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Action Motor action (Pathways (binkofski e reader)
—> exogenous =…
Action Motor action
Pathways (binkofski e reader)
—> exogenous = where what pathway
—> endogenous = medial prefrontal cortex
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exogenous (binkofski)
(terminates / end into the premotor cortex)
—> dorsal (visually guided)/ ventral stream (skill tools usage)
——> contain possible action targets (used for translation
endogenous
—> medial prefrontal cortex
——-> medial prefrontal also where final decision is made what target to persue and which one to suppress
OOMMGGG :D!!! link to neuroanatomy
exogenous from premiceus directly to premotor area cause where / how and what pathway terminate there
for endogenous voluntary movements it starts at frontal like polar frontal / and them THE WHOLE PATHWAY THAT YOJ DESCRIBED IN YOUR NEUROANATOMY MAP —>frontal —> SMA —> pre SMA —> premotor area (dorsal/ventral) —> Motor area (M1)
dorsal dorsal = grabbing (with frontal eyefield)
---> quick activation :D
---> lesion = optic ataxia (estimation of movement error , overreaching or grasping too short :3 !!)
ventral dorsal = how = memory / knowledge of how to execute movement / skill :3 !!
---> lesion = limbic apraxia (loss of skill (praxia=praxis :D!!) / impairment in use of real objects or mimicking / pantomiming how to use objects
-------> double dissociation :3 !!
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Exam relevant question :D!!
--> whats affordances, why do we need them
and
--> why does memory last longer for use function than for grasping
---> cause use function necessarily needs to invoke grasp function :D? and skill learning with economics = less brain areas used cause specialized motor programs bg and motor area
---> cause efficiency !!! and speed !!! if learning lots of brain active and basal ganglia fires all throughout!
--> once motor plan learned , only basal ganglia active at beginning to trigger motor plan and at the end to end motor plan but apart from that not much from other brain areas WHICH IS VERY EFFICIENT AND FAST !!!
---> so rather than remembering every little motor movement which would be inefficient, we just remember the use / motor plan :) !! way easier and more efficient because the tiny movements we used to learn in beginning not needed in the end when we actually know very well how to perform an action :D!!
Translation (wong)
—> action target into motor target / commands
---> USALLY happens in parallel but they discuss it serially :O !!
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Translation
--> feedback control policy= action selection + motor movement specification ---> motor goal #
---> analog to cerebellum inverse feedback
-------> responsible for smooth movement based on where limb is now and wehre it shoul dbe, how it will feel once it reached the target location/state and the cost associated with it :3 !!
Drift diffusion model
---> evidence = collects in frontal eye fields :D !! :!!:
--> frontal eye fields --> transformation of perception into motor goals --> not needed for simple tasks --> evidence accumulation (drift diffusion model) (mediated by task demands) -----> if reaches threshold = select this motor goal ---------> if asked to move before threshold reached = movement begins in direction of highest accumulated evidence -----------------> even after selection = evidence still collected (can lead to change in motor goal midway through motor movement if threshold for new goal reached or becomes bigger than previously accumulated evidence which did not reach threshold yet!!) ------------> (drift diffusion model) ---> only discrupts saccades when motor goal isnt the same site of visual attention (since not needed fo all sacadic movements FEF not likely to be involved in motoor planning (Superior colliculi = responsible for saccades btw !!
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Summer (pre-SMA+priming)
---> inhibits involuntary movement :p ,thus is responsible for voluntary control :3!!
Priming
---> damage to SMA = no negative compatibility effect
--> damage to Supplementary eye fields (SEF) = no negative compability effect in occulumotor task :D!!
Up to 100ms duration
- faster reaction time if compatible (e.g. ---> , ----> )
- slower reaction if incompatible ( e.g <--- , ----> )
Negative compatabelity effect :3 !!
they prime left, you pay attention left but they dont show stimulus --> but hten as you focus attention abck at center they show it at previously primed location
---> RT longer because you need to update motor plan and also because of inhibition as marking this area at that time as irrelevant :3 !!
more than 100ms priming = negative compatibility effect!! (reverse effects)
- slower reaction time if compatible (---> , --->)
- faster reaction time if incompatible (<--, -->
- ----> Because SMA = inhibits involuntary movement to prime location as for more than 100ms hasn't predicted anything, so when actual stimulus appears, takes longer / faster to respond to area because of that inhibition (10 to 30ms)
If lesion = no negative compability effect, cause SMA no longer inhibitits involuntary movement :D !! #
---> in effect = SMA = important for voluntary action cause inhibits unwanted/ involuntary one :D !!
----> so basically performed same as if prime only shown for 100ms :D!!
If pre-SMA lesioned
---> should not have this negative compability effet, because it wont inhibit refocusing attention back there :3 !! (but that because you always jsut do tasks :D!!) YES cause inhibits involuntary action, so if damaged you just do stuff haha :D !!
--_> cause in SMA information from precunus and PFC converge so if info damaged tehre, inhibitiory effect of PFC doesnt get trhough :p !! so also not to pre-sma thing :3!!
---> also hy cant respont to arbitary stimulie cause inhibtory effect / decision making effect of pfc not gettign through :p !!
--------> sooo PFC info also in SMA = important for task 2 where its all about PFC :D !! :!!:
Design
--> prime shown (<-- or --> ) for either 100ms or above 100ms
--> then actual location indicating button press shown (<-- or -->
-----> compatible (e.g. prime = --->, actual = ----> (same direction)
-----> incompatible (e.g. prime = <---, actual = ---> (different direction)
:!:Study repeated with SEF (suppelemtary eye fields):!:
--> same task just with moving eyes in stimulus direction instead of button press (same results of lesion = no negative compatibility if lesion to supplementary eye fields :D !!)
Two action system + exogenous action (biekofski)
--> separation of dorsal stream into:
- dorsal dorsal = where / grasp pathway
- online modification of movement
- ventral dorsal = how / skill use info
- offline modification of movement
Dorsal pathways
---> exogenous/ affording driven action selection (parietal bottom up processing)
--> both streams end in pre-SMA
--> these meant as two action system
dorsal dorsal pathway (where / grasp)
- bilateral pathway
- lesion in either hemisphere = Optic ataxia
- overreaching movements etc..
- Online modification of movement
- based on visual stimulus(optic ataxia = evidence!)
- stores info brief / transient
- shown by study = fast initiation onset
- stored in intraparietal sulcus (iPS)
Ventral dorsal pathway (how / skill use)
- left lateralized pathway
- lesion in left hemisphere = lymbic apraxia
- deficits in skill execution for object related actions
- Offline modification of movement
- as evident that lesion effects = stronger when object not visible (which doesn't happen if no lesion :P!!)
- stores info long + longer initiation time than dorsal dorsal
- cause necessarily needs to imitate grasp (dorsal dorsal) first
- economics, brain more specialized only BG to initiate + M1 activity
- stored in inferior parietal lobe (iPL)
Ventral pathway (what pathway)
--> processing of stimulus attributes (what is it/ lok like etc)
--> communicates with ventral dorsal stream #
Affordances
--> possible actions offered by environment
--> used by both dorsal dorsal + ventral dorsal
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Variable
--> affordance changes cause demand changes
--> empty bottle = lighter than full bottle --> so adjust grip strength when lifting
Medial frontal cortex (SMA/pre-SMA + MCC) + endogenous action (self generated) (passingham :D)
---> dorsal streams = exogenous /affordance driven movement
---> here = medial PFC = endogenous / self generated movement
------> both modulated by pre-SMA :D !! #-
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pre-SMA
--> inhibitiong involuntary action (thus facilitating voluntary one :3 !!) --> see summer priming study :D !!
--> response conflict/ uncertainty processing even in absence of feedback :3 !! (correlates with longer reaction time when response conflict present :3 !!)
Translation(wong)
--> from formulating a motor goal to planning movement how to achieve it to actual motor movement :3 !!
--> from perception to movement :D!!
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Task demands
--> by PFC
--> more specifically Medial PFC (punningham ereader) #
--->bias for easy things :D !!
path of least resistance :D!! eg. 2 pens but one lies closer so you pick that one instead of the one furthest away
-----> Important had that in exams!!
:!!: LOL look this shit u cause it cant be right cause says what pathway but then speaks later of parietal sulcus:!!: # #
Calculator study
- dorsal dorsal (grasp) = stores info short
- ventral dorsal = stores info long (can conflict with dorsal dorsal action
- as shown when ventral dorsal skill use first and then followed by dorsal dorsal grasp action --> initiation time = longer cause memory of use still persist and activated first # #