Schizophrenia

Define positive symptoms of schizophrenia

an excess/distortion of normal functions i.e. hallucinations (auditory/visual not present), delusions (false beliefs/paranoia), disorganised speech/behaviour

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What is used to diagnose schizophrenia?

DSM and ICD (DSM used as basis for ICD)

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Define negative symptoms of schizophrenia

decline/loss of normal functions i.e. speech poverty, lack of volition (no self motivation/desire), psychomotor disturbances (rocking/twitches)

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State a positive evaluation point of classification/diagnosis of schizophrenia

Allows doctors to communicate using similar terminology and can help them predict the outcome so suggest related treatment for patient

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State 3 negative evaluation points of classification/diagnosis of schizophrenia

Slater & Roth hallucinations least important symptom as not exclusive to schizophrenics; Scheff labels individual made lead to self fulfilling prophecy/low self esteem; possible misdiagnosis/mistreatment, loss of rights, prejudice etc

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How would the classification system for schizophrenia be reliable?

If different clinicians using the same system (i.e. DSM) gave the same diagnosis for the same individual

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Why is diagnosis difficult?

because the practitioner has no physical signs, only symptoms which the patient reports on

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Describe Jakobsen et al's study

tested the reliability of ICD-10 classification; 100 danish patients with history of psychosis and concordance rate of 98% which demonstrates high reliability of this clinical diagnosis

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What is comorbidity?

people who suffer from 2 or more mental disorders i.e. schizophrenia and depression and symptom overlap makes it more difficult to diagnose schizophrenia/problem of reliability

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Loring and Powell (gender bias)

found some behaviour psychotic in males was not regarded as psychotic in females

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How would the classification system be valid?

it should be meaningful and classify a real pattern of symptoms that result from a real underlying cause

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Give 2 evaluation problems of validity of schizophrenia

As a single disorder it is questioned (no such thing as "normal schizophrenic" w/ usual symptoms); problems with validity of diagnosis could lead to unsuitable treatment sometimes involuntary (practical/ethical issues)

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Are we really testing what we think we are testing? (problems of validity negative evaluation)

In US 20% psychiatric patients classed as schiz in 1930s but rose to 80% in 1950s, london rate remained at 20% suggests that neither had valid definition

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Give 2 more negative evaluation points of validity of schizophrenia

predictive validity (some schiz successfully treated and others not - Heather only 50% chance of predicting treatment from diagnosis); aetiological validity (all patients should have same cause but in schiz could be biological, psychological or both)

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Describe Rosenhan's study (in relation to validity of schizophrenia)

Pseudopatients led to 8 normal people kept in hospital despite behaving normally by assuming with no real evidence suggesting that doctors had no valid method for detecting schiz. Follow up study - rejected genuine patients

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Explain the issue of culture in relation to validity of schizophrenia

Asian cultutes not expected to show emotions but Arabs public emotion encouraged. Cochrane incidence of schiz in West Indies & UK 1% but people of Afro-caribbean origin x7 more likely to be diagnosed with schiz when living in UK

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Benzel et al (genetic explanations)

COMT, DRD4 and AKT1 (all associated with excess dopamine in specific D2 receptors) leading to acute episodes and positive symptoms

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Miyakawa et al (genetic explanations)

those with schiz more likely to have a defective version of PPP3CC gene (associated with the production of regulation of immune system)

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Sherrington et al (genetic explanations)

gene located on chromosone 5 linked in some extended families with schiz

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Kendler (genetic explanations)

1st degree relatives of those with schiz x18 more risk than general population

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Gottesman (genetic explanations)

schiz more common in biological relatives of a schiz and closer degree of genetic relations, higher the risk

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Give one explanation for why genetics are not entirely responsible for the development of schizophrenia

as identical twins don't have 100% concordance rates, it could be that the individual is pre-disposed to develop it so they are at higher risk (nature v. nurture)

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Give 2 weaknesses of the genetic explanation of schizophrenia

methodological problems (family/twin/adoption studies are retrospective and diagnosis may be bias - demand characteristics); reductionist (schiz is result of many genes/environmental factors and research into gene mapping is oversimplistic)

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What is dopamine?

neurotransmitter - chemical in the brain causing neurons to fire

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State the original dopamine hypothesis

schiz suffered from an excessive amount of dopamine causing the neurons to fire too often and transmit too many messages

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What does high dopamine activity cause?

acute episodes and positive symptoms

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Give evidence that supports the effects of high dopamine activity

large doses of amphetamines (increases amount of dopamine) in those w/ no psychological disorder history gives behaviour sim to paranoid schiz; small doses to schiz worsens symptoms

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State the second dopamine hypothesis

not excessive dopamine but more dopamine receptors (leads to more firing and an over production of messages)

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Owen et al/Falkai (second dopamine hypothesis)

in autopsies, large number of dopamine receptors and increased dopamine in caudate nucleus & putamen; increase in amount of dopamine in left amygdale (supports 2nd dopamine hypothesis)

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Give 3 weaknesses of the dopamine hypothesis as an explanation for the development of schizophrenia

Farde et al found no difference between schiz levels of dopamine compared to norm indivs; Noll 1/3 patients don't respond to drugs blocking dopamine so other neurotransmitters must be involved; deterministic (no free will)

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How does neural correlates explain the development of schizophrenia?

people w/ schiz have abnormally large ventricles in brain (ventricles - in the brain supplying nutrients/removing waste)

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Give a strength of neural correlates as an explanation for the development of schizophrenia

high reliability of research in highly controlled environments w/ MRI/PET scans giving accurate readings of brain regions

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Explain research support for neural correlates

Suddath et al - MRI to see brain structure of twins (one schiz) and schiz twin generally enlarged ventricles/reduced anterior hypothalamus; differences easily identified from images in 12/15 twins

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Give a weakness for neural correlates

deterministic - individual with large ventricles may not always develop schiz (not accounting for free will)

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Buckley et al (comorbidity)

around half of patients with diagnosis of schiz also have diagnosis of depression (50%) or substance abuse (47%); PTS in 29% cases and OCD in 23% - shows disorders as comorbid

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Why is diagnosis of schizophrenia ethnocentric?

different interpretations of what is normal in different cultures - any deviation from norm of own culture is wrongly misinterpreted and labelled as a symptom

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Broverman et al (gender bias)

clinicians in US equated mentally healthy adult behaviour w/ mentally healthy male behaviour (androcentric) and so women percieved as less mentally stable when not showing 'male' behaviour

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What factors in relation to differences in gender need to be considered when diagnosing schizophrenia?

males tend to suffer more negative symptoms and higher levels of substance abuse, females tend to have better recovery rates/lower relapse rates

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What is Laing's explanation for the development of schizophrenia?

believed it was the result of social pressures from life and interactions between people (especially in families)

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What is the double bind theory (Bateson et al)?

suggests that children who frequently receive contradictory messages from their parents are more likely to develop schiz i.e. expressing love whilst appearing angry

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How does the double bind theory lead to schizophrenia?

prolonged exposure to contradictory messages from parents prevents the development of an internally coherent construction reality and in the long run this manifests itself as typically schizophrenic symptoms

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What is negative emotional climate or expressed emotion?

EE is family communication style involving criticism/hostility/emotional over-involvement; but researchers concluded it's more important in maintaining it rather than causing it; those returning to high EE family more likely to relapse

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Give 2 strengths of family dysfunction as an explanation for developing schizophrenia

double bind comes from empirical support that schiz had higher rate of double bind statements by mothers (patient recall affected by schiz - relability?); EE practical applications i.e. therapy improves patient lives

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Give 2 weaknesses of family dysfunction as an explanation of schizophrenia

difference in speaking to schiz children than normal (result of living with schiz child not cause?); ethical issues of blaming family; gender bias of mother being blamed & socially sensitive

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What are cognitive deficits?

impairments in thought processes such as perception/memory/attention; evidence of deficient attention skills, understanding people's behaviours/lack of social skills

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What are cognitive biases?

when people notice/pay attention to/remember types of info better than others (selective attention) i.e. delusions of persecution associated w/ specific

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Give 2 strengths of cognitive explanations of schizophrenia

practical applications (machine w/ virtual hallucinations to show schiz their hallucinations aren't real; understanding effects of cognitive deficits improves life quality); nurture approach (behaviour is cause of environmental factors)

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Give 2 weaknesses of cognitive explanations of schizophrenia

problems w/ cause and effect (cognitive approaches don't explain the cause of them); reductionist (ignores factors such as genes i.e. low neurotransmitters could create cognitive deficits)

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What are typical antipsychotics? (dopamine antagonists)

first generation drugs i.e. chlorpromazine; stops dopamine production by blocking receptors in synapses absorbing dopamine so reduce + symptoms; tended to block all types of dopamine activity so harmful side effects

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What are atypical antipsychotics?

newer drugs (clozapine/risperidone), attempting to target range of neurotransmitters and D2 dopamine activity in limbic system but not other parts of brain so less side effects; also some effect on other neurotransmitters i.e. serotonin and glutamate

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Give 3 strengths of drug therapy

greatly improved treatment/patient's lives; relatively cheap/easy to administer; relapse rates less common with drug therapy so suggests they are effective

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Give 2 weaknesses for drug therapy

do not cure schiz just lessen symptoms; may give harmful side effects

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What is the interactionalist approach to schizophrenia?

Diathesis-stress model: may be born w/ predisposition triggered by stress but if they have supportive environment illness may not develop

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Explain Tienari's study in relation to the interactionalist approach

adopted children from families with schiz had more chance of developing it than those from norm fams (supports genetic link), but children from schiz fam less likely to develop it if placed in 'good' fam (supports environment role)

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How does stress cause the onset of schizophrenia?

causes the brain to be flooded with neurotransmitters bringing on acute episodes

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Brown and Birley (interactionalist approach)

50% people with acute episode of schiz had experienced major life event 3 weeks prior

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How does substance abuse affect chance of schizophrenia?

amphetamine/cannabis etc identified as triggers as they affect serotonin and glutamate levels

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How does living environment affect chance of schizophrenia?

risk of schiz greater in cities (probs due to stress levels), clear pattern between city environments and levels of psychosis (scandanavian villages low levels of psychosis)

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Bentall's meta analysis (interactionalist approach)

stress arising from childhood abuse increases risk of developing schiz

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What are the aims of family therapy?

to educate relatives, improve family communication, teach patients stress management

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What are the methods used in family therapy?

weekly meetings to solve problems/pinpoint stressors, interviews/observation identifying strengths/weaknesses of family members, teaching actual facts about illness, communication skills teaching aimed to lower expressed emotion

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Give 4 strengths of family therapy as treatment

Anderson (relapse rate almost 40% when drugs only, 20% when fam therapy, >5% when both used together); pharaoh meta analysis (family interventions reduce relapse rates); highly cost effective as reduce relapse rates; family members cope better

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Give a weakness of family therapy as treatment

Risk of patient stressed by therapy or over fixated

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How is token economy used as a treatment for schizophrenia?

behavioural change can be achieved by awarding tokens for desired actions and reinforcers exchanged for benefits; not punishing undesirable behaviours; alleviates - symptoms and can reduce + symptoms by not rewarding them

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Give a strength of token economy as a treatment for schizophrenia

leads to better overall patient functioning and more cost effective

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State 3 weaknesses of token economy treatment

unclear if behaviour changes are maintained beyond treatment programme (not a cure); difficult to keep treatment going once back home; ethics - dehumanising, takes away patient rights

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How is CBT believed to improve symptoms of schizophrenia?

based on belief that problems are based on incorrect beliefs and it aims to identify/alter irrational thinking to improve emotional attitudes

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What is the process of CBT as therapy for schizophrenia?

asessment (encourages patient to explain concerns), engagement (wins trust of patient i.e UPR), Actions/Beliefs/Consequences, normalisation (don't feel ashamed), critical collaborative analysis (where wrong/why developed), alternative explanations

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What is coping strategy enhancement?

aims to teach individuals to apply effective coping strategies which will reduce the frequency/duration of symptoms/alleviate accompanying distress: education/rapport training; symptom target

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Give 2 strengths of CBT

reduces relapses/readmissions, reduces symptoms especially + ones

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Give 3 weaknesses of CBT as treatment

little use in early stages of acute schiz episode (not a cure), not suitable for all patients, evidence of relapse related to stress/EE so CBT should be used alongside fam therapy to reduce pressures on individual

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What is symptom overlap?

considerable overlap between symptoms of schizophrenia & other conditions i.e. schiz/bipolar share delusions and avolition etc - questions validity of schiz diagnosis/classification

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Ellason & Ross (symptom overlap)

people with DID more schiz symptoms than those with schiz

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Ophoff et al (symptom overlap)

found 7 gene locations the genome associated w/ schiz, 3 of them also associated w/ bipolar which suggests a genetic overlap and a reason for symptom overlap

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what is the role of candidate genes in schizophrenia development?

individual genes thought to be associated w/ risk of inheritance; polygenic (a number of genes each appear to confer an increased risk/factors in combination); aetiologically heterogeneous (different candidate genes/diff combo of factors)

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Tienari et al (genetic explanations)

adoption studies show that children of schiz sufferers still at heightened risk if adopted into families w/ no history of it

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What is the issue of cause and effect in relation to the dopamine hypothesis?

post mortem and PET scans of schizophrenics have revealed higher than normal levels of D2 dopamine receptors however cause/effect cannot clearly be established

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What is hyperdopaminergia in the sub cortex?

original version of the dopamine hypothesis - possible role of high levels/activity of dopamine i.e. excess of dopamine receptors in Broca's area may be associated w/ speech poverty or auditory hallucinations

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What is hypodopaminergia in the cortex?

more recent hypothesis - abnormal dopamine systems/low levels of dopamine in prefrontal cortex in - symptoms of schiz (may be hypo & hyper are correct; high/low levels dopamine in different brain regions involved in schiz)

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Explain negative symptoms in relation to neural correlates

avolition: ventral striatum may be involved in development of avolition and measurement in this area of schiz brain found low levels of activity than control groups

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Explain positive symptoms in relation to neural correlates

brains scans of schiz with auditory hallucinations to identify pre recorded speech as their own or others compared to control group (reduced activity in superior temporal gyrus/anterior cingulate gyrus correlate of auditory halluncinations)

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Schizophrenia

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