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EMG abnormality without fasciculations. Yes. They reflect different mechanisms. It should say that absens of fasciculations is unusual in ALS, think of other diagnosis. High ampl F waves and no fasciculations. This is not studied as far as I know. Again, abscens of fasciculations in all muscles is unusual in ALS

@@jittertube so, the f wave correspond to fasciculations? And without fascinations they don’t appear?

F waves and fasciculations are completely different things. F-waves occur when the nerve it electrically stimulated. The nerve cell in the spinal cord is thenoccasionally backfiring, producing the F-wave. May be more frequent in ALS. Fasciculations occur spontaneously. They usually start in the peripheral nerve, sometimes in the nerve cell in the spinal cord, indicating a nerve hyperexcitability. Can have different reasons. Separate from Fwaves

Thank you so much for explaining this! The last question if you don’t mind: is emg able to find abnormalities at a very early stage of the als, when there are no visible weakness, hypotrophy or atrophy, and only fasciculations are present?

@@CurlsAndMadness The simple answer is YES, EMG finds abnormalities before symptoms occur. When nerve cells disappear we see that in EMG. This is initially counteracted by the outgrowth of new nerves from healthy nerves, (so efficient that no weakness occur) and we see that also in EMG. The test must be made in a few muscles (3-5) since some areas in the body may be completely unaffected early.

@Sanctuary, thanks for your question. As you correctly noticed, it is impossible for me to judge in this situation. Your doctor may use other reference values, base conclusion not only on these numbers, and many other factors. I have a question regarding your treatment you talked about. For what? I may have comments when I know this. All the best Erik Stålberg

Hi. In this article your find many details for CNE jitter recordings. Muscle Nerve 53: 351-362, 2016. If you cannot find, return to me over mail

This is not my experiencer at all. RNS during high frequency is prone to technical artifacts, both with decreasing amplitude (movement) as may have occurred in your case, and with increasing amplitude (up to 43%) due to muscle shortening and ion changes. Theoretically you may have uniquely increased decrement after long term high frequency in a patient with some type of congenital typ of MG.

Vike20. This description is not consistent with ALS. Hope that the EMG findingscan serve as a strong comforting factor for a patient that may worry

Thank you ! I know you have figured out that I'm the patient. I became concerned mostly with the "polyphasic" nature of the reinnervation and although no fasiculations on either of my EMGs, I do have them (widespread) but mostly when fatigued. I am also seemingly trying to commence recovery from B6 toxicity which can cause those as well as other sensory symptoms which I have. I had an initial EMG done by a non neuro 2 mos prior that showed +1 PSW and Fibs bilaterally in the L5/S1 myotomes . (No other abnormalities) Some of the very same muscles on the 2nd EMG were now somehow devoid of any PSW or FIBs. That seems encouraging but not sure I understand how that happen so quickly ? The Ortho who ordered 1st EMG didn't think my herniated disc in that region would have been severe enough to cause me to fail it so that's what started all this. The second was done by an actual Neuro. @@jittertube

@@Vike29 Thanks again. EDB is probably "neurogenic" more often than any other muscle. An isolated finding here is not giving any diagnosis. Some fibs and psw in L5/Si are also very common. Their disappearance at second test is reassuring. EMG is not for treatment, except in exactly in these situations. A normal finding, or disappearance of slight EMG changes over time tell us that you have no EMG signs of ALS. We all have fasciculations, so do not go for a new EMG just for fatigue related fasciculations. Hope you recover from your B6 related problems...E Stålberg

Thanks a lot Stålberg

Nice to hear that you have seen it. Have a great day Erik S

The simple answer is that prolonged F-latency and slow velocity in distal segments (forearm, leg) indicates proximal slowing. This pattern is seen in e.g. GBS. Stålberg

Thanks, Erik S

Thanks, Erik S

Thanks Erik S

If EMG has been performed accodring to standards a negative finding for ALS should be trusted. I suggest that other test should be done to find a possible treatment.

I have cervical sponlitic Myelopathy according to my cervical MRI and need surgery.My neurologist wants to do an EMG to rule out motor neuron disease.

The Munix softwarte is implemented in a few commersial system. As I know today it is found in Cadwell Sierra, Synergy and Neurosoft. Maybe elsewhere also that I have missed. Good luck ES

Thanks a lot, Stålberg

Dear Colleague. You are quite right. The short answer is that I have no firm opinion on this. It is seen mainly in Trapezius, but also in other muscles. The reason may be: 1. shortening of the signal dure to increase muscle fiber velocity. 2. Na/K ion changes after activation discussed by McComas. This is a physiological phenomenon, so it is expected to give some increase, but why more in some muscles? 3. Shortening of the muscle. 4.Artefact due to 95% stim first stimulus and then 100% for second due to changed excitability to active all axons (my speculation, but only as artefact). What to do? Change rec electrode position and try to avoid the change. Do not pay too much attention on findings in ONE muscle when this is present. Note that SFEMG does not have this problem.

2ns reply. I have actually calculated the change between stimulus 1 and 2 in trapezius and anconeus in NORMALs. For trapezius (301 studies) the mean was +3% increasem (max 20%), 75% of data were changing in positive direction. For anconeus 91 cases mean was + 0,4% (max 20%). 52% of the data were on the positive side (2nd large than the 1st)

This we seen relatively often in Trapezius. Confusing I think and difficult to understand. If the ampl increase for response nr 2 is due to changes in the muscle fibre (theoretically possible), we cannot trust a decrement. If the amplitude increase is due to some n-m junction parameter, we can trust. Until we know, try other muscles also. No patient has MG only in Trap. And try SFEMG Stålberg

Alexander I try my best to reply I agree, that there is a distributions of arrival times. Shortest latency is not necessarily fastest, since responses my come from different roots, i.e. different distance, may have different central delay. People have not agree that shortest latency represent fastest axons. I do not think that ampl or dur is related to excitability. The parameters increase after reinnervation. Each F wave is a surface recorded motor unit potential, and so parameters follow the rule. Signals between CMAPP and F. There are 2 possibilities. But first of all, an explanation. If suprastimulation is used (all axons to that muscle are stimulated), then they cannot be voluntary signals, because of proximal blocking of antidromic stim impulse and ortodromic F-wav es. Now, one possibility is that you have not been able to stimulate all axons (weak stimulation of very inexcitable axons in disease). The other possibility is that they represent fasciculations starting peripherally (like in ALS).

Does the physiological chronodispersion of F-latencies reflect the range of motor nerve conduction velocities? Or is the range of F-latencies smaller than the different nerve conduction velocities would suggest? I did not understand why chronodispersion increases in the case of spasticity. I previously thought that spasticity was a central phenomenon and therefore increased the amplitude and duration of F waves. What is the cause of the increase in chronodispersion of the F-waves?

Alexander In spasticity, more neurons are active. Without my own studies, I suggest that since the number of F waves with their distribution of latencies, it will be a large chance of increasing both latency and duration and chrono dispersion.@@alexanderrose189

Aidin. It is all dependent on sensitivity of detection. The more denervation, the weaker muscle and then later recruitment. So, in the gray zon it depends how you detect and define denervation and also what kind of quantitaion you have to detect abnormal recruitment. I cannot therefore not gie a precise answer.

In one patient, I calculated the recruitment of the patient with the raster method, it was normal, but there was PSW, the muscles looked normal, have you had such a case?

@@aidintaalimi2232 If it was minor degree of psw, and if patient did not have clinical weakness, I can imagine normal result on your way to analyze reccruitment. Erik S

Thank you very much professor 🌹🌹🌹🌹🌹

Hello, Professor, good time. I sent a clip suspected of myotonia and CRD to your wife's MAIL. I would appreciate it if you could guide me. Thank you.

I will be happy to answer your questions. Email: stalberg.erik@gmail.com

Glad to har Erik Stålberg

Good luck Erik S

Alexander. Thanks for comments. I think that ALS and inclusion body myositis, very rarely are difficult to differentiate. The clinical picture (reflexes, atrophies, development over time..) and the histochemical pictures. Unfortunately the EMGers may have confused the picture, which is the basis for your question. In some muscles in patients with myositis, (also other myopathies) we can see the very high MUPs, but they are generally short and they are stable. In ALS MUP are overall not very high, but complex and show instability, jiggle. Furthermore, the interference pattern is generally full in myopathy, contrary to the finding in ALS. The reason for the confusing high amplitude MUPs may be muscle fiber hypertrophy, well known from biopsies, or the summation of signal from split muscle fibers, a common phenomenon in myopathy. This is the most likely casque, but not experimentally directly proven. As you mention, in advanced stages of myopthy, we may see secondary nerve involvement with some degree of reinnervation, probably.among

Thanks. Happy New Year to all, all over the world. Erik

Thanks Erik Stålberg

Yes you are absolutely correct. And in addition, signals at the end-plate zone do not have the positive going "arriving phase", they start abruptly in negative direction, so the duration is cut into "half", or at least become shorter than signals recorded a few cm downstream

Thanks for the important question. Our studly long ago only included 16 muscles. Now there are a few more. Unfortunately they differed somewhat between equipment, but supposedly similar for most systems of high quality. What to do you ask. Buchthal´s original and classical "Blue book" from Copenhagen in the 50-60 ties has that same problem. For muscles where ref values are missing, they simply copied values from other similar muscles. Thus, at the moment you have to use ref values from muscles of similar size as your test muscle. A good and often used principle then is to take a small sample (210) of normals and check that those values that you have chosen, give reasonable results. This is a main problem in QEMG....In the future one will be able to define ref values for all parameters for all muscles (age height related) some high level EMG equipment, work in progress.

In our lab 5% is the 95% conf limit. It is somewhat difficult to trust RNS in nasalis, but deltoid is fine (we use 5% here also). I consider 8.7% as abnormal, dependent on good quality of the recording.

@@jittertube Thank you very much for your valuable feedback.

It is not common to see many recordings with so low jitter in a stim SFEMG study. I wonder if it is technical problem, that you are measuring on some kind of artifact. This is really my strong suspicion. Else: for surface stimulation e.g. facial nerve. Then you are always outside the muscle, and you always get axonal stim. For intramuscular needle stim - aim for a central area where you think endplates are located, close to the area of the entrance of the nerve to the muscle. Nerve stimulation gives a larger twitch than direct muscle stim. To favor axonal stim use very short stim pulse duration e.g. 0,5 msec

It's an honour to get a reply from you sir, thanks for that. Actually I barely seen twitces in the frontalis muscle (not in every study), does that denote that I'm not stimulating the nerve axon proberly, I use 5Hz and maximal intensity of 7mA . I usually use a surface stimulator to seek the highest amp of the trigger SF potential, then I insert the stimulating needle in that very spot, after that if I noted twitched I insert the recording needle in it, if not observing twitches i put the needle any where in the muscle. Please inform me what possibly is wrong with that technique

I think your method is correct, except the comment that without twitch you place the recording electrode "anywhere" in the muscle. I suggest to stimulate sufficiently strong to see the twitch, insert the electrode, and then reduce the stim strength

Ok sir, I will try this and will report the results to you. Thanks for your help.

Dear sir, I increased the stimulus intensity alittle bit as you said, and it paid of, I did see a visible twitches, inserted the recording needle and thankfully I get a normal jitter in the frontalis muscle higher than 5 msec. Thanks for that dear sir. I wanted to attach the picture of the recording for you to see, but I can't find the option here in the comments. Can I ask about the optimal sweep during recording? Again thanks for sharing your knowledge.

crystal. Thanks for your question. If the study is performed with good quality, an increased jitter is a sign for disturbed neuromuscular transmission. It may be MG but other conditions e.g with reinnervation also show this abnormality. Degree of SFEMG abnormality is related to degree of severity in tested muscle. So, un unsuspected finding of increased jitter must be investigated further; clinically, antiAch antibodies, other EDS tests.

@@jittertube thank you my dr is concerned about Als and I've been a wreck hoping that's not what it is 😔

Myokymic discharges I agree that this is a less common mechanism and therefore I did not read this word when I discussed my slide. Myokymia is the repeated contraction in the muscle detected on the surface. The generation varies. Electrophysiologically is is a subgroup under repetitive discharges or grouped discharges. Those that are seen as repetitive motor unit potentials are definitely from the axon. Those with single fiber shape (such as double discharges, CRD, ..) are from the muscle. There are situations where the generation is discussed. So, to be on the safe side, define myokymic discharges as generated in the axon, the most common. Thanks for comments.

Giant MUPs take time to generate. Their development is therefore dependent on speed of progress of denervation, as you indicated. So, in typical ALS, the time is too short for formation of Giant MUPs. In ALS we see complex unstable prolonged and often large but not very large MUPs

"Giant" is usually the term for > 10 mV, but depends on muscle. Seen in old polio. In ALS, correctly we do not see such amplitude, usually not even 5-6 mV

Thanks for your question. This technique requires training and a good technical skill, and in borderline findings, I should be very careful in judgments. I have a few comments: 1. If your clinical conditions allow, before treatment, repeat the study after 1-3 months. 2.The study should be made in weak muscles (abnormalities may be seen in one muscle, not in others) 3. Final diagnosis is always clinical (supported by the test you indicate). From your descriptions, it really sounds like myasthenia, but this is up to your physician.

@@jittertube Thank you very much for your answer! I have a new test in three months. But I wonder, if it’s above 10% abnormalities in one muscle, if I for example get three certain abnormals out of twenty pairs (15%) in frontalis, but 0% abnormalities in another muscle, is the whole test normal then? Or is the test abnormal if only one muscle is above 10%, regardless of the other muscles? At my hospital they said that it is the total percentage of all pairs from both tested muscles that count. But I found that a bit strange?

The distribution of myasthenic abnormalities is unevenly disturbed among muscles. Frontalis may be normal on one side, normal on the other and so on. So, the judgement is: if one muscle is abnormal (definitely. i.e. > 2 out of 20 recordings), the study is abnormal. We do not make statistics of all recordings performed since some normal muscles may make the total study normal if one use %. I do not use percent, but > 2 out of 20 (voluntary activation). Note 3 out of 10 is abnormal. 2 out of 8 is 25% but not abnormal since it is not > 2

@@jittertube I contacted the hospital and luckily it was just a writing error in my case summary and miscommunication between the technician and my physician. But I will try to get my next sfemg at a bigger hospital with MG specialists. Thank you very much for your time and your advices!

This is not a common situation. My guess is that a new axon is activated with incresing stimulation and give a situation that looks likes increase jitter sompared to the "clean" situation at lower stimulation strength

@@jittertube Thank you very much for taking the time to teach us.

@@aidintaalimi2232 open for more if you wish

@@jittertube 🌹🌹🌹🌹🌹

I write to you via my wife´s mail and will reply with my correct mail: stalberg.eva@gmail.com

stalberg.erik@gmail.com

Omama Please send me THE question again with other Words. I Will reply then

Rephrase your rns question

Nice to hear. Stålberg

The EMG findings in one muscle may be similar, and in early stage of ALs may be restricted to one segment. Soon, the ALS findings are spreading to other segments, not so in radix. Important clinical differences are the lack of sensory symptoms in ALS, and the signs of upper motor neurone involvement.

Thanks for the initiated question. Large MUPs "gigant" need time to build up. So, dependent on speed of progression, the MUP parameters varies. Often there is to short time in ALS, and we do not generally see these very large MUPs. c.f. sequel after polio, where you may have very large MUPs.

Unfortunately not. Technical errors, anomaly give H-reflex at sligtly different muscle. Asbcense not absolute signs of pathology. Latency difference is more reliable

Yes. For fiber diameter of 45 um , my test MUP is 327 for 55 it is 591 and for 65 it is 890. Note, this is from ONE, same MU. When we make ordinary EMG the amplitude varies a lot, at it is often difficult to obtain a good value, if we only have 20 MUPs. Usually the change in diameter is less than in my example. So, usually we do not make misinterpretations for people with normal variation in muscles. Maybe a factor in athletes.