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Nonetheless, it's not sufficient.
It's not sufficient to produce the kind of movement that we are capable of,
and that we are used to.
So if all we had was the motor hierarchy,
the movement that we would produce would be unrecognizable.
And that's because there are two critical places that modulate
the motor hierarchy and the first one is the cerebellum.
The cerebellum is, as I've said, like an orchestral conductor.
It's saying, okay, muscles, all work together.
Work well together.
When the strings start to ebb I want some real energy from the woodwinds,
and then when the woodwinds ebb then we should get some percussion.
So, in order to make sure that movements that depend on multiple joints and
multiple muscles acting across multiple joints, that they actually are smooth,
we need someone organizing that, some entity organizing that.
And that's the cerebellum.
But what makes this a modulatory pathway as opposed to
a part of the hierarchy
is that the cerebellum does not talk to the motoneurons.
It only talks to these top three areas.
The cortical control motor centers, the brain stem motor control centers, and
the central pattern generators.
It's only modulating those types of neurons.
And so the central pattern generators are found, for the most part, in the brain
stem, the ones that are modulated by the cerebellum are all in the brain stem.
So the cerebellum is only modulating places in the brainstem and the forebrain.
To do this, the cerebellum gets sensory input from the periphery,
from the muscle, from the skin, as well.
From lots of places.
And it also gets input from the motor hierarchy about what we intend to do.
And the cerebellum is all about comparing intention and actual movements.
So when the cerebellum is on the fritz, when it doesn't work, what do we get?
We get ataxia.
And that looks like, if I ask a person with ataxia to place
their finger on my finger, it's gonna look like this.
They're gonna start out okay, a little slowly, but as they get close to there,
they're going to miss the target.
That's dysmetria.
In other words, they're not measuring
the, how far they should go accurately.
They typically overshoot and then they have to come back.
And they're essentially,
instead of smoothly stopping the muscle that extends the arm and
starting to activate the muscle that pulls back the arm so
that you stop on a dime on my finger.
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The other major area that modulates movement is the basal ganglia,
the striatum and globus pallidus.
And this is even more removed from the motor hierarchy.
It only modulates the two motor control centers,
the motor control centers or the two types of motor control centers,
those the brainstem and those the cortex, in the cerebral cortex.
And it gets input from these two areas.
So this basal ganglia, the modulation of the basal ganglia,
is at a more complex level than at the modulation of the cerebellum.
It's not so much how we make the movement.
It's in part, whether we make the movement, action selection.
Do we move or do we not move?
And our default is not moving, and so when the default is,
when we can't break through that default, we don't move.
And a poverty of movement is the cardinal sign of Parkinson's.
So Parkinson's disease, which is a fairly common disease,
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involves a poverty of movement.
And that's a disease of the basal ganglia.
Another type of disease that affects basal ganglia are creaform movements.
That's sort of the opposite from Parkinson's.
Instead of having too little movement, we have too much movement.
We have extra movements.
And these are extra movements that happen and they differ in speed.
They can be chorea form, which is very dance-like, or
they could be very fast and ballistic.
And so, things like Hemiballismus, or Huntington's Chorea,
or Sydenham's Chorea, these are all examples of excess movements.
So, in part we can think of this as
not just that we have to choose a movement,
but once we choose a movement, we have to suppress all the other movements.
There are a lot of movements that we can make at any one time without falling over.
So we have to make one movement, we have to choose that.
In Parkinson's, that never gets chosen because there's this poverty of movement.
And in something like Huntington's, we choose a movement but we're unable
to suppress all these competing movements and so they happen at the same time.
So this is one way to think about the basal ganglia,
and we'll go into that in a later module.
I'm sorry, in a later unit.
Okay, so now what we're gonna do is we're gonna move on.
We're gonna look at motor neurons, and the muscle, and
the various types of motor neurons in muscle.
[MUSIC]
Peggy MasonProfessor
