Neuro - Motor Control Flashcards

(83 cards)

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
What are upper motor neurone signs of MND?
``` → Spasticity (increased tone of limbs and tongue) → Brisk limbs and jaw reflexes → Babinski’s sign → Loss of dexterity → Dysarthria (difficulty speaking) → Dysphagia (difficulty swallowing) ```
26
What are lower motor neurone signs of MND?
``` → Weakness → Muscle wasting → Tongue fasciculations and wasting → Nasal speech → Dysphagia ```
27
What are some important structures of the basal ganglia?
``` → caudate nucleus → lentiform nucleus = putamen + external globus pallidus → striatum = caudate + putamen → nucleus accumbens → subthalamic nuclei → substantia nigra = midbrain → ventral pallidum → claustrum → nucleus basalis ```
28
What are the functions of the basal ganglia?
→ 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
29
What is the cause of Parkinson's disease?
Degeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum
30
What are signs of Parkinson's disease?
→ 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
31
What is Huntington's disease? What causes Huntington’s disease?
→ Genetic neurodegenerative disorder → Chromosome 4, autosomal dominant → CAG repeat
32
What is the pathology of Huntington's disease?
Degeneration of GABAergic neurones in the striatum, caudate and then putamen
33
What are signs of Huntington's disease?
→ 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
34
What is ballism?
→ Sudden uncontrolled flinging of the extremities → Symptoms occur contralaterally. → Usually from stroke affecting the subthalamic nucleus.
35
Where is the cerebellum? What does it do?
→ posterior cranial fossa → separated form cerebrum by tentorium cerebelli → coordinator + predictor of movements
36
What does the vestibulocerebellum do?
→ Regulation of gait, posture and equilibrium | → Coordination of head movements with eye movements
37
What happens if there is damage or a tumour in the vestibulocerebllum?
causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
38
What does the spinocerebellum do?
→ Coordination of speech → Adjustment of muscle tone → Coordination of limb movements
39
What happens if there is damage in the spinocerebllum?
affects mainly legs, causes abnormal gait + wide stance
40
What is usually causes damage to the spinocerebellum?
degeneration + atrophy associated with chronic alcoholism
41
What does the cerebrocerebellum do?
→ Coordination of skilled movements → Cognitive function, attention, processing of language → Emotional control
42
What does damage to the cerebrocerebellum do?
Damage affects mainly arms/skilled coordinated movements (tremor) and speech
43
What are the main signs of cerebellar dysfunction? (DAIDS)
``` apparent only on movement: → ataxia → dysmetria → intention tremor → dysdiadochokinesia → scanning speech ```
44
What is ataxia?
General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait
45
What is dysmetria?
Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)
46
What is intention tremor?
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking
47
What is dysdiadochokinesia?
Inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms)
48
What is scanning speech?
Staccato, due to impaired coordination of speech muscles
49
What is an alpha motor neuron?
lower motor neurons of the brainstem and the spinal cord
50
What do alpha motor neurones innervate?
innervate extrafusal muscle fibres in skeletal muscles
51
What happens when you activate an alpha motor neurone?
muscle contraction
52
What contains all the alpha motor neurones that innervate a single muscle?
motor neuron pool
53
What is a motor unit?
→ single motor neuron together with all the muscle fibres that it innervates → smallest functional unit with which to produce force
54
What does stimulation of one motor neuron cause?
contraction of all muscle fibres in the unit
55
What are the 3 types of motor units?
→ Slow (S, Type I) → Fast, fatigue resistant (FR, Type IIA) → Fast, Fatiguable (FF, Type IIB)
56
What are the properties of a Type I unit?
→ smallest diameter cell bodies → small dendritic trees → thinnest axons → slowest conduction velocity
57
What are the properties of Type IIA units?
→ larger diameter cell bodies → larger dendritic trees → thicker axons → faster conduction velocity
58
What are the 3 categories by which motor units are classified?
→ amount of tension generated → speed of contraction → fatiguability
59
What are the properties of Type IIB units?
→ larger diameter cell bodies → larger dendritic trees → thicker axons → fastest conduction velocity
60
What are the 2 mechanisms the brain uses to regulate the force a single muscle can produce?
→ recruitment | → rate coding
61
What is "recruitment"?
→ 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
What is rate coding?
→ 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
What are neurotrophic factors?
→ Type of growth factor → Prevent neuronal death → Promote growth of neurons after injury
64
What was proven by cross innervation?
Motor unit and fibre characteristics are dependent on the nerve which innervates them.
65
How do Type IIB fibres become Type IIA fibres?
most commonly following training
66
How do Type I fibres become Type II fibres?
→ severe deconditioning → spinal cord injury → Microgravity during spaceflight
67
How does ageing affect motor units + muscle fibres?
→ loss of type I and II fibres → preferential loss of Type II fibres → leaves behind larger proportions of Type I fibres
68
What is a reflex?
→ 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
How is the magnitude + timing of a reflex determined?
respectively by intensity and onset of stimulus
70
How do reflexes differ volunltary movements?
once released, they can't be stopped
71
What is the Jendrassik manoeuvre?
→ 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
How are stretch reflexes regulated in the CNS?
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
What can cause rigidity and spasticity?
Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex
74
What is the pathway of descending (supraspinal) control of reflexes?
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
What is hyper-reflexia?
→ over-active reflexes → loss of descending inhibition → associated w upper neuron lesions
76
What is clonus associated with hyper-reflexia?
involuntary + rhythmic muscle contractions
77
What is the Babinski sign?
→ 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
What is hypo-reflexia? What lesions is it associated with?
→ below normal or absent reflexes | → associated w lower motor neuron diseases
79
What is bradykinesia?
Slowness of small movements e.g. doing up buttons, handling a knife
80
What is akinesia?
Difficulty in the initiation of movements because cannot initiate movements internally
81
What is meant by “rigidity”?
Muscle tone increase, causing resistance to externally imposed joint movements
82
What is tremor at rest?
Starts in one hand (pill-rolling tremor) and with time spreads to other parts of the body
83
What is hypomimic face?
Expressionless and mask-like, absence of movements that would normally animate the face