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final exam Flashcards

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1
Q

rubrospinal tract (start, end, function)

A
  • red nucleus (midbrain)
  • contralateral cervical spinal cord (upper limbs only)
  • flexor muscles of the arms
  • induces flexion and inhibits extension.
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2
Q

tectospinal tract (start, end, function)

A
  • superior (visual) and inferior (auditory) colliculi - contralateral cervical spinal cord (neck muscles only)
  • orient toward visual and auditory stimuli in the environment.
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3
Q

extrapyramidal tracts ______ through the pyramids of the medulla and are resonsible for ___________ control

A
  • do NOT pass through the pyramids of the medulla
  • responsible for involuntary control
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4
Q

pyramidal tracts pass through the __________ and are responsible for ____________

A
  • pyramids of the medulla
  • voluntary muscle control
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5
Q

medial (pontine) reticulospinal tract (start, end, function)

A
  • reticular formation in pons
  • interneurons of S.C
  • extension of legs for postural support
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6
Q

cortical spinal tract (start, end, function)

A
  • cortex (upper motor neurons)
  • medulla/spinal cord
  • lateral cortical spinal tract: distal muscles (contralateral hands and feet)
  • anterior cortical spinal tract: proximal muscles (ipsilateral trunk, neck, shoulders)
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7
Q

cortical bulbar tract (start, end, function)

A
  • cortex
  • cranial nerve nuclei in the medulla and pons
  • bilateral control over muscles of the upper head and face
  • contralateral control over muscles of the lower face, mouth, and neck
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8
Q

list the two pyramidal tracts

A
  • cortical spinal
  • cortical bulbar
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9
Q

list the four extrapyramidal tracts

A
  • tectospinal
  • rubrospinal
  • vestibulospinal (lateral, medial)
  • reticulospinal (lateral, medial)
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10
Q

lateral (medullary) reticulospinal tract (start, end, function)

A
  • reticular formation in medulla
  • interneurons of S.C
  • flexion
  • inhibit the effect of medial R.S.T
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11
Q

lateral vestibulospinal tract (start, end, function)

A
  • lateral vestibular nuclei
  • all levels of S.C
  • Biased toward extension – controls muscle tone in neck, trunk, shoulder and leg muscles involved in keeping body upright (relative to gravity).
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12
Q

medial vestibulospinal tract (start, end, function)

A
  • medial vestibular nuclei
  • upper cervical levels
  • biased toward extension in neck and shoulders
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13
Q

lesion method

A
  • if brain area X is involved in performance, then damage to X will cause movement impairment
  • what happens to the body (movement impairment) can reveal action of brain area X
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14
Q

decorticate rigidity

A

pyramidal tracts are interrupted but extrapyramidal tracts are left intact
- input from the cortex (where pyramidal tracts originate) is disrupted
- damage ABOVE midbrain

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15
Q

decorticate rigidity: posture 1)

A
  • loss of inhibitory input from cortex to red nucleus
  • Increased activity in rubrospinal tract – increases activity in flexor muscles of upper limbs.
  • Flexor activity in rubrospinal tract > extensor activity in vestibulospinal, and reticulospinal tracts
  • Posture -> Arms and hands in a flexed position
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16
Q

decorticate rigidity: posture 2)

A
  • disruption of the lateral corticospinal tract of spinal motor neurons to extensors
  • vestibulospinal and lateral reticulospinal input: extension > flexion
  • Hips extended and internally rotated, feet plantar-flexed
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17
Q

what tract is active when the arms and hands are flexed in decorticate rigidity?

A
  • rubrospinal tract = activie (does flexion)
  • this activity is more powerful than vestibulospinal and reticulospinal tracts (extension)
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18
Q

what is the reason for the extension and internal rotation of the hips, and the plantar flexion of the hips in decorticate rigidity?

A
  • lateral corticospinal tract (pyramidal) is disrupted
  • vestibulospinal and lateral reticulospinal tracts are more active (cause extension)
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19
Q

decerebrate rigidity

A

BOTH pyramidal AND extrapyramidal tracts are disrupted
- worse than decorticate (damage BELOW midbrain/red nucleus)

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20
Q

Activation method

A

If brain area X is involved in performance, then a movement task will increase the activity of X

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21
Q

Activation method: 4 examples

A
  • ELECTROPHYSIOLOGICAL RECORDINGS: in animals can see spatial (where) and temporal (when) activity in brain
  • FMRI: can show flow of blood via oxygen in brain, best spatial info (clearest picture), poor temporal (delayed timing)
  • ELECTROENCEPHALOGRAPHY: electrodes on the head, good temporal, bad spatial
  • OBSERVING DANCE: activation level is influenced by our own motor experiences
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22
Q

stimulation method

A

stimulate brain area X by applying a (low-voltage) electrical signal and observing the resulting movement

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23
Q

what is prehension?

A

reaching + grasping

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24
Q

3 steps of prehension

A
  1. LOCATE target with vision/dorsal stream (parietal cortex sends location info to PMC and M1)
  2. REACH: moving hand distance and direction
  3. GRASP: shaping fingers and generating grip force
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25
Q

ventral stream

A
  • “v” for vision (vision for recognition)
  • primary visual cortex (V1) to inferior temporal cortex
  • processes visual info: perception and recognition of objects, faces, senses
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26
Q

dorsal stream

A
  • “d” for DOING (vision for actions)
  • primary visual cortex (V1) and PMC
  • process visual info/ targets of action: location, shape, size
  • merges visual and proprioceptive info
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27
Q

patient DF

A
  • lesions in ventral stream (“V” for vision recognition)
  • couldn’t recognize objects, faces, scenes
  • Visual Form Agnosia: inability to use vision to
    determine shape
  • Visual: recognize touch, hearing, but not vision
  • Form: sees free-floating patches, can’t recognize shape
  • Agnosia: problem with perception, not with memory (not amnesia)
28
Q

Patient RV

A
  • lesions in dorsal stream (“d” for doing)
  • Optic Ataxia
  • optic: visual disorder (can use hearing and touch to reach for objects)
  • ataxia: movement disorder (can recognize objects)
29
Q

hand-path kinematics

A
  • Velocity profile has a typical “bell” shape (Start, accelerate, peak velocity, decelerate, stop)
  • Time to peak velocity (TPV)/first half of movement = ballistic stage (projectile) that depends entirely on the motor command
  • Time after peak velocity (TAPV)/second half of movement = Sensory feedback used to update and improve movement
  • outcome of reaching (certain direction over a specific distance)
30
Q

GRIP size vs type vs force

A

size: distance between thumb and index finger
type: power or pinch (determined by goal, size, weight)
force: strength of force needed to lift (determined by weight and surface properties/friction)

31
Q

PMC (premotor) and M1 (primary motor cortex) codes for _______ in reaching

A

direction
- Georgopoulos study

32
Q

M1 (primary motor cortex) codes for _________ in reaching

A

distance (force)
- Evarts study

33
Q

grasp/ grip control

A

using object size/weight information to determine grip size, type, force

34
Q

parietal cortex involvement in control loop

A

codes visual feedback and makes the sensory comparison (btw prediction and feedback)

35
Q

parietal cortex codes ______ for action

A

target location for action
(movement planning)

36
Q

parietal cortex codes_______ for sensory comparison

A

visual feedback

37
Q

structures of basal ganglia

A

Corpus striatum:
- striatum: caudate nucleus, nucleus accumbens, putamen (3)
- lentiform: putamen, globus pallidus internal, globus pallidus external (3)
– subthalamic nucleus
– substantia nigra: pars compacta, pars reticulata

38
Q

4 coritco-cortical circuits of basal ganglia

A

skeletomotor: control of voluntary movements, balance, gait
oculomotor: eye movement control
limbic: emotional control and motivation
prefrontal: planning, persistence, memory, spatial ability

39
Q

pathway of input TO the basal ganglia

A

cortex to the striatum

40
Q

pathways of output OUT of the basal ganglia

A

globus pallidus internal (GPi) to…
- cortex (via thalamus)
- spinal cord (via medulla: balance & gait)
- cerebellum (via pons: balance & gait)

41
Q

What is Parkinson’s disease?

A

a progressive degenerative disorder of both movement and stillness
- degeneration of the substantia nigra ~ lack of neurotransmitter dopamine (pars compacta)

42
Q

Negative signs of Parkinson’s disease

A
  • DIRECT ROUTE: interference with cortical excitation
  • loss of movement
  • akinesia (lack of movement, facial masking)
  • bradykinesia (slowness)
  • poor balance (postural instability)
43
Q

Positive signs of Parkinson’s

A

++ INDIRECT ROUTE: interference with cortical inhibition
+ presence of unwanted movements
+ resting tremor (uncontrollable, repetitive movements of extremities at rest)
+ rigidity (muscle stiffness associated with involuntary co-contraction around joints)

44
Q

control theory loop

A

how we use sensory information to start movements (generate motor actions) or update them (from error signals/feedback)

45
Q

high GPi output = ______ motor cortex excitability

A

decrease
(GPi inhibits cortex more)

46
Q

low GPi output = ________ motor cortex excitability

A

increase
(GPi inhibits cortex less)

47
Q

global pallidus internal

A

inhibits cortex to prevent and stop movement

48
Q

4 ways the cerebellum participates in movement control

A
  1. acts in advance of sensory feedback
  2. motor timing
  3. relies on model of body (height, weight, bone mass) to coordinate movements
  4. adaptation + learning
49
Q

how does the cerebellum control motor timing

A
  • M1 and cerebellar neurons linked
  • cerebellar firing happens before muscle contractions
  • triphasic EMG: reflects normal timing of muscle activation
50
Q

what do triphasic EMGs show us about the cerebellum controlling motor timing?

A

triphasic EMG: reflects normal timing of muscle activation
- the TEMG is disrupted after cerebellar damage
- hypermetria (overshoot target)
- oscillations at movement end

51
Q

how does the cerebellum store info about your body?

A
  • stores model of limb structure and mass for proper motor commands
  • tools that add weight to limb, the cerebellum embodies it (Katniss)
  • when the cerebellum is disrupted, no more compensation
  • coordination disorders: harder to do multijoint than single-joint movement
52
Q

cerebellar ataxia

A
  • Jerky, ungraceful, inaccurate movements
    – poor balance and gait
    – Poor learning
  • lack of coordination
  • dysmetria: over or undershoot target
  • action/intention tremor
  • disdiadochokinesis: inability to perform alternating movements
  • gait ataxia and poor balance: steps irregularly timed and placed
  • nystagmus: repetitive beating movements of the eyes
  • hypotonia: low muscle tone
  • poor proprioception
53
Q

the role of adaptation in cerebellar motor control

A
  • normal cerebellum: make errors, fix errors, return to baseline
  • damaged cerebellum: cannot adapt for errors
54
Q

posture

A

ability to control the body’s position in space to maintain orientation and stability

55
Q

postural orientation

A

maintain relationship btw segments of body and body and environment

56
Q

postural stability

A

(aka balance) ability to keep center of mass within the base of support

57
Q

base of support

A

area defined by body’s contact with the support surface

58
Q

center of mass

A

point in 3D space that is at the center of the total body mass
- usually around L2

59
Q

Center of gravity

A

the vertical projection downward from the center of mass

60
Q

Center of pressure

A

center of distribution of total forces applied to the support surface

61
Q

quiet stance postural control

A
  • goal is to maintain upright body alignment
62
Q

stability limits

A

amount of sway body can experience without changing its base of support

63
Q

3 main reactive postural adjustments

A
  • ankle strategy
  • hip strategy
  • stepping strategy
64
Q

how is the ankle strategy different from the hip strategy as reactive postural adjustments?

A
  • ANKLE: responds to small perturbations on firm surface. Distal muscles are activated first, where the body sways at the ankles
  • HIP: responds to larger and faster perturbations with a narrow BOS. Proximal muscles activated first, large rapid motions at hip (no swaying)
65
Q

locomotion

A

rhythmic, alternating activity of opposing limbs of the body that requires progression, postural stability, and adaptation

66
Q
A

kin psych final (1 decks)

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