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Year 2 - BRS > 2.6 - Motor control and movement disorders > Flashcards

2.6 - Motor control and movement disorders Flashcards

1
Q

What is hierarchical organisation?

A
  • high order areas of hierarchy are involved in more complex tasks (programme and decide on movement, coordinate muscle activity)
  • lower level areas of hierarchy perform lower level tasks (execution of movement)
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2
Q

What is functional segregation?

A

Motor system organised in a number of different areas that control different aspects of movement

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3
Q

What is the role of the motor cortex?

A

Receives information from other cortical areas and sends commands to the thalamus and brainstem

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4
Q

What is the role of the cerebellum and basal ganglia?

A

Adjust commands received from other parts of the motor control system

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5
Q

What is the role of the brainstem?

A

Passes commands from cortex to spinal cord

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6
Q

What are the two types of major descending tracts?

A
  • pyramidal tracts
  • extrapyramidal tracts
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7
Q

What are the two pyramidal tracts?

A
  • corticospinal
  • corticobulbar
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8
Q

Why are the pyramidal tracts called pyramidal?

A

They pass through the pyramids of the medulla

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9
Q

Where do the nerves of the pyramidal tracts go from and to?

A

From motor cortex to spinal cord (corticospinal) or cranial nerve nuclei in brainstem (corticobulbar)

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10
Q

What do the nerves of the pyramidal tracts control?

A

Voluntary movements of body and face

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11
Q

What are the four extrapyramidal tracts?

A
  • vestibulospinal
  • tectospinal
  • reticulospinal
  • rubrospinal
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12
Q

Why are the extrapyramidal tracts called extrapyramidal?

A

Do not pass through the pyramids of the medulla

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13
Q

Where do the nerves of the extrapyramidal tracts go from and to?

A
  • UMN in cortex
  • LMN in brainstem nuclei to spinal cord
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14
Q

What do the extrapyramidal tracts control?

A

Involuntary (automatic) movements for balance, posture and locomotion

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15
Q

What does the vestibulospinal tract do?

A
  • stabilise head during body movements or as head moves
  • coordinate head movements with eye movements
  • mediate postural adjustments
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16
Q

What does the tectospinal tract do and where is it from?

A
  • from superior colliculus of midbrain
  • orientation of head and neck during eye movements
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17
Q

What does the reticulospinal tract do and where is it from?

A
  • most primitive descending tract - from medulla and pons
  • changes in muscle tone associated with voluntary movement
  • postural stability
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18
Q

What does the rubrospinal tract do and where is it from?

A
  • from red nucleus of midbrain
  • in humans mainly taken over by corticospinal tract
  • innervate lower motor neurons of flexors of the upper limb
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19
Q

Where is the primary motor cortex located?

A

In precentral gyrus, anterior to central sulcus

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20
Q

What is the primary motor cortex responsible for?

A
  • controls fine, discrete, precise voluntary movements
  • provides descending signals to execute movements
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21
Q

Where is the premotor area located?

A

Located anterior to primary motor cortex

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22
Q

What is the premotor area responsible for?

A
  • involved in planning movements
  • regulates externally cued movements e.g. seeing an apple and reaching out for it
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23
Q

Where is the supplementary motor area located?

A

Anterior and medial to primary motor cortex

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24
Q

What is the supplementary motor area responsible for?

A
  • involved in planning complex movements (i.e. internally cued, speech)
  • becomes active prior to voluntary movement
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25
Q

Where do the neurons decussate in the corticospinal tract?

A
  • 85-90% of fibres decussate and cross over in the medulla, forming the lateral corticospinal tract
  • innervate limb muscles (contralateral)
  • 10-15% of fibres do not decussate and are uncrossed forming the anterior corticospinal tract
  • innervate trunk muscles (ipsilateral)
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26
Q

Where are the upper and lower motor neurons of the corticobulbar tract?

A
  • UMN in motor cortex
  • LMN in relevant cranial nerve nuclei (oculomotor, trochlear, trigeminal motor, abducens, facial, hypoglossal)
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27
Q

In the corticobulbar tract, what do motor nerves from the oculomotor and trochlear nucleus control?

A

Eye movements

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28
Q

In the corticobulbar tract, what do motor nerves from the trigeminal motor nucleus control?

A

Muscles of the jaw

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29
Q

In the corticobulbar tract, what do motor nerves from the abducens nucleus control?

A

Eye movements

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30
Q

In the corticobulbar tract, what do motor nerves from the facial nucleus control?

A

Muscles of the face

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31
Q

In the corticobulbar tract, what do motor nerves from the hypoglossal nucleus control?

A

Tongue

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32
Q

What are negative signs of an upper motor neuron lesion? (3)

A
  • loss of voluntary motor function
  • paresis - graded weakness of movements
  • paralysis (plegia) - complete loss of voluntary muscle activity
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33
Q

What are the positive signs of an upper motor neuron lesion? (5)

A
  • increased abnormal motor function due to loss of inhibitory descending inputs
  • spasticity - increased muscle tone
  • hyper-reflexia - exaggerated reflexes
  • clonus - abnormal oscillatory muscle contraction
  • Babinski’s sign
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34
Q

What is apraxia (UMN lesion)?

A
  • a disorder of skilled movement
  • patients are not paretic but have lost information about how to perform skilled movements
  • due to a lesion of inferior parietal lobe or frontal lobe (premotor cortex, supplementary motor area)
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35
Q

What are the two most common causes of apraxia?

A

Stroke and dementia (although any disease affecting the areas can cause it)

36
Q

What are the symptoms of a lower motor neuron lesion? (6)

A
  • weakness
  • hypotonia (reduced muscle tone)
  • hyporeflexia (reduced reflexes)
  • muscle atrophy
  • fasciculations
  • fibrillations
37
Q

What are fasciculations?

A

Damaged motor units produce spontaneous action potentials, resulting in a visible twitch

38
Q

What are fibrillations?

A

Spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination

39
Q

What is a summary of the power, tone and reflexes of an UMN vs LMN lesion?

A
  • UMN - reduced power, increased tone, increased reflexes (think upper = up for tone and reflexes)
  • LMN - reduced power, reduced tone, reduced reflexes (think lower = down for tone and reflexes)
40
Q

What is motor neuron disease (MND)?

A
  • progressive neurodegenerative disorder of the motor system
  • spectrum of disorders
  • both UMN and LMN lost
41
Q

What is MND also known as?

A

Amyotrophic lateral sclerosis (ALS)

42
Q

What are the upper motor neuron signs of MND? (6)

A
  • spasticity (increased tone of limbs and tongue)
  • brisk limbs and jaw reflexes
  • Babinski’s sign
  • loss of dexterity
  • dysarthria (difficulty speaking)
  • dysphagia (difficulty swallowing)
43
Q

What are the lower motor neuron signs of MND? (5)

A
  • weakness
  • muscle wasting
  • tongue fasciculations and wasting
  • nasal speech
  • dysphagia
44
Q

What are the parts to the basal ganglia?

A
  • caudate nucleus
  • lentiform nucleus (putamen + external globus pallidus) - together caudate and putamen are known as striatum
  • nucleus accumbens
  • subthalamic nuclei
  • substantia nigra (midbrain)
  • ventral pallidum, claustrum, nucleus basalis (of Meynert)
45
Q

What are the functions of the basal ganglia? (4)

A
  • decision to move - subthalamic
  • elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
  • moderating and coordinating movement (suppressing unwanted movements) - lentiform
  • performing movements in order - caudate + nucleus accumbens
46
Q

What should we be aware of in relation to the basal ganglia circuitry?

A

Some diseases (e.g. Parkinson’s, Huntington’s, ballism) target specific parts of the basal ganglia

47
Q

What is Parkinson’s disease?

A

Degeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum

48
Q

What are the symptoms of Parkinson’s? (5)

A
  • bradykinesia - slowness of (small) movements (doing up buttons, handling knife)
  • hypomimic face - expressionless, mask-like (absence of movements that normally animate the face)
  • akinesia - difficulty in initiation of movements because cannot initiate movements internally
  • rigidity - muscle tone increase, causing resistance to externally imposed joint movements
  • tremor at rest - 4-7Hz, starts in one hand (‘pill-rolling tremor’); with time spreads to other parts
49
Q

What is Huntington’s disease?

A

Degeneration of GABAergic neurons in the striatum - caudate and then putamen

50
Q

What is the aetiology of Huntington’s disease?

A
  • genetic neurodegenerative disorder
  • chromosome 4 has a CAG repeat
  • autosomal dominant
51
Q

What are the symptoms of Huntington’s disease? (5)

A
  • choreic movements - rapid jerky involuntary movements of hands and face first, then legs, then rest of body
  • speech impairment
  • dysphagia
  • unsteady gait
  • later stages - cognitive decline and dementia
52
Q

What is ballism?

A
  • usually from stroke affecting subthalamic nucleus
  • sudden uncontrolled flinging of the extremities (one-sided)
  • symptoms occur contralaterally
53
Q

Where is the cerebellum?

A
  • located in posterior cranial fossa
  • separated from cerebrum above by tentorium cerebelli
54
Q

What is the overall function of the cerebellum?

A

Coordinator and predictor of movement

55
Q

What are the three main regions of the cerebellum?

A
  • vestibulocerebellum
  • spinocerebellum
  • cerebrocerebellum
56
Q

What does the vestibulocerebellum do?

A
  • regulation of gait, posture and equilibrium
  • coordination of head movements with eye movements
57
Q

What does a lesion to the vestibulocerebellum cause?

A

Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia (unsteady, staggering gait) and tendency to fall (even when patient sitting and eyes open)

58
Q

What does the spinocerebellum do? (3)

A
  • coordination of speech
  • coordination of limb movements
  • adjustment of muscle tone
59
Q

What does damage to the spinocerebellum cause?

A

Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)

60
Q

What does the cerebrocerebellum do? (5)

A
  • coordination of skilled movements
  • cognitive function
  • attention
  • processing of language
  • emotional control
61
Q

What does damage to the cerebrocerebellum cause?

A

Damage mainly affects arms/skilled coordinated movements (tremor) and speech

62
Q

When are the signs of cerebellar dysfunction apparent?

A

Only on movement

63
Q

What are the main signs of cerebellar dysfunction? (5)

A
  • ataxia - general impairments in movement coordination and accuracy; disturbances of posture/gait - wide-based, staggering gait
  • dysmetria - inappropriate force and distance for target-directed movements (knocking over cup instead of grabbing it)
  • intention tremor - increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
  • dysdiadochokinesia - inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)
  • scanning speech - staccato, due to impaired coordination of speech muscles
64
Q

What is a mnemonic for the signs of cerebellar dysfunction?

A

DANISH

  • dysdiadochokinesia + dysmetria
  • ataxia (Romberg’s)
  • nystagmus (draw H)
  • intention tremor (touch nose then pen)
  • slurred, staccato speech
  • hypotonia / heel-shin test
65
Q

What are alpha motor neurons?

A
  • lower motor neurons of the brainstem and spinal cord
  • innervate the extrafusal muscle fibres of the skeletal muscles
  • their activation causes muscle contraction
66
Q

Where are the alpha motor neurons located?

A
  • anterior horn of grey matter of spinal cord
  • also located in brainstem
67
Q

What is the motor neuron pool?

A

Contains all alpha motor neurons innervating a single muscle

68
Q

What is a motor unit?

A
  • a single (alpha) motor neuron together with all the muscle fibres it innervates
  • one muscle fibre cannot be innervated by >1 neuron
  • stimulation of one motor unit = contraction of all muscle fibres
69
Q

What are the three types of motor units?

A
  • slow (S, type I)
  • fast, fatigue resistant (FR, type IIA)
  • fast, fatiguable (FF, type IIB)
70
Q

How are muscle fibre types distributed through muscle?

A

Randomly distributed - different muscles have different proportions of slow and fast twitch muscles (e.g. back = more slow)

71
Q

By which two ways does the brain regulate muscle force?

A
  • recruitment (slow –> FR –> FF)
  • rate coding (already recruited motor units increase firing rates)
72
Q

How does recruitment work?

A
  • motor units not randomly recruited - order
  • governed by ‘size principle’ - smaller (slow) recruited first
  • more force required = more units recruited
  • allows fine control (low force needed e.g. writing)
73
Q

How does rate coding work?

A
  • a motor unit can fire at a range of frequencies - slow units fire at a lower frequency
  • as firing rate increases, force produced by unit increases
  • summation occurs when units fire at frequency too fast to allow muscle to relax between arriving APs
74
Q

What are neurotrophic factors?

A
  • type of growth factor
  • prevent neuronal death
  • promote neuronal growth after injury
75
Q

What are motor unit and fibre characteristics dependent on?

A
  • nerve which innervates them
  • if a fast and slow muscle are cross innervated, they switch = motor neuron has some effect on properties of muscle fibre it innervates
76
Q

What is the plasticity of motor units/muscle fibres?

A
  • fibre types can change properties under different conditions
  • type IIB–>IIA common following training
  • type I–>II possible in severe deconditioning/SC injury/microgravity
  • ageing associated with loss of type I and II fibres - preferentially type II = larger proportion type I (slower contraction times)
77
Q

What is a reflex?

A
  • automatic response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector without reaching the level of consciousness
  • involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli
  • magnitude and timing determined respectively by intensity and onset of stimulus
78
Q

How do reflexes differ from voluntary movements?

A

Once reflexes are released, they cannot be stopped

79
Q

What are reflexes thought of as being?

A

Automatic (knee jerk) and stereotyped behaviours (sneeze, cough) in response to stimulation of peripheral receptors

80
Q

What is the Jendrassik manoeuvre and why does it happen?

A
  • if you clench your teeth, make a fist or pull against locked fingers when your patellar tendon is tapped, the reflex becomes larger
  • because descending inhibition from the brain is removed
81
Q

What is the descending (supraspinal) control of reflexes?

A
  • higher centres of the CNS exert inhibitory and excitatory regulation upon the stretch reflex
  • inhibitory control dominates in normal conditions
  • decerebration reveals the excitatory control from supraspinal areas
82
Q

What can cause rigidity and spasticity?

A

Can result from brain damage giving over-active or tonic stretch reflex

83
Q

What are the pathways that produce descending spinal reflexes? (5)

A
  • activating alpha motor neurons
  • activating inhibitory interneurons
  • activating propriospinal neurons
  • activating gamma motor neurons
  • activating terminals of afferent fibres
84
Q

What is hyper-reflexia?

A
  • overactive reflexes
  • loss of descending inhibition
  • associated with UMN lesion
85
Q

What is clonus (hyper-reflexia)?

A
  • sign of UMN dysfunction
  • involuntary and rhythmic muscle contractions
  • loss of descending inhibition
86
Q

What is Babinski’s sign (hyper-reflexia)?

A
  • when sole stimulated with blunt instrument, big toe usually curls downwards
  • curls upward - abnormal in adults = positive Babinski sign
  • associated with UMN lesions of corticospinal tract
  • note - toe curls upwards in infants - normal
87
Q

What is hypo-reflexia?

A
  • below normal or absent reflexes
  • associated with LMN diseases

Year 2 - BRS (84 decks)

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