Vestibular System: Neuroanatomy Video Lab – Brain Dissections

>>Today’s discussion will be
about the vestibular system, which is involved with our
balance and our ability to keep things in focus
while our head is moving. The vestibular system is
part of the inner ear. The external auditory canal and the middle ear are
involved with the cochlea. And this is for the
perception of sound, which will be a different
discussion. But up here you can see we have
the semicircular canals embedded in the bone. So we have a bony labyrinth, and
we have a membranous labyrinth. Let’s look at the vestibular
part in more detail. Here we have that
part of the labyrinth. It really does look like a
labyrinth, like a maze here, composed of the three
semicircular canals. And then there is a
larger vestibular area which has two areas involved
in sensing gravity as well as linear acceleration. And this is the utricle
and the saccule adjacent to this area called
the vestibule. Now these membranous canals
have sense organs inside them. And the semicircular canals
are particularly involved with sensing angular
acceleration. And these canals are oriented
in three different planes; so all three dimensions of
your movement are registered. And when we test the
vestibular system, we are almost always
testing the horizontal canal. It’s easiest to test, especially if you bend the head
forward about 30 degrees. So this will be our focus today. And let’s look at
another diagram. Here we have the
membranous labyrinth in blue. This is filled with endolymph,
and at the base of each of these semicircular canals we
have a region called the ampulla where the sensory hair cells
that are going to be responding to angular acceleration
are located. And in the saccule and
utricle in the vestibular area, or vestibule, we have
the sensory hair cells that are going to respond to
linear acceleration and gravity. We will look at those
hair cells in more detail. But first let’s look
at the skull and look at the orientation and location
of the labyrinth with respect to not only the cochlea, but to
the vessels and other structures on the internal surface
of the skull. I have here a skull, and we’re
looking at the inside of it. And it has been specially
prepared to show you the vestibular and
cochlear areas of the bone. The petrous part, this part
here, and the petrous ridge, are part of the temporal bone. And if I tilt this, you can see
the internal auditory meatus through which the
seventh, facial, and vestibuloacoustic
nerve pass. And the structures
we are interested in are deep in this bone. And this area has been
dissected from the outside, and we can look at that. Here we have the
mastoid process. You can see the air cells, and
deep in the bone you can see one of the semicircular canals. And right beneath
here is the foramen through which the
facial nerve passes after it leaves the
temporal bone. Now let’s look at
this from the inside and look at our landmarks. We have the vessels,
which are most obvious. The middle meningeal
artery comes up and splays out over the inside
of the skull. It’s really running in the dura. And it is right under
this squamous part of the temporal bone, which
is often damaged or lacerated in trauma cases, and is
the source epidural bleeds. We also have the
blue venous drainage. We can see the sinus coming
along here and then going down and entering into the jugular
foramen and returning the blood from the brain to the heart. The petrous ridge here has
been partially dissected. The yellow here represents
the facial nerve. Here is one of the
semicircular canals. And up here is the cochlea, the
little tiny structure involved with the perception of sound. So now let’s look
at the temporal bone in an isolated section. And you can see how
complicated it is. There’s the mastoid process,
the zygomatic process. This is facing anteriorly, so this is from the
left side of the skull. This is the squamous part, the
more delicate part of the bone that can be easily
lacerated in trauma. And as I turn it around, you
can see the relationship again of the internal auditory meatus where the vestibular
nerve is running. And you can see the
vestibular apparatus, one of the semicircular canals. Now let’s look at the
membranous labyrinth in detail from a large model. This giant model of the right
ear and the petrous part of the temporal bone,
which I can remove here, will expose for you
both the cochlea and the semicircular canals. So let’s just lift out and
separate the semicircular canals and the vestibule from
the rest and look at it in a little bit of detail. So now I’m holding the
labyrinth, and you can see that the white part
represents the bony labyrinth which is filled with perilymph. That would be the pink fluid
so to speak in this model. And I can lift out the
inner membranous labyrinth that is filled with endolymph. And that is the fluid that
swishes around in these canals. I only have one to
demonstrate to you. Or moves around in the utricle
and saccule and stimulates, by its movement, the hair cells. The semicircular canals have
an ampulla with hair cells. And the saccule and utricle
also have hair cells. And we’ve already mentioned
their specific functions. And you can see the nerves
coming from each part and forming part of
the vestibular nerve. Now let’s look at these hair
cells that are the transducers of the movement of the
endolymph that become the signal to the brain of position
and movement. I might mention that this
labyrinth can become infected. We call that labyrinthitis. And labyrinthitis is an
inflammation, which usually due to viral or bacterial
infections. And the patient has nausea,
disorientation, vertigo and dizziness when you interrupt
the mechanism for transduction. Here we have the hair
cells in the macula. And each one of them is
innervated by an axon of the vestibular nerve. And each of these hair cells
has one tall cilia called a kinocilium, and then
many smaller, shorter cilia, called
stereocilia. And it’s very cleverly designed so that whichever
way the cilia bend, if they bend toward
the kinocilium, the nerves (axons) are excited. If they bend away
from the kinocilium, then the nerve (axon)
is inhibited. And with this mechanism we have
a mirror image in each ear. So only one side is stimulated. If that’s so, then the other
side is always inhibited. Now on top of these hair
cells is the membrane. We usually just call it
the otolith with crystals of calcium carbonate that are
sort of embedded in the jelly. And they’re about twice
as heavy as the fluid, the endolymph that
surrounds them. So with the movement of
the body, the kinocilium and the stereocilia are deformed and produce either
excitation or inhibition. This mechanism is different
than what we see in the ampulla at the base of the
semicircular canals. Let’s look at that. At the base of each of the
three semicircular canals is an ampulla. And at the base is also a crest
here, which we call the crista with hair cells along it, each again innervated
by a vestibular axon. These hair cells have
the same arrangement with a tall kinocilium,
shown here, and the other stereocilia
are not shown. These stereocilia and
kinocilia are embedded in a gelatinous cupula. And when the fluid, pretend
that you imagine fluid in this space moving,
they deflect the cupula, and if it’s in the
direction of the kinocilium, then the nerve discharges, and if it’s in the opposite
direction, it inhibits. And since each of these on either side is a
direct mirror image, if you stimulate the right side, then you are inhibiting
the left side. And let’s talk just about
the horizontal canal. So this is the anatomy
of the cupula, and this fluid is always sort of lagging behind the
movement of the body. Now we need to bring this
nerve here into the brain, and so let’s look at where the
vestibular nerve enters the brain at the junction of
the medulla and the pons. Here I have the ventral surface
of the brain stem and cerebellum that have come out of the
posterior fossa of the skull. You can see the medulla
and the pons. And out here in the
cerebellopontine angle, you can see two nerves. The more medial facial,
or seventh nerve, and the more lateral eighth
or vestibulocochlear nerve. That nerve actually has two
parts you can sometimes see a groove in it. And we’re going to be
talking about the connections of the vestibular system
with nuclei in the brainstem and tracts that go down
into the cervical region. So the important part of
the vestibular system is in the brainstem,
not in the cortex. And this angle here, called
the cerebellopontine angle, sometimes tumors develop and
develop right in this space. There’s just room
enough for them to grow. And these tumors are often on the vestibular
or cochlear nerve. They often involve
the seventh nerve. And they come from
Schwann cells mostly or sometimes from the meninges. Now let’s look at
a cross-section. So this is a section through
the medulla with the cerebellum on either side, and you can
very nicely see the vestibular and cochlear nerve
coming in right over the inferior
cerebellar peduncle. And there are some
connections actually that go to the cerebellum from
the vestibular nerve. But most of them end up in some
nuclei right here called the vestibular nuclei. There are four of them,
and they extend all the way from the medulla
through the pons. And they have very
important connections for controlling eye movements. And we’re going to look at
some diagrams indicating that in a moment. So what I’m going to do now
is, looking at the superior or dorsal surface
of the cerebellum, I’m going to split
the cerebellum open, and now we’re going to
look down onto the floor of the fourth ventricle. So now I have split the
center of the cerebellum, and you can see the
vermis on either side. And this is the beginning
of the midbrain. And so now we’re looking
down on to the floor of the fourth ventricle. And our vestibular
nuclei are going to be located right near
the midline on either side. Let me remove the
cerebellum now. So, now we have a bit of
cerebellum, but we can look down very nicely on the floor of
the fourth ventricle and imagine where these nuclei are. There are four of them. We don’t need to
know their names. But they have connections with
tracts that ascend and descend. Because after all we have
to coordinate neck movements and eye movements with
our position in space. Very important, the
vestibular nuclei. So, in this mid-sagittal
section, we see the whole half of the right hemisphere, and
the brain stem begins here at the aqueduct and the superior
colliculus and extends down, even a little farther than you
can see here, in the medulla. So the only part of
vestibular system we’re going to talk about, although
there are connections with the thalamus and the
cortex, for diagnostic purposes, it’s the brain stem
that’s important. And we’re going to be looking
at that in more detail. And I’m going to show
you a tract that runs in this dimension here. This image shows the
vestibular nuclei, the four vestibular nuclei, in
a computer-generated graphic. So let me orient you. Down here we have our
classic cross-section through the medulla. And up here our section
through the pons. All the way up to the
rostral part of the pons. And so the vestibular
nuclei extend all the way through the pons
and the medulla. This is important, and they
give off branches to a tract that runs in the
midline on either side. This tract is called the
medial longitudinal fasciculus. The medial longitudinal
fasciculus, or MLF as we call it, is what
connects the cranial nerves with the vestibular system. Let’s look at that now. Here we have another
computer graphic, and this time showing the
medial longitudinal fasciculus, that tract to which
the vestibular nuclei contribute axons. And this green tract
runs all the way from the superior
colliculus at the level of the oculomotor nucleus, all the way down to
the high cervical level for coordinating neck muscles
and the position of the head with respect to the object
that you want to focus on. Disease of this MLF is
very pronounced and results in a variety of changes
that we’re going to discuss momentarily. So the MLF is a highly
myelinated pathway that extends all the way
through the brainstem. That means it’s also a
useful pathway to test for the integrity
or the viability or the functioning
of the brain stem. So now let’s suppose
that we have a lesion of the left vestibular nerve. What would happen, or what
would the patient report or what would you see? So let’s imagine
that this nerve, and we’re just now talking about
the horizontal portion basically of the semicircular canal. Because that’s the one
that’s easiest to understand. We would have a disparity
in the information coming to the vestibular
nuclei on the left side when compared to the right side. And so since movement on this
left side is normally balanced by inhibition of the other side,
that input is no longer there. And so the right side thinks
that it’s always moving. And so if you have your right
side moving to the right, so the brain thinks your
body and your head is moving to the right, you want to
keep the object in focus, so you slowly move
your eyes to the left. You can test that on yourself. You have something in focus, you
turn your head, and your eyes go in the opposite direction
of the head. And that is a slow phase. But pretty soon you end, your
eyes can’t go any farther to the side, and so
then you flick them back from this position
out to the side, and you have a fast flick back. And that is called a
saccade, a fast movement. And so we have a condition
where we have jiggly eyes, so to speak, in which there is
a slow phase and a fast phase. And we call this
movement of the eyes when you’re not moving,
nystagmus. And nystagmus can either be
pathological or physiological. In this case we’ve given you
an example of pathological. Nystagmus is a complicated
thing to understand. It can be in any direction. It can be up, down, roundabout,
and it can be congenital, or it can be acquired. The most common cause of
nystagmus, acquired nystagmus, are drugs, medications such
as Dilantin or Phenytoin used for controlling epileptic
seizures. And excessive alcohol
can cause this, or certain sedating medicines. So nystagmus is not normal. If the person has it, then you
need to search for the cause. So the cause could
be in the nerve. Or the cause could be toxic. And we want now to go
on and discuss the role of the vestibular system and what we call the
vestibulocular reflex. So this is a reflex that
happens when you turn your head in this diagram to the left. So we know now that
if the head goes left, the eyes should turn
to the right. But what is the connectivity
for this? We’ve already mentioned the
medial longitudinal fasciculus that runs all the way from the
medulla up to the midbrain. But we have to coordinate
cranial nerves six, the abducens, and three in the
midbrain oculomotor nucleus, and they are on opposite sides. So this is a complicated
diagram, but many of the other diagrams
you’ll see are in error. So pay attention to this one. We’re going to stimulate
now the semicircular canal, the horizontal one,
on the left side. So this is the left
vestibular nerve coming into those vestibular nuclei. And what is not very logical
is that the next neuron here in the vestibular nucleus
crosses into the MLF of the opposite side and travels up to the right abducens
nucleus. And in the right abducens
nucleus there are two types of neurons. The logical one, which you need
to turn your eyes to the right, are the motor neurons that come
out through the abducens nerve, to the lateral rectus muscle. But these other neurons,
interneurons here, go up to the third nucleus. But it has to be the third
nucleus on the other side. So these neurons cross and
travel up through the MLF on the opposite side, on
the left side, to terminate in the oculomotor nucleus. And there, motor neurons from
the oculomotor nucleus travel out on the left side
to the medial rectus. So that you have coordination,
and you can track to the right when your head is
turning to the left. Now this reflex is important
because look, it is testing from the end of the pons where
the vestibular nerve comes in, the junction there between
the medulla and the pons, all the way up to the
superior colliculus. And that’s a couple of inches. And so this is a great test for
the integrity of the brain stem, for the pons and the midbrain. And it’s useful and very
important clinically. So damage to this MLF, medial
longitudinal fasciculus, will usually result in nystagmus because you have an unequal
stimulation on either side. And we are going to look at something called an
internuclear ophthalmoplegia. This can be from a
disruption of the MLF. It could be on either side. And it could be anywhere
from the pons to the superior colliculus. And with it comes nystagmus. It’s different from the
vestibular lesion nystagmus. But it is a place where
you see nystagmus, and it’s often associated either
with a small brainstem stroke or quite often with
demyelination of this tract in multiple sclerosis. Here we have a diagram
of the pupil of a person who is looking straight
ahead at you. This is normal. And they are fixed on you. And you command them first to
look to the right down here. And both eyes move to the right. So here you’re using the
lateral rectus on one side and the medial rectus
on the other side. And there is no problem. You then ask them to
quickly look to the left, and what happens is the left eye
goes over, so there’s no problem with the left abducens. And the right does not go over. The right actually
will move a bit, but it doesn’t go
all the way over. And if you ask the patient to
look at your fingers to see if they can focus on something, you’ll see that both
eyes can converge. So it’s not a problem with
the medial rectus muscle. And that puts the
problem in the MLF that connects the
nuclei three and six. Three doesn’t move
all the way over. This is more or less paralyzed. And this eye moves
all the way over. And then it starts to oscillate. It starts to jiggle. You have nystagmus. And this is abnormal. It’s as if all the electricity
went out the abducens nerve because no stimulation is
going to the oculomotor nerve. That’s not necessarily true, but it’s a good way
of thinking about it. And this condition is called
internuclear ophthalmoplegia. Internuclear between
nuclei of six that goes to the lateral rectus,
and the nuclei of three that go to the medial rectus. And so what we have here is
a unilateral internuclear ophthalmoplegia, a paralysis
between the two nuclei three and six, producing paralysis. And in this case we have, since
it’s the right medial rectus that isn’t working, we call
this a lesion of the right MLF. Now let’s look at a patient
that has this condition.>>This patient had subacute
bacterial endocarditis with a bacterial abscess
in the brain stem. Ductions and gaze are fairly
full looking to the right, but look at this, when
looking to the left, his right eye does
not AD-duct well, and you can see these
jerk AB-ducting nystagmus of the left eye. So he has a right internuclear
ophthalmoplegia (INO). Again, the components are
medial duction abnormalities of the ipsilateral eye
and AB-ducting nystagmus of the contralateral eye. Now these are really
brought out with saccades. This is a nice technique
to bring out an INO. Ask the patient to
saccade quickly to the right as he’s done here. Normal to the left. Now look at the lag of the medial duction
of that right eye. Here, see how it just sort
of slowly drifts across. That’s a nice way to
bring out a subtle INO. I think it shows
up fairly nicely. Look at the left eye. You can see the AB-ducting
nystagmus in the left eye and medial duction of the right
eye just slowly drifts across. You can also do this with
an optokinetic drum or strip by moving the target
opposite the direction of the suspected gaze. Now here’s another
example, fairly normal when looking to the left. Now look at that left eye
medial duct slowly compared to the right eye. And again I think you can
see the prominent AB-ducting nystagmus of the right eye. This patient has
multiple sclerosis. I’m going to use myself as an
example of how you could test on a conscious person whose
cerebral cortex is working, and demonstrate the
vestibulocular reflex. And I’m going to spin around
on this stool, and it’s going to stimulate the endolymph
in my horizontal canal. And when I stop, my eyes are
going to flick back and forth. And I’m going to have nystagmus. So let’s look at that now. So now I’m going to spin around. And I’m turning to the right. So normally my eyes would
want to track to the left. And now I’m going to
look at the camera, and you should see
my eyes jiggling. That’s nystagmus. That’s physiological nystagmus. That’s normal. So now finally I want to talk
about caloric stimulation of the semicircular canals. That is irrigating the
external canal with either warm, around 44 or a little
higher degree centigrade, or cold about, 30 degrees
centigrade, and what happens when you cause with this heat or
cold, the endolymph in the canal to set up convection currents and artificially stimulate
the hair cells in the cupula, and in this case,
the horizontal canal. So the body is not moving, but
the brain thinks you are moving because you’re a
conscious person. Your cerebral cortex is working. And so the irrigation then
causes my eyes to move. And there is a mnemonic
for remembering which way the nystagmus
is beating, as we say. The fast component
is the beating phase. So we have a mnemonic for caloric testing
in an awake patient. And we say that it is COWS,
Cold Opposite, Warm Same. That refers to the
direction of the fast phase, the saccadic part
of the nystagmus. Cold opposite, meaning your
eyes beat to the opposite side. Warm irrigation, the eyes
beat to the same side. Now when we have a
comatose patient, the cerebral cortex
is not working. So when we irrigate the canal
and they’re lying on their back and their eyes are up and
looking straight ahead. You can irrigate but you
will, and again you will set up the movement of
the endolymph. But since there is no focusing,
the component of nystagmus for the fast phase, you will
only have the slow phase. And so with a comatose patient,
IF the brainstem is working, you will only have
the slow phase, and the eyes will
drift to the side. So you will only
have the slow phase when the canal is irrigated. And if you have put
in cold water, the eyes will drift
to the same side. If you put in warm water, the comatose patient’s eyes
will drift to the opposite side. And you can then move their
head to looking straight ahead. Let the eyes equilibrate and
test on the opposite side. If you get the slow movement
of the eyes, that is GOOD. That is good news. It means that the MLF
and the brainstem, at least for eye movements,
are working over the distance from the midbrain down to
the beginning of the medulla. So that’s a very good sign. If the eyes do not move,
that is a very BAD prognosis and indicates that the
brain stem is damaged. So this concludes
our discussion, our all too long discussion,
about the vestibular system. But it’s complicated. And clinically it’s
useful for testing. We’ve introduced the terms MLF,
medial longitudinal fasciculus, which coordinates
the eye movements from the midbrain all
the way down to the pons. And we’ve introduced the
role of the vestibular nerve in the vestibulocular reflex. And we’ve also talked
about nystagmus, a condition where the eyes are
moving when they shouldn’t be. So hopefully you’ll be able
to look at your patient and figure out what’s going on. Is it in their brainstem? In their vestibular nerve? Or have they been drinking?


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