So with myasthenia gravis,
signs and symptoms include
weakness of the extraocular
type 2 muscle fibers—fast switch,
eventually at 3 or 4 o’clock, what
happens? The proximal muscles
will then be affected. No doubt.
Ptosis often the first symptom.
Diplopia and improvement in strength with,
there you go, anticholinesterase agents
because by given anticholinesterase
agents such as
pyridostigmine, neostigmine, what have you,
you have increased in concentration
of acetylcholine in the cleft
in the hopes of opening up
those sodium channels.
If you do a short-acting such as edrophonium
then you might find increase in strength,
not only be positive for myasthenia gravis.
The diagnosis here is an edrophonium test,
strength because the concentration
of acetylcholine and
the longevity of acetylcholine
has been increased
and ______ bind to the receptors opening
up the sodium channels
and single-fiber EMG, electromyography,
and here you find abnormal
in 95% of patients with
myasthenia gravis as you can expect.
Management. Pyridostigmine, a longer acting
immunosuppressants because it is
an autoimmune disease,
maybe azathioprine or cyclosporine;
plasmaphereisis with short-term treatment
removes then the antibodies;
and if you’re given a chest x-ray
in which in a 40-year-old lady,
you find a thymic remnant, that
fact that in a 40 year old
that you even find a thymic remnant,
you should be thinking autoimmune disease,
and if you’re looking at the symptoms that
I’ve given you, then it’s myasthenia gravis.
What’s the one that I gave you where if
there’s a thymic remnant, for example,
and there is susceptibility to infection?
It’s called Good Syndrome.
Some of these are part of
your immune lectures.
Management. Well avoid certain medications,
beta blockers, aminoglycosides, quinolones,
and class 1 antiarrhythmics because it’s
already blocking those sodium channels.
You don’t want to make it worse.
There is a little bit of
overlap here, right,
between some of these cardiac and skeletal
muscle. You just, you never know.
These are ones that you want
to be very, very careful of.
Here we have Lambert-Eaton
Now what you want to do as you
go through this is compare
myasthenia gravis with Lambert-Eaton.
In myasthenia gravis, what was my problem?
Fundamentally, it was
They are being destroyed,
one by one by one.
Here, that is not the issue.
Yes, it’s an autoimmune disease;
however, this time it’s going after
the voltage-gated calcium channel.
Remind me where those voltage-gated
calcium channels are located.
In the presynaptic terminal. Good.
In the presynaptic terminal of the
a little bit more detail for you.
You must know that those voltage-gated
calcium channels are of the P and Q type,
and there they are.
What are they? The P and Q—yes,
he presynaptic voltage-gated
of the neuromuscular junction
is being attacked.
So ultimately between
physiology and pathology,
there are 4 different kinds of calcium
channels that you probably have heard of.
They include the L and T type, and
of course, the majority of your
calcium channels in the heart,
would be of the L type,
and then you have the P and Q in pathology.
Why do you need that calcium to
come in presynaptically again?
So that it can facilitate the fusion
of the synaptic vesicle containing what?
Acetylcholine with the membrane.
If those voltage-gated calcium channels
are not permitted
to bring the calcium in,
then how in the world
are you supposed to have
fusion and release?
Completely different from what we
can expect in myasthenia gravis
where the receptors were being
Here, in Lambert-Eaton,
those post-synaptic acetylcholine
receptors are untouched.
Untouched. Keep that in mind.
Where can Lambert-Eaton come from _______?
For example, small cell lung cancer.
Of all the lung cancers that
the one that has the most number of
or the ones that have the most
our manifestations will
be small cell. __________.
The proximal muscle weakness, again,
just like myasthenia gravis,
but this time it’s a little bit different.
What do I mean?
“Doc, I wake up in the morning,
I’m feeling pretty tired,
and then about 11 or 12 o’clock,
I feel a little bit better,
1 or 2 o’clock I feel better. Why?”
Well with use, I’m feeling better.
That would never happen
in myasthenia gravis
with use of feeling better in
The body, trust me, the body
will find a way
with increased use of releasing
into the cleft.
Once its release into the cleft, is it
going to bond to the receptor? Absolutely!
There’s no pathology there and
you will then have
an action potential and muscle contraction.
How? You may ask, is it being released?
The body is resilient, it will find a way
and the more use there is,
the better the patient feels.
Opposite in terms of
It could be autonomic dysfunction,
and how to differentiate between
Lambert-Eaton and myasthenia gravis.
As I just explained in Lambert-Eaton,
you will show improvement
with repeated use.
That will not happen with
And remind me, so in myasthenia gravis,
if you’re able to increase a concentration
of acetylcholine in the cleft,
then you would perhaps find improvement
in muscle movement
in myasthenia gravis.
Here in Lambert-Eaton,
I don’t care how much
cholinesterase inhibition that you’re
giving your patient,
the problem is not with the receptor.
So you will find no improvement with
cholinesterase inhibitor in Lambert-Eaton.
Is that understood? Those points must be
crystal clear before we move on. Please.