Control of Movement Flashcards

1
Q

Why is movement difficult to replicate electronically?

A

→ The brain predicts movement

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2
Q

What are the basal ganglia?

A

→ A group of nuclei inside the brain

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3
Q

What kind of a disease is Parkinsons?

A

→ basal ganglia degenerative disease

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4
Q

What do the basal ganglia act as?

A

→ Relay stations

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5
Q

What are the 3 different circuits in the brain?

A

→ Motor
→ Associative

→ Limbic

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6
Q

How are the basal ganglia segregated?

A

→ Anatomically

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7
Q

What is the main output of the basal ganglia?

A

→ inhibitory

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8
Q

What are the 2 basal ganglia pathways?

A

→ One decreases output activity (increases movement)

→ One increases output activity (decreases movement)

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9
Q

What sends inputs to the basal ganglia?

A

→ The striatum

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10
Q

What is the indirect stop pathway?

A

→ Activates the inhibitory nucleus and makes movement less likely to happen

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11
Q

What is the direct go pathway?

A

→ Inhibits the inhibitory pathway

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12
Q

Where is dopamine produced?

A

→ In the substantia nigra

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13
Q

What is the Alexander and Delong model?

A

→ Changes in firing rate (of the output nuclei) determine the degree of thalamic inhibition and the amount of movement possible

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14
Q

What is bradykinesia?

A

→ A lack of movement

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15
Q

What happens in Parkinsons?

A

→ Substantia nigra degenerates
→ Not enough dopamine

→ Inhibitory output of the basal ganglia turns up
→ Inhibits the thalamus and inhibits the motor cortex
→ rate of firing of the output nucleus goes up

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16
Q

What is hemiballismus and what is it caused by?

A

→ A flinging movement of one side of the body

→ caused by a subthalamic nucleus stroke

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17
Q

What role does the subthalamic nucleus have?

A

→ it is a key node in the stop pathway

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18
Q

What happens if the subthalamic nucleus is removed?

A

→ excessive inhibition of the stop pathway or an inhibitory output nucleus
→ the Gpi/SNr is not stopping the thalamus

→ excessive movement

19
Q

What is a clinical issue with the Alexander and Delong model?

A

→ lesioning the thalamus does not cause prominent akinesia

→ lesioning the GPi does not cause dyskinesia

20
Q

What is the beta frequency?

A

→ 20-30 Hz

21
Q

What is the firing like in people with motor disorders?

A

→ the neurons have a bursty pattern

→ the rate of firing is not abnormal but the pattern of firing is

22
Q

in a normal situation what do brain electrodes pick up and what happens in Parkinsons?

A

→ lots of different frequencies firing

→ Everything becomes synchronised

23
Q

When does dopamine release occur?

A

→ At the beginning of movement

24
Q

People with Parkinsons still produce dopamine, why is this not enough for movement to occur?

A

→ There is a baseline level of dopamine release
→ additional dopamine release happens at the beginning of movement

→ people with Parkinsons have low baseline dopamine
→ When a stimulus occurs the additional dopamine released it not enough to pass the threshold for movement.

25
How do you define moving?
→ Change from one stable sensory state to another stable sensory state
26
What are the 3 things required for changing sensory states?
→ Turning down current sensory state → Accurate prediction of the new sensory state → Stabilising the new sensory state
27
What is involved in stabilising sensory states?
→ Beta power
28
What is beta power like when sitting still and why?
→ It is high | → stops you having other unneeded movements such as jumping
29
If you want to move what happens to beta power?
→ It is turned down which allows you to change state
30
What allows prediction of movement in the brain?
→ The brain builds internal models of the world
31
What is the forward model?
→ Brain sends a copy of the movement to the cerebellum to check if the movement is correct
32
What does the forward model do?
→ Comparing what happened with what was expected to happen
33
What happens when there is damage to the cerebellum?
→ movement becomes steady and uncoordinated because the comparison can't happen → the brain is unprepared for obstacles
34
What is abnormal in Parkinsons?
→ initiation → Scaling → and persistence of movement
35
What is the relationship between firing rate of basal ganglia and thalamic inhibition?
inversely correlated
36
What does removal of STN do to the thalamus?
knocks out excitatory pathway of BG and thus thalamus increases in firing so more movement​
37
What does beta suppression lead to in Parkison's?
correlates with reduction in Parkinson’s symptoms​
38
In Parkinson's what about the firing determines disorders?
a particular rhythm abnormality appears to disturb control of movement, resulting in slow initiation and poor scaling (size, vigour) of movement
39
What does high beta power mean in Parkinson's?
→High beta means that the current sensory state is excessively stable, therefore can’t initiate or stabilise new movement →Actual movements in Parkinson’s disease appear normal
40
What does pathologically low beta result in?
→the current sensory state is unstable so that new, unwanted patterns of movement can arise and come out without will
41
What is the treatment for many movement disorders?
→dopamine receptor antagonists which increase beta activity.​
42
What is cerebella tremor?
→Possibly a problem with inappropriate response to sensory feedback that comes into the cerebellum​ →Things to do with corrective feedback- over correction.
43
What is chorea and dystonia?
→arise from other motor control problems →core control of movement seems normal with “noise” added