AANEM Connect

Esteemed (and much smarter than me) colleagues,

I was recently asked the following question by an AANEM member:

"Another scenario I have encountered is a relative amplitude drop from side to side of Ulnar sensory at the wrist in the presence of normal ulnar motor studies."

For this scenario (especially when needle EMG and MAC are unremarkable), i have a templated bit of text that i have been using and thought i'd run it by you folks:

In the absence of any motor conduction or needle electromyographic abnormalities, the isolated finding of relatively decreased ulnar sensory response is of unclear significance and could be attributed to:

• Ulnar sensory only neuropathy
• Old axonal injury with motor recovery (via collateral sprouting) along the course of its pathway (C8 ramus, lower trunk, medial cord, or ulnar nerve).
• Technical issue (although the test was repeated and all electrodes repositioned during testing today).

What do you think? Any problems on your end with that? 
 

Hello everyone.

A 34 yo woman was reffered to emg lab.

During puerperium she had a diagnosis of iliac vein thrombosis.
She had right leg edema, a little pain and weakness on the limb
She complainned about hyperstesia on the foot and distal third of the leg

now, about 3 months after diagnosis and symptom presentation she came to emg lab
she had suspended anticoaglutaion for the needle exam in the past 24h

- ncs:
motor, right deep peroneal: reduced amplitude
tibial nerve h reflex: absent in the right
sensory, superficial peroneal nerves normal and symetric
sensory, sural: on the right (symptomatic side) = 23 mcv  / on the left side = 44 mcv

i repeated ncs in the next day. same results

- emg:
at rest: a lot of spontaneos activity in gluteus medius,  tibialis anterior, tibialis posterior, peroneus longus
contraction: chronic neurogenic pattern in  tibialis anterior, tibialis posterior, peroneus longus

She had a normal lombossacral spine MRI.

I fisished my report suggesting lombossacral plexopathy (right sural 48% lower), thought could not eliminate pré-ganglionar etiology for sure.

I would like to hear critics and ideias about the case, and wonder if anyone has had any case similar.
thank you

 

Dear Neuromuscular Specialist,
 
 
We would like you to participate in a brief, 9-question survey research study about your use treatment approach in generalized myasthenia gravis (gMG). These survey results will be analyzed and published to inform the neuromuscular community about current practice patterns in gMG.  Please see the attached letter and link to the REDCap survey (https://redcap.vcu.edu/surveys/?s=DYYJYHLHMEFWA373) Your participation in voluntary and would require between 2-5 minutes. We will analyze the survey results and disseminate this information as a publication. If you have any questions at all, please do not hesitate to contact me.
 
 
Thank you for this consideration,

Kelly G. Gwathmey, MD
Neuromuscular Division Chair
Department of Neurology
Virginia Commonwealth University
Kelly.gwathmey@vcuhealth.org

As we prepare for EMG Talk next month, we'd love to hear of proposed EMG impressions as poems, limerics, or haiku.  There may be a prize the for best one (e.g. a EMG Talk Hat).

An example (which is admittedly not very good) to get you started

His only weak muscle is the trap
Bladder's good and he can take a c- -p
His issue is with accessory spinal
So I think this report is final.

I know many out there can do much, much better - please suggest some alternatives.
See you all next month!

is there a need to place a magnet over an ICD while performing nerve conduction studies? I have never done this before, but recently was asked to apply a magnet over the ICD while performing nerve conduction studies.

I am on this year's taskforce to increase physiatry involvement in AANEM. A colleague commented on Muscle & Nerve being a place where we can improve attractiveness or relevance to us physiatrists.

So the question is, if you had a magic wand, what would you want the Muscle & Nerve Journal articles to address? 
 

I am looking for Semiars for IONM billing. I can't find anything, we need this included in the annual conferences..... this is a rare type of billing and needs someone to lead the way... I have been doing it for 20 plus years but still can't find any type of education to help with new things or knowing what all you can bill for etc...,.

Congratulations Dr. Dumitru on Lifetime Achievement award! 

Our questions:
Is this the correct diagnosis?
Should we simply treat her with whatever rheumatology suggests (steroids plus steroid sparing agent of thier choice) or should we continue maintenance IVIg in addition to this?


62 year old woman with 6 weeks of progressive distal painful paresthesias and weakness. 
Seven weeks prior - myalgias, no weakness, ?viral illness?. No further musculoskeletal pain after this week.  
Six weeks prior - painful paresthesias in both hands and both feet. 
4-5 weeks prior - noticed progressive weakness - fell when "ankle collapsed" 
 
Exam with significant distal and proximal weakness with some distal wasting.
Absent reflexes except knees 1+.  (Exam from another MD noted present reflexes 5 days prior.)
Sensation: Stocking (to ankle) - glove (to above wrists) - LT, PP.
Decreased vibration ulnar styloid, B and medial malleolus, B.
Proprioception impaired at MP bilaterally and ankle bilaterally. 

EMG/NCS
Motor NCS - no responses - Median (APB), Ulnar (ADM), Tibial (AH), Peroneal (EDB).
Peroneal (TA) - low amplitude, no slowing of CV, no temporal dispersion, no conduction block.
Sensory NCS - no responses - Median (DIII), Ulnar (DV), Superficial peroneal and sural. 
Signs of denervation in multiple muscles with few MUPS with normal configuration, increased recruitment ratio, discrete interference patttern at full effort.

CSF
Protein - 28
Glucose normal
WBC - 4 -
52%Neutrophils
22%Lymphocytes
26%Eosinophils
RBC - 11

Awaiting VEGF results

P-ANCA 1:320
MPO (myeloperoxidase) 23.8 weakly positive (drawn after IVIg was given)
CT sinuses -  extensive paranasal sinusitis with with areas 
of hyperattenuation favored to represent inspissated secretions.
No rash
CT chest - 6 mm left apical nodule; no parenchymal abnormalities. 
CT abd/pelvis - no abnormalities.
EKG - normal
ECHO - no abnormalities
No symptoms of asthma
Peripheral eosinophil - 37%; absolute 4.7 K/uL
 

Rheumatology - given her clinical and laboratory data, they had high suspicion for eosinophilic granulomatosis with polyangiitis (EGPA - the old Churg-Strauss).  They started treating with pulse methylprednisolone 1000 mg IV daily for 3 days and now on oral steroids daily.
We gave IVIg a week prior but no response as of yet. 
 

MRI spine and brain without and with gado - no abnormalities.

Patient with some mild improvement of symptoms on steroid, noted as return of some reflexes ( 1+ Brachioradial, Biceps bilaterally and 2+ patellar bilaterally).

The rheumatologists wanted to do sural nerve biopsy and I asked them about other sites for biopsy and they said there was nowhere else to biopsy.
Sural Nerve Biopsy showed no evidence of vasculitis. Showed severe, subacute (ongoing) axonal degeneration, in the background of moderately severe axonal loss.. 

Official report summary as follows: 
This biopsy reveals severe, subacute (ongoing) axonal degeneration, in the background of moderately severe axonal loss. Numerous foct of fiber breakdown associated with phagocytotic macrophages are displayed in cross-sections. By the semi-quantitative teasing fiber analysis, 62% of the remaining fibers show active Wallerian degeneration. The demyelinating componentis displayed amongst 12% of the teased fibers in the forms of segmental demyelination/ remyelination and is thought to be indistinguishable from age-related changes. Multiple levels of sections have been investigated for possible vasculitis: this biopsied segment of the nerve shows no histological features of vasculitis.
 

Other work up: 

-B12, Mg and TSH wnl

-ESR/CRP moderately elevated

-Zn, Cu levels normal

-RPR negative

-strongllodes, toxocara, tryptase- WNL,

- Hepatitis panel negative

 

THANK YOU!!
 

Hi everyone,
I saw a 43 y/o woman with right neck and shoulder atrophy after surgical excision of a upper cervical mass in June 2021.  Needle evaluation shows decreased insertional activity and no recruitment of motor units in the trapezius and SCM, except for two MUAPs seen in the upper trapezius.  No abnormal spontaneous activity was seen.  Other scapular muscles were normal.  Ultrasound evaluation confirms marked atrophy and hyperechoic texture changes localized to these muscles.  Presentation seems consistent with near complete loss of spinal accessory nerve function.

Is this a diagnosis that may benefit from peripheral nerve surgery?  If so, are there any centers that can evaluate for this.  Location is Spokane but I'd imagine this patient would be willing to travel.  

Hi; 
I'm asking if you found during your practice any peripheral neuropathies associated with the sickle cell disease (heterozygous variant)

With kind regards

Hi; 
I'm asking if you found during your practice any peripheral neuropathies associated with the sickle cel disease (heterozygous variant)

With kind regards

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?

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