Clinical psychology Flashcards
what are the 4ds of diagnosis
Deviance
Dysfunction
Distress
Danger
what does deviance mean in the 4 d model
behaviours that are unusual, undesirable or bizarre
failure to conform to social or statistical norms
what does dysfunction mean in the 4d model
symptoms which distract, confuse or interfere with a persona ability to perform normal tasks
WHODAS ii questionnaire measures dysfunction
what does distress mean in the 4d model
when symptoms cuase emotional pain or anxiety
may be manifested as physical symptoms like aches and pains
distress can be sometimes considered normal e.g. if person has just lost their job
clinician considers length and distress
what does danger mean in the 4d model
careless, hostile or hazardous behaviour which threatens safety of person or others
in the UK if a person is considered a danger to themselves or others they can be sectioned under the mental health act
what is a strength of the 4d model (four criteria)
using all four might help to avoid errors in diagnosis
e.g. if deviance was the only part considered then those who eccentric yet harmless may be seen as abnormal while those with common debilitating symptoms of depression may be missed
why might a weakness of the 4d model be lack of objectivity
ratings are being based off of the clinicians own views of what they deem to be abnormal, this may be affected by culture
for example a clinician from a different cultural background may see someones behaviours from a different culture alien while others do not - in some cultures hearing voices is viewed as communicating with god but a non religious clinician may see this as a symptom of SZ
why is possible labelling a weakness for the 4d model
end up with negative labels for people with mental illness
e.g. using danger as a criterion leads people to associate mental illness with danger
most people with SZ are no more dangerous than people without a diagnosis (Fazel et al)
could cause self fulfilling prophecies
what is a counter arguement for labelling being a weakness of the 4d model
labelling does not neccessarily lead to a self fulfilling prophecy, some people even attempt to rid themselves of negative labels by acting the complete opposite e.g. study done on baby faced boys who are frequently called cute - more aggressive than mature faced boys
what is an application for the 4d model
used by clinicians in conjuction with dsm -5 and icd 10 to help make appropriate diagnosis
different disorders tend to display different combos of the 4ds e.g. deviance from stats norms normally associated with intellectual disability vs the other ds being present in anti social personality disorder
what is the DSM
the diagnostic statistical manual,
describes symptoms, features and assocaited risk factors of over 300 mental and behavioural disorders
22 categories
where is the DSM primarily used and is it free
USA
not free, makes revenue for the american psychiatric association
what version of the DSM are we on now
the DSM-5
what is in section one of the DSM-5
guidance on how to use the new system
what is in section 2 of the DSM-5
details the disorders and categorises them according to current understanding of causes and similarities of symptoms
what is in section 3 of the DSM-5
suggestions for new disorders e.g. internet gaming disorder
also includes info of the impact of culture on diagnosis
how does a clinician make a diagnosis using the DSM-5
-gather info about individuall through observation
- most gathered through unstructured interviews
- also many structured interview schedules like the beck depression inventory
-process often involves ruling out possible disorders before deciding which one is the “best fit”
-complicated cases may take weeks or months
how is reliability of the DSM assessed
- Kappa score for reliabilty
- refers to proportion of people who receive the same diagnosis when assessed and reassessed either at a later time (test-retest) or by another practitioner (inter rater)
how is validity of the DSM assessed (different types of validity ?)
descriptive validity - when two people with the same diagnosis exhibit similar symptoms
aetiological validity- same causal factors
concurrent validity- when a clinician uses more than one method for diagnosis and both methods lead to the same diagnosis
predictive validity- if we are able to accurately predict outcomes for an individual after their diagnosis e.g. prognosis and reaction to treatment
why is the DSM reliable
good level of agreement between clinicians shown in field trials
Regier found that PTSD had a kappa score ranging from 0.6 to 0.79 which is deemed very good and seven other disorders including SZ ranged from 0.4 to 0.59 which is deemed as good
Shows that clinicians have adapted well to changes with the DSM and diagnostic criteria for some disorders
why is the DSM less reliable
what counts as acceptable levels of agreement has diminished over the years
Cooper explained that the DSM-5 task force classified levels as low as 0.2-0.4 as acceptable - suggests that the DSM-5 may be less reliable than previous versions
why is the DSM ethnocentric
made in and for America
also have private healthcare in America which may lead to more frequent diagnosis as they will gain revenue form someone needing care - therefore less valid
why is diagnosis using a best fit approach an issue ?
may be diagnosing with wrong disorder
may be a complex disorder - possible comorbidity
each best fit will be subject to each clinicians norms and values
why is the DSM-5 more reliable than other versions
DSM-5 has fewer diagnostic categories than the previous version. In the past, patients who “ticked the boxes” automatically qualified for a diagnosis. For example, having an IQ under 70 meant you were “mentally retarded”. DSM-5 encourages clinicians to look at other factors, like functioning or distress.
what is the ICD
diagnostic manual like DSM used produced by WHO
current version is the ICD-10
includes both physical and mental disorders
freely available around the world
how is a diagnosis made using the ICD-10
clinician selects key words from an interview with a client that relate to their symptoms - e.g. hallucinations or delusions
clinician can then look up these symptoms in an alphabetic index or go straight to an obvious disorder
clinician then uses other symptoms to locate a sub category
how has the ICD been improved
presentation, communication and interpretation of symptoms is shaped by language and culture and culture bias meant that one clinician may give a different diagnosis from clinicians in another culture because of differences in language and cultural norms
The ICD-10 is now as a result available in many languages with appropriate cultural forms
what is a strength of the icd 10 compared to the icd 9 (reliability)
Ponizovsky - compared reliabilty of the two , 3000 patients assessed at each time point
was measured using positive predictive value (ppv) - this i sthe proportion of people who get the same diagnosis when reassessed, for SZ PPV increased from 68% to 94.2% in 2003
what is a counter argument for the icd-10 having high reliability
high reliability is meaningless without validity. a demonstration of a high stability of diagnoses i.e. reliability of a certain diagnostic system doesnt mean the system is valid. reliability on its own tells us nothing about the meaning of the diagnosis
why does the ICD-10 have high inter-rater reliability
has good consistency when two clincians assess the same clients using the ICD-10
Galeazzi- arranged for two researchers to conduct a joint interview to assess 100 consecutive clients - got kappa scores ranging from 0.69 to 0.97 showing high agreement
why does the ICD-10 have high predictive validity for SZ
Mason- did a study that compared different ways of making a diagnosis- ICD-9 and ICD-10 were reasonabley good at predicting disability in 99 people with SZ 13 years later - using global assessment of functioning questionnaire
what is the application to diagnosis in regards to the development of the ICD-11
- aim to improve clinical utility of the system - conducted a huge survey of clinicians and found a preference for simplicity and flexibility, suggesting the ICD-11 task force will be cautious of adding new disorders and are likely to merge existing ones that are difficult to diagnose - system should be more user friendly improving the validity.
what is schizophrenia
a psychotic disorder characterised by positive symptoms (added on) such as delusions and hallucinations , negative symptoms can also be present such as alogia (poverty of speech) or flat effect
what is a symptom
subjective experiences reported by the individual that cannot be observed
what is a feature
info about prevalence , age of onset, gender differences, prognosis etc
what are the four key symptoms of SZ
thought insertion
hallucinations
delusions
disordered thinking
explain thought insertion
when a person believes their thoughts do not belong to them and have been implanted by an external force
blurring of boundary between self and others and feel barrier is permeable
explain hallucinations
perceptual experiences which do not correspond with reality
can be visual , olfactory , somatosensory and auditory (most common)- often experienced with hearing voices
explain delusions
fixed beliefs that are not amendable to change in the light of conflicting evidence
may be related to everyday life (believing your movement is being tracked by the government) or bizarre (believing an alien is trying to get in your brain)
can take many forms - persecutory , referential, grandiose
explain disordered thinking
inferred by someones speech - characterised by derailment (unrelated ideas) or tangentiality (going completely off topic)
word salad- refers to apparently random strings of ideas
only symptomatic if it leads to dysfunctional communication
what are some key features of SZ
lifetime prevalence- 0.3-0.7%
onset- slightly earlier in males (early to mid twenties ) than females (late twenties)
males tend to have poorer prognosis
prognosis is variable and harder to predict
females are over-represented in late onset cases
why is SZ often reliably diagnosed
can be made with a high degree of consistency with both DSM-5 and ICD-10
has a good kappa value of 0.46 after field trials of dsm-5 which is consodered good
only 3.8% of clinicians said they lacked confidence in their diagnosis of SZ using the ICD-10
suggests descriptors of SZ are sufficentky detailed to allow clinicians to distiguish it from other conditions
why is the reliability of diagnosis for SZ not easy
it shares symptoms with other disorders e.g. hallucinations can be experienced by people with depression or caused by drug withdrawal , stress , sleep deprivation etc
why do cultural differences make diagnosis harder in SZ
difficult if client is of a different culture than clinician
e.g. rastafarians often use neologisms (new words) which are a play on english words such as overstand instead of understand
a clinician unaware of these may see this as a sign of disordered thinking
suggests that diagnosis of SZ requires awareness and sensitivity to cultural and linguistic differences
what is hyperdopaminergia
excessive dopamine in the mesolimbic pathway or the rewards centre of the brain
linked to positive symptoms of SZ
what are some possible causes of hyperdopaminergia
low levels of beta hydroxylase - the enzyme which breaks down dopamine may be responsible for build up of excess dopamine in the synapse
too may D2 receptors on postsynaptic neuron
what is hypodopaminergia
dopamine deficiency in the mesocortical pathway
linked to negative symptoms such as flat effect and alogia
explain the relationship between serotonin and negative symptoms of SZ
clozapine
binds to D1 and D4 dopamine receptors but only weakly to D2
the fact this drug worked in treating SZ called dopamine hypothesis into question
clozapine also binds to serotonin receptors and greatly reduces both pos and neg symptoms
suggests serotonin links to SZ
why is the use of amphetamines a strength to support the dopamine hypothesis
rats treated with amphetamines
Tenn- found that rats given nine amphetamine injections over three weeks showed SZ like symptoms
this included social withdrawal and odd movement
furthermore dopamine antagonists (block D1 receptors) were successful in reversing effects
people also report experiencing hallucinations when taking amphetamines for recreational use - amphetamines have action on dopamine- increasing its likelihood to fire more regularly - suggests that positive symptoms of SZ could be caused by excessive dopamine
what is a competing arguement for the dopamine hypothesis
apomorphine stimulates D2 receptors but does not induce psychotic symptoms in non psychotic patients or exacerbate symptoms in those already diagnosed with SZ- challenges dopamine hypothesis
what is a weakness for neural explanations for SZ
does not explain higher prevalence of SZ in certain groups
veling found moroccan immigrants were more likely to get a diagnosis than turkish immigrants
this difference correlates with actual and perceived discrimination
suggests non biological explanations such as social stress may be more effective
what application has the dopamine hypothesis had on SZ and the development of drug theories
Zhao conducted met analysis comparing 28 antipyshcotics from 56 randomised controisl with over 10,000 ppts
found antipsychotics tested had sig lower relapse than placebos
why is the dopamine hypothesis limited by the treatment aetiology fallacy
an individual with a headache would take paracetamol but the cause of the headache was not a paracetamol deficiency
therefore in terms of SZ dopamine agonists may reduce symptoms but may not be the cause of the disorder
why are biological explanations low level and reductionist
SZ is a complex disorder with patients experiencing a wide range of symptoms
unlikely a single neurotransmitter is the cause
also focus on animal research is also reductionist as animals often given higher doses blocking role of dopamine that would be ethically possible for humans
what are the aims of rosenhan classic study (clinical classic)
aimed to reveal flaws in process of psychiatric diagnosis
demostrate that psychiatrists cannot distiguish between sane and insane
support the idea that mental disorders lie not with the individual but the person making the diagnosis
what was the procedure of the initial study for rosenhan (clinical classic)
- three females and five males including rosenhan acted as pseudo patients - included a painter, psych student and housewife
-each person presented themselves at a psych hospital complaining of the same symptoms- heard same sex , unfamiliar voice that was unclear - said terms like empty hollow and thud
-approached 12 hospitals in 5 states
-some hospitals old, some new , some well staffed and one a private facility
-once administered they behaved normally
-to be let out the pseudo patients had to convince staff they were sane even though they followed orders, chatted with other patients
-kept records of observations
what was the procedure of the follow up study for rosenhan (clinical classic)
- after intial study some hospitals wanted to show that this wouldnt happen there
- rosenhan agreed to send some psuedopatients to their wards to see if they would be identified as imposters (none were actually sent)
- staff had to rate each patient on a scale of 1-10 where 1 meant there was high confidence the patient was fake
what were the findings for rosenhans initial study
- all pseudopatients admitted (7 SZ one with bipolar disorder)
-when released they were siad to have SZ in remission - length of stay ranged from 7 to 52 days - avg 19 days
- about 30% of patients on the ward were suspicious of them
what were the findings of Rosenhans follow up study
- at least one member of staff wrongly reported with high confidence that 41/193 patients were fake
23 were reported by at least one psychiatrist and a further 19 were thought to be fake by a psychiatrist and one other staff member
what did rosenhan conclude
- that we cannot distinguish the sane from insane in psych hospitals
- felt that the hospital environment created a set of situational factors which led to depersonalisation and segregation which made people seem insane
why is rosenhans study well designed (strength)
- use of covert participant observation and collection of both qualitative and quantitative data
- staff unaware of pseudopatients so their behaviour more natural - e.g. rosenhan reported physical abuse on patients that stopped when other staff members appeared
- high ecological validity enhanced by wealth of data collected
why might the validity of Rosenhans study be considered poor
- psuedopatients may have only recorded negative interactions between staff and patients as they all supported rosenhan
why might data collected in rosenhans study be unreliable
only one pseudopatient per hospital so no way of knowing if data collected was reliable
why might demand characteristics explain the diagnosis of the pseudopatients in rosenhans study
- the willingness to admit a patient on flimsy evidence may be because the psychiatrist wouldnt suspect that someone might be pretending and therefore assumes that anyone seeking admission would have a good reason
How did rosenhans study support the antipsychiatry movement
- Psychiatrist thomas Szasz argued that mental illnesses are problems in living and not diseases and it is therefore inappropriate to use a medical model
- rosenhans study supported this as it demonstrated that diagnosis of mental states was invalid
- this study drew attention to the need for reforms in psychiatry , to avoid misuse of diagnostic labels
what was the application of rosenhans study
- led to changes in the DSM 111
- the failure of psychiatrists to make accurate diagnoses led to call fro changes
what are the ethical issues that came from rosenhans study
- clinicians made to fell incompetent (psychological harm) , real patients may have been discriminated against as clinicians thought they were fake (psych harm) and the rep of psychiatry was damaged - may have led to vulnerable people failing to seek support
what is a recent estimate for heritability for SZ and what does this suggest
79%
- genetic factors play a part
what did wright indicate about genes linked to SZ
as many as 700 genes are linked to SZ
How might gene mutation occur
may be due to environmental factors or an error during cell division such as deletion or duplication
what is the link between the COMT gene and SZ
- this gene provides instructions for the enzyme that breaks down neurotransmitters such as dopamine in the prefrontal cortex
- deletion of the COMT gene would mean poorly regulated dopamine resulting in schizophrenic symptoms
what is the link between the DISC1 gene and SZ
people with an an abnormality in this gene are 1.4 times more likely to develop SZ (kim et al)
This gene codes for creation of GABA , a NT that regulates other NT’s such as glutamate and dopamine in the limbic system
what is the link between the diathesis stress model and genes that are linked to SZ
- genes create a vulnerability to SZ rather than causing it
- may possess the gene but it is only triggered by other biological or environmental factors
- still a gentic explanation as genes are the required element
- stress can include anything that risks triggering SZ
- one of concern is cannabis use - increases risk of SZ by 7 times - probably as it interferes with the dopamine system
what research support provides evidence for the genetic explanation for SZ
Gottesman et al
- analysed concordance rates for people of different genetic similarity
- clear relationship between genetic similarity and an increase in two related individuals both having SZ
In an earlier study Gottesman and Shield found a concordance rate of 42% for MZ twins and 9% for DZ
- shows biology plays a role
why should you be cautious about using data from twin studies (Gottesman and Shield)
MZ’s are more likely to be treated similarly than DZ twins due to more similar appearance and the fact they are always the same sex
(shared environment assumption)
- reduces validity
what is a weakness of the genetic explanation for SZ in terms of concordance rates
- the fact the concordance rate is not 100%
- Pedersen and Mortensen - research demostrates that the longer a person has been exposed to city life and the denser the population in that city the greater risk they have of developing SZ
- suggests rural dwelling may protect a person from developing a disorder they are genetically predisposed to
what research into the COMT and DISC 1 genes provide evidence for the genetic explanation of SZ
dahoun - did a review of 14 studies and concluded that DISC 1 is associated with pre synaptic dopamine dysregulation
egan - propes a link between a variant of the COMT gene (val gene) and decreased dopamine activity in the prefrontal cortex
concluded that inheriting two copies of the val gene increases risk of SZ by 50%
what application came from the gentic explanations of SZ
used to inform gentic counseling
when a family member is diagnosed with sz they may want more info about whether it is inheritable
‘recurrence risk’ can be calculated and the counsellor will help the family interpret the info
removes fears and allows for the correct choices in family planning
How does Tienari’s research support the diathesis stress model in terms of the genetic explanation of SZ
- did 21 year longitudinal adoption study
- adopted children whose biological mothers were diagnosed with sz were more sensitive to family dysfunction in the adoptive home than those from low risk matched backgrounds
explain social adversity
- idea that some children grow up in environments less favourable than others and this can make them more vulnerable to mental health disorders in the future
- for example families affected by unemployment and poorer standards of living will likely face more stress than other families
- people from lower socioeconomic groups may not be able to access treatement for SZ - makes them even more vulnerable and exacerbates symptoms
explain urbanicity
- the association between living in urban areas and SZ
- Eaton- suggested city life is more stressful than rural life and exposure to such stress may trigger an episode of sz
- many stressors including noise , light pollution criminality
- increased pop density makes life more competitive whether its for a seat on the tube or a job
- arguably increases experine of social defeat - stressor that may elicit sz symptoms
explain social isolation
- Faris- suggested that people with sz withdraw because they feel contact with others is too stressful
- such self imposed isolation cuts the person off from feedback about what behaviours are deemed strange or not - in absence of corrective feedback they begin to act strangely
what is the link between immigration/minority status and sz
- research in many countries has shown that first and second generation immigrants are at greeater risk of sz than the general pop
- however this risk decreases as people from same ethnic background increases (Boydell)
what does the link between minority status and sz mean
- indicates outgroup status is key
- Veling - suggests that sz may be a reaction to the chronic experience of prejudice and discrimination
why are second generation immigrants more at risk than first generation
- they have weaker cultural/ethnic identities
- they have learned more than thier parents to fit in with the norms of society
- therefore their identification with their parents and the beleifs and expectations they hold may be at odds with their parents and extended family
how does meta-analyses support the role of urban dwelling
- Vassos - performed meta analysis of four studies conducted in sweden netherlands and denmark - 24,000 cases of sz
- they correlated location with sz
- at the extremes they found that the risk was 2.37 times higher for people living in the most urban vs most rural environments
what is the competing argument for meta analyses supporting urban dwelling
- research is correlational
- social drift hypothesis - suggests people with SZ find it hard to hold down a job leading them to drift into a lower social class than their parents
- leads to them migrating into deprived inner city areas - therefore SZ leads to urbanicity rather than the other way
why is the social causation view not a complete explanation for SZ
- we know there is some genetic contribution
- gottesman and the twin study
- suggests environmental factors may only trigger the onset of sz in people genetically predisposed (diathesis stress model of sz)
what is a strength of velings explanation
- evidence from a complex analysis of self reported questionnaire data
- study found that people classed as marginalised ( weak national and ethnic identity ) and assimilated (strong national weak ethnic ) were at greater risk of sz than people classed as integrated (strong national and ethnic ) or seperated ( weak national strong ethnic )
- suggests strong ethnic identity may be a protetcive factor against SZ
how has the social causation view been applied to treating sz
- draws attention to factors which affect mental health at the community level
- housing projects which reduce overcrowding and encourage neighbourhood cohesion and celebrate cultural diversity should help communities arm themselves against mental breakdown
how does the nature nurture debate apply to the social causation view
tienaris findings
what is an example of an FGA
chlorpromazine
what is a dopamine antagonist
rduces pos symptoms by blocking postsynaptic receptors without activating them
what type of fgas are most effective
ones that bind to the D2 receptors ( one of the main receptors linked to SZ
what are the side effects of FGAs
tardive dyskinesia- uncontrollable stiff or writhing movements of the face and body
what is an SGA and give an example
second gen antipsychotics
clozapine
whats the difference between FGAs and clozapine
also acts on serotonin and glutamate receptors
how does clozapine help treat sz
reduces pos and neg symptoms
whats a side effect of clozapine
a potentially fatal blood condition- made the drug fall out of favour but is still used in treatement resistant clients providing releif for up to 60%- regular blood tests help avoid agranulocytosis
what is the protocol for prescribing anti psychotics
- in first week after psych episode the aim is to decrease hostility and return client to normal functioning
- careful monitoring of symtoms and side effects
- when symptoms subside a maintenance diose is prescribed-
what does a maintenance dose help with (SZ)
encourages socialisation and self care
- improves mood
- combats relapse - occurs in 18-32% who take meds but 60-80% in those who dont
- continued for at least a year after remission
when do medications need to be used for the most effectiveness (SZ)
the first five years after an acute episode - dont seem to help people who have experienced symptoms for many years
what empirical evidemce is there for drug use (Zhao)
-compared 18 antipsychotics using data from 56 randomised controlled trialswith over 10,000 people - found 17 antipsychotics tessted had significantly lower relapse rates than placebo
- means people can be helped to avoid emotional and financial costs of going to hospital by using drugs
what is a counter arguement for zhao et als research
20% of people with sz show little improvement after multiple fga trails and 45% experience partial or inadequate improvement and unacceptable side effects (patel)
many people with sz who take drugs still fail to function in everyday life e,g they are uemployed
why is it a weakness that most of the data comes from research with animals (SZ) (Kapur)
pointed out that high doses of meds can be given to animals to block d2 receptors but these doses produce severe side effected in humans
- animals cannot show how side effects would affect people or whether they would lead to lack of compliance
- lack validity and generalisability
- cannot replicate the lived experience of taking meds everyday
why is there bias in some reported evidence for drug treatments of SZ
publication bias towards studies showing a positive outcome of antipsychotics
- much research funded by drug compaines who promote continuing success of drugs therefore the effectiveness is exaggerated - lacks validity
how have drug treatments for sz lead to de-institutionalisation
meant an enormous change is people with sz and how they could live their lives
- had a chance to remain in the community avoiding institutionalisation
- reduced stigmatisation and segregation of people with mental health issues as they werent been isolated from the rest of the community by being put into hospitals
how are drug treatments for sz an issue for social control
‘chemical straitjackets’
- people suggest they lead to disempowerment
- believe its wrong that some people in society have the power to control others using drugs to change their behaviour
how does CBT help treat irrational thoughts in people with sz
- helps client identify irrational thoughts and change them
- altering how a person thinks can help prevent decompensation (decline from normal functioning into a psychotic episode_)
- self awareness is enhanced - can recognise specific situations preceding decompensation and learn to use coping strategies
how does cbt help treat delusions in people with sz
- helps make sense of how delusions and hallucinations affect feelings and behaviour
what is reality testing in cbt treatment for sz
- combats delusions and hallucinations by verbally challenging clients perceived reality
- client tests whether delusions are real - often better than trying to talk client out of false belief
- evidence is discussed to debunk false beliefs - helps client differentiate between confirmed and perceived reality
what is behavioural activation in cbt for sz
- sz linked to motivational deficits e.g. social withdrawal and lack of enjoyment or pleasure (anhedonia)
- can be reduced by rewarding positive behaviours
e.g. becoming more socially active and expanding the activities a client is involved in - clients sense of self also addressed e.g. helping recognise they are more than a person with sz
How does evidence from NICE support cbt
- they conducted a meta anlysis of high quality studies of CBT
- rehospitalisation rates reduced
- time spent in hospital reduced (average 8.26 days)
- symptom severity reduced at the end of treatment and twelve months later
why might cbt for sz NOT reduce symptoms or prevent relapse
- Mckenna and Kingdon
- compared CBT and routine treatment or a control nonbiological intervention
- CBT only superior in 2/9 trials
- suggests CBT may not be as effective as NICE suggests
what is a counter argument for Mckenna and Kingdons research
- only used quantitative data
- overlooks the unique experiences of people in therapy
- case studies such as Bradshaw take more of an idiographic approach
- demostrated a strong client and therapist relationship developed over many months can support the process of personal recovery
How do findings from studies on drug resistant clients support the use of CBT for sz
Kuipers et al
conducted randomised controlled trial of CBT for sz
- drug resistant clients improved when given CBT targeting their delusions and hallucinations
- importnat as many people with sz dont respond to antipsychotics so useful to have second line of therapy to offer
how has CBT for sz been used to develop independent living skills
- can develop personal and social skills improving a person quality of life
- can be achieved through challenging irrational thoughts so the person relates better to others plus specific use of social skills training
- offers more long lasting solution than drug therapy
how is ethics an issue in relation to CBT and sz
- CBT relies on colaboration between therapist and client - challenging clients delusions can be distressing so must be managed with sensitivity (same with behavioural experiments)
- must be approached with care to avoid psychological harm
