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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 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 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?
EMG Talk is coming up next month and we'd love to hear about your lived experiences in EMG - but this time from outside the lab.
Please describe a time or an experience when you were away from work and saw or heard something that made you think of an EMG waveform.
The most interesting descriptions will be highlighted at EMG Talk at the AANEM meeting. You might be asked to come up and tell us about that time and even win a coveted EMG Talk hat!
As usual, extra points for creativity (we have a very creative AANEM membership!). Figures and A-V files are also welcome.
I am a PM&R Physician who performs EMG/NCS and am interested in how other practices/ institutions approach collaboration between physiatry and neuromuscular neurologists.
Occasionally I perform initial EDX studies referred by orthopedic/ NSGY/ or primary care providers that are technically adequate for the initial clinical question, but occasionally findings are unexpected or disproportionate to the patient's exam and/ or imaging findings. (for example, more extensive widespread denervation or atypical polyneuropathies).
In these situations, my pracice has been to document the findings, my differential diagnosis, and referral to neuromuscular specialist when I feel a broader neuromuscular evaluation and work up is warrented. However, there can be a quesiton of when the performing EDX physician should be referring to a neuromuscular physician who may ultimately want additional EDX testing (whether to extend study or repeat).
I am interested to hear how other institutions handle this scenario.
1. When initial EDX study is adequate for the original referral question but revealed unexpected or clinically discordant findings, do you order work up or refer to neuromuscular neuro in the case more extensive lab work or imaging is indicated?
2. Is there an established pathway or agreed upon criteria for these referrals?
3. What challenges are there with regard to billing/ reimbursement when neurology wants to repeat or extend the initial EDX study?
4. Any other docummentation, communication, or referral practices that help avoid unnecessary duplication of studies while still allowing for initial clinical evaluation and subsequent subspecialty evaluation with repeat EDX if indicated.
My goal is to foster good collaboration between specialists to make sure patient get appropriate level of care and in a timely maner. Looking forward to this discussion.
I have a very interesting patient that has been a conundrum for me in the interpretation. I would love to hear how the literati and gliterati of the EDX world would interpret this patient's study.
Patient is 47 year old who is an inpatient in the rehab center. He was referred for evaluation of qudriplegia, atrophy and to rule out possible critical illness neuiroapthy. He has extensive history initially presented with right sided weakness to a peripheral hospital and imaging revealed left intraprenchymal hge with subacute right caudate infarct along with multivessel stenosis and left anterior cerebral artery occlusion. He developed additional left sided weakness prompting referral to the academic hospital for work up of vasculitis. He had multiple areas of diffuse intracranial vasculopathy, bilateral anterior cerebrl artery occlusion and sever posterior circulation stenosis.. Further imaging revvealed new areas of diffusion restriction along with watershed area area restriction and chronic micro hges. Another imaging almost one month later after initail presentation revealed a new infarct in left cerbellar hemishpere in PICA distribution. Thoracic and cervical MRIs normal. Work up for treponema pallidum, HIV, Sjogren, double stranded DNA, ANA, ANCA, lupus, anicardiolipin, IgA, IgG, IgG, cryoglobulin, CSF immunoglobulin panel, CSF VDRL, paraneoplastic panel CSF PCR were all normal. Sed rate was increased at 83, with increased C reactive protein. CSF electrophoresis with positive for small alpha-1 globulin and beta globulin spikes. Brain biopsy negative for vasculitis. Hence had extensive studies. exam with left cortical thumb, right gaze preference, diffuse muscle atrophy in all areas, he is unable to answer questions about sensation and has no active ROM in the limbs. Rflexes generally 3/4 in uppers, 2/4 in patellar tendons and right Achilles and 3/4 in left Achilles. Babinski flexor. Glabellar and snout reflexes are present.
Sorry I could not get the tables into the format. Hence I am giving descriptive information. Sensory latencies were borderline prolonged but normal amplitudes. The CV in superficial peronel nerves were at 33 with latencies of 4.3. All of the CMAPs revealed temporal dispersion of more than 10ms, normal upper CV, borderline to slow CV in the LL in the range of 31 to 33, normal amplitudes of tibial and peroneal to TA but significantly small peroneal to EDB on right (0.1 mA) and 0.9mA on left. There was 40% drop of the CMAP across the fibular head on right when recording from TA. Left median F latency was 31.7 with H-reflexes obtainable, the left tibial F latency was 70.9 with presence of A waves. Blink reflex studies were normal. Upper limb temperature was 34 degree C and lower limb temperature was 29.5 degree C
The MUPs were obtained mostly by facilitation techniques generally with one or two units in most of the areas or no activity. Recruitment was very good in the medial hamstrings and gastroc on the right but none in the lateral hamstring, TFL, TA and single polyphasic units in PL. There were single polyphasic units in the left TA and EDB and none in the gastroc, VM and TFL. There were fibs and PSWs in the right peroneal muscles but none in other muscles. The recruitment in the right hand muscles was normal with normal units. FCR showed spasticity and normal units. There was reduced recruitment of MUPs in clavicular PM with signle unit pattern in the deltoid (facilitated).
Is this CIDP or other motor more than sensory demyelinative neuropathy because of temporal dispersion? Reflexes are brisk in the setting of multiple strokes as outlined. I could rule out CIP as there was no generlized axon loss process. Lack of albuminocytological dissociation may be against CIDP or AIDP. Could this be a outlier and be Castleman's disease but he does not have vasculitis with brain biopsy. Normal blink reflexes rules out possibility of brainstem pathology. Am I missing some diagnosis here. I would love the input from you all in this complex patient.
I'm not sure about other AANEM members, but for me it is not uncommon to need to commuicate to patients, at the end of the exam, that EDx studies are normal. I generally don't look forward to that discussion.
This can leave patients feeling frustrated and sometimes invalidated at the end of the visit and even though we don't say this, they can hear "there is nothing wrong with you - it's all in your head". They came seeking answers for their symptoms and don't have an answer at the end of testing. Sometimes an explanation, even if it's not actionable or has a great deal of certainty attached, can be helpful.
My current strategies, and I'd be interested to hear from others include:
Looking for musculoskeletal issues during the initial H&P. Particularly commenting to the patient upon finding muscle tenderness or other MSK findings so that I can loop back to that later in the discussion "Your nerves look good today, but I think it's your muscles that are causing pain"
Setting expectations at the start of the study. "We are good at detecting damage to the nerve fibers (axons) or their insulation (myelin) but generally are not able to detect nerve irritation that does not cause nerve damage."
Validating their symptoms and indicating I believe they are really feeling what they are.
Most of us know early on when the study will be normal. I often start discussing results when I'm about 80% done (and indicate we are not done yet - things could change), so the patient has time to process information mentally and ask questions and doesn't feel rushed all at the end of the study. "We are not quite done yet, but so far things are looking really good for your nerves..."
At the end I come back to the MSK findings and "nerve irritation" possibilities discussed earlier, and sometimes discuss central sensitization as a possibility.
I will reassure patients that we found nothing serious and that's good news.
Often for patients with chronic pain I give them a handout with links to Andrea Furlan's YouTube channel on chronic pain - she covers basic pain education, as well as both pharmacologic and non-pharmacologic treatments. https://www.youtube.com/@DrAndreaFurlan
I'd be interested to hear from others what strategies they use.
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 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 came across the above normative values (see hyperlink above) and appreciate the new acceptable CV drop for the Ulnar nerve across the elbow as at least 15m/s or 23% drop in CV. This was introduced in the Spring meeting.
However,
Is the absolute value of less than 43m/s across the elbow significant as quoted in the normative value chart ? Even if there is no significant drop in CV in comparision to below / above the elbow (i.e. a drop of less that 15m/s) ?
A very large patient was referred to the lab and when he sat on the EMG table it creaked. This led us to wonder about weight limits of the tables we use in our EDX lab locations. Seems like many stanfard medical tables have a 400 pound "limit." We have researched this and there are baraiatric tables with weight limits up to 600 pounds. Is there any standard on this from AANEM? I would be curious to know if anyone else has had any issues with this or if there have been any problems. Does anyone have disclaimers about weight limits on medical exam tables, similar to what is done with MRIs? Thanks.
Will individuals with a history of Guillain Barre syndrome demonstrate abnormalities on nerve conduction studies years after the acute involvement? Can individuals with a history of Guillain Barre syndrome develope new or return of weakness years after the acute involvement after reporting a full recovery?
Wanted to hear suggestions about warming cool limbs for NCS. Recently switched from a practice adjacent to PT that we had borrowed hydrocollator warming pads as needed when limb temp was low. Any good suggestions for heating lamps or other effective methods to assist during these cool months?
Did a case of a 68yom with vague acute forearm pain from shovelling snow perhaps. EMG showed distal median motor latency of 3.6 msec, and amp of 10.3 mv, the proximal stim showed amp of 4.6 mv, velocity 52 m/s, and I repeated it a couple times. Median transcarpal was normal. Ulnar studies were normal. EMG showed spontaneous activty in the Opponens Pol, the PQ, and the FPL. Pronator Teres and all other upper limb muscles were normal. Thus a proximal median neuropathy (pronator syndrome) was suspected.
But I also wondered what would the median waveforms would look like with the MGA? I stimulated the ulnar nerve at the wrist and recorded at the ADM a CMAP of 4.6 mv. I did not do the needle EMG until after the NCVs, thus I was surprised to see any spontaneous activity as shown because his clinical presentation was more consistent with lateral epicondylitis, not pronator syndrome. Maybe any anomolus anatomy is nothing of concern....
I have noticed increasing use of MRI for evaluation of muscle weakness by my colleagues including often myself.
As a neurophysiologist, I can appreciate the information on EMG that is not appreciable on MRI, however I am keen to know what others thoughts are re what future for EMG would look like if whole body muscle MRI is easily available to look for pattern of denervation/myopathy.
Also, does anyone have any suggestions re: uptodate re: interpreting muscle MRI's and its limitations.
Hello everyone. Over the years I have examined a number of patients who present with signs and symptoms of ulnar neuropathy, but when doing their sensory examination they report abnormal sensation on the lateral half of the ring finger instead of the medial half. Many report that the medial half feels normal but the pinky finger and the lateral side of the ring finger have reduced or altered sensation. I am wondering if anyone else has observed this and if there is a good explanation for it? (some may have had coexisting CTS of course but not all of them did). Thanks!
"Nerve conduction codes 95907-95913 had their Physician Supervision of Diagnostic Procedures Indicators adjusted to 7A effective 01/01/2013 (CR 8169). Please refer to the description of 7A below. Therefore if authorized by state law Physical Therapists are allowed the technical portion and professional component of the test.
The technical component (TC) of the Neuromuscular junction testing code 95937 had its Physician Supervision of Diagnostic Procedures Indicator changed to “7A” This change is effective January 1, 2013.
“7A” = “Supervision standards for level 77 apply; in addition, the PT with ABPTS certification may personally supervise another PT, but only the PT with ABPTS certification may bill.”
“77” = “Procedure must be performed by a PT with ABPTS certification (TC & PC) or by a PT without certification under direct supervision of a physician (TC only; PC always physician)”. These changes are effective January 1, 2013."
Unfortunately I'm not able to find anything else from CMS about supervision for nerve conduction studies. And the above seems to be some sort of tangent about physical therapists doing EMG/NCS. Does anyone know of anywhere else that I can find information from CMS which clearly outlines that a nerve conduction tech may perform the NCS with supervision (I believe the proper term is "direct supervision" which would mean I'd be in the office and available though not necessarily in the exam room)?
Hi, I have a few cases in which the EMG and NC is c/w axonal Neuropathy, but I or a different MD already have sent the ganglioside antibody panel. I have repeated the panel to make sure is not a lab error. I have a few patients testing positive for GQ1b, and GD1A antibodies, both with sensory and motor axonal neuropathies, some of them progressive in symptoms and sign,s which you would like to consider as Autoimmune Neuropathies that could benefit from IVIG or other treatments; yet is difficult to get them approved since they are not the typical CIDP. Although the literature mentions cases of axonal CIDP, or rare chronic cases of Miller Fisher Syndrome, I am not entirely sure what to do with those patients, since, yes, I would like at least a 6-month trial of IVIG to see if there is response or not. In same group of patients, there are some patient s with absent sensory and motor responses and the feet ( no surals, peroneal sensory, plantar and no peroneal or tibial CMAPS) with normal or reduced peroneal response at the TA but no significant active denervation in the leg which you would think are most likely related to proximal demyelination, but yet cannnot oficiallly call the EMG as CIDP. Have you encountered similar cases, and what would you advise? Thanks.
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.
