AANEM Connect

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.  

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. 

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 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! 

See NCS chart below

 

https://www.aanem.org/docs/default-source/documents/aanem/news/thumbnails/ndtf-chart-final

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....

Hi all,

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.

Thank you,

Gaurav Singh

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!

Hello All,

I'm interested in having some of our EEG techs at our institution learn to do nerve conduction studies.  A roadblock occurred when our billing department found the following article at cms.gov (https://www.cms.gov/medicare-coverage-database/view/article.aspx?articleId=57668&ver=44) which states:

"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)?

Thanks in advance!

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. 

Lately about half a dozen patients have declined needle EMG in the upper limb side in which a mastectomy had been performed; all them said that they'd been told not to have needle insertions in that limb. 

Would appreciate thoughts and/or references to studies / practice guidelines about this issue. 

Thanks to all.

Greetings,

Has anyone encountered billing issues in the following scenario?

A patient is referred to our office strictly for an EMG study, with no evaluation and management (E/M) service performed at that time. Days to weeks later, the referring physician sends the same patient back for a full neurology consultation.

Despite the fact that we have never provided a clinical consult before and the prior encounter was EMG-only, the insurance processes the visit as a follow-up rather than a new patient visit. The insurances does not allow new patient code to be used 99203-05, I am curious how others are handling this—whether there is specific documentation, coding, or payer-specific guidance that has helped ensure the subsequent neurology visit is recognized and reimbursed appropriately as a new patient encounter.

Thank you in advance for any insight.

Autonomic disorders often go unrecognized and under-diagnosed and many clinicians struggle with the treatments of these often-complex diseases.  Most training programs do not have dedicated autonomic disorders specialists at their centers.

There is a Google form to fill out if you'd like a lecture to be arranged.  These lectures are typically done virtually. Arrangements can be made for in-person speakers, if that is preferred (the program has no funding for speaker travel).

https://docs.google.com/forms/d/1DPAzynWuQ_E_RbQwZUBXyeU6vBBGfIicgv2qdlNf1gs/viewform?edit_requested=true

Our lecturers span a variety of backgrounds, and lectures can be tailored to a program's needs and interests.  We have found that most programs benefit from an introductory lecture covering autonomic physiology relevant to clinical practice, the autonomic medical history, and the diagnosis and initial management of common autonomic disorders.  Many programs opt for a follow up lecture going into more depth on specific topics, to include alpha-synucleinopathies, autonomic neuropathies, pediatric and genetic autonomic conditions, POTS, syncope, gastrointestinal autonomic disorders, etc.

Sincerely,

Ratna Bhavaraju-Sanka, MD,FAAN

Co-Chair, Education Committee

American Autonomic Society

I’m exploring opportunities to work in Australia/New Zealand/Singapore after completing my neuromuscular fellowship. I would love to connect with any U.S.-trained physicians who are currently practicing in these 3 countries. 

I’m especially interested in learning about licensing pathways, job search strategies, and clinical practice differences.

Thank you in advance!

After 40 years of practice, I will be retiring in March and have the following equipment available.  If you are a non-profit organization or a new practitioner, just a thank you will suffice. If not, make an offer.

1. TECA TD-5

2. TECA TD-10

3. Teca Synergy, laptop and PIU - I have 2 units

Joe Lubeck

jlubeck@lubeckneurology.com

This is the case of a 66 y.o. RHD M referred for EDX evaluation of progressive right hand weakness over the last two years.  He endorses h/o neck stiffness, right shoulder pain radiating to upper arm and more recent numbness along medial aspect right forearm.  The patient denies similar symptoms in his left arm/hand or feet.  He has no h/o DM, autoimmune disease or cancer.  Interestingly, he reports family history of CIDP in his biological brother (confirmed by patient correspondence) and father (deceased).  

Physical Examination: significant atrophy right thenar eminence with more mild atrophy right FDI.  Mild right distal forearm atrophy compared to asymptomatic left side.  Hoffman's neg.  DTR's: depressed biceps bilaterally; 1+ triceps and brachioradialis reflexes.  MMT: 5/5 B/L DELT/BICEPS/Triceps/Wrist Ext; 4/5 R FDI; 2/5 R APB.  Sensation: grossly no decrement to PP between right and left hands.

First EDX Study (2024): do not have full access to

Second EDX Study (Feb 2025):

(1) minimally prolonged DL, very low amplitude & normal CV right median motor evoked response

(2) normal left median and ulnar motor evoked responses

(3) normal right ulnar motor evoked response at ADM & FDI

(4) normal PL, minimally low amplitude and normal CV b/l median SNAPs

(5) normal PL, low amplitude and normal CV right ulnar SNAP

(6) normal DL, minimally lower amplitude and normal CV right radial SNAP

(7) normal PL, low amplitude and minimal CV slowing left ulnar SNAP

(8) normal left radial SNAP

(9) normal bilateral MABC SNAPs

(10) abnormal right mid palm (lumbrical - interossei) study 

(11) chronic denervation & reinnervation in all right upper limb muscles worse in C7-8-T1 muscles and active denervatiobn right APB

IMPRESSION:

(1) very severe chronic axonal right median neuropathy distal to branch of FCR

(2) bilateral mild axonal non localizable ulnar neuropathies

(3) chronic mild right C6-7 radiculopathies

(4) chronic severe right C8-T1 radiculopathies

No EDX evidence of right brachial plexopathy.  MD made note of the possibility of a remote brachial plexopathy as evidence by the severe denervation and reinnervation of muscles innervated by AIN and prior EDX absence of MABC SNAP.

My EDX Study (Jan 2026) - one moment please :)

I had the benefit of reviewing the following studies: 

MRI Right Brachial Plexus: normal

MRI C-spine: small focus myelomalacia C4; mild to moderate spinal canal stenosis C3-7; severe bilateral NF narrowing C3-7

MRI Right Forearm: mild edema within FDP & PQ muscles

Now, my EDX study ...

(1) Right median CAMP - still very low amplitude 1.2 mV and minimal CV slowing forearm 

(2) Right ulnar SNAP - NOW ABSENT !!!

(3) Right radial SNAP - NORMAL OL/PL/CV

(4) Right median SNAP D2 - NORMAL OL/PL/CV (no segmental slowing across wrist)

(5) Right median SNAP D1 - NORMAL OL/PL/CV (minimal slowing across wrist)

(6) Right LABC SNAP - NORMAL

(7) Right ulnar CMAP - no interval change in DMLs or amplitudes but now 18 m/s slow across elbow (ADM) and 13 m/s slow across elbow (FDI)

(8) Right ulnar F-waves - proloned latency 33 ms

(9) Persistent active denervation in APB w/ PSWs & CRDs; moderate-to-severe reduced recruitment in APB & FPL muscles (MUPs firing 30 - 35 Hz); less pronounced reduced recruitment in FDI and PT muscles but with sigificant polyphasia and increased duration; deltoid still showed slightly decreased recruitment but no significant polyphasia (above what we would normally expect to see); biceps, triceps and EIP muscles normal recruitment and MUAPs; cervical paraspinal muscles negative

Unfortunately, I did not have time to study patient's contralateral limb.

My EDX Impression: EDX study highly suspicious for a chronic lower trunk and medial cord brachial plexopathy with interval development of mild, demyelinating, motor, ulnar mononeuropathy across the right elbow.

My conundrums ...

(1) When I see persistently low amplitude median nerve CMAPs + absent ulnar SNAPs I usually conclude lower trunk brachial plexopathy but AIN mononeuropathy seems valid here given the markedly decreased recruitment in FPL and PQ muscles and atrophy of thenar eminence and distal volar forearm muscles on clinical examination.  Can we see such such atrophy in lower trunk BP lesions?  The patient also had FDI weakness but with less demonstrable atrophy (perhaps from the new UNE ?)

(2) The non-localizable ulnar sensory axonal neuropathies ... could they be a precursor to UNE w/ subsequent development of segmental slowing (ie, neuropraxia) of motor fibers across the elbow?

(3) Chronic cervical radiculopathies with absence of on-going denervation and reliance on MUAP analysis ... i know enough that we need to group these neurogenic changes in myotomal distributions but relatively new finding of modestly decreased recruitment in PT muscle can be seen in medial cord BP lesions ???

(4) NMUS Examination - I tracked patient's MN from CT inlet to level of PT.  I'm good but not an US guru by any means :)   CSA MN at CT inlet 10 mm2 (wnl) -> CSA MN at PQ 13 mm2 (relatively normal as we expect CSA to slightly increase as we scan proximally) -> PQ muscle definitively hyperechoic and atrophied -> it was hard to appreciate the take off the AIN from trunk of MN.

Do you think I should make an amendment to my report ???

Thank you all !

Todd R. Lefkowitz, DO, DABPMR, DABEM, CAQSM

Hello everyone,

My name is Andrew Gibson, Ph.D., and I am a faculty member in Exercise and Sport Sciences at Keiser University. My academic and applied work sits at the intersection of neuromuscular physiology, fatigue, and wearable technology, with a particular focus on translating electrophysiological methods into clinically and practically meaningful outcomes.

I am an active member of the American College of Sports Medicine (ACSM) and recently joined the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) to further align my research and scholarship with the neuromuscular medicine community. My current work involves applied sEMG methodology, neuromuscular fatigue assessment, and collaborative projects that bridge exercise science, rehabilitation, and clinical neuromuscular practice.

I’m introducing myself here with the goal of collaborating with AANEM members to support scholarship, research initiatives, and educational efforts that advance the mission of the organization. I welcome opportunities to contribute as a researcher, collaborator, or co-author on projects that further the field and strengthen the integration of neuromuscular science across disciplines.

If you’re interested in connecting or exploring potential collaborations, I’d be glad to hear from you.

Contact:
andrew.gibson@keiseruniversity.edu

Best regards,

It is with a sad heart that we share the shocking news that Dr Jeremy Bland passed away on Sunday night during his sleep.

Jeremy was an influential and popular Clincial Neurophysiologist and wise member of British Society for Clinical Neurophysiology Council for many years as Treasurer, Webmaster and more recently as NHS England National Specialty Advisor for Neurophysiology and Visual Science.

His influence will continue to be felt through the BSCN website and his research into carpal tunnel syndrome. The Canterbury Carpal Tunnel Scale is a memorial to his use of the scientific method applied to benefit patients and a tool to guide treatment for our surgical colleagues and is used across the globe. More recently he was instrumental in creating the ANS-BSCN National Referral Guidance will influence activity in clinics in the United Kingdom.

Jeremy also had an international impact. He was an active member of the AANEM and spoke regularly at their teaching courses and conferences. The AANEM awarded him the Distinguished Researcher Award in 2021. He was also rewarded in recognition for reviewing >1000 papers for Muscle and Nerve.

He has taught at many Oxford triennial courses and was demonstrating ultrasound techniques at the European Congress of Clinical Neurophysiology in September.

We send our sympathy and prayers to the family at this difficult time.

He will be sorely missed.

Dear colleagues,

I am seeking clarification on an observation that frequently appears in my daily electrodiagnostic practice: patients with lumbosacral radiculopathies seem to demonstrate EMG evidence of denervation more often than those with cervical radiculopathies.

Clinically, this pattern appears consistent, yet I have not found a clear statement in the literature directly addressing whether lumbosacral radiculopathies are objectively more likely to show needle EMG abnormalities than cervical ones.

While reviewing available studies, I did find data suggesting a difference in detection rates. For example:

• Hassan et al. (Can J Neurol Sci, 2013) reported EMG-confirmed radiculopathy in 62% of lumbosacral cases vs 31% of cervical cases in their cohort.

• Lefkowitz, “Electrodiagnosis of Radiculopathies” (AAPMR/NOW review) summarizes typical sensitivity ranges as approximately 49–86% for lumbosacral radiculopathy and 50–72% for cervical when paraspinal muscles are included.

• Several reviews (e.g., Narayanaswami et al., 2016) note factors that may reduce the likelihood of detecting cervical denervation, including overlapping myotomal innervation, variable motor involvement in cervical root compression, and technical challenges in paraspinal sampling.

These trends seem to align with what many of us observe in practice, but I have not found a paper that explicitly states this comparison as a distinct conclusion.

My question:
Is there a definitive study, review, or consensus source that directly addresses whether lumbosacral radiculopathies produce denervation changes detectable by EMG more frequently than cervical radiculopathies? If so, I would appreciate references or guidance toward the most authoritative literature on this topic.

Thank you in advance for your insights.

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.

Does anyone have any experience with ultrasound billing? Is anyone doing it as an extension to the NCS/EMG? 
Can you still do Ultrasound when a primary asks for NCS/EMG only?