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University - Neuroscience > Motor Control and Disease > Flashcards

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
Q

What do the UMN of the brainstem do

A

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
Q

Where do UMN always synapse to

A

LMN

27
Q

Where do LMN always synapse to

A

Directly onto muscle fibres

28
Q

What does the anticipatory mechanism do

A

pre-adjusts body posture to compensate for the forces that will be generated when an object is lifted

29
Q

Why do feedforward mechanisms work

A

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
Q

What is ALS

A

Degenerative disease of motor neurons characterised by muscle atrophy and sclerosis of the lateral spinal cord

Quick degeneration and early death

31
Q

What is LMN disease characterised by

A

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
Q

What is UMN disease characterised by

A

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
Q

What are the causes of neuron degeneration

A

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
Q

What do the basal ganglia and cerebellum do

A

Influence movement indirectly by regulating the function of UMN

35
Q

Where is the basal ganglia and what is inside of it

A

Forebrain

Caudate
Putamen
Globus Pallidus
Subthalamic nucleus

36
Q

What are the key components of the initiation of movement

A 
Motor cortex (telencephalon)
Basal ganglia (forebrain)
Ventral lateral nucleus of thalamus (diencephalon)
Substantia nigra (midbrain)
37
Q

What is the motor loop

A

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
Q

What is the direct pathway of the basal ganglia

A

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
Q

Why is the direct pathway set up like this

A

Integration of cortical inputs to trigger a response

Rapidity of response – “engine is running”; inhibition of inhibition releases the “brake”

40
Q

What is the indirect pathway of the basal ganglia

A

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
Q

What is VLo

A

Ventral lateral thalamus is activated to initiate movement

42
Q

What is parkinsons disease (Symptoms and how it is passed on)

A 
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
Q

What causes PD

A

Dopamine loss due to reduction of dopaminergic neurons in Substantia Nigra

Degeneration is marked by presence of Lewy bodies (protein aggregates)

44
Q

How does L-DOPA effect PD

A

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
Q

What does Reduced dopaminergic input from substantia nigra to striatum lead to

A

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
Q

What is hypokinesis

A

Reduced movement

47
Q

What is Huntingtons disease (Symptoms and how it is passed on)

A

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
Q

What are the causes of HD

A

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
Q

What does the Substantia nigra regulate

A

caudate, putamen and globus pallidus

50
Q

What causes the first symptoms of HD

A

Degeneration of the striatum which leads to hyperkinesia and then to akinesis

51
Q

What causes PD

A

PD is due to degeneration of the substantia nigra and leads to hypokinesis

52
Q

What causes Huntingtons

A

Mutation in HTT (Huntingtin protein)

53
Q

What is the role of the cerebellum in motor learning

A

Modulates upper motor neurons – no direct connections to spinal cord
Required for the learned execution of planned, voluntary, multijoint movements

54
Q

What is motor learning

A

Predictions based on past experience of movements.

Importantly, cerebellum also compares what is intended with what actually happens – motor learning

55
Q

What is dyssynergia

A

decomposition of movement due to breakdown of normal coordinated execution of a voluntary movement.

56
Q

How doe the cerebellum form a loop with the motor cortex

A

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
Q

What is the function of the cerebellum motor cortex loop

A

to detect and correct differences between the intended movement and the actual movement - the so-called motor error.

58
Q

What can lesions in the cerebellum cause

A

Cerebella ataxia

Poorly integrated movement (dyssynergia)

University - Neuroscience (9 decks)

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