Motor Control Flashcards

(64 cards)

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
What kind of cortical input does reticular formation receive?
tonic inhibition
26
Reticulospinal tract is split into two separate paths. Name the two, and describe their function
medullary reticulospinal tract - control mostly the extensor muscles pontine reticulospinal tract - axial muscle control + postural control
27
Which part of the midbrain contributes to lateral brain pathway?
red nucleus
28
What is the role of red nucleus neurons
inhibition of mainly the flexors
29
What causes decorticate rigidity
removal of activity from all cortical inputs, losing inhibition on both red nucleus and medullary reticulospinal tract. So arms flex and legs extend
30
what causes decerebrate rigidity?
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
T/F decerebrate rigidity and progress to decorticate
False, lesion progress from midbrain to pons/medulla Can't go the other way because rubrospinal tract would have already been damaged
32
What does an abnormal babinski sign mean?
brain no longer in normal control of the spinal cord
33
Which nuclei in the brainstem do not receive bilateral inputs
hypoglossal and lower face
34
What happens if you cut the LMN innervating facial muscles
unilateral and contralateral facial weakness
35
what happens if you cut the UMN innervating facial muscles?
superior quadrant still receives ipsilateral input, so there is only unilateral, contralateral weakness in the inferior quadrant
36
what is the aetiology of spastic movement from UMN lesion
you lose the anticipatory component of movement as well as disinhibiting LMN
37
Where is the locomotor reflex circuit?
in the lumbar spinal cord
38
Swing is mostly ______ activity | Stance is mostly ______ activity
flexor | extensor
39
What senses the need to increase speed if there is no cortical control?
golgi tendon and muscle spindles provide the sensory input
40
How does the muscle spindle increase the locomotion speed with increasing treadmill speed?
a sudden increase in flexor muscle will mean the extensor muscle is fully extended, therefore the cycle can be brought forward
41
T/F during extensor activation, you get termination of flexor activity
True, because this is when the posture of the body is maintained, so flexing will only cause the individual to fall over
42
What are the two types of gait abnormality
hemiparetic gait | circumducting gait
43
What is the difference between hemiparetic and circumducting gait?
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
What kind of information does the motor association area encode?
complex movement the planning and the goal of movements the thought of movement
45
What do the neurons in the motor cortex represent?
functionally relevant movements
46
T/F if a muscle is active, then motor cortex neuron must be active
True, although the signal drops off a little bit
47
What are mirror neurons
Neurons that integrate motor and visual signals. They fire when watching or doing/mirroring a particular action
48
What is the purpose of having mirror neurons
they reflect our capacity of motor learning
49
Where does the motor cortex get its inputs from?
prefrontal area (meaning of movement) motor association area (complex movement with a goal) somatosensory cortex (proprioception) central parietal area (recognising 3D surrounding space)
50
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
what grasping where reaching
51
what are the motor functions of basal ganglia?
complex movement selection and motor learning evaluating and improving movements initiation of movement
52
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 __________
``` caudate putamen striatum globus pallidus subthalamic nucleus substantia nigra ```
53
Why is substantia nigra black?
because it produces melanin
54
What is the appearance of the brain macroscopically in patients with Huntington's Disease?
abnormally large ventricle because caudate has degenerated from massive amount of neuronal death
55
What are the four functions of the cerebellum?
optimise pattern of movement muscle tone maintenance motor learning (in smoothness of movement) planning sequence of movements
56
How many lobes are in the cerebellum?
three
57
What is the presentation of cerebellar anterior lobe syndrome
ataxic gait, loss of inter-limb coordination
58
What is the test of ataxic gait?
slide heel down opposite shin
59
What is the greatest risk factor of cerebellar anterior lobe syndrome?
chronic ethanol toxicity, which preferentially targets neurons in the anterior lobe
60
What is the presentation of cerebellar posterior lobe syndrome
dysmetria (overshoot in precision reach) Dysdiadochokinesia (inability to rapidly alternate movements) Speech abnormality
61
What is the presentation of flocculonodular lobe syndrome?
truncal ataxia
62
How do we test for dysmetria?
ask the patient to alternative touching the nose and the doctor's hand
63
How do we test for dysdiadochokinesia
the clapping test
64
Describe the "double cross" of cerebellar pathway
Cerebellar damage affects the ipsilateral side, because the output to motor cortex is contralateral, but then the descending upper neuron decussates again