Schizophrenia Flashcards
what is schizophrenia?
severe mental disorder characterised by profound disruption of cognition and emotion
affects language, thought, perception, emotions, sense of self
how is schizophrenia diagnosed?
DSM-V (used in US)
ICD (used in Europe)
what are positive symptoms?
eg?
those that appear to reflect an excess or distortion of normal functions
- hallucinations
- delusions
- disorganised speech
- grossly disorganised or catatonic behaviour
what are hallucinations?
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.
what are delusions?
what are the different types?
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.
what is disorganised speech?
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)
what is grossly disorganised/ catatonic behaviour?
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
what are negative symptoms?
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.
What is the deficit syndrome?
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)
examples of negative symptoms
speech poverty (alogia)
avolition
affective flattening
anhedonia
what is alogia
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
what is avolition?
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
what is affective flattening?
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)
what is anhedonia
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).
what is diagnostic reliability?
the diagnosis of schizophrenia must be repeatable
there should be test-retest reliability and inter-rater reliability
how do you measure inter-rater reliability?
what is it for schizophrenia
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
cultural differences in diagnosis of schizophrenia
copeland 1971
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
cultural differences in diagnosis of schizophrenia
Luhrman et al (2015)
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
Rosenhan et al 1972- being sane in insane places
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”.
what is the aim of DSMs and ICD?
problem?
to provide a standardised method of recognising mental disorders
more subjective than hoped
what is validity in diagnosing schizophrenia?
is the diagnosis an accurate reflection of the disorder/ is it distinct from other disorders?
what is gender bias in validity of schizophrenia?
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
studies of gender bias in diagnosing schizophrenia
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)
what is symptom overlap- validity of diagnosing schizophrenia
many of the symptoms are also found in disorders such as depression and bipolar
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
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)
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
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
weber et al 2009- looked at 6mil hospital discharge records and found 45% co-morbidity rate w other psychiatric disorders. also co-morbidity with non-psychiatric disorders eg type 2 diabetes
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
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
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
family studies- biological explanation
more common among bio relatives
more closely related= greater risk
gottesman and shields-
concordance rate for child with 2 schizophrenic parents= 46%
one schizophrenic parent= 13%
sibling= 9%
twin studies- biological explanation
problems
Joseph (2004)- MZ= 40.4%, DZ= 7.4%
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
problems:
- even twins reared apart shared womb so same environment for some time
- mz may be treated more similarly than dz and experience identity confusion
adoption studies- biological explanation
problem
disentangles genetics and environment
Tienari et al (2000)- of 164 adoptees whose biological mothers had schizophrenia, 11 also received a diagnosis compared to 4 of 197 control adoptees (non-schizophrenic mothers)
problem- stress of adoption. control is 2% when should be 1%. adoptees told about history of mental illness so may treat child differently
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
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
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
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
animal studies
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)
evaluate genetic explanations
evidence- Gottesman shows how genetic similarity and shared risk of sz are closely linked, adoption studies, important but not only thing (not 100% conc rates)
sz appears to run in family could be because of common rearing patterns. eg expressed emotion
joseph (2004)- mz treated more similarly than dz, more similar environment, more identity confusion. diff between mz and dz could still be environmental not just genetic
joseph 2004- unlikely that parents who adopt children with sz bio parent are no diff to parents who adopt child w normal background. Denmark and US, parents informed of bckg of children before adoption. Kringlen- ‘Because the adoptive parents evidently received information about the child’s biological parents, one might wonder who would adopt such a child.’
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
Moncrieff (2009)- evidence for the dopamine hypothesis isnt. stimulant drugs shown to induce schizophrenic episodes but these affect lots of neurotransmitters.
evidence for dopamine in post-mortem brain tissue is negative/ inconclusive
other confounding sources of dopamine release, such as stress or smoking, have rarely been considered
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
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
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
expressed emotion- psychological explanation
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
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
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
cognitive explanations of hallucinations
Hallucinating individuals focus excessive attention on auditory stimuli (hypervigilance)- 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
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
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
evaluate cognitive explanations
Sarin and Wallin (2014)- reviewed research relating to model of sz. found supporting evidence for claim that positive symptoms have origin in faulty cognition. eg delusional patients found to show various biases eg jumping 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
deals adequately with cognitive impairment but doesnt explain other aspects eg neurochemical changes. Howes and Murray (2014)- adress this with integrated model of sz. argue that early vulnerability factors combined with exposure to social stressors sensitises the dopamine system, causing it to increase the release of dopamine. increased dopamine activity results in paranoia and hallucinations. this contributes to stress experienced by individual, leading to more dopamine release, more symptoms, and so on
4 treatments for sz
drug therapy- antipsychotics
CBT
family therapy
token economy
what are antipsychotics?
typical?
atypical?
initial and most effective treatment
reduce dopaminergic transmission
typical- combat + symptoms
atypical- combat + and - symptoms
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
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
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- ethical problems
atypical better than typical as no extrapyramidal side effects, combat + and - symptoms
crossley et al- meta analysis of 15 studies to study efficacy and side effects of atypical vs typical in early phase treatment of sz- no sig diff in terms of effect on symptoms but diff side effects- atypical gained more weight, typical more side effects
dont treat cause just mask symptoms- relapse afterwards
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
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
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
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
evaluate CBTp
NICE found that 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
lack of availability due to few trained therapists, time consuming treatment, expensive
meta analysis can reach unreliable conclusions about effectiveness as study quality isnt taken into account. some dont randomly allocate ppts to CBTp/ control group, some dont do it blind. Juni et al (2001)- evidence that the problems associated w methodologically weak trials translated into biased findings. Wykes et al- more rigorous study= CBTp seems weaker
Jauhar et al 2014- only small therapeutic effect on key symptoms of sz but even these small effects 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
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
what is family therapy?
how does it work?
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%
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
evaluate family therapy
Paroah et al 2010
is it effective due to improvement in clinical markers or just because it increases medication compliance
methodological issues w family therapy studies. random allocation- most of studies in Pharoahs analysis were from People’s republic of China where random allocation is said to be used but actually isnt. bias as raters werent biased to conditions
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
what is token economy?
how does it work?
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
FINISH?
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
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.
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.
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
evaluate diathesis- stress
increased risk isnt necessarily genetic. eg can be result of brain damage caused by environmental factors. Verdoux e al (1998)- estimated risk of sz in individuals who experienced obstetric complications at birth eg long labour causing oxygen deprivation, is 4x greater than those w no complications
Romans-Clarkson (1990)- no urban rural diffs in mental health among women in new zealand. studies that did find a diff said that diffs disappeared after adjusting to socioeconomic diffs of the 2 groups. so, likely an oversimplification
difficult to determine casual stress as stressor may have occurred earlier on in life and influence how people respond to later stressful events. Hammen (1992)- maladaptive methods of coping in childhood means person doesnt develop effective coping skills which compromises resilience and vulnerability. may make life in general more stressful
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. Turkington et al (2006)- not really poss to use combo of treatments wo interactionist approach. 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
