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Neuroscience BMS153 > Motor Control and Diseases > Flashcards

Motor Control and Diseases Flashcards

1
Q

all movements produced by skeletal musculature are initiated by what?

A

lower motor neurons.

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2
Q

the spinal cord has central pattern generators meaning…

A

it can generate behaviours without brain input.

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3
Q

the neurons found in the brain that control motor function are…

A

upper motor neurons.

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4
Q

what did Fritsch and Hitzig demonstrate in the 1870s when they electrically stimulated parts of dogs’ cortex?

A

electrical stimulation of that part of the cortex caused contractions of collateral body muscles.

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5
Q

what do we now call the region of the brain that Fritsch and Hitzig stimulated?

A

the motor cortex.

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6
Q

Sherrington and Penfield in the 1900s correlated stimulation sites with muscle contraction and found that the motor cortex is what?

A

somatotopically mapped.

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7
Q

lower motor neurons in the ventral horn (of spinal cord) innervate striated muscle to control movement

A

b

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8
Q

axial muscles control what movement?

A

trunk movements.

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9
Q

proximal muscles control what movement?

A

shoulder,
elbow,
pelvis,
knee movements.

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10
Q

distal muscles control what movement?

A

hands,
feet,
digit movements

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11
Q

each muscle fibre receives input from what type of neuron?

A

a lower, alpha motor neuron - each one innervates 1 muscle

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12
Q

what is a motor unit?

A

motor neuron and the muscle fibres it innervates.

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13
Q

what is a motor neuron pool?

A

all the motor neurons that innervate a single muscle

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14
Q

lower motor neurons receive inputs locally from where?

A

the spinal cord,

and upper motor neurons.

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15
Q

upper motor neurons project axons to where?

via what?

A

they project to lower motor neurons via descending tracts in the spinal cord.

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16
Q

what tract in the spine controls voluntary movement?

A

the Corticospinal Tract (CST).

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17
Q

where is the Corticospinal Tract found?

A

in the lateral pathway in the spinal cord from the motor cortex.

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18
Q

pyramidal cells of the motor cortex project axons on the Corticospinal Tract.
how many layers is the cortex made up of?

A

6 layers.

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19
Q

where and what are the main inputs in the motor cortex?

A

they are stellate cells in layer 4.

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20
Q

where are the main out puts in the motor cortex?

A

in layers 3, 5, and 6.

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21
Q

the axons of the Corticospinal Tract derive from where and what in the motor cortex?

A

derive from layer 5 pyramidal cells.

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22
Q

Corticospinal Tract outputs to the upper body originate from where?

A

the lateral motor cortex.

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23
Q

Corticospinal Tract outputs to the lower body originate form where?

A

the medial motor cortex.

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24
Q

describe where the axons of the Corticospinal Tract go:

A

they cross the midline in the pyramidal decussation of the medulla,
they project laterally in the spinal cord,
synapse on lateral lower motor neuron circuits that control distal muscles.

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25
Q

also, there are upper motor neurons in the brainstem, they projects to medial motor pools related to postural movement.
explain the rest of this.

A

axons from the brainstem project to ipsilaterally in tracts such as:
– the vestibulospinal tract
– the reticulospinal tract,
they synapse on to medial lower motor neuron circuits that control axial muscles.

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26
Q

ventromedial tracts control posture:

what does the vestibulospinal tract control?

A

head balance and tilting - inputs from the vestibular system.

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27
Q

ventromedial tracts control posture:

what does the tectospinal tract control?

A

orienting response - inputs from the visual system (via the super colliculus).

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28
Q

ventromedial tracts control posture:

what does the reticulospinal tract control?

A

control antigravity reflexes.

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29
Q

a volunteer lifts a lever in response to an auditory stimulus,
surprisingly the muscles recorded revealed leg muscles contract first.
what is this?

A

an anticipatory mechanism that pre-adjusts body posture to compensate they forces generated when lifting the lever.

30
Q

upper motor neurons in the cortex influence spinal cord circuits through 2 route:

A

the direct route,

and the indirect route.

31
Q

in the indirect route, movement anticipation starts where?

A

the premotor area.

32
Q

in the direct route, movement initiation starts where?

A

the primary motor cortex.

33
Q

what is motor neuron disease? (simple)

A

a degenerative disease of motor neurons.

34
Q

what is motor neuron disease characterised by?

A

sclerosis of the lateral spinal cord,

and muscle atrophy.

35
Q

what neurons does motor neuron disease affect?

A

both upper and lower motor neurons.

36
Q

what are the characteristics of lower motor neuron disease?

A

muscle paresis (weakness),
loss of muscle tone due to loss of stretch reflexes,
leads to muscle atrophy,
and in severe cases lung dysfunction.

37
Q

what are the characteristics of upper motor neuron disease?

A

muscle weakness,
increased muscle tone due to failure of modulation of stretch reflex,
hyperactive reflexes,
loss of voluntary movement.

38
Q

what is an example of a neurodegenerative disease?

A

ALS.

39
Q

what is one possible explanation for neurodegenerative diseases?

A

excitotoxicity.

40
Q

what is excitotoxicity?

A

process by which neurons are damaged and killed by the overactivations of receptor,
usually for the excitatory neurotransmitter glutamate.

41
Q

when can there be too much glutamate released?

A

in hypoxic conditions,

like after cardiac arrest, a stroke, brain trauma.

42
Q

is there a drug that is effective against neurodegenerative diseases?

A

glutamate release blockers only delay the onset of the disease.

43
Q

do neurodegenerative diseases have a genetic basis?

A

only 10% of cases do,

such as mutations of genes that encode superoxide dismutase (an enzyme).

44
Q

what are key components in the initiation of movement:

A

motor cortex,
basal ganglia (caudate, globus pallidus, putamen, subthalamic nucleus),
the ventral lateral nucleus of the thalamus,
substantia nigra.

45
Q

how is the basal ganglia involved in the initiation of movement / what is the motor loop?

A

motor cortex connects to the basal ganglia,

which feedbacks to the ventrolateral complex of the thalamus (VLo).

46
Q

the motor loops has 2 pathways:

A

the direct pathway,

the indirect pathway.

47
Q

what 4 structures are involved in the direct pathway of the motor loop?

A

the globus pallidus internal segment,
the ventrolateral complex of the thalamus,
the striatum,
and the premotor area.

48
Q

describe how the direct pathway of the motor loop works:

A

the globus pallidus internal segment tonically inhibits the the ventrolateral complex of the thalamus,
when activated by inputs, the striatum inhibits the inhibitory activity of the globus pallidus internal segment,
this allows the ventrolateral complex of the thalamus to activate the premotor area of the cortex.

49
Q

describe how the indirect pathway of the motor loop works:

A

the cortex stimulates the striatum,
this causes the striatum to inhibit the globus pallidus external segment,
the output from this causes stimulation of the globus pallidus internal segment,
which inhibits the ventrolateral complex of the thalamus,
and it is prevented from stimulating the premotor area of the cortex.

50
Q

how does the substantia nigra act in the indirect pathway of the motor loop?

A

substantia nigra inhibits the striatum,
causing disinhibition of the globus pallidus external segment,
which decreases stimulation of globus pallidus internal segment,
which disinhibits the thalamus,
so overall acts to increase cortical stimulation.

51
Q

how does the substantia nigra act in the direct pathway of the motor loop?

A

substantia nigra stimulates the striatum,
causing inhibition of the globus pallidus internal segment,
which disinhibits the thalamus,
so overall acts to increase cortical stimulation.

52
Q

indirect – inhibits

direct – amplifies.

A

-

53
Q

what motor symptoms does Parkinson’s disease include?

A 
hypokinesia,
bradykinesia,
akinesia,
resting tremor,
shuffling gait and flexed posture,
impaired balance,
mask-like expression.
54
Q

what is Parkinson’s disease a result of?

A

loss of dopamine,
due to a loss of dopaminergic neurons in the substantia nigra,
due to degeneration.

55
Q

what is a possible treatment for Parkinson’s disease?

A

L-dihydroxyphenylalanine (L-DOPA).

56
Q

what are the effects of taking intravenous L-dihydroxyphenylalanine to treat Parkinson’s disease? (Oleh Horyenkiewicz)

A

provided a brief reversal of symptoms in patients.

57
Q

what are the effects of taking oral L-dihydroxyphenylalanine to treat Parkinson’s disease? (Cotzias)

A

boosted the capacity of surviving dopaminergic neurons in the substantia nigra.

58
Q

reduced dopaminergic input from substantia nigra to striatum leads to:

A

increased activity of the indirect pathway of the motor loop,
and decreased activity of the direct pathway of the motor loop.

59
Q

what does increased indirect and decreased direct pathway activity lead to?

A

increased inhibitory activity of the globus pallidus internal segment,
causing decreased activity of the ventrolateral complex of the thalamus,
and so less motor cortex activation.

60
Q

what motor symptoms does Huntington’s disease include?

A 
hyperkinesia / dyskinesia,
chorea,
lead to akinesia / dystonia,
dementia,
personality disorder / psychosis.
61
Q

what is the cause of Huntington’s disease?

A

autosomal genetic disease resulting in neural degeneration in the indirect components of the motor loop,
then in the direct pathway and globus pallidus external component.

62
Q

what happens in the basal ganglia that leads to the characteristics of Huntington’s disease?

A

degeneration in the striatum reduces inputs to the globus pallidus external input,
increasing input to the globus pallidus internal segment,
results in disinhibition of ventrolateral complex of the thalamus,
causing inappropriate initiation of movement (hyperkinesia, chorea).

63
Q

both Parkinson’s disease and Huntington’s disease have a genetic / inherited component.

A

-

64
Q

what genes are involved in Parkinson’s disease?

A

mutations to genes SNCA and GBAT predispose to the disease,

and disease genes encode proteins involved in protein degeneration pathway.

65
Q

what genes are involved in Huntington’s disease?

A

mutations in HTT genes

66
Q

what is the cerebellum responsible for?

A

modulates upper motor neurons,

required for learned execution of planned, voluntary, multi-joint movements.

67
Q

cerebellum appears to instruct motor cortex with respect to direction, timing, and force of movement.

A

-

68
Q

what are the primary functions of the cerebellum?

A

to detect and correct differences between the intended and actual movement (motor error)

69
Q

what inputs does the cerebellum receive?

A

inputs from the cortex,
corticocerebellar projection,
and sensory info from the spinal cord and vestibular system.

70
Q

where does the cerebellum project to?

A

projects to the motor cortex via the thalamus.

71
Q

what does lesions to the cerebellum result in?

A

poorly integrated movement (cerebellar ataxia).

Neuroscience BMS153 (22 decks)

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