Neuro: Control of Movement Flashcards
What does appropriate motor control require?
- Motor control requires an integrated system.
- This system includes not just the mechanisms of movement, but also aspects of motivation, cost, appropriateness, importance etc to move or act at this moment.
- The basal ganglia are a key part of this network and seem to be particularly important in switching from one state to another (when to act) and also the cost of acting (the vigour of movement), and perhaps therefore also which particular action is most appropriate at this time.
Describe the basal ganglia.
- The Basal Ganglia are a set of heavily interconnected nuclei deep in the brain which are key to successful motor control.
- A key role appears when selecting the right action for the given situation.
- Damage to the basal ganglia (by degeneration such as Parkinson’s or injury such as stroke) is a common cause of movement disorders.
- Information enters via the striatum (caudate nucleus and the putamen)
- The outputs of the basal ganglia are known as the Globus Pallidus and the thalamus.
- The Substantia Nigra (SN) are dopamine producing nerve cells which link into the basal ganglia. This is the main site of damage in Parkinson’s disease (lose dopamine going up into the basal ganglia).
Describe some concepts of movement disorders.
- Hypokinetic movement disorders - movement is too slow/not enough movement.
- Hyperkinetic movement disorders - extra unwanted movement.
There is a concept that in hypokinetic movement disorders such as Parkinson’s, there is not enough dopamine around. Whereas in hyperkinetic movement disorders there is too much dopamine around. However it is not very true.
What is the Alexander and Delong model for how the basal ganglia affects movement?
- Changes in firing rate (of the output nuclei) determine the degree of thalamic inhibition, and therefore the amount of movement possible.
- If the rate of firing in the basal ganglia is high, then this inhibits the thalamus, motor cortex so there wont be a lot of movement.
- Whereas if they turn the firing rate down then the thalamus is not inhibited as well as the motor cortex not being inhibited so there is too much movement.
- Idea is that the basal ganglia activity can turn up or turn down the output and therefore turn up or turn down the amount of movement as possible.
How does Parkinson’s affect the basal ganglia?
- In Parkinson’s, the substantia nigra is damaged, meaning that dopamine can’t be made.
- Characterised by slow and small movement. Significant difficulty in the initiation of movement and getting the movement to carry on. There is also rigidity in the muscles.
- Dopamine tends to turn on the movement pathway and turn off the non-movement pathway.
- Therefore if there is damage, 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 (dyskinesia), 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.
What would be the difference in frequencies between a normal brain and a brain with Parkinson’s?
- People found that there is an abnormal rhythm of nerve cell interaction. Oscillations picked up at around 20Hz (beta frequency). This is seen in healthy people.
- However there are pathologically enhanced beta oscillation in people with Parkinson’s disease.
- If L-dopa is given (makes people with Parkinson’s disease generally better), then there is a suppression of beta activity.
What happens when there is beta suppression in deep brain stimulation?
Reduction in Parkinson’s symptoms
So what do we need to move or not to move?
Moving is a change from one (stable) sensory state (e.g. sitting still) to another (stable) sensory state (e.g. standing up).
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 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 (higher β power)
What is the relation between movement and β power?
The higher the β power, the less movement is possible (current sensory state is excessively stable so cant initiate or stabilise new movement).
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.
Describe some different movement abnormalities.
- Some movement disorders (e.g. Parkinson’s disease, Tourette’s syndrome) fit well with a disorder of this “brake” on action, with too much present beta activity in Parkinson’s and too little beta activity in Tourette’s.
- Other disorders of movement (e.g. dystonia, chorea, certain types of tremor) may arise “noise” in the sensorimotor system
- Can also have problems with generating an appropriate response to sensory feedback such as overcorrection in cerebellar damage.
