W11 - Control of Movement (incl. Basal Ganglia) Flashcards
How is predicting helpful?
We need prediction in day to day life.
Eg. In a ball game, players predict where the ball is going to go and get into position.
What is a system approach to motor control?
movement has just happened and the sensory system picks this up and the state of the body - what position is the body in now.
This information goes into the cerebellum.
It also receives information from the top about what the organism was trying to do.
You can compare this with what is currently happening and what the organism is hoping would happen. State of estimation in the Parietal cortex.
There are other parts of the brain that plans the movement in the first place - motor & pre-motor cortex.
The Basal Ganglia determines whether the right action is selected at the right time - costs and rewards of doing that movement.
There is also the Central and peripheral motor neurones and muscles that actually allows the movement to happen.
What is the Basal Ganglia?
-The Basal Ganglia are a collection of heavily interconnected nuclei in the brain which are key to successful motor control.
-A key role appears to be in action selection: i.e. selecting the right action for the given situation.
-Damage to the basal ganglia (by degeneration or injury) is a common cause of movement disorders. This is a disorder of the quality of movement.
-Caudate nucleus and the Putamen making up the Striatum - input side.
-Global Pallidus externa and interna (GPe) (GPi) - output
-Thalamus - output structure
- Subthalamic nucleus
- Substantia Nigra - dopamine producing nerve cells - important in Parkingson’s.
What are the simple concepts of movement disorders?
Hypokinetic = not enough movement, too slow, not enough dopamine
Hyperkinetic = too much movement, too much dopamine
What isThe rate (Alexander and Delong) model for how the basal ganglia affect movement?
Changes in firing rate (of the output nuclei) determine the degree of thalamic inhibition, and therefore the amount of movement possible.
The basal ganglia is inhibitory on the thalamus and motor cortex. If the firing rate of basal ganglia is high, it is going to inhibit the two limiting movement vise versa.
What is Parkinson’s disease?
Clinically dominated by a lack of movement: bradykinesia.
- Lack of facial expression, no fidgety movement
- Difficulty in initiating and continuing movement
- Ridgidity of muscles.
Less dopamine
What is Hyperkinesia?
Hemiballismus is a flinging movement of one side of the body, typically caused by a subthalamic nucleus stroke.
Knocking out the subthalamic nucleus knocks out the excitatory pathway in the basal ganglia. There is less inhibition of the output structure (thalamus) which means more movement is possible.
Lines with the model.
What are some clinical problems with the Alexander and Delong model?
There is a man with Parkinson’s disease - has complication of having long term treatment for dyskinesia - lots of extra fidgety movements.
There is a treatment for this called deep brain stimulation surgery. This is where an electrode is put into the sub thalamic nucleus and it’s connected up to a stimulator, a pacemaker type box. The effect of this is to block the activity of the sub thalamic nucleus. According to the model, this is a bad idea to knock the subthalamic nucleus out with a stroke. But it is a brilliant treatment.
How is it not the rate that matters, but the rhythm?
There is an abnormal rhythm with nerve cell interaction. Around 20 Hz frequency - B frequency - seen in healthy people.
This is pathalogically enhanced Beta oscillations in people with Parkinson’s disease.
What does Beta suppression mean for Parkinson’s symptoms?
Beta suppression with levodopa correlates with reduction in Parkinson’s symptoms
What does the delayed return of bradykinesia mean?
Delayed return of bradykinesia after DeepBrainStimulation correlates with delayed return of beta.
Normalised both finger tapping amplitudes and beta LFP power to that recorded 2 minutes after stopping DBS. Thus movement amplitude falls as power in the beta band returns. Kűhn et al, 2008.
When you turn the device off, as you see a rise in beta activity, there is a rise in symptoms.
So what do we need to do to move or not 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 (e.g. turn down the network that is supporting you sitting still).
-To have an accurate prediction of the new sensory state. (e.g. create a plan/prediction of the new state such as standing up).
-To have a mechanism to rate how important it is to do this movement rather than to stay in the current state or do another movement.
-To have a way of stabilising the new sensory state.
What is abnormal about Parkinson’s disease?
Actual movements in Parkinson’s disease appear normal – it is their initiation, scaling and persistence which is abnormal.
High beta means that the current sensory state is excessively stable, therefore can’t initiate or stabilise new movement…all movement (action) has a high “cost”: Treatment – providing levodopa which supresses beta.
What is the common case with movement disorders?
Many movement “disorders” are in fact normal movement occurring at the wrong time: the key abnormality is the inappropriate (sensory) urge to move.
Pathologically low beta means that the current sensory state is unstable so that new, unwanted patterns of movement can arise and come out without will. Treatment: dopamine receptor antagonists which increase beta activity.
What is cerebellar tremor?
Cerebellar Tremor: Possibly a problem with inappropriate response to sensory feedback that comes into the cerebellum
In a healthy person, as we move our hands towards a target, there is a correction movement to make sure we are heading towards the real target. In this case, there is over correction causing tremors
