Task 1 Flashcards

(43 cards)

1
Q

1.1.: What brain structures/systems are involved in planning an action in response to visually
presented object?

A

Intraparietal cortex (IPC), PFC, FEF, (pre)SMA & PMd+M1

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2
Q

Function of Intraparietal cortex (IPC)?

A

‘What?’

  • Representing relevant stimuli
  • Helps selecting motor goals
  • Salience map for spatial attention
  • Guides visual attention
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3
Q

Function of (lateral) PFC?

A

‘What?’

  • Translates visual targets into motor goals
  • Encodes relationship between object & goals –> according to rules
  • Determines whether to proceed motor action or to inhibit –> influenced by priming & difficulty
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4
Q

Function of frontal eye filed (FEF)?

A

‘What?’

  • Represents motor goals selected on behalf of stimuli
  • Initially several target choices but evolves to only one goal –> Drift diffusion model
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5
Q

Function of (pre)-SMA?

A

‘How?’

  • Action selection
  • Control over voluntary actions in situations of response conflict
  • PRE-SMA: Monitoring of outcomes
  • SMA: Inhibition of primed actions
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6
Q

Function of PMd + M1?

A

‘How?’

  • Movement specification
  • Determine motor command of limb & postural adjustment
  • Activity before movement –> define how it is executed
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7
Q

1.2.: Explain Wong’s scheme –> WHAT pathway (selection of motor goals)

A

Observation of environment (LIP) –> Attention –> Object selection (LIP) –> Application of task rules to select object (PFC) –> Motor goals (FEF)

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8
Q

Explain Wong’s scheme –> HOW pathway (motor planning)

A
Action selection (pre-SMA, PMv) --> Movement specification (PMd & M1)
=> complex tasks: abstract cinematics
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9
Q

What’s the role of feedback control policies?

A

o We flexibly change plans
o Allows us to be more flexible, it’s less effortful
o Corrections to initial movement plan
o Flexibly reapplies + changes old plan rather than making a new plan
==> Inverse model: comparison between predicted vs actual sensory feedback

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10
Q

1.3.: What is the HOW-pathway? Its function? (EXOGENOUS pathway)

A
  • dorsal pathway
  • -> visuomotor integration
  • -> how to direct action with regards to stimulus
  • -> motor planning
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11
Q

Where is the HOW (dorsal) pathway in the brain?

A

visual cortex –> parietal cortex –> premotor cortex

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12
Q

Where is the dorso-dorsal stream in the brain?

A

V3a –>V6 –> V6a –> dorsal PMA

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13
Q

Function of dorso-dorsal stream? Important for what- grasp or use?

A

-Online visually guided motor control
-Processes structural characteristics (size, shape, orientation) to guide online action toward a currently visible stimulus
-Structure-based action
==> GRASP system

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14
Q

Which disorder does a lesion in dorso-dorsal stream lead to?

A

optic ataxia –> misreaching visual targets

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15
Q

Where is the ventro-dorsal stream in the brain?

A

Medial superior temporal area –> inferior parietal lobe –> ventral PMA

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16
Q

Function of ventro-dorsal stream? Important for what- grasp or use?

A

-More cognitive, based on long-term experiences with objects
-Important for ‘praxis’ + tool use
-Transforms visual inputs into representations
-Function-based actions
==> USE system

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17
Q

Which disorder does a lesion in ventro-dorsal stream lead to?

A

ideomotor/limb apraxia ==> impaired performance of skilled motor acts (without direct visual control)
(but intact sensory, motor + language function)

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18
Q

Visual pathway: Ventral ‘what’ pathway

A
  • Recognition of objects
  • ‘what am I seeing?’
  • From V1-V4 to inferior temporal cortex
19
Q

Visual pathway: Dorsal ‘how’ pathway

A
  • Involved in visually guided behaviour
  • ‘How to adjust my behaviour based on visual perception?’
  • V1-V4 to parietal cortex
  • Subdivison into 2 pathways
    1. dorso-dorsal pathway
  • -> online visually guidance of actions
    2. ventro-dorsal pathway
  • -> skill-based/tool-based action
20
Q

1.4: Endogenous action- which areas are involved in self-generated movement?

A

Medial frontal lobe: Pre-SMA, SMA, ACC + SEF (=supplementary eye field)

21
Q

Evidence from monkey studies- what happenes when you remove (pre)-SMA or cingulate motor areas?

A

Reduction in self-initiated movements + inability to learn new movements

22
Q

Evidence from Sumner study (lesioned patients)

A

one of the roles of the SMA + SEF is to contribute automatic inhibition of primed actions

23
Q

Role of SMA & SEF in voluntary behaviour

A

-involved in unconscious + involuntary motor control
-mediate automatic effector-specific suppression of motor plans
==> Automatic inhibition is an important part of flexible, volitional behaviour

24
Q

Role of pre-SMA in voluntary behaviour

A
  • parietal external + medial-prefrontal internal source of action control
  • > kept in balance from the pre-SMA
  • Activity starts earlier when self-initiated than externally motivated actions
25
Role of anterior cingulate sulcus in voluntary behaviour
- Assigning values to goals - Cells fire when action is not followed by expected reward -> alternative action must be performed next - Involved in switching between actions when no external cue specifies a switch
26
1.5: Sumner Study- Hypotheses
- SMA responsible for inhibition of manual movements | - SEF responsible for inhibition of eye movements
27
1.5: Sumner Study- Task paradigm
-subj. responded to target arrows (either left or right) - preceded by brief primes (again, either left or right) rendered invisible by the mask
28
1.5: Sumner Study- Results
hypothesized effects confirmed → therefore: dissociation between mechanisms of control undertaken by SMA or SEF and those by pre-SMA
29
What is a negative compatibility effect (NCE) & when does it occur?
at longer prime- target delays → negative compatibility effect (NCE) = response slower for compatible than for incompatible primes
30
What is NCE an index for?
an automatic inhibitory mechanism that suppresses the subthreshold motor activation evoked by the prime, stopping it from interfering with an alternative response to the target
31
Sumner study- Hypotheses about patients
CB: disrupted inhibition for both eye and manual responses | - JR: dissociation between manual and saccadic responses → only eye responses impaired
32
Sumner study- Hypotheses about patients & lesions of patients
- CB: disrupted inhibition for both eye & manual responses (CB → damaged SEF & SMA) - JR: dissociation between manual & saccadic responses → only eye responses impaired (SEF damaged; much of SMA spared)
33
What are SMA&SEF important for as shown in Sumner's study?
SMA & SEF contribute to automatic inhibition of primed actions --> important component of flexible, volitional behavior
34
1.6: Ideomotor apraxia- symptoms
Impaired performance of skilled motor acts (despite intact sensory, motor and language function) --> tool use impaired
35
1.6: Ideomotor apraxia- Causes
lesions in inferior parietal & ventral premotor cortex & connecting white matter--> networks
36
1.6: Ideomotor apraxia- linked to which stream?
ventro-dorsal stream (How stream) --> skilled, functional object-related action (long-term experience with objects & tools) --> interact, grasp, manipulate objects
37
1.6: Optic ataxia-symptoms
- Impaired use of visual information for action guidance | - Can discriminate object size, but cannot scale their grip appropriately
38
1.6: Optic ataxia- causes
Caused by superior posterior parietal lobe lesions
39
1.6: Optic ataxia- linked to which stream?
dorso-dorsal stream (How stream) --> reach component
40
1.6: Alien hand syndrome-causes
Lesions in medial (pre-)SMA --> involved in suppressing inappropriate/unwanted action plans
41
What's the role of SEF & SMA regarding affordances?
Frees from affordances of environment
42
Figure 2: Grasp vs use ==> GRASP
- structure-based action --> grasping: only slower for conflict items when preceded by use task - Grasp: Quickly activated but also decays very quickly
43
Figure 2: Grasp vs use ==> USE
-Function based actions --> use: slower for conflict object --> more related to longer processing; we also take memory & knowledge into account