Basal Ganglia: Neuroanatomy Video Lab – Brain Dissections

>>Today’s subject
is the basal ganglia. One of the major motor pathways
along with the cerebellum and the corticospinal tract. It’s complicated. And the name basal ganglia
is really a misnomer, because it’s not a ganglion. Let’s look at what you
think a ganglion looks like and then compare it
to what we’re going to be talking about today. We’ve associated ganglia
with these collections of nerve cell bodies outside
the central nervous system such as these dorsal root
ganglia along the spinal cord. But today we’re going to
talk about the basal ganglia in the base of the brain. So, now let’s look at a
model of the basal ganglia, principal components, before
we go to the gross specimens. This fun color-coded brain
is useful for orientation to the major players that we’re
going to be talking about today. The basal ganglia consist of
two large nuclei, the caudate and the putamen in
brown, here separated by this rainbow colored
internal capsule. Next to it is the
large thalamus. And one of the nuclei of
this thalamus will be part of the circuitry that
we’re discussing. Nicely shown on this
model is the fact that these rainbow colors
represent axons going to and coming from the cerebral
cortex in a color-coded fashion. So, here you have fibers from
the frontal lobe and here fibers from the occipital lobe. A very important point
to keep in mind today as we discuss these
basal ganglia is that basal ganglia
disease is associated with involuntary movements. Movements you cannot control. And the key diseases
that you can think of are Huntington’s disease
and Parkinson’s disease. Another important point we
can make on this model is that basal ganglia
disease is manifested on the opposite side
of the body. Whereas cerebellar
disease that we have talked about is manifest usually on
the same side of the body. So, we have two consultants to
the corticospinal tract coming from these red and orange areas. One is the basal ganglia,
for involuntary movements. And the other is the
cerebellum involved with voluntary movements. And so diseases for the motor
system can be categorized as either basal ganglia-type
diseases, cerebellar-type diseases,
or motor cortex diseases. Let’s go to an animation
showing parts of the basal ganglia
made in 1998. And it’s still the best
three-dimensional graphic description that I can show you
of the green caudate nucleus, which is part of the
basal ganglia as it curves around the blue ventricular
system. You can see it curves from the
frontal lobe where it is large down into the temporal lobe
where it is very, very small. And as it comes down, it can be
seen to have a body and a tail and a very large head. So, the caudate nucleus
curves around and follows the ventricle. The second animation adds the
structure called the putamen. The putamen is large and green. And this base here represents where our rainbow internal
capsule was located and here’s the caudate that
we’ve already looked at. And now let’s introduce
another term. The putamen and the
caudate together are called the striatum. Now, let’s rotate this. And you can see the tail
of the caudate coming around and the putamen. And we can look through
this phantom brain. And, by the way, the red
structure is the amygdala. In this animation, we’re going
to peel back the cerebral cortex and look in a coronal
view at the structures and another new structure
we’re going to add called the
globus pallidus on the inside of the putamen. So, here’s the putamen. Watch as we rotate,
peel back the cortex, and separate the putamen with its globus pallidus
out to the side. This is the globus pallidus. You see how it’s tucked into
the inside of the putamen. And then we have a new
structure up front here. This is part of what’s
called the ventral striatum or nucleus accumbens. And this is an important
area associated with reward seeking behavior,
pleasure, and addiction. Now, let’s go to
the gross specimens. In this hemisphere, I can show
you the caudate, very poorly, because it’s inside and next
to the ventricle as we saw. If this is the corpus callosum. This is the lateral ventricle. This bulge that I’m
running my probe over inside the ventricle
represents the head the caudate. Now, let’s look at
a coronal section. This is the first of four
coronal sections we’re going to look at briefly just
to see the structures. Here we have the caudate
nucleus, which is bulging, into the lateral ventricles
separated from each other by the septum pellucidum
and the corpus callosum is above and below. So, that’s pretty
straightforward. Now, we’re going to look
at these structures, and I’m going to turn this over. And as we look at
them, we are going to just sort of recognize them. And then later we are going to talk a little bit
about the circuitry. So, on the other side of this,
what we see now is the head of the caudate is just this
part here, it’s getting smaller. And another structure is
coming in over on the side. This is that putamen. So, together, the putamen
and the caudate make up the corpus striatum. Why is it striatum? It’s striped. It’s striated by these white
fibers of the internal capsule. The anterior part of
the internal capsule that separates the
caudate and the putamen. So, now let’s look
at the next section. Going caudally now, we’ve added
our temporal lobes down here. And this area down here around
the junction of the putamen and the caudate is the area
called the ventral striatum. This is where that nucleus
accumbens is that is so important in reward and
pleasure seeking behaviors. And it’s not very clear here, but that’s the region
where it’s located. So, on the other side of this
same section, we can see now that our caudate nucleus
continues to get smaller. And the internal capsule
is getting larger. And off to the side
we have our putamen. And now do you see
this paler area sort of triangular in shape? That is paler than the putamen. That is the globus
pallidus, paler, pallidum. All right. And then coming across here, we
can see the anterior commissure. And this part of
the pallidum that is down beneath the
anterior commissure is the ventral pallidum. It works together
with the limbic system and that nucleus accumbens. And down here, we see the optic
chiasm and temporal lobes. So, this section has a
nice large temporal lobe. We’re moving caudally. The ventricular system,
the lateral ventricle, is out here to the side. And here, always in relationship
to it, is the caudate nucleus. Do you see how small
it’s getting? This is a part of the body, and
it’s going to get even smaller such that we can hardly see it. Now, between the
internal capsule here and the third ventricle
in the midline, we have the large thalamus. The thalamus plays a large
part in the circuitry that we’re going to be
discussing later on. So, our players are
thalamus, caudate, putamen, and here is our globus
pallidus down here. Here is the mammillary body. It’s just a landmark
for us at this moment. And the last section
we’re going to look at is back a little
farther through the thalamus and the internal capsule. And our basal ganglia,
mostly putamen out here, is getting harder to see. And there’s just a
little bit of the caudate, but you may not be
able to recognize it. And what I want you
to see is this sort of greyish-black smudge here. This is the substantia
nigra that is going to play an important
part in our discussion. And you can see that it’s
actually moving down. It’s going to be
also seen together with the cerebral peduncle. And I can imagine and see,
but I don’t know if you can, there is a little nucleus
out here, just sort of above and a little bit lateral to the substantia nigra called
the subthalamic nucleus. And that’s also going to
be part of our discussion. Now, let’s look at
the substantia nigra for a moment before we
go to the circuitry. So, now we are looking at the ventral surface
of the brain stem. This is the medulla. This is the midbrain. The cerebellar hemisphere
is out here. And I am going to turn this so that you can see the
rostral part of the brain stem, which is the midbrain. You recognize the aqueduct,
the cerebral peduncles. And here we have the
black substantia nigra. So, this part that is
filled with dopamine cells, which can degenerate and cause
basal ganglia disease is an important component of
today’s instruction. Let’s quickly just look
at these same structures in an axial section. So, now we have an axial
section where I’m going to point out some of these
same structures. Up top here we have
the frontal pole and back here the
occipital pole of the brain. And we have the ventricular
system. This is back in the
occipital horn. Here is the frontal horn. And here are our caudate nuclei
separated from the putamen out here by the internal
capsule. So, caudate, internal
capsule, putamen, then this pale area is
the globus pallidus. And on this side, the
pallidus can be seen divided into two parts. At least I can see it. There’s an external part
and an internal part to the globus pallidus. And then this is the
internal capsule. And the thalamus is starting
to blend into the midbrain. Let’s look at one more section
a little bit lower, or ventral. This section is a
bit asymmetric. But it shows us what
we want to see. Here again is the frontal
lobe, the occipital lobe, part of the ventricular system. And right here in the
middle is our midbrain. You can see how it sits right in
there with the mammillary bodies and the hypothalamus and the
optic tract right around it. And, again, now you can
see the substantia nigra. This black substance right
between the cerebral peduncles and the rest of the midbrain. There is an area that you can’t
really see very well right about in between the
substantia nigra and the level of the midbrain called the
ventral tegmental tract. It, like the substantia nigra, is filled with dopamine
containing cells, but these in the ventral
tegmental area project up to that ventral area of the
striatum, the nucleus accumbens. Now, let’s look at the circuitry
using a computer diagram. So, now we’re about to
tackle the hard part of this. And we’re going to do it in
the simplest form I know how with some excellent diagrams
from my college, Stephen Voron. So, let’s look at the structures
that we’ve already identified on the gross sections. Striatum, which would be
your caudate and putamen. The globus pallidus,
which is the pallidum. The thalamus, which I showed
you on the large model. The cerebral cortex, which
we’re already acquainted with. And the midbrain with
the substantia nigra and the ventral tegmental
area in between. So, we have two circuits. The first circuit is the
cortex-to-cortex circuit. So, remember, this
is a consulting loop. So, the cortex is
consulting the basal ganglia in order to improve movement. So, cortex to striatum,
to globus pallidus, to thalamus, to cortex. Right? And then the
corticospinal tract comes down and remember our motor pathway. All the way down. Crosses at the top
of the spinal cord and becomes the corticospinal
tract in the spinal cord. And that is the way all
movements are basically executed on a voluntary basis. The second loop involves
the substantia nigra, the pars compacta
as it’s called. We’ll just call it the nigra. And it also involves the
ventral tegmental area, but let’s just talk
about the nigra. And it projects, with
dopamine, a dopamine pathway, called the nigrostriatal
pathway using dopamine. All right? And that is the other pathway. It is these nigral cells
that tend to degenerate in Parkinson’s disease. Now, let’s add another level of
complexity to this same diagram. Here are three main points
I want you to remember when we talk about
the basal ganglia. The first is this
cortex-to-cortex circuit. And I’m going to
show you in a minute, there are actually
two parallel circuits. This substantia nigra dopamine
circuit, and I want you to remember now that
the signs and symptoms of basal ganglia disease
are on the opposite side because they influence
the corticospinal tract. So, basal ganglia signs are
expressed on the opposite side of the body due to the
pyramidal or corticospinal tract that they influence
as it descends. Now, let’s make this circuitry over here a little
bit more complicated. So, now the story gets a little
more complicated when we look at the trajectory of these
dopamine-containing cells in the substantia nigra that
project to the striatum. In this case, the putamen, which is quite involved
with motor activity. We have a light and
a dark pathway. And they represent excitation
and inhibition, in this case. And that is to say, that
dopamine, the transmitter, has two opposite
effects on these D1 and D2 cells in the striatum. In one case the transmitter is
excitatory to certain neurons. And in another case it’s
inhibitory to other neurons. In addition, we also have
acetylcholine in some of the neurons in the striatum. And they also have different
effects and opposing effects on these cells in the striatum. So, this leads to the idea that
we have two pathways, a direct and an indirect pathway
to the globus pallidus. This is the globus pallidus. The internal part of it. And here we have in this
indirect pathway another station, or another synapse,
not only with the outer part of the globus pallidus but
with that subthalamus and then onto the globus pallidus,
internal part. So, we have a direct
and an indirect pathway. And then from the
globus pallidus, most of these neurons going to the thalamus inhibit
the thalamus. That is to say the thalamus is
normally inhibiting the cortex keeping extraneous
movements from occurring. And only if you have the
right combination of direct and indirect stimulation
do you get the decrease in the inhibition, which allows
the increase in the excitation and for the action to be
carried out by the cortex. Now, don’t sit there and fret about is this inhibitory
or excitatory. They are just two things
that you need to remember. That the indirect pathway is
usually inhibitory to movement and the direct pathway
facilitates movement. All right? The indirect inhibits. And the direct facilitates
movements. And these both act through
the thalamus to the cortex. So, that’s not so difficult. Now, let’s look at
certain diseases. You might expect, and
this is what we see, that if you interrupt a
pathway that is inhibitory, the patient ends up with too
much movement or hyperkinesia. And if you interrupt a
pathway that is facilitatory or excitatory, you might end up with not enough
movement or hypokinesias. So, we have a whole variety
of movement disorders that have combinations
or primarily too much or too little movement. And so now what I’d
like to do is to move on to the videos I have
giving you some examples of hypo- and hyperkinesia. Along with this, changes
in muscle tone occur. Basal ganglia disease is
associated with rigidity. This is something you
cannot show in a movie, but you certainly can feel it
when manipulating the patient. Now, let’s look at some examples
of Parkinson’s disease beginning with a pathological picture
of what the midbrain looks like in patients with severe and
late stage Parkinson’s disease. This pathological picture
compares a normal midbrain with the midbrain of a patient with a severe end-stage
Parkinson’s disease. The most striking feature is the
melanin black pigment is absent in the midbrain of the patient. And melanin is a precursor to
the production of dopamine. I can also point out to you,
this ventral tegmental area between the two cerebral
peduncles and recall this is a dopamine
projection, not to the striatum that we’ve looked at before,
but to the ventral striatum and the nucleus accumbens,
which is just loaded with dopamine receptors, is
involved with eating, sex, drugs, nicotine, and is a very
important pathway associated with emotion and the limbic
system as well as reward, in a behavioral sense. So, this is a very
important pathway, but difficult to show you. Much literature deals
with this pathway as part of the limbic system. This Parkinson’s disease
patient has a resting in his right arm greater
than his left arm. And when he is asked to raise
his arms above his head, notice that the tremor in his
right arm decreases remarkably. This is basically the
opposite of cerebellar disease. And notice now on the
finger-to-nose test, his accuracy is quite good. He’s a big slow because he’s
a little bit rigid and stiff, but he does fine and
doesn’t have a tremor. This is a different patient
with Parkinson’s disease. You’ll notice that the
resting tremor in his arm, he’s not asked to use his arms. He’s using his legs. This resting tremor
is a typical four to eight cycle frequency
per second tremor. And notice his legs. When he turns he takes
two or three steps. He doesn’t just swivel
180 degrees on one foot. Look at his face. And you notice his face, he
has very little expression. He doesn’t blink very often. And that goes along with
the paucity of movements that these patients have. And he’s quite rigid
but we can’t assess that in this short clip, because
we cannot manipulate his arms or legs. This woman is asked, to
as quickly as possible, but her finger and thumb
together repeatedly. And you’ll notice that she’s a
little slower on her right side but much slower and lower
amplitude on her left side, which is more affected with
rigidity and decreased ability to execute rapid movements. They are not as high in
amplitude or as quick as they should be
in a normal person. Previous examples
of bradykinesia or too slow movement
or decreased movement, were associated together
with the tremor with Parkinson’s disease. But now I want to
show you examples of hyperkinesia,
too much movement. This gentleman at rest has
writhing fingers and sort of a sinusoidal movement
called athetosis. He is asked not to move his
hand, but he cannot prevent it. This is mild in this
gentleman, and it can be due to a whole number of things. One of them is anoxia. Another cause can be due
to let’s say a stroke in the thalamus or
even high bilirubin as jaundice in a neonatal. It’s also a precursor to Huntington’s disease
in many cases. And I’m going to show you
next a more advanced stage of Huntington’s disease. Athetosis is the more distal
part of the extremities. Here is an example of
Huntington’s disease and choreiform movements. Big, broad, jerky movements
of all parts of the body. And unfortunately, this
is also accompanied with major subcortical dementia. This is a postmortem specimen
from a patient who died of Huntington’s disease. This disease involves
degeneration of the neurons in the caudate nucleus, which
is a mere remnant in this image. And in turn, the
ventricles have enlarged. Recall that before
the caudate bulged, very large into the lateral
ventricle, it’s totally gone. In addition, the
putamen is smaller and accompanying these
wild movement disorders, is a dementia, a
very severe dementia that is called subcortical
dementia and it’s part of this very severe
autosomal dominant disease which does not manifest
itself in most patients until they have reached
their childbearing years or even slightly beyond that. So, early diagnosis is important
together with counseling. Another movement disorder of the
hyperkinesic type is myoclonus. This young gentleman
has had an infection. So this is the result
of an infection. Post-infectious myoclonus. Now, he is trying to do
the finger-to-nose test. And as he concentrates on that, his body makes these wild
jerks that interrupt it. So, it’s not that he’s
got a cerebellar problem; he could complete it if his body
didn’t jerk on him all the time. If it doesn’t jerk, then
he’s able to complete it. These myoclonic twitches or
jerks can be due not only to an infection but they
can come with head injuries, strokes, brain tumors, kidney
or liver failure and chemical or drug poisoning among
many, many disorders. So, myoclonic jerks like
you just see here is typical of a variety of etiologies. And one of the more common
etiologies is severe hypoxia. So, you may see something
called post-hypoxic myoclonus. Phew, that was a lot, wasn’t it? Pretty difficult. And I know you can’t
remember it all right away. If you can only keep
a few things in mind, think of the patient symptoms
and signs that you looked at. And remember that those signs
and symptoms from the left half of the basal ganglia are
going to be expressed on the right side of the body because the corticospinal
tract comes down and crosses to the other side and
influences the spinal cord. Also remember that if the
corticospinal tract is damaged, then you won’t be able to see
these basal ganglia subtleties of movement because the
corticospinal tract damage will overwhelm, if it’s
severe, the expression of these basal ganglia diseases. And also remember that
the basal ganglia work with the cerebellum. Both of them are consultants
to this corticospinal tract. And you need to only try to sort out if your diseases
are cerebellar in signs and symptoms, basal
ganglia in signs and symptoms, or corticospinal. If you only have those three
sorts of bins to put the signs and symptoms in,
you’ll be a long way to achieving neurological
localization, which is our goal.

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