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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
Define Reality Distortion by Liddle 1987
Delusions | Hallucinations
26
Define Disorganisation Syndrome by Liddle 1987
Inappropriate affect Distractibility Poverty of content of speech Thought disturbances
27
What 5 factors did Liddle expand to in 2002
1. Psychomotor poverty 2. Reality distortion 3. Disorganisation 4. Psychomotor excitation 5. Anxiety/Depression
28
Developed world what are the 4 leading causes lost year of healthy life aged 15-44
1. Major depressive disorders 2. Alcohol use 3. Road traffic accidents 4. Schizophrenia
29
What are the cognitive symptoms a target for
Applied research | Drug companies
30
What did Fletcher and Frith 2009 identify as voices in the head
Audible thoughts - after own thought head another voice. Embodied Voices arguing Voices commenting on actions Influence on body - somatic positivity
31
What did Fletcher and Frith 2009 identify as thoughts in the head
Thoughts of withdrawal Inserting Broadcasting Delusional perception
32
What did Fletcher and Frith 2009 identify as “made”
Made feelings Impulses Volitional acts - delusions of control
33
Outline enlarged ventricles in twins with Schiz
Structural physical change Replicated Maguire - hippocampal size increased London taxi drivers. Physical difference not always due to illness can be down to experience
34
Criticisms of enlarged ventricles in Schiz
Other causes not specific to Schiz Brain plasticity Must ppts medicated being tested If not medicated often unusual condition
35
What studies investigate frontal cortex brain activation during executive tasks in Schiz
N back task Haying task
36
Outline the N back Task
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
Outline results N Back task
Activation across frontal cortex | Activation lower in Schiz
38
Outline Haying Task
Test Inhibition Given part of sentence Asked to complete sentence by providing an extra word
39
Results of Haying Task
Activation across Frontal Cortex Brain | Activation lower in Schiz
40
How can we correct for medication use in studies
See if higher doses produce higher effects than lower doses If they do probably effect of medication
41
Outline fMRI study looking at the activation of the brain whilst people are hallucinating
Ppts press button when felt hallucinations coming on Experiencing hallucinations as if they are real activating specific brain regions
42
Outline early and late gray matter deficits in Schiz by Thompson et al 2001
Loss gray matter as disease progresses Down to long term drug use Different social environments, being treated differently, don’t have a job
43
Outline Bressler and Menon 2009 faulty connectivity in Schiz Ventral Medial PFC -> PCC
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
Outline Bressler and Menon 2009 faulty connectivity in Schiz Salience Network AI -> ACC
Dynamic switching Associated emotion VTA = reward Orientation most salient things in environment
45
Outline Bressler and Menon 2009 faulty connectivity in Schiz Central Executive Network Dorsal Lateral PFC -> PPC
Exogenously drive Cognitively demanding mental activity Switching between activities = WM loaded Faulty connectivity leads positive symptoms
46
What is the % of general population getting Schiz
1
47
What is the likelihood of getting Schiz if your identical twin has it
48
48
What is the likelihood of getting Schiz if your fraternal twin has it
17
49
What is the likelihood of getting Schiz if your children has it
13
50
What is the likelihood of getting Schiz if your siblings have it
9
51
What is the likelihood of getting Schiz if your parents have it
6
52
What are the approaches to investigating the neurochemistry of Schiz
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
Outline the dopamine theory of Schiz
Overactivity in brain dopamine transmission Hyperactivity Mesolimbic dopamine rise to positive symptoms Hyperactivity frontal cortex rise negative
54
How does the effectivity of antipsychotic drugs parallel support the dopamine theory of Schiz
Effective antipsychotics parallels their pharmacological potency in blocking dopamine binding
55
How does the dopamine theory account for the role of Amphetamine
Amphetamine which releases dopamine Induces psychosis Responds to neuroleptics
56
What is the link between the Dopamine Theory and Parkinson’s
Parkinson’s is a side effect of neuroleptic Reduce dopamine in striation Restricting movement of body Develop Parkinson’s
57
Outline post mortem study support for the dopamine theory of Schiz
Receptor affinity studies increased D2 but not D1 receptors in striatum Mixed results D4 receptors - 6 fold in Schiz others no D4 receptors
58
Outline Abi Darghone et al increases striatal dopamine transmission support of dopamine Theory
``` Binding in PET Compounds displace amphetamine Give amphetamine binds to dopamine Greater effect those with Schiz Hyperactivity dopamine System in Schiz ```
59
Outline the dopamine systems
VTA - thalamus areas and cortex - pre frontal region Substantia Nigra region - extremely involved motor behaviour Blocked causes motor side effects
60
Outline Howes et al 2009 elevated striata dopamine function linked to Prodromal signs of Schiz
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
Outline Metabolite Measurements - Peripheral Markers
Brain DA turnover reflected by plasma Homovanillic acid concentrations Chronic antipsychotic treatment lowers plasma HVA related good treatment outcomes
62
Outline In Vivo Methods Animal Studies
Mesolimbic dopamine System implicates animal models of disrupted selective attention in Schiz Latent Inhibition Pre pulses Inhibition
63
Outline In Vivo Methods Animal Studies findings on antipsychotics
Chronic antipsychotic decrease dopamine firing A9 naac and A10 striatum Chronic atypic antipsychotics decrease firing in A10
64
Outline animal models of Schiz
Selective attentional models be disrupted by augmentation of dopamine function Latent Inhibition disrupted by amphetamine - reversed by antipsychotic drugs: Haloperidol clozapine
65
Outline D-amphetamine abolishing latent Inhibition
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
Outline In Vivo Methods of Patient Studies
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
What is the neurochemistry of Glutamate and Schiz
Drugs block glutamate receptors such as PCP Produce psychosis
68
What is the neurochemistry of Serotonin and Schiz
Atypical antipsychotic drugs high affinity for 5-HT2 receptor Via modularity role on DA function
69
What is the neurochemistry of GABA and Schiz
Modulators role on DA function
70
Outline abnormalities of NMDA and Kainate receptors of Schiz and glutamate
Abnormalities NMDA and Kainate receptors in Schiz prefrontal cortex Associated up regulation of NR1 subunit
71
Outline decrease in glutamate synthesis and Schiz
Decrease glutamate synthesis release in cortex Decrease certain receptor sites for glutamate in certain areas brain Such as Cingulate and hippocampus
72
Links between cognitive deficits glutamate and Schiz
``` Cog deficits consequence reductions in transcript mRNA for receptor subunits NMDAR1 GLUR1 GLUR7 KA1 In frontal cortex ```
73
Links between glutamate PCP and Schiz
PCP induces psychosis | Is a non competitive NMDA antagonist

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