AANEM Connect

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,

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.

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.

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!

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

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

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? 

I am trying to find out the fair market value of my Natus Elite Synergy EMG that I purchased new 5 years ago.  Does anybody know how I might find this information?

Colleagues,

During routine practice I’ve encountered several patients with classic ocular myasthenia features (fluctuating ptosis and/or diplopia, fatigability, diurnal variation). However, single-fiber EMG (SFEMG) performed in frontalis and orbicularis oculi (OO) yielded:

Mean jitter: normal

No blocking

Number of spikes with abnormal individual jitter < 3

Given the strong clinical suspicion but a “negative” SFEMG, I’d appreciate your input on next steps. In your experience, how often do you see false-negative SFEMG in ocular MG ?

35 y/o F with severe ankle sprain sent for EDX 4 mos after injury. Strength in ADF 4-/5, APF 3/5,  in particular she is unable to plantar flex 2-5th toes, strength in  FDL 1-/5, FHL 3-/5, EHL 4/5, foot inversion 5-/5, eversion 2/5, she has tingling in planter foot and some dorsal foot. No proximal weakness. MRI ankle nc with complete ATFL tear, tarsal tunnel wnl. 

NCS- Tibial CMAP wnl, Fibular CMAP from EDB  was low 3.5 mv( opposite 8mv) , Fibular from TA intact bilateral. Sural, Sup fibular, Saphaneous wnl. Lateral and medial plantar mixed nerves were intact (but opposite side was not done ) needle emg intact in Tib ant, Med gastroc, EHL, vastus med, biceps short head, but she could not activate any MUPs in FDL and Peron longus. she couldnt tolerate EDB, tried Abd Hallucis but she couldn't activate any units. All her weakness in foot started after this ankle injury. Lumbar spine MRI unremarkable. I am puzzled with multiple nerves affected after ankle injury, distal Tibial, superficial and deep fibular? any thoughts on localization? what is also baffling no MUP duration/amp changes, no denervation in any of the muscles. She says she has gained ADF strength, it was about 2/5 early on, but no improvement in toe plantaflexion. 

Greetings all, 

I'm an adult neurologist who inherited a patient from a colleague who has Becker Muscular Dystrophy. The patient was started on Prednisone 50mg daily and believes it helped him. He ambulates with a rolling walker and has bilateral foot drop. 

I have an idea that one could use steroids for " a few years" but that's a vague recommendation/concept. Studies in the literature tend to be one year at most.  I'm starting to taper because of side effects in this patient, but am wondering specifically for Becker Muscular dystrophy..... how long would one generally treat such patients? 

I appreciate the input of the " hive mind"....

Why are the sensory axons affected first in carpal tunnel syndrome?  I know that in acute compression, motor axons are typically affected first. Is it different for carpal tunnel syndrome or in chronic compression in general. Is it the location of the axons?

Hello, 

I am looking for a Neuromuscular physician in South India, specifically in Hyderabad or Vishakapatnam. This is for one of my family member whose symptoms concern me for ALS. 

Any recommendations would be of great help. 

Thank you.

Dear AANEM community (and the handful of fans of EMG Talk out there),

In honor of our 30^th anniversary of EMG Talk, we desperately need an EMG Talk theme song.

As an example, just to get the creative juices flowing, we have an initial draft set of lyrics to be sung to the theme of Gilligan’s Island (a TV show probably too old for most of you to remember).  Our colleague Gautam Malhotra has even expertly sung the lyrics (listen here). 

Judging from prior years submissions, we know we have a VERY creative group out there in AANEM-land. 

We ask you to submit other, even better, ideas for EMG Talk Theme songs – performance (audio or video) gets extra credit! 

EMG Talk theme song #1

Now sit right back and you'll hear a tale
About our specialty
With two guys we call Wave and Spike
Who love their EMG

At AANEM each year
They entertain their guests
With snacks and jokes and quizzes that
Could stump even the best
They stumped even the best

At times the questions got too tough
Sometimes the jokes fell flat
If not for the knowledge of the residents
No one would get a hat
No one could win a hat

For 30 years now Spike and Wave
Have been the show to see
For snacks and jokes and sometimes hats
And even CMEs
Yes! even CMEs

So sit back now and enjoy the show
For two hours on the clock
And learn while you are entertained
Here on EMG Talk.

 

 

 

 

I'm wondering if anyone believes neurapraxia can give small distal motor amplitudes. 

We recently had a case of ulnar neuropathy at the elbow with distal CMAPs of 0.7 mV to ADM and 0.2 mV to FDI with only 1/5 strength in those 2 muscles.  She had surgery which released marked compression under the FCU and only 2 months later she had 4/5 strength.  I think it's too early for axon regrowth (she's 65 y/o and diabetic) so I'm wondering if the neurapraxia somehow affected the axons distally, giving small CMAPs?

Larry Robinson

 

I'm working to purchase a new ultrasound machine for my practice - the hospital system where I work has contracts in place with sonosite and GE. Was wondering if anybody in this community had insight in working with machines like the sonosite LX, GE Logiq E, GE venue go and impressions on how they compare to one another? Thanks!

I'm transitioning from a solo private practice office to a strictly EDX practice serving orthopedic groups in the St. Louis metro area.

My challenge is how to manage my medical records and coding/billing/collections remotely now that I am closing my general practice office and will not have a physical office and office staff. I will still have my practice LLC, business banking, etc. but need services that include scheduling, managing the medical records, as well as billing & collections. 

What 'remote office' resources are available to support a physician like me?

I would like to have a colleague review an EDX study with a diagnosis of "severe demyelinating sensory motor polyneuropathy" in a patient with severe diabetic polyneuropathy.  

Clifford Schostal MD, FAAN

Hi everyone,
Looking for your thoughts on a puzzling case.

I'm seeing a 54-year-old right-handed woman on long-term disability.

Her history includes type 2 diabetes, hypertension, hypothyroidism, OSA (on CPAP), nodular thyroid hyperplasia, DVT/PE and, most importantly, a lateral medullary stroke in 2021. She also underwent bariatric surgery and has bilateral knee prostheses.

She is a past smoker, and drinks only rarely.

After her stroke, she had stable non-painful hypoesthesia of the right face and left hemibody. However, in late May 2025, she experienced rapid onset (over a few days) of paresthesias in all fingertips, followed shortly by paresthesias in the soles of both feet. She also reported left hand weakness—mainly grip issues, such as difficulty holding a knife. Around the same time, she developed new low back pain (not clearly radicular), worsening balance (now needs two canes instead of one), and four falls in the span of a few weeks—whereas she hadn't fallen at all in the preceding year.

She has long-standing urinary urgency since her stroke, but feels it has worsened; more concerningly, she now reports new-onset fecal incontinence. No orthostatic hypotension is present. MRI cervical spine showed only mild spondylosis, without myelopathy. Brain MRI revealed no new findings.

On exam, there’s mild atrophy of the left first dorsal interosseous with 2/5 weakness in that muscle, the ADM, and APB on the left. The rest of the motor exam is intact. Reflexes are symmetric at 2+ except for an absent right Achilles. Light touch is reduced over the fingertips bilaterally and soles of the feet. Vibration at the toes lasts 6–7 seconds.

EMG/NCS revealed severe bilateral median neuropathies at the wrist (markedly prolonged distal motor latencies, at 13-14 ms, and collapsed CMAPs), bilateral ulnar neuropathies at the elbow (more severe on the left, with both demyelinating and axonal features), and absent median and ulnar SNAPs. Tibial and right fibular motor responses are intact, as well as radial, sural (6-7 microvolts) and superficial fibular sensory responses.

Needle EMG showed chronic neurogenic changes in the left FDI and APB, with normal C5-C7 muscles. In the legs, there were chronic neurogenic changes in bilateral TA and medial gastroc, with the left TA and right MG more affected and showing active denervation. There were also changes in the left vastus lateralis, equivocal findings in the left tensor fascia lata, and mild denervation in the left L5 paraspinals.

Altogether, we’re looking at:

• Bilateral median and ulnar entrapment neuropathies 

• Axonopathic changes suggestive of chronic L5 > S1 > L4 involvement (bilateral, asymmetric), possibly radicular in origin

I interpreted the relatively robust sural amplitudes (6–7 µV) as not suggestive of an obvious large-fiber polyneuropathy.

Although the simplest hypothesis would be a combination of mechanical entrapment neuropathies and lumbar radiculopathies, I remain somewhat puzzled by the rapid and simultaneous onset of symptoms in all four limbs, which seems hard to reconcile with purely mechanical explanations like cane use.

It makes me wonder whether something more systemic is at play, amyloidosis being one of the possibilities I'm considering, especially given the massively prolonged median motor latencies and fecal incontinence. 

My plan is to pursue a workup for amyloidosis (including serum protein electrophoresis, free light chains, etc.), inflammatory/vasculitic workup, and to push for expedited carpal tunnel release surgery with biopsy of the flexor retinaculum—though this isn’t always straightforward to obtain in my setting.

I would appreciate any insights—particularly on whether you'd explore additional imaging, consider nerve biopsy, or look into other systemic causes. Any suggestions or advice would be very welcome.

Many thanks!

MB

I just sent a case last week and got NO response. Would you please read it and help with any idea or differential. 

I have another case of a 25 year old who had a right leg DVT and saddle PE s/p thrombectomy. Found to have Factor V Leiden. Started Elequis. He slept all the time after D/C. A week later noticed right foot drop followed a week later with left foot drop . 

EMG for this patient showed normal sural and super peroneal sensory with severe denervation of all muscles below the knees. I do not want to do a biopsy as his surals are normal. I do not want to add to his problems an iatrogenic numbness. 

It can be vasculitis but how can you explain bilateral vasculitis at the same exact location. 

I m very concerned about these 2 very young adults with severe bilateral and symmetric feet drop

Am I missing something?

Report attached. 

Hi all,

I lead a PM&R training program for doctors across Sub-saharan Africa through the International Rehabilitation Forum www.rehabforum.org.  November is our neuromuscular month and I'm hoping to get some on-line teachers.  Also, if anyone has interest in teaching other areas, or in self-funded road trips to teach, please let me know: andyhaig@umich.edu.

The details:

With zero PM&R trained doctors in the region, we launched this 2-year, mostly on-line fellowship for physicians who are either already board certified (FP, neuro, ortho, etc.) or have a few years working in a rehab setting.  It's now the official board-certification in Ghana and Ethiopia, and we've got about 220 graduates in South Africa, with other countries joining in.  Under fellowship director Yunna Sinskey (Mary Free Bed PM&R) Fellows do local 'rotations', attend 3 hours of on-line lectures wednesday morning 7-10 a.m. EST, have research and other requirements, exams, etc.

The training is a challenge because of the mixed experience and current exposure of the clinicians. One might be world-class in amputee but not know where the median nerve is. Another may be doctor for a national soccer team but never run into a polyneuropathy.  At this stage most do not have access to an EMG machine. Yet we (the African leaders and I) feel that its critical that they all become competent in diagnosing and treating focal nerve issues and neuromuscular disorders.  We also feel that this first generation needs to at least know the language and logic of EMG, so that those who follow may choose a career.

Very basic EMG/neuromuscular is contained in 5 lectures I put YouTube (BTW, the technical intro video and EMG-1 video are great intro for American med students rotating through your lab...). However they need to get a pragmatic sense of diagnosis and treatment. so we're hoping to get experts who can do an hour of teaching-semi-lecture but cases and audience participation. If you're interested, drop me a note with your area of focus.  Great for your fellows/junior faculty to get some CV-fillers.

Also, though...working with West Virginia's Ken Wright, M.D., we're trying to organize longer-term mentorships and road trips for neuromuscular experts to visit and teach in person.  No, we have no money whatsoever for travel. but we know places to get good fu-fu, Ethiopian Coffee, and visit the South African elephants!  so let me know that, too.  

Thanks,

Andy