How are we going to diagnose it?
How are you going
to diagnose it?
CSF, mildly elevated protein,
gamma globulin is increased,
and most importantly,
What does oligo mean?
So here, I want you to think of your
clonal bands or the bands, in general.
And as you’re interpreting a band,
you have these little bands
called oligoclonal bands,
and those are quite indicative
of multiple sclerosis if found
by investigating your
Visual evoked potentials.
Remember, you do have vision issues.
Useful in demonstrating evidence of prior
optic neuritis, but keep in mind though,
frequently, the visual
evoked potentials are found
and there’s no history of the visual loss.
Just keep that in mind as well.
So you could have such
abnormalities taking place
but there is no history
of optic neuritis.
So these are things that you
want to put everything together.
Obviously, they’re not just
going to give you one fact
and expect you to
know what’s going on.
They’ll give you multiple clues and
then you have to make sure that
you use your clinical judgment
to come to the proper diagnosis.
What about treatment and such?
If it’s acute relapse, you’re thinking
about high dose IV corticosteroids.
And then you have disease
These include your
I repeat that multiple times
here because you don’t want to
confuse this with alpha
interferons or gamma interferons.
These are beta.
Then you have something
called glatiramer acetate,
and you have one of the monoclonal
is something that you
want to keep in mind.
In the parenthesis here
are the trade names,
but more importantly, you want to know
about the generic names, obviously.
In refractory cases,
you’re not really left with much
of an option except to start using
chemotherapeutic drugs, in other
and that of course has its
own host at adverse effects.
At this point, I'd really like for
you to focus on acute relapses
and the disease modifying agents
such as your monoclonal antibodies
and the beta interferons.
And we also have, as I said, the
glatiramer type of acetate.
To summarize the multiple sclerosis:
Risk factors: Caucasian,
the genetic predisposition I told you about
family history that increase 15-fold risks.
Preventative medicine; really,
we don’t know of any,
really difficult, unless there’s
a family history already.
Signs and symptoms: We’ve
talked about this quite a bit.
We talked about the blurred
vision, the optic neuritis.
We talked about internuclear ophthalmoplegia,
the conjugate gaze type of issue,
and then also medial
In addition to that, there might be ataxia,
numbness, remember, CNS types of issues.
Differential diagnoses includes
infections, maybe vasculitides.
And I showed you an imaging study where
I showed you these plaques
around your ventricles.
What do those plaques
White matter degeneration.
And we talked about the treatment.
What kind of interferon?
Beta interferon and
And if it’s an acute
type of relapse,
then you’re thinking about
high dose IV corticosteroids.
So, once we’ve done --
You’ve noticed now over and
over again in neuropathology
that I have these topics in these
pages in which I’ve summarized
the pinpoint information or details
that you want to take out of
each one of these diseases
These are important.
Now, the variants,
just very quickly.
I don’t want to spend
too much time here.
Rarely, if ever asked, but just
to make sure that you’re clear,
you can have neuromyelitis
or Devic’s disease.
It’s a bilateral optic neuritis,
very rare but variant nonetheless,
just to make sure
that we’re clear.
Then you have acute, this
is called Marburg form
in which this is in young individuals,
maybe even lesser or younger than 20.
Fulminate course during the
period of several months.
What does that mean?
it usually takes years and decades
and decades and decades for this to
use your most common clinical course, my
goodness, this is rapidly acting, months.
Large and numerous plaques,
widespread destruction of myelin.
It’s the variants that
are extremely difficult
in terms of deriving
a diagnosis quickly,
but nonetheless, they exist
for multiple sclerosis.