Polyneuropathy: Introduction

by Carlo Raj, MD

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    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.

    About the Lecture

    The lecture Polyneuropathy: Introduction by Carlo Raj, MD is from the course Polyneuropathy. It contains the following chapters:

    • Polyneuropathy
    • Acute Inflammatory Demyelinating Polyneuropathy (Guillain-Barré)
    • Chronic Inflammatory Demyelinating Polyneuropathy
    • Multifocal Motor Neuropathies

    Included Quiz Questions

    1. Infectious peripheral polyneuropathy
    2. Acute inflammatory demyelinating polyneuropathy
    3. Multifocal motor neuropathy
    4. Chronic inflammatory demyelinating polyneuropathy
    5. Paraneoplastic and monoclonal gammopathy–associated peripheral neuropathy
    1. Elevated protein in the CSF and demyelinating features on nerve conduction studies
    2. Elevated leucocytes in the CSF and demyelinating features on nerve conduction studies
    3. Decreased protein in the CSF and demyelinating features on nerve conduction studies
    4. Elevated lymphocytes in the CSF and demyelinating features on nerve conduction studies
    5. Elevated protein in the CSF and normal findings on nerve conduction studies
    1. Response to both steroids and IVIG
    2. Response to IVIG only
    3. Elevated protein in the CSF
    4. Demyelinating features on nerve conduction studies
    5. Raised protein with an absence of WBCs
    1. Areflexia and relapsing course
    2. Ascending paralysis and acute course
    3. Descending paralysis and relapsing course
    4. Steroids ineffective
    5. Involves hip flexors
    1. Anti-GM1 antibodies
    2. Anti-Ro antibodies
    3. Anti-dsDNA antibodies
    4. Anti-La antibodies
    5. Anti-GM2 antibodies
    1. Weakness proportionate to atrophy
    2. Asymmetric weakness in individual nerve distributions
    3. Sparing of the sensory nerves
    4. More prominent in the arms
    5. Positive for anti-GM1 antibodies.

    Author of lecture Polyneuropathy: Introduction

     Carlo Raj, MD

    Carlo Raj, MD

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    Bad Lesson Arrangement and Leccturing
    By stassia s. on 21. December 2023 for Polyneuropathy: Introduction

    Where is pathophysio, the arrangements of these lessons are bad .i cant even understand and Osmosis is better

    Concise and straight to the point! :)
    By Danica L. on 01. December 2018 for Polyneuropathy: Introduction

    I really enjoyed watching this lecture versus having to listen to hours of lecture on these topics.