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Neurology > Control of Movement (Incl. Basal Ganglia) > Flashcards

Control of Movement (Incl. Basal Ganglia) Flashcards

1
Q

What are basal ganglia?

A

The basal ganglia are a group of interconnected nuclei deep inside the brain

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2
Q

What is the function of the basal ganglia?

A

The basal ganglia take massive input from multiple cortical and brainstem regions, and output to selected parts of these same areas: Focusing function

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3
Q

How are basal ganglia categorised?

A

The basal ganglia are segregated anatomically and functionally between different loops (motor, associative, limbic) and within loops (e.g. different motor areas retain topographic separation)

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4
Q

What is the main effect on movement of basal ganglia?

A

The main output of the basal ganglia is Inhibitory, so more activity = less movement

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5
Q

How do basal ganglia cause movement?

A

Two pathways through the basal ganglia exist, one which DECREASES output activity (increases movement) and one which INCREASES output activity (decreases movement)

Dopamine has different effects on these two pathways

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6
Q

Where does basal ganglia get their input from?

A

Input to the basal ganglia is called the striatum

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7
Q

Describe the pathway promoting movement

A

The direct ‘go’ pathway inhibits the inhibitory output nucleus to promote movement
=> inhibits subthalamic nucleus (STN) allowing inhibition of inhibitory output for movement to occur

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8
Q

Outline the pathway inhibiting movement

A

The indirect ‘stop’ pathway through a complicated system enables excitation of the inhibitory nucleus, preventing pathway

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9
Q

What is the SNc?

A

The substantia nigra (SNc) is the brain region that produces dopamine which is released into the basal ganglia - substantia nigra is damaged in Parkinson’s disease

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10
Q

What determines the amount of movement possible according to the rate model?

A

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

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11
Q

What causes Parkinson’s Disease?

A

Clinically dominated by a lack of movement: bradykinesia

The substantia nigra (SNc) degeneration leads to a lack of dopamine

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12
Q

How does dopamine affect the control of movement?

A

Dopamine activates the inhibitory pathway causing movement

Dopamine inactivates excitatory pathway inhibiting movement

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13
Q

How does damaged SNc lead Parkinson’s disease?

A

Damage to the SNc causes the inhibitory output nucleus of the basal ganglia to turn up as high as possible causing inhibition of the thalamus and motor cortex - stops movement occurring

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14
Q

Give an example of hyperkinesia

A

Hemiballismus is a flinging movement of one side of the body, typically caused by a subthalamic nucleus stroke

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15
Q

Explain what causes Hemiballismus in stroke patients

A

The subthalamic nucleus is a significant node in the movement pathway causing inhibition. When damaged, there is an excessive inhibition of the inhibitory output nucleus
⇒ the inhibitory output nucleus is no longer stopping the thalamus or motor cortex causing excessive movement

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16
Q

What are the anatomical issues of the movement model?

A

There are many more connections between basal ganglia than the model suggests

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17
Q

What are the clinical inaccuracies of the movement model?

A

When clinically investigating movement disorders, lesioning the relevant brain regions produces unexpected results from the model

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18
Q

Give an example of unexpected outcomes, deviating from the movement model

A

⇒ lesions to the output nucleus of the basal ganglia stops any abnormal movement developed even though this is not the expected outcome (would expect more movement as we’ve knocked out the inhibitory output of movement)

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19
Q

What can be concluded about the movement model?

A

It is not the level of basal ganglia output but its pattern that is important

20
Q

When investigating rate of firing in PD, what pattern was seen?

A

Was seen that there was a particular frequency that the nerve cells discharged (firing) which is dominant - abnormal
> not just bursts of neurones but excess synchrony in PD

MPTP monkey: especially tremor frequencies <12 Hz

Parkinsonian rodent & human: <30 Hz

21
Q

How is basal ganglia output measured?

A

Using a deep brain stimulation electrode under imaging guidance
When the electrodes are in, we can record the activity of nerve cells around them - local field potentials (LFPs)

Can process lFPs to identify a firing rate
This is done in patients with Parkinson’s etc.

22
Q

Describe the recorded output (LFPs) in normal healthy patients

A

In a normal STN there are lots of different frequencies of firing occurring in different nerve cell populations - carries more info

23
Q

How does the firing rate of PD patients differ than normal?

A

In PDs everything is more synchronised around beta-frequency - reduces the amount of info carried in those signals

24
Q

What is the factor causing movement inhibition in PD patients?

A

Beta activity is high in PD patients and is thought to affect motor control

25
Q

How was beta activity limited in PD patients

A

When patients administered levodopa, beta activity is suppressed - amount of suppression correlates with therapeutic outcome (improved movement control)

26
Q

What other method is used to suppress beta activity?

A

Beta suppressed by deep brain stimulation surgery

Can turn a deep brain stimulation electrode on/off

27
Q

How is deep brain stimulation surgery used to suppress beta activity?

A

Whenever the deep brain stimulator is turned on ⇒ suppression of beta power
When it is turned off beta power returns and symptoms prevail

28
Q

What can worsen the onset of PD?

A

Causation: Direct stimulation of STN at beta band frequencies worsens Parkinsonism

High beta activity makes it difficult for patients to initiate and continue movements
But effect is small (≤ 20% slowing)

29
Q

When is dopamine released to aid movement?

A

Baseline tonic level of dopamine released in basal ganglia

DA release occurs mainly at the beginning of a change in movement state i.e, rest → movement

DA release also occurs during salient changes in environment i.e, someone walks through the door

30
Q

How does dopamine release differ in PD Patients?

A

In PD, reduction of DA release means DA levels never reach threshold
Medication enables the phasic levels of DA release to occur

31
Q

What factors control amount of movement?

A

Firing rate aids movement but clinically doesn’t control movement

Beta activity in basal ganglia is significant - firing of nerve cells at particularly frequency inhibits movement (aids movement control)

DA release also modulates the signal

32
Q

What is movement?

A

Moving is a change from one (stable) sensory state to another (stable) sensory state

33
Q

What are the requirements for movement to occur?

A

In order for movement to work you need:

  • To turn down the current sensory state (lower beta
    power)
  • To have an accurate prediction of the new sensory state
  • To have a way of stabilising the new sensory state
    (higher beta power)
34
Q

How can we predict movements to aid how we actually move?

A

Sensory system picks up info about the world ie. moving objects
The sensory system enables us to predict movements even if we’ve never encountered them by estimating how heavy an object is likely to be

35
Q

What is the consequence of incorrect predictions?

A

Any inconsistencies in the prediction and actual observation can be learnt for future to avoid mistakes → don’t have to wait for slow sensory feedback to reach brain

36
Q

What enables us to make predictions of movements?

A

Internal models of the world simulated in our brain to predict movement for faster responses

37
Q

What is the significance of internal models?

A

Current sensory state has lots of possibilities of movement to go into - need to be able to filter out inappropriate movements and enable specific movements quickly - action selection

38
Q

How do we decide which movement to follow through?

A

Competition between current sensory state and prediction to create a future movement state
We require a mechanism to either continue the current state or to move into the future state via predictions → beta activity significant in this

39
Q

What are the 2 possibilities of movement?

A

Possibilities of movement:

  1. Stay in current state
  2. Move into future state
40
Q

How does the brain enable us to remain static?

A

One way of staying in the current state is to upregulate the current sensory state to keep you static → high beta activity to prevent movement occurring

41
Q

How do we move into a future state from the current state?

A

Other option is to move by allowing the prediction of the future state to come through - beta activity reduced to down-regulate strength of current state allowing you to move

42
Q

What is the significance of basal ganglia in movement?

A

Basal ganglia play a significant role in turning on/off movements and require lots of external input from other brain regions e.g. emotion centres, sensory regions, reward centres etc.

43
Q

What is the role of sensory afferents in movement?

A

Sensory inputs via afferents provides info about any unexpected movements

44
Q

What is the effect on movement of damage of sensory afferents?

A

Sensory neuropathy causes unsteady movement due to loss of sensory feedback - control is difficult

45
Q

What role does the cerebellum play in movement?

A

Cerebellum uses forward model to double check if the movement caused by sensory afferents is what was expected - any error is picked up by cerebellum

46
Q

How does cerebellum damage effect movement?

A

Damage to the cerebellum leads you to be unsteady and uncoordinated - little errors aren’t adjusted for and cannot learn to adapt

47
Q

What is the issue in PD movement?

A

Actual movements in Parkinson’s Disease appear normal - it is their intention, scaling and persistence which is abnormal

Many movement ‘disorders’ are in fact normal movement occuring at the wrong time: the key abnormality is the inappropriate (sensory) urge to move

Neurology (20 decks)

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