00:01
Let me put this into a
perspective for you.
00:04
Polyneuropathy:
many nerves that are
being affected.
00:09
It all comes down to the organization
of peripheral neuropathy.
00:12
And if you go back to a
particular schematic
that I showed you of the spinal cord.
00:19
And from the spinal cord, you
had your anterior horns,
and you had the motor,
and as you pass
through your motor,
you made your way out into
your peripheral neuropathies,
and it’s basically where we are.
00:32
And then with peripheral neuropathy,
we talked about mononeuropathy,
went through individual
nerve injuries,
went through mononeuropathy
multiplex or mononeuritis multiplex
where you have one nerve in multiple
locations that are being injured.
00:48
The biggest section of it
all will be polyneuropathy.
00:52
Let’s begin.
00:53
Differential diagnoses of peripheral
polyneuropathy include the following:
immune mediated,
metabolic issues,
hereditary,
toxic,
infectious.
01:03
We’ll be spending a lot of time
with a lot of these differentials.
01:08
If it’s immune mediated,
I’m going to slow down here, make
sure that you’re very, very clear
how to identify Guillain-Barre,
you’ve heard before.
01:17
Guillain-Barre is an acute type of
inflammatory demyelinating polyneuropathy.
01:24
Hopefully, you know that.
01:25
If you haven’t,
please understand that Guillain-Barre
is an acute inflammatory,
considered to be inflammatory
demyelinating type of polyneuropathy.
01:36
Once we have discussed our AIDP,
we will then go into CIDP.
01:42
Instead of acute, it will be chronic
inflammatory demyelinating polyneuropathy.
01:48
We’ll walk through multifocal
motor neuropathies,
paraneoplastic and associated
with monoclonal gammopathies,
vasculitic type of neuropathy, and
associated with other autoimmune diseases.
02:02
Let’s take a look at Guillain-Barre,
a.k.a, acute inflammatory
demyelinating polyneuropathy.
02:11
You must understand that you
may have many infections
that predispose this patient,
such as gastroenteritis,
maybe even influence of virus.
02:21
And then thereafter,
the pattern of demyelination
will be an ascending paralysis.
02:28
Now, not as benign
as one would think,
because if it ascends enough, what are
you going to hit at some point in time?
Your breathing apparatus, in
other words, the diaphragm.
02:39
And if that’s been knocked out, your
patient is in serious compromise.
02:42
Has absent reflex, even
before, full weakness,
and often have low
back pain early.
02:50
It can result in respiratory
failure because as I said,
as you ascend at some point in time, you
are at risk of injuring your diaphragm.
02:59
Monitor your FVC closely.
03:01
What does that mean to you?
You've heard of pulmonary
function test,
so therefore, you want to make sure,
if you’re suspecting Guillain-Barre,
to make sure that the respiratory system is
not being compromised with the diaphragm.
03:15
Intubate if less than 15
milliliters per kilogram.
03:20
That’s important.
03:22
Let’s diagnose Guillain-Barre.
03:24
On CSF, it shows elevated protein.
03:26
That of course is non-specific.
03:29
The demyelinating features,
what does that mean
to you when you do a
nerve conduction test?
As a next step, you should perform a nerve
conduction test. It will show mainly decreased
conduction velocity and increased latency,
for example in a demyelinating issue. And raised
protein with absence of WBCs. Just keep in
mind your clinical history becomes the most
important component of Guillain-Barre. Was there
a prior infection? Was an ascending type
of paralysis and is your patient in a state
of respiratory compromise? Acute inflammatory.
04:05
IVIG or plasmapheresis would be management
and steroids are not at all useful in acute
inflammatory demyelinating polyneuropathy.
Chronic inflammatory demyelinating
polyneuropathy. The opposite of Guillain-Barre
syndrome. Or chronic meaning to say slowly
progressing weakness often involves the
neck flexors. Chronic relapsing course. Areflexia,
common. May have lost of vibration sense as well.
Diagnosis: Once again, elevated protein in
CSF, it is going to be nonspecific. Demyelinating,
your nerve conduction test will be abnormal.
04:45
And raised protein with absence of WBCs.
Management here, steroids are effective whereas
in acute inflammatory it's not. IVIG also useful.
What's IVIG? Intravenous immunoglobulin.
05:01
Management require for many years. Chronic inflammatory.
It will take a look at multifocal
motor neuropathy. What are clinical features here?
Slowly evolving, asymmetric weakness
in individual nerve distribution. Multifocal motor neuropathy.
Usually more prominent in the
arms, weakness out of proportion to atrophy.
This then tells you that this is more of a nerve
issue. Is that clear? The weakness is out
of proportion to atrophy. Sparing of the sensory
nerves. Strictly motor neuropathy.
Diagnosis: Motor nerve conduction block on nerve
conduction study. So you're looking for motor.
Positive anti-GM1 antibody in approximately
60-80% of your patients. Guess what?
You're memorizing this GM1 antibodies. Management:
IVIG and perhaps immunosuppressive therapy is required.