Schizophrenia Flashcards

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1
Q

Diagnosis and Classification in Schizophrenia - AO1

A

Most common in men, city-dwellers and lower socio-economic groups. Experienced by 1% population.
Classification either DSM-5 (one positive symptom) or ICD-11 (two negative symptoms are sufficient.) Previous editions recognised subtypes of schizophrenia.

Positive symptoms:
Hallucinations - unusual sensory experiences - voices or visual hallucinations.
Delusions - also known as paranoia - irrational beliefs. Delusions of grandeur - thinking they are famous historical figures like Jesus. Conspiracies about aliens or government.
Disorganised speech and behaviour - changing topic mid-sentence or behaving in a way that does not make sense.

Negative symptoms:
Speech poverty - delay in verbal responses. Reduction in amount and quality of speech.
Avolition - inability to keep up with goal-directed activity - lack of personal hygiene, lack of persistence in work or school, lack of energy.

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2
Q

Diagnosis and Classification in Schizophrenia - AO3

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+ Good reliability within DSM-5 - inter-rater reliability +0.97 and test-retest +0.92. Osorio et al. study of 180 people.

  • Low criterion validity between ICD and DSM - out of 100, 68 had Sz under ICD and 39 with DSM
    C.P - good criterion validity when using one diagnostic manual - see above Osorio study.
  • Rosenham experiment demonstrates poor validity in diagnosis - 11/12 participants left with ‘schizophrenia in remission.’
  • Co-morbidity - Buckley et al. 50% have depression, 47% substance abuse, 23% OCD. Means that Sz may not exist as a distinct condition.
  • Symptom overlap - shares positive symptoms with bipolar disorder (delusions and avolition.) Overlap with depression and OCD symptoms. Classification and diagnosis are flawed
  • Gender bias - more men than women are diagnosed, ratio of 1.4 to 1. Could be because of biology or women having better social support groups so can manage symptoms. Underdiagnosis may mean women are not receiving treatment.
  • Culture bias - African-Caribbean British 9 times more likely to receive diagnosis than white-British, but living in Afro-Caribbean countries are not. Some cultures believe that hearing voices is their ancestors.
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3
Q

Genetic Explanation for Schizophrenia - AO1

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Family studies - risk increases with genetic closeness. Grossman showed correlation. 2 percent for aunt. 9 percent for sibling. 48% for identical twins.

Candidate genes - polygenetic and aetiologically heterogenous. Genes coding for dopamine most important. 108 genetic variations.

Mutation - genetic vulnerability in people with no family history - mutation in parental DNA caused by radiation or poisoning - e.g. 2% risk factor in men over 50 - risk of sperm mutation.

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4
Q

Genetic Explanation for Schizophrenia - AO3

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+ Research support - strong evidence base - family studies - 33% concordance MZ but 7% DZ in recent study by Hilker et al.
C.P - identical twins treated more similarly. Not 100% for MZ twins shows environment also relevant.

  • Environmental influences - cannabis use, childhood trauma, birth complications such as C-section. 67% people with Sz or related psychotic disorder had childhood trauma compared to 38% with non-psychotic disorders. Suggests an interactionist model is better. (diathesis-stress.)
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5
Q

Neural Correlates with Schizophrenia - AO1

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Dopamine - DA levels in different brain regions correlate with SZ symptoms.

Original DA hypothesis - SZ caused by high dopamine levels in subcortex. Hyperdopaminergia. Explains positive symptoms eg. high DA receptors in pathways between subcortex and Broca’s area explains speech poverty.

Updated DA hypothesis - high DA in subcortex plus low DA in cortex. Hypodopaminergia. Explains negative symptoms like avolition. DA levels affected by genetic vulnerability and childhood and adolescent stress.

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6
Q

Neural Correlates with Schizophrenia - AO3

A
  • Environmental influences - cannabis use, childhood trauma, birth complications such as C-section. 67% people with Sz or related psychotic disorder had childhood trauma compared to 38% with non-psychotic disorders. Suggests an interactionist model is better. (diathesis-stress.)
  • Glutamate - high correlation with Sz - post-mortems and scanning studies. Candidate genes associated with glutamate. Ignored by DA hypotheses.

+ Application - anti-psychotics reduce intensity of symptoms and typical ones are dopamine antagonists (chlorpromazine.) Demonstrates application and validity.

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7
Q

Family dysfunction - AO1

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The schizophrenogenic mother - psychodynamic explanation. Cold, rejecting and controlling. Conditional love. Leads to distrust and paranoid delusions.

Double-bind theory - contradictory family communication, child can’t win. Fear doing the wrong thing - don’t know what this is. Punished for doing wrong. Understanding of the world as dangerous and confusing. Not a cause - just risk factor.

Expressed emotion - families with high levels of hostile EE create stress. Verbal criticism, hostility, emotional overinvolvement. Big factor in Sz relapse.

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8
Q

Family dysfunction - AO3

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+ Research support - many have insecure attachment - type C or D. More than 50% have history of abuse. Large portion experience childhood trauma. Suggests family dysfunction causes vulnerability.

  • Lack of support - little evidence for schizophrenogenic mother or double binds except informal assessments. No empirical, clinical support. Explanations lack validity.

+ Family therapy - proven effectiveness. Relapse rates down 50-60%, more effective at beginning of symptoms. Clinical advice from NICE recommends family therapy to everyone with Sz diagnosis.

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9
Q

Cognitive explanations for schizophrenia - AO1

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Dysfunctional thinking - lower levels of functioning in some brain areas - e.g. reduced in ventral striatum, linked to negative symptoms. Reduced processing of information in the temporal and cingulate gyri associated with hallucinations.

Metarepresentation dysfunction - inability to recognise thoughts as our own. Leads to positive symptoms - hearing voices and delusions through insertion - thoughts projected into mind.

Central control dysfunction - cant suppress automatic responses (each word triggers other thoughts) - leads to speech poverty and derailment of thought.

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10
Q

Cognitive explanations for schizophrenia - AO3

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+ Research support - people with Sz took much longer to complete Stroop task (colours and words) - shows impaired cognition. Schizophrenics also struggle with abstract concepts - see things as literal.

  • A proximal explanation - explains the origins of symptoms but not the root cause of Sz - incomplete explanation. A distal explanation would look at what caused the disorder - family dysfunction or genetics.

+ CBT - 34 studies reviewed showed positive and negative symptoms decrease. Pontillo - auditory hallucinations reduce in severity and frequency.
C.P - different studies use different CBT techniques, so difficult to measure effectiveness.

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11
Q

Biological therapy for schizophrenia - AO1

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Typical antipsychotics - associated with original DA hypothesis.
Dopamine antagonists - Chlorpromazine - block dopamine receptors, normalising transmission. 400-800mg taken orally. Reduced dopamine activity reduces positive symptoms.
Sedation effects - affects histamine receptors, has calming effect.

Atypical antipsychotics - aim to reduce symptoms without side effects. Used since 1970s.
Clozapine - not taken as injection due to rare complication of a blood disease - agranulocytosis. 300-450mg. Binds to dopamine receptors as well as serotonin and glutamate. Improves mood regulation, so used for suicidal patients (30-50% schizophrenics.)

Risperidone - syrup or injection, 4-8mg. Less side effects with smaller dosage. Binds to DA, serotonin and glutamate, but more strongly to dopamine, hence the smaller dosage.

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12
Q

Biological therapy for schizophrenia - AO3

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+ Research support - Chlorpromazine more effective than placebo - Thornley et al. - 1121 participants. Clozapine more effective than typical antipsychotic, especially treatment-resistant cases, where it works 30-50% of the time.
C.P - issues in pharmaceutical industry + studies published multiple times, short-term studies.

  • Serious side effects - mild (sleepiness, mood, stiff jaw.) Serious (tardive dyskinesia) - causes involuntary face movements. Fatal (neuroleptic malignant syndrome) - caused when dopamine is blocked in hypothalamus - results in delirium and coma.
  • Mechanism unclear - most antipsychotics based on DA hypothesis which may be wrong. Theoretically they should not work. Some other factor is involved in their effectiveness - maybe the sedation effect.
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13
Q

Cognitive behaviour therapy for schizophrenia - AO1

A

5-20 sessions individually or in groups. Deals with thoughts (delusions) and behaviour.

Therapist helps client make sense of symptoms e.g. understand origins of voices. Normalisation used to reduce anxiety and reality testing used to challenge delusions. Voices come from malfunctioning speech centre.

Case example - client believed Mafia were trying to kill him, other possibilities explored. Delusions challenged.

Behavioural element - encouraging participants to get out and engage in goal-directed activities.

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14
Q

Cognitive behaviour therapy for schizophrenia - AO3

A

+ Evidence of effectiveness - 34 studies reviewed showed positive and negative symptoms decrease. Pontillo - auditory hallucinations reduce in severity and frequency.
C.P - high relapse rates, meaning therapy might have to go on for a while, which is a drain on the NHS.

  • Quality of evidence - different studies focus on different CBT techniques so not clear which ones help the most.
    Different techniques for positive and negative symptoms.
  • Potentially not suitable for severe cases - may think therapist is in on the conspiracy.
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15
Q

Family therapy and schizophrenia - AO1

A

Related to psychological theory - double bind and schizophrenogenic mother.

Reduces negative emotions - reduces EE levels such as anger, guilt. Helps prevent relapse.
Improves family’s ability to help - helps balance caring and maintaining own lives.

(don’t need to remember all) A model of practise:
(1) share info
(2) identify resources
(3) mutual understanding
(4) identify unhelpful patterns of understanding
(5) skills training
(6) relapse prevention
(7) maintenance

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16
Q

Family therapy and schizophrenia - AO3

A

+ Evidence of effectiveness - relapse rates down 50-60%, more effective at beginning of symptoms. Clinical advice from NICE recommends family therapy to everyone with Sz diagnosis.

+ Benefits to whole family - reduces negative impact on everyone. Families provide the bulk of care for schizophrenics. Strengthens their ability to support.

+ Economic Benefits: Family therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources. The NICE review of family therapy studies demonstrated that it was associated with significant cost savings when offered to patients alongside the standard care – Relapse rates are also lower which suggests the savings could be even higher.

17
Q

Token economies in schizophrenia - AO1

A

Token economies used in 60s and 70s Britain, still used elsewhere.

Rationale for token economies - tackles institutionalised behaviours such as poor personal care and antisocial behaviour that develop in prolonged hospitalisation.
Improves quality of life and ‘normalises’ behaviour to prepare for life outside hospital.
Does not alleviate positive symptoms - just manages behaviour.

Tokens are given for desirable behaviours (most effective when immediate). Later swapped for rewards - food, luxuries, outdoor time.

Behaviour modification through operant conditioning.
Tokens are secondary reinforcers, rewards are primary reinforcers.
Strengthen effect by pairing together at start, and pairing with multiple primary reinforcers.

18
Q

Token economies in schizophrenia - AO3

A

+ Evidence for effectiveness - seven high quality studies showed reduction in negative symptoms and unwanted behaviours. Glowacki et al.
C.P - difficult to continue outside a hospital setting, may cause behaviours to re-emerge.

  • Ethical issues - professionals have power to control behaviour - also restricting pleasures for seriously ill people. Imposing norms of the institute. May worsen depressive symptoms.
  • Alternatives - other alternatives better like art therapy. Lacks side effects or ethical abuses. NICE guidelines recommend art therapy but not token economies.
19
Q

Interactionist approach to schizophrenia - AO1

A

Diathesis-stress model - vulnerability + stressor = Sz.

Meehl’s model - schizogene creates vulnerability to effects of stress. Lead to schizotypic personality. No schizogene - will never develop the disorder. ( Stressor is especially a schizophrenogenic mother)

Modern understanding of diathesis - not a single gene, may not even be genetic. Polygenetic and aetiologically heterogenous. Early trauma can alter brain development and become the diathesis.
Modern understanding of stress - any potential trigger - psychological (parenting) or biological (cannabis). Cannabis interferes with dopamine system - 7x more likely to get Sz.

Treatment - combine antipsychotics and CBT. More common in UK than US.

20
Q

Interactionist approach to schizophrenia - AO3

A

+ Support for vulnerability and triggers - Finnish study - Sz more likely in children with genetic vulnerability AND adoptive parents with low empathy, high criticism and hostility.

  • Diathesis and stress are complex - Meehl’s model is hopelessly simplistic - many different stressors. Stressors can be biological and diathesis can be psychological. Childhood trauma a stress but can change brain development and act as diathesis.

+ Real-world application - greater effectiveness for medication plus psychological therapy than medication alone. No difference in hospital readmission however.
C.P - successful treatment doesn’t logically mean explanation was correct. Treatment-causation fallacy.