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Neuroscience and behaviour > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

historical background SZ

kraepelin (1898)

A
  • dementia praecox
  • impairments in att, mem & goal-directed beh
  • progressive, no return to premorbid functioning
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2
Q

historical background SZ

bleuler (1911)

A
  • coined term SZ
  • characterised fragmented thinkning
  • +ve & -ve symptoms
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3
Q

SZ according to DSM

A
  • syndrome
  • combination of variable degrees of +ve, -ve & cog deficits
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4
Q

+ve symtpoms SZ

type I

A
  • delusions
  • hallucinations
  • disorganised beh
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5
Q

delusions

A
  • false belief despite ev to contrary
  • distorting reality
  • Thought insertion
  • Thought withdrawal
  • Thought broadcasting
  • Not being in control of own actions
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6
Q

hallucinations

A
  • perceptual experience seems real in absence of physical proof
  • Most common: auditory, visual, olfactory
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7
Q

disorganised beh

+ve symptoms

A

Can affect speech, difficulties with routine tasks, inappropriate emotions

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8
Q

-ve symptoms

type II

A
  • 2 subdomains (Lim et al.)
  • diminished emotional expression
  • avolition
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9
Q

diminished emotional expression

-ve symptom

A
  • Affect: blunted affect, mood or emotional state, limited range of emotions
  • Alogia: poverty of speech, lack of conversation
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10
Q

avolition

-ve symptoms

A
  • Apathy (lack of motivation)
  • Social withdrawal
  • Anhedonia: inability to feel pleasure
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11
Q

cog deficits

SZ symptoms

A
  • can be variable (selective or general)
  • Executive functions/cog control (incl. verbal fluency & problem solving)
  • Attention (incl. vigilance)
  • Processing speed
  • Memory (working mem, episodic mem)
  • Social cognition
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12
Q

SZ as a neurodevelopmental disorder

A
  • +ve/-ve symptoms during late adolescence
  • Cog deficits detectable in childhood/adolescence
  • Slow emergence of brain abnormalities (neuro-developmental)
  • Combination of genetics & environment (~80% heritable)
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13
Q

genetics role in SZ

neurodev disorder

A
  • Prevalence = 1%
  • Children or siblings of affected inds 10x more likely to develop SZ
  • Polygenic disorder: at least 108 genes implicated
  • Genetics only explain small percentage of cog variance
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14
Q

environmental risk factors SZ

neurodev disorder

A
  • Adverse events prenatally or perinatally e.g. poor maternal nutrition, infection
  • Contact with certain viruses in early childhood might increase risk
  • Growing up in urban environment
  • Air pollution
  • Drugs: some inds develop SZ after taking certain drugs e.g. cannabis
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15
Q

NT systems involved in SZ

A
  • dopamine
  • acetylcholine
  • glutamate - excitatory NT
  • GABA - inhibitory NT

also serotonin & adrenalin

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16
Q

dopamine system in SZ

A
  • +ve symptoms
  • att
  • WM
  • cog control
17
Q

acetylcholine system in SZ

A
  • att
  • mem
18
Q

dopamine hypothesis

A
  • Important role of mesocortical dopaminergic pathway (from tegmentum)
  • Typical antipsychotic medication reduces DA levels in brain
  • Dissociation: cortical vs striatal DA
  • DA levels fluctuate in inds with SZ over time, cog symptoms much more stable –> close link is unlikely
19
Q

role of mesocortical dopaminergic pathway

dopamine hypothesis

A
  • DA agonists can induce psychotic symptoms
  • Disturbances in DA system: impaired cog functions
20
Q

cortical vs striatal DA

dopamine hypothesis

A
  • Hypodopaminergic state in cortex - too little
  • Hyperdopaminergic state in striatum - too much
21
Q

glutamate & SZ

A
  • Dysregulation of DA system only secondary to impaired Glu function
  • Postmortem brains of SZ patients: loss of Glu neurons in ACC (& other brain areas)
  • 2 phases of Glu modulations
  • decreased glu in patients (meta-analysis of MRS studies)
22
Q

2 phases of Glu modulations

SZ (Moghaddam & Javitt, 2012)

A
  1. NMDA-mediated interneuron dysfunction –> loss of inhibitory control, increased Glu levels
  2. Glu-induced excitotoxicity –> loss of Glu connections; decreased Glu levels
23
Q

magnetic resonance spectroscopy

MRS

A

measure neurometabolites in vivo

24
Q

neuroanatomical diffs SZ

A
  • weigh less
  • Enlarged ventricles
  • Reduced neuron numbers in prefrontal cortex
  • Thinner parahippocampal gyri
  • Abnormal cellular structure in prefrontal cortex & hippocampus
  • grey matter loss
25
Q

grey matter loss in SZ

meta-analysis chronic SZ

A
  • Medial frontal cortex, anterior cingulate cortex
  • Insular cortex bilaterally
  • Left thalamus and caudate
  • Amygdala bilaterally
26
Q

cog control SZ

barch & ceaser (2012)

A
  • Hypothesis: common mechanism across cog domains ‘context processing’, ‘WM’ & ‘episodic mem’
  • –> impairment in representing goal info in WM to guide beh
  • = impairment in proactive control
  • Proactive control associated with representation of info in dorsolateral prefrontal cortex (DLPFC)
27
Q

working mem in SZ

A
  • no general WM deficit but impairments in specific components
  • central executive
  • visuo-spatial sketchpad & phonological loop
28
Q

central executive & SZ

A
  • associated with DLPFC in healthy inds
  • patients show difficulties with this area
  • e.g. goal-representation
  • patients have reduced DLPFC activity
29
Q

visuo-spatial sketchpad & phonological loop in SZ

A
  • no strong ev for selective impairment in these components
  • associated with ventrolateral prefrontal & central parietal brain areas in healthy inds
  • fMRI studies - intact activity in these areas in patients
30
Q

processing speed in SZ

dickinson et al. (2007) meta-analysis

A
  • impairments in processing speed in patients
  • Processing speed measured with digit symbol coding-type tasks
  • Slowed processing speed in patients might be due to lack of integrity of white matter fibre tracts
  • Or due to possible WM aspects in test
31
Q

episodic mem in SZ patients

A
  • Relational mem more impaired than item mem
  • Associated with reduced DLPFC activity (but hippocampus might play a role as well)
  • Recollection more impaired than familiarity during remembering
  • Supports hypothesis that encoding items in relation to their context is disrupted in SZ
32
Q

decision-making in SZ

A
  • Motivational impairments in SZ
  • Culbreth et al.: atypical effort-based decision-making may contribute to motivational impairments
  • Effort-based decision-making: inds with SZ less willing to exert effort to get monetary rewards in experiments
33
Q

motivational impairments in SZ

A
  • affects social & occupational functioning
  • No effective treatments
  • Underlying mechanisms not clear
34
Q

neural correlates of effort-based decision-making

SZ

A
  • Structures involved in effort-based decision making in healthy inds: Medial frontal cortex, Ventral striatum, Dopamine systems
  • Inds with SZ: reduced BOLD activity in ventral striatum, posterior cingulate & medial frontal cortex during effort-based decision-making
35
Q

anticipatory pleasure & SZ

A

studies have shown correlations between anticipatory pleasure & effort in patients: those who reported more anticipatory pleasure, expended more effort

36
Q

defeatist performance beliefs

SZ

A
  • -ve beliefs about their ability to complete a task successfully
  • Belief influences precision of estimated effort (task might be a lot harder than you thought if you are not good at something)
37
Q

dopaminergic medication

SZ

A
  • Antipsychotics block dopaminergic (D2) receptor sites
  • Antipsychotics might modulate activity in brain areas involved in effort-based decision making
  • Culbreth et al.: D2 affinity of patient’s drug correlated with willingness to put effort in a task

Neuroscience and behaviour (17 decks)

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