Neuro - Motor Control Flashcards

1
Q

What is the hierarchal organisation of motor control?

A

→ high order areas of hierarchy = more complex tasks (programme + decide on movements, coordinate muscle activity)
→ lower level areas of hierarchy = lower level tasks (execution of movement)

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2
Q

What is functional segregation?

A

motor system organised in a no. of different areas that control different aspects of movements

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3
Q

How is the hierarchy organised for motor systems?

A
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4
Q

What are the 2 types of major descending tracts?

A

→ pyramidal tracts : passes thru the pyramids of the medulla

→ extrapyramidal tracts : do not pass through the pyramids of the medulla

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5
Q

What are pyramidal tracts? What are 2 examples of pyramidal tracts?

A

→ pass through the pyramids of medulla
→ motor cortex to spinal chord or cranial nerve nuclei in brainstem
→ voluntary movements of body and face
→ corticospinal + corticobulbar

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6
Q

What are extrapyramidal tracts? What are 4 examples of extrapyramidal tracts?

A

→ doesn’t pass through the pyramids of medulla
→ brainstem nuclei to spinal chord
→ involuntary movements for balance, posture and locomotion
→ vestibulospinal + tectospinal + reticulospinal + rubrospinal

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7
Q

Where is the primary motor cortex and what does it do?

A

→ located in precentral gyrus, anterior to the central sulcus
→ controls fine, discrete, precise voluntary movements
→ provides descending signals to execute movements

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8
Q

What is the premotor cortex and what does it do?

A

→ located anterior to primary motor cortex
→ involved in planning movements
→ regulates externally cued movements e.g. reaching for something after seeing it

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9
Q

What is the supplementary motor area and what does it do?

A

→ located anterior + medial to primary motor cortex
→ involved in planning complex movements e.g. internally cued, speech
→ becomes active prior to voluntary movements

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10
Q

What route does the corticospinal tract take from the brain to the muscles?

A
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11
Q

What is a part of the lateral corticospinal tract? What does it do?

A

→ 85 - 90% crossed fibres

→ innervates limb muscles

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12
Q

What is a part of the anterior corticospinal tract? What does it do?

A

→ 10-15 % uncrossed fibres

→ innervates trunk muscles

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13
Q

What does the corticobulbar tract do?

A

principal motor pathway for voluntary movements of face and neck

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14
Q

What route does the corticobulbar tract take?

A

v

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15
Q

What does the reticulospinal tract do?

A

→ Most primitive descending tract - from medulla and pons
→ Changes in muscles tone associated with voluntary movement
→ Postural stability

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16
Q

What does the tectospinal tract do?

A

→ From superior colliculus of midbrain

→ Orientation of the head and neck during eye movements

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17
Q

What does the rubrospinal tract do?

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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18
Q

What are the negative signs of upper motor neurone lesions?

A

→ Loss of voluntary motor function
→ Paresis: graded weakness of movements
→ Paralysis (plegia): complete loss of voluntary muscle activity

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19
Q

What are the positive signs of upper motor neurone lesions?

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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20
Q

What is apraxia?

A

→ disorder of skilled movement

→ Patients are not paretic but have lost information about how to perform skilled movements

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21
Q

What can cause apraxia?

A

stroke, dementia or disease of these areas:
→ Lesion of inferior parietal lobe
→ the frontal lobe (premotor cortex
→ supplementary motor area - SMA)

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22
Q

What are the signs of a lower motor neurone lesion?

A

→ Weakness
→ Hypotonia (reduced muscle tone)
→ Hyporeflexia (reduced reflexes)
→ Muscle atrophy
→ Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
→ Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination

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23
Q

What is motor neurone disease?

A

→ Progressive neurodegenerative disorder of the motor system

→ Spectrum of disorders

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24
Q

What is MND also known as?

A

ASL (Amyotrophic Lateral Sclerosis)

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25
Q

What are upper motor neurone signs of MND?

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)
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26
Q

What are lower motor neurone signs of MND?

A
→ Weakness
→ Muscle wasting
→ Tongue fasciculations and wasting
→ Nasal speech
→ Dysphagia
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27
Q

What are some important structures of the basal ganglia?

A
→ caudate nucleus
→ lentiform nucleus = putamen + external globus pallidus
→ striatum = caudate + putamen
→ nucleus accumbens
→ subthalamic nuclei
→ substantia nigra = midbrain
→ ventral pallidum
→ claustrum
→ nucleus basalis
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28
Q

What are the functions of the basal ganglia?

A

→ Decision to move
→ Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
→ Moderating and coordinating movement (suppressing unwanted movements)
→ Performing movements in order

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29
Q

What is the cause of Parkinson’s disease?

A

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

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30
Q

What are signs of Parkinson’s disease?

A

→ Bradykinesia - slowness of (small) movements (doing up buttons, handling a knife)
→ Hypomimic face - expressionless, mask-like (absence of movements that normally animate the face)
→ Akinesia - difficulty in the initiation of movements because cannot initiate movements internally
→ Rigidity - muscle tone increase, causing resistance to externally imposed joint movements
→ Tremor at rest - 4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body

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31
Q

What is Huntington’s disease? What causes Huntington’s disease?

A

→ Genetic neurodegenerative disorder
→ Chromosome 4, autosomal dominant
→ CAG repeat

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32
Q

What is the pathology of Huntington’s disease?

A

Degeneration of GABAergic neurones in the striatum, caudate and then putamen

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33
Q

What are signs of Huntington’s disease?

A

→ Choreic movements (chorea - dance)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body
→ Speech impairment
→ Difficulty swallowing
→ Unsteady gait
→ Later stages, cognitive decline and dementia

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34
Q

What is ballism?

A

→ Sudden uncontrolled flinging of the extremities
→ Symptoms occur contralaterally.
→ Usually from stroke affecting the subthalamic nucleus.

35
Q

Where is the cerebellum? What does it do?

A

→ posterior cranial fossa
→ separated form cerebrum by tentorium cerebelli
→ coordinator + predictor of movements

36
Q

What does the vestibulocerebellum do?

A

→ Regulation of gait, posture and equilibrium

→ Coordination of head movements with eye movements

37
Q

What happens if there is damage or a tumour in the vestibulocerebllum?

A

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

38
Q

What does the spinocerebellum do?

A

→ Coordination of speech
→ Adjustment of muscle tone
→ Coordination of limb movements

39
Q

What happens if there is damage in the spinocerebllum?

A

affects mainly legs, causes abnormal gait + wide stance

40
Q

What is usually causes damage to the spinocerebellum?

A

degeneration + atrophy associated with chronic alcoholism

41
Q

What does the cerebrocerebellum do?

A

→ Coordination of skilled movements
→ Cognitive function, attention,
processing of language
→ Emotional control

42
Q

What does damage to the cerebrocerebellum do?

A

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

43
Q

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

A
apparent only on movement:
→ ataxia
→ dysmetria
→ intention tremor
→ dysdiadochokinesia
→ scanning speech
44
Q

What is ataxia?

A

General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait

45
Q

What is dysmetria?

A

Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)

46
Q

What is intention tremor?

A

Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking

47
Q

What is dysdiadochokinesia?

A

Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)

48
Q

What is scanning speech?

A

Staccato, due to impaired coordination of speech muscles

49
Q

What is an alpha motor neuron?

A

lower motor neurons of the brainstem and the spinal cord

50
Q

What do alpha motor neurones innervate?

A

innervate extrafusal muscle fibres in skeletal muscles

51
Q

What happens when you activate an alpha motor neurone?

A

muscle contraction

52
Q

What contains all the alpha motor neurones that innervate a single muscle?

A

motor neuron pool

53
Q

What is a motor unit?

A

→ single motor neuron together with all the muscle fibres that it innervates
→ smallest functional unit with which to produce force

54
Q

What does stimulation of one motor neuron cause?

A

contraction of all muscle fibres in the unit

55
Q

What are the 3 types of motor units?

A

→ Slow (S, Type I)
→ Fast, fatigue resistant (FR, Type IIA)
→ Fast, Fatiguable (FF, Type IIB)

56
Q

What are the properties of a Type I unit?

A

→ smallest diameter cell bodies
→ small dendritic trees
→ thinnest axons
→ slowest conduction velocity

57
Q

What are the properties of Type IIA units?

A

→ larger diameter cell bodies
→ larger dendritic trees
→ thicker axons
→ faster conduction velocity

58
Q

What are the 3 categories by which motor units are classified?

A

→ amount of tension generated
→ speed of contraction
→ fatiguability

59
Q

What are the properties of Type IIB units?

A

→ larger diameter cell bodies
→ larger dendritic trees
→ thicker axons
→ fastest conduction velocity

60
Q

What are the 2 mechanisms the brain uses to regulate the force a single muscle can produce?

A

→ recruitment

→ rate coding

61
Q

What is “recruitment”?

A

→ Motor units are not randomly recruited. There is an order to this.
→ Governed by the “size principle”. Smaller units are recruited first (these are generally the slow twitch units).
→ As more force is required, more units are recruited.
→ This allows fine control (e.g. when writing), under which low force levels are required

62
Q

What is rate coding?

A

→ A motor unit can fire at a range of frequencies.
→ Slow units fire at a lower frequency.
→ As the firing rate increases, the force produced by the unit increases.
→ Summation occurs when units fire at frequency too fast to allow the muscle to relax between arriving action potentials.

63
Q

What are neurotrophic factors?

A

→ Type of growth factor
→ Prevent neuronal death
→ Promote growth of neurons after injury

64
Q

What was proven by cross innervation?

A

Motor unit and fibre characteristics are dependent on the nerve which innervates them.

65
Q

How do Type IIB fibres become Type IIA fibres?

A

most commonly following training

66
Q

How do Type I fibres become Type II fibres?

A

→ severe deconditioning
→ spinal cord injury
→ Microgravity during spaceflight

67
Q

How does ageing affect motor units + muscle fibres?

A

→ loss of type I and II fibres
→ preferential loss of Type II fibres
→ leaves behind larger proportions of Type I fibres

68
Q

What is a reflex?

A

→ involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli
→ 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 (as a muscle or gland) without reaching the level of consciousness

69
Q

How is the magnitude + timing of a reflex determined?

A

respectively by intensity and onset of stimulus

70
Q

How do reflexes differ volunltary movements?

A

once released, they can’t be stopped

71
Q

What is the Jendrassik manoeuvre?

A

→ clenching the teeth, making a fist, or pulling against locked fingers when having patellar tendon tapped
→ reflex becomes larger
→ proves that reflexes can be influenced

72
Q

How are stretch reflexes regulated in the CNS?

A

higher centres of the CNS exert inhibitory + exhibitory:
→ inhibitory control dominates in normal conditions (N)
→ decerebration reveals the excitatory control from supraspinal areas (D)

73
Q

What can cause rigidity and spasticity?

A

Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex

74
Q

What is the pathway of descending (supraspinal) control of reflexes?

A

1) activates alpha motor neurons
2) activates inhibitory interneurons
3) activates propiospinal neurons
4) activates gamma motor neurons
5) activates terminals of afferent fibres

75
Q

What is hyper-reflexia?

A

→ over-active reflexes
→ loss of descending inhibition
→ associated w upper neuron lesions

76
Q

What is clonus associated with hyper-reflexia?

A

involuntary + rhythmic muscle contractions

77
Q

What is the Babinski sign?

A

→ the curling upwards of the big toe when sole is stimulated with blunt instrument in adults
→ meant to curl downwards
→ upwards curling is normal in children

78
Q

What is hypo-reflexia? What lesions is it associated with?

A

→ below normal or absent reflexes

→ associated w lower motor neuron diseases

79
Q

What is bradykinesia?

A

Slowness of small movements e.g. doing up buttons, handling a knife

80
Q

What is akinesia?

A

Difficulty in the initiation of movements because cannot initiate movements internally

81
Q

What is meant by “rigidity”?

A

Muscle tone increase, causing resistance to externally imposed joint movements

82
Q

What is tremor at rest?

A

Starts in one hand (pill-rolling tremor) and with time spreads to other parts of the body

83
Q

What is hypomimic face?

A

Expressionless and mask-like, absence of movements that would normally animate the face