Schizophrenia Flashcards

(67 cards)

1
Q

what is schizophrenia?

A

severe mental disorder characterised by profound disruption of cognition and emotion
affects language, thought, perception, emotions, sense of self

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2
Q

how is schizophrenia diagnosed?

A

DSM-V (used in US)
ICD (used in Europe)

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3
Q

what are positive symptoms?
eg?

A

those that appear to reflect an excess or distortion of normal functions
- hallucinations
- delusions
- disorganised speech
- grossly disorganised or catatonic behaviour

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4
Q

what are hallucinations?

A

bizarre, unreal perceptions of the environment that are usually auditory but may also be visual, olfactory (smells) or tactile

Many report hearing a voice(s), telling them to do something/ commenting on their behaviour.

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5
Q

what are delusions?
what are the different types?

A

Bizarre beliefs that seem real to the patient

Paranoid- eg a belief that the person is being followed or spied upon/ their phone is tapped/ there are cameras hidden
Delusions of grandeur- eg believing they are famous/ have special abilities
Delusions of reference- events in the environment appear to be directly related to them, e.g. special personal messages are being communicated through the TV or radio.

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6
Q

what is disorganised speech?

A

result of abnormal thought processes, where the individual has problems organising thoughts- shows up in speech.

slip from one topic to another (derailment)
extreme cases- speech may be so incoherent that it sounds like gibberish (word salad)

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7
Q

what is grossly disorganised/ catatonic behaviour?

A

inability or motivation to initiate a task, or to complete it once it’s started- leads to difficulties in daily living and decreased interest in hygiene
May dress or act in ways that appear bizarre eg wearing heavy clothes on a hot day

Catatonic behaviours are characterised by a reduced reaction to the immediate environment, rigid postures or aimless motor activity

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8
Q

what are negative symptoms?

A

reflect a reduction or loss of normal functions, which often persist even during periods of low (or absent) positive symptoms

Weaken ability to cope with everyday activities- affects quality of life/ ability to manage without significant help
unaware of the extent of their negative symptoms, less concerned about them than their relatives may be.

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9
Q

What is the deficit syndrome?

A

Enduring negative symptoms characterised by the presence of at least 2 negative symptoms for 12 months or longer

Individuals have been found to have more pronounced cognitive deficits and poorer outcomes

Milev et al, 2005 reported worse functional outcomes in individuals with more prominent negative symptoms
Negative symptoms respond poorly to antipsychotic treatment (but atypical better than typical)

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10
Q

examples of negative symptoms

A

speech poverty (alogia)
avolition
affective flattening
anhedonia

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11
Q

what is alogia

A

speech poverty
lessening of speech fluency and productivity- reflects blocked thoughts

produce fewer words in a given time on a task of verbal fluency (e.g. name as many animals as you can in one minute)- know words but cant spontaneously produce them

less complex syntax e.g. fewer clauses, shorter utterances- associated with long illness and earlier onset

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12
Q

what is avolition?

A

reduction of interests and desires, inability to initiate and persist in goal-directed behaviour

distinct from poor social function or disinterest, which can be the result of other circumstances

reduction in self-initiated involvement in activities that are available

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13
Q

what is affective flattening?

A

Reduction in the range and intensity of emotional expression, voice tone, eye contact and body language

When speaking, may show a deficit in prosody (intonation, tempo, loudness and pausing)

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14
Q

what is anhedonia

A

loss of interest in pleasure in activities
lack of reactivity to normally pleasurable stimuli.

may be pervasive or confined to a certain aspect of experience

Physical anhedonia- inability to experience physical pleasures

Social anhedonia- inability to experience pleasure from interpersonal situations

social overlaps with other disorders, physical doesn’t, so is considered a more reliable symptom of schizophrenia (Sarkar et al 2010).

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15
Q

what is diagnostic reliability?

A

the diagnosis of schizophrenia must be repeatable
there should be test-retest reliability and inter-rater reliability

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16
Q

how do you measure inter-rater reliability?
what is it for schizophrenia

A

using a kappa score
1= perfect inter-rater reliability
0.7 + is good
0= no agreement
In the DSM-V field trials (Regier et al 2013), the diagnosis of schizophrenia had a kappa score of only 0.46

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17
Q

cultural differences in diagnosis of schizophrenia
copeland 1971

A

gave 134 US and 194 British psychiatrists a description of a patient
69% US psychiatrists diagnosed schizophrenia 2% of British ones gave the same diagnosis

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18
Q

cultural differences in diagnosis of schizophrenia
Luhrman et al (2015)

A

interviewed 60 adults diagnosed with schizophrenia, 20 each in Ghana, India and the US

asked about the voices they heard. many African and Indian reported positive experiences eg playful/ advice, US reported violent and hateful

Luhrman said harsh violent voices might not be an inevitable feature of sz- suggests lack of consistent characteristics

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19
Q

Rosenhan et al 1972- being sane in insane places

A

interested in investigating whether 8 pseudo patients would be diagnosed based on objective symptoms and behaviours, or if the nature of the environment would influence the interpretation of their behaviours by the professionals who were diagnosing them

12 patients admitted into 12 different hospitals on East and West coasts of US. only symptom they were told to give the hospitals was hearing voices from a stranger that was the same gender as them, and the voices were unclear

11 were diagnosed with schizophrenia and one was diagnosed with manic-depressive psychosis. They remained in the hospitals for a range of 7 to 52 days- avg of of 19 days

Once the pseudo patients were admitted, they carried on behaving normally and told staff their symptoms had stopped. They took notes and made other observations, at first hiding this in case the staff found out, but after they realized the staff weren’t paying attention to them, they took notes freely

“Once a person is diagnosed abnormal, all of his other behaviours are coloured by that label”.

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20
Q

what is the aim of DSMs and ICD?
problem?

A

to provide a standardised method of recognising mental disorders
more subjective than hoped

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21
Q

what is validity in diagnosing schizophrenia?

A

is the diagnosis an accurate reflection of the disorder/ is it distinct from other disorders?

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22
Q

what is gender bias in validity of schizophrenia?

A

when accuracy of diagnosis is dependent on gender of individual

occurs to gender biased diagnostic criteria or clinicians basing judgement on stereotypical beliefs about gender

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23
Q

studies of gender bias in diagnosing schizophrenia

A

Broverman et al (1970)- clinicians in the US equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour- so women often perceived as less mentally healthy

Longenecker et al (2010)- reviewed studies of the prevalence of schizophrenia- found since the 1980s, men have been diagnosed with schizophrenia more often than women

Cotton et al (2009)- female patients typically function better than men, more likely to work and have good family relationships- could explain why some women have not been diagnosed with sz where men with similar symptoms may have been- better interpersonal functioning may bias practitioners to under-diagnose (symptoms masked or quality of interpersonal functioning makes case seem too mild to diagnose)

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24
Q

what is symptom overlap- validity of diagnosing schizophrenia

A

many of the symptoms are also found in disorders such as depression and bipolar

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25
research into symptom overlap
Ellason and Ross (1995)- people with DID have more schizophrenic symptoms than people schizophrenics Read (2004)- most people diagnosed with schizophrenia have sufficient symptoms of other disorders that they could also receive at least one other diagnosis
26
what is co-morbidity- validity of diagnosing schizophrenia?
the extent that 2 or more conditions occur at the same time If 2 occur together lots, then validity questioned- might be a single condition (very severe depression and sz look very similar so may be 1 condition)
27
research into co-morbidity
Buckley et al (2009)- co-morbid depression occurs in 50% of patients, and 47% of patients also have a lifetime diagnosis of co-morbid substance abuse Swets et al (2014)- meta analysis found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant obsessive-compulsive symptoms but as both uncommon, would think only a few people with schizophrenia would develop OCD and vice versa as roughly 1% of the population develop schizophrenia, and roughly 2-3% develop OCD
28
evaluate validity
research support for gender bias- Loring and Powell (1988)- 290 male and female psychiatrists used DSM. 56% diagnosed schizophrenia when patient was male/ no info about gender. 20% when female. gender bias not as evident from the female clinicians comorbidity research- 50% depression, 47%(?) substance abuse, 12% OCD 25% severe OC symptoms symptom overlap research- DID patients have more sz symptoms than sz patients schizophrenics rarely share same symptoms or outcomes. 20% completely recover, 30% some improvement, 10% significant improvement. if each person has such diff outcomes, how can we be sure they have schizophrenia
29
evaluate reliability
whaley 2001 found interrater reliability correlations for diagnosing sz as little as 0.11. also illustrated in Rosenhan study. beck et al- interrater reliability only 54% unreliable symptoms- only one characteristic symptom is required for a diagnosis if delusions are bizarre but 50 senior psychiatrists asked to differentiate bizarre and not and only had 0.4 interrater reliability barnes 2004- cultural and racial differences- ethnic minority experienced less distress associated w mental disorders due to protective characteristics and social cultures. brekke and barrio 1997- 184 sz people- white americans more symptomatic than the 2 non-white minority groups
30
what are the biological explanations for schizophrenia?
genetic (biological predisposition, polygenic)- family studies, twin studies, adoption studies neural correlates- dopamine hypothesis, neural imaging, animal studies
31
outline genetic explanations
family study- genetic element- passed on more closely related= greater risk twin study- gottesman and shields- 2 sz parents= 46% conc rate one sz parent= 13% conc rate sibling= 9% conc rate Joseph (2004)- MZ= 40.4%, DZ= 7.4% polygenic- multiple genes that contribute together 108 candidate genes
32
evaluate genetic explanations
more recent studies where the researcher is blind to whether twins are mz or dz shows lower concordance rate for mz but still higher than dz. also similarities between mz could still be environment because joseph (2004)- mz treated more similarly than dz, more similar environment, more identity confusion scientific- post mortems and genomes studied adoption study (disentangles genes and environment) - Tiennari-164 adoptees whose biological mothers had schizophrenia, 11 also received a diagnosis compared to 4 of 197 control adoptees (non-schizophrenic mothers)- but control 2% not 1% Tienari also suggests environment plays a role- all those that developed sz had dysfunctional family
33
problems with twin studies
- even twins reared apart shared womb so same environment for some time - mz may be treated more similarly than dz and experience identity confusion - common rearing patterns in family
34
revised dopamine hypothesis- biological explanation
Davis and Khan (1991)- excess of dopamine in mesolimbic pathway causes positive symptoms and deficit of dopamine in mesocortical pathway causes negative and cognitive symptoms schizophrenics have more D2 receptors on receiving neurones so more dopamine binds so more neurones fire so more positive symptoms
35
drugs that increase dopaminergic activity
dopamine agonists- stimulate nerve cells containing dopamine, causes synapses to be flooded with it normal individuals- delusions and hallucinations parkinsons- have low levels of dopamine. take these drugs and end up developing schizophrenia type symptoms (Grilly 2002) eg L-dopa and amphetamine
36
drugs that decrease dopaminergic activity
antipsychotics block activity of dopamine in the brain so eliminate delusions and hallucinations dopamine antagonists these work- evidence for dopamine being a cause
37
neural imaging
patel et al 2010- used PET scans to assess dopamine levels in schizophrenics and controls found lower levels of dopamine in dorsolateral prefrontal cortex of schizophrenics compared to controls
38
animal study of dopamine hypothesis
Wang and Deutch (2008)- induced dopamine depletion in prefrontal cortex in rats. resulted in cognitive impairment that the researchers were able to reverse using olanzapine (atypical antipsychotic thought to have beneficial effects on negative symptoms in humans)
39
evaluate dopamine hypothesis
evidence from treatment- Leucht et al (2013)- meta-analysis of 212 studies that had analysed effectiveness of diff antipsychotics compared with placebo. all drugs tested were significantly more effective than placebo in treatment of positive and negative symptoms, achieved through the normalisation of dopamine prac aps- drug treatments animal studies- dopamine in brain of rats Noll (2009)- evidence against original and revised dopamine hypothesis. antipsychotics dont alleviate hallucinations/ delusions in 1/3 of people. some have hallucinations/ delusions despite normal dopamine (blocking D2 receptors has little effect on symptoms). other neurotransmitters may play a role
40
what are psychological explanations for sz?
family disfunction (abnormal patterns of communication)- double bind, expressed emotion cognitive (schemas that see world in more threatening way
41
double bind- psychological explanation
Gregory Bateson et al (1956) suggest children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia eg 'I love you' whilst turning head in disgust- conflicting messages child fears doing wrong thing but dk what that is believe world is confusing and dangerous- reflected by disorganised thinking and paranoid delusions just a risk factor
42
expressed emotion- psychological explanation and 3 pieces of research
primarily an explanation for relapse negative emotional environment, family communication style where family members talk about patient in critical/ hostile way that indicates over concern or over involvement Kuipers et al (1983) found that high EE relatives talk more and listen less patient returning to a family with high EE is 4x more likely to relapse that a patient whose family is low in EE (Linszen et al 1997) (Noll, 2009)- family environment that is relatively supportive and emotionally undemanding may help the person with schizophrenia to reduce their dependence on antipsychotic drugs and help reduce the likelihood of relapse
43
what are the elements of EE?
verbal criticisms often accompanied by violence hostility including anger and rejection emotional over-involvement leads to stress in patient
44
cognitive explanations of delusions
interpretations of experiences controlled by inadequate information processing critical characteristic is degree to which individual perceives themself as central component in events (egocentric bias) so jumps to conclusions- relate irrelevant events to themselves and arrive at false conclusions (whispering is about them, flash of light is from God) unwilling/ unable to consider that they are wrong (Beck and Rector, 2005) impaired insight, an inability to recognise cognitive distortions and substitute more realistic explanations for events
45
cognitive explanations of hallucinations
Individuals focus excessive attention on auditory stimuli- have a higher expectancy for occurrence of voice than normal individuals Aleman (2001)- hallucination-prone individuals struggle to distinguish between imagery and sensory-based perception inner representation of an idea can override actual sensory stimulus and produce an auditory image that is as real as the transmission of actual sound hallucinating patients significantly more likely to misattribute source of self-generated auditory experience to an external source than are non-hallucinating patients (Baker and Morrison, 1998) dont go through the same processes of reality testing (such as checking external sources) than others would do
46
Christopher Frith et al (1992) 2 kinds of dysfunctional thought processes (underlie hallucinations)
meta representation- cognitive ability to reflect on thoughts/ behaviour gives us insight into goals/ intentions, allows us to interpret actions of others. dysfunction in meta representation means cant recognise own actions/ thoughts as being carried out by self- explains thought insertion central control- cognitive ability to supress automatic responses whilst performing deliberate actions instead. inability to leads to disorganised speech and thought disorder. derailment of thought
47
evaluate family dysfunction
Tienari et al (1994)- adopted children w sz bio parents were more likely to become ill than those with non bio parents. but, diff only occurred in situations where adopted family was rated as disturbed. ie illness only manifested under appropriate conditions- genetic vulnerability not enough Berger (1965)- szs reported higher recall of double bind from mother. but, their recall may be affected by sz. Liem (1974)- measured patterns of parental communication in families w sz child and found no diff Read et al (2005)- reviewed 46 studies of child abuse and sz and concluded 69% adult women in patients with sz had history of physical/ sexual abuse. men- 59% evidence for double bind is weak- based on clinical obs and (in the past) assessing mother for 'crazy-making characteristics'. also leads to parent blaming- parents have already seen child suffer and is now being blamed- ethics
48
evaluate cognitive explanations
Sarin and Wallin (2014)- found evidence to support positive symptoms having origin in faulty cognition, eg delusional patients found to show various biases (jump to conclusions). szs with hallucinations were found to have impaired self monitoring. patients w negative symptoms also displayed dysfunctional thought processes eg low expectations regarding success cognitive based therapies work so must be cognitive. eg CBTp was found to be more effective in reducing symptoms severity and improving levels of social functioning than antipsychotics reductionist- doesnt take into account neurochemical changes. But, Howes and Murray- early vulnerability factors combined w social stressors sensitises dopamine system so increased release - leads to paranoia, hallucinations which cause stress and cycle repeats not so good at explaining negative symptoms
49
4 treatments for sz
drug therapy- antipsychotics CBT family therapy token economy
50
what are antipsychotics? typical? atypical?
initial and most effective treatment reduce dopaminergic transmission typical- combat + symptoms atypical- combat + and - symptoms
51
what are typical antipsychotics? side effects?
reduces effects of dopamine so reduces (positive) symptoms dopamine antagonists- bind to receptors but dont stimulate effectiveness lead to dopamine hypothesis Kapur et al (2000) estimate that between 60% and 75% of D2 receptors in the mesolimbic pathway must be blocked for these drugs to be effective- to do this D2 receptors in other pathways are blocked so results in side effects - symptoms similar to parkinsons- stiff, tremors) - in 30% this leads to tardive dyskinesia- facial ticks - low bp, blurred vision, constipation
52
what are atypical antipsychotics? side effects?
- lower risk of extrapyramidal side effects - beneficial for negative and cognitive symptoms - suitable for treatment resistant patients only temp blocking of D2 receptors so less extrapyramidal side effects littel effects on dopamine systems that control movement stronger affinity for serotonin receptors and less for D2 - only used if typical doesnt work as can cause blood condition (agranulocytosis) so need reg blood tests. can be fatal
53
evaluate drug therapies
leucht et al- meta analysis of 65 studies where patients stabilised on typical/atypical antipsychotics, some placebo- in 12m, 64% with placebo relapsed compared to 27% on medication typical- extrapyramidal side effects (movement problems) as drugs affect extrapyramidal area of brain which controls motor skills. parkinsons related symptoms. experienced by over 50%. may also have tardive dyskinesia- involuntary movements of tongue, face, jaw, atypical- blood condition- ethical problems ross and reid- when prescribed antipsychotics, reinforces belief something is wrong. prevents patient from thinking about poss stressors so reduces motivation to look for poss solutions. reid and haslam- when asked what causes sz, public say social factors, poverty, trauma more than biological factors masks symptoms not remove- relapse however- economy
54
what is CBTp?
all patients should have CBT to treat residual symptoms that persist despite medication - correct faulty thoughts - provide coping strategies NICE recommend at least 16 sessions patient encouraged to trace origins of symptoms and evaluate content of delusions etc
55
what are the steps of CBTp?
assessment- express thoughts about experiences, discuss realistic goals engagement- therapist empathises w patients perspective and distress and explanations of distress developed together ABC- activating event, beliefs, consequences- change beliefs normalisation- say that many experience hallucinations and delusions in diff circumstances- reduces anxiety and isolation- recovery seems more possible critical collaborative analysis- gentle questioning to help understand illogical deductions and conclusions eg if voices real, why cant others hear? remain non judgemental and empathetic developing alternative explanations- healthier explanations can be thought of by patient/ together
56
2 types of strategies developed in therapy
cognitive - distraction - focus on specific task - positive self talk behavioural - relaxation techniques - loud music - behavioural experiments (test faulty thoughts) - ignore hallucinations - hw - social withdrawal/ opposite
57
evaluate CBTp
NICE- compared to just drugs, CBTp effective in reducing rehospitalisation rates up to 18m following end of treatment. also effective in reducing symptom severity and improves social functioning. however, tests of CBTp have been done when patient is taking drugs too so dk effect of CBTp alone more effective when available at diff stages. addington and addington- in initial acute phase, self reflection not really appropriate. benefit more when have group CBTp after drugs have stabilised symptoms. group means their experiences are normalised Juni et al (2001)- evidence that the problems associated w methodologically weak trials (eg not blind, not randomly allocated) translated into biased findings. Wykes et al- more rigorous study= CBTp seems weaker Jauhar et al 2014- only small effect on key symptoms of sz but even these disappeared when tested blind. uncertainty over if it works or not has led to conflicting guidance on drugs vs therapies between countries in the UK
58
what are the sz specific barriers to the success of CBTp?
- negative symptoms make it difficult to be open to change - hallucinations/delusions may make it difficult to trust that the therapist isnt working against them - poor memory recall- forget hw tasks - must be stabilised on drugs first - got to want it to work but some have relationship w voices - voices may distract them from therapists guidance - not effective in initial stages but more effective as you get more experienced w sz
59
outline family therapy
provides support for carers in attempt to make family life less stressful and reduce hospitalisation and relapse. given with drug treatment & outpatient clinical care - psychoeducation- help person and carers understand and deal w illness - form alliance w relatives who care for patient - reduce emotional climate in family and burden of care for family members - enhance relatives ability to anticipate and solve problems - reduce expressions of anger/ guilt from family - maintain reasonable expectations - encourage relatives to set appropriate limits - patient talk to family and say what support is helpful Garety et al 2008- relapse rate for individuals w family therapy- 25%, w/o- 50%
60
Pharoah et al 2010- family therapy
reviewed 53 studies on effectiveness of family intervention in europe, asia, N.america. compared outcomes from family therapy to standard care - some studies reported improved mental state, some didnt - increased compliance w medication - didnt have much effect on social functioning eg living independently/ employment - reduced risk of relapse and hospitalisation during and 24m after family therapy
61
evaluate family therapy
Paroah et al 2010 but is it effective just due to increased drug compliance. economy- back to work as less relapse, less relapse means less hospital so less money. but expensive to train/ give family therapy helps family members as well as patients. Lobban et al (2013)- analysed results of 50 family therapy studies that included intervention to support relatives. 60% had positive impact on family members eg coping and problem solving, relationships etc. however, the studies had methodological flaws Garety et al (2008)- failed to show better outcomes for patients given ff than those who just had carers. both groups had low relapse. for many people, family intervention may not improve outcomes further than good standard treatment as usual Garety et al 2008- relapse rate for individuals w family therapy- 25%, w/o- 50%
62
outline the use of token economy as a treatment for sz
using operant conditioning and positive reinforcement to reduce negative symptoms and encourage positive behaviours 2 types of reinforcer - primary- gives pleasure/ removes unpleasant states. dont depend on learning - secondary- initially no value but aquire reinforcing properties when paired w primary reinforcer. tokens are secondary reinforcer has to be given as soon as poss after target behaviour as another behaviour may have happened in between and this could be reinforced instead targets- brush hair, dress, help someone reward- food, privileges, activity token traded for reward- has to happen soon to work best
63
allyon and azrin 1968 token economy
token economy on ward of female sz patients given plastic tokens, each saying ‘one gift’ for behaviours eg making their bed/ chores. tokens exchanged for privileges eg movie. found that the number of desirable behaviours performed each day increased dramatically
64
evaluate token economy
research support- Dickerson et al (2005)- reviewed 13 studies of use of token economy in psychiatric setting. 11 reported beneficial effects directly attributed to the token economy. however, many of the studies have methodological limitations so limit impact in overall assessment Comer (2013)- major prob in assessing effectiveness is that studies tend to be uncontrolled. when a token economy is brought in, all patients take part in programme rather than having a control group. as a result, behaviours compared to past behaviours not control group. other factors may be improving patients behaviour eg increased attention from staff alloyn and azrin ethical concerns dk if it actually works. very few randomised trials carried out to support effectiveness. so, not used much as no evidence. McMonagle and Sultana (2000) suggest it may still be important if randomised trials could be carried out.
65
what is the interactionist approach?
diathesis-stress- combo of psychological/environmental and biological/genetic influences. symptoms of sz are triggered/ made worse when stressors combine w biological vulnerability. explains why not all w genetic predisposition go on to develop sz diathesis- genetic/ any biological factors in terms of vulnerability. supported by conc rates w twins. however, not 100% so environmental part too. stress- childhood trauma, living in highly urbanised environment. Varese et al (2012)- children who experienced trauma before 16 were 3x more likely to develop sz. relationship between level of trauma and likelihood of developing sz. Vassos et al (2012)- meta analysis found risk of sz in urban environments was estimated to be 2.37x higher than most rural environments. reason not clear but environment may be a contributory factor. many people live in deeply populated urban areas but only a small minority develop sz. relationship between urban stress and sz is conditional on some other factor eg biological vulnerability. several ways the combo of diathesis and stress can lead to onset of sz. eg relatively small stressors may lead to onset who is highly vulnerable or major stressor in someone w low vulnerability. they add together.
66
Tienari et al 2004- interactionist approach
procedure- hospital records for nearly 20000 women admitted to Finish psych hospitals 1960- 1979. identified those diagnosed at least once w sz. list checked to see mothers who had one/more offspring adopted. resulting sample 145 adopted offspring (high risk group) were matched w 158 wo genetic risk (low risk group) both groups independently assessed after 12yrs then followed up after 21yrs. family functioning is adoptive families was assessed- interviewers were kept blind whether mother had sz or not findings- 14/303 adoptees developed sz. 11 from high risk and 3 from low risk. however, being in healthy adoptive family appeared to have protective effect even if high genetic risk. in families of high risk group, adoptive family stress was signif predicot of development of sz conclusion- biology plays a role but environment provides protective factors
67
evaluate diathesis- stress
Tienari study limitations of Tienari study eg when assessing family functioning, this was only at one point in time- fails to reflect developmental changes in family functioning. support for usefulness of combos of biological and psychological treatments vs bio alone. Tarrier et al (2004)- studied 315 patients randomly allocated to med + CBT, med + supportive counselling, control (med only). patients in 2 combo groups showed lower symptoms than control. superior treatment outcomes shows importance of this approach Turkington et al- good logical benefit between interactionist and using combo treatments. however, fact combo is more effective doesnt necessarily mean interactionist approach is correct just like drugs working doesnt necessarily mean sz has biological origin. this is the treatment-causation fallacy mz twins not 100%