NEURO: Control of Movement Flashcards
Describe the basal ganglia.
a group of nuclei deep inside the brain that are all interconnected.
The basal ganglia take massive input from multiple cortical and brainstem regions, and output to selected parts of the same areas: focusing function.
While the motor functions of the basal ganglia have been highlighted (e.g. Parkinson’s), non-motor processing (such as sensory, emotional, cognitive) is just as important.
How are the basal ganglia split up?
They are split into three circuits:
- motor circuit (movement control)
- associative circuit
- limbic circuit (emotional information)
The basal ganglia are segmented anatomically (and functionally) between different loops (motor, associative, limbic) and within loops (e.g. different motor areas retain topographic separation).
Describe the simplified output of the basal ganglia.
The main output of the basal ganglia is largely inhibitory, so more activity in the basal ganglia leads to less movement.
There are two pathways that exist through the basal ganglia: one which decreases output activity (increasing movement), and one which increases output activity (decreasing movement).
Dopamine has different effects on these two pathways; it tends to promote movement.
What does the Alexander and Delong model of movement based on basal ganglia state?
It states that changes in the firing rate (of the output nucleus) determine the degree of thalamic inhibition, and therefore the amount of movement possible.
If the firing rate goes up, it tends to inhibit movement, and vice versa.
How does Parkinson’s affect the basal ganglia?
In Parkinson’s, the substantia nigra is damaged, meaning that dopamine can’t be made.
Dopamine tends to turn on the movement pathway and turn off the non-movement pathway. Thus, if you get damage to it, the inhibitory output of the basal ganglia turns up as high as possible. This inhibits the thalamus, which in turn inhibits the motor cortex.
So, it stops movement from happening.
Explain hyperkinesia and how it ties in with the basal ganglia.
Hemiballismus is a flinging movement of one side of the body, typically caused by a subthalamic nucleus stroke.
If the subthalamic nucleus is knocked out, you get excessive inhibition of the inhibitory output nucleus. This means that it’s not stopping the thalamus or the motor cortex, so we get excessive movement.
What is wrong with the Alexander and Delong model of movement based on basal ganglia?
It’s been proven not to be clinically correct.
For example, there was someone with extreme uncontrolled fidgety movements, and you would expect that lesioning the basal ganglia would make it worse (as the basal ganglia majorly inhibit movement). However, in that scenario, lesioning the output nucleus of the basal ganglia managed to make him much better.
After research, it was found that it was not the level of basal ganglia output but its pattern that was important.
How would you record the level of firing in humans?
You can put electrodes on the brain, and from that, we can record the activity of nerve cells around them; these are called local field potentials.
We can process the images and see the firing rate.
What would be the difference in frequencies between a normal brain and a brain with Parkinson’s?
In a normal brain, there are lots of different frequencies of firing that are happening in different nerve cell populations. They are multiple channels with independent temporal codes. Hence, they can carry a lot of different information.
In Parkinson’s, the channels become synchronised, so there is less information processing and transfer.
What is the evidence that β activity is antikinetic?
β suppression with levodopa correlates with a therapeutic outcome.
Proving the causation, direct stimulation of the subthalamic nucleus at β band frequencies worsens Parkinsonism.
So what do we need to move or not to move?
Moving is a change from one (stable) sensory state to another (stable) sensory state.
In order for this to work, you need:
- to turn down the current sensory state (lower β power)
- to have an accurate prediction of the new sensory state
- to have a way of stabilising the new sensory state (higher β power)
What is the relation between movement and β power?
The higher the β power, the less movement is possible.
This makes sense with Parkinson’s, where there is always high β power, so it is hard to turn down to get into a new state. Thus, it’s hard to move.
How do brain predictions help us in day-to-day life?
The brain allows us to make internal models of the world, how the world is meant to work and how our body will then respond.
Based on previous experiences, the body doesn’t need to rely on slow, sensory feedback, but instead it can call on those experiences and learn from them.
What is the cerebellum’s role in controlling movement, and what happens if it is damaged?
The cerebellum checks if what you expected to happen did actually happen, since it is is a hub of a lot of sensory information running through.
If the cerebellum is damaged, you find that you can’t coordinate movements well because you can’t adjust or adapt based on the little errors in movement (meaning you can’t learn normally).
