Join this vibrant community of professionals eager to exchange ideas, share resources, and engage in meaningful discussions. Use this platform as a sounding board to seek advice for navigating challenging cases or career decisions, and receive expert guidance from generous peers who want to help you succeed.
In order to comment on posts and view posts in their entirety, please login with your AANEM member account information.
I am interested to know whether this pattern of sensory involvement is a clue to a particular aetiology or pathology? This is a patient referred several months after prolonged ICU admission with suspected recovering critical illness myoneuropathy on a background of poorly controlled diabetes mellitus. The upper limb sensory responses revealed an unexpected relative sparing of the ulnar nerve. See attached image for sensory study results.
Hi,
Our old EMG machines were overdue for replacement and now we finally new EMG machines in the department.
We have 4 neurophysiologists and 1 senior neurophysiology scientist, all of whon have trained with slightly different normative values ie slightly different measurements and corresponding normal ranges.
We had a discussion around using the same values for the whole department but I thought I'd ask at this forum.
1. Is there a gold standard reference value we all should be using/adapting our individual practices to ? The AANEM published data on normative values in 2018, but some of us have inherited normative values from where our trainers trained in ie Mayo or others, all of which seem slightly different.
2. Is there merit in sticking to your own slightly different values as you've trained in them ?
3. Has anyone had this issue in their group practice or department and what reference values did you use ?
Thank you so much for your inputs.
Regards,
Gaurav
I have a question about bleeding from puncture sites on the needle exam. I've been practicing for many years. In the past year it seems like all my puncture sites bleed. In the past maybe 1 of 6 or 7 sites would bleed. I have been using new needles- Rhythmlink monopolar 37 mm x 26 g or Ambu neuroline 50 x 0.45 mm for the larger folks. These Ambu needles seem to be "teflon" coated and slip in and out nicely but bleed way more than previous needles. Is anyone else noticing this?
Trainees seem to like self-directed learning better these days.
They can do more good out there than on my hard drive.
I really don't want to "perform" these anymore
Please share this with your program directors so that they can share with their trainees.
Be sure to click "show more" in the video descriptions to see the clickable chapter links:
https://photos.app.goo.gl/uBhdCLm57mPsp3KSA
https://photos.app.goo.gl/vszpwBchYA9LitBq7
THANKS to Dr. Dumitru who i persistently plagiarized over the years for many of the baics EDx lectures. (i won't apologize for using the amazing source he put out there for all of us!)
I am trying to do some office hours in a day rehab facility where it would be difficult to get vital signs on each patient. Are vital signs before electrodiagnostic testing necessary, and if so, which signs are a must?
The NIH-supported Rare Disease Clinical Research Consortium (RDCRC) for myasthenia gravis (MGNet), which is part of the Rare Diseases Clinical Research Network (RDCRN), views standardization of MG outcome measures as a critical need for clinical trials. To address this issue, MGNet convened an outcome measure symposium and a working group charged with refining specific MG outcome measures and their instructions for administration, based on consensus opinion. The goal was to improve the clarity of instructions and scoring and reduce outcome measure variability. The outcome measures included in this effort were the Quantitative Myasthenia Gravis Score (QMG), MG Activity of Daily Living Scale (MG-ADL), MG Quality of Life-15 (MG-QOL15 and MGQOL15 revised), MG Foundation of America Post Intervention Status (MGFA-PIS), MG Composite, and the MG Impairment Index (MGII). Ultimately, implementing these recommendations is expected to lead to less data variability, greater efficiency, and fewer errors at clinical sites.
As the next step in the process, we are holding a public commentary period to help ensure that the views of all stakeholders are heard. We would value your input on the proposed revisions. The revised instruments and a link to a survey where you can provide feedback for each outcome measure are located on the MGNet website at: https://www.rarediseasesnetwork.org/mgnet/outcomes
The public commentary period was opened on May 9, 2022 and will end on June 24, 2022.
Following the public commentary period and final revisions, MGNet intends to develop a comprehensive set of training materials and case report forms for each outcome measure that reflect the recommended changes. MGNet anticipates holding training sessions for study teams at future meetings and offering initial and renewal certification processes for clinical trial raters.
Thank you for your input on this important effort to improve clinical trial conduct in MG.
Sincerely,
On behalf of the MGNet Clinical Trial Outcome Measure Working Group
I am a clinical neurophysiology trainee from UK (yup, they created such such speciality where we do NCS/ EMG and also EEG)
Just wondering if I can apply for any post doctoral fellowships in neuro muscular electrophysiology in US without USMLE exam please. Not only to get
more experience, but also to see the practice on other side of pond.
After almost 20 years in the VA, i am leaving. My day consisted of various general PMR clinics (MSK, EDx, amputee, mTBI, wheelchair, etc), teaching residents almost all day long, and working on process improvement within the VA.
I will now be doing a full week of outpatient EDx and MSK evals in a private/group setting (medicare and private insurances). I am going out there with an open mind & heart but will be cautious about letting the new incentive structure affect my clinical decision making.
I am wondering if any of you who have been out there for a while could impart any advice, wisdom, or cautions.
Does anyone just stimulate below the fibular head and the ankle as a standard in their lab? We have some techs doing this and I have never learned it this way and cannot find anything in the literature. We do above the fibular head and ankle stimulations as standard and a 3 point with foot drop.
This is an ordinary fibular nerve motor conduction study recorded from EDB. The CMAP responses to ankle and fibular head stimulations were perfectly fine (top two traces (see attached). However, the popliteal fossa stimulation resulted in a double peaked CMAP (the third trace) with lowered peak amplitude. I think it is from a tibial muscle (due to coactivation/costimulation of tibial motor nerve). The question is which muscle is responsible for the extra peak? Thanks.
p. s. I don't want this to turn into discussion of volume conduction of the stimulation. There is no conduction block. Needle stimulation was later used and a perfectly matching CMAP morphology as the top two traces was obtained.
Is any one aware of where I can obtain St Marks Electrodes as it is not available from the usual source I used to get. When I used Google nothing pops up as to where I can obtain them. Appreciate your help.
Thanks
I would appreciate input on a recent patient referred by one of our nerve surgeons. The patient is a 31 y/o male with a longstanding perineurioma of the femoral nerve and profound weakness and loss of function of his quadriceps muscle. Even though this has been going on for a long duration there is still ongoing spontaneous activity but with no recruitable motor units. Our surgeon is asking if a nerve transfer from the obtutator is feasible. My thought is that this far out there is little chance of nerve regeneration but told her I would check with colleagues who have more experience in this area.
Hello!
Does anyone have any recommendations for finger clip electrodes? The current ones I use are Chalgren finger clip electrodes. They USED TO BE great, but since they got bought out by another company last year, they are less durable.
NOW, they only last for 1-1.5 months. They short out or can't provide a stable baseline (interference) even though I clean thoughly, use gel, and a stable ground. I will post a picture of the ones that I use. I have contacted the new company that bought Chalgren and alerted them about the issue.
Once I replace the old finger cip electrodes with new ones, they work fine...for 1 month or so. They used to last a lot longer before they were bought out. https://www.google.com/search?q=finger+clip+electrodes&rlz=1C5CHFA_enUS899US910&sxsrf=APq-WBtkvc4KkQaZ3cpeUmBoGBO9eq6rkw:1648916928469&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjr_qOe5vX2AhV_gnIEHa6yAQ4Q_AUoAnoECAEQBA&biw=1440&bih=708&dpr=1#imgrc=PfMLjZ8BB22vEM
If I am not on a particular insurance panel but the patient wants to see me anyway and pay the "self pay" rate, do I have to do anything differently? It seems this would not be balance billing. Sometimes my self pay rate is higher than the insurance rates, sometimes lower depending upon the insurance (the self pay amount does not change). We submit the bill as my usual charges with a courtesy discount to the self pay rates. Thoughts? JMB
2 questions:
We had a patient with prior CTS surgery (about 8 years prior) who had delayed distal latency (6.8ms) on the median motor with low amplitude of 1mV. The proximal CMAP was low amplitude and the CV was slow. The median sensory digit II was 3.3ms at a distance of 14cm with an amplitude of 12uV. Pt also has a C8 radiculopathy on EMG.
1. Was I dreaming or have I heard of a "purely motor only" CTS at an AANEM meeting. Is that a real thing?
2. Does the median motor and median sensory recover, after CTS surgery, at different rates for remyelination and axonal regrowth? As in the situation above, could the sensory segment have remyelinated and recovered (even with shortened internodal distances) quicker than the motor component? Could that contribute to the sensory being normal and the median motor abnormal?
Thanks to all you smart doctors in advance!
Carrie REPT, RNCST, CNCT
I am a long time user of TECA elite monopolar needles and have significant difficulty or delays in obtaining needles for my last 2 quarterly shipments to the point where I was on the verge of postponing or delaying scheduled EDx. I am wondering if this problem is widespread with all suppliers. I have a small backup cache of Ambu needles which I put into service but have avoided using them as they are very prone to 60Hz interference.
Hello
I have a patient who would like to be enrolled in an ALS clinical trial.
She is 43 yo and has C9ORF72 expansion, and she has family living in UK.
She has an excellent perfomance status, with no Dementia, and only lower limb signs and symptoms.
What would be your recommendation for a recruting center for this kind of trial, preferably in the UK?
Thanks for your help
We are conducting a survey on teaching preferences for the diagnosis of mild distal entrapment neuropathies. We would greatly appreciate your time to complete our survey via the following link. Please feel free to forward the link to other EDX practitioners.
I would be grateful for any wisdom or advice on this case as I have found little in the literature. I have a female in her 40s who is otherwise healthy whom I saw for the first time after a 12 month history of insidious 'boring' pain in her right upper trapezius and SCM, with some fasciculation and cramping and then more recenty marked wasting and weakness. No history of neuropathic type pain at onset to support neuralgic amyotrophy and course seems much more protracted that I would expect.
By the time I saw her she has lost essentially all right SCM and trapezius function and I was unable to needle traps on EMG, going straight through it into rhomboid minor when attempted. No sensory symptoms and UL NCS otherwise normal (I confess, I did not attempt NCS of spinal accessory itself). MRI including fine slices through region of jugular foramen, CSF analysis (protein, cells) and CT chest abdomen and pelvis have all been unrevealing.
Are any of the systemic autoimmune diseases prone to picking off the accessory like that? What else do I need to consider? At this stage, feeling rather deflated and will be looking at orthopaedic referral as only means of addressing her poor function and mechanically induced significant pain.
hello,
I have had a cluster of myositis cases in the hospital lately that I shared care with rheumatology and they are fairly univerally ordering myositis specific antibody pannels. These pannesl came out after my fellowship training and I don't feel like I have great comfort in interpreting the pannel results. Does anyone have a resource that they feel is helpful in decipering these panels and how the data impacts diagnosis, management or prognosis in clinical patient care? Addtionally, any experience/pearls would be welcome and appreciated.
Recently I saw a 31 year-old male showing involuntary muscle twitch isolated in right brachioradialis (around elbow) for 2 months almost interfering his daily life. Normal neurological examination except large muscle twitch in right arm. (normal sensory and muscle strength)
He was diagnosed with type 2 diabetes mellitus before 1 week visiting our clinic. (hemoglobin A1c 10%). His hemoglobin level was elevated (17.2 g/dL), but normal thyroid function test, metabolic panel, and serum CK.
NCS was unremarkable.
EMG only showed spontaneous discharges as below with normal MUAP in right brachioradialis muscle. (sensitivity 500 uV/division, sweep speed 10ms/division)
Can it be considered as fasciculation potentials? Too long duration and followed by small positive sharp wave-like discharges ...
But it does not seem to be categorized to well-known, typical abnormal spontaneous activity by definitions.
Does anyone have guidance on the relationship of vitamin B6 toxicity and laboratory reference range of this vitamin? Our lab measures B6 in mcg/L with a normal range of 2-32.8mcg/L. In our workup of axonal polyneuropathy, we frequently receive results slightly outside of the range (40mcg/L) and infrequently much higher (156mcg/L is the highest we've seen). My understanding is that B6 neurotoxicity is very rare and generally occurs with supplementation above 1000mg daily. As we see these abnormal results in patients frequently and in those who do not take high dose supplement, I question the lab cutoff as a marker for neurotoxicity.
I'd appreciate any insight others have in addressing this issue.
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.