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.
Does anyone know of any issues with doing NCV studies on an extremity that has a Dexcom monitor? This came up for the first time today. The patient had it on the medial arm and I had planned to test that extremity, but held off.
As I approach retirement I find that I have about 45 years worth of Continuum issues. I hate to throw these away but haven't found a home for them. Does anyone have any ideas.
The Myositis International Health and Research Collaborative Alliance (MIHRA) is hosting a scientific seminar on Inclusion Body Myositis on March 26, 8-10 am CST, dedicated to both providers and patients. It is cost free.
A 76-year-old male with a remote history of a lumbar decompression at L5, presented to the Sports Medicine Clinic for a painless right foot drop that presented acutely November 2024. Of note, the patient also had a left-side foot drop with prolonged recovery after lumbar decompression in 2023. Exam on the right side demonstrated 4/5 dorsiflexion and big toe extension but 5/5 foot eversion and inversion.
A recent MRI of the lumbar spine still demonstrated bilateral right greater than left L5-S1 foraminal stenosis in the setting of grade 1 degenerative spondylolisthesis.
The NCS/EMG findings revealed the following abnormalities: decreased right superficial fibular sensory nerve amplitude, bilaterally decreased fibular CMAP amplitudes with slowed conduction velocity but no conduction block or focal slowing, and abnormal spontaneous activity with decreased recruitment only in the right tibialis anterior and extensor digitorum brevis. The other L4-S1 muscles were WNLs.
The spine surgeon is ready to do a decompression; however, these findings suggest a right fibular neuropathy at the knee level with ongoing denervation but no evidence of radiculopathy or tibial neuropathy.
I would appreciate your thoughts on this case to help guide management. I have never seen a painless fibular neuropathy predominately involving the deep branch at the knee.
What do you use to warm limbs. I have seen and read about heating lamps, heating pads, hydocollators, hair dryers. Are there any standards on this issue from AANEM?
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?
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!
Hello everyone! Thank you for taking the time to read this.
It seems that many practices want a NM neurologist to perform autonomic testing and muscle/nerve biopsies.
How would a neuromuscular practitioner/fellow obtain training in this if not offered by the fellowship in which they were/are trained? Also where can one be trained to do core needle muscle biopsies?
Baylor Scott and White Medical Center - Baylor College of Medicine (Temple) still has 1 Clinical Neurophysiology Fellowship position opening for 7/1/2025.
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......
When billing NCS/EMG and NMUS Limited study 76882, (performed on the same day), Medicare ( for Northeast region) is returning the bills as incomplete claim, as MODIFIERS were not used with 76882. They do not specify which Modifiers ( 59,? XU, ? RT...????) are missing.
Does anyone have any specific experience to advise which modifiers to use for Medicare when NCS/EMG is performed on the same day, (same limb) for example.
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:
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.
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.
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.
I would like the experts in the forum to weigh in on this issue. I would appreciate input to get help with my patient.
I recently had a patient who has clinically an UMN syndrome (PLS like). Onset of symptoms less than a year and evolving. Patient had EMG done by another neuromuscular provider, admittedly had technical difficulties, only limb muscles were tested. No craniobulbar or thoracic paraspinal muscles were tested. No LMN features on EMG (no PSW or fibs) or fasciculations. The patient was sent to me for a 2nd opinion. Since then (8 months), the patient has developed mild spastic/flaccid dysarthria. The whole picture is clinically confounded by a coiled basilar tip aneurysm, cerebellar stroke, C5 corpectomy and cervical fusion due to osteomyelitis of cervical vertebrae and epidural phlegmon 6 years ago.
I am trying to get NMUS to check for fasciculations. At my practice, the radiology department is the only one who is allowed to to NMUS. I am trying to get radiology to do NMUS of 5 muscles (see link below) which some of you are aware to see for fascics which I can use to clinically diagnose ALS. I am meeting some resistance by some who feel they can only use EDx proven fascics and not NMU proven fascics to get patient's enrolled in clinical trial and avail the diagnosis of ALS. Al Awaji criteria is applicable for EDx fascics and not shown for NMU fascics. I find it rather confusing to parse out the logic.
I would appreciate if the experts in the forum can weigh on this issue. Below are some links to articles, I had quoted.
How much does trying to normalize the temperature, to avoid slowing of conduction velocity and dista latencies, have an inpact on patient care? I do not think that cool (not extreme) skin temperature will create the characteristic abnormalities noted by demyelinating polyneuropathies with quite prolonged temporal dispersion and significant slowing of velocities. Trying to warm up extremities cause delay and dyscomfort on patients given the extra time spent on performing the studies. Has there been a study that address this issue?
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?
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?
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:
Is the absence of fibrillations at this stage consistent with a plexopathy, or should I consider an alternative explanation?
Could the lack of EMG activity be attributed to technical factors or perhaps a central nervous system contribution?
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.
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
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.
