AANEM Connect

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?

WHAT: I have created a Youtube playlist of all of my lectures for anyone to watch, quote, steal, share, cook, clean, to their hearts' desires. 

WHY: Many reasons.

1. Trainees seem to like self-directed learning better these days.
2. They can do more good out there than on my hard drive. 
3. 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
 

Hi all, 


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. 

Best regards

Satya Duddu

Life Question

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. 

Thank you for your comments!
Michael Fredericson 

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

Dear EDX Colleagues

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.

Thank you.


https://forms.gle/hkzRN98QrLe5vyds8

Hello, 

How long on average would you say a SFEMG takes and how many do you usually do in a day?  Do you know the reimbursement/RVU?

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.

All comments very welcome!

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 am hoping that some of you have some insight as to how to sell a private neuromuscular dz/ EMG practice. I have built up a very enjoyable and profitable practice centered in Duluth MN. I have been here for 30 years and will retire fairly soon. I don't want to shut the practice down; it is successful enough that I ought to be able to sell it. Just as important, I have a very large referral basis of orthopedic and neurosurgeons plus primary care that will be in a lurch if I leave. I did find a business that made up a website for me https://sellingapractice.com/nnm but that's about all they do. I am not sure how to proceed from here. Thoughts/ suggestions?

Thanks in advance: Has anyone treated patients with chilblain lupus who have severe symptoms of small fiber neuropathy? See questions at end of post. Appreciate your help.

The patient is a 45-year-old woman with 5 years of symptoms in the hands and 3 years of symptoms in the feet. Symptoms are sensitivity, swelling, pain with activity, redness with activity, and neuropathic pain. On exam she has visible edema and rubor in the extremities. No neuro deficits apart from altered temperature sense in feet. 

1) Derm workup: Skin biopsy with dermatology revealed chronic cutaneous lupus erythematosus, compatible with chilblains lupus. 
2) Neuro workup: Abnormal QSWEAT. Normal Therapath skin biopsy. Normal NCS (sural 15-20 uV). 
3) Rheum workup: CRP 0.6 (ULN 0.5), ESR 36 (ULN 20). Otherwise, extensive labs are normal including WashU sensory neuropathy Ab, paraneoplastic panel, CBC, CMP, cryoprotein, B12 681, CK 76, ferritin, C3, C4, proteinase 3, myeloperoxidase Ab, ANA, SSA, SSB, Sm, RNP, Scl70, Jo1, cANCA, pANCA, SPIE, FLC, HIV, Hep C Ab. A1c 5.5.  

Treatment trials:
1) For vascular component: Nifedipine caused swelling. Pentoxyfylline (Trental) 400 TID is helping with toe swelling. 
2) For neuropathic pain component: Duloxetine and pregabalin are helping a little. Side effects from low dose venlafaxine, gabapentin. Compound cream (ketamine and amitryptyline) didn't help. 
3) For immune process: On plaquenil 300 mg daily - unclear if helping. Prednisone 40 mg daily caused severe foot pain.

Questions:
- Have you treated patients like this?
- Any other ideas for workup? Genetic testing for small fiber neuropathy is pending. Genetic testing for genetic causes of chilblain is also pending (maybe her case isn't immune)
- Do you know how to order plexin antibody testing? 
- Any other ideas for treatment? We are going to try prednisone again at a lower dose of 10 mg daily.  

Thanks again. She is grateful for your input. 
 

Sarada

 

 

I finally have a clinical case question worthy of this community.  All the relevant details of the presentation are below. This was not an easy diagnosis. I had to reflect on it overnight to realize what it was because I'd never seen it before. If you want to skip ahead, the quesiton is at the bottom of this post. 

CLINICAL HISTORY
79 year old left handed male with PMH of prior carpal tunnel releases 2013 who began dropping things from both hands 2019 and suffered associated right neck shoulder pai. Epidural offered 2 days of pain relief. MRI 8/2021 revealed "multilevel severe DDD/spondylosis with extensive flowing anterior osteophytosis suggestive of DISH and mild abnormal cord signal at C5-6 suggesting an element of cord atrophy." His neurologist sent him to a spine surgeon who documented rt deltoid/biceps/triceps/grip and finger flexor weakness with right thena atrophy. For this reason 10/2021 he underwent C7-T1 and T2-3 lami and C5-T3 posterior fusion. 

The pain has resolved but he has noted winging of his scapula, inability to comb hair, elevate arm and use fingers rt>lt.

CLINICAL EXAM
On exam, his CTR incisions are strangely distal in the palm (?). He has an extensive cervical incisional line which is healed. Right grip, D3 DIP flexion, and bilateral D1/5 abduction are 4/5. Right D3 DIP flexion 3/5. Otherwise 5/5 bilateral humeral ext rotation, shrug, and elbow/wrist extension/flexion.

At rest the scapulae are nearly symmetric. With forward flexion more than abduction, there is medial deviation and prominence of the lower medial border/angle of the scapula. He is unable to get to 90 degrees with these due to weakness but this is correctable with assisted scapular depression by the examiner. NO pain reported with these motions. 

ELECTRODIAGNOSTIC FINDINGS
There were no borderline findings. SNAPs and CMAPs in ulnar nerves were normal. CMAPs bilat MEDIANs revealed prolonged onsets, mildly slowed NCVs, and normal left but severely diminished right amplitudes without significant drops in amplitude with proximal stimulations.  Meidan SNAPs also revealed prolonged latencies, slowed conduction velocities at the wrists, and normal left amplitudes but significant drop in amplitude when going from palm to wrist. 

NEE: Parapsinals were avoided due to recent incision. Fibs/PSWs in bilat FDI, rt EIP/Triceps (latter two had diminished recruitment). Otherwise NORMAL bilateral delboids, biceps, pronator teres. NORMAL left triceps, trapezius, Rhomboid Major, Infraspinatus. I did attempt needling the SERRATUS anterior but it was my first time doing so since residency. Whatever i needled was normal

ELECTRODIAGNOSTIC IMPRESSION:
This is an abnormal study. There is EDx evidence at this time of bilat rt>lt lower cervical (possibly C8) radiculopathy. There is EDx evidence at this time of bilat demyelinating sensorimotor median neuropathies at the wrists. 

CLINICAL IMPRESSION
IMPAIRED HAND STRENGTH/DEXTERITY: from an electrodiagnostic perspective, there appears to be a prominent bilateral C8 radiculopathy superimposed over bilateral median mononeuropathy which is compromising his hand function. The findings today do not support a plexus lesion of the C8 ramus, lower trunk, or medial cord. Pre-operatively, this was also evident. Hand therapy to improve strength and function are indicated while awaiting the results of neural regeneration/reinnervation.

LEFT SCAPULAR WINGING: clinically presents with compromised trapezius more than serratus or rhomboid involvement. Spinal accessory, suprascapular, and generally upper cervical roots (C5-6) and
upper plexus (C5/6 rami, upper trunk) appear unaffected on today’s electrodiagnostic testing. On inspection, the location of the extensive cervical spine scar suggests that there could be a compromised trapezius from direct incisional injury to the trapezius. This could certainly explain the winging and, after consideration for potential reattachment by the surgeon, should be addressed with scapular stabilizer strengthening in physical therapy. Despite this and the findings on physical exam, serratus anterior (long thoracic nerve) remains on the differential and could be further evaluated by bringing the patient back in for needle EMG of the serratus anterior muscle.

QUESTION FOR AANEM COMMUNITY
The surgeon reviewed the MRI and was able to confirm that there are about 2 inches of trapezial fascia and muscle that have retracted away from the spinous processes (per surgeon, this is a very small percentage of the incision). A reputable surgeon, he has done numerous laminectomies with extensive incisions and never faced this. I have never heard of this before. If anyone on the forum has, what did you do for them?

If not, the question is, 3 months out, would it be better to just start working on scapular stabilizaiton in therapy or would there be value in re-attaching the trapezial fibers. The downside to the latter is delay of rehabilitation while healing and subjecting him to potential complications of a second surgery.  

please don't be shy and thanks in advance