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I just had 28 year old man referred for an EMG. Symptoms started about 6 months ago. Numbness in arms and legs . All the same. He was much worse at the beginning and was unable to walk. He uses a cane currently. Poor historian. 2+ upper and absent lower. Full strength.
All thought to be alcoholic. He was a heavy drinker for few months per his report???
could not get any sensory in 4 rextremities. LE motor, very low amplitude or absent. Upper motor is normal. No delayed latency or slow conduction velocity.
No pain at the onset.
EMG is the confusing part. Quads with 3+ fibs. Legs with no fibs but slightly large and polyphasic units. Upper is ok. Lumber paraspinal with no fibs.
I was thinking sensory neuronopathy until I stuck the needle in the quads.
My emg machine finally died, so I borrowed my friend's Cadwell Sierra Ascent. Works great besides for a phantom waveofrm with sensory studies. It always occurs around 1.2 ms at 8 cm or 1.5 ms at 10 cm. I think it's shock artifact but I'm not sure. I have the notch filter on, exam table unplugged, use a shielded shuttle cable, keep the electrode and stimulus cables away from each other, tried using the machine in different rooms, etc.
I attached the waveforms below (or at least I hope I did).
Does anyone know what this wavefore is and how I might get rid of it?
Hi there. I run a quite busy EMG lab that is accredited and I am employed under a huge medical system. I am wondering about venturing to establish my own independent EMG lab. Are there any guidance or resources out there that can help me? Thank you in advance.
Does anyone have any experience with ultrasound billing? Is anyone doing it as an extension to the NCS/EMG?
Can you still do Ultrasound when a primary asks for NCS/EMG only?
How should increased ulnar distal sensory latency, with normal sensory nerve action potential and normal ulnar motor NCS, and otherwise normal NCS of the median and radial nerves, be interpreted?
There have been references to "muscle pairs" for example in the Peripheral Nerve questions (question 3 on my set), it said that fibularis brevis and fibularis longus (peroneus brevis and peroneus longus) are a muscle pair.
There was another question suggesting that coracobrachialis and pectoralis are another muscle pair. Also, extensor pollicis longus and latissimus dorsi as another pair.
Please can anyone explain the defintion of a muscle pair.
hi
we know that Hx , clinical features & temporal course are important integral parts in EMG report , but i wonder if EMG could easily differenciate between two conditions ( AIDP & CIDP ) depending on EDX findings only away from Hx ! ?
I'm seeing a 50 y/o man with painful asymmetric polyneuropathy whose exam suggests severe weakness and sensory loss involving left median and left tibial myotomes/dermatomes. Very weak DIP flexion in left hand digits 1-3 suggesting AIN involvement. Only significant past medical history includes heroin use. Negative or normal: anca, esr, crp, hiv, hep Bs Ag, hep c ab, Ana, sjogrens abs, cryoglobulins, CBC, cmp. Last reported use of heroin February 2020, symptom onset September 2020. Nerve and muscle biopsy planned. Has anyone ever seen mononeuritis multiplex without any abnormalities on the serum lab tests? NCS/EMg confirms asymmetric polyneriopathy with subacute denervation in left APB, left FCR, left gastric. Chronic denervation in left TA.
Is swelling and blisters can be a side-effect after NCS?
I did NCS of both lower limbs to my 68 y/o woman lasts Wednesday, possibly poly neuropathy. She didn't complain of any untowards pain during the test.
Today, Saturday the patient came back and she had right foot swelling and blisters. Are these a side effects of NCS?
Blisters location are not on the stimulation site.
I was reading about the the new bill being introducecd into the house of repersentatives. I am excited there is action being taken to ensure EMG quality. I was suprised to see a requirement of 3 months of EMG during trianing. Where I trained EMG was only one month, does this mean the average neurlogist would no longer be able to perform EMG's upon graduation? I am fellowhip trained so I dont have to worry but it made me wonder, how this effects the average resident going into practice?
Also as somone not in a large hospital system the prospect of accreditation is worrisome from a financial perspective. Has this been taken into consideration?
I would like to hear from you guys about you routine on repetitive nerve studies for patients reffered with the hypothesis of Musk+ MG with proeminent bulbar symptoms and signs.
I had a patient in particular had a lot of bulbar symptons, no ocular abnormalities, and the repetitive nerve stimulation on orbicular oculis and nasalis was normal.
Well, we always learn how important it is to study the weak muscles in MG. So I wonder if I had studied orbicular oris or mentalis I could have found decremental pattern.
Does anyone have experience in repetitive nerve stimulation on these muscles or any other suggestion?
Hello
I would like to hear some sugestions regarding investigation in this patient.
65 yo male, with long standing distal paresis in 4 limbs, almost with bilateral dropped foot. Wife says he allways walked funny, and she knows him since teenage. No pain, no atrophy, weak osteotendinous reflexes, distal tetraparesis (3/5) , simmetric, multimodal sensation, even distally, preserved, no cranial nerve involvement.
EMG with normal conduction studies, but with myopathic signs in all muscles studied, no myotonic discharges, no dennervation.
CK with slightly above normal value.
Any sugestions on further investigation or possible diagnosis?
Thanks
I was wondering if anybody has any thoughts about whether
TWO patients can have EMG's done at the SAME time in a very
large room (designed for THREE patients
in three separate cubicles) and where
the TWO patients are on the opposite ends of the room
(in the far cubicles) and are about 20 feet apart.
Assuming all other COVID parameters are followed, such as
face masks and face shields, etc. what anyone's thought is
about whether it's okay to do the two EMGs at the same time.
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 2nd 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 2nd 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 2nd 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 2nd 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 2nd 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?
I was permorming the exam of a 57yo female, with trauma with multiple fractures on right leg 20 years ago. There was evidence of chronic neurogenic alterations on tibial, deep peroneal and superficial peroneal muscles and the I ran into this discharge while evaluating right abdutor hallucis
I had some doubts about describing this discharge and wanted your opinion about it. It does wax and wane in frequency and amplitude... could it be a myotonic discharge in traumatic neuropathy?
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.
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?
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?
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 enjoy participating in the AANEM Connect Forum for a number of reasons. There are very fundamental questions posed on a frequent basis that cause me to pause and ask myself, ‘Why didn’t I think of that?’ Also, I continue to learn
new things when others contribute their thoughts and experiences. Connect is an excellent opportunity for members to interact and to address any topic, including those that may not be discussed
at an annual meeting or journal article.
