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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

What is the output of neurons of the pyramidal tracts?

A

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

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8
Q

What is the output of the extrapyramidal tracts?

A

Brainstem nuclei to spinal cord

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9
Q

What are the pyramidal tracts responsible for?

A

The voluntary movements of the body and face

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10
Q

What are the 4 extrapyramidal tracts?

A
  • Vestibulospinal
  • Tectospinal
  • Reticulospinal
  • Rubrospinal
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11
Q

What are the extrapyramidal tracts responsible for?

A

Involuntary (automatic) movements for balance, posture and locomotion

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12
Q

Where are the motor neurons of the extrapyramidal tracts?

A
  • UMN = motor cortex
  • LMN = brainstem nuclei to the spinal cord
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13
Q

Where is the primary motor cortex?

A

In the precentral gyrus, anterior to the central sulcus

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14
Q

What does the primary motor cortex control?

A

Controls voluntary movement

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15
Q

Where is the premotor area located?

A

anterior to the primary motor cortex

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16
Q

What does the premotor area do?

A
  • involved in planning voluntary movements
  • regulates externally cued movements
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17
Q

Where is the supplementary motor area?

A

anterior and medial to the primary motor cortex

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18
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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19
Q

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

A

85%-90% crossed fibres
10%-15% uncrossed fibres

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20
Q

What is the vestibulospinal tract responsible for?

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

What is the reticulospinal tract responsible for?

A
  • changes in muscle tone associated with voluntary movements
  • postural stability
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22
Q

What is the tectospinal tract responsible for?

A

orientation of the head and neck during eye movements

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23
Q

What is the rubrospinal tract 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 voluntary movements of the head/neck?

A

corticobulbar

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30
Q

What motor spinal tract is responsible for motor information to the trunk?

A

anterior corticospinal tract

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31
Q

What motor spinal tract is responsible for motor information to 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 of medulla
  • corticospinal tracts
  • synapse with LMN in the ventral horn of spinal cord
  • LMN via the ventral root to effector
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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

Where do upper motor neurones travel to?

A

from the brain to the spinal cord

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36
Q

Where do the lower motor neurones travel to?

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 examine 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 a nucleus?

A

collection of neurones in the brain that have a similar function

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41
Q

What is Parkinson’s disease?

A
  • degeneration of dopaminergic neurones projecting from the substantia nigra (midbrain) to the striatum (basal ganglia)
  • basal ganglia cannot process motor programmes correctly
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42
Q

What are the symptoms of Parkinson’s?

A
  • rigidity
  • tremor at rest
  • hypomimic face
  • bradykinesia
  • akinesia
  • shuffling gait
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43
Q

What is Huntington’s disease?

A
  • degeneration of GABA and acetylcholine neurones in the striatum
  • leads to hyperexcitability because GABA is inhibitory
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44
Q

What are the symptoms of Huntington’s disease?

A
  • choreic movements
  • speech difficulty
  • dementia
  • dysphagia
  • unsteady gait
  • hallucinations
45
Q

What lies in the posterior cranial fossa?

A

cerebellum (below the tentorium cerebelli)

46
Q

What is the role of the vestibulocerebellum ?

A

regulation of gait, posture and coordination of head/eye movement

47
Q

What is the role of the spinocerebellum?

A

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

48
Q

What is the role of the cerebrocerebellum?

A

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

49
Q

What happens when the vestibulocerebellum is damaged?

A
  • gait ataxia
  • tendency to fall
50
Q

What happens when the cerebrecerebellum is damaged?

A
  • Damage to arms/skilled coordinated movements and speech
  • tremor
51
Q

What are the general cerebellar dysfunction signs?

A 
D - Dysdiadochokinesia (inability to perform rapidly alternating movements)
A - Ataxia
N - Nystagmus
I - Intention Tremors
S - slurred staccato speech
H - Hypotonia
(Dysmetria)
52
Q

Where are the effects of cerebellar disease seen?

A

In the limbs ipsilateral to the lesion

53
Q

What is a motor unit?

A
  • basic unit of motor control
  • involves a single lower 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 motor units are needed to function in day to day living?

A

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

58
Q

What motor unit 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 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
65
Q

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

A
  • precentral gyrus
  • cerebral peduncle
  • midbrain
  • medulla (cross over)
  • lower motor nuerones
66
Q

What makes up the lateral corticospinal tract?

A

decussated upper motor neurones

67
Q

What makes up the anterior corticospinal tract?

A

ipsilateral upper motor neurones (innervate trunk muscles)

68
Q

Where do UMN in the corticobulbar tract synapse?

A

the brainstem cranial nuclei

69
Q

What is motor neurone disease?

A

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

70
Q

What is motor neurone disease also known as?

A

amyotrophic lateral sclerosis (ALS)

71
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

72
Q

What are the upper motor neurone disease signs?

A
  • spasticity
  • brisk limbs
  • babinski’s sign
  • loss of dexterity
  • difficulty speaking (dysarthria)
  • dysphagia
73
Q

What are the lower motor neurone disease signs?

A
  • weakness
  • muscle wasting
  • tongue fasciculations and wasting
  • nasal speech
  • dysphagia
74
Q

What is the basal ganglia?

A

a number of subcortical nuclei primarily responsible for motor control

75
Q

What is the role of the basal ganglia?

A
  • decision to move and conduct voluntary movements including elaborating associated movements
  • Moderating and coordinating movement through suppression
  • Performing movements in order.
76
Q

What does the basal ganglia consist of?

A

.

77
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
78
Q

What happens when the spinocerebellum is damaged?

A

affects mainly the legs

  • abnormal gait
  • wide based stance
79
Q

What can cause damage to the spinocerebellum?

A

chronic alcoholism

80
Q

What is an intraparenchymal bleed?

A

within the substance of the brain

81
Q

What are the clinical features of an Intraparenchymal bleed?

A
  • rapid onset headache
  • Hx of hypertension
  • no trauma
82
Q

How do you treat a Intraparenchymal bleed?

A
  • anti-hypertensives
  • ?surgical intervention
83
Q

What is an alpha motor neurone?

A

LMN of the brainstem and spinal cord

84
Q

What do alpha motor neurones innervate?

A

extrafusal muscle fibres of skeletal muscles (contractile)

85
Q

What is an innervation ratio?

A

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

86
Q

What is the innervation ratio of fine control?

A

low (nuanced movement)

87
Q

What is the innervation ratio of coarse control/ strong movements?

A

high

88
Q

Describe slow twitch (T1) motor units?

A
  • small diameter
  • slow conduction velocity
  • minimal fatiguability
  • small force
89
Q

Describe fast, fatigue resistant (T2a) motor units?

A
  • larger diameter
  • faster conduction velocity
  • increased ATP hydrolysis
  • eg: oxidative fibres
  • fatigues in minutes
  • moderate force
90
Q

Describe fast, fatigable (T2b) motor units?

A
  • largest diameter
  • insignificant amount of myoglobin
  • Glycolytic fibres generate ATP through anaerobic glycolysis
  • fatigues in seconds
  • large force
91
Q

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

A

slow type muscle fibres

92
Q

What is recruitment?

A

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

93
Q

In what order are motor units recruited?

A

from slow to fast

94
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

95
Q

What are neurotrophic factors?

A

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

96
Q

What do neurotrophic factors do?

A
  • prevent neuronal death
  • promotes the growth of neurone post-injury
97
Q

What is the palsticity of motor units?

A

Muscle fibres can change types under different conditions

98
Q

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

A

post-training

99
Q

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

A

severe deconditioning or spinal cord injury

100
Q

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

A

from slow (T1) to fast (T2)

101
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
102
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
103
Q

What are the steps involved in a reflex arc?

A
  • sensory receptor
  • sensory neuron
  • integrating center (spinal cord)
  • motor neurone
  • effector
104
Q

What is decerebration?

A

Loss of inhibtion due to motor neurone damage causes hyper-excitability of relflexes

105
Q

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

A
  • rigidity
  • spasticity
    (due to brain damage)
106
Q

What causes hyper-reflexia?

A
  • loss of descending inhibition
  • UMN lesions
107
Q

What causes clonus?

A
  • loss of descending inhibition
  • UMN lesions
108
Q

What is Babinski’s sign?

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

BRS YR2 (67 decks)

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