Good afternoon

first time posting although have followed for many years with interest and valuable education. Would like to present a case which has left me quite puzzled.

This is a 63 year old lady seen for EMG 3/22 for arm and hand pain and numbness. Findings st that time showed left CTS, but also had multiple muscles with 1-2+ fibs and PWs in C-6,7 bilaterlly (PT, FCR, ECRL, APB and C-PS) without clinical symptoms. Had left CTS surgery with good outcome. Returned 3/29/2023 with right digit 2,3 pain and numbness. No cervicall pajn but intermittent right shoulder and upper arm pain. Nerve conductions, including right axillary, MC and radial to triceps all normal, both motor and sensory. However, Emg today showed diffuse 1-2+ rest activity in all muscles, including bilat C-PS bilaterally.  No neck pain, normal MMT, nl stretch reflexes, nl sensation (light touch and pin), no myotonia or fascics. No family history of NMDZ, negative drug including excessive caffeine history.

Appreciate thoughts on etiology, differential diagnosis and further testing. Thanks in advance for all your input.

Good afternoon,
 
I am writing as the principal investigator of a research team at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell. We are conducting a survey on the teaching preferences on the diagnosis of mild distal entrapment neuropathies. 
 
As an electromyographer, we are hoping you would be able to provide us with some insight into your clinical practices. Some of you may have already filled out our survey before prior to its updated IRB approval so there is no need to do it again.  If you are interested in participating, please use the following link on: https://redcap.northwell.edu/surveys/?s=Y73FEPXFKMTC4PMR
 
Please complete our survey only once.
 
We are also interested in hearing from any of your colleagues who perform NCS/EMGs regarding the diagnosis of mild distal entrapment neuropathies. If you feel they would be interested in participating, please feel free to forward them this survey.
 
This research has been reviewed by the Northwell Health Institutional Review Board (IRB). If you have any questions about your rights as a participant, or if you feel that your rights have been violated, please contact the IRB at 516-465-1910.
 
Thank you so much for your time.
 
 
Sincerely,
 
Todd R. Lefkowitz, DO, DABPMR, DABEM, CAQSM
Assistant Professor & Associate Program Director, Dept. PMR
Donald & Barbara Zucker School of Med at Hofstra/ Northwell

 

I've recently diagnosed a patient with LEMS, however the patient also has generalized epilepsy, partially controlled on AEDs. Does anyone have experience with Amifampridine in patients with epilepsy? Amifampridine is contraindicated in patients with epilepsy, however there are no other good options.

thx

What does everyone use for warming?? I have used hydrocollator since my fellowship 10 years ago. It is great and easy to use. I did not find the IR lamb helpful. The disposable heating cools fast and is not efficient. My new workplace is resistant to get a hydrocollator . They say that they moved on as it causes burning. Just want to check what everyone uses

Brain trust,
Wondering if anyone has experience doing facial nerve palsy studies for plastic surgeons who have the intent to do reanimation procedures. Specifically they would like testing of all the branches and commentary on if the injury is more neuropraxic vs other. Bonus points if you see kids. One of my concerns is that it is nearly impossible to do a good facial study in a young child without sedation which then limits the usefulness of the EMG portion. (Also not confident in how to be sure it is more neuropraxic vs other). Without sedation you likely could not needle a young child's face successfully anyway. Seeing more referrals for this and would love guidance on the best approach and tips and tricks from the experts. Also anyone using neuromuscular ultrasound and has it been a useful adjunct? Thanks!

Brain trust,
Wondering if anyone has experience doing facial nerve palsy studies for plastic surgeons who have the intent to do reanimation procedures. Specifically they would like testing of all the branches and commentary on if the injury is more neuropraxic vs other. Bonus points if you see kids. One of my concerns is that it is nearly impossible to do a good facial study in a young child without sedation which then limits the usefulness of the EMG portion. (Also not confident in how to be sure it is more neuropraxic vs other). Without sedation you likely could not needle a young child's face successfully anyway. Seeing more referrals for this and would love guidance on the best approach and tips and tricks from the experts. Also anyone using neuromuscular ultrasound and has it been a useful adjunct? Thanks!

I recently saw an interesting and confusing right median nerve injury and I am hoping somebody may have a similar experience and/or can explain the findings. Healthy 29-year-old male fell about 10 feet from a ladder in September 2022 resulting in a radial head fracture treated nonoperatively. He developed pain in the elbow but otherwise no numbness or paresthesias. However, he developed weakness with pronation, and flexion of the DIP joint of only the index finger.  He was evaluated by orthopedics with MRI of the hand and forearm performed about 2 months post injury showing inflammation in the pronator teres and FDP as well as the radial head fracture.  There was no evidence of tendon injury to the index finger.  I saw him in December, 3 months post injury for electrodiagnostic consultation.  He stated he had no numbness and tingling, and weakness had not improved.  Physical examination notable for essentially 0/5 pronator strength (he was substituting shoulder internal rotation), no active motion of the PIP joint of the index finger.  There was obvious atrophy over the pronator teres compared with the contralateral side.  There was normal strength to the FDI, FPL, APB, wrist flexion, wrist extension, finger extension, FDS and FDP to the small, ring and middle finger.  Nerve conduction studies done bilateral showed normal and symmetric median sensory and motor.  I performed NCS to the bilateral pronator quadratus using surface electrodes and stimulating at the elbow.  The latency and amplitude were symmetric although the waveform morphology was different.  Needle EMG showed extensive positive sharp waves/fibrillation potentials and no active motor units in the pronator teres, pronator quadratus and FDP to the index finger.  Needle EMG was normal to the FCR, FDS, FPL, extensor indicis and APB.  Regarding the FDP exam, I was able to localize motor units to each finger as I advanced the needle.  After passing through the fibers to the middle finger, I encountered spontaneous activity and no motor units.

I saw him back a few days ago for repeat needle EMG. He stated other than feeling his pronation strength was somewhat better, there were no interval changes. Exam continues to show significant atrophy over the pronator teres with the FCR now showing hypertrophy. He demonstrated some active pronation but continued to have no active flexion of the DIP joint of the index finger.(I believe the FCR is now performing pronation duties). Needle EMG again showed extensive spontaneous activity with no active motor units to the pronator teres, pronator quadratus and FDP to the index finger.

Functionally, he is minimally impaired and not inclined to do anything invasive, such as exploratory surgery.

Questions/Observations:
1. Given the trauma resulting in a radial head fracture, I assume the median nerve was injured at the level of the elbow. Given the severity of denervation to the pronator muscles and FDP to the index finger, I do not have a good explanation for why other muscles were spared and why no median sensory injury occurred. Any thoughts on this?
2.  Does anybody know of anatomic variant of the anterior interosseous nerve where the pronator teres would also be innervated, and/or the AIN comes off as proximal as the elbow?
3. Regarding the FDP, I find it interesting that the only denervation is to the index finger. I assume the muscle could have more ulnar dominance with the median nerve only innervating the index finger portion of the muscle, which would explain the findings and also explain why reinnervation is not occurring from collateral sprouting of the surviving median fibers to the middle finger. Any thoughts on this?
4. Regarding the nerve conduction study to the pronator quadratus, I was surprised to have an intact conduction on the affected side, given the clinical and needle EMG findings. This is not a study I do very often. The waveform was different from the intact side, and my assumption is the electrode may have picked up signal from the FPL and/or other distal median muscles. Doing the study using a needle pickup probably would have been useful. does anybody have experience or comments on this?

Hi everyone, 
I have an inquiry concerning the electromyography study of the carpal tunnel syndrome
Does the median–ulnar sensory amplitude difference to the ring finger have any positive predictive value in the diagnosis of CTS besides the latency difference?
If it's the case, how much this difference will be?

Thank you

I'm graduating pediatric rehabilitation fellowship this summer and will be starting my new job in the fall. An EMG machine is going to be purchased for me and I am being asked which one they should get. Any suggestions/insights into choosing a machine/software are greatly appreciated! I've use both Natus and Caldwell machines at various points during my training, slightly leaning toward Natus as I used it a lot during residency but it was a much older model. 

Any things you wish you would have known when choosing a machine?

I will be working in NJ, have connected with a Caldwell rep, but if anyone knows a Natus rep there I could speak with please send their info!

Hello all, 

I would like to collect the thoughts and opinions on the interpretation of jitter study/single-fiber EMG. 

Short version: In an otherwise normal jitter/SFEMG study performed with disposable concentric needle electrode, does having 1 pair (out of 20) with increased jitter WITH blocking make the study abnormal?  If so, I am looking for some literature supporting this statement. May be I am missing it while it is in plain sight. I need some help finding this info. 

Long-version: 
Clinical history: 48-year-old African-American woman presenting with 15-year history of generalized weakness, 2 years of fatigable ptosis, 1 year of dysarthria, intermittent binocular diplopia, shortness of breath.  Reports having exposure to Pyrethrin (organophosphate) since the age of 11.  Neurological examination at the time of jitter/SFEMG study was only notable for some dysarthria but ocular and general motor examination was within normal limits.

Current medication regimen: IVIG q. monthly and mestinon with subjective improvement. 

Prior work up: Underwent serological testing for myasthenia gravis X3 times.  One of the times was noted to be positive for  AchR modulating antibodies but on repetietion negative.  Prior EMGs with repetitive nerve stimulation was negative. Also had a muscle biopsy reported to be normal. 

She was evaluated by at least 4 different neurologists and our group is the fifth.

Jitter studies: Patient does not have any history of botulinum toxin.  No more exposure to pyrethrin.  She had been off pyridostigmine for more than 24 hours prior to her study.

Study was performed on the right frontalis muscle with voluntary activation using disposable concentric needle electrode.  Data as documented in the tabular format,  and videos.

Apart from the single pair that shows increased jitter with blocking, rest of the study is normal.  From what I remember, having a block even in a single pair makes the study abnormal.  But, I am not able to find any data supporting the statement.  Here are my questions: 

1.  Is it commonly accepted that having a block (ofcourse with increased jitter) on a single pair makes the study abnormal ? Like I said before, I may be missing it in plain sight. If so, I would like to get some literature evidence to support the statement.  I remember hearing this, but I also remember hearing other views. 

2.  If it is felt that this particular pair has a quality issue and should be excluded out of the analysis, in that case would like to understand why and what could have been done better.

Please note: This question is strictly related to interpretation of single-fiber EMG/jitter studies and would appreciate limiting the discussion towards electrodiagnostic interpretation rather than clinical.

Thank you in adavnce for your time and expertise.

Best,
Sri Raghav Sista, MBBS
Asst. Prof of Neurology - UTHouston

Hello,
Does everyone have patients sign an informed consent prior to performing NCS/EMG?

Thanks,
Iram

Hi all,
I was hoping to get some advice on an ultrasound finding. The patient is a 50-year-old quite muscular male with a history of prediabetes presenting with typical CTS symptoms. Symptoms and electrodiagnostic findings were much more prominent on the non-dominant left side. Left side DL/amp = 11.9ms/3.5mV, right side = 5.6ms/8.9mV. Ultrasound of the left median nerve at the distal wrist crease showed intrusion of the FDS muscle belly into the carpal tunnel when opening the hand and extending the fingers. On short axis, the muscle belly displaces and appears to compress the median nerve. Left median CSA was 24 mm2, right was 15 mm2. See youtube video link below. I was able to find a 2012 case report by Terasnoudis with similar findings but otherwise didn't see much in a pubmed search. I have not seen this before and am not certain about its incidence in general or its relationship to CTS. Does anyone have experience with this? How have you managed such patients? 

https://www.youtube.com/watch?v=QVyZuwsPChc

Dan

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