AANEM Connect

I am hoping that some of you have some insight as to how to sell a private neuromuscular dz/ EMG practice. I have built up a very enjoyable and profitable practice centered in Duluth MN. I have been here for 30 years and will retire fairly soon. I don't want to shut the practice down; it is successful enough that I ought to be able to sell it. Just as important, I have a very large referral basis of orthopedic and neurosurgeons plus primary care that will be in a lurch if I leave. I did find a business that made up a website for me https://sellingapractice.com/nnm but that's about all they do. I am not sure how to proceed from here. Thoughts/ suggestions?

Thanks in advance: Has anyone treated patients with chilblain lupus who have severe symptoms of small fiber neuropathy? See questions at end of post. Appreciate your help.

The patient is a 45-year-old woman with 5 years of symptoms in the hands and 3 years of symptoms in the feet. Symptoms are sensitivity, swelling, pain with activity, redness with activity, and neuropathic pain. On exam she has visible edema and rubor in the extremities. No neuro deficits apart from altered temperature sense in feet. 

1) Derm workup: Skin biopsy with dermatology revealed chronic cutaneous lupus erythematosus, compatible with chilblains lupus. 
2) Neuro workup: Abnormal QSWEAT. Normal Therapath skin biopsy. Normal NCS (sural 15-20 uV). 
3) Rheum workup: CRP 0.6 (ULN 0.5), ESR 36 (ULN 20). Otherwise, extensive labs are normal including WashU sensory neuropathy Ab, paraneoplastic panel, CBC, CMP, cryoprotein, B12 681, CK 76, ferritin, C3, C4, proteinase 3, myeloperoxidase Ab, ANA, SSA, SSB, Sm, RNP, Scl70, Jo1, cANCA, pANCA, SPIE, FLC, HIV, Hep C Ab. A1c 5.5.  

Treatment trials:
1) For vascular component: Nifedipine caused swelling. Pentoxyfylline (Trental) 400 TID is helping with toe swelling. 
2) For neuropathic pain component: Duloxetine and pregabalin are helping a little. Side effects from low dose venlafaxine, gabapentin. Compound cream (ketamine and amitryptyline) didn't help. 
3) For immune process: On plaquenil 300 mg daily - unclear if helping. Prednisone 40 mg daily caused severe foot pain.

Questions:
- Have you treated patients like this?
- Any other ideas for workup? Genetic testing for small fiber neuropathy is pending. Genetic testing for genetic causes of chilblain is also pending (maybe her case isn't immune)
- Do you know how to order plexin antibody testing? 
- Any other ideas for treatment? We are going to try prednisone again at a lower dose of 10 mg daily.  

Thanks again. She is grateful for your input. 
 

Sarada

 

 

I finally have a clinical case question worthy of this community.  All the relevant details of the presentation are below. This was not an easy diagnosis. I had to reflect on it overnight to realize what it was because I'd never seen it before. If you want to skip ahead, the quesiton is at the bottom of this post. 

CLINICAL HISTORY
79 year old left handed male with PMH of prior carpal tunnel releases 2013 who began dropping things from both hands 2019 and suffered associated right neck shoulder pai. Epidural offered 2 days of pain relief. MRI 8/2021 revealed "multilevel severe DDD/spondylosis with extensive flowing anterior osteophytosis suggestive of DISH and mild abnormal cord signal at C5-6 suggesting an element of cord atrophy." His neurologist sent him to a spine surgeon who documented rt deltoid/biceps/triceps/grip and finger flexor weakness with right thena atrophy. For this reason 10/2021 he underwent C7-T1 and T2-3 lami and C5-T3 posterior fusion. 

The pain has resolved but he has noted winging of his scapula, inability to comb hair, elevate arm and use fingers rt>lt.

CLINICAL EXAM
On exam, his CTR incisions are strangely distal in the palm (?). He has an extensive cervical incisional line which is healed. Right grip, D3 DIP flexion, and bilateral D1/5 abduction are 4/5. Right D3 DIP flexion 3/5. Otherwise 5/5 bilateral humeral ext rotation, shrug, and elbow/wrist extension/flexion.

At rest the scapulae are nearly symmetric. With forward flexion more than abduction, there is medial deviation and prominence of the lower medial border/angle of the scapula. He is unable to get to 90 degrees with these due to weakness but this is correctable with assisted scapular depression by the examiner. NO pain reported with these motions. 

ELECTRODIAGNOSTIC FINDINGS
There were no borderline findings. SNAPs and CMAPs in ulnar nerves were normal. CMAPs bilat MEDIANs revealed prolonged onsets, mildly slowed NCVs, and normal left but severely diminished right amplitudes without significant drops in amplitude with proximal stimulations.  Meidan SNAPs also revealed prolonged latencies, slowed conduction velocities at the wrists, and normal left amplitudes but significant drop in amplitude when going from palm to wrist. 

NEE: Parapsinals were avoided due to recent incision. Fibs/PSWs in bilat FDI, rt EIP/Triceps (latter two had diminished recruitment). Otherwise NORMAL bilateral delboids, biceps, pronator teres. NORMAL left triceps, trapezius, Rhomboid Major, Infraspinatus. I did attempt needling the SERRATUS anterior but it was my first time doing so since residency. Whatever i needled was normal

ELECTRODIAGNOSTIC IMPRESSION:
This is an abnormal study. There is EDx evidence at this time of bilat rt>lt lower cervical (possibly C8) radiculopathy. There is EDx evidence at this time of bilat demyelinating sensorimotor median neuropathies at the wrists. 

CLINICAL IMPRESSION
IMPAIRED HAND STRENGTH/DEXTERITY: from an electrodiagnostic perspective, there appears to be a prominent bilateral C8 radiculopathy superimposed over bilateral median mononeuropathy which is compromising his hand function. The findings today do not support a plexus lesion of the C8 ramus, lower trunk, or medial cord. Pre-operatively, this was also evident. Hand therapy to improve strength and function are indicated while awaiting the results of neural regeneration/reinnervation.

LEFT SCAPULAR WINGING: clinically presents with compromised trapezius more than serratus or rhomboid involvement. Spinal accessory, suprascapular, and generally upper cervical roots (C5-6) and
upper plexus (C5/6 rami, upper trunk) appear unaffected on today’s electrodiagnostic testing. On inspection, the location of the extensive cervical spine scar suggests that there could be a compromised trapezius from direct incisional injury to the trapezius. This could certainly explain the winging and, after consideration for potential reattachment by the surgeon, should be addressed with scapular stabilizer strengthening in physical therapy. Despite this and the findings on physical exam, serratus anterior (long thoracic nerve) remains on the differential and could be further evaluated by bringing the patient back in for needle EMG of the serratus anterior muscle.

QUESTION FOR AANEM COMMUNITY
The surgeon reviewed the MRI and was able to confirm that there are about 2 inches of trapezial fascia and muscle that have retracted away from the spinous processes (per surgeon, this is a very small percentage of the incision). A reputable surgeon, he has done numerous laminectomies with extensive incisions and never faced this. I have never heard of this before. If anyone on the forum has, what did you do for them?

If not, the question is, 3 months out, would it be better to just start working on scapular stabilizaiton in therapy or would there be value in re-attaching the trapezial fibers. The downside to the latter is delay of rehabilitation while healing and subjecting him to potential complications of a second surgery.  

please don't be shy and thanks in advance

Wondering what other experience the group may have.
I saw a 61 YO man who came in today for routine annual followup and med refills for a small fiber neuropathy. He mentioned that he was being treated for a left rotator cuff tear.
In late October he received Moderna #2 in left deltoid. About 36 hours later he developed intense pain in the shoulder lasting 48 hours followed by weakness in shoulder musculature. He had a followup with an orthopod who had performed a left TKR and diagnosed him with a RC tear (no comment). On exam, only had forward and lateral flexion of LUE to 90 degrees and weakness of infraspinatus, but full passive ROM. EDX with fibs in deltoid, BC, supraspinatus and infraspinatus. Rhomboids and PS clean. 
Diagnosis seems clear. I read a couple case reports. Also curious if there is any predilection for post-vaccine plexitis to develop in the injected arm. 

Hello All,
Looking for resources or apps to learn about EMG

Thank you for your help
 

I have a 72 y/o patient who presented to EMG for my colleague with
weakness of both legs. EMG is showing absent superficial peroneal bilaterally. Sural is 5.5 bilaterally. Peroneal motor amplitudes were 1.4 and 1.2 going down to 0.7 bilaterally with no slowing across the knees .

abnormal muscles on needling are TA, PL, EHL. 

everything else is normal. 

brought her in for a full Neuro exam. Only dorsiflexion, eversion and big toe extension are weak. Sensation diminished on dorsum of the feet only. 

Mri of the knees showed faint edema with no atrophy of the TA
of note , she had bilateral injection in both knees for pain just before this started (medial approach)

Just not comfortable with all of sudden, bilateral painless peroneal neuropathy. 

ALS ruled out. Needling everywhere, negative. No other weakness or symptoms

I would greatly appreciate any comments or thoughts regarding the further management of a patient who has given me permission to present his case in this forum. 

He is a 66yo male who underwent a liver transplant for alcoholic cirrhosis complicated by hepatocellular carcinoma in February 2018. He noted difficulty walking immediate post transplant with progressive sensory loss and imbalance. In early 2021, this became signifiantly worse and culminated in a fall with an ankle fracture. During admission, I was consulted and he was noted to have a sensory > motor polyneuropathy with lower limb predominance and nerve conduction studies confirmed a generalised demyelinating polyneuropathy. This was in the context of being on tacrolimus and mycophenolate therapy. Initial consideration was given to the possibility of a tacrolimus associated neuropathy given the onset at the time of transplant with possible worsening in the setting of dose escalation.

He was subsequently found to have IgM kappa paraprotein (3g/L) and positive high titre MAG antibodies on both ELISA and Western blot.

He had significant but incomplete clinical response to IVIg therapy with improvement in balance and distal strength. He remains on mycophenolate and a reduced dose of tacrolimus. He is on maintenance IVIg and notices his foot "slapping" more when walking in the week prior to his 4 weekly infusions.

Is there cause to push to switch his tacrolimus to an alternative - such as cyclosporin which will put him at risk of developing diabetes? Would anyone consider rituximab therapy for MAG neuropathy given persisting gait dysfunction - taking into account he is already immunosuppressed for his liver transplant? What are your thoughts on the development of a presumably autoimmune neuropathy in the setting of immunosuppression?

Thank you for your wisdom!

Today I saw a 25-year-old woman complaining of generalized numbness, tingling and itching over her trunk, extremities and scalp. This started a year ago , and she was treated as if this were an allergic reaction since she had severe allergic reactions to medications in the past. She was treated with antihistamines, IV steroids, etc. with only temporary improvement. She was seen by several dermatologist and neurologists , initially without change in her symptoms. She was started on gabapentin for the possibility that this was a neuropathy. This finally did markedly improve her symptoms . Most of the paresthesias in her trunk and extremities cleared, although they  are  still present over her face and scalp. Her physical exam today was essentially normal. The electrodiagnostic studies done today showed normal electromyography of all extremities. The nerve conduction study showed normal motor and sensory conduction studies in the distal extremities. Median and ulnar sensory amplitude's were 60 to 80 µV, and sural amplitude's were greater than 30 µV. Medial and lateral plantar sensory studies were easily obtainable and also showed large amplitudes. However, when testing proximal sensory conduction, a completely different picture arose. I was unable to obtain medial or lateral antebrachial cutaneous sensory studies in either arm. I have always found these easy to obtain in young patients who have large distal sensory responses. Since I began doing  the procedure for lateral antebrachial cutaneous sensory conduction in 1978, I was sure I was performing this correctly. In the lower extremities, I could not obtain a response in the lateral femoral cutaneous nerve, although it too  is usually obtainable in thin patients  with large distal sensory responses.

Motor artifact can be an annoy to SNAP (antidromic sensory study). It was told that moving the recording electrode away from the muscle would minimize it. This worked when possible. 

I wonder if longer stim duration ( say 0.2 ms instead of default setting of 0.1 ms) while lowering the stimulation intensity (60% perhaps) would stimulate sensory fibers preferentially to motor fibers, hence lesser motor interference?

Why or why not? Thanks

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 am considering buying my new sierra summit from current practice to use in a new job. Is there an additional cpt code or tech fee for owning the machine?

thanks

Does anyone have any experience of using simulation in training? I am aware of Dr Nandedkar's website, but are there any limbs or programmes that have been developed for use in training?

I did an emg on a patient that has had three thoracotomies, The last one included   and a Lat  Dorsi and serratus ant transfer. Post of pt had some scapular winging. No change  with shoulder abduction or protraction. NCS of the LTN was compared side to side. There was  a decreased amplitude of the NCS and normal latency. EMG  MUAPs showed small polyphaisc potentials,  and  reduced recruitment  or  poor activation without large MUAPs.  There were no fibs or positive waves. I thought there were a few CRDs. With the previous surgeries a dn msucle flaps , I am reluctant to call this a LT neuropathy as there is signifciant anatomical changes with the previous surgery. I  am not confident that this is a LT neuropathy. Perhaps the CRDs and small polyphasic MUAP were false postives becuase of muscle damage from the surgeries. 

Can Covid induced NMJ Blockade be named under Myasthenia? Or it is considered a different entity?

I am interested in purchasing a Neuromax, 2 or 4 channel, any year except a white model.  Prefer with the cart, but not necessarily.

I was wondering how many of our members have been monitoring or requiring their staff members to receive COVID-19 vaccination.With regard to patients, we have been administering antigen rapid testing in the office to all the unvaccinated . While  this is not as accurate as laboratory PCR testing, at least it gives us some information. Regardless of the patient's vaccination status, we still require masking of all staff members and patients.

59 yo female with numbness on the the thenar eminence following a repeat CTS release in 01/2021 (first release surgery was in 2005). Both open release. The numbness pre-op was on the median fingers. NCS (median SNAP with mid palm stim, median CMAP, median-radial thumb comparison) and EMG (including APB, OPPONENS) are normal. Suspecting damage to the palmar cutaneous branch of the median nerve. I do not know how to assess this branch. Help me please. 

I was hoping to get some input on this interesting EMG case that I saw the other day.  The patient is 65 year old female who was referred for an electrodiagnostic study to evaluate the bilateral lower extremities.  Patient presented to the hospital on 4/19/21 s/p being down for 2 days secondary to shock requiring intubation and pressor support.  She had a complicated hospital course and ultimately was suspected to have an acute spinal cord process causing paraplegia, however, MRI C/T/L-spine was unrevealing (MRI limited by motion artifact, body habitus, and body wall edema).  There were no sensory or motor impairments in the bilateral upper extremities.  She was referred for EMG of the bilateral lower extremities due to concern for critical illness neuropathy vs. spinal cord infarct. 　

EMG of the bilateral lower extremities was performed on 8/16/21.
Physical exam: 0/5 strength in the bilateral lower extremities (hip flexors, hip adductors, hip abductors, knee flexors, knee extensors, ankle dorsiflexors, ankle plantar flexors), absent sensation to light touch distal to the groin bilaterally, and absent patellar and achilles reflexes bilaterally.  There was significant pitting edema in the bilateral lower extremities to the knee bilaterally.
NCS: Sural and superficial sensory responses were unobtainable bilaterally.  Fibular and tibial motor responses were unobtainable bilaterally.  Right median sensory, ulnar sensory, and superficial radial sensory responses were normal.  Right ulnar motor and median motor responses were normal.  Right ulnar F wave was slightly prolonged at 33.2ms.
Needle EMG: There was active denervation in proximal (TFL) and distal lower extremity muscles (vastus lateralis, tibialis anterior, fibularis longus, medial gastrocnemius, and short head of biceps femoris) bilaterally with no evidence of axonal continuity in any sampled muscles of the bilateral lower extremities.  There was active denervation in the right middle/lower lumbar paraspinal muscles.  The left middle/lower lumbar paraspinal muscles were normal.  The right first dorsal interosseous and right deltoid muscle were normal. 
Conclusion:

1. Abnormal study.  Technically challenging study due to significant bilateral lower extremity edema and limited mobility due to bilateral paraplegia.  
2. Bilateral lower extremity sural sensory, superficial fibular sensory, fibular motor, and tibial motor nerve conduction studies showed no response.  Needle EMG examination of the bilateral lower extremities showed diffuse active denervation in proximal and distal muscles with no evidence of axonal continuity in any sampled muscles.  Taken together, these findings localize the pathologic process distal to the level of the dorsal root ganglion, and could be explained by severe bilateral lumbosacral plexopathies vs. a severe axonal, sensorimotor peripheral polyneuropathy.  
3. There is a possible superimposed right lumbosacral radiculopathy that is non-localizable.  
4. There is no electrodiagnostic evidence of a superimposed left lumbosacral radiculopathy.  
5. There is no definitive electrodiagnostic evidence of median neuropathy, ulnar neuropathy, or myopathy in the right upper extremity.  

I appreciate any thoughts that you may have. 

  

I am trying to get other physician confirmation regarding EMG NCV being a superior test to MRI in diagnosis of a bracial plexus disorder.

Thank you, 
S. de Lanerolle, M.D.

My practice is devoted exclusively to EMG/NCS testing.   I do not provide ongoing care for any patients and all my testing is non-urgent.  During this time of the delta variant surge, and in the interest of the safety of my vaccinated patients and staff, I am considering limiting my practice to vaccinated patients.
What are the thoughts in the AANEM community regarding this?   Has anyone limited their practice in this way? 

Do we have a consensus for the standard of practice for IVIg treatment small fiber neuropathy?
Some insurers will cover, others not. I understand the literature, such as it is, does not clearly support IVIg one way or the other.

Thanks for any opinions!

 

I would like to open a discussion about the p-value fallacy.
 
As a preface – The p-value fallacy has been known and discussed for many years.  Yet, little to no change seems to be happening in the medical sciences with regards to how we use and interrupt p-values (though alternate solutions have been proposed). I have only recently read into this topic and feel the implications for medical research are large and unpromising (hence my desire to hear the community’s opinion on the matter).
 
My understanding is such:
 
The common way (in medical sciences) p-value is taught/understood is categorically wrong. P-value was developed as part of significance testing. However, it has been erroneously applied to represent a type I error rate (or alpha level) in hypothesis testing. In hypothesis testing - null and alternative hypothesis are developed. Then an alpha level is set (usually and arbitrarily set at .05 or 5%) and an experiment is done. If the observed difference between the null and alternative hypothesis meets or exceeds a p-value of 5%, we reject the null hypothesis in favor of the alternative hypothesis (with the understanding that there is a 5% chance that the observation we made was by chance alone).

The problem is that assumptions made in significance testing (p-value) cannot be seamlessly transitioned to hypothesis testing (type I errors). Yet, this is exactly how it is taught and what is routinely done in medical sciences. Specifically, the null hypothesis in significance testing is assumed to be true. Therefore, it is categorically incorrect to apply it to hypothesis testing where the null hypothesis can be rejected. To bridge the p-value of significance testing with the type I error rate of hypothesis testing, and to mathematically quantify the p-value fallacy, researchers have used a Bayesian framework. Conclusions resulting from Bayesian analysis are multifold with two notable issues, 1) p-values routinely (and at times wildly) underestimate the false positive rate, and by extension, 2) p-values cannot give a specific percentage to uncertainty without considering priors (i.e., if we reject the null hypothesis, we cannot say there is a 5% probability what we are seeing is from chance alone without considering the prior probability the hypothesis was true pre-experiment).  

Taken together this would argue the p-value is widely misunderstood and misused with one corollary being we are routinely reporting “statistically significant” findings when none exist. This problem is superimposed on a myriad of other potential problems in medical research – some related to p-values (the reproducibility, or lack thereof, of p-values under theoretically identical experimental conditions) and some not (wide-spread bias, confounding, small sample sizes, lack of reproducibility of new research findings, conflicts of interest, etc).
 
Below are some resources that have shaped my view. I am very interested to hear the community’s thoughts and the possible implications for medical research.
 
 
 
Colquhoun, D. (2017). The reproducibility of research and the misinterpretation of p-values. Royal society open science, 4(12), 171085.
 
Gao, J. (2020). P-values–a chronic conundrum. BMC medical research methodology, 20(1), 1-8.
 
Wasserstein, R. L., & Lazar, N. A. (2016). The ASA statement on p-values: context, process, and purpose.
 
Goodman, S. (2008, July). A dirty dozen: twelve p-value misconceptions. In Seminars in hematology (Vol. 45, No. 3, pp. 135-140). WB Saunders.
 

Hey all, I'm in the process of starting up a PM&R EDX Lab in the context of an existing academic EDX lab and I would like to set things up so that patients can electronically enter their history information prior to the visit to help with clinic flow.  Does anyone have a patient intake form that they really like that we can use as a template that they would be willing to share?  We are also giving a talk on Building a  Successful Neuromucular practice at the fall meeting and would love to share it there as well or share a composite of the ones that we find.  Thanks everyone and happy Friday!  JWN

Hi all,
I wanted to ask for community/expert input on how you approach interpretation of distal latency with regards to demyelination, in the setting of severe axonal loss and muscle atrophy?
 
I believe it’s generally accepted that distal latency can be prolonged up to about ~130% of the upper limit of normal in the setting of axonal loss (without implying superimposed demyelination)-- largely due to loss of the fastest fibers.  For more proximal conduction velocities, ~75% of the lower limit of normal is used, which seems roughly commensurate.
 
However, when amplitudes are extremely low (e.g., 0.1 mV for a motor NCS), it seems plausible that other factors (beyond loss of fastest fibers) could cause further latency prolongation (without implying demyelination). Some of these include:
(a) distal collateral sprouting: increased NMJ transmission time
(b) distal collateral sprouting: more slowly conducting immature myelin (and decreased spacing of nodes of Ranvier)
(c) increased electrical transmission time through muscle due to atrophy
(d) inability to accurately measure motor onset latency (only seeing "tip of the iceberg" of the motor response
 
Importantly, it seems to me that all of these factors would affect the terminal portion of the study (distal latency) disproportionately (relative to the more proximal conduction velocity measurements)-- without implying demyelination-- and that these mechanisms bring us beyond what's expected for loss of the fastest fibers. In this context, 130% of the upper-limit-of-normal as a threshold seems too low/lax (might overcall demyelinating disease in the setting of end-stage axonal loss?).  I don't know if this has systematically been explored: the range of latency prolongations expected in extreme axonal loss.  
 
In this context, do you have a threshold for assessing distal latencies potentially concerning for focal demyelination in the setting of extreme axonal loss?  (A relevant clinical application would be looking for evidence of superimposed ulnar neuropathy at the wrist in a patient with established ulnar neuropathy at the elbow with severe and chronic end-stage axonal loss).   
Sandra
 

I am curious if anyone in the audience is a Medical Director of all Electrodiagnostic Services at a large hospial system (preferably academic medical center), particulary where neurology and PM&R labs are combined under this Medical Director? What are the job responsibilities of the Medical Director in this situation, who do they report to in the hospital? Do they receive any compensation for their time? What has been some of the pros/cons of this arrangement? Thanks for your help!