Psychology - Schizophrenia

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AQA Psychology Schizophrenia

65 Terms

1

positive symptoms of SZ (+ definitions of them)

  1. hallucinations - bizarre, unreal perceptions of the environment that are usually auditory but may also be visual or tactile

  2. delusions - bizarre beliefs that seem real to the person but are not. They may be paranoid or inflated beliefs about a person’s power and importance

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2

negative symptoms of SZ (+ definitions of them)

  1. avolition - the reduction of interests and desires for activities that are available to the person as well as an inability to initiate and persist in goal-directed behaviour

  2. speech poverty - characterised by a lack of speech fluency and productivity in order to reflect slowing or blocked thoughts

  3. catatonia - staying in the same position for hours

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3

reliability of diagnosis of SZ

  1. inter-rater reliability = a diagnosis may be given by one doctor and therefore the same diagnosis should be given by another

  2. test-retest reliability = the same diagnosis should be given at two points in time

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STRENGTHS of reliability of diagnosis (x3)

  1. CHENIAUX ET AL = 2 psychiatrists independently diagnosing 100 patients using DSM (26 vs 13) and ICD (44 vs 24)

  2. different treatment may be given so important to be right

  3. READ - test-retest reliability was poor (38% concordance)

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5

validity of diagnosis of SZ

the extent that the diagnosis represents the disorder accurately

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STRENGTHS of validity of diagnosis (x4)

  1. ROSENHAN = ‘psychiatrists could not distinguish the sane from the insane’ as they diagnosed ‘pseudo-patients’ who claimed to hear voices saying ‘thud’, ‘empty’ and ‘hollow’

  2. different treatment may be given so important to be right

  3. ROSENHAN - pseudopatients given drug treatment and labelled with SZ even when not exhibiting symptoms + follow up study = 21% real patients detected as fake

  4. may be due to co-morbidity, symptom overlap, culture bias and gender bias

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symptom overlap of SZ

where there is considerable overlap between symptoms of SZ and other disorders so hard to know which disorder to diagnose

e.g. bipolar = positive symptoms like delusions + depression = avolition

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8

STRENGTHS of symptom overlap (x2)

  1. ELLASON + ROSS - people with dissociative identity disorder show more schizophrenic symptoms than those diagnosed with SZ

  2. most people with a diagnosis have enough symptoms of other disorders that they could receive at least one other diagnosis

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9

co-morbidity in SZ

where patients may suffer from two or more mental disorders at a time so difficult to know if symptoms are due to SZ

e.g. SZ + anxiety/depression

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10

STRENGTHS of co-morbidity (x2)

  1. SZ + OCD - roughly 1% of population develop SZ vs 2-3% for OCD but evidence says they appear together more often than 1%

  2. SWERS - meta-analysis shows 12% of SZ patients fulfilled almost all the diagnostic criteria for OCD and 25% displayed significant OCD symptoms

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11

culture bias and SZ

there is significant variation between countries of what is viewed as schizophrenic

e.g. hearing voices is considered normal in African cultures during grief as believe they are communicating with ancestors but in the UK that would receive a diagnosis

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12

STRENGTH of culture bias (x1)

  1. KEITH ET AL - 2.1% of African-Americans are diagnosed with SZ compared to 1.4% of white Americans (may be due to stress as strong evidence suggests immigrants are more likely to suffer from mental disorders than indigenous population)

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13

gender bias and SZ

accuracy of the diagnosis depends upon the gender of the individual

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14

STRENGTH of gender bias (x1)

  1. LONGENECKER - reviewed studies of the prevalence of SZ and since the 1980s, significantly more men have been diagnosed than woman (may be due to men being more genetically vulnerable or gender bias i.e. women function better)

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15

family studies of SZ

GOTTESMAN - concordance rate between degree of closeness and risk of developing SZ

sibling = 9%

DZ twin = 17%

MZ twin = 48%

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16

STRENGTH of family studies (x2)

  1. impossible to seperate genes and upbringing as relatives share the same environment so may be a psychological explanation instead

  2. most SZ patients did not have an SZ parent

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17

twin studies of SZ

MZ twins share 100% of genes and so we would expect they would both exhibit or not exhibit SZ if genetic basis

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18

STRENGTH of twin studies (x1)

  1. GOTTESMAN - concordance rate is higher for MZ than DZ twins suggesting a genetic basis

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19

LIMITATION of twin studies (x1)

  1. not 100% concordance rate for MZ twins but would expect to see this if genes was the only factor as they share 100% of genes

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20

adoption studies

removes environmental factor as share genes with those in another household/environment

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21

STRENGTH of adoption studies (x1)

  1. TIENARI - 6.7% of adoptees whose biological mother had SZ also had SZ vs 2% of adoptees whose biological mother wasn’t diagnosed (strong likelihood of genetic component as high above the baseline measure of 1%)

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LIMITATION of adoption studies (x1)

  1. not as high a risk as when the children lived with their mothers (increased to 13%) suggesting environmental impact

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23

neural correlates

assuming a relationship between measurements of the structure of the brain/incidence of neurotransmitter activity and schizophrenic symptoms

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24

decreased brain weight

enlarged ventricles meant larger cavities in the brain which contain cerebrospinal fluid

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25

STRENGTHS of neural correlates (x3)

  1. SUDDATH - MRI scans on identical twins showed the one with SZ had enlarged ventricles (vs one without)

  2. JUCKEL - reduced levels of activity in the ventral striatum (controls anticipation) in SZ patients compared to control group

  3. ALLEN - lower levels of activation in the superior temporal gyrus when brain scanned those experiencing auditory hallucinations

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LIMITATIONS of neural correlates (x2)

  1. those with bipolar also have enlarged ventricles so could be too simplistic

  2. correlation causation problem - cannot be certain an area of the brain that is low in activity is causing the symptoms as symptoms may be causing less information to flow through that brain area

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27

dopamine hypothesis for positive symptoms

caused by an excess of dopamine in the mesolimbic pathway in the centre of the brain

possibly due to neurons that transmit dopamine firing too easily or too often as schizophrenics thought to have abnormally high numbers of D2 receptors on receiving neurons

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dopamine hypothesis causing negative symptoms

caused by a deficit of dopamine in areas of the prefrontal cortex

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STRENGTHS of dopamine hypothesis (x5)

  1. anti-psychotic drugs inhibit symptoms of SZ and found to block dopamine receptors = correlational result

  2. drug L-dopa used for Parkinson’s disease increases dopamine + a side-effect is schizophrenic like symptoms

  3. post-mortem examinations revealed more dopamine receptors in certain parts of the brain for SZ patients

  4. biochemical explanations complimentary to genetic ones as an inherited gene could cause dopamine receptor abnormalities

  5. neural imaging using PET scans found lower levels of dopamine in the prefrontal cortex of SZ than controls

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LIMITATIONS of dopamine hypothesis (x3)

  1. correlational result + drugs don’t work for everyone and mainly only for positive symptoms meaning not the only factor

  2. psychological explanations reject view it is physical factors as a lack of concordance of 100% shows it cannot account for all causes of SZ

  3. interactionist approach may be better (biology only predisposes)

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typical anti-psychotics (how they work + an example)

they are dopamine antagonists meaning they bind to but do not stimulate the D2 receptors in the mesolimbic pathway. this prevents the dopamine reaching the receptors to stimulate them, eliminating positive symptoms within a few days

e.g. chloropromazine

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KAPUR

estimates about 70% of D2 receptors in the mesolimbic pathway must be blocked for effective treatment

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atypical anti-psychotics (how they work)

also block D2 receptors but only temporarily and then rapidly dissociate to allow normal dopamine transmission (reducing positive symptoms)

act on serotonin receptors which may explain why they improve mood and cognitive functioning (reducing negative symptoms)

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STRENGTHS of drug therapy (x3)

  1. THORNLEY - better overall functioning, reduced symptom severity and lower relapse rates for those taking chloropromazine vs control

  2. now a ‘short stay’ condition meaning permanent hospitalisation is unnecessary as can manage own condition

  3. MELTZER - atypical psychotics are effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed (target both positive + negative symptoms)

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LIMITATIONS of drug therapy (x3)

  1. side effects could lead to stopping taking the medication - typical antipsychotics = dry mouth + tardive dyskinesia (involuntary jerky movements of the mouth) develops in 24% of those who take it for 7 years + atypical antipsychotics decrease number of white blood cells = AGRANULOCYTOSIS

  2. not effective for everyone as about 30% of patients either do not respond or are intolerant to drugs

  3. reinforces the view that there is ‘something wrong with you’ and thus prevents patient from taking responsibility and seeking other solutions

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36

family dysfunction as a cause of SZ (x3)

  1. double bind

  2. psychodynamic explanation

  3. high expressed emotion

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37

double bind theory (+ example)

BATESON - children who frequently receive contradictory messages from their parents are more likely to develop SZ as they develop an understanding of the world that is confusing, leading to the development of disordered thinking and withdrawal (avolition)

e.g. mother telling son she loves him whilst turning her head in disgust

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38

psychodynamic explanation

FROMM-REICHM = ‘schizophrenogenic mother’ - cold, rejecting and controlling leading to a family climate characterised by tension and secrecy - leads to distrust that later develops into paranoid delusions

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39

high EE

family communication style where the schizophrenic is talked about in a hostile or critical manner or in a way that indicates emotional over-involvement or over-concern

more likely to increase relapse rates suggesting families play a role in maintaining the disorder

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40

STRENGTHS of family dysfunction (x5)

  1. VAUGHN + LEFF = 51% relapse rate when returning to a high EE home vs 12% if low EE (contact time is significant as relapse rate was 92% if high contact)

  2. READ = adults with SZ are disproportionately more likely to have had an insecure resistant attachment + 68% of women and \595 of men had a history of physical and/or sexual abuse

  3. MORKVED = 67% of people with SZ had at least one childhood trauma (vs 38% of control group)

  4. TIENARI = adoption study - high levels of criticism and conflict with low levels of empathy was only implicated in the development of SZ when there was a genetic risk

  5. family therapy had some success in reducing hospital admission so must be valid to some extent

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41

LIMITATIONS of family dysfunction (x2)

  1. ALTORFER - 25% of patients showed no physiological response to stressful comments made by relatives meaning some patients do well regardless of family environment

  2. can lead to parent-blaming meaning it is socially sensitive (parents already watch unpleasant symptoms and take responsibility)

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42

cognitive explanations of SZ (x2)

dysfunctional thought processing

  1. metarepresentation

  2. central control

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43

metarepresentation

the cognitive ability to reflect on thoughts and behaviours allowing insight into our own intentions and goals

dysfunction means they don’t monitor their thoughts correctly and attribute them to someone or something else in the external world trying to communicate with them

links to hallucinations as hearing voices is seen as a misrepresentation of our ‘inner speech’ and delusions (our own thoughts attributed to an outside influence)

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44

STRENGTH of metarepresentation

STIRLING ET AL - 3 groups must product simple drawings while their arm is behind a screen and then asked to select the picture they had drawn (one was correct with the others rotated)

  1. SZ with hallucinations and delusions

  2. SZ without hallucinations and delusions

  3. control group with SZ

group 1 had more incorrect identifications so poor at monitoring their own output

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45

central control

a breakdown in the normal filtering system of thoughts means SZ patients can’t suppress automatic thoughts that are usually filtered out due to being irrelevant or unimportant

now interpret these thoughts in conscious awareness which may account for disordered speech (occurs due to disordered thinking)

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STRENGTHS of central control (x2)

  1. STIRLING ET AL = Stroop task - participants are timed on their ability to correctly identify the colour of a word when it conflicts the words meaning (e.g. white word that says blue = white) - SZ patients took 2x suggesting harder to suppress saying the word

  2. reinforced by the success of CBT which helps patients take control of their thought processes

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LIMITATION of central control

cause or effect issues - not clear if the cognitive defects cause SZ or neuro-chemical changes cause the cognitive impacts

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48

CBT therapy (aims,

aims to help the patients identify and correct these

e.g. patients noticed that a van parks outside their flat everyday at 12:15pm for 30 minutes so they conclude the van is a disguised MI5 van (delusion of persecution) but it could just be a driver parks to eat his/her lunch every day at a spot close to work

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method of CBT

  1. trace back the origins - allows a better idea of how they might have developed

  2. evaluate the content of their delusions or of any choices to consider ways they may test the validity of their faulty beliefs e.g. may dispute the beliefs to change them to healthier ones

  3. set behavioural assignments to try improve their general level of functioning - uses coping strategies to develop alternatives to previous faulty beliefs

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STRENGTHS of CBT (x2)

  1. NICE = found evidence it reduced rehospitalisation rates, symptom severity and improved social functioning up to 18 months follow end of treatment

  2. PILLING = reviewed 8 random control trials and found it is superior to drugs only in terms of long-term outcome as CBT patients maintained gains for longer

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LIMITATIONS of CBT (x3)

  1. most studies conducted with patients treated alongside medication so difficult to assess CBT alone

  2. KINGDON + KIRSCHEN = many patients not deemed suitable for CBT as they must actively engage with it (e.g. younger patients are more suitable meaning doesn’t benefit everyone)

  3. ADDINGTON + ADDINGTON = initial acute phase of SZ means self-reflection is not appropriate but once the condition has been stabilised with medication, benefits are seen (therefore dependent on stage of disorder)

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52

family therapy

family intervention programmes mean family members are involved over at least 10 sessions in order to reduce the level of expressed emotion within the family

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53

method of family therapy

  1. psychoeducation - inform the family on why they behave as they do meaning the family can understand what the patient goes through, lessening feelings of anger, shame and guilt

  2. managing stress levels - creates a more tolerant environment as it aims to provide calm but frank discussion of the problems so workable solutions can be found

  3. problem-solving and communication skills

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54

STRENGTHS of family therapy (x4)

  1. PHARAOH - reviewed 53 studies and found family therapy led to reduce hospital readmission over the course of a year and improvements in quality of life for both patient and family

  2. LEFF ET AL - studied families involved in a program of educational sessions, group meetings with successful families and sessions where professionals met family at home = significant decrease in high EE characteristics with only 14% readmission rates vs 78% in control

  3. 65% of those with SZ return from hospital to live with families so important to reduce EE levels (economic benefits as therapy cost lower than hospitalisation)

  4. LOBBAN - 60% of 50 studies led to significant benefits for relatives

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LIMITATION of CBT

not effective on its own as needs to be in conjunction with drug therapy

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56

token economy

behavioural therapy based on operant conditioning in order to replace unwanted behaviours with more desirable ones (management strategy)

usually used in an institutional setting as involves getting tokens for behaving in appropriate ways

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tokens in token economy systems

act as secondary reinforces as they only have value once the patient learns that they can be used to obtain rewards such as sweets and cigarettes

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AYLLON + AZRIN study

female SZ patients that were hospitalised for 16 years were given token s for actions such as making their beds or combing their hair

led to pleasant activities such as seeing a film or an additional visit to the canteen

VERY successful as the number of chores performance increased from 5 to over 40

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STRENGTH of token economies

PAUL + LENTZ - patients placed into a ‘learning group’ which operated around a token economy system vs a control group who had ‘general institution treatment’

100% in control were receiving drug treatment 4.5 years later (increased from 90%) vs only 11% in the learning group + did better in the community

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LIMITATIONS of token economies (x4)

  1. limited effectiveness as only works while the behaviour is being rewarded meaning difficult to implement with outpatients in the community

  2. only focuses on negative symptoms instead of hallucinations or delusions

  3. doesn’t deal with the cause of SZ as it isn’t used with the view of freeing the patient from the disorder

  4. ethically inappropriate as the ‘desired behaviours’ are decided by psychologists or institutions so might not be acceptable to the patient if they had free choice

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interactionist approach

both a biological predisposition and psychological/stress experience is required for the development of SZ (diathesis = vulnerability e.g. genetic + early psychological trauma whilst stress = a negative psychological experience e.g. parenting and critical life events)

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STRENGTHS of interactionist approach (x3)

  1. GOTTESMAN - 48% concordance rate for MZ twins and the disconcordance may be explained by no environmental trigger (despite a genetic vulnerability)

  2. TIENARI - low levels of empathy and high levels of criticism only implicated the development of SZ for those with a genetic risk

  3. HAMMEN - maladaptive methods of coping with stress in childhood means people are unable to develop effective coping skills (compromising resilience and increases vulnerability)

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treatment for the interactionist approach

combination of antipsychotic drugs and CBT

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STRENGTHS of combination treatment (x2)

  1. TARRIER - randomly allocated patients to (1) medication + CBT, (2) medication + counselling or (3) medication only - patients in 1 and 2 had lower symptom levels

  2. many psychological treatments require motivation and engagement with therapist and many can’t do this during psychotic periods so drugs may allow more effective psychological therapies

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LIMITATIONS of comvination therapy (x2)

  1. just because combined therapy works, doesn’t mean it is the cause (may only help symptoms)

  2. practical problem of increased cost may make it less accessible

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