schizophrenia

Question 1

define schiz

Answer 1

a type of psychosis - a severe mental disorder characterised by a profound disruption of cognition + emotion so that contact w external reality + insight = impaired
–> this affects one’s language // thought // perception // emotions // sense of self

it affects 1% of the pop

Question 2

types of symptoms

Answer 2

positive symptoms: [atypical symptoms in addition to normal experiences / behaviour –> an excess / distortion of normal functioning]

• eg -> hallucinations [disturbances of perception on any of the senses - they’re false perceptions that have no basis of reality or is a distorted perception]
• auditory = most common hallucination
• many ppl report hearing voices // seeing ppl that tell them things or comment on their behaviour
• eg -> delusions [firmly held irrational beliefs that have no basis in reality //
• many types:
  – delusions of persecution -> others want to harm // threaten // manipulate them (like gov)
  – delusions of grandeur -> they’re important (even god-like) & have powers
  – delusions of control -> their body = under external control (by aliens // gov thru a chip)
  – delusions of reference -> event in the environment = directly relate to them (special messages to them thru TV or newspapers)

negative symptoms [atypical experiences that show the loss of a usual experience] -> (lack of functioning properly)

• eg -> avolition [a lack of purposeful + willed behaviour -> the inability // difficulty // reduction of goal-directed behaviour]
• schiz patients = reduced motivation => lowered activity levels
  -=> staying + poor hygiene + lack of persistence in education / work –> lack of meaning for life
  – co-morbidity for depression –> (D) wrong diagnosis?
• eg -> speech poverty [limited speech w limited + repetitve content]
• involves reduced freq + qual of speech + diff to spontaneously produce words

Question 3

classifications

Answer 3

[organising symptoms into categories based on which symptoms patients display]

international clasification of disease (ICD) {over diagnoses}
- mostly used in Europe
- 2 or more (-)ive symptoms = sufficent for diagnosis // 1 (+)ive symptoms
- recognises range of subtypes
– paranoid schiz (powerful hallucinations + delusions) & hebephrenic schiz (mostly neg symptoms)

associations’ diagnostic + statistical manual (DSM) {under diagnoses}
- mostly used in USA
- 2 (+)ive symptoms = present to be diagnosis
– but only if delusions = bizarre // hallucinations = voice = running commentary of one’s behaviour / thoughts or 2 or more voices conversing
- there must continuous signs of disturbance for (at least) 6 months
- interpersonal relations + self-care must be low

Question 4

define reliability

Answer 4

how consistent the results / findings are

Question 5

validity

Answer 5

[the extent to which we measure what we intended to measure]

• Cheniaux’s study -> schiz = more likely to be diagnosed by ICD (over-diagnosing) > DSM (under-diagnosing)

Question 6

(inter-rate) reliability

Answer 6

[the extent to which diff assessors agree on their assessments to diagnose a patient]
– eg -> diagnosing schiz according to ICD + DSM

• cheniaux has 2 psychiatrists (independently) diagnose 100 patients using DSM + ICD
  – found: poor inter-rater reliability -> one = diagnosing 26 w schiz according to DSM + 44 according to ICD & the other one = 13 w DSM + 24 w ICD
• questions the relaibily -> (D) for the diagnosis of schiz

Question 7

co-morbidity

Answer 7

[when 2 or more conditions occur together]
- this questions the validity of their diagnosis + classifications as there may be a single condition

• system overlap:
  –> eg -> avolition in schiz + depression
  –> eg -> hallucinations + delusions in schiz + bipolar
  … refer to table in notes
  (D) - this questions validity -> under ICD, patients may have schiz but ppl w similar symptoms may be diagnosed w schiz under DSM
• people w schiz also have:
  – 50% = depression
  – 47% = substance abuse
  – 29% = PTSD
  – 23% = OCD
• health professionals can make mistakes => misdiagnoses
  (D) this questions the validity of the classification + diagnosis of schiz as psychiatrists may not be able to distinguish schiz + depression // dep + schiz may be seen as 1 single condition

Question 8

evaluate classifications / the diagnosis of schiz

Answer 8

(D) co-morbidity / system overlap
- Bucky et al found that people w schiz also have:
– 50% = depression
– 47% = substance abuse
– 29% = PTSD
– 23% = OCD
- health professionals can make mistakes => misdiagnoses
(D) this questions the validity of the classification + diagnosis of schiz as psychiatrists may not be able to distinguish schiz + depression // dep + schiz may be seen as 1 single condition

(D) cultural bias
- research illustrates a significant diff between cultures
– african-american + english ppl w caribbean origin = more likely to be diagnosed w schiz
– (+) symptoms {like hearing voices} = more acceptable in african cultures -> due to cultural beliefs of communication w ancestors –> hence, ppl = ready to acknowledge such experiences
– when reported to a psychiatrist (of a diff culture) - this experience = bizarre + irrational
- this questions the validity of diagnoses, as psychiatrists may be influenced by their cultural standards onto those from other cultures (IMPOSED ETIC) –> and are biased towards the ‘norm’ in their culture
- this questions the reliability of diagnoses –> it suggests that there may not be agreement of the diagnoses across cultures –> so methods may not be suitable globally {as there won’t be consistent classifications / diagnoses)
– suggesting that patients can display the same symptoms but get diff diagnoses due to their ethnic background)

(D) gender bias
- Longnecker et al (2010)
– reviewed studies of the prevalence of schiz –> since the 80s, men = diagnosed w schiz more often than women
- women = more high functioning than men - so their symptoms = overlooked
- Loring and Powell (1988) found some behaviour = regarded as psychotic in males but not regarded as psychotic in females.
[add more detail]

Question 9

what are all of the biological exps

just list them

Answer 9

genetic explanations {twin + adoption + family studies}
the dopamine hypothesis
neural correlates

Question 10

briefely describe genetic explanations

Answer 10

how ppl w SZ carry allels that inc the risk of developing SZ

Question 11

family studies for biological explanations

Answer 11

[finds individuals w schiz + determines whether their bio relatives = similarly affected more often > non-relatives]

• schiz runs in families
• as genetic similarity increases = probability of sharing schiz incs

(A) strong evidence from Gottesman (1991) for genetic vulnerability
- kids w 2 schiz parents = CC rate of 46%
– 1 schiz parent = CC rate of 13%
– siblings w schiz = CC rate of 9%
-> (CP) twin studies may over-exaggerate the importance of genetics environment can be an influence
– eg -> if they’re bullied or overworked this incs stress (diathesis-stress model?)

Question 12

twin studies for bio exp

Answer 12

[if MZ twins = more concordant than DZ twins => similarity = due to genes]

• Joseph (2004)
  – meta-analysis of twin studies before 2001 = combined CC rate of 40% for MZ twins & 7% for DZ twins

(D) twin studies may over-exaggerate the importance of genetics environment can be an influence
– eg -> if they’re bullied or overworked this incs stress (diathesis-stress model?)

Gottseman + Shields (1960s)
- CC of 74% for MZ twins
- CC of 24% for DZ twins

Question 13

adoptions studies for bio exp

define + study?

Answer 13

[studies of genetically related individuals that = reared separately]

• Tienari et al (2000)
  – found 164 adoptees w/ schiz mums -> 11 (6.7%) = diagnosed w schiz {compared to the 2% in the control grp of 197 adoptees}
• shows that genetics > environment –> There are particular gene alleles that increase the risk of developing schizophrenia.

Question 14

briefly describe what the D hypothesis shows

Answer 14

ppl w SZ experience an imbalance of neurotransmitters in the brain

Question 15

the dopamine hypothesis

Answer 15

can be seen if one’s SZ = treated w APs (shows that D = main factor for development of SZ)
- dopamine = invloved in attention + processing reward
- SZs have high D in + near the basal ganglia
- (the mesolimbic system) -> high levels of dopamine => more electrical acticity (due to excitiory D)

original H:
- claims that excess D in certain brain reigons = associated w (+) symptoms
- suggests that SZ = due to abnormal brain function (from neurotransmitters)
- **excess of D (over-active neruons) in mesolimibic pathway => (+) symptoms **
- research -> schiz ppl = abnormally high D2 receptors (@ receptor site) on recieveing neurons
=> more D binding => more neurons firing => overstimmed

revised H:
- claims there’s excess D in mesolimbic pathway => overactive neurons (+) symps
- Davis et al (1991)
- **D deficit in pre-frontal cortex **areas
– responsible for descision making // thinking .. => (-) symptoms
(A) neural imaging -> Patel et al (2010)
– used PET scans -> found low D levels in dorsolateral prefrontal cortex of schiz ppl

Question 16

evaluate the dopamine hypothesis

Answer 16

(A) - research support from drug studies
- healthy ppts = given D inducing drugs
– they experience (+) symps
- SZs ppl = given D decs drugs
– it reduced their (+) symps

(D) drugs that dec D levels don't always prevent (+) symps
- Noll (2009) reviewed drug studies where SZs = given D decs drugs
- for most = it worked
- for 1/3 -> drugs didnt reduce (+) symps => meaning symps = not caused by high D in mesolimbic system => could be other causes

(D) supporting evidence = sometimes inconclusive
- Moncrieff (2009) reviwed studies abt D hypothesis
- D incing drugs also impact other neurotransmitters (like S // noradernaline) => hallucinationscan be caused by other neurotransmitters
- also post-mortem studies showed SZ’s brains dont always have inced D compared to control grps

Question 17

breifly explain what neural correlates show

Answer 17

SZ = caused by abnormal brain structure

Question 18

neural correlates

(+) & (-) symptoms for it

Answer 18

[measurements of structure / function of the brain that correlates w symptoms of schiz]

• • low* activation levels in superior temporal gyrus + anterior cingulate gyrus = found when experiencing auditory hallucinations
    – hence -> reduced activity = in these areas = neural correlate of auditory hallucincation {(+) symptom}
• ventral striatum = involved in anticipation of reward
• Juckel et al (2006)
  – found negative correlation between activity levels in VS & the severity of (-) symptoms -> hence - activity in VS = neural correlate of the (-) symptoms of schiz
  
  • low activity = high avolition

Question 19

evaluate biological explanations

Answer 19

(A) strong supporting evidence for family studies
- Tienari et al (2004) -> adoption study found kids of SZ = heightened risk of SZ - even if adopted into noSZ families
- shows genetic factors make ppl more vulnerable to develop SZ
– doesn’t mean it’s purely genetic -> but available evidence => genetic susceptibilty = v important

(A) supporting research for D influence
- evidence for D hypothesis comes from drug treatment success
- Leucht et al (2013) found APs = more effective > placebo when treating symptoms
- Curran et al (2004) D agonists that inc D => worsen SZ + produces SZ-like symptoms in non-sufferers
(CP) ethical issues taking away medicantion + replacing w placebos can make ppl relapse = unethical
(CP) the evidence shows only high correlation -> not causality
(CP) Noll (2009) argues AP drugs don’t alleviate (+) symps
- sometimes, (+) symps occur w/out abnormal D levels -> hence blocking D2 receptors won’t effect symptoms

(D) there’s flaws in twin studies
- MZ = treated more similarly but DZ & encounter more similar environemnts (same friendship grps …)
– environ factors of DZ + MZ twins = diff (not standardised) => diff outcomes that arent’ caused by genetics
- hence, TS may show inly environmental differences -> undermines research
- also, TS = never 100% -> shows that bio = not only . main factor and evironment = clearly has influence over development of schiz

(D) neural correlates don’t show causality
- doesn’t prove brain activity in certain reigons causes the symp
- possible tht another factor causes it
- cannot support int val

(D) SZ = more likely caused by family dynamic > genetics
- due to common rearing patterns & not heredity
- (-) emotional climate => stress beyond coping mechanisms => triggering schiz episode
- suggests than psych factors = important

Question 20

what is the excess of
D?

Answer 20

hyperdopminergia

side effects = symptomatic of Parkinson’s disease

Question 21

cognitive explanations of schiz

dysfunctional thought processes

Answer 21

[dysfunctional mental processes => schiz symps]

dysfunctional attention
- ppl w DA -> easily distracted + hyperfocuses on irrelevant details

dysfunctional reasoning -> 2 types of DR:
- jumping to conclusions bias -> [irrational reasoning // asumptions based on little evidence]
- persecution bias -> [the irrational belief people want to harm them // treat them unfairly] {can be seen in (-) symps - delusions of persecution}

positive symptoms:
- the combination of DA + DR => delusions
– DA => patients overfocus on small irrelevant details of real events / coincidences {making the events seem more important than it acc is}
– when patients explain these coincedences - DR makes it irrational => delusional belief

• DA -> one may overfocus on their thought -> may seem bizzare & won’t realise they generated the thought -> believes it’s someone talking to him {auditory hallucination}
  – or they may overfocus on a mental image -> believe that’s happening IRL (can’t distinguish that it’s a thought) {hallucination}
  overall: (overfocused on thoughts => they feel real => cant differentiate what’s real and what’s imagined => hallucination)

negative symptoms:
- tries to ignore / shut down their thoughts -> this is v draining => stop wanting to talk (communicating) {speech poverty}
– difficult for them to socialise whilst battling mental processes
- patients = overwhelmed by Ds + Hs + abnormal experiences => they want to avoid this - done thru isolating {negative reinforcement} -> hence avolition

Question 22

evaluate the cognitive explanations of schiz

Answer 22

(A) study support from O’Carroll
- he reviewed studies that examined schiz patients’ mental processes
– tested for DA (aking ptts to press a button when a red dot appeared on the screen - has to ignore blue dots)
– tested for DR (ptts had to solve logic puzzles - to test reasoning)
- found: 75% of patients = dysfunctional mental processes (AR + impaired working memory + low IQ + impaired R)
–> hence supporting cog exps as DMP => symptoms of schiz

• O’Carroll also reviwed studies abt ppl at risk of schiz w no symps yet
• longitudinal study (to see if they would dveleop schiz)
• those who developed schiz had DMP - which existed before they displayed schiz symps
  – maybe cause + effect relationship

(D) ignores biological factors
- genetic causes & how APs are effective = ignored
– states that only DMP cause symps if schiz - despite research (Gottseman + Shields …) supporting bio exps

Question 23

cognitive treatments

Answer 23

CBT
- aim = to challenge + correct patients’ irrational beliefs + thought processes - which cause symps of schiz
– ppl w schiz have constant irrational beliefs (delusions)
- doesnt treat SZ -> but does treat DMP
- not appropriate for all patients
– severe symps -> APs

process:
- explanation / assessment -> therapist explains process & patient shares their (irrational) beliefs + esperiences + concerns & realisitic goals = set
- engagemet -> therapist = empathetic w patient’s perspective
- normalisation -> tells patient that others experience this too - they’re not alone
– reduces feelings of alienation => less isolated => decreased negative symps (avolition)
- challenges patients thoughts -> can be done thru ABC model
– Activating event & irrational beliefs & behavioural + emotional Consequesnces
– Dispute thoughts thru critical collaborative analysis [gentle questioning => patient acknowledges + understands irrational thoughts, w/out causing stress] & patients come up with alternative explanations w logical reasoning
– patients idetify the bias (JTCB // PB) in their reasoning (DR)
– Effects of this on their new behaviour (how this impacts them to act diff -> corrected thoughts that = use logical reasoning)

• can use reality testing - [places them in sitch so they can react normally] -> {high validity} => induces rational thoughts
• patients can be given beavioural assignments - outside of sessions to maintain what is taught (doesn’t forget) => longer-lasting effets

*explanation -> normalisation -> challenging -> alt exps

Question 24

evaluate the cognitive treatment

Answer 24

(A) study support from review from NICE (national insitute for health + care excellence) (2014)
- when CTB = compared w APs alone -> it was effective in decs rehospitalisation rates - up to 18 months
- also reduces symp severity + improves social functioning
- CBT = effective LT therapy > APs -> as it provides strategies to manage symps beyond therapy
(CP) most studies investiagte CBT whilst patients = using APs -> hard to establish how effective CBT is

(D) difficult to access
- estimated that 1/10 in UK that can benefit from CBT have access
- Haddock et al (2013) found: only 6.9% of patients in NW England = offered CBT
- thus, limiting the effectiveness as patients = unable to participate

(D) requires motivation for full length + effectiveness
- also requires commitment to many sessions + self-awareness + willingness to engage
- patients may lack this (avolition) (positive symps -> lack of sekf-awareness)
- CBT may not be appropriate for all
(CP) CBT = more effective @ certian stages of schiz
- Addington (2005) claim: self-reflection = no appropriate during intial phase of SZ
- after stabling symps w APs - ppl may then benefit from group-based CBT
– helps to normalise their experience
– those w better realisation + undertsnadng of their symps = benefit more (in latter stages of SZ)

(D) provokes ethical issues
- when challenging one’s paranoia => intefering w their freedom thought (may impose therapist beliefs onto them)
-> eg -> challenging delusions abt contolling gov can stray into modifying their politics

Question 25

(nurture) what are the family disfunctions?

the 3 theories

Answer 25

[refers to any forms of abnormal processes within a family: conflict, communication problems, cold parenting, criticism, control and high levels of expressed emotions -> may be risk factors for the development + maintenance of schiz]

schizophregenic mother
- Fromm-Reichmann (1948)
- mother = cold + controlling & father = often passive
- leads to excessive stress + distrust as family = filled w tension + secrecy
- triggers disorganised thinking + paranoidb delusions -> ultimately schiz

double-bind theory
- Bateson et al (1972)
- child recieves mixed messages -> one parent may allow smthin while the other doesn’t (2 diff messages from parents) => child can’t please both -> feel trapped // confused
- this can also be done thru just one parent (if what things they say conflict)
– their punishment = withdrawal of love
- this causes stress + confusion (incs risk of developing schiz)
- leads to understanding the world as confusing + dangerous
- triggers psychotic thinking + paranoid delusions (schiz)

expressed emotion
- Brown et al (1958)
- EE = negative emotions + critism
- family = exaggerated involvement in their life
– needless self-sacrifice + critical + controlling + hostility -> inlcuding anger + rejection (sometimes can be violent)
- leads to excessive stress beyond impaired coping mechanisms
– anxiety may cause them to isolate
- triggers relapse in schiz patients // may trigger onset in a genetically vulnerable person (due to their genetic make-up) {diathesis-stress model}

Question 26

eval psychological exps

Answer 26

(A) supporting evidence from Read et al (2005)
- reviewed 46 child abuse studies
– found: 69% of SZ adult women & 59% of SZ adult men = history of pshysical // sexual abuse in childhood
- Berry et al (2008)
– adults w insecure attatchments = more likely to have SZ
- this clearly portrays FD as a risk factor for SZ
(CP) most evidence = gathered after development of SZ symptoms -> patients may have distorted view of memories (not accurate) => low validity
– reductionist + deterministic?

(D) Harrington (2002) claimed there’s not enough evidence to claim mums provoke SZ
- little evidence for schizophregenic mother + double bind theories
– = based on clinical observations & early evidence of assessing mum’s personality {they’re not studying like w bio, they can only go off behvaiour and infer - some bias? may not always be objective}
- ‘parent-blaming’ = large issue
– parents = likely to bear life-long responsibilty for their child & may undergo further trauma {from recieving blame of the condition}
(CP) this is a socially sensitive issue
- from hospital to community care (often involving parental care) => decline of schizophregenic mothers + double bind cases {parents no longer tolerate them}

(A) Stirling et al (2006) for research support
- compared 30 SZs w 18 control ppl on a range of cognitive tasks
- used the stroop test [name the colour of the words]
– this shows how ppl suppress the impulse to read the word first {testing the central control function}
- found: SZ ppl = twice as long to answer correctly (compared to ctrl grp)
(CP) lack of credibility -> it doesn’t expand on the origin of cognitions {shows proximal causes but not distal}

(D) hard to distinguish psych + bio exps {they have the same / similar outcomes + symptoms}
- the exps (on their own) provides partial // inconclusive evidence to confirm theories
- can refer to diathesis-stress model -> diathesis (enviro trigger) can be bio or psych

(D) bi-direction of causality
- it’s unclear whether cognitive factors = cause or result of neural correlates + abnormal neurotransmitter levels in SZ
- this decs val of both exps & effecs which treatements used to treat the cause of SZ

Question 27

what is metarepresentation

Answer 27

[insight into our intentions -> interprets actions

• Frith et al (1992) -> identified 2 types of dysfunctional thought processing
• if there’s a dysfunction in metarep means it disrupts ability to recognise / identify one’s actions + thoughts
  – thinks that this = done by someone else - not themsleves
• this explains (+) symptoms {like Ds + thought insertion}

Question 28

Central Control

define

Answer 28

[cognitive ability to supress automatic responses as we peform actions w intent instead]

• inability to suppress automic thoughts => disorganised speech + thought disorder
• for SZ patients - certain words may trigger association, and they cannot suppress their expressions for these automatic assosiations

Question 29

what is a type of biological treatment

how does it help

Answer 29

• drug therapy [use of antipsychotic medication to reduce SZ symptoms
• helps ppl to function + improves feeling of subjective mental health
• antipsychotic = lowers dopaminergic in brain areas associated w SZ symptoms {nerual correlates}

Question 30

what are the 2 types of drugs

APs

Answer 30

typical antipsychotics (traditional)
- lowers the amount of D {in mesolimbic system}
- they bind to D (post-synaptic) receptors => blocks receptors (doesn’t stimulate them) => decs actions of D
– less D entering post-synaptic neuron => less neurons firing => less stimulated + less (+) symptoms
- suffers from side-effects
- eg -> chlorpromazine = D antagonist

atypical antispychotics (newer)
- there is less disruption to dopamine activity in all areas of the brain
- bind + block D receptors - only temporarily -> then quickly dissociate to allow norm D transmission
– thought to be resposible for less side effects
- it also impacts S
– adresses both types of symptoms
- eg -> clozapine + rosperidone

Question 31

side effects of APs

Answer 31

traditional (traditional) APs:
- according to D hypothesis, high D in mesolimbic system => schiz
- APs block D receptors (they block all receptors - not just in the mesolimbic system
– Tardive Dysinesia [involuntary neurological movement disorder] -> caused by D blocking drugs effecting the motor cortex {can lose control over movement => muscle spasms}

• APs can inc risk of heart problems // obesity // diabetes
• (-) symps = caused by low D in pre-frontal cortex
  – APs dont inc D in frontal cortex => hence it doesn’t treat (-) symptoms {may even worsen them}

newer (atypical) APs:
- fewer side effects (as D receptors = onyl temporarily blocked)
- more effective at reducing (-) symptoms

Question 32

evaluate APs

Answer 32

(A) Lecuht (2001)
- meta analysis [when reserachers combine results + studies w simillair aims] of 65 studies that compared the effects of APs w placebos
- ppl that took APs = less (+)ive symptoms > control grp (placebos)
– these ppl = less likely to relapse to (+) symps

(D) Crossley (2010)
- meta analysis from 15 studies comparing T + AT APs
- found no significant diffs when preventing symps
- T APs = side effects (muscle spasms + stiff muscles + health risks {heart probs + diabetes …})
- AT APs = less side effects
– the only one SE = weight gain

(D) limited effectiveness of AT APs
- sometimes don't prevent relaspe 

(D) relapse
- ppl w schiz = a high likelihood of relapsing if they stop taking their medication
– This is important because drugs might not be treating the underlying cause of the disorder - they may just be blocking the symptoms -> may be in need of CBT instead

Question 33

token economies

Answer 33

[patients = given tokens when they display positive adaptive behaviours - which can then be used in exchange for rewards] -> encourages patient to repeat behaviour {operant conditioning so the oatient learns new positive behaviour -> thru (+) reinforcement}

classical conditioning {used to associate the token w reward to motiavte patient}
- at first token = NS
- after he develops a CR - it becomes CS (and a reinforcer)

Question 34

evaluate token economies

Answer 34

(A) research support
- reviewed 13 TE studies
- 11/13 = improvement in patients’ behaviours
- effective when used alongside APs + CBT -> implies they’re effctve in managing behaviours

(D) no control group
- in most studies TE was used w all patients @ the same time -> there’s nothing ot compare the behaviours to - to show the difference TEs make {could be due to extraneous variables}
– can’t guarentee causality (could be just correlation)

(D) can be considered unethical
- can be humiliating + disrespectful towards adults {they’re treated like children - condesding manner}
- causes (-) emotions

(D) may not be useful outside hospital setting -> they have limited use

{over dependant on rewards -> they would not behave well if there’s no rewards (which there aren’t IRL)
- patients would expect to be rewarded fr correct behsviour -> if this doesn’t happen they could relaspse -> can’t manage behaviour w/out external help}

• patients should be given tickets immeditaely after (+) behaviour = shown -> if it;s goven mcuh after, the patient may have forgotten their good behaviour and will not associate (+) behaviour w rewards (no CS)
  – to do this - bhevaiour needs to be monitored contasntly -> easier in hospital setting & unlikely in normal settings

Question 35

interactionist exp

define + D-S model (brief)

Answer 35

[acknowledges there’s a range of factors (including bio + psych) = involved in development of schiz]
- bio exps = more reductionist

• diathesis = increased risk of developing illness due to biological factors {pre-diposed to illness}
• stress (from environment)
• IA believes bio + psych therapies / treatments should be used (APs + CBT)
  – Turkington (2008) suggest bio meds + use of CBT to relieve psych symptoms

diathesis - stress model
- this exp argues you can only develop schiz if u have bio risk and a stressor (have to have both) -> if they only have one then they won’t develop schiz
- ppl w diathesis only develop schiz if they experience enough psych stress (environmental)

Question 36

diathesis stress models?

Answer 36

original D-S model:
- bio + stressor = needed
- Meehl (1962):
– diathesis = only genetic -> there’s a single schizogene => development of schizotypic personality
– no gene = can’t develop SZ

modern D-S model:
- many genes (208) can cause schiz {polygenic}
- Ripke (2014) argues: there’s no single schizogene
– range of factors can make one vulnerable -> both bio + psych (eg -> psychological trauma)
- Read (2001) suggested: if psych trauma = severe enough + @ young age => alters brain development => less resitant tp stress (easily distressed)
- there are stressors beyond family dysfunctions (like cannabis) -> x7 more likely to develop schiz

Question 37

evaluate the interactionist explanation for schiz

Answer 37

(A) Tiernari et al (2004) - research support
- investiagted combos of gentic vulnerability + parenting styles w adoption studies
- 19,000 Finnish mums w SZ -> their child rearing methods (from new family) = conflict + critism
- kids only developed schiz if they had diathesis + environment stress
- compared adoptees w control grp -> experimental grp = more likely to develop schiz
– significant risk factor of development of schiz for kids w only genetic risk

(A) Houston (2008) - research support
- found childhood sexual trama = vulnerability whilst use of cannabis = stress factor

(A) Brown + Birley (1968)
- iterviwed patients ( & their families) who had recently developed SZ
- found: 3 weeks prior to SZ devlopment, 50% = experienced stressful life event
– support how stress acts as trigger for development of schiz

(A) Dury (1996)
- IA suggests to combine treatments (due to the 2 diff natures of schiz devlopment)
– APs (for decs (+) symps + CBT (for dysfunctional mental processes + decs (-) symps) + family therapy (prevents relapse + decs stressful environments)
- found 25-30% reduced recovery time + (+) symps for patients w a combo of CBT + meds
(CP) hard to distinguish the effectiveness of psych and bio treatments and which cause had more of an impact
(CP) therapies = expensive and sometime low availability