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Block 4 Neuro > Motor Control > Flashcards

Motor Control Flashcards

1
Q

Stellate cells

A

Receive thalamocortical input.

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2
Q

What are areas with lots of stellate cells called?

A

Granular cortex

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3
Q

Is the primary cortex more granular or agranular?

A

Agranular (small layer 4, with a large 5th layer)

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4
Q

Where are stellate cells found?

A

Layer 4 of the 6 layers

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5
Q

Where are pyramidal cells found?

A

Layer 5

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6
Q

Pyramidal cells

A

Neurons that project out of the cortex. Projects out of the brainstem and into the spinal cord.

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7
Q

Betz cells

A

Really big pyramidal cells, distinguish the motor cortex

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8
Q

Area 4

A

Primary motor cortex

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9
Q

Area 6

A

Premotor cortex

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10
Q

Parts of area 8

A

Visual field

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11
Q

What do the frontal eye fields do?

A

Gaze control, image stabilization, changing fixation

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12
Q

How do the frontal eye fields work on image stabilization?

A

Fixation, VOR, optokinetic response

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13
Q

How do the frontal eye fields change fixation?

A

Saccades, smooth pursuit, vergence, cancellation of VOR

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14
Q

What is the horizontal component of gaze control?

A

Paramedian pontine reticular formation (PPRF)/ horizontal gaze center

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15
Q

What is the vertical component of gaze control?

A

Rostral interstitial nucleus of the medial longitundinal fasiculus/ vertical gaze center

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16
Q

Saccades

A

Ballistic eye movements occur (can’t stop once they start). Can be voluntary or automatic. Need to be bilateral

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17
Q

PPRF projects where?

A

To the ipsilateral abducens and contralateral CN III (via medial longitudinal fasciculus)

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18
Q

Where do the frontal eye fields project?

A

To the contralateral PPRF and the vertical gaze center. Does this directly or via the superior colliculus

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19
Q

Frontal eye field injury

A
  • Loss of voluntary saccades to the contralateral side
  • Eyes deviate to the side of the lesion
  • Can’t move gaze away from stimulus
  • Symptoms may resolve over time
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20
Q

Superior colliculus

A

Important for orienting to a stimulus (via tectospinal tract) for involuntary saccades

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21
Q

Functional organization of primary motor cortex (M1)

A
  • Stimulation usually evokes simple movement of ind. body part (NOT ind. muscle)
  • Movement evoked at low stimulus intensity
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22
Q

What is movement being evoked at a low stimulus intensity indicative of?

A

Large, direct pathway to brainstem and LMNs

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23
Q

Primary motor cortex function

A

Force, direction, extent, velocity

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24
Q

Premotor cortex inputs

A

Supplementary motor area
Cingulate motor area
Prefrontal cortex (planning, learning, executive function)
Posterior parietal cortex
Cerebellum and basal ganglia via thalamus

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25
Q

Premotor cortex organization

A

Dorsal–reaching

Ventral–grasping, cognitive control

26
Q

Premotor cortex function

A

Higher level of motor coordination, multijoint motions that are more complex, stereotyped actions, transforming sensory cue into motor actions

27
Q

Sensorimotor transformations

A

Transforming sensory cues into motor actions by premotor cortex. Externally driven.

28
Q

Does the primary motor cortex or the premotor cortex produce a higher level of coordination?

A

Premotor cortex. Also has more complex, multi-joint actions.

29
Q

Mirror neuron example

A

Monkey watches another primate picking up food. Neurons respond as if the monkey was picking up the food himself.

30
Q

How does the premotor cortex respond in a behavioral context? Coffee cup example

A

Bigger response when hand reaching in to pick up the full coffee cup. Much slower response when moving to pick up the empty coffee cup.

31
Q

Premotor cortex lesions

A

Inability to:

  • Respond properly to stimuli
  • Plan appropriate movements based on circumstances
  • Learn new sensory-motor associations
  • Steer arm correctly
32
Q

Supplementary Motor area functional organization

A

Evokes motion in multiple joints (fewer than premotor, but more than M1). Involved in posture changes

33
Q

Supplementary motor inputs

A

M1, Prefrontal cortex, posterior parietal cortex, basal ganglia and cerebellum

34
Q

Supplementary motor area function

A

Internal movement generation (no direct response to external stimulus). Activity linked to: learning sequences of movements, performing learned movements, mental rehearsal.

35
Q

What happens when tasks become highly proficient (become habits)?

A

Supplementary motor control decreases and M1 assumes control

36
Q

Supplementary Motor area lesions

A

Reduction in internally driven movements
Loss of suppression of motor programs triggered by visual stimuli (alien hand syndrome and utilization behavior)
Neglect of the affected limb

37
Q

Alien hand syndrome

A

Contralateral “semi-purposeful” movements that are outside the patient’s volitional control

38
Q

Utilization behavior

A

Use of objects in an inappropriate setting (excessive response to stimuli)

39
Q

Corticobulbar and corticospinal tracts pathway (until they split)

A

M1, premotor, SMA + somatosensory cortex–>internal capsule–> cerebral peduncle –> pons –>pyramidal tracts on ventral side of medulla

40
Q

Where does the corticobulbar tract go when it splits from the corticospinal tract?

A

To the cranial nerve nuclei (CN III, IV, V3, VI, VIII, IX, X, XI, XII)–nuclei with motor components

41
Q

Corticobubar projections–bilateral, ipsilateral, or contralateral?

A

Most are bilateral (depends on the target nucleus)

42
Q

Corticobulbar tract and voluntary facial movements

A

Lower face: contralateral M1

Upper face: bilateral control (indirect connections through reticular formation)

43
Q

Emotional facial movements

A

Controlled by the cingulate
Upper face: bilateral
Lower face: contralateral

44
Q

What type of lesion does it have to be when the entire side of face is paralyzed?

A

Lower motor neuron

45
Q

What happens with an upper motor lesion in the corticobulbar tract?

A

Facial paralysis on the contralateral lower face.

46
Q

Corticospinal tract after split from corticobulbar?

A

Sends collaterals to the red nucleus and the reticular formation. Cont. to medulla and then to spinal cord

47
Q

Lateral corticospinal tract

A

Controls lateral parts of body. Innervates distal limbs

48
Q

Ventral (anterior) corticospinal tract

A

Primarily innervates axial and proximal limb muscles. Don’t decussate

49
Q

How many of the corticospinal tract fibers decussate? What type are they?

A

90%. Lateral corticospinal tract.

50
Q

Corticospinal tract branches to contact what?

A

Alpha-motorneurons that contact many muscles or interneurons that connect to alpha-motorneurons

51
Q

Where are most of the direct contacts with aplha-motorneurons and corticospinal tracts?

A

In the forearm and hand

52
Q

What is the benefit of the corticospinal tracts connecting to interneurons?

A

The can regulate a larger number of muscles and it allows for multi-jointed movement coordination

53
Q

Rubrospinal tract function and location

A

Primary motor pathway in lower vertebrates. Control of arms in humans. Will become more active if the corticospinal tract is damaged. Involves red nucleus. Terminal is the upper half of spinal cord

54
Q

Magnocellular input and output

A

Input: motor cortex
Output: spinal cord

55
Q

Parvocellular input and output

A

Input: cerebellum
Output: inferior olive

56
Q

Vestibulospinal tract inputs

A

Vestibular organs and cerebellum

57
Q

Medial vestibular nucleus termination point and function

A

Termination: bilaterally in the medial ventral horn. Reg. head position

58
Q

Lateral vestibular nucleus

A

Activates physiological extensor muscles when deviations from stable posture detected.

59
Q

Reticulospinal tract function

A

Coordinate movements of trunk and proximal limbs

60
Q

Reticulospinal tract nuclei

A

Pontine reticular formation

Medullary reticular formation

Block 4 Neuro (8 decks)

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