AANEM Connect

One of the techs here posed a question regarding the MAC and median mixed sensory nerve.

Years ago, I *think* I remember someone (maybe Dr. Dumitru?) at a maybe(?) AANEM meeting mention that  when testing the MAC that it is possible to record the median mixed sensory instead.  Is that correct? If yes, how do you avoid recording from the median mixed sensory when stimulating the MAC?

Can someone answer that one for me?

Any recommendation to use relate for EMG boards

di they have any Board review courses for EMG board 

Hello!

My name is Christine Gou, and I’m currently a third-year Physiatry resident at Washington University School of Medicine. I’m applying for Neuromuscular Medicine fellowships this cycle and would love the opportunity to connect with individuals in this field to gain a deeper understanding of what a career in Neuromuscular Physiatry could look like. You can reach me at cgou@wustl.edu. Thank you in advance for your time and guidance!

Best regards,
Christine Gou

Attn Neurology Residents and Program Directors:

Baylor Scott and White Medical Center - Baylor College of Medicine (Temple) still has 1 Clinical Neurophysiology Fellowship position opening for 7/1/2025.

Contact:

Tina.Miller@BSWHealth.org (Program Coordinator) or

Seyed.Jalali@BSWHealth.org (Program Director)

Neurology Residency – Temple, TX | BSWHealth.med

Hello, 

Soon I will be tasked with setting up a new EMG lab at a satellite hospital. I've been thinking about choice of location of the lab in the new hospital and have been wondering about electrical interference. 

Is there a way to measure/predict if this will be a problem? That is, short of setting up the EMG machine and using it in the new location? 

I know folks are familiar with this problem in ICU settings, but once or twice I've run across the problem during inpatient studies, and have concluded the interference must have come from a room above or below where I was located......

What are the upper limits of a patient's blood pressure, if any, beyond which you would consider it unsafe to perform an EMG/NCS ?

I got trained in analogue era on oscilloscope and am very comfortable in qualitative EMG in motor unit analysis including interference pattern with 10-10k filter and monopolar needle for patient comfort and compliance. Time base 10 ms/div, gain 100 uv/div for spontaneous activity and 500 uv to 1 mv for MUP and IP analysis. Do I need to go into quantitative mode of turn-amplitude analysis also- am I missing too much in my understanding. My training by my Guru is unless and until I am good in quality- quantity is irrelevant - Om Peace. Dr Hans Raj

Hi all- I occasionally get requests from my movement disorders colleagues for EMG/NCS for tremor or myoclonus. I have done a cursory review of the literature and tried to help. Seems like I can help with hertz measurement, etc. They seem to use mostly surface electrode EMG.  I have more recent requests that are a bit more advanced. Does anyone feel really good about neurophys techniques in movement disorders? How do you bill for surface EMG? I would be interested in a lecture on this at the AANEM from any experts. 

Below is an article that I was sent to see if we can do at our lab: 

https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mdc3.14306

Thanks, !

Thy 

Hi all,

I have had two cases recently which I would love the group's thoughts on. Both patient's had an atraumatic onset of severe pain through the shoulder/scapular/lateral arm region. This involved some sensory symptoms and weakness. The pain was so severe to keep them awake for a few days. They both then developed significant atrophy through C5 myotomes in the coming months with scapula winging. 

I saw them month approx 5 months post event. The NCS demonstrated recordable lateral cutaneous nerve responses, both within allowable symemtry of the contralateral side. The remainder of the NCS were normal (sensory/motor studies of median, ulnar, radial, antebrachial bilaterally). 

The EMG demonstrated involvement of seemingly fairly isolated C5 muscles (Rhomboids, supraspin, infraspin, deltoid, biceps with sparing of brachioradialis, triceps, EDC, FDI, serratus anterior) with both spontaneous neurogenic changes and neurogenic units with reduced recruitment. 

The MRI Cx spines for these patients demonstrated a mild, and a moderate (respectively) C5 formainal stenosis without nerve impingement. 

The MRI plexus was normal (but this was a delayed scan post my assessment, so approx 5-6 months post event)

My questions for the group

1) Historically, involvement of Rhomboids was used to demonstrate pre-plexus localisation. There have been a number of case reports in recent times, with people documenting involvement in later diagnosed plexopathies. How many people would still use Rhomboid involvement as evidence of pre-plexus localisation? 

2) Severe onset, atraumatic pain keeping patients awake with then progressive atrophy is not restricted to Brachial Plexopathies, but would make one think this, rather than a Radiculoapthy. These two patients have a very C5 isolated picture, Rhomboid involvement, seemingly spared peripheral nerves (including LABC), with mild and moderate formainal stenosis. Acknolwedging that you would be trusting my  ncs skills/report, who would lean towards a radiculopathy and who towards a C5/very early upper plexoapthy. 

Thank you all

I intend to retire next year. I will see patients through March, then use the next 3 months to get rid of office equipment, computers, printers, one functional Natus EMG machine, examination tables, electrodes, needles,computers, pictures, books, all of it. I am willing to give any, and preferably all of this away after March. After 41 years of a primarily EMG practice, you accumulate a lot of stuff. All I ask is that the recipient arrange for packaging and transport. I can be contacted at jad1715@mac.com. 

To All,

I am wondering if anyone has and would be willing to share any needle EMG recordings in a patient (s) with hyperkalemic periodic paralysis (or paramyotonia) showing the so called florid "fibrillation" potentials that can occur with a reduction in temperature as the recording transistions from myotonic discharges to the noted fibrillation potentials, or both waveforms occurring simultaneously.  I am working on a project attempting to correlate the intracellular action potentials with the extracellularly recorded waveforms in these patients.  You can contact me off this forum through my email at the aanem directory.

Thank you for your kind attention

Dan Dumitru

Dear Colleagues

We have a question and would like help from Connect readers and Prof. Dumitru.

In a neuroconduction examination of the lower limb, we did not record compound muscle action potentials in the posterior tibial nerve and in the deep peroneal nerve when captured in the extensor digitorum brevis muscle, but in the latter, when we stimulated the medial malleolus, we obtained a response.

The question is: Was the answer obtained due to the presence of the accessory peroneal nerve or the posterior tibial nerve? Or another explanation? 

Thanking you for your time and help.

Hello

Has anyone experienced infraorbital and inferior alveolar nerve injuries after plastic surgery?

Do you have any recommendations for reading about how to conduct nerve conduction studies and needle EMGs?

Thank you

For many years, I have used the Kendall Nutab (ER88007) electrode for my EMGs.  It's a disposable, inexpensive, reliable, 14 mm round electrode that attaches with an alligator clip, similar in dimension to the standard bar electodes we all trained on.  The manufacturer has discontinued these, and has recommended a replacement electrode that is a18mm x 22mm, rectangle.  I typically measure from the center of the electrode to my stimulation site, not the near edge of the electrode.  

Does anyone know of a similar small round disposable electrode?

Does anyone know if measuring from the center of the larger electrode will make a difference in the recorded latencies and or the morphology of the waveforms?

Thanks for any input.

Case Presentation:
I am presenting the case of a 44-year-old male who sustained an anterior shoulder luxation while playing football. After reduction by an orthopedist, he developed noticeable deficits in shoulder and arm strength, as well as paresthesias in the hand.

Clinical Findings:

• Motor Deficits: Weakness in arm flexion, shoulder abduction, wrist extension, abductor pollicis brevis (APB), and abductor digiti minimi (ADM).
• Sensory Deficits: Diminished sensation in the distribution of the radial, third digit, and fifth digit nerves.

NCS Findings:

• Slightly reduced amplitude in APB.
• Markedly reduced amplitude in ADM.
• Reduced sensory responses in digit 3, radial nerve, and digit 5—more pronounced in radial and digit 5.

EMG Findings (15 Days Post-Injury):
This is where I encountered a puzzling observation:

• Muscles Examined: Deltoid, biceps, wrist extensors, APB, first dorsal interosseous (FDI), long supinator, and ADM.
• Findings: No fibrillations or spontaneous activity were observed.
• Recruitment Activity: Absent in all muscles except the biceps, where limited activity was present.

Given the deficits and the NCS findings, I initially suspected a brachial plexopathy, likely affecting the upper trunk. However, the absence of fibrillations 15 days post-injury raises questions, as one would typically expect early signs of denervation by this time.     

My Questions:

1. Is the absence of fibrillations at this stage consistent with a plexopathy, or should I consider an alternative explanation?
2. Could the lack of EMG activity be attributed to technical factors or perhaps a central nervous system contribution?
3. Would you recommend any additional studies (e.g., imaging, repeat EMG at a later time) to clarify the diagnosis?

I appreciate any insights or similar experiences the community can share, as I aim to better understand the underlying mechanisms in this case.

Thank you

Seen a lady with mild diabetes
2 months back
Perineal area pain.No fever,skin rash
Followed by asymmetrical sensory involvement
Left more than right of lower limbs of acute onset
She is a known case of post polio residual paralysis
No increase of motor deficit
MRI spine and brain is normal it is a contrast MRI
NCV sensory normal
Bilateral Sural snaps are normal
Considering acute sensory Lumbo sacral radiculitis
What can be the possibly etiolgies please guide

Good afternoon,

I'm interested in hearing others' thoughts on this case I have.

25yoM with severe back injury while lifting a heavy object in August but with worsening weakness and clumsiness in his legs thereafter. Exam with preserved reflexes except absent achilles and reduced patellars. 2/5 ankle dorsiflexion, otherwise 4- great toe extension 4+ knee flexion and 5s elsewhere. Romberg with step off and decreased proprioception in toes and patchy temp/LT loss in legs. Normal MRI L-spine x2. I did an EMG/NCS 1 month after injury and found (abnormals bolded):

LUE:

- Median digit 2 SNAP latency 3.9 amplitude 5.2, motor distal latency 5.2, amplitude 8.1

- Ulnar digit 5 SNAP latency 3.9, amplitude 4.6, motor CV 24 across elbow, amplitude 11.6 distally

- Radial SNAP latency 2.6, amplitude 11.6

LLE:

- Sural latency 4.7, amplitude 4.4

- Superficial peroneal latency 3.8, amplitude 6.3

- Peroneal - EDB distal latency 8.0, amplitude 2.6, distal segment CV 34, across fibular head 42

- Tibial AH distal latency 6.7, amplitude 2.8

RLE

- Sural peak latency 5.3, amplitude 5.9

- R superficial peroneal latency 4.2, amplitude 6.6

- R peroneal - EDB latency 7.3, amplitude 1.2, distal segment CV 37, across fibular head 46

- R tibial - AH latency 7.5, ampliotude 1.9, NR at popliteal fossa

I (regretably but due to time constraints did not do any F-waves or H-reflex)

EMG

- L FCR 1+ fibs/positives, 1+ amplitude

- L APB 1+ fibs/positives

- L tib ant 2+ fibs/positive, 2+ amplitude/duration, reduced recruitmet

- L gastroc medial head 2+ fibs/positives, 1+ amplitude/duration

- R tib and 2+ fibs/positives, 1+ amp/duration

- R gastroc medial 2+ fibs/positives, 1+ amp/duration

- Normal: L delt, L biceps, L triceps, L FDI, L vastus, L EIP, R vastus, R lumbar paraspinals

At this point I was concered about a mixed polyneuropathy but also noted the severe ulnar at the elbow and median at the wrist (FCR spontaneous noted...) and sent genetics for HNPP. No M-spike, B12 238 (started supplementation), TSH >16 (started thyroid replacement), A1c 5%.

He deteriorated and became wheelchair bound with 2/5 dorsiflexion, inversion/eversion, and some scattered weakness elsewhere. Reflexes went away even in the uppers. I did an LP and whites were 9 with protein 150-170. Admitted for IVIG 2g/kg. Second outpatient IVIG 1g/kg reflexes returned but strength remained the same, L leg slightly worsening (dorsiflexion/inversion/eversion 1/5).

Genetics returned HNPP positive for heterozygous PMP22 deletion.

So now here I am left with a variety of questions, and I'm wondering the thoughts of the community. Does he have CIDP? There are some arguments for this, but it isn't clean. Could this be a nodopathy justifying Ritux? I'm gearing up to send for the antibodies but haven't pulled the trigger yet. Could this all be HNPP? It seems unlikely, but so is HNPP + an acquired mixed polyneuropathy. It's almost as if the arms look like HNPP and the legs look like an acquired polyneuropathy (maybe DADS-I looking at L peroneal EDB and R sural, but I can't ignore the axon loss).

I will also repeat the EMG after his next dose of IVIG.

Thanks for any thoughts on this complex case!

Currently two of our emg labs reside in multi-disciplinary outpatient buildings considered non facility. My employer is looking to change this to facility based. We use technologists for nerve conductions but they are directly supervised. Do you know what, if any, impact this will have on the physicians working in our labs from a wrvu standpoint or where I might find this information? Currently the ambulatory physicians receive the wrvu for the ncv and the emg. 

A patient is asking me to prescribe topical testosterone for inclusion body myositis. Is there evidence behind this? Do you prescribe this? Why or why not?

Looking for someone who does Botox injection into piriformis muscle (ultrasound guided or not). Need to refer a patient. I am practicing in Virginia, but patient is willing to travel.  Thanks.

39 year old man came in a few days ago for history of weakness in all four extremities worse in the left leg proximally. He has a long history of months of being bed bound in hospitals after undergoing many GI procedures/sugeries with many complications requiring more surgeries ICU admissions for months and rehab inpatient for months with little resolution. He has pain, sensory deficits and weakness in limbs. The clinical picture and exam suggested critical care neuropathy. EMG showed no response to stimulation of any of the motor nerves in the legs (no response at all). Interestingly, all the muscles tested (seven in each leg) showed no spontaneous activity whatsoever. There is decreased recruitment in all muscles but normal motor units and a few polyphasic ones. No PW or fibs or fascs! The study was limited to the legs. Can I make this a demyelinating type of neuropathy? Would he be a candidate for IVIg? I may bring him back for upper extremities study. Thoughts?

Hey all,

Im not sure if this is the right forum for this question, but I figured I'd give it a shot.

I did an EMG on a young patient with a clinical history of left UNE, and the nerve studies confirmed that localization. I proceeded to a root screen with the needle to evaluate for additional radiculopathy, and all muscles were normal except for one finding. When I inserted the needle in the left biceps at rest, I saw/heard what looked like a fib firing quite regularly at around 1 hz. There was some subtle variability to it, and it remained as I moved the needle around to sample different regions. 

He was wearing a zio patch, and while I didn't think this device put out any signal (just read), I put my finger on his radial pulse and the "fib" seemed to follow his pulse. 

The above led me to consider that maybe this could somehow be a zio-patch related artifact. Has anyone seen this?

I think a true fib is less likely because of the subtle variability (not just linear slowing or speeding up) and the fact that it continued as I moved the needle around.

I think a volitional motor unit is less likely because of the morphology and firing speed.

Thank you for any thoughts!

I have a peculiar case on which i would like to have sought some advice. 

30y old male, electrician with no medical Hx. with since 3 weeks abducted little finger on the right side. Unable to bring the finger in adduction. No paresthesia, no other loss of strength. Doesn't remember a trauma or pain. 

 Clinical examination shows preserved reflexes, strength (FDI / ADM / FPL / FCU / FDP5 / Orther interossei), esthesia. Tests for UNE are negative  No UMN signs. 

Needle Emg: no denervation potentials in FCU / FDI / ADM / APB / EIP/ 3rd palmaf IO, decreased recruitment in 3rd palmar IO with two rapid firing MUAPs  

Ultrasound: normal configuration ulnar nerve from the axilla down to just distal of the pisohamate lig. Further course could not be evaluated but no ganglion cyste or other masses in the palm. Impression of possible myotendinous injury 3rd palmar IO on US but this is not my expertise so MRI is planned.

I had 2 questions about this case:

- Could you have a selective neuroraxia of the branch to the 3rd palmar explaining the clinical image a d findings on EMG? Patient reported repitive use of clipper the day he noticed the paresis  

-What would your findings be on needle emg after of musculotendinous / muscular injury? I've searched pubmed but can't find any literature on this. I think this woud give a dcreased recruitment but would this also influence firing rate?