Thank you for your videos and explanations! Do giant potentials (> 5-6 mV) occur in normal courses of ALS? Or do the MU die within the framework of the underlying disease before they become so large?
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
Hello Dr.: What if you had no UMN signs on clinical exam and normal EMG of both upper and lower right extremities with no Fibs, PSW, or Fascics or signs of active denervation/reinnervation with the exception of one muscle (EDB) that reinnervated that showed "slightly increased motor potentials amplitudes with polyphasic configuration." No loss of Motor Neurons detected. Consistent with early ALS ?
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
I have extreme muscle fatigue, muscle and tendon pain, fasiculations and muscle wasting. My EMG was normal. I know I have a severe parasite load and mould, very bad live blood test in terms of sludge. I'm being told I don't have ALS but I keep getting worse. Taking herbal cleanse for the parasites made my fasiculations and body pain much worse.
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.
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.
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
Extremely informative Content. Thankyou very much Dear Sir!
Wonderful lecturer
I appreciate your great effort
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May Allah bless you ❤
GO On
Thanks
Erik S
Thank you for your videos and explanations! Do giant potentials (> 5-6 mV) occur in normal courses of ALS? Or do the MU die within the framework of the underlying disease before they become so large?
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
Hello Dr.: What if you had no UMN signs on clinical exam and normal EMG of both upper and lower right extremities with no Fibs, PSW, or Fascics or signs of active denervation/reinnervation with the exception of one muscle (EDB) that reinnervated that showed "slightly increased motor potentials amplitudes with polyphasic configuration." No loss of Motor Neurons detected. Consistent with early ALS ?
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
I have extreme muscle fatigue, muscle and tendon pain, fasiculations and muscle wasting. My EMG was normal. I know I have a severe parasite load and mould, very bad live blood test in terms of sludge. I'm being told I don't have ALS but I keep getting worse. Taking herbal cleanse for the parasites made my fasiculations and body pain much worse.
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.
Thanks, How can we differentiate between EMG findings in AHC lesion and root lesion?
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.
Hello professor thanks for your education is It possible to provide a direct link for questions
I write to you via my wife´s mail and will reply with my correct mail: stalberg.eva@gmail.com
stalberg.erik@gmail.com
Hello, good time, I had a question, is it possible to have active denervation with normal recruitment in radiculopathy?
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
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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.