Test 6 Flashcards
3 stages of control of movment
- Determines what needs to be done (ready)
-identiy the goal of the movement and best strategy to accomplish the goal - PLans the specific movement (set)
-Specific sequences of muscle acitvations and patterns required to do the movement - Execute the plan (GO)
-activation of the motor neurons to do the movement and make minor adjustments
(Prefrontal cortex–> motor cortex–> spinal cord) decreasng complexity
0basal ganglia nad cerebellum complicate things
The preforntal cortex
-Highest in the chain of command and greatest complexity
-Identifies a goal and determines what needs to be done to accomplish this- “what you need to do”
-highly connected woth sensory cortex
–Executive function
Is the “head coach”
executive function
-higher cognitive processes for planning, organizing, and controlling thoughts, speech and behaviours
-involves a wide0range of skills
Executive function an movement
1.Goal directed actions
-Organizing: what is the goal and hoe does this realte to the current sensory state
-Planning: what will need to be done to accomplish the goal
-Directing: sending this information to the next processing statin (ie motor cortex)
2.Attention
-multitasking: allocating attention amoung tasks performed simultaneously
-Response inhibtion: respond effectively with distractions/irrelvant information. Similar to a second level of “sensory gating: (thalamus filtering)
Executive function and aging
EF declines woth age (volume: lesions in whote matter, loss of grey matter; connectivity: loos of dendrtiic brnaching)
Changes are highly variable: can be minimal in healthy aging- influecned by lifestyle, education, genectics, ect
Aging realted declines in: overall processing speed, problem solving (organzing, planing, directing- goal-directed actions), controlling attentional resources (multitasking and response inhibiton)
-decline is not to level of dysfunction in healthy aging
Changes in gait parameters with age
in general: decreased: gait speed, step length; increased: step time and variability in these parameters
however, healhy older adults may have little to know changes (relates to fall risk). Reduced executive functionign may be an important driver of these changes
Executive function and gait
Gait is a complex motor task that uses executive function
-Not fully managed by GPGs (especially in humans)
-therefore executive function is needed to plan, organize and direct movements
-often must also divide attention to toehr tasks
EF allows effective division of attention between gait and other taks
-dual-task or multi-tasking (eg walking and talk/text)
motor cortex
Now that you have decided what ypu need to do, you need to decide how you will do it
-supplmeentart motor area (SMA)
-premotor area (PMA)
-Primary motr cortex (M1)
Is the offensive manager- plans movments from info from the head coach
The planning of movmeent- PMA and SMA
Creates movment plans and holds them until ready to execute
-Actuve just BEFORE movment occurs
-Up to 1s before voluntary movement
Plans must be highly integrated with sensory information
Details of coding taking place remains unclear
Pre-motor area
selection of best motor plans based on current sensory infomation
-react to sensory info
Supplementary motor area
More complex motor sequences often with bilateral connections
may be more internally driven (remebered sequences)- ie dance routine, plays
Measuring the planning of movement
INstruction stiumuls
-Red light where movment will need to be
-PMA neruons begin firing
Trigger stimulus
-Blue light tells it to act
-PMA neruon stops firing soon after the action is made
Specific to the side required for movement
The planning (or even watching) of movement
“mirror neurons” exist in the PMA
-Respond when movement is imagined or watched
-each cell has very specific movement preference
May be part of an extensive brain system for understanding actions and intentions of others
The PRimary motor cortex (M1)
Transforms the motor plan into specifc movemnt patterns
motor map masks the deeper complexity
Very diferent from lower motor neurons
-complex and overlapping neruons work together to control specific movments (ie, not indivdial msucles- not a 1:1 ratio)
-coding realted to direction and force of movment
The quaderback- on the feild driving movement
Lesions of the premotor region (area 6)- SMA and PMA
-difficulty choosing the correct or appropriate sequnce of muscle actions neede to accomplish a goal
lesions of the primary motor regions (area 4)
-While the appropriate action may be taken, there is difficulty in the execution of the task
-Weakness, lack of coordination, or even complete paralysis
lesion of the PFC
-deficits in goal directed movment
The coding of movement primary motor cortex
Movement direction is encoded by the collective activity of neruons
-Many neurons are active for every movement
-activity of each cell represents a single “vote”
-direction of movment is based on a tally (and averaging) of votes
direction vector
A single cell’s vote
population vector
Tally of all cell votes
(sum of direction vectors)
what is a direction vector
recodings from a single cell in M1 create a driection vector
-Each cell has a “preferred” direction where furing rate is highest
-Firing rate reduces as movment direcion cahnges
–Direction fo the arrow stays the same for a given cell but the length changes base on the direction of movment
populating vectors created from many cells
Populating vectors (pruple) created from many direction vectors recorded from individaul cells in M1
-Each cluster is placed in area where the movment was directed to
population vectors and forces
population vectors generated in the direction in which force is needed
need a larger poplation vector if resiting an external force
Neural decoding in M1
We have a greater understanding of signals in M1
-Compared to prefrontal, SMA and PMA
Still decoding these overlaps signals remains extremly complex:
-requires intrepreting inputs from potentially thousands of neurons
-relating to multiple msucle movements
Decoding these signals would allow us to read the brains motor output
-artifical intelligence to support neuroprothestics
How would you train neural decoding AI algoryhtm
Data must have inputs:
-Brain-computer interface
-signals from neurons in brain (motor cortex)
-EEG and/or fNIRs, impplants,ect
Data must have outputs:
-Know of the resulting movmeent related to the recorded electrical signal
Need lots of data
(NOT THAT SIMPLE)
Flaws with recoding only cerebral cortex activity
Missing sensoy feedback
Maybe missing out on complete information from out 2 loops- basal ganglia and cerebellum
“artififical” movments lack the smoothness of real movments
Rapidly growing area with advancements cosntantly being made- ie elon musk
Basal ganglia
Group of subcortical nuclei which support the selection and initation of willed movements while preveting unwanted movments
cortex–>nasal ganglia–>thalamus–>cortex loop
input form many areas of the cortex
Loop with major input to area 6 (premotor region)
4 main nuclei of the basal ganglia
In the telenchephalon:
-Striatum (caudate nucleus, putamen)
-Globus pallidus
In the diecephalon
-Subthalmic nucelus
In the mibrain:
-Substantia Nigra
2 motor patheays of the substatia nigra
direct (excites) and indirect (inhibits)
need a healthy balance between the 2
Direct pathway of the substantia nigra
Facilitates movment
helps select motor plans
indirect pathwyas of the substantia nigra
inhibits movment
helps supress competing or inappropriate motor plans
Disorders of the direct pathway: parkinson’s disease
Difficulty stimulating wanted movment
-Reduced direct pathway release of thalamus inhibtion
-Arises from a loss of dopaminergi neurons acting on the striatum in the direct pathway
-heavy braking on movment- hypokinetic
Hypokinestic disorder- reduced voluntary motor activity
-Bradykinesia: slowness of movment
-Akinesia- lack of movement (eg freezing of gait)
Levodopa helps maintain this pathway
Disorders of the indirect pathway: huntingstons’s disease
Diffuculty supressing unwated movments
-Reduced indirect pathway= reduction in thalamus inhibtion
-Arises from a loss of striatum neurons acting on the globus pallidus external in the indirect pathway
Hyperlinestic disorder- excessive involuntary motor activity
-Chorea- spontaneous and uncontrollable movments
additonal inof on huntington’s disease
-Rare genetic disorder (<0.01% of people)
-symtoms arise in 30s-40s
-neuron loss will also occur in other areas in cerebral cortex leasing to: dementia, personality changes, death (~20yrs after diagnosis)
Atrophy of neurn=ons in basal ganglia and cerebral cortex- see enlarged ventricles
cortico-cerebellar loop
prper execution of planned, voluntary multi-joint movments
-necessart to fine tune the sequences (ie timing) of muscle contractions
Discussed in 3 parts:
1cortex to cerebellum,
2within cerebellum,
3cerebellum to cortex
Cortico-cerebellar loop: cortico-ponto-cerebellar pathway
-sensory and motor cortex axons from massice projection on pons
-pontine nuceli relay information to cerebellar cortex
Cortico-cerebellar loop: within the cerebellar cortex
Ganule cells:
-most numerous cells in cerebellum
Perkinje cells
-largest cells in cerebellum
-Receive thousands of synaptic inputs
Deep cerebellar nuceli
-Excitatory or inhibitory outputs to thalmus
Cortico-cerebellar loop: cerebello-thalmo-cortical pathway
-Deep cerebellar nuclei relay to thalamus (VL)
-VL realys info back to M1: basal ganglia was area 6 (premotor); here, M1 (area 4) signifies last change tuning (timing, direction, force)
Cerebellar lesions- Ataxia (2 types)
Ataxia: uncorrdinated and inaccurate movments (missing fine tuning)
Sysmetria: overshoot or undershoot target
Dyssynergia: decompensation of synergistic movments
