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BRS YR2 > Motor Control and Movement Disorders > Flashcards

Motor Control and Movement Disorders Flashcards

1
Q

What are the 2 principles of motor control?

A
  • Hierarchical organisation

- Functional segregation

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2
Q

What is hierarchical organisation?

A

higher order areas are involved in complex tasks (programming and deciding on movements, co-ordinating muscle activity)
lower order areas are involved in lower level tasks (execution of movement)

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3
Q

What is function segregation?

A

Different areas control different aspects of movement

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4
Q

What are pyramidal tracts?

A

tracts that pass through the pyramids of the medulla

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5
Q

What are extrapyramidal tracts?

A

tracts that do NOT pass through the pyramids of the medulla

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6
Q

What are the 2 pyramidal tracts?

A
  • Corticospinal

- Corticobulbar

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7
Q

Where are the output neurons of the pyramidal tracts?

A

In the motor cortex, to the spinal cord or cranial nerve nuclei in the brainstem

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8
Q

What is the pyramidal tracts responsible for?

A

The voluntary movements of the body and face

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9
Q

What are the 4 extrapyramidal tracts?

A
  • Vestibulospinal
  • Tectospinal
  • Reticulospinal
  • Rubrospinal
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10
Q

What are the extrapyramidal tracts responsible for?

A

Involuntary (automatic) movements for balance, posture and locomotion

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11
Q

Where are the motor neurons of the extrapyramidal tracts?

A

Upper motor neurons:
- motor cortex
Lower motor neurons:
- brainstem nuclei to the spinal cord

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12
Q

Where is the primary motor cortex?

A

In the precentral gyrus, anterior to the central sulcus

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13
Q

What does the primary motor cortex control?

A

Fine, discrete, precise, voluntary movements

provides descending signals

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14
Q

Where is the premotor area located?

A

anterior to the primary motor cortex

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15
Q

What does the premotor area do?

A
  • involved in planning voluntary movements

- regulates externally cued movements

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16
Q

Where is the supplementary motor area?

A

located anterior and medial to the primary motor cortex

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17
Q

What does the supplementary motor area do?

A
  • involved in planning complex movements (internally cued, speech)
  • becomes active prior to voluntary movement
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18
Q

What is the proportion of crossed fibres in the corticospinal tract?

A

85%-90% crossed fibres

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19
Q

What is the precentral gyrus responsible for?

A

Principal motor pathway for voluntary movements of the face (and neck)

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20
Q

What is the vestibulospinal extrapyramidal tracts responsible for?

A
  • stabilise the head during body movements, or as head moves
  • co-ordinate head movements with eye movements
  • mediate postural adjustments
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21
Q

What is the reticulospinal extrapyramidal tracts responsible for?

A
  • most primitive descending tract (from medulla and pons)
  • changes in muscle tone associated with voluntary movements
  • postural stability
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22
Q

What is the tectospinal extrapyramidal tracts responsible for?

A
  • from superior colliculus of midbrain

- orientation of the head and neck during eye movements

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23
Q

What is the rubrospinal extrapyramidal tracts responsible for?

A
  • from the red nucleus of the midbrain
  • In humans mainly taken over by the corticospinal tract
  • Innervate lower motor neurons of flexors of the upper limb
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24
Q

What are the negative signs of the effect of a upper motor lesion?

A
  • loss of voluntary motor function
  • paresis: graded weakness of movements
  • paralysis (plegia): complete loss of voluntary muscle activity
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25
Q

What are the positive signs of an upper motor lesion?

A
  • Babinski’s sign
  • Clonus (abnormal oscillatory muscle contraction)
  • Hyper-reflexia (exaggerated reflexes)
  • Spasticity (increased muscle tone)
  • Increased abnormal motor function due to loss of inhibitory descending inputs
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26
Q

What is apraxia?

A

A disorder of skilled movement, not paretic but have lost information on how to perform skilled movements

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27
Q

What are the causes of apraxia?

A 
lesions at:
- inferior parietal lobe
- the frontal lobe
(premotor cortex, supplementary motor area)
- stroke 
- dementia
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28
Q

What are the impacts of the lower motor neuron lesion?

A
  • weakness
  • hypotonia (reduced muscle tone)
  • hyporeflexia (reduced reflexia)
  • muscle atrophy
  • fasciculations (damage motor units produce spontaneous action potentials, resulting in a visible twitch)
  • fibrillation (spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination)
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29
Q

What motor spinal tract is responsible for the head/neck?

A

corticobulbar

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30
Q

What motor spinal tract is responsible for the trunk?

A

anterior corticospinal tract

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31
Q

What motor spinal tract is responsible for the limbs?

A

lateral corticospinal tract

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32
Q

What cranial nerves are controlled by the corticobulbar tract?

A
  • oculomotor
  • trochlear
  • abducens
  • trigeminal
  • facial
  • hypoglossal
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33
Q

what is the route of the corticospinal tracts?

A
  • motor cortex
  • cerebral peduncle (midbrain)
  • pyramids
  • corticospinal tracts
  • synapse in the ventral horn
  • LMN via the ventral root
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34
Q

Which part of the corticospinal tract decussates at the pyramids?

A
  • anterior stays ipsilateral

- lateral goes contralateral

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35
Q

What are upper motor neurones?

A

from the brain to the spinal cord

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36
Q

What are the lower motor neurones?

A

from the spinal cord to the effector

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37
Q

What happens when there is upper motor neurone lesion?

A

increased tone
reduced power
increased reflexes

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38
Q

How do you examen patients?

A
  • inspection
  • tone
  • power
  • reflexes
  • sensation
  • co-ordination
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39
Q

What happens when there is lower motor neurone lesion?

A

muscle atrophy and fasciculations (twitch)
reduced tone
reduced power
reduced reflex

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40
Q

What is the basal ganglia?

A

a group of nuclei in the brain with functions associated with motor

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41
Q

What is a nucleus?

A

collection of neurones in the brain that have a similar function

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42
Q

What is Parkinson’s disease?

A

degeneration of dopaminergic neurones projecting from the substantia nigra (midbrain) to the striatum (basal ganglia)
(normally have inhibitory effect)

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43
Q

What are the symptoms of Parkinson’s?

A
  • rigidity
  • tremor at rest
  • hypomimic face
  • bradykinesia
  • akinesia
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44
Q

What is Huntington’s disease?

A

degeneration of GABA neurones in the striatum, caudate and putamen

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45
Q

What are the symptoms of Huntington’s disease?

A
  • chorea
  • speech difficulty
  • dementia
  • dysphagia
  • unsteady gait
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46
Q

What lies in the posterior cranial fossa?

A

cerebellum (below the tentorium cerebelli)

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47
Q

What is the role of the vestibulocerebellum part of the cerebellum?

A

regulation of gait, posture and head/eye movement

48
Q

What is the role of the spinocerebellum part of the cerebellum?

A

Coordination of speech, adjustment of muscle tone and coordination of limb movements.

49
Q

What is the role of the cerebrocerebellum part of the cerebellum?

A

co-ordination of skilled movements and cognitive functions (attention, language processing and emotions)

50
Q

What happens when the vestibulocerebellum is damaged?

A
  • gait ataxia

- tendency to fall

51
Q

What happens when the cerebrecerebellum is damaged?

A

affects the arms and ckilled, co-ordinated movements (tremor) and speech

52
Q

What are the general cerebellar dysfunction signs?

A 
D - Disdiadochokinesia
A - Ataxia
N - Nystagmus
I - Intention Tremors
S - slurred staccato speech
H - Hypotonia
(Dysmetria)
53
Q

What is a motor unit?

A

basic unit of motor control

involves a single motor neurone and all the motor fibres that it innerveates

54
Q

What are the three different types of fibres?

A
  • slow (1)
  • fast, fatigue resistant(2a)
  • fast, fatiguable (2b)
55
Q

What is the fatiguability of slow (1) fibres?

A

minimal

56
Q

What is the maximum force of slow (1) fibres?

A

small

57
Q

What type of neurones needed to function day to day living?

A

a combination of fast, fatigue resistant (2a) and slow (1)

58
Q

What neurone transition happens in spinal injury?

A

from fast, fatigue resistant (2a) to fast, fatiguable (2b)

59
Q

What colour do slow neurones tend to be?

A

red

60
Q

What is the fatiguability of fast, fatigue resistant (2a) fibres?

A

medium

61
Q

What is the maximum force of fast, fatigue resistant (2a)fibres?

A

large amount

62
Q

What are reflexes?

A

automatic protective responses to dangerous stimuli that don’t reach consciousness and are unstoppable

63
Q

What is descending control?

A

descending pathways (UMN) that can inhibit or increase reflexes

64
Q

What happens in decerebration?

A 
UMN that normally are inhibitory, lose control and become excitatory
decerebral posture (constant tensing)
65
Q

What is the Jendrassik Manoeuvre?

A

to relax the UMN effect - LMN reflexes more obvious
clench teeth, lock hands and pull hard
increased UMN firing overflows to increase excitability of LMNs

66
Q

Describe the path of the lateral corticospinal tract from the brain?

A
  • cerebral peduncle
  • midbrasin
  • medulla (cross over)
  • lateral and anterior corticospinal tract
67
Q

What is lateral corticospinal tract responsible for?

A

limb muscles

68
Q

What is anterior corticospinal tract responsible for?

A

trunk muscles

69
Q

What makes up the lateral corticospinal tract?

A

decussated upper motor neurones

70
Q

What makes up the anterior corticospinal tract?

A

ipsilateral upper motor neurones (innervate trunk muscles)

71
Q

How is the body represented somatotopically in a coronal section of the motor cortex?

A

in -> out

  • foot
  • leg
  • hipp
  • trunk
  • neck
  • head
  • arm
  • eblow
  • hand
  • fingers
  • eye
  • nose
  • face
  • lips
  • tongue
72
Q

Where do UMN in the corticobulbar tract synapse?

A

the brainstem cranial nuclei

73
Q

What is motor neurone disease?

A

progressive neurodegenerative disorder of the motor system characterised by progressive muscle weakness

74
Q

What is motor neurone disease also known as?

A

amyotrophic lateral sclerosis (ALS)

75
Q

What are the affects of motor neurone disease?

A
  • voluntary contractions of upper and lower limb muscles
  • upper and lower motor neurones (contraction of tongue)
  • respiratory intercostal movements
76
Q

What causes upper motor signs in motor neurone disease?

A

damage to the UMN which extend from the primary motor cortex via the pyramids of the medulla and down the corticospinal tract

77
Q

What are the upper motor neurone disease signs?

A
  • spasticity
  • brisk limbs
  • babinski’s sign
  • loss of dexterity
  • dysarthria
  • dysphagia
78
Q

What are the lower motor neurone disease signs?

A
  • weakness
  • muscle wasting
  • tongue fasciculations and wasting
  • nasal speech
  • dysphagia
79
Q

What is the basal ganglia?

A

a number of subcortical nuclei primarily responsible for motor control

80
Q

What is the role of the basal ganglia?

A
  • decision to move and conduct voluntary movements including elaborating associated movements
  • Moderate and coordinating movement through suppression
  • Performing movements in order.
81
Q

What does the basal ganglia consist of?

A
  • caudate nucleus
  • lentiform nucleus
  • striatum (putamen and caudate)
  • nucleus accumbens
  • subthalamic nucleus
  • substantia nigra
  • ventral pallidum
  • claustram
  • nucleus basalis
82
Q

What causes Huntington’s disease?

A
  • due to excessive (>35) CAG repeats in the HTT gene on chromosome 4
  • elongated polyglutamine tail of the huntington protein, interfering with normal cellular function
83
Q

What is Hemiballismus?

A

a basal ganglia syndrome characterised by aggressive involuntary limb movements

84
Q

What causes Hemiballismus?

A
  • injury to the subthalamic nucleus of the basal ganglia (stroke)
  • discharges signals down motor tracts to the contralateral skeletal muscles causing uncontrollable swinging
85
Q

What is the subthalamic nucleus like in normal physiology?

A
  • regulates motor function

- connected to the internal globus pallidus

86
Q

What happens when the spinocerebellum is damaged?

A

affects mainly the legs

  • abnormal gait
  • wide based stance
87
Q

What can cause damage to the spinocerebellum?

A

degeneration and atrophy due to chronic alcoholism

88
Q

What is an intraparenchymal bleed?

A

within the substance of the brain

89
Q

What are the symptoms of an Intraparenchymal bleed?

A
  • rapid onset
  • Hx of hypertension
  • no trauma
90
Q

How do you treat a Intraparenchymal bleed?

A
  • anti-hypertensives

- ?surgical intervention

91
Q

What is an alpha motor neurone?

A

LMN of the brainstem and spinal cord

92
Q

What do alpha motor neurones innervate?

A

extrafusal muscle fibres of skeletal muscles (with contractile elements)

93
Q

What is an innervation ratio?

A

the number of muscle fibres innervated by a single motor neurones (inversely proportional to the level of control)

94
Q

What is the innervation ratio of fine control?

A

small (nuanced movement)

95
Q

What is the innervation ratio of coarse control?

A

high

96
Q

Describe slow (T1) motor units?

A
  • small diameter

- slow conduction velocity

97
Q

Describe fast, fatigue resistant (T2a) motor units?

A
  • larger diameter
  • faster conduction velocity
  • increased ATP hydrolysis
  • eg: oxidative fibres
98
Q

Describe fast, fatigable (T2b) motor units?

A
  • largest diameter
  • forceful contractions
  • insignificant amount of myoglobin
  • Glycolytic fibres generate ATO through anaerobic glycolysis
99
Q

What motor units are prevalent in the muscles for postural stability?

A

slow type muscle fibres

100
Q

What is recruitment?

A

the activation of additional motor units to accomplish an increase in contractile strength in muscle

101
Q

In what order are motor units recruited?

A

from slow to fast

102
Q

What is rate coding?

A

the concept that the force produced by a single motor unit is determined by the number of muscle fibres that it innervates and the frequency of innervation

103
Q

What are neurotrophic factors?

A

growth factors that support growth, survival and differentiation of developing/mature neurones

104
Q

What do neurotrophic factors do?

A
  • prevent neuronal death

- promotes the growth of neurone post-injury

105
Q

What can cause the conversion of motor units from type 2b to type 2a?

A

post-training

106
Q

What can cause the conversion of motor units from type 1 to type 2?

A

severe deconditioning or spinal cord injury

107
Q

What is the impact of microgravity on the type of muscle fibre types?

A

from slow (T1) to fast (T2)

108
Q

How does microgravity cause a change in the muscle fibre types?

A
  • diminished load on the MSK system
  • hydrostatic pressure difference
  • muscular atrophy of postural muscles
109
Q

What happens to muscle fibre types in ageing?

A
  • loss of type 1 and type 2 (2 preferentially)

- larger proportion of T1 therefore slower contraction time

110
Q

What are the steeps involved in a reflex arc?

A
  • sensory receptor
  • sensory neuron
  • integrating center (spinal cord)
  • motor neurone
  • effector
111
Q

What can cause an over-active or tonic stretch reflex?

A
  • rigidity
  • spasticity
    (due to brain damage)
112
Q

What happens in the descending control of reflexes?

A
  • alpha motor neurones
  • inhibitory interneurones
  • propriospinal neurones
  • gamma motor neurones (alters sensory sensitivity)
  • terminals of afferent fibres
113
Q

What causes hyper-reflexia?

A
  • loss of descending inhibition

- UMN lesions

114
Q

What causes clonus?

A
  • loss of descending inhibition

- UMN lesions

115
Q

What is Babinski’s sign?

A
  • stimulate sole with blunt instrument
  • normal: curls downwards
  • positive: curls upwards
  • in infants, upwards normal

BRS YR2 (70 decks)

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