Motor Control Flashcards

1
Q

What are the observable signs of decreased quality of movement?

A

Paralysis, Weakness

Stiffness

Increased reactivity

Ticks, Twitches and Jerks

Fibrillations and fasciculations

Loss of coordination and smoothness

Loss of the effectiveness of movements

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2
Q

What is a “sign”, in relation to disorders of motor control?

A

Observable or measurable motor abnormalities, the presence of abnormalities, or the absence of normal motor actions.

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3
Q

What is a symptom, in relation to disorders of motor control?

A

Problems of motor function reported by patients Syndromes: associated or clustered signs and symptoms

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4
Q

Where are motor neuron cell bodies located?

A

Brainstem (cranial motor neurons) and spinal cord

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5
Q

Why are motor neurons able to produce 1:1 transmission?

A

Highly myelinated axons

Large synapse spread across muscle fibres

Ruffled post-synaptic membrane for increased SA

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6
Q

Where do motor neurons sit in the spinal cord?

A

Ventral horn

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7
Q

What are motor columns?

A

The topographically organised motor neurons in the spinal cord that belong to one muscle.

They tend to be organised into a pool in the ventral spinal cord, spanning multiple segments.

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8
Q

What is a motor unit?

A

All muscle fibres innervated by a single alpha motor neuron.

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9
Q

What is Henneman’s size principle?

A

The smallest motor neurons are recruited first, then gradually larger motor units are recruited with the largest being recruited last.

This ensures low force contractions are initially made and large force contractions made last, allowing fine movements to take place.

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10
Q

What types of muscle fibres are recruited first?

A

Slow fatiguing, because they’re active for all movements, whereas larger motor units are recruited only in large force movements, and therefore are fast fatiguing.

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11
Q

What is myasthenia gravis?

A

Autoimmune disease whereby the action of the NAChR is blocked.

ACh therefore can’t get to the receptor, blocking contractions.

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12
Q

What happens to muscles if they are un-innervated?

A

Fibrillations, fasciculations and eventually atrophy and degeneration.

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13
Q

What are fibrillations?

A

Tiny contraction cause by activity of a single muscle cell - can be due to hypersensitivity, increased AChR expression (including extra-junctional).

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14
Q

What are fasciculations?

A

Groups of muscle fibres contracting involuntarily, probably a motor unit synaptically activating due to spontaneous activation of a degenerating MN/axon.

Can be measured on surface (cf. fibrillations - need extracellular electrode).

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15
Q

What will happen to a muscle if it is denervated for a long time?

A

Atrophy and degeneration.

Atrophy can occur in catabolic states (diabetes, Cushing’s disease) but complete denervation will lead progressively to irreversible muscle loss.

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16
Q

When is the only time muscles are naturally inactive?

A

During REM sleep

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17
Q

What causes involuntary muscle activation?

A

Lower motor neurons connected to muscle spindles and Golgi tendon organs.

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18
Q

What does the muscle spindle do?

A

Sensory axons sit within the intrafusal muscle fibres and send signals back to the spinal cord to report on length of the muscle.

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19
Q

What is the Golgi tendon organ?

A

The Golgi tendon organ is embedded within the collagen matrix of the tendon with nerves that respond to how much force is experienced in the muscle.

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20
Q

What are the signs and symptoms of low motor neuron lesions?

A

Weakness or paralysis

Decreased superficial reflexes

Hypoactive deep reflexes

Decreased tone

Fasciculations and fibrillations

Severe muscle atrophy

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21
Q

Where can the monosynaptic reflex pathway be tested?

A

Anywhere there’s an exposed tendon.

This allows elucidation of where the lesion is in the spinal cord.

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22
Q

What is an upper motor neuron?

A

Any neuron that controls the excitability of lower motor neurons.

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23
Q

What is most of the input to the lower motor neurons via?

A

Local interneurons

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24
Q

What are the 2 main pathways by which axons get from the brain to the spinal cord?

A

Ventromedial and lateral pathways.

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25
Q

Which tracts sit in the ventromedial pathways?

A

Tectospinal

Vestibulospinal

Pontine and medullary reticulospinal.

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26
Q

What types of motor neurons do ventromedial tracts tend to control?

A

More medial motor neurons

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27
Q

What types of motor neurons do lateral tracts tend to control?

A

More lateral neurons

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28
Q

What tracts sit in the lateral pathways?

A

Corticospinal and rubrospinal tracts

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29
Q

Which tract does the reticular formation give rise to?

A

Reticulospinal tract in the ventromedial pathway.

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30
Q

What is the pathway for axons in the lateral corticospinal tract?

A

Axons originate from cerebral cortex, travel down through the internal capsule, through the brainstem (some make connections in pons and medulla), decussates at the medullary pyramids and travels down in the lateral white matter.

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31
Q

What type of movements is the lateral corticospinal tract most for?

A

Voluntary movements

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32
Q

What 3 tracts originating in the brainstem give rise to the ventromedial pathway?

A

Vestibulospinal, reticulospinal and colliculospinal.

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33
Q

What is the main function of the vestibulospinal tract?

A

Postural control with inputs from the vestibular apparatus at the vestibular nuclei.

These nuclei have a large role in postural maintenance.

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34
Q

What is the main function of the reticulospinal tract?

A

Maintaining muscles of the midline, the axial muscles.

These affect postural control.

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35
Q

What is the main function of the colliculospinal tract?

A

The superior colliculus is a structure related to our orientation in space and receives input from auditory and visual systems.

It subserves orienting reflexes – if a sound is hear or a flash of light seen, movement towards the source is done by the superior colliculus.

It’s also important in visual looming – if something is getting bigger, you’re falling towards it.

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36
Q

What are most medial motor tracts for?

A

Posture

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37
Q

What are most lateral tracts for?

A

Voluntary, skilled movements

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38
Q

True or false: when the brain can no longer influence the spinal cord, the spinal locomotor circuits can still be activated.

A

False.

In humans, the spinal locomotor circuits cannot be activated, even by activation of the muscle sensory inputs which can initiate locomotion in spinal quadrupeds.

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39
Q

What happens to the excitability of lower motor neurons when upper motor neuron modulation is lost?

A

They become more excitable, because upper motor neurons normally inhibit.

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40
Q

What are the signs and symptoms of upper motor neuron lesions?

A

Weakness

Spasticity - increased tone, hyperactive deep reflexes, clonus

Babinski’s sign

Loss of fine voluntary movements.

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41
Q

Why do gait and reflex control systems reveal more than the immediate causes of upper motor neuron syndromes?

A

Because these circuits are inexorably enmeshed in a motor control system that comprises significant proportion of the brain, spinal cord and the periphery, these most simple of movements interrogate the entire nervous system.

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42
Q

What are the postural signs of decerebrate rigidity?

A

Extension of the upper and lower limbs. Extensor muscles dominate.

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43
Q

What are the postural signs of decorticate rigidity?

A

Upper limbs flex, lower limbs extend.

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44
Q

Where are the motor control parts of the reticular formation?

A

In the pons and medulla

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45
Q

Where is the red nucleus?

A

In the midbrain.

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46
Q

What does the red nucleus control?

A

More lateral spinal neurons

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47
Q

What does the reticular formation excite?

A

Extensors

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48
Q

What does the red nucleus excite?

A

Flexors

49
Q

What form of modulation do the reticular formation and red nucleus receive from the cortex?

A

Inhibitory inputs

50
Q

What happens if cortical inhibition to the red nucleus is released?

A

The red nucleus will excite the flexors

51
Q

What is the rubrospinal tract?

A

The short tract between the red nucleus to motor neurons at cervical levels of the spinal cord.

52
Q

What must be released for the rubrospinal tract to excite flexors?

A

Cortical inhibition

53
Q

What is decorticate rigidity?

A

Removal of cortical input to all levels of the brainstem (red nucleus and reticular nucleus), resulting in a free running reticular nucleus and red nucleus, leading to dominance of extensors, but with flexion as well in the arms because flexors dominate over extenors.

54
Q

What is decerebrate rigidity?

A

The level of disruption is below of the midbrain, meaning only the red nucleus has been compromised. Therefore, extensors dominate.

55
Q

What is rostrocaudal demise?

A

If there’s progression from the decorticate state to the decerebrate, it means the lesion is affecting more and more of the brainstem.

As it progresses towards the medulla, death is imminent as it will inevitably affect the CV and respiratory centres.

56
Q

When does the rubrospinal tract decussate?

A

Immediately after the nucleus at the midbrain.

57
Q

What is a positive Babinski sign indicative of?

A

Descending tract damage, somewhere related to the UMN.

58
Q

Why is the motor neuron described as the final common pathway?

A

For all movement to happen, irrespective of what it is, it must pass through the motor neuron.

Thus, the monosynaptic stretch reflex tells you if this pathway is operating in the correct way and in the case of the Babinski sign, if it’s excitable then input has been lost from higher up the neural pathway.

59
Q

True or false: LMN and UMN signs apply to a neuron or group of neurons.

A

False.

Each is a clinically recognisable functional system that allows you only to say where something is going wrong in the system.

60
Q

How are UMN vs LMN lesions distinguished for cranial nerves?

A

There is a pattern of loss rather than the LMN/UMN signs seen with spinal motor output.

61
Q

What are the only cranial nerves of the face and tongue that receive contralateral innervation?

A

Hypoglossal and lower facial nerve.

62
Q

How will an UMN lesion present in the face?

A

Loss of innervation to a quadrant of the face, i.e. lower left.

63
Q

How wll a LMN lesion present in the face?

A

Loss innervation to half of face - weakness of superior and inferior facial muscle.

64
Q

What are anticipatory and reflex movements?

A

Anticipatory: knowledge that the task is going to occur and what sorts of forces are going to contact the limb, leads to feed-forward contractions to stabilise the body and limbs.

Reflex: muscle contraction correcting for the disturbance when an object contacts the limb or weight on the body shifts.

65
Q

What percentage of cortical fibres in the corticospinal tract remain ipsilateral?

A

10-15% - the ventral corticospinal tract

66
Q

What are the ipsilateral fibres of the ventral corticospinal tract involved in?

A

Anticipatory postural maintenance

67
Q

Where is the basic locomotor pattern kept?

A

In the lumbosaccral spinal cord.

68
Q

What are the two phases of locomotion?

A

Swing phase: flexion - the limbs get shorter, swing off the ground and then there’s extension for placement.

Stance phase: extension - keeps the leg straight during weight bearing on the limb.

69
Q

How is locomotion still possible in decerebrate cats?

A

Because the spinal cord receives information from muscle spindles and Golgi tendon organs.

If the muscle is fully extended, then the leg will move into the flexion swing phase.

The periphery informs the spinal cord on where in the locomotion cycle the limbs are based on muscle position and the force on the tendon.

70
Q

What happens to the flexor muscle when the extensor is contracting?

A

It is inhibited.

71
Q

When would UMN input to locomotion centres in the spinal cord be necessary?

A

If there’s an increase in speed desired or an upcoming obstacle.

72
Q

Which types of abnormal gait patterns are associated with cerebellar disorders?

A

Ataxic gait.

73
Q

Which types of abnormal gait patterns are associated with basal ganglia disorders?

A

Choreaform and Parkinsonian gait

74
Q

Which types of abnormal gait patterns are associated with cerebral disorders?

A

Hemiparetic and circumducting gait

75
Q

What role does the motor cortex play in movement?

A

Initiation of voluntary movement, skilled, dextrous movements, integration of movement with goals and the physical environment.

76
Q

What comprises the motor cortex?

A

Primary motor area and motor association areas that are organised in various topographic maps.

77
Q

Where is the motor cortex?

A

Immediately anterior/rostral to the central sulcus

78
Q

How is the body mapped in the primary motor cortex?

A

Into a topographic representation of movements - homunculus.

79
Q

Which artery supplies the medial aspect of the longitudinal fissure?

A

Anterior cerebral artery

80
Q

What effect will an occlusion of the middle cerebral artery have on movement?

A

The lower limb and trunk will be affected resulting in, for example, circumduction.

81
Q

What happens when motor association areas are stimulated?

A

More complex movements are produced, suggesting the more complex movements reside in the motor association areas.

82
Q

What sorts of movements are stored in the primary motor cortex?

A

Simple movements, e.g. finger flexion.

83
Q

What do motor association areas do?

A

Hold and string together more complex movements, holding them as individual whole movements.

For example, stimulating one area of the motor association area always results in the hand being brought to the face, irrespective of where in space it originated.

The end-point is important, not the pathway.

84
Q

What does the motor cortex receive input from?

A

Rostral cortical regions associated with goal representation and planning and caudal cortical regions associated with the representation of egocentric space and our encounterable environment.

85
Q

How are upper motor neurons different to lower motor neurons?

A

UMNs are organised into clusters for particular tasks/movements whereas LMNs are organised into clusters for a particular muscle.

86
Q

What are mirror neurons?

A

Visually guided motor neurons in the lateral premotor cortex whose activity is related to specific actions required to be made to copy an observed task.

87
Q

Why are parietal cortical areas important for motor tasks?

A

Because they synthesise the model of the space the body is in, i.e. where everything is in relation to you.

88
Q

How do the “where” and “what” pathways of the primary visual cortex feed into the motor cortex?

A

The where stream controls reaching towards an object and the what stream controls grasping of the object itself.

89
Q

What is the functional role of primary motor cortex?

A

Activation of lower motoneurons or spinal interneurons.

Neurons encode simple movements and force.

90
Q

What will result from a lesion in the primary motor cortex?

A

Weakness

91
Q

What results from stimulation of the primary motor cortex?

A

Simple movements, mainly extremities

92
Q

What is the functional role of motor association areas?

A

Planning and sequence (multi-joint)

93
Q

What will result from a lesion in the motor association area?

A

Apraxia - can’t sequence movements into patterns.

94
Q

What results from stimulation of motor association areas?

A

Complex movements (bilateral/pre-emptive)

95
Q

What are the 3 major functions of the basal ganglia?

A

Allow the selection of complex patterns of voluntary movements

Evaluating the success of actions in achieving the goals of those actions - learning movements better, getting better at movements

Initiating movements - Parkinsonian patients can’t initiate, for example.

96
Q

True or false: the basal ganglia are associated only with movement.

A

False.

Movement is just a component.

97
Q

Which part of the basal ganglia is reduced in Parkinsonian patients?

A

Substantia nigra in the midbrain

98
Q

What are the two traditional pathways through the basal ganglia?

A

Direct and indirect; excitatory and inhibitory.

These pathways operate together in the onset and offset of movement.

99
Q

Why is the traditional view of the basal ganglia not so reliable anymore?

A

Because complete removal or stimulation (i.e. opposite therapies) can ameliorate the tremor symptoms of Parkinson’s disease.

100
Q

What are the functions of the cerebellum?

A

Coordinating the timing and sequence of muscle actions and movements

The maintenance of muscle tone

Motor learning

Planning sequences of muscle activation for complex movements

101
Q

What is the gross structural anatomy of the cerebellum?

A

Tightly folded, three main divisions (lobes), the cerebellar peduncles that attach the cerebellum to the brainstem are fibres connecting with medulla, pons and midbrain

102
Q

Describe the histology of the cerebellum.

A

Cortex, sub-cortical white matter, sub-cortical grey matter (the deep nuclei), massively iterated canonical neural circuit.

103
Q

How is the cerebellum functionally organised?

A

From medial to lateral with some fragmented somatotopy.

104
Q

What is ataxia?

A

Inability to appropriately integrate/coordinate movement.

105
Q

Which side of the body will a unilateral cerebellar lesion be seen?

A

Ipsilateral

106
Q

What are 2 anterior cerebellar lobe syndromes?

A

Ataxic gait (“drunken sailor”)

Loss of inter-limb coordination (slide heel down opposite shin)

107
Q

Which cerebellar neurons are preferentially lost with chronic ethanol toxicity?

A

Anterior Purkinje cells

108
Q

What does posterior progression of anterior cerebellar lobe syndromes result in?

A

Begins to involve upper limbs and facial muscle dys-coordination (ataxic speech).

109
Q

What are 3 posterior cerebellar lobe syndromes?

A

Dysmetria (overshoot in precision reach)

Dysdiadochokinesia (inability to rapidly alternate movements)

Speech abnormality (loss of natural rhythm, slurring across syllables, over compensation by explosive speech)

110
Q

What is a flocculonodular lobe syndrome?

A

Truncal ataxia (difficulty walking, even standing or sitting in severe cases)

111
Q

What are the signs of chronic alcoholism and damage to the anterior vermis?

A

Ataxic gate, but few other signs.

112
Q

What are the 3 main cerebellar disorders?

A

Dysmetria

Dysdiadochokinesia

Ataxia

113
Q

Why are cerebellar lesions ipsilateral deficits, not contralateral?

A

Axons decussate twice after leaving the cerebellum - once at the VL nucleus of the thalamus or red nucleus and then again at the pyramidal decussation.

114
Q

In summary, what are the functions of the spinal cord in motor control?

A

Segmental and intersegmental reflexes, pattern generation

115
Q

In summary, what are the functions of the brainstem in motor control?

A

Integration of sensory information for postural control

Adaptive descending modulation of spinal circuits for adaptive reflex activity

116
Q

In summary, what are the functions of the cerebellum in motor control?

A

Optimisation of sensory motor integration - acquisition of motor skills (coordination).

117
Q

In summary, what are the functions of the basal ganglia in motor control?

A

Learning and selection of motor programs and strategies

118
Q

In summary, what are the functions of the cerebral cortex in motor control?

A

Initiation of voluntary movement, skilled movements, integration of movement with goals and the physical environment. Abstract motor representations, planning