Task 1: Response Selection Flashcards
A1: What brain structures/systems are involved in planning an action in response to visually presented object?
Visual targets --> Intraparietal Cortex Motor goal --> FEF Combining them --> lPFC Action selection --> PreSMA Movement specification --> dPreMC/PMC
A2: Explain Wong’s scheme
(1) Identifying the motor goal
name steps/functions + brain regions
What: perceptual decision-making/selection of motor goals: generally takes time
o 1) Observation of environment (Occipitoparietal cortex)
o 1a) Attention (lateral intraparietal area), salience/priority map for spatial attention
o 2) Task Rules (encoded in lateral PFC), higher order decisions to define the motor goal
o 1 & 3 kind of form a dorsal attention system
o 3) Object selection (FEF), transition from decision about stimulus to decision about motor action
A2: Explain Wong’s scheme
(2) executing an action to achieve the motor goal
name steps/functions + brain regions
How: movement decision-making/motor planning; set of processes describing how motor goal will be achieved; generally very fast, despite 4)
o 4) Abstract Kinematics (parietal cortex)
Stores multiple movement options to reach goal –> how movement will look; optional/for complex tasks
o 5) Action Selection (vPreMC, (Pre)SMA; related to ventrodorsal pathway)
Choice & decription of motion of the end-effector (e.g. body part, tool) independent of arm posture
o 6) Movement Specification (dPreMC, PMC; related to dorsodorsal pathway)
Complete motor command of limb and any posture adjustments are determined
A2: What dos the Drift Diffusion Model say about how motor goals are reached?
Evidence about motor goal is accumulated until a threshold is reached to make a decision.
- relates to FEF (object selection)
- Can be seen in movements of uncertain individuals
- Study with jumping target
• Response briefly after switch: still old response, somewhat certain
• Response after switch: new response, somewhat certain
• Response long after switch: new response, very certain
Motor planning vs. Motor execution
Keywords: Null space & Dynamic Systems Model
Same areas: mPMC and PreMC
Different firing-rate space
Motor planning: average firing rate remains constant –> null space
Motor execution: drives muscle activity –> moving away from null space
Dynamic Systems Model (DSM)
Motor Cortex is a dynamic system: it can be active without movement execution–> aka it can be active without leaving the null space –> this is the case in motor planning
A2: Clarify the role of feedback control policies (draw parallel with inverse models from the course Functional Neuroanatomy)
Optimal Feedback Control
Determines complete movement trajectory taking into account:
current state of the limb
motor target (endpoint)
cost between the two
–> inverse model (process defined based on goal)
A3: Where does the exogenous path of action run along?
Exogenous path/How pathway
- overlaps with dorsaldorsal stream
Visual Cortex -> IPS (LIP/MIP) + SPL -> PostCS
A3: What is the function of the exogenous pathway? Why is it called “how” pathway
Dorsal stream –> How –> action/movement initiation
Lesion in superior PPC –> Optic Ataxia
- inability to use visual info to guide action
- still intact visual/spatial perception
- can be unilateral
e. g. can tell where something is but cannot point to it
A3: Describe the dorso-dorsal subpathway (Binkofski & Buxbaum, 2013)
Mention its anatomical organization & functional relevance
Dorsodorsal –> exogenous path
Visually guided motor control
(e.g. reaching)
Movement specification
Via V1 –> IPS –> SPL –> PostCS
Lesion in sPPC –> optic ataxia
(impaired use of visual info to guide action)
A3: Describe the ventro-dorsal subpathway (Binkofski & Buxbaum, 2013)
Mention its anatomical organization & functional relevance
Ventrodorsal –> endogenous path
Praxis, skilled motor acts & tool use, more cognitive/based on LTM
(e.g. grasping & manipulating)
Action selection
Via V1 –> Angular Gyrus –> SMG
Lesions in IPC, vPreMC & connections–> Ideomotor apraxia/limb apraxia
(cannot fulfill instructed movements, interact with an object or mime those actions,
intact reflexive/unconscious movements)
Briefly describe the ventral pathway
Function & What if lesion?
Ventral stream –> what –> object identification
Lesion –> visual form agnosia
A4: What is self-generated movement? (vs. non-self-generated action)
Self-/internally generated action
- Operant behaviour: response on own accord –> initial change inside respondent
vs. respondent behaviour: response to external stimulus –> initial change in environment
Flexible depending on goal
- change in goal –> change in action
- failed to obtain goal –> change in action
Automatic inhibition mechanism of prepotent responses
–> needed for flexible voluntary behaviour
In accordance with rules/task demands
- representation of goal to retrieve correct action
Other conditions for self-generating actions
- specified by time they needed
- one action can cue the next one
A4: What is the role of the (Pre)SMA in self-generated movement?
Activity in (Pre)SMA
- -> neurons fire earlier & only for self-initiated movements
- -> code for time intervals needed
- -> code for specific transaction between actions
Lesion (Passingham)
- Monkeys tested in the dark to eliminate cues for exogenous actions
- -> reduced self-initiated movements & inability to learn movements
- -> anarchic hand syndrome/Dr. Strangelove Syndrome
A5: Explain the study by Sumner et al (2007)
- Task paradigm
Masked-prime task
- “invisible” primes cueing target location followed by actual target
–> trigger automatic cue-response associations
- Conditions:
Button-press (motor) vs. saccades (oculomotor)
Compatible vs. incompatible trials
A5: Explain the concepts of Positive and Negative compatibility effect
Time between prime & stimulus < 100ms
- -> PCE/facilitatory priming
- -> compatible trials vs. incompatible –> faster RTs
Time between prime & stimulus > 100ms
- -> NCE/automatic inhibition
- -> compatible trials vs. incompatible –> slower RTs
- -> due to auomatic inhibitory mechanism
-> we expect a difference between compatible & incompatible trials in how the NCE affects RTs in healthy people
A5: Explain the study by Sumner et al (2007)
- Hypotheses & results
CB: lesion in SMA & right SEF
- Hypothesis
Impaired saccades & manual movements
- Result:
No NCE, but always PCE for both type of movements
JR: left SEF
- Hypothesis:
Impaired saccades only
- Results:
No NCE, but PCE for saccades only
AG: no relevant lesion (PreSMA)
- Hypothesis:
No impairment of NCE
- Results:
Normal NCE in both
RS, VC: no relevant lesion (lPreMC)
- Hypothesis:
No impairment of NCE
- Results:
Normal NCE in both
In summary:
- -> Automatic inhibition is effector-specific
- -> Unilateral lesions lead to loss of automatic inhibition (NCE) on both sides of body –> thus, important for self-initiated movement
- -> SMA lesion –> issues with manual tasks
- -> SEF lesion –> issues with oculomotor tasks
Explain object affordances
Object affordances:
Association between potential actions & perceived object
–> link between object selection & action selection
Determined by:
- Pragmatic features of objects (e.g. size, shape, …)
- Motor capacities (e.g. strength, agility of limb…)
- Context
No semantic knowledge needed
Takes effort to override strong object-action associations
- Needs top-down control
A6: Describe Ideomotor (IMA)/limb apraxia
- Lesions
- Dysfunction
- Conclusions about motor system
Ideomotor apraxia/limb apraxia
Lesions
- dorsoventral pathway (V1 -> AngularG -> SMG)
- IPC (includes AG & SMG), vPreMC & parieto-premotor-connections
Dysfunction
- impaired fulfillment of instructed movements
- Impaired interaction with an object (tool use)
- Impaired pantomiming/miming of interactions with objects
- intact reflexive/unconscious movements
Conclusions
- > both HPs store gesture representation
- > left BG controls spatial & temporal features of learned movements/sequences & inhibition
- > PPC involved in preparation & execution of eye movement, grasping, reaching & hand position
A6: Describe Optic Ataxia
- Lesions
- Dysfunction
- Conclusions about motor system
Optic Ataxia
Lesion
- dorsodorsal pathway (V1 -> IPS -> SPL -> PostCS)
- sPPC (mainly SPL & IPS)
(impaired use of visual info to guide action)
Dysfunction
- impaired coordination between visual input & motor outputs
- intact general motor abilities
Conclusions
- -> PPC (+ part of frontal cotex that follows it) is involved in reaching, saccades, grasps, attention & state estimation
- -> these functions are important for hand-eye movement
A6: Describe Dr Strangelove Syndrome
- Lesions
- Dysfunction
- Conclusions about motor system
Anarchic hand syndrome/Dr. Strangelove Syndrome
Lesion
- PreSMA (also ACC and PCC)
- also caused by callosum surgery
Dysfunction
- contrallesional hand is not under voluntary control
- dysfunctional hand performs complex, goal-oriented actions
- often oppositional behaviour
Conclusions
–> damage to parietal cortex can cause lack of awareness of movements due to loss of feedback
What is the relation between dorsodorsal & ventrodorsal pathways with the area AIP
What is the relation between ventral & dorsal
Relevance of area AIP
- has motor dominant cells, visuomotor cells & visual dominant cells
- -> combine visual info with motor info for action
Ventral connected with dorsal
But dorsodorsal & ventrodorsal are dissociated
Describe light-motor sensitivity in the intraparietal area (AIP)
Area AIP (anterior intraparietal) Motor dominant cells - Active for manipulation in light & dark - Doesn’t fire when there’s no movement -> only motor
Visuomotor cells
- Fire when manipulating in light, bit less in dark
- Even just object fixation has some activation
- > both visual & motor response
Visual dominant cell
- Fire when manipulating in light and when just fixating
- > only visual
