Dear colleagues 
I would be grateful for thoughts on the ulnar-mixed-fibres waveform (lowermost trace) across the elbow on the left.
Woman, mid-forties, good health.
Numbness affecting left hand, mostly ulnar half, suspected to be related (having followed) soft-tissue injury to the neck ten years earlier. Neck normal on imaging.
Referred specifically for the possibility of nerve entrapment in the cubital tunnel. 
No wasting or weakness in the upper limbs. 
Conduction mildly slow (43m/s) across elbow, and only in fascicles to FDI. 
I have seen similar two-peaks waveforms in several ulnar elbow-neuropathies, and I would be grateful for your thoughts on whether the dissociated peaks do reflect pathology in a subset of the “mixed fibres”.
 
 

Does anyone know of billing code changes for neuromuscular ultrasound?

Our lab has been using 76882.    But I am told that payers are not paying on that code.    

I'm being told to use 76883

Any advise?

sorry.  I just discovered the conversation regarding this issue.  

the new code and the definition is very helpful.  It will be interesting to see the reimbursement. 

Hi all –
I'd like to open an interesting debate and get some input from experts here! In full disclosure, a few of us are working on a monograph for AANEM that may speak to this point in some form.
There are differing opinions in the literature as to whether the amplitude of fibrillation potentials can be meaningfully used in inferring the (a) duration of a lesion and (b) viability of muscle fibers.  Some references of interest:

• Jiang et al. (2000)
• Dumitru and King (1998)
• Kraft (1990)
• (poster #15 at 1997 AAPM&R annual meeting): Park DS, Joo MC, Lee SJ, Kim DH, Park YG. Amplitude of fibrillation potential and positive sharp wave following peripheral nerve injury. Arch Phys Med Rehabil. 1997;78:1035

What does this community think?  Can we glean any information from fibrillation amplitudes, in practice?  Should these be used in broad strokes and with caution, quantitatively, or never at all? 

How long after starting eculizumab do you usually see a clinical improvement in your myasthenia gravis patients?  What’s the average and what’s the range?

 

45 yo man with a h/o AChR Ab positive myasthenia gravis who began to have symptoms about a year prior.
He initially presented to us on 12/4 with diplopia, ptosis, "neck pain", dysphagia, and nasal regurgitation.  These were also his presenting symptoms upon initial diagnosis but he had been normal for several months without any symptoms until 9 days prior to admission.  He had been taking prednisone 10 mg daily and pyridostigmine 60 mg QID plus TS 180 mg QHS at home. 
Work up in his home country: 
May 2022 - AChRAb 5.85 (< 0.45)
May 2022 - CT Chest - "Thymus not enlarged"
Initial exam was significant for:
Diplopia in all directions of gaze.  Impaired up gaze.  Ptosis - R > L - significantly worse with EOM for about 20 seconds and improved with rest for about 20 seconds.  Face - orbicularis oculi weakness, B.  Strong orbicularis oris.  Smile - normal. Palate elevates normally.  No nasal speech.  Swallows 90 cc of liquid with no difficulty or coughing. NF/NE - limited due to discomfort but definite neck extension weakness.  Delt 4+ and HF 4 with some fatigability. Other muscles are 5/5.

He improved and then had significant worsening again within a few days while getting IVIg.

He was later treated with plasma exchange and slightly improved and then significantly worsened.

He never had any respiratory complaints.  During his stay he developed worsening dysphagia and weakness in chewing which was new.  

During his stay, pyridostigmine was increased to 120 mg QID, and he was continued on TS 180mg at night.   Prednisone was slowly increased to 40 mg daily.  Lowering the pyridostigmine resulted in a significant worsening of all symptoms.  
 
Work up by us:
Anti-striated muscle Ab was + 1:320.
TSH normal.
CT chest - "3.2 cm isodense lesion is noted in the prevascular space/anterior mediastinum. Primary differential diagnostic consideration includes a thymoma.


Most recent exam:
Mild bilateral orbicularis oculi and orbicularis oris weakness.  
No nasal speech. 
Neck extension 4-  --> 4
L/R       Deltoid  4+ --> 5, B initially and then fatigues to 4/4    Biceps   5/5      Triceps  5/5         Wrist Extension 5/5   Wrist Flexion  5/5    Grip  5/5 
finger flexion 5/5, finger extension 5/5
L/R         Hip Flexion  4-/4-     Knee Extension  5/5  Dorsiflexion  5/5      Plantar Flexion 5/5 
All weakness is fatiguable weakness. 

We are awaiting insurance approval for eculizumab.

We are obviously thinking about several factors when deciding on timing:
Since he is still having significant bulbar symptoms, we would wait.  
Would you do a thymectomy soon in this patient who likely has a thymoma and has been refractory to treatment?
We will get full formal PFTs prior to considering any surgery.
Since symptomatic improvement is usually seen 6 months or more after thymectomy,  there is no emergency in performing thymectomy but waiting longer has its downside also.  

When would you recommend doing a thymectomy in this patient? 

Thank you and happy holidays. 

Cary

Hello all, I am hoping for some help with diagnosis and management from people much smarter than I am with this complicated (and long) EMG/NCS and case I encountered recently.  The background is a 57 year old patient who had started lamotrigine for mood related issues.  After about 2 weeks she developed diffuse hives for 4-5 days.  She stopped the lamotrigine and used diphenhydramine and topical creams for treatment.  She then woke up one day with trouble using her hands a day or two after the hives resolved.  She also reported numbness in her hands.  She had bad pain in her shoulders and upper back.  The pain lasted about 2 weeks.  She had Xrays of her cervical spine that showed mild degenerative changes.  EMG/NCS performed prior to formal neurological consultation and about 2.5 weeks after onset of the weakness showed normal sensory responses in the bilateral median, ulnar, and radial nerves, and reduced amplitudes of the bilateral median and ulnar motor responses (right median 2.1 mV, left median 1.7 mV, right ulnar 2.1 mV, left ulnar 1.4 mV) and right radial (2.5 mV) without evidence of conduction block or LEMS and with normal distal latencies and conduction velocities.  Left peroneal motor response was normal (latency of 4.5 ms and amplitude 4.7 mV).  Needle exam showed a few fibs and PSWs in the bilateral FDIs and the left pronator teres.  Reduced recruitment of normal units was found in the bilateral FDI, FPL, PT, EDC, and left EIP and right APB, with normal proximal muscles and paraspinals.  Neuro consult performed the next day confirmed the history of an abrupt onset of symptoms (no weakness prior to the lamotrigine and hives) and found 4/5 strength in the bilateral triceps, deltoids, wrist flexion, wrist extension, 3/5 in bilateral finger abduction and flexion and 4+/5 in bilateral finger extension.  Reflexes were normal throughout.  Sensory exam revealed patchy decrease in temperature in the distal forearms and hands symmetrically with normal modalities otherwise.  She was started on a 10 day tapering course of prednisone (60 mg for 5 days then quick taper).  MRI cervical spine and brachial plexus ordered and performed about 4-5 weeks after symptom onset.  These showed T2/STIR hyperintensity in the bilateral T1 and possibly right C7 without clear enhancement (though post contrast images were degraded by artifact).  MRI C spine showed multilevel degenerative disc disease, C5-6 canal stenosis without cord compression and patchy T2 hyperintensity at C5-6 possibly extending to C6-7 without enhancement - radiologist opined that this could be from remote trauma from a disc herniation that resolved or from demyelination.  Lab testing was unremarkable (HIV, SPEP, immunofixation, Sjogren's antibodies, ACE, light chains, celiac panel, B1, ESR, CRP, TSH, B12, CMP - ANA or ANCA were not sent). Lumbar puncture then performed - WBC -2, RBC-21, no differential performed, protein 36.5, glucose 71, negative HSV and CMV and negative gram stain and culture, oligoclonal bands were not sent.  Repeat EMG/NCS performed 8 weeks after initial test (patient reported maybe very minimal improvement in subjective numbness and weakness in the right hand though exam showed no changes) showed again normal sensory responses in the arms bilaterally, left median motor amplitude 3.1 mV, right median 1.5 mV, with normal distal latencies (less than 4.4 ms), left ulnar 1.9 mV and right ulnar 3.5 mV (with minimally prolonged distal latencies 3.5-3.7 ms) and left radial 3.3 mV and right radial 3.7 mV (normal distal latencies 2.7 ms) with no evidence of conduction block or LEMS.  Needle exam showed more insertional and spontaenous activity with expected neuropathic changes (larger units with polyphasia and increased duration) in the motor units in the bilateral FDI, EIP and pronator teres.  Proximal muscles were normal.  Repeat MRI brachial plexus is pending.  I am sorry for the long presentation but this is complicated and I wanted to present as clear a picture as I could.  Thank you!

Hi guys! I'm trying to see if neuromuscular ultrasound makes sense from a business perspective. 
Cadwell quoted us 23K for the ultrasound software and upgrading our laptop(apparently our current laptop which we use for EMG is insufficient?). 
Seems that the RVUs/Medicare reimbursement rates for 2023 are as follows:

The RVU’s and CMS reimbursement for each beginning in 2023 will be:

76881—1.56 ($51.57)

76882—1.20 ($39.67)

76883—2.15 ($71.08)

So ultimately it all depends on time, patient volume, and return. 
I would like to hear from those who have had experience regarding this matter. 
Thank you. 

Hi everybody

A 25 years old woman presented paresthesias in her right hand ascending to the shoulder, 20 days after her marriage (minding that she wore a traditional wedding dress that is considered heavy), few minutes later she presented sudden muscle weakness on the right upper limb, and then a gradual recovery 4 days after, without a real pain!
The NCS: All neurophysiological parameters are normal, including the lateral antebrachial cutaneous and the medial antebrachial cutaneous
In EMG: ongoing denervation (spontaneous activity +++) just in 3 muscles Deltoid, extensor communis digitorum and supinator with moderately reduced recruitment
No denervation in these muscles: biceps brachii, 1st interosseous and infraspinatus
No imaging at the moment (in progress)
note that she is thin (39kg for 1m57!) There was a bruise on the back of her shoulder! Now is it a slight trauma that she didn't pay attention to or something else, we don't know.
Note also that the incident occurred 20 days ago and it is in the recovery phase.
What do you think dear colleagues?
Do you think it is plexopathy even if all SNAPs are within normal limits or cervical radiculopathy? or maybe a Rucksack Paralysis? looking at the rapid recovery!  
Thank you so much
 

Hi all,

A med student is writing a review with me on how text books describe cervical paraspinal EMG. The problem is that their med school and my solo practice don't have all the texts or the most recent versions.  If anyone has any of the following (most recent edition) could you email me andyhaig@umich.edu with either a photocopy or answers to these questions?  (Yeah, so far most books don't get specific, I know. )

Do they mention cervical paraspinal anatomy? what do they say?

do they mention a technique?  what technique if any?

do they have a scoring system? what is it? are there norms?

What utility do they claim for cervical paraspinal EMG?

Missing most recent versions of these books:
Fishman
Pease
EMG Pearls    
Binnie 
Misulis
Bertorini         
Dumitru           
Kimura

Thanks!  Andy

Good Morning,
The Annual Meeting Workshop Committee received a proposal to start a new workshop on US guided lumbar puncture to be performed on a body model. I just wanted to gauge the interest of the AANEM members in the topic. Please let me know your thoughts or if you have any questions or concerns.

Hi everybody
we realised an EMG to a 14 year old girl today, presented to the Electrodiagnostic unit for muscle weakness and fatigue, she has Hodgkin lymphoma who received a chemotherapy with this OEPA scheme ( Vincristine Sulfate, Etoposide Phosphate, Prednisone,  Doxorubicin Hydrochloride) she is in the fifth session now; started from august, 
In the EMG we found a pure diffuse motor neuropathy, and an ongoing denervation in the abductor policis previs and anterior tibialis with poor recruitment, and very prolonged F waves in lower limbs (60ms), my question is: is it only a neuropathy induced by chemotherapy, is it described in the literature? and why sensory fibers are spared in this case?
Can neurotoxicity affect motor fibers and not sensory fibers and vice versa? 

Thank you so much




 

ACNS CNP Fellowship Match Townhall
Tuesday, November 29, 2022 • 7:00 - 8:00pm ET

The American Clinical Neurophysiology Society (ACNS) will convene another townhall meeting of Clinical Neurophysiology, Epilepsy, and Neuromuscular fellowship Program Directors on Tuesday, November 29, 2022, 7:00 – 8:00pm ET (6:00 – 7:00pm CT; 4:00 – 5:00pm PT).
The goal of this meeting is to convey information to and answer questions from programs related to options for fellowship recruitment for the 2024-25 fellowship year, including the Epilepsy Match (led by AES), the Neuromuscular Portal (administered by AANEM) and ACNS’s Fellowship Finder resource.
A tentative agenda is as follows:

7:00pm ET	Introduction to the Overall Recruitment Landscape and the ACNS Fellowship Finder Saurabh R. Sinha, MD, PhD, FACNS
7:05pm ET	Overview of the AANEM Portal Ruple Laughlin, MD, FACNS
7:15pm ET	Overview of the Epilepsy/CNP Match Sara E. Schmitt, MD, FACNS
7:25pm ET	Overview of Other Options Lynn Liu, MD, MS (HPE) FACNS
7:35pm ET	Panel Discussion

 
The discussion will be recorded and made available on the ACNS website, along with slides from each of the presenters.

CLICK HERE to join the Zoom meeting.

Meeting ID: 838 0154 5776
Passcode: 353886
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Hello everyone

I was wondering if any of you has experience with trigeminal motor neuroconduction study using digastric muscle. 

I heard about this technique but I could not find any paper nor book chapter describing it. It was cited in the context for repetitive stimulation in patients with myastenhia with bulbar symptons. 

Thank you for your time

If a patient was sent to get NCS EMG by another physician on a certain date, then referring physician asks the patient to come back for full neurological work up and consultation on a different date after EMG is completed. Can you bill a new visit code like 99204 when you see the patient the second time?

I have been having issues with insurance refusing to pay a new visit code for a patient whom I had seen previously for EMG. I am forced to use a follow up codes for the patient even though I never bill for a new visit before when i see the patient for EMG. 

Any advice?

I am interested in learning Neuromuscular ultrasound and would appreciate any advice regarding courses and equipment.    I am located in New York City, so courses in the Northeast would be preferable.    I have also seen some online courses, e.g. sonocampus.org. Does anyone have experience with theses? 

With respect to equipment, are there specific machines, models that are preferred? I have seen ones that work with smart phones. Is their quality adequate for this purpose?

Hello everyone
I'm impressed with the cases and ultrasound discussions at this years AANEM conference.  A few presenters mentioned high frequency ultrasound for better visualization of the nerve fascicles.   Our office plans to purchase another ultrasound; currently we have a GE P9.  Does anyone know the GE ultrasound version that is optimal for peripheral nerve visualization, specifically the high frequency option?

thanks in advance!
Ryan

This is an EMG in a person in their 40s with a 3 year history of progressive weakness in their right arm. NCS and clinical exam supports a working diagnosis of an acquired demyelinating motor neuropathy. This EMG video was recorded from the pronator teres (clinically weak) at rest. He reported no pain during the study.

See other post with attached video

I recently had an young individual with a lacerated ulnar nerve at the elbow who retained good hand function, particularly of FDI.  It turns out he had a HUGE Martin Gruber Anastamosis (see figure from 1 year post injury and repair) that saved his intrinsic function. 

I am thinking that this redundant innervation is an evolutionary advantage.  I've also heard that MGA is associated with higher levels of intelligence and good looks (unpublished observations).  It's present in 20% of people.  Not sure if I mentioned I personally have MGA.

What do others think?  Evolutionary advantage or random mutation?  Not sure I see any downsides to MGA.

Is there any situation where the fibular/peroneal CMAP and superficial fibular/peroneal SNAP can be absent normally? I was asked to evaluate a 22 y.o. for potential foot drop. he had an anoxic brain injury from an overdose with a prollonged period of low cognative and physical function, but has made a pretty profound recover. he has poor dorsiflexion of his right foot, but clinically this appears to be more related to a mild plantar flexion contracture than dorsifelxion weakness. on needle examination he had normal activity in the tibialis anterior, peroneous longus and ext. digitorm brevis. He has no sensory loss of the right calf or foot, but I was unable to obtain a fibular CMAP at the ankle, fibular head or proximal to the fibular head. At the time, I did not think to get a CMAP from the T.A. Before I bring him back to test for a fibular response to the T.A., I wanted to see if it possible to be unable to obtain a fibular response to the EDB without some sort of pathology. he did have a normal fibular CMAP on the left.

Dear Colleagues,
I am hoping to enlist your expertise in a case that is perplexing me.

23 yo M admitted for focal swelling of left forearm and pigmenturia. He had done some light upper body resistance exercises 3 days prior (10 lb dumbbells) and was sore following this. CK on admission was 14,000. MRI left forearm showed edema and enhancement in the left brachioradialis muscle only. He was hydrated and his CK came down slowly to 700 over the next week. He did not receive steroids. About 2 weeks prior to admission, his PCP noted elevated AST/ALT to 75/91 (his GGT was later normal). 

I saw him 1 week after discharge. His CK at that point was 106.There was some loss of bulk in the left brachioradialis and very mild weakness of elbow flexion, but the remainder of the exam was normal. His HMGCR antibody (ARUP) was positive at 49 (normal <20). The ARUP extended myositis antibody panel was negative. 

He is scheduled to get a muscle biopsy to see if he has changes consistent with necrotizing myopathy, then EMG to assess other muscles for subclinical abnormalities. Will recheck HMGCR antibody in about 3 months. 

After searching the literature, I found only one case report of immune mediated necrotizing myopathy presenting focally like this. I'm not sure which is more likely - an atypical presentation of a rare disease or a false positive antibody despite a reportedly very high specificity. 

My questions for this community:
1. Has anyone seen this before? Is focal-onset IMNM a reasonable conclusion?
2. If CK has returned to normal but the affected muscle remains weak, does that justify treatment with steroids? How aggressively would you treat this?
3. What kind of exercise restrictions would you recommend, if any?

Your expertise, as always, is highly valued!
Dan Simmons

Any advice on how to find an NCS tech?  We might be posting a position, just curious high yield places to post it, entities to reach out to, etc.  We are an orthopedic practice with studies being performed by our physiatrists and fellows.

Thanks,

Brian Steinmetz DO
York, PA

Hi, I need help on explaining two cases I have seen last week of paralysis after spine surgery at my institution....
Case ONE: 53 year old man with NSPMHx who was admitted 10/7 for elective cervical spine decompressive Sx. For C5-7 HNP with cord compression.  Pt had chronic cervical pain associated to paresthesias and mild weakness of the Ues and also chronic LBP associated to paresthesias in the Les and weakness in the Les, states, however, was able to ambulate without any aid  able to function on a day to day activities. Pt underwent C5-7 Anterior Cervical Decompression and Fusion with general anesthesia. Pt states when He woke up from the surgery was not able to move his arms or legs and had pain in the cervical and lumbar spines, also complained of numbness in the entire Les, LUE, and also bilateral face L>R. 
States has been able to control the urine though. On the following AM  there is partial improvement in the mobility of the Ues but no improvement in the Les . Exam shows initially 4/5 RUe and 4-/5 LUE weakness of the UEs with both proximal deltoids 4-/5 , and 0/5 in the entire both LEs except for minimal wiggling of the toes bilaterally, there is generalized hyperreflexia ( which as per report was present prior to Sx) with mute plantars and there is sensory loss LEs> UEs> face and L>R, no definite level. 
The first sets of MRIs brain, c, T, and L spines shows good cervical decompression, normal cord, and no significant lumbar stenosis although has disc disease, interestingly the brain showed L frontal cortical dysplasia and partial agenesis of the C Callosum , ( Pt was a post office worker and had no disabilities) . Started on decadron and 3 days later a repeat set of studies including Brain and entire spine, this time with Diffusion and with T2 spin Echo sequences to exclude cord ischemia was done and again were negative. after 3 days Pt strength improved in the UEs to 5/5 but remain unchanged in the LEs 

Case TWO: 67 y.o. RH female with a history of HTN, HLD, OSA, DM who was admitted on 10/10 for partial L2 and complete L3-L4 lumbar laminectomies.  Preoperatively, she was ambulating without issue, but suffered from back pain.  She had no preceding weakness, numbness, or urinary symptoms. She underwent surgery 10/11  afternoon and upon waking, was unable to move her legs.  A foley catheter needed to be placed due to urinary retention. 
The exam showed normal CNs and UEs, Motor: Ues : 5/5 
Les: Hip flexion 1/5, hip adduction and abduction 2/5, knee flexion 3-/5 and knee extension 0/5 , feet and toes 1/5 bilaterally. Reflexes are 2 in the Ues and absent in the Les , plantar responses were mute. 
Sensory: has a sensory level at T7 bilaterally.
MRI of the L spine showed good decompressive surgery and no other pathology. C and MRI T spine with contrast were also negative with normal cord!!!  was placed on steroids...
This second patient received Liposomal Bupivacaine ( Exparel) for analgesia into the paraspinal muscles for post-op analgesia...I have not found any reports of permanent paraparesis with this medication so far....

The Dx concerns were cord edema, cord infarct, white cord syndrome and even I considered Periodic paralysis ( normokalemic since both patients had normal K) ..however, the first Pt is been plejic for 9 days now and then the second for 5 days. 

Please, anybody, have seen something like this? I will be looking forward for your comments and your help

33 yr otherwise healthy female had mild COVID in April 2022 and in May began experiencing bilateral perinasal numbness that progressed to involve anterior tongue and lower face. Also with some mild abnormalities in vision. No MG symptoms but with increased fatigue during the day. Neuro exam otherwise normal besides facial and tongue numbness. Outside provider did LP, rheum panel, infectious panel and MRI brain - all normal. 
I'm checking lyme ab for completion and MRA but is anyone else see insolated cranial nerve involvement following COVID?

..this is the question I'm struggling with. 

Hi Everyone,
This is the first time I'm using this forum but figured it would be a great place to pick everyone's brain. I'm currently a Cancer Rehab Fellow at MSKCC in NYC. I had the pleasure of meeting a few of you at the recent AANEM conference (first time atendee) and left feeling super inspired and excited to learn more and dive into NMM/EDX. 

I'm currently in the process of looking for academic-based job in NYC area to specialize in cancer rehab. I envision my practice to include EMG studies - as we know patients with cancer develop a lot of NM effects related to diseae/treatments/ etc.  While I had a good amount of practice as a resident, my current fellowship focuses on general cancer rehab and not much hands on EMG practice, unfortunately.  My concern is that I won't feel prepared to take on complicated EMG cases when I start my job.  I'm also between a rock and a hard place in that I'd consider another fellowship for the additional in-depth training but feel that there is such a need for cancer rehab physicians now. Also I believe I'm too late in applying for a fellowship for 2023. 

That's my story. Was wondering if anyone here has any advice? Any tips on asking my potential employer for strategies and support to develop my skills?  

I appreciate any input/ guidance. 

Chanel