AANEM Connect

During the last 4 months I have seen 4 patients with fibular mono- neuropathies, a very high percentage for my practice. Two had foot drop with a sudden painless onset and an electrically confirmed lesion at the fibular head. Two others had paresthies in a fibular distribution but no definite electrical abnormalities. All 4 had,for the first time, been working at home on their computers. All confirmed that they sat for long periods with the symptomatic leg crossed underneath the other. ( See the photo of our president  on the cover of EDGE ) Since I usually only see patients once for a diagnostic evaluation, I rarely receive follow up. However, one of the patients with only paresthies told me they have improved since avoiding leg crossing.
Let's tell all those on-line workers to ge up and walk around

 Digital Antidromic SNAPs Are NOT an Exception to Volume Conductor Theory
 
Please Note:  In another post on “Atypical Waveform”, a question arose about antidromic SNAPs and I was requested to address why an antidromically recorded SNAP from upper limb digits is NOT an exception to volume conductor theory, i.e. it is biphasic initially negative and not triphasic initially positive as would be predicted for a propagating action potential.  Rather than extend that particular post, I am initiating this post to address the previously noted issue as requested.
 
Specifically, it is well recognized that a propagating action potential (nerve or muscle) on a sufficiently long enough segment of excitable tissue can be represented as a tripole (+-+) and even better a quadrupole (+- -+) [see Dumitru et al:  Electrodiagnostic Medicine 2^nd Ed: Electrical Sources and Volume Conduction, pp 27-67].  Another way of saying this is that a negative sink (-) is preceded and followed by positive source currents “feeding” the negative sink.  The associated current/voltage distribution associated with the three “poles” extends out into the volume conductor with the leading and trailing source currents extending out in front of, and behind the negative sink respectively thereby representing the “leading/trailing dipole:  +- -+” model. 
 
A recording electrode located at some location away from the propagating action potential will initially detect the leading positive source current by describing a downward or positive deflection on the instrument’s screen [Dumitru et el:  Electrodiagnostic Medicine 2^nd Ed: Figs. 2-5 & 2-6, pp 32-33].  This positive source voltage extends some distance physically both radially away from, and longitudinally in front of/behind, the negative sink.  When the negative sink arrives at the recording electrode an upward or negative spike is described by the instrument.  Further action potential propagation results in the recording electrode now detecting the terminal positive source current again defining a downward or positive deflection smaller in magnitude, but somewhat longer in duration than the leading positive spike (areas are the same) thereby defining the typical triphasic positive/negative/positive configuration of a propagating action potential traveling toward and passing by an electrode in a volume conductor.  There are no exceptions to this theoretical construct. 
 
Similarly, if an action potential is initiated at a location coincident with the recording electrode, then it is at the initiation site of the negative sink and the instrument first describes the upward negative deflection associated with the negative sink.  With propagation, the action potential departs the electrode location in both directions with the terminal positive source currents now detected with the instrument defining a downward or positive deflection.  The end result is a biphasic initially negative waveform.  This is true for all waveforms initiated at a location coincident with the recording electrode (biphasic initially negative) to include:  end-plate spike, CMAP, MUAP, Fibrillation potential, Myotonic Discharge, CRD, Fasciculation, etc.  There are no exceptions to this fundamental aspect of action potential propagation and volume conductor theory.
 
There is, however, an “apparent exception”.  Specifically, if you record an antidromic SNAP from the third digit, for example, subsequent to median nerve activation at the wrist, you will indeed record a biphasic initially negative waveform [Dumitru et el:  Electrodiagnostic Medicine 2^nd Ed: Figs. 2-7, pp 34].  Recall, volume conductor theory states that any waveform with an initial negative onset must originate at the recording electrode and propagate away.  However, it is clear that the antidromic SNAP does not originate at the recording electrode.  Rather, it originates away from the recording electrodes, that is at the wrist, and then propagates toward the two ring electrodes consistently describing the familiar biphasic initially negative waveform.  Isn’t this either a violation, or at the very least, an exception to standard volume conductor theory?  It sure seems like it is.  Specifically, as noted above, when an action potential approaches, reaches, and then passes the recording electrode it must produce a triphasic waveform.  The antidromic SNAP approaches, reaches, and passes the recording electrode to be sure, but generates a biphasic initially negative waveform.  Herein lies the conundrum
 
Well, indeed no, it is not a violation of volume conductor theory.  In order to understand what is going on one must conceptualize the voltage field distribution associated with the propagating action potential as it extends out into the volume conductor both longitudinally and radially.  Imagine if you will, that the nerve is in the center of a cylinder filled with normal saline.  Now, imagine the radius of the cylinder is reduced symmetrically about the center line [Dumitru et el:  Electrodiagnostic Medicine 2^nd Ed: Figs. 2-6, pp 33].  As the cross-sectional area of the cylinder declines, the associated voltage field lines become compressed radially and “stretched or distended” longitudinally.  Imagine squeezing a water balloon.  As you squeeze the balloon in one direction, the balloon expands in the direction perpendicular to the force applied, i.e. it grows longitudinally.  If one were to reduce this imaginary cylinder’s radius until it was just a few millimeters thick around the nerve, then the action potential’s associated voltage field distribution would be concentrated around the nerve radially as well as extending  some distance more longitudinally.  If one were to locate two electrodes along the nerve within relative close proximity to each other (say 4 cm), then the approaching compressed positive source voltages would essentially be detected simultaneously at both electrodes and with very similar magnitudes.  The compression of the longitudinal field doesn’t leave much voltage difference between these compressed isopotential positive voltage lines with respect to the distance within the spatial confines of our recording electrodes, i.e. 4 cm.  In other words, both E-1 and E-2 detect virtually the same positive source voltages because they are comparatively close together with respect to the difference between the actual voltages of the compressed isopotential lines.  Since E-1 and E-2 record very similar positive voltages, they are eliminated through differential amplification.  So, no potential is described on the instrument, and the baseline remains flat.
 
However, the voltages transition between the leading positive source and subsequent negative sink, unlike the similar positive source voltages at the two recording electrodes, is detected.  This is because the time frame of sodium activation is comparatively abrupt and manifests at
E-1 while E-2 still records the leading positive source current.  This difference in voltage leads to the detection of the abrupt onset of the negative sink and manifest on the instrument’s screen as a rapid upward, or negative spike since E-1 is now coincident with the negative sink while E-2 is not.  Just like the leading source voltages, the negative sink also has a spatial expanse.  The spatial expanse of the leading source currents extends a considerable distance out in front of the negative sink (theoretically it’s along the entire volume conductor ahead of the sink), while that of the negative sink is rather confined.  In other words, the negative sink is “sandwiched” between the leading and trailing source voltages (+ - +; or equivalently:  +- -+).  We can calculate the spatial expanse of the negative sink with respect to how much of the nerve it approximately occupies relevant to the parameter of interest to us as electromyographers:  i.e. the SNAP’s amplitude.  Amplitude, of course, is important because its magnitude is an approximate representation of the number of axons excited.  This issue of amplitude and number of axons activated in a sensory nerve can be quite different from that of the CMAP:  why?
 
So, if we are interested in how much distance along the nerve the negative sink occupies with respect to its maximum amplitude, then we need to know how long it takes from negative spike onset to its maximal peak.  That time is close to about 0.8 ms.  If the nerve is guestimated to propagate at roughly 50 M/s, then the distance of the negative sink from its initiation to maximum peak is about 4 cm.  This is where that 4 cm number comes from.  You want your two recording electrodes to be at least if not greater than 4 cm to avoid differential amplification from truncating the SNAP’s amplitude thereby yielding a possible false positive axonal loss lesion without demyelination (amplitude decline without latency prolongation).  The onset latency will not be affected if the E-1 and E-2 difference are closer than 4 cm (E-1 remains a constant distance from the cathode), but the peak will be shortened (waveform stopped from reaching it maximal amplitude) and the amplitude reduced.  Hence, no demyelination but supposed axonal loss.
 
There are several natural outcomes of the preceding issue of inter-electrode separation.  Axons are certainly traveling faster than 50 M/s which has consequences of measuring the waveform’s true amplitude.  Specifically, if the fastest axons are traveling at 60 M/s, then the optimal inter-electrode separation is 4.8 cm (NCV=D/T); and the 4 cm distance is too close which will result in differential amplification truncating the response magnitude.  On the other hand, if a patient with a peripheral neuropathy and has a CV of 40 M/s, then 3.2 cm of inter-electrode separation is tolerable.  The saving grace in all of this, is the concept of replicating the exact conditions under which the original reference population data was obtain.  Again, we do not have “normal” values but rather “reference” values.  If you use the exact filter, gain, inter-electrode separation, distance, temperature, etc. as that of the original data collection, then you should be just fine.  If not, then your data cannot be compared to that of whatever reference population you are using.  This is why it is critical for investigators to clearly define the instrument/environmental parameters under which they collected their data so it can be used by others.
 
Ok, now let’s return to reality.  The sensory nerves in the digit occupy a relatively small region of the volume conductor compressed between the skin and underlying bone.  Hence, the anatomy “squeezes” the propagating action potential’s voltage distribution as noted above. 
E-1 and E-2 both record virtually the same voltage simultaneously associated with the approaching action potential.  As a result, nothing is detected because of differential amplification.  Then, the action potentials’ negative sinks arrive at E-1 but not yet at E-2.  There is an ensuing initially upward negative spike with subsequent propagation and termination at the fingertip, thereby describing a biphasic initially negative and NOT triphasic initially positive waveform as would be predicted by theory.  But wait, there’s more!  You can accept the above explanation and move on, or you can rightfully expect some evidence for all this theory stuff.  Fortunately, this can all be “proved” quite easily.  First, record the typical antidromic SNAP with your two ring electrodes placed as noted above [Dumitru et el:  Electrodiagnostic Medicine 2^nd Ed: Figs. 2-7, pp 34].  You then obtain the anticipated biphasic initially negative SNAP.  Now, quite simply, move E-2 to the fifth digit, stimulate the median nerve again; low and behold the waveform now becomes larger (less differential amplification) and clearly displays an initial positive deflection fully supporting volume conductor theory.  All is well!  (An alternative approach would be to move E-2 further along the finger until such a distance is reached so as to manifest the small voltage differences between E-1 and E-2 pursuant to the initial source current.  The problem is that you would need a really really long digit.)
 
Now you can also ask, why do I get an initial positive deflection (triphasic waveform) when doing orthodromic or mixed nerve studies: e.g. stimulating the proper digital nerves and recording the response from the wrist?  Well you do most times but not always.  It depends how much subcutaneous tissue is present so as to permit the radial expansion of the source currents ahead of the negative sink allowing them to manifest differently at the two recording electrodes.  The more subcutaneous tissue present, the more the source currents expand radially and the less compressed longitudinally, thereby permitting their associated voltages to be recorded somewhat differently and hence now observed.  This concept applies to all recordings whether using bar, ring, or separate disc electrodes.  Volume conductor theory is preserved.
 
[Note:  I hope this helps.  I apologize for the lengthy explanation, but this is rather complicated stuff and I am attempting to address this issue at the request of a reader.  I tried to include practical examples which also leads to a more lengthy, but hopefully more clear explanation.  Also, I could not include figures and hence only refer to them because of copyright issues.]
 

52 yo female s/p chemo for breast ca 2017. Bilateral LE markedly absent PP, vibration, LT distal to her shins bilaterally.  High arches and hammer toes, thin ankles, calfs not atrophied. MMT 5/5 bilateral LE, but weak heel raise bilaterally.

Bilateral LE tibial and fibular motor responses were normal, but elicited only upon increasing the PW to 200-700 us, and 100 mA (patient insensate so not painful). Bilateral superficial peroneal and sural responses were absent, H-reflexes absent, fibular F wave absent. Tibial F waves normal.

Needle EMG was normal.

What is the significance, if any, of the requirement of strong stimulation to elicite a normal motor response in this setting?

Thank you,
Robert

Dear colleagues,

I've recently seen a patient who's NCS results like this: increased CMAP duration in all elicited nerves with reduced CMAP amplitude significantly, but without conduction block, slow CV, prolonged distal motor latency or F-waves (mild slow CV or prolonged late responses were observed, but not compatible to demyelination criteria). 

That also was not temporal dispersion. All segment was increased in CMAP duration. (for example, R median 10.2 / 9.6 / 10.5 ms, R ulnar 12.3 / 12.7 / 12.5 / 13.0 ms, R tibial 24.5 / 23.9 ms , and so on.)

Is it reasonable that this patient is under demyelinating process of neuropathy? or else?

For your information, He is 50-yo and found to be paraparetic after prolonged sedation and tracheostomy (over 1 week) in ICU care. I would suspected critical illness polyneuropathy but the NCS's was a little bit confusing. 

Thanks in advance.

 

Hello,

I have a 44 year old male with no PMH who was referred to rule out radiculopathy.  His MRI demonstrates foraminal narrowing on the opposite leg, the left, but nothing notable on the right.

He definitely was enhancing his discomfort because of the continued pain in spite of pain management and multiple doctors attempting management with limited success.

His NCV demonstrated delayed surals in the ball park of 5.2.  He had absent H reflexes bilaterally.  The remainder of the sensory and motor NCV was WNL.  His EMG was within normal.

I am just wondering if there is a diagnosis or further work up that would be warranted from this?

Thank you in advance.

Female in 30s with non-specific fatigue but normal neurological examination and nerve conduction studies. Normal CK. Normal thyroid function. No objective weakness or clinical muscle fatiguability. No bulbar or ocular symptoms. Several very short (<3ms) MUAPs in triceps and deltoid, though not small and didn't seem to have early recruitment.

Is this definitely mild myopathy or could it be a normal finding?

Hello,

I am part of a group practice. Some of the doctors have been sending patient for bilateral studies but the patinet only has symptoms in 1 limb. The way I trained we focused on performing a few NCS or needle sticks to make the diagnosis or rule something out. 

I requested calrification on what they were looking for and was told that patient with chornic pain and pateint with neuropathy should always have bilateral studies beacuse this is what  previous EMG clinic has told them. 

There certanly are cases where you need to study the other limb for referance or determine a more systemic proccess such as neuropathy. However , I have some concerns especilly when sent for Bilateral UE studies and 1 limb has no symptoms.

has anyone else run into this and if so how did you handle it. 

I recently saw a lady very early on (11 days) from onset of neck pain, arm pain, paresthesias and subjective weakness of the hand. I saw her for EMG at the request of her PCP due to travel and timing issues. Clearly this is not the ideal time from for EDX evaluation of radiculopathy. Her ulnar CMAP to ADM/FDI was reduced (~3.5 mv) with normal median CMAP, normal median, ulnar, radial and MABC/LABC sensory responses. No conduction block or slowing at the elbow. Needle examination showed mildly reduced recruitment in Extensor Indicis, triceps and maybe ADM. Normal paraspinals. I suspect cervical radiculopathy, possibly in C8 distribution. Has anyone seen this presentation and type of finding before? Any thoughts about the process involved?

We need a ground electrode to provide a safe path for leakage current away from our patients. But why, given that we are using differential amplifiers with very high CMRR's, is the 60 hz artifact so overwhelming when the ground electrode is disconnected. You would think that the effects of extraneous 60 hz interference would be equal to the two pre amplifier inputs and thus cancel.

I had a patient present the other day with back and buttocks pain for EMG. The patient was in her 30's. symptoms had been going on for almost a year. no weakness. no complaints of numbness or tingling in her toes or feet. NO radiating symptoms intot the leg. normal examination for strenth and sensation (light touch and vibration). no family hx of neuropathy. 

Her nerve conduction studies and needle exam were normal with exception of inability to otbain sural responses bilaterally. I moved the electrode 3 times on each side. I rolled across the calf with changes ,in stimulator alignement for several minutes and could not find anything that appeared consistant. 

Can this ever be a normal varient or is this signsof neuropathy that is not symptomsatic yet? 

April Yuki

Dear Colleagues, I was hoping for some advice on this one...

I was referred a 70 yo non-diabetic man by a neuro-ophthalmologist for vertical diplopia who in the course of his workup was found to have positive AChR antibodies. The patient woke-up with isolated fixed binocular diplopia, has had no fluctuation since onset, and has no ptosis, fatiguability, or generalized weakness on exam. MRI of the brain was normal. Repeat MRI and AChR antibodies two months later were unchanged (normal and positive, respectively). No response to pyridostigmine. Interestingly, his brother has symptomatic MG with positive antibodies, diagnosed >20 years ago. 

Given the history and exam, the working diagnosis is an MRI-negative posterior circulation stroke. But what to do about the antibodies? Pre-symptomatic MG? Epiphenomenon of underlying autoimmunity? 

In  a patient with a severe inherited peripheral neuropathy- if the distal CMAPs (and SNAPs) are absent from the lower and upper limb nerves - how do we define whether it is predominantly demyelinating or only pure axon degenerative? 
We could think of the following :
1.Recording over the FCR /FCU muscle and stimulating the Median/Ulnar nerve at the elbow and mid arm : any data available for defining when it should be called demyelinating?
2. R1 & R2 components of  blink reflex if prolonged is it demyelinating ?
Could not find any defined criteria for this -would appreciate inputs please 

Second question from the same patient （brachial plexopathy)

say, the thumb is in C6 dermatome. Does it mean all C6 sensory fibers go to this dermatomes and only C6 fibers go to this dermatomes? 

this patient has completely normal median SNAP amplitude from the thumb ( comparable to the normal side) but completely unobtainable from the long finger ( including mid palm stim). 

This is a real question. When there are two roots innervating a muscle and there is complete axonopathy to one of the two roots but not the other, do the axons from the unaffected root reinnervate (via collateral sprouting) the muscle fibers originally innervated by the other root? This question arose from seeing a patient with brachial plexopathy today. 

I thought of this waveform after the recent posting. I made this video in 2012 for my residents to drive home the same point as the last one.  Enjoy

https://youtu.be/RCdd8QM9YjY

Every patient scheduled for an elective surgical procedure in Baltimore area hospitals is required to have a COVID-19 pcr study done preoperatively,  and if negative, quarantine themselves until admitted. Since reopening my EMG practice,I have adopted this procedure  and also required a pcr study, mainly because of my age, my wife's age ,and her comorbidities. I have not insisted on the quarantine. Virtually all patients have understood and complied with this request. We are now able to obtain the nasal swab in our office with results returned from Quest within 3 days. This allows the patient to choose where they would like to have the swab done. A very few rare patients have refused to be tested, but for no consistent reason, other than for fear.
i wonder how others feel about pre procedure pcr testing. It is certainly not as good without quarantines,but if someone becomes ill, at least we will have some record of the patient's status and it should be of help in contact tracing.

What is the difference in area and duration on a CMAP and what does it mean? Is one more important than the other?

This is a waveform that a member recorded last week from the APB in a 66 year old woman.  We are sharing it as an 'unknown' waveform to see what others think.  More information and the 'answer' will be shared later.

Does such a diagnosis objectively exist?

 Is there evidence based literature that supports this offered diagnosis in a 55 yo with normal clinical and edX exams of an upper limb with diffuse pain?

I can recall being told by Neil Spielholtz, PhD, when I was  a resident/fellow in neuromuscular medicine in 1970, that facilitation of peripheral motor nerve conduction can be seen, especially when performing proneal/fibular motor studies. Stimulating the peroneal nerve at the ankle,will  occasionall cause  no response from the Edb .However, stimulating at the fibular head produces a response, and after this is done, stimulating at the ankle now produces a response. I recall being told that this was "facilitation." No further explanation was given, as much as I can recall. I recently have looked this up in the literature, since I have been doing this for 40 years, and have never given it much thought. If any of the  basic scientists out there can explain this to me, I would be very appreciative 

I am seeking the opinion of fellow neurologists/neurophysiologists as to whether you consider clinical examination, history taking and explanation of results and discussion of management as part of the neurophysiology study or is it considered as a separate consultation?  In my clinic I (as a Neurologist) personally exam the patient and take their history and based on this, set a test protocol which a neuroscientist then performs.  I then see the patient in my office after the study is completed for discussion of the results and management recommendations, and I provide a detailed report back to the referring physician.  

I would appreciate a simple yes or no response to the question:  does the above process allow billing of an EDX study and a consultation?

Thanking you in advance. 

John 

In various Maryland medical institutions, the degree of testing for Covid 19 before surgeries and diagnostic procedures varies greatly from one institution to another. With most surgical procedures patients are required to have a PCR test done during the week prior to their surgery, and they are asked to isolate themselves after their test until their surgery is done. Patients having MRI or other imaging procedures are not usually required to have any testing done, and are simply asked basic questions about Covid exposure, and their temperature is measured on arrival at the facility. Inside the facility, no procedures seem to be taken other than everyone wearing facemasks. In our office we perform only electromyography and nerve conduction studies. All patients are required to have a PCR 19 study done prior to being seen, but we do not require the patient to isolate themselves after this is done. We have turned away patients who arrived without having been tested. During the procedure I wear gown, mask, shield, head cover and gloves on each patient and even though the COVID-19 test is negative, I assume that the patient could have been  infected after the test was done.I suppose I am halfway between the surgical procedure and the imaging studies with regard to precautions. I wonder how others are handling safety precautions now that we are much further into the pandemic then earlier this year. Patients wonder why I am being so strict, but since we spend so much time in close quarters with the patients, I believe our degree of caution is appropriate. 

hi
could RNS be used for following up patients with MG !? 
assessing recovery or response to treatment ?
by comparing  pre  & post medication results 

What policies does your lab follow in regard to archiving raw data from EMGs/waveforms?  Do you archive for a certain length of time?  Any recommendations are welcome.