EMG Testing axonal vs peripheral & more

    • jk
      June 7, 2016 at 6:06 pm

      An article from the University of Washington titled “An Electrodiagnostic Approach to the Evaluation of Peripheral Neuropathies” by Mark B. Bromberg, MD,PhD includes-

      Axonal Injury
      Loss of axons disconnects fibers from their receptors (sensory nerves) or muscles (motor nerves). Not all fibers may be affected, and the remaining unaffected fibers conduct normally, or all fibers may be affected in severe neuropathies. Generally, axonal loss occurs at the distal ends of fibers, a process called “axonal dying-back.” This results in reductions in both SNAP and CMAP amplitudes.

      and then,

      Damage to myelin affects nerve conduction at multiple sites along nerve fibers and nerve roots, resulting in varying degrees of slowed conduction in affected fibers. Thus, distal latency and F-wave latency are prolonged, and conduction velocity is slowed.

      the article is here: http://depts.washington.edu/neurolog/images/emg-resources/Peripheral_Neuropathies.pdf

      EMG and NCV testing and the interpretation of the testing results is complicated. For example, temperature of your skin is important. Think back- did anybody care what the temperature of your extremities were?

      According to Bromberg, “Correction factors can be applied when limb temperature is low, but the factors are approximate and diagnostic interpretation uncertainties can be avoided by warming limbs to approximately 31C.”

    • GH
      June 12, 2016 at 3:21 pm

      The temperature of the skin might come into play if one were an outpatient, but as I was in hospital it was not a factor. That’s up to the doctor anyway, but interesting.

    • November 2, 2016 at 11:00 am

      I was thinking about this the other day. Everything I read talks about how difficult it is to diagnose CIDP and my doc said my EMG results were textbook; is he right? What if it is axonal damage and not demyelination. What if I am being treated wrong. I only started thinking about this because I am on my third month of IVIG and I have yet to seem any improvement in my symptoms and I am starting to get concerned. I see my doc tomorrow anyway so I hope he can explain some things to me.

    • jk
      November 2, 2016 at 7:31 pm

      You may have already been to see your doctor before you sign in here again. A surprising percentage of CIDP patients do not respond to IVIG. For those who do not respond, there are other treatments available. Ask your doctor about them.

      Textbook EMGs might only be a part of the ‘classic’ diagnosis. For example, according to Dr. Lewis, patients may also have:

      “Pertinent physical findings are limited to the nervous system, except when the condition is associated with other diseases. Such findings may include the following.

      Signs of cranial nerve (CN) involvement (eg, facial muscle paralysis or diplopia)
      Gait abnormalities
      Motor deficits (eg, symmetric weakness of both proximal and distal muscles in upper and lower extremities)
      Diminished or absent deep tendon reflexes
      Sensory deficits (typically in stocking-glove distribution)
      Impaired coordination”

      Your post mentions things you have read. There is a comprehensive and complicated article in Medscape by Dr. Lewis. The link is here:


      There is another article in the Journal of Neurology…. “Clinical diagnosis

      The diagnosis of CIDP relies on a combination of clinical and electrophysiological criteria. A number of criteria have been proposed. The European Federation of Neurological Societies (EFNS)/Peripheral Nerve Society (PNS) guidelines were developed for clinical and research use.7 The criteria combine clinical features and electrophysiological evidence to define CIDP, with supportive criteria including elevated cerebrospinal fluid (CSF) protein, gadolinium enhancement of nerve roots or plexus on MRI or nerve biopsy findings providing supplemental diagnostic evidence. Electrodiagnostic evidence of peripheral nerve demyelination in motor nerves is required for diagnosis, including distal latency prolongation, reduction of motor conduction velocity, prolongation of F-wave latency and partial motor conduction block and must be identified in at least two nerves for a diagnosis of ‘definite’ CIDP”

      Here: http://jnnp.bmj.com/content/early/2015/02/12/jnnp-2014-309697.full

      In other words, the clinical presentation combined with the appropriate lab work is an important part of the diagnosis.

      From a different source: “The most important laboratory studies that support of the diagnosis of CIDP are the cerebrospinal fluid (CSF) examination, NCS, and nerve biopsy. Of these three, the CSF evaluation is the most sensitive as protein is elevated in up to 94 % of cases with normal white cells”

      Nerve biopsy is not considered so important these days. As stated, elevated CSF and abnormal nerve conduction studies narrow down the diagnosis. However, not all patients initially have elevated CSF, some have reported their CSF elevated later on.

      In my case, the CSF has never been elevated.

      Continued, two way conversations with your doctor should lead you in the right direction.