AANEM Connect

How much does trying to normalize the temperature, to avoid slowing of conduction velocity and dista latencies, have an inpact on patient care? I do not think that cool (not extreme) skin temperature will create the characteristic abnormalities noted by demyelinating polyneuropathies with quite prolonged temporal dispersion and significant slowing of velocities. Trying to warm up extremities cause delay and dyscomfort on patients given the extra time spent on performing the studies. Has there been a study that address this issue?

Manuel.

What do you use to warm limbs. I have seen and read about heating lamps, heating pads, hydocollators, hair dryers. Are there any standards on this issue from AANEM? 

Hello, 

Soon I will be tasked with setting up a new EMG lab at a satellite hospital. I've been thinking about choice of location of the lab in the new hospital and have been wondering about electrical interference. 

Is there a way to measure/predict if this will be a problem? That is, short of setting up the EMG machine and using it in the new location? 

I know folks are familiar with this problem in ICU settings, but once or twice I've run across the problem during inpatient studies, and have concluded the interference must have come from a room above or below where I was located......

Hi all,

I have had two cases recently which I would love the group's thoughts on. Both patient's had an atraumatic onset of severe pain through the shoulder/scapular/lateral arm region. This involved some sensory symptoms and weakness. The pain was so severe to keep them awake for a few days. They both then developed significant atrophy through C5 myotomes in the coming months with scapula winging. 

I saw them month approx 5 months post event. The NCS demonstrated recordable lateral cutaneous nerve responses, both within allowable symemtry of the contralateral side. The remainder of the NCS were normal (sensory/motor studies of median, ulnar, radial, antebrachial bilaterally). 

The EMG demonstrated involvement of seemingly fairly isolated C5 muscles (Rhomboids, supraspin, infraspin, deltoid, biceps with sparing of brachioradialis, triceps, EDC, FDI, serratus anterior) with both spontaneous neurogenic changes and neurogenic units with reduced recruitment. 

The MRI Cx spines for these patients demonstrated a mild, and a moderate (respectively) C5 formainal stenosis without nerve impingement. 

The MRI plexus was normal (but this was a delayed scan post my assessment, so approx 5-6 months post event)

My questions for the group

1) Historically, involvement of Rhomboids was used to demonstrate pre-plexus localisation. There have been a number of case reports in recent times, with people documenting involvement in later diagnosed plexopathies. How many people would still use Rhomboid involvement as evidence of pre-plexus localisation? 

2) Severe onset, atraumatic pain keeping patients awake with then progressive atrophy is not restricted to Brachial Plexopathies, but would make one think this, rather than a Radiculoapthy. These two patients have a very C5 isolated picture, Rhomboid involvement, seemingly spared peripheral nerves (including LABC), with mild and moderate formainal stenosis. Acknolwedging that you would be trusting my  ncs skills/report, who would lean towards a radiculopathy and who towards a C5/very early upper plexoapthy. 

Thank you all

I performed EMG with nerve conduction study on a lady who is treated regularly with Botox for dystonia due to Parkinsonism. From an electrical standpoint she had L5-S1 radiculopathy, With fibrillations and positive sharp waves in limb muscles, as well as the paraspinous musculature. I do not know what muscles are injected with Botox (she receives it at a different institution) So I do not know what percentage of electrical changes could be due to Botox. Proximal muscles that are involved make me comfortable diagnosing radiculopathy, but I felt a little uncertain with some of the distal findings. How much of a concern do you think this is, and how do you handle this?

Hello,

What ICD 10 code should I use for a long thoracic neuropathy?

G58.9? 

Thanks

While recording F waves on left APB, stimulating at wrist, I noticed the waveforms in question. I made the screen capture at two different sweeps, with increased F-wave gain for better visualization. The patient is a 69 year-old female that had a left carpal tunnel release aprox. 13 weeks prior. She did well after CTR for around 4-5 weeks when she developed worsening hand symptoms.

Good evening,

I recently encountered an unusual case of carpal tunnel syndrome (CTS) that I found quite challenging, and I am seeking some insights from this esteemed group.

A 77-year-old right-handed woman presented with various right hand symptoms, including paresthesias, stiffness, and coldness, which were sometimes worse at night. A cursory examination was normal, except for mild APB atrophy.

Her nerve conduction studies (NCS) showed the following:

• Median motor potential: Normal latency (3.8 ms), low amplitude (3.0 mV), and normal velocity (53 m/s)
• Right median SNAP: Borderline increased peak latency (3.60 ms), borderline low amplitude (19.5 μV), and normal velocity (53 m/s)
• Radial SNAPs were normal
• Palmar studies and studies to the fourth digits were entirely normal

I did not perform the ulnar motor potential or a needle EMG due to time constraints and the assumption that the low median motor potential was artefactual. I concluded with an essentially normal report, attributing her symptoms to musculoskeletal issues.

She was later evaluated at another institution, where her history was described as more typical of CTS. Their NCS results were also normal, but a restricted EMG examination revealed severe chronic neurogenic changes in the APB and a normal FDI. They diagnosed severe CTS and referred her for surgery.

I was surprised by this conclusion and would have considered a radicular or myeloradicular origin, likely imaging the cervical spine.

My questions are:

• Can CTS present solely with axonal motor findings, even with sensory symptoms?
• Is this potentially a case of isolated thenar motor branch involvement?
• How would you have proceeded with a case like this?

Thank you for your guidance.

Sincerely,
Repentant EMGer

I have a peculiar case on which i would like to have sought some advice. 

30y old male, electrician with no medical Hx. with since 3 weeks abducted little finger on the right side. Unable to bring the finger in adduction. No paresthesia, no other loss of strength. Doesn't remember a trauma or pain. 

 Clinical examination shows preserved reflexes, strength (FDI / ADM / FPL / FCU / FDP5 / Orther interossei), esthesia. Tests for UNE are negative  No UMN signs. 

Needle Emg: no denervation potentials in FCU / FDI / ADM / APB / EIP/ 3rd palmaf IO, decreased recruitment in 3rd palmar IO with two rapid firing MUAPs  

Ultrasound: normal configuration ulnar nerve from the axilla down to just distal of the pisohamate lig. Further course could not be evaluated but no ganglion cyste or other masses in the palm. Impression of possible myotendinous injury 3rd palmar IO on US but this is not my expertise so MRI is planned.

I had 2 questions about this case:

- Could you have a selective neuroraxia of the branch to the 3rd palmar explaining the clinical image a d findings on EMG? Patient reported repitive use of clipper the day he noticed the paresis  

-What would your findings be on needle emg after of musculotendinous / muscular injury? I've searched pubmed but can't find any literature on this. I think this woud give a dcreased recruitment but would this also influence firing rate? 

Good morining everyone. I wanted to reach out to anyone interested in presenting at a small conference virtually. We are looking for someone who can speak about the growing need for EMG/NCS and challenges of availability in both urban and rural communities. Anyone intersted please reach out to me at

cory.hansen2@imail.org

Hey all,

Im not sure if this is the right forum for this question, but I figured I'd give it a shot.

I did an EMG on a young patient with a clinical history of left UNE, and the nerve studies confirmed that localization. I proceeded to a root screen with the needle to evaluate for additional radiculopathy, and all muscles were normal except for one finding. When I inserted the needle in the left biceps at rest, I saw/heard what looked like a fib firing quite regularly at around 1 hz. There was some subtle variability to it, and it remained as I moved the needle around to sample different regions. 

He was wearing a zio patch, and while I didn't think this device put out any signal (just read), I put my finger on his radial pulse and the "fib" seemed to follow his pulse. 

The above led me to consider that maybe this could somehow be a zio-patch related artifact. Has anyone seen this?

I think a true fib is less likely because of the subtle variability (not just linear slowing or speeding up) and the fact that it continued as I moved the needle around.

I think a volitional motor unit is less likely because of the morphology and firing speed.

Thank you for any thoughts!

I have posted on this before.  The AANEM office suggested I post this to the forum to see if there are other physicians experiencing this issue.

I am starting to see billing warnings from other insurance companies (besides Humana who flat out denies) saying a patient can’t have carpal tunnel syndrome and cervical radiculopathy at the same time.  This combination frequently occurs in patients. 

And now the software system is also saying/warning that patients can’t have lumbosacral plexopathy and radiculopathy, even though there are patients with symptoms and findings that could be possible plexus and possible radiculopathy clinically where the EMG doesn’t definitively rule out one or the other and additional anatomical imaging or other work up is needed. 

This is looking like a trend where the insurance company will deny if these diagnoses are submitted together but will also deny higher nerve conduction codes like 95913 saying it isn’t necessary for “just” carpal tunnel or “just” cervical radiculopathy or any other limited diagnosis codes submitted. 

Perhaps AANEM would have more clout in going to insurance companies on this.  I have submitted position letters from AANEM with appeals, but many times it doesn’t work.  The insurance companies don’t give a s… about me as a solo practitioner and they have no incentive to do what is fair. 

 Thank you. 

Janet Balbierz, M.D.

I have a patient with a small fiber neuropathy who started with constant severe burning pain in his feet. After 2 or 3 infusions of Rituximab his pain intensity is now 20% of the original intensity and his pain is no longer constant with the pain lasting from 2 or 3 hours a day up to 11 hours (2 or 3 hours the most common duration.

He has a sustained response to the Rituximab but seems to be hitting a plateau in terms of response. Would switching him to another agent possibly produce additional benefit? If not how long should I continue the Rituximab. He has had 3 infusions so far?

We had a 40 years old male with no previous co-morbids in our edx lab for evaluation of non-specific generalized weakness since childhood which he noted has worsened recently with ho of neck pain. There was no radiation to arms, no reported sensory or motor weakness or bladder and bowel dysfunction.

OE: strength was good in all 4 limbs, relatively brisk reflexes (more in upper limb), hoffmans negative, plantars-down, no sensory level, was able to walk tandem, could walk few steps on toes and heels.

On NCS, right median sensory latencies and SNAP were normal, bilateral median motor were not-recordable bilaterally from APB. Ulnar motor and sensory were normal.

On needle examination few neurogenic units (polyphasic, broad) were found in right APB and bilateral ADM with no active denervation. Apart from these muscles, no EMG abnormalities found in bilateral upper limbs (including right EIP, PT, PQ, PL, FPL, biceps, triceps and left APB, FDI, FCU and EIP) and bilateral cervical paraspinals.

Since no significant abnormality was found in median SNAPs and EMG of median innervated muscles,

we did additional studies recording ulnar motor nerve from thenar (to rule out riche cannieu anastomosis) and median from hypothenar muscles (for MGA) which were inconclusive. Median nerve was then recorded from FPL which mostly showed ulnar motor wave form.

MRI cervical spine was reported multilevel disc degenerative disease most marked at C4-C5 level, resulting in mild compressive myelopathy (as reported )

Is this remote inactive cervical C8-T1 radiculopathy or proximal CB of bilateral median nerves but again EMG is normal in all median innervated muscles except minimally abnormal APB and, yes normal SNAPs?

Appreciate your input to understand this.

Thanks.

 

There is somewhat disputed different opinions about the ideal CMAP recording elctrode size, shape and type (metal vs. disposable) and relation to different muscle size. I appreciate experts discussion of this issue . 

Bassam A. Bassam, MD, FAAN

Looking for someone who does Botox injection into piriformis muscle (ultrasound guided or not). Need to refer a patient. I am practicing in Virginia, but patient is willing to travel.  Thanks.

Hi all,

I am hoping for some input on the following case.

The patient is a 70F with no known medical history.

Left lower extremity weakness and pain for ~ 8 months. Progressed slowly; ~4 months ago the left lower extremity symptoms started to improve but patient developed weakness of the right lower extremity. Has had multiple falls. Some burning pain and numbness of right leg (not well characterized). No back pain. No upper extremity complaints.

Exam

LLE strength 2-3/5

RLE strength 1-2/5 proximally; 0/5 dorsiflexion, toe extension; trace plantarflexion

Sensation intact to pinprick and light touch, decreased to vibration on the right

Achilles/patellar reflexes absent

 

Patient has been seen by neurology. There was concern for CIDP.

Has not had extensive labs; ESR/CRP, CMP, CBC normal.

MRI lumbar spine and LP with CSF studies unremarkable

Electrodiagnostic results:(technically limited by lower extremity edema and obese body habitus)

NCS

Absent sural sensory responses bilaterally (there was moderate edema)

Left fibular CMAP: normal latency and CV; decreased amplitude 0.5 mV at EDB, 1.1 mV at TA

Right fibular CMAP: absent at EDB and TA

Left tibial CMAP: normal latency and CV; decreased amplitude (3.0mV)

Right tibial CMAP: normal latency; dec CV (28m/s); decreased amplitude (0.4mV)

Normal right radial SNAP and normal ulnar/median CMAPs

F waves-normal right median, normal left fibular, prolonged left tibial, absent right tibial

H reflex-borderline left tibial, absent right tibial

EMG: TA, FL, gastroc, VM, RF bilaterally: fibs/psws in all muscles; unable to activate the right TA or FL; there were mild-moderate neuropathic changes in all other muscles.

I'd like to call it an axonal polyneuropathy but am thrown by the relatively rapid onset, waxing/waning left lower extremity symptoms, and extent of proximal muscle involvement without any upper extremity involvement.

From reviewing Preston and Shapiro, the relapsing/remitting nature, stepwise progression, and asymmetry suggest mononeuritis multiplex or a CIDP variant. But would these present with findings isolated to the lower extremities and abnormal findings in all muscles tested?

Thank you and I appreciate any input!

 

67F Patient referred for right hand weakness and numbness/pain over the past year.  She reports it started in digit 5, now numb in digit 4 also. She is having progressive difficulty with gripping things, bending her fingers and thumb, but also weakness with extending her wrist and thumb. She has a histroy of stroke with right sided residual deficits a few years ago, but those were improving until the last year. Her exam is notable for 4/5 RUE  shoulder abduction, elbow flexion, elbow extension. 3/5 RUE wrist extension, finger extension, DIP flexion, thumb opposition, and 2nd/5th digit abduction. 5/5 throughout the LUE. Decreased sensation in right ring and pinky fingers. 3+ reflex throughout the RUE. Has a positive Tinel's at the elbow but also positive Spurling and Adson+Roos test (she really reported symptoms with any movement of that arm).

NCS notable for absent right ulnar SNAP with robust median, radial and contralateral ulnar signals. Very low amplitude right ulnar CMAP (0.2 mV) and slowing across the elbow (59 m/s to 48 m/s) without conduction block.  Also slowing of the right median SNAP at D2 (4.4 ms), with normal right median CMAP.

EMG with neuropathic changes in FDIH, OP, EIP (p waves, fibs, large polyphasic units with markedly reduced recruitment, with most spontaneous activity at FDIH). Normal biceps, triceps. 

The lesion seems to be post ganglionic, and with pattern of numbness and weakness, the most parsimonious location would be inferior trunk. No trauma, no cancer history. However, she also has slowing across the elbow, so considered seperate severe ulnar neuropathy and a cervical (C8?) radiculopathy. 

I sent for an MRI brachial plexus with contrast, which returned as essentially normal. Then got an MRI C-spine with findings of "Severe right foraminal zone stenosis C6-C7 due to uncinate osteoarthropathy and moderate degenerative disc disease.  Tiny right paramedian disc protrusion C5-C6. There is no central canal compromise at any level". Nothing notable at C7/T1.  I've referred her to both a hand surgeon to discuss her ulnar elbow, and a spine neurosurgeon for her neck. 

Any suggestions on interpretation of localization in this patient? Things that would have helped electrodiagnostically to point in the right direction for management? Looking back I probably should have done a MABC. 

Thanks!

In the evaluation of a person with LMN spina bifida (ie S1), who is referred for query S1 radiculopathy, can we be sure that if we see spontaneous activities on needle EMG that there is something acute going on? Or could that be a remnant of the underlying spina bifida? 

Hello colleagues,

I have a 16M patient with complicated history, presumed CIPD but also found to have MFN2 gene mutation. He came to me for PM&R consult, he has persistent distal weakness and atrophy requiring AFOs, hand splints and scoliosis. He has seen multiple neuromuscular specialists over the past few years, but now they are looking for referral to a neuromuscular specialist in CIDP who they can get another opinion regarding his medications (IVIG, rituximab). He likely needs a repeat EMG but I didn't want to do it if he was going to go to a new neuromuscular doctor who would probably want to repeat the study themselves anyway. He lives in central NJ. Any recommendations for a CIDP specialist in this area? Thank you

Hello All,

Looking for input/data for safety of NCSs in cardiac patients with external pacers/ defibrillators/ LVAD. there is plenty of literature on implanted devices, any insight for external devices.

Thanks.

I am requesting all of your help to better define both the audience and outreach for this forum via the AANEM Connect discussion venue.  Would you be so kind as to please give your thoughts on the following:

 

• Continue to keep the AANEM Connect forum open only to the AANEM membership as it currently exists as a benefit of a paid membership only.

Or

• Open up the AANEM Connect forum a bit for viewing purposes only, to Neurology/PM&R residents/neuromuscular fellows who are not members of the AANEM, but without the ability to ask questions or perform searches and free of charge.  A support letter from a program director would ensure the status of the resident/fellow.

 

Greetings EMGers,

 Do you have any old EMG or SSEP equipment or parts?  ASET--The Neurodiagnostic Society (Technologist society) is collecting old EMG and EP parts and equipment for the virtual museum of the  Smithsonian Institute Neurodiagnostic Museum. I'm on the ASET Historical committee for the Smithsonian Institute.  I'm working on the EMG/EP section.  If you have anything that looks like it should be thrown in the trash or old equipment you are trying to get rid of , please consider donating these old items to ASET for the virtual museum. 

I am posting this in part out of frustration, and also to generate discussion regarding training and philosophy on performing history/physical during EDx consult.

I recently saw a 63 y/o male, smoker, with pmxh from pcm note copd/chronic hep c with about 1 year of progressive subjective decreased balance, dropping items, shoulder weakness, numbness/tingling equal bilateral volar forearms into hands d1-3 (constant but improved with gabapentin) night cramps in thighs and calves.  He had seen local neurologist shortly before I saw him (fellowship trained neuromuscular) who did NCS but could not do needle study due to patient refusal.  NCS normal other then ulnar slowing across elbow, felt to be indicental given lack of ulnar symptoms.  This doctor did no history or physical exam, nor did he make any comments regarding potential diagnoses or workup.

My exam notable for deltoid and scapular muscle atrophy and weakness with distal UE muscles and quad/hip flexors normal. Reflexes spastic with Hoffman, no clonus.

I orderd c-spine MRI:  Severe central stenosis C3-5 with cord signal changes.

• I was trained as PM&R to always do H&P; discuss findings with the patient; discuss clinical correlation, need for additional workup/treatment in my report. I will make the surgical referral or order additional workup within my scope of practice because that's how I learned and it's good for the patient and their referring provider.
• However, I have seen many studies over the years, all done by neurologists, where none of the above is done.  The patients have confirmed this as well.  Doctor told them to get on the table, no exam, test was done, no discussion, minimal or no discussion in the report, sent back to PCM so they can try to figure it out.
• I have had neurologists tell me this is how they were taught.
• I struggle with the concept that at least some neurologists don't practice EDx medicine per the guidelines from AANEM, especially considering that the AAN seems to use the AANEM guidelines.
• I'm frustrated:  how can a fellowship trained neuromuscular specialist miss what should be a pretty simple diagnosis?  
• Does anyone in this community also not do H&P as part of the test?  If so, why?
• Can we as a community do anything about this problem?

I've been looking for the ideal pen to use for studies -- a combination of visible, somewhat resistant to electrode gel, and washable.  I've used Zebra Clickart Water-Based Pen Calm Dark 12 Colors Set, Wyss22-12Cdk that has the advantage of being clicked open/closed but does smear a bit when patients sweat or when too much electrode gel is present.  Does anyone else have a product that they are happy with?