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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? It is going to come back to be abnormal, non-specific.

    03:36 You would find that with Lou Gehrig as well.

    03:39 And raised protein with absence of WBCs.

    03:42 Just keep in mind, your clinical history becomes the most important component of Guillain-Barre.

    03:48 Was there a prior infection? Was there an ascending type of paralysis? And, and, is your patient in a state of respiratory compromise? Acute inflammatory.

    03:59 IVIG or plasmapheresis would be management, and steroids are not at all useful in acute inflammatory demyelinating polyneuropathy.

    04:09 Chronic inflammatory demyelinating polyneuropathy, the opposite of Guillain-Barre syndrome.

    04:14 Chronic, meaning to say slowly progressing weakness, often involves neck flexors.

    04:21 Chronic, relapsing course, areflexia common, may have loss of vibration sense as well.

    04:29 Diagnosis.

    04:31 Once again, elevated protein CSF.

    04:33 It is going to be non-specific.

    04:35 Demyelinating, your nerve conduction test will be abnormal.

    04:39 And raised protein with absence of WBCs.

    04:43 Management here, steroids are effective, whereas, in acute inflammatory, it’s not.

    04:50 IVIG also useful.

    04:51 What’s IVIG? Intravenous immunoglobulin.

    04:55 Management required for many years, chronic inflammatory.

    05:00 Here, we’ll take a look at multifocal motor neuropathy.

    05:03 What are clinical features here? Slowly evolving, asymmetric weakness in individual nerve distribution, multifocal motor neuropathy.

    05:14 Usually more prominent in the arms, weakness out of proportion to atrophy.

    05:21 This then tells you that this is more of a nerve issue, is that clear? The weakness is out of proportion to atrophy.

    05:29 Sparing of the sensory nerves, strictly motor neuropathy.

    05:36 Diagnosis: motor nerve conduction block on nerve conduction study.

    05:41 So, you’re looking for motor.

    05:42 Positive anti-GM1 antibody in approximately 60% to 80% of your patients.

    05:48 Guess what? You’re memorizing this, GM1 antibodies.

    05:56 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-Barre)
    • Chronic Inflammatory Demyelinating Polyneuropathy
    • Multifocal Motor Neuropathies

    Included Quiz Questions

    1. Neuropathy with leukodystrophy
    2. Acute inflammatory Demyelinating Polyneuropathy
    3. Multifocal neuropathy
    4. Chronic inflammatory Demyelinating Polyneuropathy
    5. Paraneoplastic and associated with monoclonal gammopathy
    1. Increased protein without leucocytes.
    2. Increased leucocytes with increased protein.
    3. Decreased glucose with increased proteins.
    4. Increased opening pressure and increased proteins
    5. Increased neutrophils and decreased glucose
    1. Response to steroids
    2. Amount of proteins in the CSF
    3. Amount of leucocytes in the CSF
    4. Nerve conduction studies
    5. Immune-mediated polyneuropathy
    1. Loss of vibration sense and complete absence of reflexes.
    2. Ascending paralysis occurs in the patient.
    3. Rapidly progressing to develop respiratory paralysis.
    4. There is no response to steroids.
    5. Patient presents with low back pain early in the course of the disease.
    1. Anti-GM1 antibodies
    2. Anti-Ro antibodies
    3. Anti-SSA antibodies
    4. Anti-jo1 antibodies
    5. Anti-GM2 antibodies
    1. Loss of vibration sense and complete absence of reflexes
    2. Asymmetric weakness in individual nerve distributions
    3. Sensory nerves are spared
    4. Weakness is out of proportion to atrophy
    5. Positive for Anti-GM1 antibodies

    Author of lecture Polyneuropathy: Introduction

     Carlo Raj, MD

    Carlo Raj, MD


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