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Aneesha Flashcards BRS 2 > Motor control & movement disorders > Flashcards

Motor control & movement disorders Flashcards

1
Q

what are the main principles of motor control?

A

hierarchical organisation and functional segregation

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2
Q

what is hierarchical organisation?

A

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

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3
Q

what is functional segregation in terms of motor control?

A

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

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4
Q

Motor system hierarchy diagram

A
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5
Q

what are the two major types of descending tracts?

A

pyramidal tracts (pass through the pyramids of the medulla)
extrapyramidal tracts (do not pass through the pyramids of the medulla)

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6
Q

what is the function of the pyramidal tracts?

A

voluntary movements of body and face

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7
Q

what are the 2 the pyramidal tracts

A

corticospinal and corticobulbar

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8
Q

What are the four extrapyramidal tracts?

A

Vestibulospinal
Reticulospinal
Tectospinal
Rubrospinal

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9
Q

What is the broad function of the extrapyramidal tracts?

A

involuntary (automatic) movements for balance, posture and locomotion

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10
Q

what is the pathway for pyramidal tracts?

A

pass through pyramids of the medulla
motor cortex to spinal cord or cranial nerve nuclei in brainstem

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11
Q

what is the pathway for extrapyramidal tracts?

A

brainstem nuclei to spinal cord
do not pass through pyramids of the medulla

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12
Q

where is the primary motor control area located

A

precentral gyrus, anterior to the central sulcus

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13
Q

what is the role of the primary motor cortex?

A

controls fine, discrete precise voluntary movement - sends descending signals for execution of movement

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14
Q

where is the premotor control area?

A

anterior to primary motor cortex, lateral to the supplementray motor area

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15
Q

what is the role of the premotor area?

A

involved in planning movements, regulating externally cued movements (e.g seeing an apple and reaching out for it)

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16
Q

where is the supplementary motor area?

A

Located anterior and medial to primary motor cortex

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17
Q

what is the role of the supplementary motor area?

A

planning complex movements and regulating internally cued movements (e.g. internally cued, speech)
becomes active prior to voluntary movements

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18
Q

what is the corticospinal tract split into?

A

lateral (limb muscles) and anterior (trunk) corticospinal tract

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19
Q

which corticospinal fibres cross in the pyramids of decussation?

A

lateral corticospinal tract (85-90%) of corticospinal

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20
Q

which corticospinal fibres don’t decussate in the pyramids?

A

anterior corticospinal tract (10-15%)

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21
Q

Corticospinal tract pathway

A
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22
Q

Somatotopic representation

A
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23
Q

what is the function of the corticobulbar tract?

A

principle motor pathway for voluntary movements in the face and neck

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24
Q

what nuclei do eye movements originate from?

A

oculomotor, trochlear and abducens nucleus

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25
Q

what nucleus controls the muscles of the jaw?

A

trigeminal motor nucleus

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26
Q

what nucleus controls the muscles of the face?

A

facial nucleus

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27
Q

what nucleus controls the tongue?

A

hypoglossal nucleus

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28
Q

what is the role of the vestibulospinal tract?

A

stabilise head during body/head movements
coordinates head & eye movement
mediates postural adjustments

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29
Q

what is the reticulospinal tract, where does it originate from and what is its role?

A

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

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30
Q

Where does the tectospinal tract originate from and what is its role?

A

From superior colliculus of midbrain
Orientation of the head and neck during eye movements

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31
Q

Where does the rubrospinal tract originate from and what is its role?

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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32
Q

what are the negative signs of upper motor neuron lesions?

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 associated with upper motor neuron 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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34
Q

what are the signs of a lower motor neuron 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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35
Q

what is apraxia?
Lesions in which brain regions can cause apraxia?
What diseases cause apraxia?

A

A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements
Lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area - SMA)
Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes

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36
Q

what is motor neuron disease also known as?

A

ALS (amyotrophic lateral sclerosis)

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37
Q

what is ALS?

A

Progressive neurodegenerative disorder of the motor system
spectrum of disorders

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38
Q

what are the upper motor neuron signs of ALS?

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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39
Q

what are the lower motor neuron signs of ALS?

A

Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia

40
Q

what does the basal ganglia consist of?

A

Caudate nucleus
Lentiform nucleus (putamen + external globus pallidus) – together caudate and putamen are known as the striatum
Nucleus accumbens
Subthalamic nuclei
Substantia nigra (midbrain)
Ventral pallidum, claustrum, nucleus basalis (of Meynert)

41
Q

what is the striatum?

A

caudate and putamen combined

42
Q

what is the function 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

43
Q

look at this picture of the basal ganglia hehe

A
44
Q

what type of neuronal degeneration causes parkinsons disease?

A

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

45
Q

what are the symptoms of parkinsons 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

46
Q

what type of neuronal degeneration causes huntingtons disease?

A

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

47
Q

what is the genetic component of huntingtons disease?

A

Genetic neurodegenerative disorder
Chromosome 4, autosomal dominant
CAG repeat

48
Q

what are the symptoms of huntingtons 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

49
Q

what causes ballism? What symptoms does this result in?

A

Usually from stroke affecting the subthalamic nucleus.
sudden, uncontrolled flinging of extremities
symptoms occur contralterally

50
Q

what is ballism the result of?

A

usually stroke subthalamic nucleus
symptoms appear contralaterally

51
Q

Which cranial fossa contains the cerebellum and what seperates it fromthe cerebrum above?

A

Posterior cranial fossa
Tenterium cerebelli

52
Q

what is the function of the cerebellum

A

coordinator and predictor of movement

53
Q

what is the function of the vestibulocerebellum?

A

Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements

54
Q

what does damage to the vestibulocerebellum cause
What is a common cause of vestibulocerebellar damage

A

syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
Tumour can cause vestibulocerebellar damage

55
Q

what is the function of the spinocerebellum?

A

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements

56
Q

what is a common cause of damage to the spinocerebellum?

A

degeneration and atrophy associated with chronic alcoholism

57
Q

what does damage to the spinocerebellum present as?

A

affects mainly legs, causes abnormal gait and stance (wide-based)

58
Q

what is the function of the cerebrocerebellum?

A

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

59
Q

what does damage to the cerebrocerebellum present as?

A

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

60
Q

Main signs of general cerebellar dysfunction

A

Ataxia
Dysmetria
Dysdiadokinesia
Intention tremor
Scanning speech

61
Q

what is ataxia?

A

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

62
Q

what is dysmetria?

A

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

63
Q

what is an intention tremor?

A

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

64
Q

what is dysdiadochokinesia?

A

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

65
Q

what is scanning speech?

A

staccato, due to impaired coordination of speech muscles

66
Q

what are the signs of cerebellar dysfunction?

A

ataxia
dysmetria
intention tremor
dysdiadochokinesia
scanning speech

67
Q

what are alpha motor neurons

A

lower motor neurons of the brainstem and spinal cord that innervate extrafusal muscle fibres of skeletal muscle
Activation causes muscle contraction

68
Q

What is motor neuron pool

A

Motor neuron pool contains all alpha motor neurons innervating a single muscle

69
Q

What is the smallest functional unit with which to produce force?

A

Motor unit

70
Q

what is a motor unit?
WHat happens on stimulation of a motor unit

A

a single motor neuron together with all the muscle fibres that it innervates.
Stimulation of one motor unit causes contraction of all the muscle fibres in that unit.

71
Q

How many muscle fibres are supplied by a single motor unit on average?

A

600

72
Q

what are the main classifications of muscle fibre

A

slow S type I
fast fatigue resistant FR type IIA
fast fatiguable FF type IIB

73
Q

what are the features of type I muscle fibres?

A

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

74
Q

what are the features of type IIA muscle fibres?

A

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

fast fatigue resistant

75
Q

what are the features of type I muscle fibre contractions?

A

least force, slow to contract but maximal force is maintained

76
Q

what are the features of a type IIA muscle fibre contraction? (fast fatigue resistant)

A

more force, fairly fast contraction but held for long time

77
Q

what are the features of a type IIB muscle fibre contraction?

A

most force, fast contraction but fairly short

78
Q

what are the mechanisms by which the brain regulates force of a single muscle?

A

recruitment- number of motor units involved
rate coding- how fast the units contract

79
Q

what is the principle of recruitment for muscle fibres?

A

size principle - smaller units recruited first(usually slow twitch fibres), as more force is required, more units recruited
allows fine control when low force levels are required (e.g. when writing)

80
Q

what is rate coding?
When does summation occur

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.

81
Q

What are neurotrophic factors?

A

Are a type of growth factor
Prevent neuronal death
Promote growth of neurons after injury

82
Q

What happens if a fast twitch and slow twitch muscle fibre are cross innervated?
What does this indicate?

A

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

If a fast twitch muscle and a slow muscle are cross innervated, the soleus becomes fast and the FDL becomes slow.

The motor neuron has some effect on the properties of the muscle fibres it innervates.

83
Q

when is the most common change of IIB to IIA?

A

muscular endurance training

84
Q

what can cause a change of I to II fibres?

A

Type I to II possible in cases of severe deconditioning or spinal cord injury. Microgravity during spaceflight results in shift from slow to fast muscle fibre types

85
Q

how does ageing affect muscle fibre types?

A

Ageing associated with loss of type I and II fibres but also preferential loss of type II fibres. This results in a larger proportion of type I fibres in aged muscle (evidence from slower contraction times).

86
Q

What is a reflex?
WHat determines the magnitude and timing of a reflex?

A

An 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.
“…….the magnitude and timing of which are determined respectively by the intensity and onset of the stimulus”.

87
Q

describe the course of a monosynaptic reflex?

A

sensory receptor - sensory neuron - motor neuron = action

88
Q

what is the jendrassik manoeuvre?

A

creating larger reflexes by clenching teeth, making a fist, pulling against locked fingers and then testing a reflex

89
Q

What signals are exerted by higher CNS centers on reflex action?
Which of these dominate under normal circumstances?
What then happens with decerebration?

A
89
Q

What signals are exerted by higher CNS centers on reflex action?
Which of these dominate under normal circumstances?
What then happens with decerebration?

A

Higher centres of the CNS exert inhibitory and excitatory regulation upon the stretch reflex.
Inhibitory control dominates in normal conditions (N).
Decerebration reveals the excitatory control from supraspinal areas (D).
Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex.

90
Q

what type of lesion is hyperreflexia associated with?

A

upper motor neuron lesions (loss of inhibition)

91
Q

what is clonus?
What type of lesion is this associated with?

A

rhythmic involuntary muscle contraction after manual stretch
upper motor neuron lesions (loss of inhibition)

92
Q

what is the babinski sign?

A

When sole stimulated with blunt instrument the big toe:
Curls downwards - normal
Curls upwards – abnormal in adults. This is a positive Babinski sign.
Note: Toe curls upwards in infants – this is normal.

93
Q

what is a positive babinski sign?

A

big toe curls upwards (but normal in infants)

94
Q

What is hyporeflexia?

A

Below normal/ absent reflexes

Aneesha Flashcards BRS 2 (47 decks)

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