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Jonathan's Neuroscience > Motor Control > Flashcards

Motor Control Flashcards

1
Q

What is fibrillation

A

undetectable, unexpected movements of muscle sub-divisions

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2
Q

What is scanning speech caused by?

A

cerebellum lesion

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3
Q

Why does the NMJ have a “secure synapse”

A

because of the spread out synaptic cleft with plenty of embedded Nic receptors, an impulse is guaranteed to cause a contraction

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4
Q

Which muscles are recruited first when straining?

A

the smaller muscle units are recruited first. These units are slow twisting and resistant to fatigue

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5
Q

T/F Muscle strength grows in increments

A

True, neurotransmitters are released in discrete units. The more neural signal = more muscular contraction

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6
Q

T/F each muscle is made up of a number of identical motor units

A

False, muscle is made of motor units of varying sizes so there is a fine control of the force applied

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7
Q

With 50% of motor neuron recruitment, how much force can be generated?

A

25% of max force

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8
Q

What are the short term consequences of denervation on lower motor neurons?

A

fibrillation and fasciculation

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9
Q

What is fasciculation?

A

measurable, spontaneous twitching of muscle fibre

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10
Q

Why do muscles fibrillate?

A

Where there is denervation, the initial compensation is to increase sensitivity to Ach, which means increased Ach receptors and moving receptors outside the junction. Therefore, muscles are more likely to be activated spontaneously in very small magnitude

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11
Q

What is the long term consequence of denervation?

A

atrophy and degeneration (irreversible

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12
Q

T/F muscles are inactive if not used

A

False, all muscles have a resting tone, allowing anticipation of contraction

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13
Q

Which part of the brain regulates muscle tone?

A

cerebellum

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14
Q

The UMN communicates with the LMN via which two pathways?

A

lateral pathway: for distal muscles

ventromedial pathway: for axial muscles

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15
Q

What are the symptoms of LMN lesion?

A 
reduced superficial reflex (withdraw reflex)
reduced tone
weakness/paralysis 
atrophy 
fasciculation
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16
Q

What are the symptoms of UMN lesion?

A 
spastic weakness
abnormal resting tone
hyperactive reflex 
clonus 
abnormal babinski 
loss of fine movements
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17
Q

What does the lateral pathway include?

A

corticospinal tract

rubrospinal tract

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18
Q

What does the ventromedial pathway include?

A

vestibulospinal tract
pontine reticulospinal tract
medullary reticulospinal tract
tectalspinal tract

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19
Q

What does the vestibulospinal tract control?

A

postural maintenance

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20
Q

what does the reticulospinal tract control?

A

maintains muscles of the midline for posture of the body

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21
Q

what does the colliculospinal tract control?

A

reflex movement triggered by sound and vision. All information is integrated in the superior colliculus

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22
Q

What does decerebrate mean?

A

without cerebellum

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23
Q

What is decerebrate rigidity?

A

A rigid posture in an unconscious individual where extensors dominate on both upper and lower limbs

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24
Q

What is decorticate rigidity?

A

rigid posture where lower limbs are extended and upper limbs are flexed

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25
Q

What kind of cortical input does reticular formation receive?

A

tonic inhibition

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26
Q

Reticulospinal tract is split into two separate paths. Name the two, and describe their function

A

medullary reticulospinal tract - control mostly the extensor muscles

pontine reticulospinal tract - axial muscle control + postural control

27
Q

Which part of the midbrain contributes to lateral brain pathway?

A

red nucleus

28
Q

What is the role of red nucleus neurons

A

inhibition of mainly the flexors

29
Q

What causes decorticate rigidity

A

removal of activity from all cortical inputs, losing inhibition on both red nucleus and medullary reticulospinal tract. So arms flex and legs extend

30
Q

what causes decerebrate rigidity?

A

level of disruption is below the mid brain.
Rubrospinal tract compromised, so flexors cannot be excited.
Inhibition to reticulospinal tract lost, so extensors are overly active

Extensors therefore dominate

31
Q

T/F decerebrate rigidity and progress to decorticate

A

False, lesion progress from midbrain to pons/medulla

Can’t go the other way because rubrospinal tract would have already been damaged

32
Q

What does an abnormal babinski sign mean?

A

brain no longer in normal control of the spinal cord

33
Q

Which nuclei in the brainstem do not receive bilateral inputs

A

hypoglossal and lower face

34
Q

What happens if you cut the LMN innervating facial muscles

A

unilateral and contralateral facial weakness

35
Q

what happens if you cut the UMN innervating facial muscles?

A

superior quadrant still receives ipsilateral input, so there is only unilateral, contralateral weakness in the inferior quadrant

36
Q

what is the aetiology of spastic movement from UMN lesion

A

you lose the anticipatory component of movement as well as disinhibiting LMN

37
Q

Where is the locomotor reflex circuit?

A

in the lumbar spinal cord

38
Q

Swing is mostly ______ activity

Stance is mostly ______ activity

A

flexor

extensor

39
Q

What senses the need to increase speed if there is no cortical control?

A

golgi tendon and muscle spindles provide the sensory input

40
Q

How does the muscle spindle increase the locomotion speed with increasing treadmill speed?

A

a sudden increase in flexor muscle will mean the extensor muscle is fully extended, therefore the cycle can be brought forward

41
Q

T/F during extensor activation, you get termination of flexor activity

A

True, because this is when the posture of the body is maintained, so flexing will only cause the individual to fall over

42
Q

What are the two types of gait abnormality

A

hemiparetic gait

circumducting gait

43
Q

What is the difference between hemiparetic and circumducting gait?

A

The location of lesion. Circumducting gait only affects the lower limb, whereas hemiparetic gait involves flexion of the upper limb and extension of the lower limb

44
Q

What kind of information does the motor association area encode?

A

complex movement
the planning and the goal of movements
the thought of movement

45
Q

What do the neurons in the motor cortex represent?

A

functionally relevant movements

46
Q

T/F if a muscle is active, then motor cortex neuron must be active

A

True, although the signal drops off a little bit

47
Q

What are mirror neurons

A

Neurons that integrate motor and visual signals. They fire when watching or doing/mirroring a particular action

48
Q

What is the purpose of having mirror neurons

A

they reflect our capacity of motor learning

49
Q

Where does the motor cortex get its inputs from?

A

prefrontal area (meaning of movement)
motor association area (complex movement with a goal)
somatosensory cortex (proprioception)
central parietal area (recognising 3D surrounding space)

50
Q

In terms of visual signals, the dorsal stream is responsible for knowing ______ the object is, and the _______ action. On the other hand, the ventral stream is responsible for knowing ______ the object is, and the ______ action

A

what
grasping
where
reaching

51
Q

what are the motor functions of basal ganglia?

A

complex movement selection and motor learning
evaluating and improving movements
initiation of movement

52
Q

In basal ganglia, the ______ is the C shape area around the ventricles, which wraps around the _______. These two are collectively known as ______, and ________ is found medial to it. The thalamus is medial to basal ganglia, but a component of basal ganglia, ________, can be found inferior to the thalamus. The last component is located in the brainstem, and it’s called __________

A 
caudate 
putamen 
striatum 
globus pallidus 
subthalamic nucleus
substantia nigra
53
Q

Why is substantia nigra black?

A

because it produces melanin

54
Q

What is the appearance of the brain macroscopically in patients with Huntington’s Disease?

A

abnormally large ventricle because caudate has degenerated from massive amount of neuronal death

55
Q

What are the four functions of the cerebellum?

A

optimise pattern of movement
muscle tone maintenance
motor learning (in smoothness of movement)
planning sequence of movements

56
Q

How many lobes are in the cerebellum?

A

three

57
Q

What is the presentation of cerebellar anterior lobe syndrome

A

ataxic gait, loss of inter-limb coordination

58
Q

What is the test of ataxic gait?

A

slide heel down opposite shin

59
Q

What is the greatest risk factor of cerebellar anterior lobe syndrome?

A

chronic ethanol toxicity, which preferentially targets neurons in the anterior lobe

60
Q

What is the presentation of cerebellar posterior lobe syndrome

A

dysmetria (overshoot in precision reach)
Dysdiadochokinesia (inability to rapidly alternate movements)
Speech abnormality

61
Q

What is the presentation of flocculonodular lobe syndrome?

A

truncal ataxia

62
Q

How do we test for dysmetria?

A

ask the patient to alternative touching the nose and the doctor’s hand

63
Q

How do we test for dysdiadochokinesia

A

the clapping test

64
Q

Describe the “double cross” of cerebellar pathway

A

Cerebellar damage affects the ipsilateral side, because the output to motor cortex is contralateral, but then the descending upper neuron decussates again

Jonathan's Neuroscience (22 decks)

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