AANEM Connect

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  I've also heard that MGA is associated with higher levels of intelligence and good looks (unpublished observations).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 

Esteemed (and much smarter than me) colleagues,

I was recently asked the following question by an AANEM member:

"Another scenario I have encountered is a relative amplitude drop from side to side of Ulnar sensory at the wrist in the presence of normal ulnar motor studies."

For this scenario (especially when needle EMG and MAC are unremarkable), i have a templated bit of text that i have been using and thought i'd run it by you folks:

In the absence of any motor conduction or needle electromyographic abnormalities, the isolated finding of relatively decreased ulnar sensory response is of unclear significance and could be attributed to:

• Ulnar sensory only neuropathy
• Old axonal injury with motor recovery (via collateral sprouting) along the course of its pathway (C8 ramus, lower trunk, medial cord, or ulnar nerve).
• Technical issue (although the test was repeated and all electrodes repositioned during testing today).

What do you think? Any problems on your end with that? 
 

Hello everyone.

A 34 yo woman was reffered to emg lab.

During puerperium she had a diagnosis of iliac vein thrombosis.
She had right leg edema, a little pain and weakness on the limb
She complainned about hyperstesia on the foot and distal third of the leg

now, about 3 months after diagnosis and symptom presentation she came to emg lab
she had suspended anticoaglutaion for the needle exam in the past 24h

- ncs:
motor, right deep peroneal: reduced amplitude
tibial nerve h reflex: absent in the right
sensory, superficial peroneal nerves normal and symetric
sensory, sural: on the right (symptomatic side) = 23 mcv  / on the left side = 44 mcv

i repeated ncs in the next day. same results

- emg:
at rest: a lot of spontaneos activity in gluteus medius,  tibialis anterior, tibialis posterior, peroneus longus
contraction: chronic neurogenic pattern in  tibialis anterior, tibialis posterior, peroneus longus

She had a normal lombossacral spine MRI.

I fisished my report suggesting lombossacral plexopathy (right sural 48% lower), thought could not eliminate pré-ganglionar etiology for sure.

I would like to hear critics and ideias about the case, and wonder if anyone has had any case similar.
thank you

 

Dear Neuromuscular Specialist,
 
 
We would like you to participate in a brief, 9-question survey research study about your use treatment approach in generalized myasthenia gravis (gMG). These survey results will be analyzed and published to inform the neuromuscular community about current practice patterns in gMG.  Please see the attached letter and link to the REDCap survey (https://redcap.vcu.edu/surveys/?s=DYYJYHLHMEFWA373) Your participation in voluntary and would require between 2-5 minutes. We will analyze the survey results and disseminate this information as a publication. If you have any questions at all, please do not hesitate to contact me.
 
 
Thank you for this consideration,

Kelly G. Gwathmey, MD
Neuromuscular Division Chair
Department of Neurology
Virginia Commonwealth University
Kelly.gwathmey@vcuhealth.org

As we prepare for EMG Talk next month, we'd love to hear of proposed EMG impressions as poems, limerics, or haiku.  There may be a prize the for best one (e.g. a EMG Talk Hat).

An example (which is admittedly not very good) to get you started

His only weak muscle is the trap
Bladder's good and he can take a c- -p
His issue is with accessory spinal
So I think this report is final.

I know many out there can do much, much better - please suggest some alternatives.
See you all next month!

is there a need to place a magnet over an ICD while performing nerve conduction studies? I have never done this before, but recently was asked to apply a magnet over the ICD while performing nerve conduction studies.

I am on this year's taskforce to increase physiatry involvement in AANEM. A colleague commented on Muscle & Nerve being a place where we can improve attractiveness or relevance to us physiatrists.

So the question is, if you had a magic wand, what would you want the Muscle & Nerve Journal articles to address? 
 

I am looking for Semiars for IONM billing. I can't find anything, we need this included in the annual conferences..... this is a rare type of billing and needs someone to lead the way... I have been doing it for 20 plus years but still can't find any type of education to help with new things or knowing what all you can bill for etc...,.

Congratulations Dr. Dumitru on Lifetime Achievement award! 

Our questions:
Is this the correct diagnosis?
Should we simply treat her with whatever rheumatology suggests (steroids plus steroid sparing agent of thier choice) or should we continue maintenance IVIg in addition to this?


62 year old woman with 6 weeks of progressive distal painful paresthesias and weakness. 
Seven weeks prior - myalgias, no weakness, ?viral illness?. No further musculoskeletal pain after this week.  
Six weeks prior - painful paresthesias in both hands and both feet. 
4-5 weeks prior - noticed progressive weakness - fell when "ankle collapsed" 
 
Exam with significant distal and proximal weakness with some distal wasting.
Absent reflexes except knees 1+.  (Exam from another MD noted present reflexes 5 days prior.)
Sensation: Stocking (to ankle) - glove (to above wrists) - LT, PP.
Decreased vibration ulnar styloid, B and medial malleolus, B.
Proprioception impaired at MP bilaterally and ankle bilaterally. 

EMG/NCS
Motor NCS - no responses - Median (APB), Ulnar (ADM), Tibial (AH), Peroneal (EDB).
Peroneal (TA) - low amplitude, no slowing of CV, no temporal dispersion, no conduction block.
Sensory NCS - no responses - Median (DIII), Ulnar (DV), Superficial peroneal and sural. 
Signs of denervation in multiple muscles with few MUPS with normal configuration, increased recruitment ratio, discrete interference patttern at full effort.

CSF
Protein - 28
Glucose normal
WBC - 4 -
52%Neutrophils
22%Lymphocytes
26%Eosinophils
RBC - 11

Awaiting VEGF results

P-ANCA 1:320
MPO (myeloperoxidase) 23.8 weakly positive (drawn after IVIg was given)
CT sinuses -  extensive paranasal sinusitis with with areas 
of hyperattenuation favored to represent inspissated secretions.
No rash
CT chest - 6 mm left apical nodule; no parenchymal abnormalities. 
CT abd/pelvis - no abnormalities.
EKG - normal
ECHO - no abnormalities
No symptoms of asthma
Peripheral eosinophil - 37%; absolute 4.7 K/uL
 

Rheumatology - given her clinical and laboratory data, they had high suspicion for eosinophilic granulomatosis with polyangiitis (EGPA - the old Churg-Strauss).  They started treating with pulse methylprednisolone 1000 mg IV daily for 3 days and now on oral steroids daily.
We gave IVIg a week prior but no response as of yet. 
 

MRI spine and brain without and with gado - no abnormalities.

Patient with some mild improvement of symptoms on steroid, noted as return of some reflexes ( 1+ Brachioradial, Biceps bilaterally and 2+ patellar bilaterally).

The rheumatologists wanted to do sural nerve biopsy and I asked them about other sites for biopsy and they said there was nowhere else to biopsy.
Sural Nerve Biopsy showed no evidence of vasculitis. Showed severe, subacute (ongoing) axonal degeneration, in the background of moderately severe axonal loss.. 

Official report summary as follows: 
This biopsy reveals severe, subacute (ongoing) axonal degeneration, in the background of moderately severe axonal loss. Numerous foct of fiber breakdown associated with phagocytotic macrophages are displayed in cross-sections. By the semi-quantitative teasing fiber analysis, 62% of the remaining fibers show active Wallerian degeneration. The demyelinating componentis displayed amongst 12% of the teased fibers in the forms of segmental demyelination/ remyelination and is thought to be indistinguishable from age-related changes. Multiple levels of sections have been investigated for possible vasculitis: this biopsied segment of the nerve shows no histological features of vasculitis.
 

Other work up: 

-B12, Mg and TSH wnl

-ESR/CRP moderately elevated

-Zn, Cu levels normal

-RPR negative

-strongllodes, toxocara, tryptase- WNL,

- Hepatitis panel negative

 

THANK YOU!!
 

Hi everyone,
I saw a 43 y/o woman with right neck and shoulder atrophy after surgical excision of a upper cervical mass in June 2021.  Needle evaluation shows decreased insertional activity and no recruitment of motor units in the trapezius and SCM, except for two MUAPs seen in the upper trapezius.  No abnormal spontaneous activity was seen.  Other scapular muscles were normal.  Ultrasound evaluation confirms marked atrophy and hyperechoic texture changes localized to these muscles.  Presentation seems consistent with near complete loss of spinal accessory nerve function.

Is this a diagnosis that may benefit from peripheral nerve surgery?  If so, are there any centers that can evaluate for this.  Location is Spokane but I'd imagine this patient would be willing to travel.  

Hi; 
I'm asking if you found during your practice any peripheral neuropathies associated with the sickle cell disease (heterozygous variant)

With kind regards

Hi; 
I'm asking if you found during your practice any peripheral neuropathies associated with the sickle cel disease (heterozygous variant)

With kind regards

I am interested to know whether this pattern of sensory involvement is a clue to a particular aetiology or pathology? This is a patient referred several months after prolonged ICU admission with suspected recovering critical illness myoneuropathy on a background of poorly controlled diabetes mellitus. The upper limb sensory responses revealed an unexpected relative sparing of the ulnar nerve. See attached image for sensory study results.