L18 - Schizophrenia 1 Flashcards

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1
Q

What is schizophrenia/psychosis?

A
  • Neurodegenerative disorder in the young
  • Cog impairment central to the concept
  • Madness can be divided into a small number of diseases with different types of brain pathology and with differing aetiologies
  • Splitting of the mind, not personalities
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2
Q

What are the positive symptoms?

A
  • Those additional to normal experience and behaviour
  • Positive symptoms’ describe psychosis and typically include delusions, hallucinations and thought
    disorder
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3
Q

What are the negative symptoms?

A
  • The lack or decline in normal experience or behaviour
  • Negative symptoms’ describe inappropriate or non-present emotion, poverty of speech, and lack
    of motivation
  • Factor analysis puts symptoms into 3 semi-independent factors i.e. three-factor models of
    ‘schizophrenia’
  • Hallucinations and delusions = reality distortions e.g. thought insertion, thought withdrawal,
    delusions of control. Can occur in any modality, typically auditory (hearing voices)
  • Negative symptoms = psychomotor poverty, flattened affect
  • Disorganised = disorganised behaviour, inappropriate affect
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4
Q

What are the criteria for schizophrenia? (According to the DSM)

A

Criteria A: Characteristic symptoms = 2+ for a month
- Delusions
- Hallucinations
- Disorganised speech
- Grossly disorganised or catatonic behaviour
- Neg symptoms
Criteria B: social/occupational dysfunction
C: Duration (6+months)
D: Schizoaffective/mood disorder exclusion
E: Substance exclusion
F: Relationship to global development delay/autism

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5
Q

How does the DSM 5 deal with these categories?

A
  • Rates severity from 1-5 inc additional symptoms like impaired cognition
  • Severity of depression and mania taken into account
  • Goal is to help clinicians and researchers - recommended
  • Criticism of going for high reliability at the expense of validity
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6
Q

What are diagnostic controversies pt 1?

A
  • Ignores cognitive symptoms despite
  • Decreased IQ, loss of recall/recog memory and EF and Problems with attention, info processing, eye movement
  • Lack of clear distinctions between various types as subtypes have poor diagnostic stability over time and >5% research studies on subtypes
  • DSM had hierarchical structures for those fitting more than one subtype
  • Sep subtypes not supported genetically
  • Key diagnostic features cannot be measured objectively
  • Needs to break down some categories
  • Cog changes not added to list of symptoms despite prominence
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7
Q

What are the subtypes?

A
  • Disorganized type - where thought disorder and flat or inappropriate affect are present
    together
  • Paranoid type - where delusions and hallucinations are present but thought disorder,
    disorganized behaviour, and affective flattening is absent
  • Catatonic – odd fixed postures, negative symptoms
  • Undifferentiated type - psychotic symptoms are present but the criteria for paranoid,
    disorganized, or catatonic types has not been me
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8
Q

What are the risk factors for Schiz/Psychosis?

A
  • Gender: males
  • Social Class: lower socioeconomic status
  • Urbanisation: rates increase as you get closer to city center
  • Immigrant groups: unusually high rates in immigrant groups: London rates vary with proportion of ethnic minority in area
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9
Q

What are the Perinatal Risk Factors?

A
  • Link with winter births/viral events
  • Stress in pregnancy – 67% increased risk of schiz in offspring exposed to ++stress when inutereo
  • Risk signs include low birth weight, pre-eclampsia
  • Perinatal complications: complications of pregnancy, abnormal fetal growth, complications of delivery
  • Perinatal effect remains after SES accounted for
  • Birth complications more common in schiz member of
    discordant twin
  • Rhesus (Rh) Incompatability: Rh –ve mother and Rh-+fetus =
    increased risk of schiz
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10
Q

How can childrearing env affect schiz?

A
  • A typical communication in family - higher verbosity and vagueness
  • Expressed emotion – Number of critical comments- hostility, over concern, overprotectiveness. = EE higher relapse rates
    ❖ ‘Double bind’ theory of parent-child communication. Where a person gets 2 contradictory messages and is prevented from talking about the contradiction = could lead to people feeling ‘insane’, uncertain
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11
Q

What are issues with assigning childrearing env to schiz?

A
  • Problems of studying family interactions = bidirectional effects – cause/effect issues,
    retrospective designs, control group
  • Childhood Adversity, Maltreatment and Abuse: Over the last two decades a growing body of research has highlighted the potentially causal role that childhood trauma may play in the development of psychosis/schiz
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12
Q

What is the role of expressed emotion in schiz?

A
  • Low EE families can be protective, but high EE can impose additional stress and affect relapse
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13
Q

What is a neurodevelopmental perspective?

A
  • Evidence of lengthy period of abnormality prior to diagnosis - ‘prodromal’ state e.g. longer to
    walk, more speech problems, low educational scores at 8, 11, 15, solitary play preferences.
  • Home videos of adults with schiz and a non-schiz sibling show more neuromotor problems, less +ve facial expressions, odd hand positions
  • 50k+ Male Swedish army conscripts assessed prior to Dx. Found fewer than 2 friends; prefer socialising in small groups; more sensitive than other people; no
    steady girlfriend; ever used drugs (incl. cannabis); low IQ
  • Similar study of Israeli army
    and found deficits in social function, low IQ, lack of organisation ability
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14
Q

What is the role of recreational drug use in Schiz?

A
  • Cannabis linked to increased Schiz
  • Longitudinal study in NZ: early use by 15yo led to greater risk 10.3% had psychosis/schiz = heavy use by 18 associated with 6x risk increase
  • Meta-analysis found that those who used cannabis in adolescence but not alcohol had earlier onset symptoms
  • Increases risk but cannabis use also associated with worse outcomes = more admission for longer periods
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15
Q

What is the role of genetics in schiz?

A
  • Concordance rates for schiz increases the more genes you share with that person
  • Twin studies show people can have an unexpressed schiz gene
  • MZ twins have the same percentage of schiz, but this is much smaller in DZ twins
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16
Q

What were adoption studies?

A
  • Find adopted children with schiz then look at rates in biological mothers
  • In Denmark, all children born 1924 -1947 adopted early
  • Adopted cases admitted for schiz versus control group of adoptees not admitted
  • Significantly higher rates of psychotic admissions in biological parents than adopted parents
  • Classical adoption, twin and family
    association studies from the 1960’s/1970’s highlighted the potentially important role of genetic factors in the development of schizophrenia
17
Q

What is further evidence for genes?

A
  • First risk gene Neuregulin 1
  • 12 candidates plus 6 more
  • 13 new risk loci
  • Over 100 potential gene variants
    BUT
  • New candidate genes still emerging
  • The ‘schizophrenia gene’ findings are not well replicated and a complex POLYGENIC
    picture is emerging
  • Increasing notion that genetic risk not specific for schizophrenia, but for other
    psychiatric disorders as well
18
Q

What are the broad conclusions for the genomics revolution

A
  • Psychiatric disorders are polygenic i.e. many
    genes involved
  • Extensive pleiotropy at level of clinical
    diagnosis
  • Increasing evidence for convergence onto
    plausible biological systems, e.g,. glutamate
    neurotransmission
  • Pleiotropy occurs when one gene influences multiple, seemingly unrelated phenotypic traits, an example
    being phenylketonuria, which is a human disease that affects multiple systems but is caused by one gene
    defect