach (2018) Model of Practice
* Describe each phase from 1 to 7
* Phase 1- Sharing basic information and providing emotional and practical support
* Phase 2- Identifying resources, what different family members can and cannot offer
* Phase 3- Encourage mutual understanding creates safe space for family to express their feelings
* Phase 4- Identifying unhelpful patterns of interaction
* Phase 5- Skills training such as stress management techniques
* Phase 6-Relapse prevention planning
* Phase 7- Maintenance for the future
54
Evaluation for CBT
* Evidence of effectiveness (Jauhar et al 2014)
* Reduction in recovery time (Drury et al 1996)
55
Evidence of effectiveness (Jauhar et al 2014)
* Jauhar et al 2014 reviewed 34 studies, concluded there is clear evidence of small but significant effects on positive and negative symptoms
* Pontillo et al (2016) found reductions in frequency and severity of auditory hallucinations
* Suggests both research and clinical experience support the benefits of CBT
56
Reduction in recovery time (Drury et al 1996)
* Drury et al (1996) found 25-50% reduction in recovery time for patients given antipsychotics and CBT
* Demonstrates CBT alongside drugs make more rapid improvements
* Free will of individual to have CBT
* Both Nature (Drugs) and Nurture (CBT)
57
Evaluation of Family Therapy
* Evidence of effectiveness (McFarlane 2016, Pharoah et al 2010)
* Benefits to the whole family (Lobban and Barrowclough 2016)
* Cost effective (Economical benefits)
58
Evidence of effectiveness (McFarlane 2016, Pharoah et al 2010)
* McFarlane concluded family therapy most consistently effective treatment
* Relapse rates reduced typically by 50-60%
* Pharoah et al found family therapy increased patients’ compliance with medication
* Reduction in risk of relapse and hospital admission up to 24 months after
* Demonstrates family therapies benefit to people with both early and full-blown schizophrenia
* Patients willing to take medication, relapse a lot less likely
59
Benefits to the whole family (Lobban and Barrowclough 2016)
* Lobban and Barrowclough concluded that this therapy helps all family members
* Families provide bulk of care for people with Sz
* Strengthening the functioning of whole family, lessens negative impact of Sz on other family members
* Strengthens ability of family to support person with Sz
* Suggests family therapy has wider benefits beyond obvious positive impact on Sz individual
60
Cost effective (Economical benefits)
* Lowers need for hospitalisation due to lower relapse rates
* Educates family members of medication regime, decrease need for medical help
* Therefore, makes treatment cost effective
* Cheaper than standard care (Drugs alone)
* Higher availability to people with less money
* Better for the economy, less medical assistance required
61
Management of Schizophrenia
* What is used to manage schizophrenia?
Token economies are used to manage schizophrenia as opposed to treating it, aim is to make behaviours more socially acceptable rather than reduce symptoms.
62
Token economies for Schizophrenia
* What are these?
* Which individuals is this particularly useful for?
* These are reward systems used to manage behaviour of schizophrenics
* Particularly those who have patterns of maladaptive behaviour (caused by long hospitalizations)
63
Developing token economies with schizophrenia (Ayllon and Azrin 1968)
* Describe Ayllon and Azrins study
* How much was the system used in the 60s and 70s. why?
* How much is the system used in the present day, why?
* Ayllon and Azrin (1968), trailed token economy system into ward of women
* Every time ppts carried out task (clean bed etc), given plastic token
* When given, embossed with words “one gift”
* Tokens then swapped for ward privileges (watch film), resulted in increase of tasks being done
* System extensively used in 60s and 70s when norm for treating Sz was long term hospitalisation
* Use declined in UK due to growth of community-based care, closure of psych hospitals
* Also, ethical issues, restricting rewards to people with mental disorders
* Still standard approach of maintenance of Sz in other parts of the world
64
Rationale for token economies (Matson et al 2016)
* What develops due to prolonged hospitalization?
* What does this lead to?
* What did Matson et al identify?
* What are the benefits of this?
* Institutionalisation develops as circumstance to prolonged hospitalisation
* One outcome, bad habits such as bad hygiene, stop socialising
* Matson et al (2016) identified 3 categories of institutional behaviour tackled with TE
* Personal care, condition-related behaviours (apathy for example) and social behaviour
* Modifying these does not cure Sz, has two major benefits
* Improved quality of life within hospital setting, example below
* Make up for individual takes pride in appearance, social interaction for sociable person
* Normalises behaviour, easier to adapt back to life in the community, examples below
* Getting dressed in the morning, making the bed
65
Requirements for successful token economy
* When are tokens given, how long till reward received?
* How are target behaviours decided?
* Give an example of a reward given in a hospital setting
* Tokens (Coloured disks) given immediately when individual carried out desirable behaviour
* Target behaviours decided on individual basis, important to know person
* In order to identify most appropriate target behaviours for them (Cooper et al 2007)
* Immediate reward important, delayed rewards less effective
* Tokens administered as soon as possible, rewards in hospital setting may include a walk or magazine
66
Theoretical understanding of token economies
* What is TE an example of?
* What type of reinforcers are tokens?
* When does a token become of value?
* What type of reinforcers are meaningful rewards?
* What is a powerful secondary reinforcer called?
* How do tokens become secondary reinforcers?
* TE example of behaviour modification (Behv therapy based on operant conditioning)
* Tokens are secondary reinforcers (sr), Meaningful rewards are primary reinforcers (pr)
* Tokens only valuable when person learns they can be used for meaningful rewards
* Tokens that can be traded for range of different pr are powerful sr
* Powerful sr are called generalised reinforcers
* For tokens to become sr, must be paired with pr
* At start of token economy programme, tokens and pr administered together
67
Evaluation of Token Economies
* Evidence of effectiveness (Glowacki et al 2016)
* Counterpoint (File drawer problem)
* Ethical Issues
* Alternative approaches (Chiang et al 2019)
* Benefits and Drawbacks
68
Evidence of effectiveness (Glowacki et al 2016)
* Strength, evidence demonstrates effectiveness
* Glowacki et al (2016) identified seven high quality studies published between 1999, 2013
* All studies showed reduction in negative symptoms, decline of unwanted behaviour’s
* Supports value of token economies
69
Counterpoint (File drawer problem)
* Seven studies, small evidence, file drawer problem
* Phenomenon leads to bias towards positive published findings
* Undesirable results “filed away”, problem in reviews that only include small number of studies
* Questions if evidence is a fair reflection of effectiveness of token economies
70
Ethical Issues
* Limitation, ethical issues
* Professionals have considerable power to control behaviour of patients
* Imposing one person’s norms on to others
* Problematic if target behaviours not identified sensitively
* For example, restricting availability of pleasures (film) for people who don’t behave
* Seriously ill people, already experiencing distressing symptoms have even worse time
* Legal action from families, major factor in decline of token economies
* Suggests, benefits may be outweighed by impact on personal freedom and short-term reduction in quality of life
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Alternative approaches (Chiang et al 2019)
* Limitation, more pleasant and ethical alternatives
* Chiang et al (2019), art therapy may be good alternative
* Evidence small and had some methodological limitations
* Appeared to show art therapy is a high-gain low-risk approach of management
* Even if benefits are modest, pleasant experience without major risks (side effects, ethical abuses)
* NICE guidelines recommend art therapy for schizophrenia
* Suggest art therapy good alternative to token economies
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Benefits and Drawbacks
* Problem with TE, difficult to continue outside hospital setting
* Target behaviours cannot be monitored closely, tokens cannot be administered immediately
* Likely leads to benefit of TE to be lost, undesired behaviour’s increase again
* Some people only have chance to leave hospitals if personal care and social interaction improves
* TE may be the best way to do so
* Even though there is a risk of losing effects of TE outside hospital
* Risk worth taking to give individual chance outside who otherwise would remain institutionalised
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The interactionist approach to schizophrenia
* What 3 factors are involved with development of schizophrenia?
* Give examples of each of the 3
* Interactionist approach acknowledges there are biological, psychological and social factors in the development of schizophrenia
* Bio factors include genetic vulnerability, neurochemical and neurological abnormality
* Psych factors include stress resulting from life events and daily hassles for example
* Social factors include poor quality interactions in the family for example
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The Diathesis-stress model
* What does diathesis mean?
* What does stress mean?
* What is necessary to develop schizophrenia?
* A way to present an interactionist approach
* Diathesis means vulnerability, in this context stress is a negative experience
* Both vulnerability and stress trigger necessary to develop schizophrenia
* 1+ underlying factors make person vulnerable to developing Sz, onset of condition triggered by stress
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Original Diathesis-stress model (Meehl 1962)
* What did the original model suggest about diathesis?
* What did Meehl suggest?
* What could result in the development of schizophrenia?
* Diathesis (vulnerability) entirely genetic, result of single “schizogene”
* According to Meehl, no amount of stress leads to schizophrenia without schizogene
* In carriers of gene, chronic stress through childhood adolescence (particular schizophrenogenic mother) could result in development of disorder
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Modern understanding of diathesis
* What do we know now about genetic vulnerability?
* What factors have now been introduced?
* What did Read et al (2001) come up with?
* Give an example
* Clear now that many genes increase genetic vulnerability, no single gene (Ripke et al 2014)
* Psychological trauma (Ingram and Luxton 2005) now a factor, trauma is the diathesis rather than stressor
* Read et al (2001), neurodevelopmental model, early trauma alters developing brain
* Early, severe enough trauma (child abuse) seriously affects aspects of brain development
* For example, hypothalamic-pituitary adrenal system (HPA) can become overactive, more vulnerable to later stress
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Modern understanding of stress
* What is the modern definition of stress?
* What is recent research concerned with?
* Why may () trigger schizophrenia?
* What does research show, what does this suggest?
* Modern definition of stress is anything that risk triggering schizophrenia (Houston et al 2008)
* Recent research concerned with cannabis use, cannabis is a stressor
* Increases risk of schizophrenia by up to 7x according to dose
* May be because it interferes with dopamine system
* Most people do not develop Sz after smoking cannabis, may be because they lack the vulnerability factors
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Treatment according to interactionist model
* What does interactionist model acknowledge?
* What does this mean for treatment?
* What did Turkington et al (2006) suggest?
* What is standard practice in Britain compared to the US?
* Acknowledges both bio and psych factors in Sz, therefore compatible with bio and psych treatments
* In particular combining antipsychotic medication and psych therapies (usually CBT)
* Turkington et al (2006), possible to believe bio causes of Sz and still practice CBT to relieve psych symptoms
* In Britain, standard practice to combine antipsychotic drugs and CBT
* Not as common in US (Tend to use drugs only in some cases, no CBT)
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Evaluation for interactionist approach
* Support for vulnerability and triggers (Tienari et al 2004)
* Diathesis and stress are complex (Houston et al 2008)
* Real World Application (Tarrier et al 2004)
* Counterpoint (Jarvis and Okami 2019)
* Urbanisation
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Evaluation for interactionist approach
* Support for vulnerability and triggers (Tienari et al 2004)
* Diathesis and stress are complex (Houston et al 2008)
* Real World Application (Tarrier et al 2004)
* Counterpoint (Jarvis and Okami 2019)
* Urbanisation
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Support for vulnerability and triggers (Tienari et al 2004)
* Strength, evidence supporting both vulnerability and triggers
* Tienari et al (2004), investigated impact of genetic vulnerability and psych trigger (dysfunctional parenting)
* 19,000 Finnish children, bio moms diagnosed with Sz, in adulthood high genetic risk group compared to control group (adoptees without history of Sz, low genic risk)
* Adoptive parents assessed for child rearing style
* Found high levels criticism, hostility, low levels empathy associated with development of Sz
* Only in high genetic risk group (not in control group)
* Shows combo of genetic vulnerability and family stress, lead to increased risk of Sz
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Diathesis and stress are complex (Houston et al 2008)
* Limitation, original DS model oversimplicity
* Clear original portrayed diathesis single schizogene, stress schizophrenogenic parenting, simplistic
* Multiple genes, multiple combo influence diathesis, stress comes in many forms also
* Diathesis also influenced by psych factors; stress can be bio as well as psych
* Houston et al (2008), childhood sexual abuse major influence on vulnerability to Sz
* Cannabis use major trigger, suggests multiple factors both bio and psych affect diathesis and stress
* Supports modern understanding of diathesis and stress, limitation for original DS model
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Real World Application (Tarrier et al 2004)
* Strength, combo of bio and psych treatments
* Practical application combo drug treatment and psych therapies, studies demonstrate advanced effectiveness
* Tarrier et al (2004) randomly allocated 315 ppts, 3 groups
* Med + CBT, (2) Med + Counselling (3) Control group (Med only)
* Ppts in (1) and (2) showed lower symptoms than (3), no difference in hospital readmission
* Suggests clear practical advantage with interactionist approach to Sz, superior treatment outcome
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Counterpoint (Jarvis and Okami 2019)
* Jarvis and Okami (2019), point out that successful treatment for disorder justifies particular explanation
* Logical equivalent to alcohol reduces shyness, shyness caused by lack of alcohol
* Logical error is called treatment-causation fallacy
* Therefore, cannot automatically assume success of combined therapies means interactionist is correct
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Urbanisation
* Sz more commonly diagnosed in urban than rural areas, sometimes used to justify interactionist position
* Assumes urban living more stressful, more psych stressful (crowds’, noise), stressors may be bio (pollution)
* May be because people with diathesis for Sz tend to migrate to cities
* Greater population density in cities, more people witness early symptoms, refer to a doctor
