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I recently attended the AANEM annual meeting. At one of the sessions they discussed rating scales for carpal tunnel syndrome. I was not aware of the specifics of the Bland scale, so did not ask this question at the session. I tend to see loss of an identifiable median sensory response before significant motor conduction changes. I tend not to consider it severe unless there are significant motor conduction changes, either significant prolonged motor distal latencies or a reduced amplitude of the motor action potential. I would appreciate any insite into my approach of not calling CTS severe based only on an absent median sensory response without significant motor changes.
Speaking as a technologist, after 30 years of doing NCS, it occurred to me that I have some questions as to the why of intensity and duration, and I’m looking for some expert insight regarding how you optimize stimulation parameters during nerve conduction studies. Specifically, I want to see how you balance current intensity (mA) against pulse duration (ms) to get a supramaximal response while avoiding unwanted volume conduction.
When you run into a technically challenging patient for a median motor study at the wrist—whether it's due to severe localized swelling, thick or calloused skin or tissue, or advanced neuropathy—which troubleshooting strategy do you find more reliable for keeping your response selective to the median nerve, for example?
Maintaining a strict 0.1 ms default pulse duration and ramping up the current intensity (mA).
Widening the pulse duration to 0.2 ms (or higher) while keeping the current intensity at a lower amplitude.
As a technologist, I'm trying to look at the science of what happens when we tweak these knobs. On one hand, a higher intensity physically pushes the electrical field deeper into the tissue volume, risking a direct stimulus spread to an adjacent nerve (like hitting the ulnar while trying to get the median CMAP, which completely alters the takeoff and morphology of the waveform).
On the other hand, lengthening the duration keeps the gate open longer and lowers the minimum current needed to fire a nerve over a longer period. My concern there is that the weaker current naturally bleeding into the surrounding tissue might suddenly have enough time to charge and trip those neighboring ulnar axons anyway.
In your practice and opinion, how do you weigh the physical spread of higher current against the lowered firing thresholds of a longer pulse window when trying to avoid costimulation? Additionally, how do you handle the trade-off with larger stimulus artifacts when choosing a wider duration?
Speaking with other techs, and pushing myself to perform even better studies, what is the best mental model or analogy you use to think about this dynamic? If you were explaining the i ntensity, duration, and volume conduction to a resident or fellow in the simplest, most practical terms, how would you frame it to help them become better at NCS?
Thanks in advance for your insight! I'm looking forward to insightful conversation on this topic :)
I am sure this is not the first time this question comes up and it won't be the last time.
33 yo female (very thin) hospitalized six months ago for unrelated illness ( brainstem meningeoma). She had to have PICC line placement through left arm. Allegedly, the needle hit some nerve in the mid medial arm. Now she came for nerve study for a small mass in the same area she had the needle. It is painful to touch. There is sometimes shooting pain down the medial elbow to the anterior medial forearm.
on exam, there is a small (2-3 mm approximately ) round subcutaneous mass, 10 cm proximal to the elbow crease and anterior to the mid axillary line. Tender with no Tinel's sign. Pinprick sensory is basically normal in this arm and forearm.
Suspected partial laceration of left medial antebrachial cutaneous nerve with neuroma formation.
Routine NCS/EMG done. Normal median, ulnar sensory motor studies. Normal needle EMG left UE muscles.
Here comes the question: left medial antebrachial sensory study. Conventional setup. Recording at 10cm distal to the elbow crease on the anterior medial forearm. Stimulation (stimulation "d" for distal to the mass) at 4cm proximal to the crease (14cm in total). This places the stimulation "d" distal to the mass of in question. Second stimulation (stimulation "p" for proximal to the mass) was done 8cm proximal to the stimulation "d".
There is 65% amplitude drop comparing proximal SNAP to distal SNAP respond. Is this normal temporal dispersion or partial conduction block? Considering the fact of 8 cm separation between the proximal and distal stimulations.
thank you. Perhaps, you will ask me to do a contral lateral comparison study. Why?
Anybody having difficulties getting regular EMG NEEDLES? According to my office manager they are back orders along with depmedrol and kenalog! Any help or advice is welcome. Thanks
Have any of you encountered physical therapists doing nerve conduction studies and EMG?
One of my neurosurgeon colleagues said PT's are reaching out to him to get his NCS/EMG business. I asked him if they were getting reimbursed for their studies and he said yes. I don't understand how they are allowed to perform these without the training neuromuscular neurologists and physiatrists have.
Is there a position statement that has been issued by the AANEM (or other societies) regarding the bundling of 76883 with EMG/NCS codes? I know there was some confusion with regards to this when the 76883 code first was introduced but our billing department informed me that the 76883 code is being regularly denied by commercial carriers in our area. I tried to look this up to no avail.
Controversy in paraspinal muscles needle EMG in cases of compressive radiculopathy exist. For example a patient with radicular neck pain and paresthesia radiating along the medial upper limb down to the ulnar side of the hand, with needle EMG neurogenic abnormality in more then two muscles innervated by C8 by different nerves, normal sensory conduction study of the ulnar and medial antebrachial nerve. In similar cases I believe that these NCS/NEMG findings, and inview of the clinical symptoms provides specific diagnosis of C8 radiculopathy. However, is there a need to perform paraspinal muscles NEMG as well?.
I believe that NEMG in similar cases only adds more pain, technical challenge in case of limited muscles relaxation and possibility of findings multiple levels or bilateral NEMG abnormality, especially in elederly patients. However, I greatly appreciate other electromyographers input and/or different view in this somewhat contrversial issue.
Hi everyone—Sandra & Shawn here! Following this fall's AANEM Meeting, we are excited to step into our roles as Co-Chairs of the AANEM Connect Committee.
We’re here to support this community and keep the conversation flowing. Whether you want to discuss an unusual EDX case, unpack a recent presentation or article, or ask for peer input on a clinical puzzle, this space is yours.
If you’ve mostly been reading without posting, consider this your official invitation to jump in! Questions on all topics/levels drive great discussion.
Please help us welcome our new Trainee Committee Members:
Dr. Meena Meyyappan
Dr. Fanny Marmol
Dr. Bao Nguyen
We encourage lively, collegial, and respectful discourse and conversation across all practice backgrounds. Check out the Rules of Engagement & Terms of Use for details.
The other committee members supporting this team include: Drs. Bassam, Dumitru, Katirji, Robinson, Stalberg, Malhotra, Sridhara & Chiodo.
I am just going to throw this out there. I do have a physician near by who performs EMGs, and reports are almost always read as: Abnormal study. Bilateral peroneal neuropathy. Can not exclude neuropathy. Can not exclude lumbosacral radiculopathy.
How would you address this ongoing inadequate studies?
I have a group of colorectal surgeons around me, and I’ve been getting referrals to evaluate patients for possible pudendal nerve disorders. Common issues include pelvic floor dysfunction, fecal incontinence, and constipation. They’ve specifically ask about pudendal nerve terminal motor latency (PNTML) testing. Needless to say, this was not part of my fellowship training :)
I’d like to help as much as I can, especially since there really isn’t anyone or academic place nearby who performs this testing. Do you have any good resources you’d recommend for learning the technique, interpretation, and appropriate clinical use of PNTML?
I retired in March with 2 functional EMG machines and have already donated one. I hung onto one machine thinking that I may be engaging in some limited EMG work but retirement has pulled me in a different direction. I have a fully functional TECA Synergy EMG unit with laptop and deluxe stimulator which I am willing to donate to a non-profit organization. Recipient pays for shipping. All inquires to jlubeck@lubeckneurology.com
Hi everyone. I am dual trained in neuromuscular medicine and movement disorders. I am thinking about proposing a workshop for AANEM 2027 on the use of botulinum toxin (BoNT) injections for neuromuscular disorders, particularly about spasticity and sialorrhea. I am hoping to introduce the different BoNT products used for these conditions, injection techniques, and other practical considerations. Current practice often involves referring patients with these problems, particularly those with motor neuron diseases, to PM&R or movement disorders specialists. I think learning spasticity injections could be relatively straightforward for practicing NM specialists, given their familiarity with anatomy.
I am posting this to get a sense of whether people would perceive this as a valuable skill to learn. I am also looking for 1–2 collaborators who are already performing these injections, as we could potentially work together on the workshop.
I have an odd case I would love the experts here on AANEM Connects help with. A 70 yo male patient presented initially with diagnosis of Notalgia Paresthetica over a year ago of which pruritus was the main complaint, and responded to steroid injection for quite a qhile (8+months). Then the pruritus returned with a vengence and more widespread including the extensor forearms. He was referred to me for possible brachioradial pruritus. Considering he had the pruritus also over the entire peri-scapular/ thoracic region and arms (more extensor surface) I was dubious of this diagnsosis.
Physical exam shows no significant weakness in upper limbs, relatievly normal sensory exam, normal reflexes.
Suprisingly EMG did show small amplitude PSW and Fibs in multiple muscles on both sides, most notable in biceps, triceps, brachioradialis, FDI bilaterally. I reviewed MRI of the cervical/thoracic spine which had been done just prior to seeing me and they were relatively benign.
Other things to note:
-70lb weight loss in last 6 months, but has been on wegovy during that time.
-Has complained of generalized mild weakness, but he attributed it to losing muscle mass with weight loss
-No new sensory complaints
Any ideas or other things you would check? Could this be a weird para-neoplastic presentation? Thank you in advance!
I would like to explore what is recommended, or is the best to say when nerve conduction study are normal or with low normal sensory action potentials amplitude in a patient with clinical symptoms consistent with small fiber sensory neuropthy?. Is it enough to say a normal NCS may not exclude small fibers sensory neuropathy, or should additional comments such as " additional diagnostic studies such as skin biopsy or QSART test are suggested", or saying a follow-up NCS is advised.
This is a sensitive issue when the patient is referred only for NCS, and additional recommendations may possibly place the referring physician at odds. I know there is no standared answer or specific guidelines for this common issue that the electromyographer deals with frequently, and would like to explore the expert opinion.
I would like to encourage commenting to Regulations.gov by September 14th regarding the new CMS cut. It is my understanding that Medicare will reimburse 50% of all codes but the highest valued code if billing E/M and a procedure on the same day. Provided you perform a one limb EMG and nerve conduction studies, it would be more costly to bill a lower level E/M code than not to biill an E/M code under the new regulations. This is essentially a 20% cut on all medicare reimbursement. For busy private practice electromyographers like myself, this $70,000+ cut will cause a severe strain on my practice. I can't imagine how to keep the doors open when private insurers follow suit like they did after the 66% cut to nerve conduction codes not too many years ago.
I'm curious as to the clinical and physiological significance of this large (1mV peak-to-peak) discharge seen in a woman in her 40s with clinical and neurophysiological evidence of bilateral ulnar neuropathies at the elbows with otherwise normal NCS and neurological examination. There were no signs to suggest a central or upper motor neuron component. She was fairly anxious during the study. This is her ulnar-ADM F wave study. Any suggestions on what this discharge represents?
As a more junior neuromuscular colleague (having completed fellowship in 2025), I would really appreciate some assistance from the wider neuromuscular community. I have a 68 year old patient who has clinical features of bilateral ulnar nerve compression: atrophy of ADM and FDI bilaterally, with sensory loss in the bilateral ulnar nerve distribution, not extending into the forearm. Her job involves a signficiant degree of manual labour. NCS bilaterally: unobtainable ulnar SNAPs (antidromic), low ampltiude ulnar motor responses at the ADM and FDI, with some temporal dispersion in the BE and AE responses. No conduction block or focal slowing across the elbow. Median motor responses and median F-responses normal. Median and radial SNAPs normal. EMG of FDI showed fibrillation potentials and chronic neurogenic change. FPL and EIP, triceps and deltoid were all normal. Ulnar innervated FDPs were clinically not weak and normal on EMG. MRI of her C-spine shows "Bilateral moderate to severe foraminal stenosis at C7/T1 and foraminal perineural cysts, dynamic impingement of the C8 roots is suspected". I asked for imaging of the right arm and the following is reported "possibility of cubital tunnel pathology should be considered as there is a prominent osteophyte arising along the medial aspect of the elbow joint, impinging with into the cubital tunnel and displacing the ulnar nerve. There is mild thickening of the ulnar nerve with increased signal seen along the course of the proximal ulnar nerve, extending up to the level of the flexor carpi ulnaris heads".
The surgeon is considering an ACDF, but I am wondering, based on the clinical and EMG findings, and now the MRI of the one arm, whether these findings can be explained by peripheral pathology alone (bearing in mind she has an almost identical presentation on the other side), or whether she may have a double crush syndrome. What more can I do to try and tease the two out? Any input would be much appreciated.
If you could recommend just one resource to someone about to start a Neuromuscular Medicine fellowship, what would it be? It could be a textbook, review book, article series, website, podcast, or any other resource that you found invaluable.
More importantly, why? Was there a particular “pearl” or concept that made you think, “I wish I had read this before fellowship”?
I’m hoping to build a list of high-yield resources for incoming fellows like myself, so I’d love to hear what made the biggest difference in your training and what you would recommend to the next generation.
Hello everyone, I would like your opinion on my approach to patients referred by gynecology for endometriosis. I have incorporated pudendal nerve sympathetic skin response (SSR) testing to demonstrate autonomic fiber dysfunction at the S2–S4 levels, and I use plantar SSR to detect autonomic fiber dysfunction at the T10–L1 levels. I perform tibial and pudendal nerve SSEPs; motor nerve conduction studies on the ilioinguinal, tibial, and peroneal nerves; and sensory nerve conduction studies on the sural and superficial peroneal cutaneous nerves. Regarding EMG, I assess the bilateral paraspinal muscles from T10 to L5 and their respective myotomes to confirm or rule out neuropathies involving the ilioinguinal, iliohypogastric, and obturator nerves. I have found radiculopathies in the majority of these patients that account for part of the pain; the high number of spinal abnormalities in young women has been striking, but I attribute the visceral pain, dysmenorrhea, and dyspareunia to these findings and correlate them with the SSR results, while using SSEPs to rule out or confirm pudendal nerve abnormalities. I have attached my protocol for your review. Thank you very much.
I was recently asked to do a follow up study for carpal tunnel syndrome. the patient had an electrodiagnostic study 16 months ago. she had been recieving injections since than with declining benefit. she had just recieved an injection 2 weeks before the my study. I proceeded with the electrodiagnostic study as she noted limited benefit from the injection and I was not aware of any research evaluating the effects of injections on electrodiagnostic results. Is anyone aware of any research that does look at the effects on electrodiagnostic studies from carpal tunnel injections?
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.
