Schizophrenia Flashcards

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1
Q

Diagnosis and Classification of Schizophrenia- AO1

A
  • SZ=severe mental disorder contact with reality and insight are impaired
  • Diagnosis and classification:
    Diagnosis=distinguish one disorder from other by identifying symptoms
    Classification=organising symptoms into categories
    ICD-10=two negative symptoms
    DSM-5=one positive symptom
  • Positive symptoms=in addition to normal experiences
    =Hallucinations=sensory experiences no basis in reality/distorted perceptions things that are there
    =Delusions=beliefs that have no basis in reality
  • Negative symptoms=loss of usual experiences
    =Speech poverty=reduced frequency and quality of speech
    =Avolition=loss motivation carry out tasks=lowered activity levels- poor hygiene/lack of persistence in work/lack of energy
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2
Q

Diagnosis and Classification of Schizophrenia- AO3

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  • Good reliability +
    Inter-rater reliability=different clinicians same diagnosis
    Test-retest reliability=same diagnosis same person different occasions
    Osorio=excellent reliability SZ in 180 DSM-5- inter-rater=0.97 test-retest=0.92
  • Low validity -
    Criterion validity
    Cheniaux=two psychiatrists 100 clients using ICD-10 and DSM-4
    68 SZ ICD and 39 SZ DSM
  • Co-morbidity -
    Two conditions occurring together=question validity
    1/2 SZ=depression or substance abuse
  • Gender bias in diagnosis -
    Men diagnosed more than women
    Women less vulnerable due to genetic factors
    Women closer relationships and get more support
    Women with SZ function better than men
  • Culture bias -
    Symptoms different meanings in different cultures
    Hearing voices=communication from ancestors
    British afro-caribbean origin=9x likely diagnosis as white british
    Culture bias by psychiatrists from different cultural background
    Overinterpretation symptoms black british
  • Symptom overlap -
    Between symptoms of SZ and other conditions
    Both SZ and bipolar=positive and negative symptoms
    May not be two different conditions but variations of same one
    SZ hard to distinguish from bipolar
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3
Q

Biological Explanations for Schizophrenia- Genetic Basis- AO1

A
  • Family studies=risk SZ in line genetic similarity relative with disorder
    Gottesman:
    General population=1% risk
    Parents=6% risk
    Children=13% risk
    MZ twins=48% risk
  • Candidate genes
    SZ=polygenic=multiple genes involved=coding for dopamine
    Ripke=37,000 SZ 113,000 controls
    108 genes=increased risk SZ
    Aetiologically heterogenous=different combination of factors can lead to SZ
  • Role of mutation
    Parental DNA caused by radiation, poison or viral infection
    Positive correlations=paternal age and risk of SZ
    0.7% risk under 25 2% risk over 50
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4
Q

Biological Explanations for Schizophrenia- Genetic Basis- AO3

A
  • Research support +
    Family studies=risk increases with genetic similarity to family with SZ
    Tienari=bio. children of parents SZ=heightened risk if grow up in adoptive family
    Hilker=concordance rate 33% MZ and 7% DZ twins
  • Environmental factors -
    Biological and psychological influences
    Birth complications / smoking THC-rich cannabis when teenager / childhood trauma=more vulnerable mental health problems respectively
    Morkved=67% SZ and related psychotic disorders=childhood trauma as opposed to 38% control
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5
Q

Biological Explanations for Schizophrenia- Neural Correlates- AO1

A
  • Neural correlate=patterns of structure/activity in brain that occur in conjunction with an experience- SZ=dopamine (DA)
  • Original dopamine hypothesis:
    Drugs used to treat SZ (antipsychotics reducing DA) cause symptoms similar to those in Parkinson’s (low DA levels)
    SZ due to hyperdopaminergia=high DA in subcortical areas of brain
    Excess of DA receptors from subcortex to Broca’s area explains speech poverty
  • Updated dopamine hypothesis- Davis:
    SZ also due to hypodopaminergia=low DA in brain’s cortex
    Low DA in prefrontal cortex explains cognitive problems
    Cortical hypodopaminergia leads to hyperdopaminergia
    =both genetic variations and early stress=more sensitive to cortical hypo and thus subcortical hyper
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6
Q

Biological Explanations for Schizophrenia- Neural Correlates- AO3

A
  • Evidence for dopamine +
    Amphetamines increase DA, worsen symptoms in SZ and induce symptoms in people without
    Antipsychotic drugs reduce DA and intensity of symptoms
    Some candidate genes act on production of DA or DA receptors
  • Glutamate -
    Post-mortem and live scanning studies=raised levels glutamate in brain regions of people with SZ
    Several candidate genes for SZ involved in glutamate production/processing
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7
Q

Psychological Explanations for Schizophrenia- Family Dysfunction- AO1

A
  • Family dysfunction=abnormal processes within family may be risk factors for development and maintenance of SZ
  • Schizophrenogenic mother:
    Fromm-Reichmann=psychodynamic expansion patients and childhoods
    =cold, rejecting, controlling, family environment of tension and secrecy
    Leads to distrust=paranoid delusions=SZ
  • Double-bind theory:
    Bateson=role of communication style within family important development SZ
    Child fears doing wrong thing but mixed messages what is actually wrong- unable comment on unfairness or seek clarification
    When get it wrong=punished by withdrawal of love- world is confusing and dangerous
    =risk factor in developing SZ
  • Expressed emotion:
    Level of emotion expressed towards patient by carers who are often family members
    =verbal criticism- accompanied by violence
    =hostility- anger and rejection
    =emotional over-involvement- needless self-sacrifice
    High levels expressed emotion=serious source stress- explanation relapse SZ patients
    Source of stress triggers onset SZ in already vulnerable person (due to genetic makeup eg)
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8
Q

Psychological Explanations for Schizophrenia- Family Dysfunction- AO3

A
  • Research support +
    Indicators family dysfunction=insecure attachment and exposure to childhood trauma
    Read=adults SZ disproportionately likely insecure attachment, type C/D
    Read=69% women 59% men SZ history of physical/sexual abuse
    Morkved=most adults SZ at least one childhood trauma
  • Explanations lack support -
    No evidence to support importance traditional family-based theories like schizophrenogenic mother and double bind
    Theories based on clinical observations and informal assessment of personality of mothers of patients but no systematic evidence
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9
Q

Psychological Explanations for Schizophrenia- Cognitive Explanations- AO1

A
  • Cognitive explanations=focusing on mental processes such as thinking, language and attention
  • Dysfunctional thinking:
    Dysfunctional thought processing=information processing does not represent reality accurately and produces undesirable consequences
    Reduced thought processing ventral striatum=negative symptoms
    Reduced processing info in temporal and cingulate gyri=hallucinations
  • Metarepresentation dysfunction:
    Frith=cognitive ability to reflect on thoughts and behaviour- insight into intentions and goals and allows us to interpret actions of others
    Disrupt ability to recognise own actions and thoughts as carried out by ourselves- explaining hallucinations and delusions like thought insertion
  • Central control dysfunction:
    Frith=issues with cognitive ability suppress automatic responses while perform deliberate actions
    Speech poverty result from inability suppress automatic thoughts and speech triggered by other thoughts
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10
Q

Psychological Explanations for Schizophrenia- Cognitive Explanations- AO3

A
  • Research support +
    Stirling=performance cognitive task 30 SZ and 30 control
    Stroop task
    Frith=people with SZ took longer, over twice as long, to name font colours
    Cognitive processes of SZ=impaired
  • Proximal explanation -
    Proximal=explain what happening now to produce symptoms- distinct from distal explanations which focus on initial cause of condition
    Distal explanations=genetic and family dysfunction
    Unclear and not well addressed=genetic variation/childhood trauma lead to metarepresentation/central control
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11
Q

Biological Therapy for Schizophrenia- AO1

A
  • Drug therapy:
    Antipsychotic drugs as psychosis=characteristic of SZ
  • Typical antipsychotics=first generation- tablets, syrup, injection- max 1000mg- gradually increased
    =Dopamine antagonists:
    Chlorpromazine and dopamine hypothesis
    Blocking dopamine receptors in synapses- normalising it in key areas of brain to reduce symptoms
    =Sedation effect:
    Effective sedative maybe due to effect on histamine receptors- calm individuals- syrup absorbed faster than tablets
  • Atypical antipsychotics=developed after typical second generation- improve effectiveness and minimise side effects
    =Clozapine:
    Regular blood tests to ensure no condition resulting in deaths in past
    Not available as injection
    Daily dosage=300-450mg
    Binds to dopamine receptors and acts on serotonin/glutamate receptors- improve mood reduce depression
    =Risperidone:
    Tablets, syrup, injection lasting two weeks
    Small dose initially but built up to 4-8mg and max 12mg a day
    Binds to dopamine and serotonin receptors- binds stronger to dopamine=more effective
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12
Q

Biological Therapy for Schizophrenia- AO3

A
  • Evidence for effectiveness +
    Typical/atypical moderately effective tackling SZ symptoms
    Thornley=chlorpromazine to controls- associated with better functioning and reduced symptom severity than placebo
    Meltzer=clozapine more effective than typical and other atypical
  • Serious side effects -
    Typical=dizziness, sleepiness, weight gain
    Long term=tardive dyskinesia=involuntary facial movements
    Most serious=neuroleptic malignant syndrome- blocked dopamine action in hypothalamus (regulation body systems)=high temp, delirium, coma, fatal
  • Mechanism unclear -
    By which antipsychotics work tied up with original dopamine hypothesis- symptoms SZ hyperdopaminergia in subcortex brain
    Dopamine levels other parts brain too low rather than too high=most antipsychotics should not work
    Adds to argument they are ineffective
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13
Q

Psychological Therapy for Schizophrenia- CBT- AO1

A
  • 5-20 sessions of challenging irrational beliefs
  • How CBT helps:
    =make sense of how irrational thoughts impact behaviour
    =doesn’t eliminate symptoms but better able cope with them- reducing stress and improving functioning
    =normalisation=voice hearing an extension of of ordinary experience of thinking
    =examine likelihood delusions are true
    =tackle anxiety and depression
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14
Q

Psychological Therapy for Schizophrenia- CBT- AO3

A
  • Evidence of effectiveness +
    Jauhar=34 studies CBT and SZ=small but significant effects positive and negative symptoms
    Pontillo=reduction frequency and severity hallucinations
    NICE recommends CBT for SZ
  • Quality of evidence -
    Thomas=different studies use different CBT techniques and different combos of positive and negative symptoms
    Modest benefits CBT conceal these
    Hard to comment on effectiveness
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15
Q

Psychological Therapy for Schizophrenia- Family Therapy- AO1

A
  • All or some family members with aim of improving communications and reducing stress of living as family
  • How family therapy helps:
    Pharoah=range of strategies use to improving functioning of family
    =reduces negative emotions- reducing stress reduces likelihood of relapse
    =improves family’s ability help- therapeutic alliance all agree on aims of therapy, improve family’s belief and behaviour about SZ, balance between caring and maintaining own lives
  • Model of practice- Burbach:
    =sharing basic info and providing support
    =identifying resources of what can(not) offer
    =encourage mutual understanding
    =identifying unhelpful patterns of interaction
    =skills training- stress management
    =relapse prevention planning
    =maintenance for future
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16
Q

Psychological Therapy for Schizophrenia- Family Therapy- AO3

A
  • Evidence of effectiveness +
    McFarlane=consistently effective treatment for SZ
    Relapse rates reduce 50-60%
    Using it as mental health starts decline is particularly promising
    NICE recommends
  • Benefits whole family +
    Lobban+Barrowclouh=effects important as family provides bulk of care
    Strengthening functioning of family lessens negative impact SZ on family members and strengthens ability to support person
17
Q

Management of Schizophrenia- AO1

A
  • Developing token economies with SZ:
    =trialed token economies with SZ women
    =positive task then given token could be swapped for ward privileges
    =number of tasks carried out increased significantly
    =TE declined due to community-based care and complex ethical issues
  • Rationale for token economies:
    =Matson- personal care, condition-related behaviours and social behaviour=institutional care tackled by TE’s
    =improves QoL within hospital setting
    =normalises behaviour making it easier adapt back to community life
  • Tokens given immediately for target behaviour and swapped later for more tangible rewards
  • Behaviour modification regarding operant conditioning
    =token is secondary reinforcer
    =reward is primary reinforcer
18
Q

Management of Schizophrenia- AO3

A
  • Evidence of effectiveness +
    Glowacki=7 high quality studies effective TE with SZ and hospital setting
    Reduction in negative symptoms and decline frequency unwanted behaviours
  • Ethical issues -
    Power control people’s behaviour- imposing your own norms on someone else
    Already distressed people will have even worse time due to restricting pleasure
    =legal action major factor in TE decline
  • Alternative approaches -
    Chiang=art therapy good alternative- high-gain low-risk approach
    Most managements have modest benefits but art therapy is pleasant with no side effects
    NICE recommends art therapy
19
Q

Interactionist Approach to Schizophrenia- AO1

A

=recognises biological (genetic vulnerability), psychological (stress) and social factors (poor quality interactions) develop SZ

  • Diathesis-stress model:
    =when an underlying genetic vulnerability is expressed by an environmental stressor that results in SZ
    =Meehl- originally diathesis entirely genetic (schizogene)- no gene then no amount of stress causes SZ
    =Ripke- many genes increase vulnerability as well as psychological trauma
    =Houston- stress was psychological but now seen as anything risks triggering SZ- cannabis increases up to 7 times
  • Treatment:
    =combining antipsychotics and CBT
20
Q

Interactionist Approach to Schizophrenia- AO3

A
  • Support for vulnerability and triggers +
    Tienari=19,000 Finnish children, mothers SZ
    High genetic risk group compared to adoptee control
    High criticism and hostility linked with development SZ but only in genetic risk group
  • Diathesis and stress are complex -
    Multiple genes and combos of genes influence diathesis
    Stress comes in many forms
    Houston=childhood sexual abuse major influence vulnerability to SZ / cannabis use major trigger
  • Real-world application +
    Combo of drug treatments and psych therapies
    Tarrier=randomly allocated 315 participants to: drugs+CBT / drugs+counselling / drugs
    Two combo groups=fewer symptoms