motor systems 2 Flashcards

1
Q

which lobe is involved in motor control?

A

all of the frontal lobe

parietal lobe

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2
Q

what is the relationship between the position on the cortical region and the complexity of movement?

A

the more anterior the cortical region, the more complex role in movement

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3
Q

what is area 4?

A

primary motor cortex

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4
Q

where is the primary motor cortex?

A

immediately anterior to the central sulcus

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5
Q

what do lesions of the primary motor cortex cause?

A

cause initial paralysis or paresis of specific muscle groups

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6
Q

why is some recovery of function possible after lesions of the primary motor cortex?

A

bc of cortical plasticity

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7
Q

why is there a smaller chance of recovery with bigger lesions?

A

more muscle groups are involved

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8
Q

what part of the brain do strokes with MCA occlusion affect? what effect does this have and why?

A
  • affects almost all of one side of the frontal lobe
  • leads to severe motor disability in the contralateral body (apart from lower limb bc lower limb is supplied by the anterior cerebral artery)
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9
Q

what does an MI of the proximal MCA affect the blood supply to?

A

o Basal ganglia via lenticulostriate arteries

o Motor cortex

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10
Q

what is area 6?

A

premotor cortex

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11
Q

what is area 8?

A

supplementary motor cortex

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12
Q

what does damage to area 6 or 8 cause?

A

motor apraxia

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13
Q

how does motor apraxia present?

A

o Normal reflexes + no muscle weakness

o Difficulty performing complex motor tasks e.g. tying shoelace

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14
Q

why does damage to one side of the brain cause minimal symptoms?

A

bc the contralateral area can take over some functions of the damaged tissue

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15
Q

what are areas 7 and 19?

A

posterior parietal cortex

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16
Q

what does damage to areas 7 and 19 cause?

A

sensory apraxia

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17
Q

what is sensory apraxia?

A

Difficulty performing complex motor tasks when triggered by sensory input (e.g. when asked verbally to do something)

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18
Q

where are the FEFs and Broca’s area?

A

adjacent to the premotor area

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19
Q

what do the FEFs do?

A

motor control of extraocular eye muscles - controls voluntary eye movements

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20
Q

what is the function of Broca’s area?

A

muscles regulating speech

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21
Q

what does damage to Broca’s area cause?

A

motor aphasia

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22
Q

what is motor aphasia?

A

patient struggles w motor programmes to construct meaningful word sequences

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23
Q

what is oculomotor apraxia?

A

difficulty moving eyes horizontally + quickly

  • Either have to turn head to follow object or use peripheral vision
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24
Q

what causes oculomotor apraxia?

A

bilateral lesions of the FEFs

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25
Q

what causes sensory apraxia?

A

caused by damage to connections from posterior parietal lobe to premotor cortex

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26
Q

what are areas 1, 2 and 3?

A

somatosensory cortex

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27
Q

where do 40% of corticobulbospinal tract axons come from? what do the axons do?

A

somatosensory cortex

Axons send instruction to spinal cord that modulate sensory input – modulate spinal reflexes (e.g. suppress nociceptive reflexes)

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28
Q

what are areas 9 and 10?

A

dorsolateral prefrontal cortex

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29
Q

what are the functions of areas 9 and 10?

A

Areas 9 & 10 – executive functions;
o Plan movement
o Evaluate possible future actions and decide which is best
o Involved in problem solving, judgement

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30
Q

what do lesions of the dorsolateral prefrontal cortex cause?

A

apathy, personality changes and lack of ability to plan or to sequence actions/tasks

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31
Q

what difference does it make if the dorsolateral prefrontal cortex lesion affects the left lobe vs the right lobe?

A

o Left hemisphere mainly affected – poor memory for verbal info
o Right hemisphere mainly affected – poor memory for spatial info

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32
Q

what is the wisconsin card sorting test?

A

common test for frontal lobe function - tests perseverence

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33
Q

what can cause frontal cortex damage?

A

impact w frontal bone e.g. road traffic accident or blow to the head that causes contusions

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34
Q

what are contusions?

A

brain bruising

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35
Q

what is area 11?

A

orbitofrontal cortex

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36
Q

what does the orbitofrontal cortex control?

A

control (inhibition) of motor responses associated w the limbic system
o E.g. responses to hunger, thirst, sexual drives etc

37
Q

what does damage to the orbitofrontal cortex cause?

A

pesudopsychopathic behaviour

38
Q

what is pseudopsychopathic behaviour?

A

impulsiveness, puerility, a jocular attitude, sexual disinhibition, and complete lack of concern for others

39
Q

what is an orbital personality?

A

people with pseudopsychopathic behaviour

40
Q

what does stroke damage to the motor thalamus cause?

A

severe paralysis

41
Q

what does the corticobulbospinal tract pass through on its way to the brainstem?

A

internal capsule

42
Q

what does the corticobulbar component of the CBS tract terminate on?

A

o CN nuclei V + VII for cortical control of the head muscles
o Occulomotor nuclei III, IV + VI for control of eye movements
o Pontine nuclei
o Reticular formation
o Red nucleus

43
Q

what is the red nucleus?

A

large nucleus in the midbrain next to the oculomotor nuclei

44
Q

where does the corticospinal component of the tract decussate and what does it become?

A

continues to the lower medulla and decussates at C1-C5 to form large lateral CST and small medial CST

45
Q

what deficit occurs with a brain injury above the spinal cord/medulla junction?

A

contralateral motor deficit

46
Q

what deficit occurs with a brain injury in the spinal cord?

A

motor deficit on the same side

47
Q

where does the lateral CST run?

A

in the dorsolateral cord near motor neurons supplying distal muscles

48
Q

what does the CST have monosynaptic connections with?

A

thumb and the digits

49
Q

what is inhibition of flexion reflexes mediated by?

A

corticospinal tract

50
Q

where does the anterior corticospinal tract run?

A

in the medial ventral cord

51
Q

what does the lateral corticospinal tract control?

A

voluntary movements of the neck

52
Q

what does damage to the CST cause? why?

A

loss of control of hands and fingers but not loss of posture or locomotion and gait (bc these are controlled by the extra-pyramidal systems (descending motor tracts)

53
Q

where do the extra pyramidal systems originate?

A

from groups of cell bodies in the brainstem

54
Q

what are the main components of extrapyramidal systems?

A

lateral vestibulospinal tract and reticulospinal tracts

55
Q

where does the lateral vestibulospinal tract originate?

A

vestibular nuclei in the upper medulla/lower pons

56
Q

what does the lateral vestibulospinal tract do?

A

controls posture and balance

tonically active during upright posture

57
Q

where does the reticulospinal tract originate?

A

reticular formation of pons and medulla

58
Q

what is the reticulospinal tract responsible for?

A

o Autonomic control – drives sympathetic preganglionic neurons
o Drive to respiration (phrenic nerve)

59
Q

what is the origin of the rubrospinal tract?

A

red nucleus in the brainstem

60
Q

what does the red nucleus mainly receive input from?

A

the cerebellum

61
Q

what is the red nucleus?

A

large nucleus in the midbrain

62
Q

what is the function of the rubrospinal tract?

A

needed for control of movement velocity and transmitting motor commands from cerebellum to the musculature

63
Q

what do lesions of the rubrospinal tract cause?

A

movement slowness

64
Q

what does the tectospinal tract do?

A

coordinates voluntary head and eye movements

activates reflex movements of the head in response to visual and auditory stimuli

65
Q

where does the tectospinal tract originate and where does it project and terminate?

A
  • originates in the superior colliculus

- projects to the contralateral cervical spinal cord to terminate in the rexed laminae VI, VII and VIII

66
Q

what is the medial vestibulospinal tract a continuation of?

A

medial longitudinal fasciculus

67
Q

what does the medial vestibulospinal tract mediate?

A

reflex co-ordination of the head and neck muscles with the extraocular eye muscles to maintain objects in view even if the body moves

68
Q

what do major descending motor tracts do?

A

modulates strength and activity of reflex pathways in the spinal cord

69
Q

which motor neurons are the ones driving the muscles of the thumb and fingers and lips and tongue?

A

Only UMNs that act directly on LMNs in the spinal cord

70
Q

define spasticity

A

abnormally increased muscle tone

o Spastic muscles have increased tendon reflexes

71
Q

what is characteristic of UMN lesions?

A

spasticity

72
Q

what is clonus?

A

series of jerky contractions of a particular muscle following sudden stretching of the muscle

73
Q

what is hyperreflexia?

A

pathologically brisk tendon reflex is seen in one or more muscles

74
Q

what is decorticate posturing?

A

arms are adducted and flexed w wrists and fingers flexed on the chest
o Legs may be internally rotated and stiffly extended w plantar flexion of the feet

75
Q

what does decorticate posturing indicate?

A

Indicates damage to the corticospinal tract in the midbrain

76
Q

describe decerebrate posturing?

A

adducted and extended arms w wrists pronated + fingers flexed. Legs internally rotated and stiffly extended, with plantar flexion of the feet

77
Q

what causes decerebrate posture?

A

bc of excessive activity (disinhibition) in extrapyramidal system esp vestibulospinal tract

• If red nucleus is damaged by severe midbrain injury  decerebrate posturing

78
Q

what keeps the vestibulospinal tract under tonic inhibition?

A

corticobulbospinal tract

red nucleus

79
Q

what patients show decerebate posturing?

A

ONLY unconscious patients

80
Q

what patients show decorticate posturing?

A

usually seen in unconscious patients

81
Q

what do discrete acute lesions cause?

A

initial paralysis followed by variable degree of recovery

82
Q

what occurs during recovery from a lesion?

A

weakness, clumsiness and fatigue of movements

83
Q

what is hemiplegic dystonia?

A

persistent flexion of arms and extension of the legs

84
Q

what can cause hemipleic dystonia?

A

• If there’s persistent spasticity following a motor cortex lesion, spasticity is invariably combined w motor weakness

85
Q

what is the clasp knife reflex?

A

characteristic of chronic cerebral motor lesions

86
Q

what is spinal shock?

A

clinical condition that occurs after acute damage to the spinal cord that includes any damage to the descending tracts

87
Q

how long can spinal shock last for?

A

Can last for days, weeks or months depending on severity

88
Q

what are the acute effects of lesions of the motor tracts in the cord?

A

paralysis or paresis and reduced reflex responses in all muscles below the region of injury

89
Q

what are the chronic effects of lesions of motor tracts in the cord?

A

spinal shock wears off and monosynaptic reflexes reappear
o Crossed extensor reflexes may also recover
o In severe injury, these reflexes aren’t controlled by the brain and may become exaggerated and hyperactive
o Clonus may be present
o Babinski sign will normally be present.