So what I'm going to do over the next 42
minutes is to talk a little bit about
common pathology of the temporal bone
and we'll first talk a little bit about
technique.  Now I assume everybody's got
a multi-detector CT you know at our
institution we've got 64 slice--anywhere
from 4 to 64 is fine.  Our CT we do
perform axial 0.65 millimeter thick
sections.  We obtain our acquisitions in
the axial plane and then what we do is
reconstruct--now we reformat in the
coronal plane and we also look at the
Stenvers and the Poschl view so all
of our studies are now reconstructed in
those coronal and parasagittal views and
this is the first--I still remember this,
I still get cringed when I see this, but
this is the first CT I ever read at UNC
when I was a junior faculty and it was
literally my first day and I was
recruited by the ENT surgeons and they
said what do you think about this CT
and there are a lot of things wrong with
this that I just didn't have the
tenacity to fix yet because I was used
to very very thin sections and so on and
so forth but when I looked at this you
know it's a large field of view it's
bone windows not bone algorithms and the
slice thickness was 2 millimeters and I
said well there's a little soft tissue
right here I don't think there's any
cholesteatoma so on and so forth and the
head of ENT who recruited me there put
his arm around me and said you know that
was a huge cholesteatoma, it extended up
into the middle cranial fossa and oh by
the way don't worry you can't see
ossicles on CT anyway so that kind of
pissed me off.  So then what I did--then
what I did is I went to the
technologists and redid our protocols
and this really is the type of imaging
that you can get on your multi-detector
imaging and this year we didn't do the
normal temporal bone anatomy, I'll probably
redo an extra step every one through
it, but just to give a couple of
highlights, here's the cochlea apical in
the middle turn, here's the modiolus,
cochlear canal, here's the canal for the
superior vestibular nerve,
there's the vestibule anterior and
posterior crus of the stapes, here's a
lenticular process of the incus, the
manubrium, and the malleus.  Now that's a
fair amount of detail, but you can see
all this stuff if you do your technique
just right.  In fact this is the tensor
tympani and with a leap of faith there
is the
little cochlea form process, but the
point is is that all of this anatomy you
can see if you do your technique just
right so before I would suggest you even
contemplate really delving into your
temporal bone about the pathology.  A lot of
the stuff that I'll be showing you is going
to be only visible if you do the right
technique so especially you residents
or fellows the first thing to do is
learn your anatomy and make sure if
you're a staff member somewhere optimize
your technique.  I can't emphasize it as
much.  So now all of our studies are
reconstructed in the Poschl and the Stenvers view and this really harkens back
to the day of conventional tomography so
you know radiologists we don't get older
we get more experienced.  Are there any
experienced radiologists in here besides
myself?  Right so you remember the days of
conventional tomography and in
conventional tomography the planes that
we used to use were the Poschl and
Stenvers view and you know what's new
is old and what's old is new right?  And
then all of a sudden with the
understanding that you can't have
dehiscence of the superior semicircular
canal and you are best seeing these in
planes that are parallel and orthogonal
to the superior semicircular canal all
of a sudden the Poschl and Stenvers
viewer were rediscovered so and you know
in our practice it's one of the common
reasons we do get temporal bone CTs is
to look for superior semicircular canal
and again with the reconstructions we
now perform it's quite easy to do.
You know I won't spend too much time on
IAC MRI, I think everyone at your
institution is doing and is doing it
quite well.  Just to reiterate, just cover
the full course of the eighth nerve make
sure your slice thickness is not greater
than three millimeters, always perform
pre contrast T1 we do post contrast the
axilla coronal plane and don't forget
there are other causes you know for me a
head neck radiologist I can get tunnel
vision, I just start looking at the IAC and
looking for vestibular schwannoma but
there are the things that can cause
hearing loss, surprisingly enough, and
this can occur in the accessory organ
called the brain because for me every
organ is an accessory organ to the neck
you know like the chest and the brain are
accessory organs to the neck.
So there are some incidental lesions
that involve accessory organs that can
cause hearing loss, things like strokes
or multiple sclerosis too, so just remember
to take a look at the brain real quickly
and make sure you don't--things have MS
causing hearing loss.  We now routinely
perform the heavily weighted T2 weighted
imaging through the internal auditory
canal and when you do this you can
really see the anatomy very very nicely
so we all remember there are four nerves in
the internal auditory canal, the anterior
superior one--remember 7up, Coke down,
right?  I don't know if you still learn that as
residents or not but the seventh nerve
is anterior and superior so here's the
facial nerve, this is the labyrinthine
segment, there's the anterior genu--
geniculate ganglion and the heavily weighted
T2-weighted images there is the facial
nerve here and on this coronal image
this is posterior this is anterior so
it's a sagittal view there's our facial
nerve.  At the same level of the facial
nerve is one of the vestibular nerves
and that's the superior vestibular nerve
so here it is on the axial plane and
then here it is on the parasagittal
plane.  Beneath the seventh nerve i.e. Coke
down is the cochlear nerve so here's our
cochlear nerve heading through the
cochlear canal extending into the
modiolus and we look on the heavily T2-
weighted images there's our cochlear nerve
which is located inferiorly and then the
inferior vestibular nerve is posterior
inferiorly as is seen here on the sagittal
images and seen here on the axial
images as well.  Now this little
thickening of the ganglion right here
that's actually Scarpa's ganglion so
we're getting to the point now where we're not--
we can see Scarpa's ganglion.  Now for
vestibular schwannomas I think we now do
the heavily T2-weighted images routinely
and we can see vestibular schwannomas
you just look for replacement of the
normal CSF.  This is a pair of sagittal
view here in this case all of the CSF is
replaced by vestibular schwannoma and
this is more the size of a rock.
However these very very small vestibular
schwannomas I would argue you can
probably see better with these very very
thin section T2-weighted images because
on a bad day it's possible you can miss
that, but I would argue on
T2-weighted images you'll be able to see
these two millimeter schwannomas easier
on these images as opposed to the
contrast enhanced studies.  Yeah you know
what, you guys probably figure out like
I dig head and neck radiology, like I love it.
I want all of you to become a head and neck
radiologist.  Nothing would make me
happier and forget about all the other
accessory organs of the body.  So the way
that we learned the template bone in the
cochlea in medical school is through
histology textbooks.  So we would learn
the apical turn, the middle turn, and the
basilar turn.  We'd learn about the inner
scalar septum that essentially
provided if you will this bosselated
appearance to the cochlea.  The channel of
the cochlea is separated by the basilar
membrane into a scala vestibuli and a scala
tympani and eventually you have the
organ of Corti.  Well this is the way on
the right we learned in medical school
through these histologic specimens where
we see the basilar membrane but now when
you do your T2-weighted images on the
and the 3T system we can start seeing a
lot of this anatomy that we could only
see on histology.  So in fact here's our
apical turn, here's our middle turn,
here's our basilar turn, we can see the
inner scalar septum here and lo and
behold there is the basilar membrane
right here separating the scala
vestibuli and the scala tympani.  We
haven't gotten down yet to the organ of
Corti, but we're getting pretty close.  Now
having said that, we're actually now to
the point where we can see the macula of
the utricle, so when we talk about
imbalance problems the way we balance
ourselves is through the various
otoliths etc and these are located in the
saccule and the utricle and now when we
do our heavily weighted T2-weighted
images work just right you can actually
see this little area of increased signal
within the vestibule and you can see
this in three planes and years ago we
actually described the normal morphology
and these are just you know one
millimeter, two millimeter thicknesses
involving the macula and the utricle and
we're able to see that on our
T2-weighted images.  Okay so that's our
technique and we talked a little bit
about the anatomy, now let's go through
some common pathology that you'll be
seeing and I'll take the remainder of
the time to again really try to focus on
the applied anatomy since we didn't have
a dedicated anatomy lecture this year.  So
otosclerosis is actually a unique
disease of the otic capsule and no one's
really quite sure what causes it.  They
say there is some genetic predisposition,
primarily autosomal dominant, a little
bit more common in females and males and
its bilateral up to 60%.  Now otosclerosis
is felt to be due to abnormal resorption
deposition of bone in the middle ear
cavity.  Otosclerosis is still a
clinical diagnosis, now having said that
I think radiologically we see little
deposits of otosclerosis now than before
in fact if you go back and read Shutnik's book he described otosclerosis and
ten percent of the quote unquote
asymptomatic population.  Having said that,
some otologist just won't get CTs before
performing surgery so I'm gonna break
from the script right?  So this one guy I
played basketball with every Sunday
morning, he's an otologist he works at
Michigan Ear, right?  So one of the other
guys that would play basketball has known
otosclerosis, so my buddy the otologist
decides to perform a stapedectomy on the
other guy and I'm like, you know, why
don't you get a CT scan to look to see
if it's fenestral or retrofenestral, he said
yeah that's not gonna change what I do
anyway and the guy is young I mean if he
was my age, he was an old fart I'd say
all right you can't you know teach an
old dog new tricks but you know the guys
like in his late 30s and he's been
operating for you know a few years but he just
won't change what he does so he still
believes that otosclerosis is primary--primarily a clinical diagnosis based on
classic audiological findings.  So what do
we say radiologically?  Well on the right
here is a illustration from Shutnik's
book, the classic book and this is what
we see on CT.  So this axial image was
taken through the level of the oval
window anterior and posterior and what
we see at the most anterior aspect of
the oval window is a region here called
a fistula ante fenestram and the
fistula ante fenestram is supposed to be
the first area of the deposition or the
creation of otosclerosis.  So on this
histologic specimen and it--obviously in
a different patient here is the oval
window and this is the
fistula ante fenestram so the first place
that you look for is a little bit of
rarefaction right here in the fistula ante fenestram, the most anterior
portion of the oval window.  Now because
this deposition occurs in the window
this is what's referred to as finestral
otosclerosis so when I'm looking at a
temporal bone potentially for
otosclerosis that's where my eye goes to
so that's the approach.  So if you have
fenestral then you could have retrofenestral
and what's retrofenestral?
Retrofenestral is essentially this
resorption of bone along the pericochlea, these are what we refer
to as the pericochlear lucencies so
because it's below the oval window or
deep to the oval window this is why it's
called retrofenestral otosclerosis.  Now
back here when I went over this there was
something called the Schwartze sign and this
was a class clinical finding
associated with otosclerosis, the
Schwartze sign is probably due to when
you have retrofenestral otosclerosis
leading to increase vascularity
involving the the cochlea itself.  Now you
can perform MR for this and I have to
admit my sensitivity for picking up
otosclerosis on MR is lacking from what
has been reported in the literature.  I
know years ago there were many people in
Europe that felt that MR was a good way
of identifying retrofinestral otosclerosis.  I haven't found it to be, now
having said that I always do check for
cochlear enhancement in patients that
come with unexplained hearing loss but
if you do perform MR what you look for
is increased enhancement involving the
cochlea following administration of
gadolinium but again it sort of
correlates to--radiologically with the
Schwartze sign.  So what has been described
most recently is the third window.  So
sometimes the classic teaching for
otosclerosis is that you look at the
fistula ante fenestram and maybe with a
leap of faith we can see a little bit of
rarefaction of bone then we have the
pericochlear lucencies but we are
starting to see more and more areas of
rarefaction along the petrous bone, the
petrous apex and this is what has been
referred to as if you will the third
window and you know we started seeing
this and lo and behold
I went back and I have Shutnik's book you
know that was 60 years old and when he
did his--when he did his histologic
specimens he did describe rarefaction of
bone and the petrous apex along the
internal auditory canal so if you see
something like this along the IAC and
you think well maybe it's a little
fibrous dysplasia or something
unusual, that's actually otosclerotic
deposits that have been--that have
been described and if you wait long
enough or theoretically you wait long
enough it can eventually cavitate and
sometimes this is a term that's been
given to cavitary otosclerosis so this is
sometimes what's referred to as a third
window for otosclerosis.  Well let's move
on now and talk a little bit about
labyrinthitis.  So what exactly is
labyrinthitis.  Labyrinthitis is pure and
simply an information of the membranous
labyrinth then there's an acute phase
and there is a chronic phase.  So the acute
phase of labyrinthitis has been
classified by the bug and the bugs can
be bacterial, viral, syphilitic, fungal,
toxic, or autoimmune or it can be
characterized by the route of spread and
that route of spread can be from the
middle ear tympanogenic, from the brain,
Meningogenic, blood-borne, or
post-traumatic so again depending on
what you read there are different ways
to classify labyrinthitis.
So what is that different types of
labyrinthitis?  Well acute labyrinthitis
pure and simply as is seen here on your
right from Shutnik's book is just pus in
the cochlea.  It's just an acute
inflammation in the cochlea and again a
lot of what we see in the head and neck can
be seen elsewhere in the body.  It's the
same pathologically, it's the same
disease process.  It's just that when
it occurs in the head and neck we
start to get palpations and nervous
because it's the head and neck right?  I don't know
if you all feel that way but I feel that
way sometimes but if you just remember
the basic principles and apply it to the
head and neck then things kind of make sense.
So what would you see if you had an
inflammation anywhere else in the body?
You would end up seeing abnormal
enhancement right?  Anywhere else in the body
and that's what you see in acute
labyrinthitis.  So the pathophysiology is
that you have pus and acute inflammation
in the cochlea and so what we would see
on MR is abnormal enhancement of the
cochlea on the involved side compared to
the opposite side.  Also we can make some
type of guess--I don't think guess is the
right word, but we can make an assumption
here that--look at this--the cause of the
cochlea here, the cause of this is due to
tympanogenic cause of labyrinthitis
you see all this abnormal enhancement
in the middle ear cavity so the cause of
this acute labyrinthitis is probably due
to direct spread from the middle ear so
this would be tympanogenic
labyrinthitis.  Yeah what's obliterative
labyrinthitis?  Or sometimes referred to
as labyrinthitis ossificans?  So the
way that I think about it and again a lot of
what I do is trying to conceptualize
things because if I can conceptualize it,
it makes it easier to understand, so if
you continue to cut yourself and you--and
your cut never heals you eventually
develop a scar right?  So what happens in
labyrinthitis ossificans or obliterative
labyrinthitis is that if you have
acute labyrinthitis and it persists for
a long time or it's never properly
treated your body has to react in a
certain way.  And the way that it reacts
in your inner ear is that you have the
deposition of fiber osseous material and
eventually sclerosis so you can see on
this histologic section about how these
normal channels within the cochlea
become replaced by this fiber osseous
matrix and this can be fiber osseous
tissue or it can eventually go on for
frank sclerosis.  So what we see here
radiologically is here's the internal
auditory canal, here's the cochlear canal
and I think I can convince you with a
leap of faith there's something in here
replacing the cochlea.  So this is what's
referred to as obliterate--obliterated--
obliteration of the labyrinth or
labyrinthitis ossificans with deposition
of ossific material.  Similarly if you
look at the vestibule, the vestibule
should be back here, it should have the
same attenuation as the IAC but we can
see that has been replaced too with this
increased attenuation.  So again
labyrinthitis
ossificans.  The most common location
to look for labyrinthitis ossificans is
in the basilar turn of the cochlea.  That's
what's been described for the first
location.  So
your eye should first go to the basilar turn
but eventually if it's untreated it can
go ahead and involve the apical in the
middle turns and this is just another
example of very severe labyrinthitis
ossificans on the right hand side,
complete replacement of the cochlea and
the vestibule.  On the CT scan you can't
even see the cochlea and a little bit of
the vestibule and on the heavily
T2-weighted images here's the internal
auditory canal.  Remember the inner ear of
the labyrinth contains fluid, right?  And
you should have fluid here but there's
no fluid at all because it's been
replaced with the ossific and fiber
osseous material.  The next thing that we
want to talk about is--if you will take a
similar clinical approach and say well
what happens if someone comes in or what
do we look for if someone has a red
retrotympanic mass or a little red mass
behind the tympanic membrane so the
otologist may see this and they think of
different things that it could be and
our job as a radiologist is to be
familiar with what may occur.  So the
first thing that we'll look at is a
glomus tympanicum so this thing could be
caused by a glomus tympanicum tumor
so what's the glomus tympanicum?  So
doctor Saab and I both talked about
glomus tumors and essentially a glomus
tumor that arises in the middle ear
cavity is a glomus tympanicum tumor if
it's isolated to the middle ear so here
we have this well-defined soft tissue
mass that's located on this prominence
of the cochlea hence the term cochlear
promontory.  On the axial images again we
see a soft tissue mass.  Now this could be
cholesteatoma, it very well could be but
we cannot say radiologically and we'll
see why later.  But this and of itself is
a differential diagnosis but if they
say a retrotympanic mass and we see a
focal soft tissue mass along the
cochlear promontory then we have to
consider glomus tympanicum.  Here's
another example of a glomus tympanicum.
Again right along the cochlear
promontory, the glomus tympanicum is
associated with this nerve right here
which forms a l--which runs along the
cochlear
promontory and it's a branch of cranial
nerve nine--does anybody remember the
name of that nerve?  Starts with a "J".
Jacobson's nerve, right.  Doctor Saab earlier mentioned
Arnold's nerve which is a branch of
cranial nerve 10.  Jacobson's is a branch
of cranial nerve nine.  In here we have
this mass right here on the cochlear
promontory.  Pretty typical location for
a glomus tympanicum.  You can perform CT
or MR, here's a CT again demonstrating
glomus tympanicum and on MR glomus tympanicum's typically
densely enhanced with contrast so here's
a coronal imaging demonstrating the
known hyper vascularity of a glomus tympanicum tumor.  So you know why do we
do MR?  Again from a value-added
standpoint, if you say to the surgeon
and they say well you know I can see
that little red retrotympanic mass and
I think it's a glomus tympanicum
you know they very well may be right but
occasionally what'll happen, it'll be the
whole tip of the iceberg phenomena
because if they see a red retro-tympanic
mass occasionally this will be a
glomus tympanicum that also has a
significant component of the tumor
extending into the jugular foramen and
that's what's referred to as a glomus
jugulotympanicum.  So typically with small tympanicums they can just go
in and literally pick off--pick off the
the glomus tumor.  They tried to do that
here, it's not going to be happy because
you can see this thing is growing deeply
and eroding the skull base so that's
another thing we have to look for
obviously.  See that mass but note--make
sure there's no deep extension.  Another
example of a glomus jugulotympanicum,
this is in the middle ear cavity and we
can see all this disease extending deeply.
The one point I want to mention too is
that here's a normal jugular bulb on the
uninvolved side and look at the jugular
bulb on the involved side.  The jugular
bulb was enlarged and we have this
permeative bone appearance.  This on the
other hand as a pure glomus jugulare.
Here's a normal jugular bulb on
the right side and look on the left side.
What are we missing here?  What tells you
there's something else going on?  The
absence of what?
Yeah, see on the left-hand side, see
this nice corticated bone here?  See
how that bone is all eroded and that
permeative appearance?  That tells you that is
not right and again like in the head and
neck you have a pretty good comparator
to the opposite side so if you're not
sure just look to the opposite side and
when we perform the MR here's a pre
contrast and a post contrast enhanced
T1-weighted images.  This is a glomus
jugulare so the glomus tumors that
are just purely limited to the jugular
foramen that arrives in the superior
cervical ganglion, this is a glomus
jugulare and then when we look
internally we see these black dots right
here which are what?  Flow voids exactly
right so that's where the flow voids
come into place.  So we talked about
glomus tympanicums, glomus jugulotympanicums and glomus jugulares.
All of things that--two of those things
can cause a retro-tympanic mass.  Well the
other thing that can cause a retro-tympanic mass is the persistent stapedial artery
and again I didn't really
understand this it took me a while but
here's the deal with the persistent stapedial artery--in fact, Hugh Kurt and I were
talking about this ad nauseam last week.
In order to have a persistent stapedial artery
it has to be attached to the
middle meningeal artery so you can have
aberrant vessels running in the middle
ear cavity but the only way we can say
it's a persistent stapedial if it gives
rise to the middle meningeal artery.  So
normally what happens is that there's
this hyoid artery which eventually has
an upper and lower division.  Over time
this segment that runs through the stapes
becomes resorbed and essentially
this component ends up translocating to
the external carotid artery which
eventually gives rise to the middle
meningeal but what happens in a
persistent stapedial artery is that this
artery--this hyoid artery persists and
then gives rise to the middle meningeal
artery so that's the true definition of
a middle meningeal artery and because
this is running in the middle ear cavity
you could see how this artery could give
you a red retro-tympanic mass so what we
look for on CT are a couple of things:
First of all because--the middle
meningeal normally arises from the
external carotid artery so it has to get
through the skull base and the way that
it gets through the skull base is
through this foramen which is what?
Foramen spinosum.  So on this side there's
absence of foramen spinosum.
The next thing that we have to see is
once we see this artery we can't say for
sure that this is a persistent stapedial artery unless we can see it's attached
to the middle meningeal artery so we
have to follow the artery out or perform
an angiogram or an MRA just to be sure.
So we can say maybe in an aberrant vessel
but it can only be a persistent stapedial artery if it gives rise to the middle
meningeal and one more example here, here
is a persistent stapedial artery and this
little vessel right here, there should be
no artery on the cochlear promontory at
all, it should be nice, smooth, and bony so
again in this particular case another
abnormal vessel--this was attached to the
middle meningeal artery so again a
persistent stapedial artery.  So the first
thing we look for are retro-tympanic
tumors like a glomus tumor then we want
to make sure there's no persistent stapedial artery
and then the third thing
is the aberrant carotid artery and I
think all of you in the room are
familiar with the aberrant carotid
artery.  Again, presenting as a retro-tympanic mass.  So how does the embryology
work you know embryology is fascinating
to me it's quite amazing so
in the normal area we have the internal
carotid artery coming up and piercing the
skull base and we can have a branch
right here that's referred to as the
inferior tympanic artery that eventually
goes through the inferior tympanic
canaliculus.  What happens in an aberrant
carotid artery is that this segment of
the internal carotid artery from here to
here becomes resorbed
or it never forms.  Well eventually the
brain needs blood, it's got to get it
from somewhere.  So what ends up happening
is that this inferior tympanic artery
becomes the route of blood flow to the
brain so this inferior tympanic artery
now anastomoses with this caroticotympanic artery.  So now you have, if you
will, this collateral pathway.  So what
ends up happening is instead of having
this direct communication, we end up
having this aberrant course with this
little acute turn and that mimics the
pathophysiology or the embryology, if you
will, of 
the development of the inferior tympanic
artery and the hyoid artery.  So what we
typically see is this aberrant course,
there's typically bony dehiscence and we
can see the carotid artery extending
into the middle ear cavity.  Again here's
the MRA normal on the left side and
here's this aberrant course on the
involved side.  So the three things we
have to look for when we see the retro-tympanic mass are the glomus tumors
involving the skull base, the persistent stapedial artery and the aberrant carotid
artery.  These can be indistinguishable on
otoscopic exam.  Well the next thing that
we'll talk about is mastoiditis and
with mastoiditis what we have to look
for is--be careful again--and when you're
looking at that accessory organ of the
brain, just be careful if you ever see
this unilateral effusion so you can have
this unilateral effusion and you have to
make sure when you see this that we look
at the nasal pharynx because the
earliest formation of nasopharyngeal
carcinoma is if we see an early
nasopharyngeal carcinoma in the fossa of
rosenmuller.  Very, very subtle T-1
lesion and why does that result in a
unilateral effusion?  The reason is is
that there's a channel that communicates
the back of the pharynx with the middle
ear and that's the eustachian tube and
if this tumor ends up pushing or
invading the torus tubarius since
the opening of the eustachian tube is right
here and right here that can include
that eustachian tube and you develop a
unilateral effusion.  So anytime that you
see unilateral serous otitis or
unilateral fusion you--your eye has to go
to the nasal pharynx to make sure
there's no early nasopharyngeal
carcinoma.  If this is untreated or it
becomes infected this can
eventually go on to erode some of the
fine bony labyrinth of the mastoid ear
cell and this is what's referred to as
coalescent mastoiditis.  Now I'm going to
show a couple of cases of cholesteatoma
later that can have a similar appearance,
so radiologically you can't have overlap,
but remember diagnosis such as mastoiditis
are not radiological diagnosis,
they're clinical diagnosis.  It's pain and
tenderness over the the mastoid tip so
with us we can
be descriptive but we have to be careful
about making this diagnosis without the
relevant clinical history but having
said that what we look for is erosion of
the fine labyrinthian bone of the
mastoid air cells.  If this goes
untreated, this can go on and erode the
inner cortex in the inner table of the
petrous bone resulting potentially
in dural sinus thrombosis so this is a
page that went on to develop dural
sinuses thrombosis from the coalescent
mastoiditis.  If this is untreated, it can
get--erode the outer cortex of the
mastoid bone.  Now this was referred to
currently as Bezold's abscess, now if you
actually go back and, again, you can see
what I do in my free time right?  So
Friedrich Bezold described Bezold's
abscesses--I think it was in 1845 or
something and again long before the days
of CT and MR and what he ended up doing was
describing a complication of mastoiditis but he specifically described this
as an abscess involving the region
just deep to the sternocleidomastoid
muscle.  So if you're a purist what a
Bezold's abscess is is coalescent
mastoiditis that extends inferiorly and
gives rise to an abscess in the neck.  Now,
you know, we've sort of changed the
definitions and I've been to conferences
where essentially any type of phlegmon
or abscess formation that extends
through the outer cortex of the mastoid
bone and involves the soft tissues in
the regions surrounding the ear or the
perimastoid soft tissues is referred to
as a Bezold's abscess so if you go to
conferences sometimes you'll see this,
but if you're a purist just realize that a true
Bezold's abscess involves the deep
neck musculature and if it continues to
go on worse and worse you can have
extension into the temporal lobe and this
is just a frank intracranial abscess.
Well the last thing that we'll end with
is cholesteatoma.  Now, cholesteatoma is
probably the main reason that you
perform CTs in your practice and so I
think it's important to learn a little
bit about
cholesteatoma from a pathophysiological
standpoint so the definition for
cholesteatoma is keratinizing debris
that arises from the desquamation of the
squamous epithelial lining.  I have no
idea what that means--no clue, no clue.
Essentially I remember cholesteatoma as
skin growing in the wr--in the wrong
place, that's the way I remember it.
So cholesteatomas can be congenital
or they can be acquired and we'll first
talk about congenital cholesteatoma.
If we're clenched, congential cholesteatomas are
fundamentally a different process than
acquired cholesteatomas.  So congenital
cholesteatomas are sometimes referred
to as epidermoid and there is no history
of tympanic membrane perforation and
there's no history of middle ear
infection.  Whoops sorry about that, there we go.
So this is an example of a congenital
cholesteatoma so we see this focal soft
tissue mass here in the middle ear
cavity.  Now what does the surgeon see or
the pediatric otologist or the
pediatrician?  They look in the tympanic
membrane and they see the retro-tympanic
white mass--not the red mass but the
white mass, the pearly white mass and the
key thing here is that you see this soft
tissue, it's separate from the cochlear
promontory and clinically it's white.  The
other thing to point out--and this will
become more pertinent in just a couple of
slides--is look at the mastoid boats.  Yeah
it's completely aerated, it looks
beautiful right?
So whatever process is happening here
does not appear to be related or
associated with the mastoid air cells so
this is what we mean: a radiographic
evidence that there's no history of
another acquired ear infection so it's
separate.  So this is a congenital
cholesteatoma.  It's typically felt to be
due very close to the plane of the
ossicles and I've seen books both ways--
some people say it's deep to the plane of the
the ossicles, some people say it's
lateral, but for me it's generally pretty
close to the plane of the ossicles.
Now what's an acquired cholesteatoma?
A fundamentally different disease.  So an
acquired cholesteatoma is--just the
way I think about it conceptually.  So you
know with our skin right?  You know our
skin is a very active organ, it's rapidly
turning over and there's a lot of
desquamation that's coming off so that's
why, you know, you may go--I may get a pedicure,
manicure or whatever -cure I get, you know,
you use a dermabrasion right?  You
know?  So what it is is to try to clean up
your skin because it's rapidly turning
over right?  So we have skin involving our
external auditory canal so it's
hard to think of it, but all that skin
turnover in our--that's turning over in our
ears got to go somewhere, right?  So it
should go somewhere and it's probably coming
out of your ear.  You may not want to
think about that but that's sort of what
happens.  So normally your eustachian tube
should be patent so remember the
eustachian tube communicates with the
back of your pharynx and it communicates
with your middle ear so there should be
good patency with that.  So as a result
the vectors from your middle ear cavity
should be pointing outwards.  So if you
have the desquamation of the skin, the
stuff should be going out, right?  But on
the other hand if you have a chronic ear
infection and you eventually go on to
have obliteration of the eustachian tube,
this is what's referred to as eustachian
tube dysfunction.  So essentially what
happens there is that the vectors
reverse and now it's coming internally
like this.  So instead of all the stuff
going out, this can come internally like
this.  Now once it comes internally it's
going to run into this structure right
here which is what?  The tympanic membrane.
You know how many parts of the tympanic
membrane are there?  It's two parts right?
Is there anybody that remembers the names of them?
There's a par something and a par
something.  Pars flaccida and the pars tensa,
exactly right.
So the pars tensa--it really comprises the majority
of the tympanic membrane but there is this
flaccid part which is located in the
superior portion of the tympanic
membrane and if indeed the vectors are
reversed the sucking sound--this negative
vector starts to have the greater
influence on the flaccid part of the
tympanic membrane and this is what's
referred to as the invagination theory of
acquired cholesteatomas.  So as the
sucking sound comes in, the pars flaccida
starts to become--guess what--retracted,
and this is what's referred to as a
retraction pocket.  Now if the vectors
continue and you form this retraction
pocket it can eventually get
filled in with a bunch of junk--all that
squamous debris, etc.  And what do you
think the space is called right here
that's located in the lateral epitympanic recess, take a while guess.
Prussak's space, but yeah it's not the masticator
space it's a Prussak's space right?  So
that's where Prussak's space is.  So if you
ever wondered why it's felt that
cholesteatoma is a rise in Prussak's space,
that's why, because the vectors are
reversed and the pars flaccida is along
the superior aspect of the tympanic
membrane and this is what gets retracted
into this area here and if it goes
unabated all of the epitympanum can
eventually become filled with
cholesteatoma.  So this is a
pathologically proven case of a
retraction pocket, we can see the soft
tissue mass, here's our scutum, here's the
malleus and we can see the soft tissue
mass right here and on the axial images
that's a retraction pocket.  Could this be
early cholesteatoma?  Sure but we can't be--
we can't say for sure but how can we
make the diagnosis of cholesteatoma?  For
us as radiologists to make the diagnosis
of cholesteatoma, it's an equation.
We have to see a focal soft tissue mass
associated with some type of bone or
ossicular erosion.  So if we see a focal
soft tissue mass and there's no erosion
it could still be a cholesteatoma but we
cannot say that as a radiologist but on
the other hand if we see a focal soft
tissue mass associated with ossicular
erosion then we can make the diagnosis.
So in this particular case here's our
soft tissue mass, here's the manubrium,
the malleus, we should see another dot
right here.  This is what I call a 2 dot
level and what would that dot be here,
anybody?  Your long process of the incus,
exactly right and then on the axial
images this is the level of the
ice-cream cone, so here's the head of the
malleus and what should comprise this
portion of the ice-cream cone?  What
process of the incus, anybody?
Short process of the incus, so notice how
that's absent.  So there's our equation:
soft tissue mass plus ossicular erosion
cholesteatoma.  Another example here,
cholesteatoma but look at it--a large
mass here and notice how there is
erosion of this bone right here.  Anybody
remember the name?  It's name--it's a
septum, starts with a K.  Koerner's septum,
exactly right.  So notice how Koerner's
septum is eroded along with all the
other fine labyrinthian bone.  Now if you
have a really sharp eye you can also see
the cholesteatoma here and look what's
happening to the long process of the incus.
It's becoming demineralized and some
people claim that the earliest sign of
cholesteatoma is demineralization of the
long process of the incus.  I still have
residents and other folks tell me, well
the scutum was intact.  This, for me, the
scutum erosion is a very very late
finding and sometimes I wonder--I just
wonder the reason why the scutum
became associated with cholesteatoma is--
I just wonder if that's the one reliable
finding that you could see on
conventional tomography because when we
look at a conventional tomography we
have to have consistent landmarks.  So the
scutum was pretty easily seen but now
that we have CT we can pick up earlier
bone erosion or ossicular erosion before
the scutum is eroded so for me I
actually rarely see scutum--
scutal erosion.  I see ossicular erosion much
more commonly than I see scutum erosion
so if you have a soft tissue mass, you're
not sure, and you say well the scutum is
intact so it can't be cholesteatoma, I
don't think that's a very reliable way
to exclude cholesteatoma.  What about on
MR?  Cholesteatomas tend to be high
signal or intermediate signal on T1 and
do not enhance with contrast and you
know, we routine--although I'd love to as
a chair of a department, I'd love to get MRs
on every cholesteatoma that came through
but it's really--it's really not
indicated but what can be helpful is
this and I think this is gaining greater
acceptance in the otology literature is
that if you do have a patient that's
undergone multiple ear surgeries and
normally to get a temporal bone CT, and
it can be challenging, there's no doubt
about it, especially if we don't have
history, but if you do have a patient
that has multiple surgeries and we start
seeing this mass here and we're not sure
what it is then I think diffusion
imaging certainly can be helpful so
there's a little bit of increased signal
here and there's a restricted ADC.  If you
go and read the literature, and I agree
with the literature on this, the best
diffusion technique to use is line scan
diffusion
and really only one of the vendors
offers this--I think on their
off-the-shelf product--there are other
vendors that have diffusion but not line
scan.  So at our institution we don't have
the vendor that offers line scan
diffusion but we still perform diffusion
imaging and I think Kevin, would you
agree, we get--it's not a bad way to
look at it may--yeah we can still see if--
it's not as good as a line scan but when
you have these very complex cases with
multiple surgeries we routinely do
perform diffusion and we do find it
helpful in particular cases.  So in
summary what I've tried to do is to go
over the technique, a little bit of
temporal bone, we talked about the
anatomy, and just to review the pathology
we went over--remember otosclerosis
finestral--retro-finestral in the third
window, we talked about acute and chronic
labyrinthitis, right?  These three things
were for the red retro-tympanic mass and
we talked about glomus tympanicum,
glomus jugulotympanicum and glomus jugulare and we talked about
persistent stapedial artery, the aberrant
carotid artery, mastoiditis and it's
complications and we ended with
cholesteatoma.
