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Neuroscience > Lecture 7 - Introduction to Schiz > Flashcards

Lecture 7 - Introduction to Schiz Flashcards

1
Q

Outline Falvet 1851 on discovery schizophrenia

A 
Falvet circulaire 
Circular madness 
Extremes highs and lows mood 
Looked isolation 
Distinguish subtypes
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2
Q

Outline Hecker 1871 on discovery schizophrenia

A 
Hebephrenia
First describe Schiz symptoms 
Early onset 
Deteriorating over time 
Problems emotion 
Sub types symptoms
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3
Q

Outline Emil Kraeplin 1898 on discovery schizophrenia

A

Combined into single disease - dementia Praecox
Seeing psychiatric diseases biological
Dissecting brains
First describe illness progressive no return

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4
Q

How does Kraeplin 1898 describe dementia

A

Global disruption of perceptual and cognitive processes

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5
Q

How does Kraeplin 1898 describe Praecox

A

Early adulthood onset

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6
Q

Who coined the term dementia Praecox

A

Emil Kraeplin 1898

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7
Q

Outline Eugen Bleuler 1911 on discovery schizophrenia

A

Reformulated dementia Praecox
Coined term schizophrenia
Characterised: fragmented thinking, breakdown of integrated functions coordinate affect and behaviour
Disturbances of association primary symptoms of Schiz

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8
Q

Who coined the term schizophrenia

A

Eugen Bleuler 1911

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9
Q

What did Bleuler 1911 identify as primary symptoms of Schiz

A

Disturbances of association

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10
Q

What does Bleuler 1911 believe schizophrenia Stands for

A

Schizo = split

Phrene = mind

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11
Q

What are Bleuler 1911 4 As

A

4 elements understand symptoms

Association
Ambivalence
Autism
Aspesticity

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12
Q

Outline Positive Type 1 symptoms of Schiz by Tim Crow 1980

A

Delusions
Hallucinations
Thought disorders

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13
Q

Outline Negative Type 2 symptoms of Schiz by Tim Crow 1980

A

Anhedonia
Flattened affect
Avolition
Alogia

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14
Q

Outline cognitive symptoms of Schiz by Tim Crow 1980

A

Working memory
Executive dysfunction
Attentional deficits

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15
Q

Outline delusions as positive symptoms of Schiz

A

False belief despite evidence contrary

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16
Q

Outline Bizarre delusions as positive symptoms of schizophrenia

A

Bizarre delusion = thought insertion withdrawal thought broadcasting made actions

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17
Q

Outline examples of delusions as positive symptoms of schiz

A 
Persecutory 
Paranoid 
Control 
Grandiose 
Reference
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18
Q

Outline hallucinations as positive symptoms of Schiz

A

Perceptual experience real in absence physical proof

Most common auditory visual olfactory

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19
Q

Outline thought disorders as positive symptoms of Schiz

A

Inventing words
Trouble understanding common words
Changing topic

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20
Q

Outline negative symptoms of Schiz

A

Blunted affect
Mood or emotional state
Limited range emotions
Anhedonia: inability to feel pleasure

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21
Q

Outline cognitive thought symptoms of Schiz

A

Avolition - unable begin tasks lack motivation
Alogia - unable speak
Problems working memory planning learning
Problematic - prevent joining workforce

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22
Q

What did Peter Liddle 1987 conduct

A

Re examined positive negative dichotomy

Included 3rd factor disorganisation Syndrome - attributed to positive dimension

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23
Q

What 3 Syndrome categories did Liddle 1987 identify

A

Psychomotor poverty

Reality distortion

Disorganisation Syndrome

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24
Q

Define Psychomotor Poverty by Liddle 1987

A

Poverty of speech
Decreased spontaneous movement
Blunted affect

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25
Q

Define Reality Distortion by Liddle 1987

A

Delusions

Hallucinations

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26
Q

Define Disorganisation Syndrome by Liddle 1987

A

Inappropriate affect
Distractibility
Poverty of content of speech
Thought disturbances

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27
Q

What 5 factors did Liddle expand to in 2002

A
  1. Psychomotor poverty
  2. Reality distortion
  3. Disorganisation
  4. Psychomotor excitation
  5. Anxiety/Depression
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28
Q

Developed world what are the 4 leading causes lost year of healthy life aged 15-44

A
  1. Major depressive disorders
  2. Alcohol use
  3. Road traffic accidents
  4. Schizophrenia
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29
Q

What are the cognitive symptoms a target for

A

Applied research

Drug companies

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30
Q

What did Fletcher and Frith 2009 identify as voices in the head

A

Audible thoughts - after own thought head another voice. Embodied

Voices arguing

Voices commenting on actions

Influence on body - somatic positivity

31
Q

What did Fletcher and Frith 2009 identify as thoughts in the head

A

Thoughts of withdrawal

Inserting

Broadcasting

Delusional perception

32
Q

What did Fletcher and Frith 2009 identify as “made”

A

Made feelings

Impulses

Volitional acts - delusions of control

33
Q

Outline enlarged ventricles in twins with Schiz

A

Structural physical change
Replicated
Maguire - hippocampal size increased London taxi drivers.
Physical difference not always due to illness can be down to experience

34
Q

Criticisms of enlarged ventricles in Schiz

A

Other causes not specific to Schiz
Brain plasticity
Must ppts medicated being tested
If not medicated often unusual condition

35
Q

What studies investigate frontal cortex brain activation during executive tasks in Schiz

A

N back task

Haying task

36
Q

Outline the N back Task

A

Asked press key if target letter appears
Then if the target letter is same as 1 letter before press key
Same as 2 letters before etc

Go back increases load on working memory

37
Q

Outline results N Back task

A

Activation across frontal cortex

Activation lower in Schiz

38
Q

Outline Haying Task

A

Test Inhibition
Given part of sentence
Asked to complete sentence by providing an extra word

39
Q

Results of Haying Task

A

Activation across Frontal Cortex Brain

Activation lower in Schiz

40
Q

How can we correct for medication use in studies

A

See if higher doses produce higher effects than lower doses

If they do probably effect of medication

41
Q

Outline fMRI study looking at the activation of the brain whilst people are hallucinating

A

Ppts press button when felt hallucinations coming on

Experiencing hallucinations as if they are real activating specific brain regions

42
Q

Outline early and late gray matter deficits in Schiz by Thompson et al 2001

A

Loss gray matter as disease progresses

Down to long term drug use

Different social environments, being treated differently, don’t have a job

43
Q

Outline Bressler and Menon 2009 faulty connectivity in Schiz Ventral Medial PFC -> PCC

A

Default mode. Endogenous mediated. Self referential mental activity
Deactivated doing cognitively engaging demanding tasks
Activated social tasks
Self monitoring - know where things are coming from
Abnormality - disruption tell where things coming from

44
Q

Outline Bressler and Menon 2009 faulty connectivity in Schiz Salience Network AI -> ACC

A

Dynamic switching
Associated emotion
VTA = reward
Orientation most salient things in environment

45
Q

Outline Bressler and Menon 2009 faulty connectivity in Schiz Central Executive Network
Dorsal Lateral PFC -> PPC

A

Exogenously drive
Cognitively demanding mental activity
Switching between activities = WM loaded

Faulty connectivity leads positive symptoms

46
Q

What is the % of general population getting Schiz

A

1

47
Q

What is the likelihood of getting Schiz if your identical twin has it

A

48

48
Q

What is the likelihood of getting Schiz if your fraternal twin has it

A

17

49
Q

What is the likelihood of getting Schiz if your children has it

A

13

50
Q

What is the likelihood of getting Schiz if your siblings have it

A

9

51
Q

What is the likelihood of getting Schiz if your parents have it

A

6

52
Q

What are the approaches to investigating the neurochemistry of Schiz

A
  1. Post Mortem studies
  2. Peripheral markers
  3. Mechanism of action of antipsychotic drugs - animals and humans radioactive labelling
  4. In vivo receptor binding PET Scan
53
Q

Outline the dopamine theory of Schiz

A

Overactivity in brain dopamine transmission

Hyperactivity Mesolimbic dopamine rise to positive symptoms

Hyperactivity frontal cortex rise negative

54
Q

How does the effectivity of antipsychotic drugs parallel support the dopamine theory of Schiz

A

Effective antipsychotics parallels their pharmacological potency in blocking dopamine binding

55
Q

How does the dopamine theory account for the role of Amphetamine

A

Amphetamine which releases dopamine
Induces psychosis
Responds to neuroleptics

56
Q

What is the link between the Dopamine Theory and Parkinson’s

A

Parkinson’s is a side effect of neuroleptic

Reduce dopamine in striation
Restricting movement of body

Develop Parkinson’s

57
Q

Outline post mortem study support for the dopamine theory of Schiz

A

Receptor affinity studies increased D2 but not D1 receptors in striatum

Mixed results D4 receptors - 6 fold in Schiz others no D4 receptors

58
Q

Outline Abi Darghone et al increases striatal dopamine transmission support of dopamine Theory

A 
Binding in PET 
Compounds displace amphetamine 
Give amphetamine binds to dopamine
Greater effect those with Schiz 
Hyperactivity dopamine System in Schiz
59
Q

Outline the dopamine systems

A

VTA - thalamus areas and cortex - pre frontal region

Substantia Nigra region - extremely involved motor behaviour
Blocked causes motor side effects

60
Q

Outline Howes et al 2009 elevated striata dopamine function linked to Prodromal signs of Schiz

A

High people Schiz signs coming on but not yet developed

Measuring dopamine function through displacement activity in PET scanning

ARMS - at risk mental state

61
Q

Outline Metabolite Measurements - Peripheral Markers

A

Brain DA turnover reflected by plasma Homovanillic acid concentrations

Chronic antipsychotic treatment lowers plasma HVA related good treatment outcomes

62
Q

Outline In Vivo Methods Animal Studies

A

Mesolimbic dopamine System implicates animal models of disrupted selective attention in Schiz

Latent Inhibition
Pre pulses Inhibition

63
Q

Outline In Vivo Methods Animal Studies findings on antipsychotics

A

Chronic antipsychotic decrease dopamine firing A9 naac and A10 striatum

Chronic atypic antipsychotics decrease firing in A10

64
Q

Outline animal models of Schiz

A

Selective attentional models be disrupted by augmentation of dopamine function

Latent Inhibition disrupted by amphetamine - reversed by antipsychotic drugs: Haloperidol clozapine

65
Q

Outline D-amphetamine abolishing latent Inhibition

A

Amphetamine disruption still occur when absence of dopamine but not for locomotor activity

Creates hyperactive state reliant D2 receptor
But locomotor activity is not - other neuromechanisms involved

66
Q

Outline In Vivo Methods of Patient Studies

A

In vivo methods of D2 receptors affinity in humans using PET scanning

Increase D2 binding no change in other studies

Reasons discrepancies: specificity of ligands and patient populations

67
Q

What is the neurochemistry of Glutamate and Schiz

A

Drugs block glutamate receptors such as PCP

Produce psychosis

68
Q

What is the neurochemistry of Serotonin and Schiz

A

Atypical antipsychotic drugs high affinity for 5-HT2 receptor

Via modularity role on DA function

69
Q

What is the neurochemistry of GABA and Schiz

A

Modulators role on DA function

70
Q

Outline abnormalities of NMDA and Kainate receptors of Schiz and glutamate

A

Abnormalities NMDA and Kainate receptors in Schiz prefrontal cortex

Associated up regulation of NR1 subunit

71
Q

Outline decrease in glutamate synthesis and Schiz

A

Decrease glutamate synthesis release in cortex
Decrease certain receptor sites for glutamate in certain areas brain
Such as
Cingulate and hippocampus

72
Q

Links between cognitive deficits glutamate and Schiz

A 
Cog deficits consequence reductions in transcript mRNA for receptor subunits 
NMDAR1
GLUR1
GLUR7
KA1 
In frontal cortex
73
Q

Links between glutamate PCP and Schiz

A

PCP induces psychosis

Is a non competitive NMDA antagonist

Neuroscience (12 decks)

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