Flashcards in Schizophrenia Deck (106):
What is sz
Psychotic disorder, the sufferer looses touch with reality and lacks insight- they have no awareness that they are ill.
How common is sz and who is most likely to get it
1% of the population will suffer from sz
Early 20s in males but slightly later in females.
More common in men who are working class
Define classification and Diagnosis
Classification - the process of organising symptoms into categories based on which symptom clusters together eg- deciding that sz is a distinct mental illness different to others and what the symptoms actually are.
Diagnosis- deciding where or not particular individuals has those symptoms and therefore is suffering with the illness
What are the two major classification systems for psychological disorders
DSM V - diagnostic and statistical manual, volume 5- produced by the American psychiatric assocation
ICD 10- international classification of disease update 10 - produced by the world health association
How do the DSM and the ICD differ for diagnosing sz
-The DSM requires at least one of the positive symptoms
-ICD requires to or more of the negative symptoms
-ICD includes a number of subtypes such as paranoid sz and hebephrenic sz but the latest addition no longer includes these subtypes
What criteria would someone need to meet to be diagnosed with sz by the DSM
A: two or more of the following symptoms
-grossly disorganised or catatonic behaviour
-negative symptoms eg- avolition
( only one symptom is required if symptoms are bizarre)
- social occupational dysfunction
- signs are present for 6 month including one month of symptoms that meet criteria A.
Describe hallucinations as a symptom of sz
Bizarre perceptions of stimuli in the environment or have no relation to reality. May include auditory voices, visual- seeing someone who's not there, olfactory - smelling things that other people can't smell.
Most common- voices telling them to do something or commenting on their behaviour
Describe delusions as a symptom of sz
Give 3 examples
Eg- delusion of grandeur where they may belief they are an important historical political or religious figure such as Jesus or the queen.
Eg- delusion of persecution where they believe that an individual or organisation is conspiring against the
Eg- delusion of reference when events in the environment seem to be directly related to them eg- personal messages being communicated through he TV
Describe avolition as a symptom of sz
Lack of purpose
Loss of motivation to carry out tasks
Become apathetic and find it difficult to begin or maintain goal directed activity
Poor hygiene and grooming, lack of persistence in work or education and lack of energy
Describe speech poverty as a symptom of sz
What does the DSM place emphasis on
Reduction in the Amount and quality of speech
Often repetitive content
Slow to respond during conversation
One word answers
On tasks of verbal fluency they produce fewer words in a given time than none sufferers
Not due to poor vocab but the difficulty in spontaneously producing words
The DSM places emphasis on speech disorganisation, speech may become Incoherent (word salad). Changes topic mid sentence. Reflects abnormal thought process. Individual struggles to organise their thoughts.
How can positive and negative symptoms be explained
Positive - additional to normal behaviour eg hallucinations
Negative - lack or absence of normal behaviour eg avolition
What is reliability in classification of sz
The extent to which the classification of sz is consistent over time and across the different classification and diagnostic systems
How may the classification of sz lack reliability
DSM and ICD have different criteria's to be diagnosed with sz
Bizarre is objective
What is meant by inter- rater reliability in diagnosing sz
The level of agreement on the diagnosis by different psychiatrists across time and culture eg- when different clinicians make identical diagnoses independently of each other.
What study may criticise inter rater reliability in sz
Elie Cheniaux et Al
2 psychiatrists independently diagnosed 100 patients using the DSM and ICD criteria
1. 26 with sz according to the DSM
44 according to the ICD
2. 13 according to the DSM
What study supports the argument that 'bizarre is objective "
Mojtabi and Nicholas 1995
50 senior psychiatrists were asked to differentiate between bizarre and non bizarre delusions
Inter rater correlations of only 0.4
Showing - even this central characteristic of sz lacks the reliability sufficient for it to be a reliable method of distinguishing between sz and none sz behaviour
What might be the implications of poor reliability in diagnosis
- receiving the wrong treatment
- people who don't have sz being diagnosed with it - going through pointless treatment
- some people who actually have sz and are not being diagnosed with it
What is test retest reliability in sz
Stability of diagnosis over time given no change in symptoms eg- a clinician makes the same diagnosis on separate occasions based on the same info
What is validity in classification
The extent to which schizophrenia exists as a mental illness that is distinct from other illnesss. The extent to which the symptoms of sz are actually symptoms of sz.
What is validity in diagnosis in sz
The accuracy of diagnosis - the extent to which people with sz are diagnosed as such while those without sz do not receive diagnosis
What is co morbidity
What does the Buckley et al show
The occurrence of two illness or conditions together. If two illness are frequently diagnosed together then it calls to question the validity of the classification.
Concluded that around half the people diagnosed with sz also have a diagnosis of depression (50%) or substance abuse (47%)
What other illness is common in those with sz despite depression
Alone effects 1% of the population
Swets et al
The two conditions appear together more often than chance would predict
12% of sz patients also fulfilling symptoms for OCD
26% displaying significant obsessive compulsive symptoms
Why might co morbidity be a problem when diagnosing
If symptoms are similar they may fit the criteria of more than one illness and Therefore be diagnosed incorrectly depending on who diagnoses when meaning they will receive the wrong treatment
What is symptom over lap
Two or more condition share the same symptoms
Eg- Sz and bipolar
According to the ICD - diagnosed with sz
DSM - diagnosed with bipolar
How can copeland show us how diagnosing sz is culture bias
Copeland 1971- gave US and British psychiatrists a description of a patient
69% of the U.S Diagnosed them with sz only 2% of the British did
Why may African Americans and Afro Caribbean English people be more likely to be diagnoses with sz
Back this up using Luhrmann et al
Hearing voices maybe considered ore acceptable among people from Afro Caribbean cultures due to beliefs about communication with ancestors. Therefore they are more ready to acknowledge and report such experiences
Luhrmann et al
Interviewed 60 sz patients from Ghana, India and the U.S.
African / Ghana - heard voices which were playful and offered advice
U.S.- voices were violent and hateful
Who can support that sz is more common in men
Longenecker et al
Found that men were more likely to be diagnosed with sz only appears to be the case since 1980s
Why may men be more likely to be diagnosed than women
Cotton et al
Cotton at El
Female patients typically function better than men they are more likely to work and have good family relationships. This high level of functioning may mask the symptoms of sz and mean the practitioners feel that they are not severe enough to be diagnosed
How does the biological explanation explain genetics in the explanation of sz
Unlikely that it is one gene
Different combinations of genes
What have family studies shown about the diagnosis of sz
How does Gottesman support this
That it is more common among the biological relatives of someone with sz than a general population
The closer you are relate the greater the risk of developing sz
Gottesman - children with 2 sz parents have a Concordance rate of 46%
Children with one 13%
Siblings had 9%
Why are twin studies better than family studies and what did Joseph find
As twins share 100% DNA can see whether it is biological
Joseph - concordance rate 40.0% in MZ twins
7.4 for DZ twins
This gives limited support for the biological explanation
What study can support the statement that " your more likely to get as if your mother has it"
Tienari et al
Adoption study in Finland
164 adoptees who's biological mother had sz
11 (6.7%) also received a diagnosis
4 (2%) of the 197 control group
What is meant by polygenic and why is sz a polygenic
- a number of genetic factors are required for an individual to develop sz
How is sz aetiologically heterogeneous
Different studies have identified different candidate genes. Different combinations of different genes can lead to the illness
What is the dopamine hypothesis
Excess dopamine is associated with the positive symptoms of sz, people with sz are thought to have high dopamine receptors on receiving neurones resulting in more dopamine binding and therefore more neurones firing.
What is dopamine important for
The functioning of several brain systems
What did Davis and Khan propose about dopamine and sz
What did Goldman- Rakic et Al find
The positive symptoms of sz are caused by access dopamine in the subcortical areas of the brain, particularly in the mesolimbic pathway. While the negative and cognitive symptoms arise from a deficit of dopamine In areas of the prefrontal cortex
Goldman- Rakic - low dopamine levels in the prefrontal cortex as an explanation for the negative symptoms of sz
How can Grilly support that dopamine levels cause sz
People who suffer from Parkinson's disease who take the drug l dopa to raise there dopamine levels have been found to develop sz like symptoms.
How do antipsychotic drugs help dopamine levels
Block the activity of dopamine in the brain.
Leucht et Al
Meta analysis 212 studies
All antipsychotic drugs tested were significantly more effective than placebo in the treatment of positive and negative symptoms
What stimulant drugs can effect other neurotransmitters effect
Effect other transmitters as well as dopamine Such as a co founding source of dopamine releases stress and smoking haven't been considered
What does noll 2009 argue against antipsychotics
That they do not alleviate hallucinations and delusions in about 1/3 of patients experiencing these symptoms. These symptoms are sometimes present despite dopamine being normal. This suggest that other neurotransmitter systems, acting independently of the dopamine system at a,so produce the positive symptoms of sz
What is a neural correlate
Measurements of the structure or functions of the brain that correlate with an experience
What part of the brain is avolition associated with
Motivation is associated with the ventral striatum, an area of the brain that is involved in the anticipation of reward.
The ventral striatum is in the basal ganglia, an area of the brain involved in the facilitation of voluntary movement. The ventral striatum contains the nuclear accumbens which is associated with reward, it is activated when we do or anticipate Doug something we know will be pleasurable
What did Juckel et al find about activity in the ventral striatum in people with sz
He found lower activity in the ventral striatum of people with sz. They also found a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms.
This makes sense as low activity in this area will mean the individuals does not anticipate reward and will therefore experience a lack of motivation.
Where did Allen et al find lower activation levels
-In the superior temporal gyrus ( which contains the primary auditory cortex and wernicke's area.
- anterior cingulate gyrus
In the hallucination group who also made more errors than the control group.
What did costain et Al find about grey matters in the anterior cingulate gyrus
Study in patients with sz and there first and second degree relatives which revealed a significant difference in grey matters. Sz patients had smaller volume of grey matter than their second degree relatives but not in comparison to their first degree relatives. Both sz and first degree healthy relatives have smaller grey matter volume than the second degree healthy relatives. It appears that genres are responsible for he decreased volume of grey matters in sz patients.
This show that sz can't be just from a small amount of grey matters and it must be something else
What did fujiwara et Al find about the size of the anterior cingulate gyrus
The smaller the size of the anterior cingulate gyrus the lower as the level of social functioning and the higher the psychopathology in sz patients.
What is a problem with all the research into the neural correlates in sz
The brain in malleable and we can't be certain that these symptoms and these neural correlates came before the symptoms of sz it could be a result of sz. We don't know if it's a cause or a consequence of anti psychotic medication.
What type of ventricles is associated with negative symptoms of sz
Enlarged ventricles. These are fluid filled cavities due to the loss of subcortical brain cells. The ventricle of a person with sz are on average 15% bigger than a normal person (Torrey)
This implies that the brain area around the border of the ventricles have shrunk or decreased in volume, the ventricular space becoming larger as a result and also decreases in brain weight.
What are the problems in drawing conclusions about the cause of sz from research into neural correlates
None of the neural correlates can be used diagnostically to distinguish between those who do and do not have disorders for example research has shown that enlarged ventricles are found in non sz which contradicts his as a physical cause.
And while MRI studies provide conclusive evidence of structural abnormalities, it is worth nothing that they do not always agree on the regions of the brain affected. For example flaum found no abnormalities in the temporal lobe regions whereas woodruff found quite significant reductions in the temporal lobe, compared with controls. This could suggest that neural correlates are actually unrelated to sz or question the extent to which it is one condition or many.
What are two strengths with the biological explanation for sz
- scientific methods -FMRI scans, this generates testable hypothesis eg- that people with sz have higher levels of dopamine than people without. It uses empirical methods eg- pet scans and FMRI which are objective and have value therefore it's not open to interpretation in comparison to the psychological explanation, therefore less open to researcher bias. It also takes a nomothetic approach in explaining sz as testing the hypothesis enables research to contest a theory providing us with general laws about the likelihood to develop sz.
- it has useful application and the development of antipsychotic meditation transformed the way in which people with sz were treated, the explanation has economic implications and people with sz are less likely to be hospitalised which reduced the cost of the economy this may also enable them to work which wouldn't mean they would be contributing to the economy.
Give two limitation of the biological explanation of sz
- determinists - patients maybe passive and rely on drugs that the doctors provide
- reductionists - reduces sz which is a complex set of emotions, cognitive and behaviour symptoms down to the action of neurotransmitters and genes.
- antipsychotics don't believe it's an illness. The biological approach adopts a medial model when explaining and treating the illness however anti psychotics such as Thomas szasz would argue that it is inappropriate as he would argue that mental illness's reflect problems with living or simply different ways of behaving.
What are the three psychological explanation for sz
The schizophrenogenic mother
How is family dysfunction and explanation for sz
How may this be socially sensitive
Refers to abnormal processes within a family such as poor communication, cold parenting and high levels of expressed emotions
As it blames the parent
What how the schizophrenicogenic mother explain sz
How may this explanation be criticised
Fromm- reichman 1948
Focus on the role of the mother in causing there child to develop the illness due to being cold, rejecting and controlling. This type of mother often creates a family climate characterised by tension and secrecy which leads to distrust and paranoia in the child.
The explanation came about it in 1948, it may well be a product of its time from when mothers stayed at home. Furthermore it is gender bias as it blames the mother and not the father.
How does the double bind theory explain sz
Bateson et al 1972
Suggested that children who receive contradictory messages from there parents are likely to develop sz. For example a mother may tell her child she loved them whilst turning away In disgust. These conflicting messages mean that the child is unsure how to behave and often gets it wrong which is then punished by the withdrawal of love from their parent. The contradictory messages invalidate each other and prevents the child from developing and internally coherent construction of reality. They are left perceiving the world as dangerous and confusing which ultimately manifests itself into symptoms such as paranoia, withdrawal and flattened affect. This is a view similar to that of R.D Laing who argued that sz was a reasonable response to the insane world.
How does Berger 1965 support the double bind theory
How can the study be criticised
Found that sz patients had higher recall of double bind statements than non sufferers.
The study maybe criticised as people are recalling there childhood and this is retrospective. There current state of well being may bias the recall. If there parents have but them forward to the doctors for being ill there maybe tensions in the family.
How may may hall and Levin 1980 challenge the double bind theory
They analysed data from previous studies and found no different between family's with and without a member suffering sz in the degree to which verbal and non verbal communication were in agreement.
How does expressed emotions explain sz
Refers to the level of emotions that are expressed towards a child by their parent. Including
-criticism- verbal criticism of the individual which may be accompanied by violence
- hostility- anger and rejection
- emotional over involvement - including needless self sacrifice on the part of the parent.
The negative emotional environment can ,was to high levels of stress from the individual and. An trigger a sz episode
How does linszen et al support the idea of expressed emotions
Why is it still a problem
- pointed out that a patient returning to a family with high expressed emotions is about 4 times as likely to relapse than a patient returning to a family with low EE
However - this doesn't mean that it is EE causing the sz. Not a cause but a perpetuating factor.
What does Tienari et al tell us about family dysfunction
Found that the difference in the rate of sz between those adopted with a biological sz parent compared to those without one only occurred in family homes which were rated as disturbed.
The links to the diathesis stress model that there is a genetic vulnerability but only once theirs a trigger in the environment e.g.- a disturbed home
Name a strengths of family dysfunction if as cause for sz and how this can also be a weakness
Environmental determinist- this is good as it doesn't blame the individual however this can be an issue as it can cause the patient to be passive and believe that they can't get better and therefore have no hope to get better and always have a negative thought process, furthermore it may lead the diagnosed to blame those around them for instance their parents and reject them at a time of need leaving them to become more ill.
What are 2 criticism of family dysfunction as an explanation for sz
- socially sensitive - ethical implications, can make parents anxious and worthless. The research is quite poor as it's mostly correlate and therefore we can't establish a cause and effect. Individuals may resent there parent and become even more isolated with society and reality then before.
- nature - nurture - ignored biological factors e.g.- dopamine
What did Frith et al identify as two types of dysfunctional thought processing that could account for some symptoms of sz (cognitive )
What symptom could his explain?
-dysfunctional metarepresentation - the ability to reflect on thoughts and behaviours that allow us to interpret the action of others and have insight into our own intentions. If this process is dysfunctional then the individual maybe unable to recognise their own thoughts and actions and make mistakenly attribute them to being carried out by some else.
- dysfunctional central control- ability to suppress automatic responses while we perform actions instead. Problems with his ability can lead to derailment of thoughts and difficulty of sustaining a conversation as words will trigger automatic associations which the individual cannot suppress
- this could explain disorganised speech
What was slade and bentalls five factor model
What were the 5 factors ?
Theory of hallucinations, highlights the mechanisms responsible for the failure of
-stress induced arousal - in a time of stress we are in a state of arousal and information is not processed easy making it difficult to decide what is real
-predisposition- more likely to hallucinate because they are easily led
-environmental stimulation - hallucination are more likely to occur in a quiet place where people experience sensory deprivation or when there is a constant noise which is meaningless
- reinforcement - hallucinations maybe reinforced because they reduce arousals
- expectancy - people see or hear what they believe exists, for example, hallucinations tend to be influences by cultural expectations.
Who objected slade and bentals model
Close and Garety - argue that hallucinations actually increase anxiety and are therefore unlikely to be reinforced.
Tarrier supports this as he found an escalation of disturbed feelings following hallucinatory experiences.
What was maher's 1970 anomalous experience model
This suggests that delusions are a result of anomalous experiences of the individual rather than faulty interpretations of their experiences. Therefore they are a product of abnormal perceptions and an adaptive and rational response to abnormal internal events such as hallucination.
- the same cognitive processes lead to delusional and normal beliefs
- delusions act as mini theories and provide order and meaning to the world
- mini theories are needed when events are not predictable
- unpredictable events can cause anxiety- the delusion explanations for these bring relief. Any data that is inconsistent with the delusional belief will be ignored or made to fit with the delusion and data confirming the belief will be sought.
How does zimbardo et al support the anomalous experience model
Found that normal individuals became increasingly paranoid when made partially deaf through hypnotic suggestions, but were kept unaware of the source of there deafness
- supports that paranoia is due to unexpected events
What is the most common form of drug treatment for sz
What are they effective with
What do they reduce
- reduction positive Symptoms such as hallucinations
- dopaminergic transmission
What is a typical antipsychotic
'First generation antipsychotics'
Reduces dopamine and therefore reduces the hallucinations and the delusions
Dopamine antagonists- they bind to dopamine receptors in the mesolimbic area but do not stimulate them and therefore block the actions.
Taking chlorpromazine results in dopamine levels building up and then it's production is reduced through normalising the neurotransmission of dopamine
What is an Atypical antipsychotic
Later developed 'second generation'
Eg- clozapine - binds in the same way as chlorpromazine however it also acts in serotonin and glutamate receptors.
Effective in improving mood, reducing depression and anxiety and improving cognitive functioning.
Often proscribed when patient is at high risk of suicide.
A lower risk of extrapyramidal side effects (problems with movement) because of there rapid dissociation ( they only temporary bind to dopamine receptors, allowing the normal dopamine transmission)
What is an example of a newer A typical antipsychotic
What does it do
Binds to dopamine w and serotonin receptors. However it binds more strongly than clozapine and therefore is effective in smaller doses = fewer side effects
What is the key differences between typical and a typical antipsychotics
Typical- chlorpromazine, first gen, blocks dopamine receptors therefore positive against positive symptoms, can cause problems with movements as it stops the flow of dopamine.
Atypical - clozapine, second gen, bind receptors and acts in serotonin and glutamate, improves mood, reduces depression and anxiety, lower extrapyramidal side effects
What study would support that typical antipsychotics are effective
Why is this a good study
Thornley et at 2003
Reviewed studies comparing chlorpromazine to placebo.
Showed that chlorpromazine was associated with better overall functioning and reduced symptom severity.
- large sample size, reliable and credible
What study would argue that atypical drugs are more effective that typical drugs
Concluded that clozapine is more effective than typical antipsychotics and that it is effective in 30-50% of treatment resistant cases where typical antipsychotics have failed.
What study shows the effectiveness of antipsychotic drugs for sz
How can his study be evaluated ad credited
Leucht et al
Meta analysis of 65 studies published between 1959 and 2011 - 6000 patients
All patients given either typical or a typical drugs. Some where taking off and giving a placebo instead.
Within 12 months ..... 64% who had been giving the placebo relapsed compared to 27% who staye on the antipsychotics.
- large sample- reliable - more confident
- even in the relapse 36% are still ok meaning there are psychological factors
- drugs are only effective to certain people, people still relapse despite being on medication.
What side effects have antipsychotics
How does kapur et al say about why side effects occur
- kapur estimated that between 60 and 75% of dopamine receptors in the mesolimbic pathway have to be blocked for the typical antipsychotics to be effective, dopamine receptors in the brain are also blocked and this leads to side effects
What can some long term effects of antipsychotics be
Dyskinesia - which is caused by dopamine super sensitivity and manifests as involuntary facial movements e.g. Blinking
What is the most serious side effect of antipsychotics drugs for sz
Neuroleptic malignant syndrome - caused by blocked dopamine action in the hypothalamus. This can result in high temperature, delirium, coma's and can be fatal.
What is a consequence of antipsychotic side effects
Lead to none compliance of medication therefore it doesn't work
How common is treatment discontinuation
74% of patients have problems with this
What does Healy argue about antipsychotics
That the evidence of the effectiveness is over exaggerated. The data from some successful trails has been published several times, the calming affects of antipsychotic has been mistaken as having positive effect of the patients despite not knowing the severity of the the psychosis has reduced. Most studies have focused on the short term effects comparing patients who keep taking antipsychotics with those suffering from withdrawal having just stopped taking them.
Antipsychotics rescue the neurotransmission of dopamine, what are the problems with this
This assumes that dopamine causes sz and if that's not the case all antipsychotics are flawed
How would the psychological explanation for sz treat sz
Psychological al therapies - CBT
What does sz CBT aim to do
Helps the individual recognise their irrational thoughts that lead to delusions and faulty interpretations associated with hallucinations and change these.
Recognising the link between their delusions and hallucinations and their feelings and behaviour.
They are encouraged to evaluate the content of the hallucinations and delusions and test the validly of these.
Take place in groups to perform their functioning
NICE recommend at least 16 sessions of CBT when it is used to treat sz
How did turkington et al evaluate CBT
- statistically significant improvements were seen in the CBT intervention group in overall symptoms, insight and depression.
- insight will make the individual more open to treatment
- there were more drop outs in the treatment as usual groups.
- 57% rated CBT as having helped them understand there illness more than anything previous
- CBT can be used to treat or just encourage people to take medication.
How does NICE 2014 support the effectiveness of CBT
Reviewed the treatments of CBT ad found consistent evidence that when compared to antipsychotics, CBT was effective in reducing rehospitalisation rates up to 18 months following the end of treatment. (economic implications) CBT reduces symptoms severity when compared to standard care, it also improved social functioning
When do addington and addington believe CBT should be used?
Once psychotic symptoms have been stabilised through medication as CBT will help normalise their symptoms. CBT will benefit those who have a greater realisation of their problems.
Why can research into the effectiveness of CBT be criticised
Some studies have not randomly allocated participants to the CBT or control group (haven't controlled for severity of illness) while others haven't masked the treatment condition for the interview who carry out the assessment interviews.
Wykes et al found that the more rigorous the study the weaker the effect of CBT
One advantage and one disadvantage of CBT
Ad- insight into the illness and encourages them to take the medication
Dis- time consuming - 12 to 20 sessions on average and homework could lead to symptoms getting worse and possible lead to self harm or suicide. Therefore drugs maybe more effective as they take less time to have an effect. Also, levels of engagement could decrease and the participant could drop out before CBT has been given chance to work. Furthermore, it would be costly to pay trained specialist therapists for 20 sessions
How do family therapies aim to improve sz
Aim to improve the quality of commination in the family and reduce levels of stress. They aim to reduce the levels of expressed emotions in the family and therefore prevent relapse of symptoms
What strategies does family therapy include
-Pyschoeducation - individual and family are helped to understand the weakness
-A therapeutic alliance is formed between the therapist and the family's members
- the stress of caring for someone with sz is reduced improving emotional climate
- the ability of family members to anticipate and solve problems is increased
- the level of anger and guilt felt by family members is rescued further improving emotional climate
- family members are helped to achieve balance between caring for the individual and maintaining their own lives
- the family members are encouraged to make more realistic expectations of the individual in terms of heir behaviour and the recovery
What is the individual encouraged to do in family therapy
What are family members encouraged to do?
Encouraged to be part of the therapy and share with their family and their experiences and what kind of support they find helpful. They should reduce any suspicions they have about there treatment.
Encouraged to listen to each other, openly discuss there problems and negotiate solutions. His helps to improve communication while providing the family with practical solutions to some of the issues they face.
What did pharoah et al find when comparing family therapies to standard treatment (antipsychotic)
Reviewed 53 studies published between 2002-2010
Carried out in Europe, Asia and North America.
The effect on the overall mental state was inconsistent- some studies found improvements compared to standard care others had not.
Family intervention did not find compliance with medication and there was a reduction in relapse and hospital admission during the treatment and the 24 months after.
Family therapy improved general functioning but there was no effect on concrete measures such as living independently or employment
What do Mari and streiner say about family therapy
It has declined over time. This could be due to the charisma and enthusiasm of the early proponents of family intervention. However it could also be due to general improvements in mental health care when comparing against treatment as usual it is harder to show an effect
Give one strength and one limitation of family therapy
Ad - economic implications- taking medication out of hospital
Dis - requires family members to be open and honest
What is token economy
Based on behaviourist principles - intended to improve the general level of functioning of individuals with sz rather than actually treat the conditions. They are aimed at improving the negative symptoms of sz such as avolition. Take a are rewarded when the patients do positive tasks, the tokens can be exchanged for various rewards and privileges such as mags and watching a film
What is a primary reinforcer
What is a second reinforcer
Give examples in terms of token economy
Anything that gives pleasure or removes an unpleasant state. They do not depend on learning to acquire their reinforcing value.
Initially have no value on the individual, they acquire their reinforcing properties as a result of being paired with primary reinforces
Secondary- tidying room
What needs to happen for token economy to be effective
Why may this have practical implications
They need to be awarded immediately after the target behaviour was performed otherwise another behaviour could have been performed in the intervening period and it would be this behaviour that would be reinforced
Staffing reasons- don't have enough staff to watch all the patients at once
What did sran and borrero find about token economy
Patients had higher rates of responding when tokens could be exchanged for a variety of items
What did ayllon and Azrin find about the use of token economy
What did Dickerson et al
Token economy on a ward of female patients with a diagnosis on sz. They found that the use of token economy drastically increased the number of desirable behaviours that the patient performed each day.
Reviewed 13 studies of the effectiveness of token economies. 11 of which reported beneficial effects directly attributable to the use of the token economy.
What does comer say about studies which have reviewed token economy
There has been a lack of control and therefore it's difficult to draw conclusions about there effectiveness. Token economies are often implemented on a whole ward without the use of a proper control group therefore patients improvements are simple being compared to their previous behaviour.
What might be an alternative explanation for improvements of patients that's not token economy
The fact that they are just getting better due to medication
The passage of time
More attention from members of staff
Name 2 limitation of toke economy
-When the patients leave the hospital and stop getting rewarded, he desirable behaviours may decrease
-doesn't actually treat sz just manages it so it should be used with drug therapy
In the original diathesis stress model what was the diathesis and what was the stress
How have these notions changed
How does tienari support the diathesis stress model sz
How can we use the findings of twin studies to support the diathesis stress model
Diathesis - vulnerability
Stress- psychological experience
It is now clear that many genes each appear to increase genetic vulnerability slightly not just one single gene .
He found both genetic vulnerability and family related stress are important in the development of sz. This is important for adopting and interactionist approach to sz
They both share the same genes and environment therefore they should be similar as the diathesis stress model suggests. Never found 100% concordance rate