Motor Control and Disease Flashcards

1
Q

What are all movements produced by the skeletal muscles initiated by

A

Lower motor neurons

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2
Q

What are central pattern generators

A

Part of the spinal cord which can generate complex behaviors without brain input

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3
Q

What does stimulation of the motor cortex do

A

Elicits muscle movement

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4
Q

What are neurons found in the brain which control motor function called

A

Upper motor neurons

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5
Q

How is the motor cortex mapped in the lower body

A

Lower body - medially

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6
Q

How is the motor cortex mapped in the upper body

A

Laterally

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7
Q

What do axial muscles control

A

Trunk movement

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8
Q

What do proximal muscles control

A

Shoulder, elbow, pelvis, knee movement

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9
Q

What do distal muscles control

A

Hands, feet, digits

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10
Q

Where does each muscle fiber receive input from

A

A single lower alpha motor neuron

Each lower motor neuron innervates the fiber of one muscle but can innervate more than one fiber

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11
Q

What is a motor unit

A

Motor neuron and all the fibres it innervates

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12
Q

What is a motor neuron pool

A

All the motor neurons that innervate a single muscle

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13
Q

How are motor pools organised

A

Organised spatially in the spinal cord

All motor neurons innervating a particular muscle are grouped into rod-shaped clusters within the spinal cord extending over vertebral segments

Somatotopic - organization reflects the organization of the body

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14
Q

How do Upper motor neurons project to lower motor neurons

A

Via descending tracts

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15
Q

Where do axons of the corticospinal tract derive from

A

layer 5 of the motor cortex

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16
Q

Where do pyramidal cells of the motor cortex project axons to

A

The corticospinal tract

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17
Q

How many layers in the cortex

A

90% is 6 layered
Main input is through stellate cells in layer 4
Main output from layers 3,5 and 6

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18
Q

where do brainstem upper motor neurons project

A

To medial motor pools primarily concerned with postural movement

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19
Q

How do axons in the brainstem project

A

Ipsilaterally in the vestibulospinal and reticulospinal tract

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20
Q

How do axons in the brainstem project

A

Medially and medially synapse onto lower motor control circuits that control axial muscles –> ventromedial pathway

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21
Q

What is the vestibulospinal tract used for

A

Head balance and turning

Project mainly ipsilaterally and medially

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22
Q

What is the tectospinal tract used for

A

Orienting response

Project mainly ipsilaterally and medially

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23
Q

What is the reticulospinal tract used for

A

Control antigravity reflexes

Project mainly ipsilaterally and medially

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24
Q

What do UMN of the motor cortex do

A

Initiate complex voluntary movement

Project mainly contralaterally via the corticospinal tract primarily to muscles involved in precise limb movements, particularly those of the hands in humans – one of the lateral pathways of the spinal cord
(Also, project via the corticobulbar tract to the hypoglossal nucleus in the brainstem, which controls movements of the tongue - important for speech in humans)

25
What do the UMN of the brainstem do
More concerned with the maintenance of posture and balance Located in several nuclei including Reticular formation Vestibular nucleus (vestibular co-ordination) Superior colliculus (visual co-ordination) Project mainly ipsilaterally to lower motor neurons controlling axial muscles concerned with maintaining posture – the ventromedial pathways of the spinal cord
26
Where do UMN always synapse to
LMN
27
Where do LMN always synapse to
Directly onto muscle fibres
28
What does the anticipatory mechanism do
pre-adjusts body posture to compensate for the forces that will be generated when an object is lifted
29
Why do feedforward mechanisms work
UMN of the cortex are influenced by 2 spinal cord circuits: Anticipation of movement activates an indirect projection to the axial muscles via reticular formation Activation of voluntary movement direct to spinal cord via corticospinal tract Anticipation activates first --> movement initiation
30
What is ALS
Degenerative disease of motor neurons characterised by muscle atrophy and sclerosis of the lateral spinal cord Quick degeneration and early death
31
What is LMN disease characterised by
Muscle paresis (weakness) or paralysis Loss of muscle tone due to loss of stretch reflexes Ultimately, leads to severe muscle atrophy Patients usually die from lung dysfunction (due to atrophy of intercostal muscles)
32
What is UMN disease characterised by
Muscle weakness Spasticity due to increased muscle tone (due to failure of modulation of stretch reflex) Hyperactive reflexes Loss of fine voluntary movement Patients usually die from loss of input to the bulbar muscles (tongue and pharynx) via the corticobulbar
33
What are the causes of neuron degeneration
Exitotoxicity is one possibility, where overstimulation, typically by glutamate, leads to neuronal cell death Sometimes a blocker of glutamate can decrease effects of ALS and motor neuron disease
34
What do the basal ganglia and cerebellum do
Influence movement indirectly by regulating the function of UMN
35
Where is the basal ganglia and what is inside of it
Forebrain Caudate Putamen Globus Pallidus Subthalamic nucleus
36
What are the key components of the initiation of movement
``` Motor cortex (telencephalon) Basal ganglia (forebrain) Ventral lateral nucleus of thalamus (diencephalon) Substantia nigra (midbrain) ```
37
What is the motor loop
The motor cortex connecting to the basal ganglia which feedsback to the premotor area via the ventrolateral complex of the thalamus to control the initiation of movement 2 pathways indirect and direct
38
What is the direct pathway of the basal ganglia
Globus pallidus inhibits the VLo --> input from many cortical regions converge on the striatum --> when activated by the input the striatum inhibits the inhibitory activity of the GPi releasing VLo which activates area 6 and initiates movement
39
Why is the direct pathway set up like this
Integration of cortical inputs to trigger a response | Rapidity of response – “engine is running”; inhibition of inhibition releases the “brake”
40
What is the indirect pathway of the basal ganglia
Involves substantia nigra which acts via the striatum to maintain the balance between inhibition and activation of the VLo Excitatory input from the SN stimulates VLo activation by activating inhibition of the GPi through direct pathway In the indirect, inhibition of GPi by GPe is inhibited by the striatum and so VLo is inhibited However inhibitory input from the SN decreases striatum inhibition of the GPe which inhibits the GPi allowing activation of VLo So the SN is balancing/tuning the activation of the VLo
41
What is VLo
Ventral lateral thalamus is activated to initiate movement
42
What is parkinsons disease (Symptoms and how it is passed on)
``` 2nd most common ND disorder Sporadic (85-90%) Familial cases (10-15%) Symptoms: Hypokinesia - paucity/insufficiency of movement Bradykinesia - very slow movements Akinesia - no movements Increased muscle tone - rigidity Resting Tremor - @4-5Hz- ‘pill rolling’ Shuffling gait and flexed posture, impaired balance Mask-like expression Non-motor symptoms (i.e. mood disorders, loss of sense of smell) ```
43
What causes PD
Dopamine loss due to reduction of dopaminergic neurons in Substantia Nigra Degeneration is marked by presence of Lewy bodies (protein aggregates)
44
How does L-DOPA effect PD
Works by boosting capacity of surviving DA-ergic neurons in substantia nigra (SN) to make dopamine (DA) However, does not stop the degeneration of SN neurons Eventually there are insufficient SN neurons left to make DA Also has side effects: increase in motor response fluctuations and drug related dyskinesias. Only around 5 years
45
What does Reduced dopaminergic input from substantia nigra to striatum lead to
Increased activity of the indirect pathway Decreased activity of the direct pathway Less inhibition of the GPi and so inhibitory activity is increased so less activation of VLo so less motor cortex activation
46
What is hypokinesis
Reduced movement
47
What is Huntingtons disease (Symptoms and how it is passed on)
Rare, hereditary, progressive and fatal Early: hyperkinesia or dyskinesia, ‘chorea’ (involuntary jerking or twitching movements) Late: akinesia and dystonia (muscle spasms), dementia, personality disorder (psychosis)
48
What are the causes of HD
Autosomal dominant genetic disease resulting in neuronal degeneration: initially in the indirect pathway components of the striatum, subsequently in the direct pathway components & in the GPe
49
What does the Substantia nigra regulate
caudate, putamen and globus pallidus
50
What causes the first symptoms of HD
Degeneration of the striatum which leads to hyperkinesia and then to akinesis
51
What causes PD
PD is due to degeneration of the substantia nigra and leads to hypokinesis
52
What causes Huntingtons
Mutation in HTT (Huntingtin protein)
53
What is the role of the cerebellum in motor learning
Modulates upper motor neurons – no direct connections to spinal cord Required for the learned execution of planned, voluntary, multijoint movements
54
What is motor learning
Predictions based on past experience of movements. | Importantly, cerebellum also compares what is intended with what actually happens – motor learning
55
What is dyssynergia
decomposition of movement due to breakdown of normal coordinated execution of a voluntary movement.
56
How doe the cerebellum form a loop with the motor cortex
The cerebellum receives massive input from many areas of the cortex, corticopontocerebellar projection, and sensory information from the spinal cord and vestibular system In turn, it projects back to the motor cortex via the thalamus (VLc), but it has no direct output to spinal cord.
57
What is the function of the cerebellum motor cortex loop
to detect and correct differences between the intended movement and the actual movement - the so-called motor error.
58
What can lesions in the cerebellum cause
Cerebella ataxia Poorly integrated movement (dyssynergia)