How are we gonna diagnose it… how are you going to diagnose it?
CSF, mildly elevated protein. Gamma globulin is increased and most importantly oligoclonal bands. What do oligo mean?
Little. So here I want you to think of your clonal bands or the bands in general and as your interpreting a band,
you have these little bands called oligoclonal bands and those are quite indicative
of multiple sclerosis if found by investigating the cerebrospinal fluid.
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 abnormalities 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.
These are things that you wanna put everything together,
obviously, they're not just gonna give you one fact and expect you to know what's going on.
I'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 as such?
If it’s acute relapse you're thinking about high dose IV corticosteroids
and then you have disease modifying agents and these include your beta interferons.
Beta interferons, beta interferons. I'll repeat that multiple times here
because you don’t want to confuse this with alpha interferons or gamma interferons – it’s your beta.
Let me add something you call glatiramer acetate and you have monoclinic antibodies
That's something that you want to keep in mind.
In the parenthesis here are the trade names or more importantly you wanna know about the generic names obviously.
In refractive cases, you do not really left with much of an option except to start using chemotherapy to drugs
in other words immunosupressants and that of course has its own whole host and adverse effects.
At this point, really to agree to focus on acute relapses and disease modifying agents
such as your monoclonal antibodies and the beta interferons.
It also have as I said, the glatiramer type of acetate.
To summarize your multiple sclerosis, risk factors – Caucasian, female population.
The genetic predisposition I told you about family history, may increase 15 fold risks.
Preventive 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 opthalmoplegia, the conjugate gaze type of issue.
And then also medial longitudinal fasciculus.
In addition to that there might be ataxia, numbness. Remember, CNS type of issues.
Differential diagnoses include infections maybe vasculitis
and I showed you an imaging study where I showed you these plaques around your ventricles -- ventricles.
And what those plaques represent please, again, white matter degeneration.
And we've talked about the treatment. What kind of interferon? Beta interferon and glatiramer acetate.
And if it’s an acute type of relapse, then you're thinking about high dose of IV corticosteroids.
So once we've done, you've noticed now over and over again your pathology that it have these topics
and these pages in which I've summarized the pinpoint information
or details that you wanna take out of each one of these diseases, these are important.
Now the variants, just very quickly, I don’t want to spend so much time here.
Rarely, if ever asked, but just to make sure that you're clear, you can have neuromyelitis.
It’s called or Devic’s disease. It’s the bilateral optic neuritis, very rare but variants nonetheless –
just to make sure that we're clear.
Rapid progressive in the acute this we call, Marburg form in which this is in young individual,
maybe even lesser or younger than twenty.
Fulminant course during the period of several months – what does that mean?
Remember, it usually takes years and decades and decades and decades for this to usual most common clinical course,
my goodness, this is rapidly acting – months.
Large and numerous plaques, wide spread destruction of myelin,
it’s the variants that are extremely difficult in terms of to arrive at a diagnosis quickly
but nonetheless they exist for multiple sclerosis.