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Neuroscience > Control of Movement > Flashcards

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
Q

How do you define moving?

A

→ Change from one stable sensory state to another stable sensory state

26
Q

What are the 3 things required for changing sensory states?

A

→ Turning down current sensory state
→ Accurate prediction of the new sensory state

→ Stabilising the new sensory state

27
Q

What is involved in stabilising sensory states?

A

→ Beta power

28
Q

What is beta power like when sitting still and why?

A

→ It is high

→ stops you having other unneeded movements such as jumping

29
Q

If you want to move what happens to beta power?

A

→ It is turned down which allows you to change state

30
Q

What allows prediction of movement in the brain?

A

→ The brain builds internal models of the world

31
Q

What is the forward model?

A

→ Brain sends a copy of the movement to the cerebellum to check if the movement is correct

32
Q

What does the forward model do?

A

→ Comparing what happened with what was expected to happen

33
Q

What happens when there is damage to the cerebellum?

A

→ movement becomes steady and uncoordinated because the comparison can’t happen
→ the brain is unprepared for obstacles

34
Q

What is abnormal in Parkinsons?

A

→ initiation
→ Scaling

→ and persistence of movement

35
Q

What is the relationship between firing rate of basal ganglia and thalamic inhibition?

A

inversely correlated

36
Q

What does removal of STN do to the thalamus?

A

knocks out excitatory pathway of BG and thus thalamus increases in firing so more movement​

37
Q

What does beta suppression lead to in Parkison’s?

A

correlates with reduction in Parkinson’s symptoms​

38
Q

In Parkinson’s what about the firing determines disorders?

A

a particular rhythm abnormality appears to disturb control of movement, resulting in slow initiation and poor scaling (size, vigour) of movement

39
Q

What does high beta power mean in Parkinson’s?

A

→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
Q

What does pathologically low beta result in?

A

→the current sensory state is unstable so that new, unwanted patterns of movement can arise and come out without will

41
Q

What is the treatment for many movement disorders?

A

→dopamine receptor antagonists which increase beta activity.​

42
Q

What is cerebella tremor?

A

→Possibly a problem with inappropriate response to sensory feedback that comes into the cerebellum​

→Things to do with corrective feedback- over correction.

43
Q

What is chorea and dystonia?

A

→arise from other motor control problems

→core control of movement seems normal with “noise” added

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