Task 1 - Voluntary Motor Control Flashcards

1
Q

CNS

A

Cerebrum
Cerebellum: movement control center
Brain Stem: vital functions + relay station from cerebrum to spinal cord
Spinal cord: communication between brain & skin, joints, muscles
-> dorsal root: afferent, ventral root: efferent

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2
Q

PNS

A

Somatic PNS: all spinal nerves innervating skin, joints muscles under voluntary motor control

  • motor axons
  • sensory axons
  • ANS/Visceral PNS: neurons innervating internal organs, blood vessels, glands
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3
Q

Motor System levels

A

High: association areas of neocortex & basal ganglia
-> Strategy
Middle: motor cortex & cerebellum
-> tactics
Low: brain stem & spinal cord
-> execution
all relies on sensory information except for ballistic movements

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4
Q

Ballistic movements

A

Brief all-or-none high speed movements

-> don’t rely/ are not influenced by sensory feedback

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5
Q

High level motor systems

A

Association areas of neocortex & basal ganglia

  • > strategy: fiture out goal of movement and best strategy
  • sensory info from cortex about spatial information and alternatives are filtered through basal ganglia
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6
Q

Middle level momtor systems

A

Motor cortex & cerebellum

  • > tactics: sequences of muscle contractions to smoothly and accurately achieve goal
  • basd on memory of sensory info fom past movements
  • translation of action goals into movement instructions for lower level
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7
Q

Low level motor systems

A

Brain stem & spinal cord

  • > Execution: activate neurons generating the goal directed movements & necessary adjustments of posture
  • motor neurons + interneurons
  • sensory feedback used to maintain posture, muscle lenght + tension before & after each voluntary movement
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8
Q

Posterior Parietal Cortex

A

Directs behavior by providing spatial information,
Area 5: input from primary somatosesnroy cortical areas
Area 7: input from higher order visual areas
-largely connected to PFC
-> damage produces deficits in perception and memory of spatial relationships (Apraxia, Contralateral negleect)

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9
Q

Apraxia

A
  • loss of skilled action
  • Difficulty of performing movements when asked about it out of context, can readily perform movement in natural situations
  • > results from parietal cortex lesions
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10
Q

Contralateral Neglect

A

inability of a person to process and perceive stimuli on the opposite side of the brain damage even though they can be subconsiously perceived

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11
Q

Prefrontal Cortex

A

Makes decisions about what actions to take & their likely outcome

  • > evaluation of external stimuli perceived by parietal cortex
  • > Posterior parietal + PFC together encode what actions are desired and send axon to area 6
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12
Q

Planning (secondary motor areas)

A

Supplementary Motor Area (SMA)
Premotor Area (PMA)
-convert info about what action is desired into how the action will be carried out
-> programming specific patterns of movment after receiving instructions from PFC,
-output to primary motor cortex
-each has own somatotopic map
-> lesions lead to apraxia

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13
Q

Supplementary Motor Area (SMA)

A
  • sends axons directly to innervate distal motor units
  • interconnected with M1/area 4
  • strong connections with PFC
  • fires about a second before action
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14
Q

Premotor Area (PMA)

A

Primarily connects with reticulospinal neurons innervating proximal motor neurons

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15
Q

Ideomotor Apraxia

A

still have rough sense of desirec action but problems with proper execution

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16
Q

Ideational Apraxia

A

Don’t know how to perform actions anymore

17
Q

Ready-set-go principle

A

Ready: depends on parietal & PFC activity
Set: depends on SMA & PMA
Go: depends on M1

18
Q

Initiation Primary Motor Cortex

A

M1

  • only fires when doing, not when imagining (like secondary areas)
  • precentral gyrus (motor strip)
  • strongest connections with motor neurons
  • input: cortical areas (6), cerebellum through thalamus
  • output: to spinal cord
  • rostral neurons: terminate on spinal interneurons
  • caudal neurons: terminate on alpha neurons
19
Q

Hemiplegia

A

Loss of voluntary movement on contralateral side due to lesion to primary motor cortex

20
Q

Motor Action Coding

A

Cells encode force & direction of movement by population coding

  • > each cell has tuning curve + activity of cell represents direction vector
  • > direction of movement depends on average of direction vectors of cells: population vector
  • the larger the population the finer the possible control
21
Q

Spinal Tracts

A
Corticospinal tract
Rubrospinal tract
Vestibulospinal trac
Tectospinal tract
Pontine & medullary Reticulospinal tracts
22
Q

Lateral Pathways

A

Corticospinal trct
Rubrospinal tract
-> voluntary movement of distal muscles (direct cortical control

23
Q

Ventral Pathways

A

Vestibulospinal tract
Tectospinal tract
Pontine & Medullary Reticulospinal tracts
-> control, maintenance, of posture & locomotion
-> proximal muscles (brainstem control)

24
Q

Corticospinal tract

A

-longest & largest in CNS
-direct
-2/3 originate in motor cortex (areas 4,6), 1/3 in somatosensory areas
Trajectory:
cortex -> internal capsule -> cerebral peduncle -> pons -> medulla -> forms medullary pyramid (pyramidal tract) where it decussates at junction to spinal cord -> runs down lateral column of spinal cord
-> terminates in dorsolateral region of ventral horns & intermediate grey matter
-> controlls distal muscles

25
Q

Rubrospinal Tract

A
  • indirect
  • originates in red nucleus of midbrain
  • decussates in pons and joins corticospinal tract
  • no major role
  • compensates when corticospinal tract is lesioned
26
Q

Vestibulospinal tract

A

keeps head balanced and turns in response to stimuli

  • originate in vestibular nuclei of medulla
  • bilateral tract: controls neck & back muscles -> head movement
  • ipsilateral tract: runs down lumbar spinal cord to maintain posture (up to motor neurons of legs)
27
Q

Tectospinal tract

A
  • originates in superior colliculus (input from retina)

- colliculus creates map of environment: stimulation of one point on map leads to orienting response

28
Q

Pontine & Medullary Reticulospinal tracts

A

Origin: reticular formation

  • pontine: enhances antigravity reflexes of spinal cord (standing posture, maintains muscle length)
  • medullary: frees antigravity muscles from reflex control (opposite of pontine)
29
Q

Effector

A

Part of body that can move as result of muscle contraction e.g. finger, neck,

30
Q

Alpha motor neurons

A

Innervate muscle fibers & provide physical basis for translating nerve signals into mechanical action
-spinal cord -> ventral root -> muscles fibers -> ACh -> contraction

31
Q

Spinal interneurons

A

integrate sensory feedback with motor commands resulting in voluntary movement

  • input from descending motor fibers
  • output to motor neurons
32
Q

Brain Machine Interface (BMS)

A

Microelectrode implanted, spike patterns analyzed to see how they encode movement

  • > decoded activity used to move e.g. a cursor on a screen
  • > video game can be played only using neural signals from M1, bypassing usual pathway involving muscles
  • works with cells in M1, PMA, SMA, parietal cortex
33
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Muscle weakness & atrophy

  • > degenration of large alpha motor neurons & neurons innervaing them
  • cognitive functions and intelligence unchanged
  • possible causes: genetic mutation affecting enzyme superoxide dismutate (normally reduced toxic superoxide radicals; Excitotoxicity: elevated levels of glutamate lead to overstimulation (cell death)
  • Treatment: Roluzole: blocks glutamate release, can only slow progress of disease
34
Q

Duchenne Muscular Dystrophy

A

Progressive weakness & deterioration of muscle in boys (passed on from mothers)
-defective region on X chromosome encoding dystrophin contributing to cytoskeleton under muscles -> lack mRNA
Treatment: gene therapy; replacing defective gene by sending virus or transplanting stem cells

35
Q

Myasthenia Gravis

A

Weakness & fatigability of voluntary muscles (typically facial expression)

  • severity fluctuates a lot
  • fatal when respiration compromised
  • causes: autoimmune disease: system generates antibodies against own receptors; less effective ACh release at neuromuscular junction
  • Treatment: drugs reinhibiting reuptake (leads to desensitization
  • suppression of immune system (drugs, removal of thymus gland)
36
Q

Premotor - primary motor area order

A

Info influencing movement must first be processed by association and higher order sensory cortices

  • > then info must be communicated to non-primary motor areas
  • > premotor areas coordinate output lvel of M1 & spinal cord (primary motor areas)