EMG case

[Myofascist]

Hi all, I guess I'll try and get this forum going a bit with an EMG case I had this AM. I am a PGY-4 and am currently doing an outpt MSK/EMG rotation at a Kaiser which has very little attending supervision and I am on my own for EMGs.
38 yo female (looking much older than age) w/ long h/o numbness/tingling in right hand. Had CTR on the right in 2006 with no relief of sx's. Was sent to pain mngmnt and had multiple CESIs w/ no relief (she c/o some arm pain as well up to shoulder). A few mnths ago, began noticing similar sxs on the left ans was sent back to hand surgeon. Hand surgeon did steroid inj and, again, no relief. Sent to me for LUE NCS for eval of CTS.

NCS data
sensory studies:
digit 2: DL 3.1 amp 5.9
digit 3: DL 3.3 amp 6.0
digit 5: DL 4.0 amp 8.1
superficial radial: DL 2.1 amp 6.1

motor studies:
median motor: latency 3.2 (7cm) amp 14.28/14.10 CV 51 m/s
ulnar motor: latency 2.3 amp 11.28/9.2 (3cm below elbow)/6.02 (above elbow) CV 52 m/s between wrist and below elbow and 43 between below and above elbow
Martin-Gruber study showed NR at elbow and wrist

At this point I asked if she has any LE sxs and she said she has had paresthesiae in her feet for the past mnth or so...

Sural: DL 4.1 amplitude 7.1
Superficial peroneal: NR???

I was running outta time so I will probably be bringing her back for more studies and I know I coulda done a heck of alot more, but at this point I thought it looked like a pure sensory axonal polyneuropathy affecting her UEs > LEs and a superimposed ulnar neuropathy at the elbow with conduction block and no signif axonal loss. Cervical radiculopathy is not likely w/ the abnormal SNAPs and normal CMAPs so I didnt really see the need for a needle exam. Any thoughts on this data and what I should do when/if she comes back?

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[drusso]

Hmm...Interesting. Would like to know more family and past medical history. Any family history of PN? Any history of environmental exposure. Could it be a pure sensory mononeuritis multiplex -- a Wartenberg's migrant sensory neuritis.

http://www.ncbi.nlm.nih.gov/pubmed/11353434?dopt=Abstract


I would have done the needle exam...

 

[neglect]

Great post. So I hope I understand you: these are low amplitude sensory, nl motor responses except the LE, with preservation of all conduction velocities? Electrically this is an axonal neuropathy. How many years has she had DM?

The other, rare possibility here is the low sensory amplitudes are coming from a more proximal source like a plexopathy, but I think you've excluded this by doing another limb and with normal motor amplitudes.

In this context, my only question is why bother to try to demonstrate a M-G and how in the world did you obtain the sural?

(I would do an EMG to find anything worth chasing into the cervical spine).

 

[Myofascist]

Thanks Drusso, I will bring her back for the needle and maybe some contralateral studies soon. I just found a very similar case 26-2 on page 406 in Preston and Shapiro. They say that if this were to be a pure sensory neuronopathy, it would be quite rare. Some cases of Sjogren's, Friedrichs ataxia, and other neurodegenerative disorders can cause this. But in this case it was due to a paraneoplastic syndrome from small cell lung cancer. As I stated she was looking much older than her age and I have a feeling she is a smoker. I'll find out more tomorrow. Thanks again.

 

[PMR 4 MSK]

So far I agree with your tentative Dx. In addition to studying the right side, try doing some proximal sensory antidromics - you stimulate same points as for motor and calculate CV the same - not everyone agrees it's worth it, but in sensory axonopathies, you'll often see a drop in CV in the forearm, similar to what you see in diabetic neuropathies in the motors.

LE motors neccesary too. Also do bilateral H-reflexes. In pure sensory neuropathies, they should be normal, but in early motor neuropathies, they are often slightly prolonged.

Needle exam should be normal, even L FDIM since it's mainly demylinating CuTS with a little CB.

Patients like this, I study the **** out of them. I have a PPN case coming back next week - legs look like classic CMT type 1, but everything normal except many fasiculations in most muscles below the knees, on needle exam and some visible, and also mildly delayed H-reflexes bilateral. He was referred for BLE's, but I'm bringing him back for some UE studies, possibly face (if he'll let me), more Hx taking, probably labs and review the MRI brain - c/o facial twitches, none seen by myself in the face or tongue, also has c/o back and leg pains, no N/T, MRI L-Spine shows mild DDD L4-5 and L5-S1.

 

[Myofascist]

Hi Neglect, I must have been reading/posting when you replied. Not sure what you mean by the M-G. The sural was very difficult to obtain and I may go so far as to say equivocal but they seemed to be reproducible, then drop, and eventuall I think I teased it out but cant be sure. No such luck with the superficial peroneal.
PMR 4 MSK thanks for the input... I definitely will shock and poke the $!#%^ outta her... wait a minute that doesnt sound so good... no disrespect meant there. I'll write more data soon.

 

[drusso]

Keep us posted.

 

[caedmon]

A neuronopathy secondary to Sjogren's is a good thought. That's what I've heard mentioned frequenlty as a differential in the setting of isolated sensory changes. I would have done a needle exam as well, but it never hurts to bring people back when your time limited.

 

[SSdoc33]

Hi all, I guess I'll try and get this forum going a bit with an EMG case I had this AM. I am a PGY-4 and am currently doing an outpt MSK/EMG rotation at a Kaiser which has very little attending supervision and I am on my own for EMGs.
38 yo female (looking much older than age) w/ long h/o numbness/tingling in right hand. Had CTR on the right in 2006 with no relief of sx's. Was sent to pain mngmnt and had multiple CESIs w/ no relief (she c/o some arm pain as well up to shoulder). A few mnths ago, began noticing similar sxs on the left ans was sent back to hand surgeon. Hand surgeon did steroid inj and, again, no relief. Sent to me for LUE NCS for eval of CTS.

NCS data
sensory studies:
digit 2: DL 3.1 amp 5.9
digit 3: DL 3.3 amp 6.0
digit 5: DL 4.0 amp 8.1
superficial radial: DL 2.1 amp 6.1

motor studies:
median motor: latency 3.2 (7cm) amp 14.28/14.10 CV 51 m/s
ulnar motor: latency 2.3 amp 11.28/9.2 (3cm below elbow)/6.02 (above elbow) CV 52 m/s between wrist and below elbow and 43 between below and above elbow
Martin-Gruber study showed NR at elbow and wrist

At this point I asked if she has any LE sxs and she said she has had paresthesiae in her feet for the past mnth or so...

Sural: DL 4.1 amplitude 7.1
Superficial peroneal: NR???

I was running outta time so I will probably be bringing her back for more studies and I know I coulda done a heck of alot more, but at this point I thought it looked like a pure sensory axonal polyneuropathy affecting her UEs > LEs and a superimposed ulnar neuropathy at the elbow with conduction block and no signif axonal loss. Cervical radiculopathy is not likely w/ the abnormal SNAPs and normal CMAPs so I didnt really see the need for a needle exam. Any thoughts on this data and what I should do when/if she comes back?

ok, i got a few problems with the data here. first of all, ive done about 400 studies, and have yet to see anything really wacky, so bare in mind that the more common stuff is the most likely.

i'd be wary to rely on sensory amplitudes. this often varies greatly with temperature and stim intensity.

also, you have several NORMAL sensory studies. how are you calling this a sensory axonal polyneuropathy? the left digit 5 sensory showed an INCREASED amplitude.

as far as the conduction block across the elbow, try not to call that unless there is greater than a 10 m/s difference across the elbow. also, you really need to have symptoms in an ulnar distribution and some even argue that the across-elbow segment needs to have a CV of < 39 m/s to be considered ulnar neuropathy at the elbow. make sure to measure that segment with the elbow bent. this will increase the CV across that segment.

always do the needle. it is the most sensitive indicator of axonal damage. plus, you get to bill for it.

i hate to burst your bubble, but i think the changes you are seeing are more likely technical that truly pathological.

i totally commend your actually thinking about the data, and what they mean. that is a lot more than i can say for a good deal of residents out there.

 

[neglect]

ok, i got a few problems with the data here. first of all, ive done about 400 studies, and have yet to see anything really wacky, so bare in mind that the more common stuff is the most likely.

I'm afraid I have some problems with what you posted. I'm not trying to come off as a know-it-all (or even as a know something) and I'm not questioning your game, just working on my own. Here are my thoughts.

You have to rely on sensory amplitudes. To my mind, all NCV data must make sense within the clinical context. Otherwise what's the point of doing it? You can't ignore widespread decreases in sensory amplitudes just because you don't like the data. Case in point, my partner saw a man who had a NCV/EMG two days before coming to the ER with clear Guillian Barre (after the LP). He had been given the diagnosis of mild CTS, but the NCV showed multiple areas of demyelination and the overall diagnosis was missed.

In our lab, a normal antidromic sensory ulnar amplitude is greater than 20. Am I incorrect in "digit 5" = sensory ulnar anti? Or was this orthodromic?

And as far as conduction across an elbow, I certainly agree this area is fraught with danger. If there are no symptoms, then an abnormal response requires remeasurement, restimulation, re-examination and basically you've got to convince yourself that this is no fluke. Agree: distance should be measured slightly flexed (45 degrees off 180 extension). You should be your harshest critic. As an aside, I've been having technical problems in the setting of obesity here. Boy, fat people get fat all over, don't they?

What I question here is that the motor nerve across the elbow should have a faster NCV than the forearm segment. (Our lab uses 50 distal and 52 proximal). The reasons are a wider nerve here and generally warmer nerve here (more so with fat people). So, in the proper clinical context, even slowing into the high 40's is probably pathologic. In this case, we have loss of amplitudes as well, possibly indicating block. If there had been chronic neurogenic chages in the FDI, but none in the APB, then it would have really implicated the ulnar nerve. Such a patient, with axonal damage, would be unlikely to respond to bracing.

Your thoughts?

 

[neglect]

Hi Neglect, I must have been reading/posting when you replied. Not sure what you mean by the M-G. The sural was very difficult to obtain and I may go so far as to say equivocal but they seemed to be reproducible, then drop, and eventuall I think I teased it out but cant be sure. No such luck with the superficial peroneal.

Sorry, Martin-Gruber. I always have to work these out in my mind when I think I have one.

I definitely will shock and poke the $!#%^ outta her

Myofascist!

 

[SSdoc33]

I'm afraid I have some problems with what you posted. I'm not trying to come off as a know-it-all (or even as a know something) and I'm not questioning your game, just working on my own. Here are my thoughts.

You have to rely on sensory amplitudes. To my mind, all NCV data must make sense within the clinical context. Otherwise what's the point of doing it? You can't ignore widespread decreases in sensory amplitudes just because you don't like the data. Case in point, my partner saw a man who had a NCV/EMG two days before coming to the ER with clear Guillian Barre (after the LP). He had been given the diagnosis of mild CTS, but the NCV showed multiple areas of demyelination and the overall diagnosis was missed.

In our lab, a normal antidromic sensory ulnar amplitude is greater than 20. Am I incorrect in "digit 5" = sensory ulnar anti? Or was this orthodromic?

And as far as conduction across an elbow, I certainly agree this area is fraught with danger. If there are no symptoms, then an abnormal response requires remeasurement, restimulation, re-examination and basically you've got to convince yourself that this is no fluke. Agree: distance should be measured slightly flexed (45 degrees off 180 extension). You should be your harshest critic. As an aside, I've been having technical problems in the setting of obesity here. Boy, fat people get fat all over, don't they?

What I question here is that the motor nerve across the elbow should have a faster NCV than the forearm segment. (Our lab uses 50 distal and 52 proximal). The reasons are a wider nerve here and generally warmer nerve here (more so with fat people). So, in the proper clinical context, even slowing into the high 40's is probably pathologic. In this case, we have loss of amplitudes as well, possibly indicating block. If there had been chronic neurogenic chages in the FDI, but none in the APB, then it would have really implicated the ulnar nerve. Such a patient, with axonal damage, would be unlikely to respond to bracing.

Your thoughts?

well, now we're talkin!!!!!

the ulnar nerve at the elbow is more superficial than in the forearm, so while it is thicker, it is actually colder. should even out. next-to-impossible to get an accurate measurement on the fatties.

im not saying you should ignore sensory amplitudes, but you have be sure to stimulate at the appropriate level, or you will get a false-low response. you have to be meticulous to call a neuropathy on that.

also, tmeporal dispersion should show up in the SNAP waveform, which we dont know about. and we'd see F-wave abnormalities.

i have no problem drawing conclusions from the data, but its gotta be legit and obtained cleanly.

 

[PMR 4 MSK]

ok, i got a few problems with the data here. first of all, ive done about 400 studies, and have yet to see anything really wacky, so bare in mind that the more common stuff is the most likely.

i'd be wary to rely on sensory amplitudes. this often varies greatly with temperature and stim intensity.

also, you have several NORMAL sensory studies. how are you calling this a sensory axonal polyneuropathy? the left digit 5 sensory showed an INCREASED amplitude.

as far as the conduction block across the elbow, try not to call that unless there is greater than a 10 m/s difference across the elbow. also, you really need to have symptoms in an ulnar distribution and some even argue that the across-elbow segment needs to have a CV of < 39 m/s to be considered ulnar neuropathy at the elbow. make sure to measure that segment with the elbow bent. this will increase the CV across that segment.

always do the needle. it is the most sensitive indicator of axonal damage. plus, you get to bill for it.

i hate to burst your bubble, but i think the changes you are seeing are more likely technical that truly pathological.

i totally commend your actually thinking about the data, and what they mean. that is a lot more than i can say for a good deal of residents out there.

I use 10 mcV as my sensory threshold for normal, so I would say these are abnormal. If the patient were cold, they'd be even higher.

Also, even though we artificially use 10 m/s delta b/w forearm and elbow, I think < 45 m/s across-elbow with forearm > 50 m/s may be legit if measured well - difficult in itself. To test the conduction-block hypothesis he presents, stim the ulnar in the axilla - if true conduction block, the amplitude should be much closer to the wrist amplitude.

 

[Myofascist]

First of all thanks for all the responses. The attending I worked with on EMG for 6 straight mnths M-F was clinically OCD!!! This may be good for an electrodiagnostician but not so much for the resident doing the tech work on a 2 1/2 hr brachial plexopathy study in a hot room. With that said... all the responses were at supramaximal stimulation, the elbow was bent at 45 deg for the study and the measurement, the ulnar study was done twice and measured twice, G1 was moved several times looking for the best response, the pt was sufficiently warmed prior to the study and remained under a blanket, and a study was done just prior to this one using the same everything and showed large SNAPs (65 uv median index). I am definitely not trying to be arrogant here by any means, just stating the facts.

At our institution we use 10 uv for ulnar digit 5 (antidromic) and 5 uv if age > 60 so all the SNAPs in the LUE were abnormal.

PMR 4 MSK... please explain the stimulating in the axilla thing to confirm conduction block. I would think the response would be similar to the above elbow recording.

SSdoc33... please explain the temporal dispersion you would see in the SNAPs in an axonal PN. I would think if its uniform axonal loss without signif demyelination the ratio of the fast conducting fibers to slow ones would be similar to a normal nerve or if the fast ones were preferentially affected wouldnt there be a loss in CV but not an increase in temp disp?

neglect... I was taught to always check for a M-G if you see a possible UNE as the ulnar fibers will cross over from the median in the forearm creating a larger CMAP at the wrist in an ulnar motor study.

Side note... if this pt does have a PN wouldnt it be much more common to see mononeuropathies especially at common entrapment sites such as CTS or UNE? And since there wasnt axonal loss (6mv above elbow) could it be asymptomatic or masked by her sxs of the PN?

The pt will be coming back 1/31 for more thorough testing and I will definitely perform a needle exam as well as many other studies that you all have suggested. I will also get a more detailed H+P because I have a feeling this case may end up being quite interesting (hopefully my bubble wont burst).
Thanks again for all the responses.

 

[neglect]

First of all thanks for all the responses. The attending I worked with on EMG for 6 straight mnths M-F was clinically OCD!!!

I think that if this is any indication, it shows the futility of being OCD in the electrophysiology lab. We all have different approaches. If you put about 10% of your effort into being OCD, and 90% into putting the NCV/EMG data into clinical context, you're doing great.

Was this patient fat? Technical errors on the obese are a thread unto itself. I've had two patients this year whom I've been unable to elicit reliable radial sensory responses! Too much fat!

M-G: I get it now. I check it if there is a difference in wave form from median wrist and elbow. Otherwise not. Perhaps I should increase my suspicions.

I think this patient has an axonal neuropathy and an ulnar neuropathy at the elbow. She's got something - like DM. All you need is an exam that fits with a neuropathy.

 

[neglect]

well, now we're talkin!!!!!

the ulnar nerve at the elbow is more superficial than in the forearm, so while it is thicker, it is actually colder. should even out. next-to-impossible to get an accurate measurement on the fatties.

Fatties. There is no way one can get reliable data from them. I had one who really had GBS last year. And it really mattered to get good data - and how are you supposed to go to the ICU (limited environment) and get this data? It is SO frustrating! As I recall, she had what I thought was conduction block within the ulnar nerve, but as you can imagine, this was so difficult to elicit that I basically gave up.

Ulnar nerve. What you say makes sense. The segment that passes through the cubital fossa does come close to the cooler skin - and it is part of neuro lore that leprosy can give rise to a mononeuropathy for exactly that cooling reason. I have Kimura at the office and I'll look up some normalized data. In the proper clinical context and with R/L comparisons, I think that slowing along the ulnar nerve at the elbow can be significant even in the high 40s m/s.

An electrophysiologic axonal neuropathy is so common, but I'd say that instead of showing an attachment to form, it is better to put the data into context. I don't generally do F-waves.

 

[Myofascist]

Sorry i meant to state in my last post that she was thin. Responses were easily obtainable at low stimulus. I will check on the diabetes thing but i think she had a normal glucose tolerance test recently. Thorough H+P on 1/31.

 

[Myofascist]

So the pt came back on thurs and I checked the other arm. Sensory NCS was very similar except no response in median index and superficial radial at thumb base. Motors were again totally normal. Lower extremity motors were normal too. Couldnt check other leg sensories as she was wearing a short leg cast due to breaking her ankle. She didnt tolerate the needle exam but I was able to sample TA and MG, both were totally normal. Maybe I should of went right to EDB and AH for more distal sampling?

History:
Symptoms of pain and numbness started in her right hand in 1998 mainly affecting her index finger and thumb. Pain was described as throbbing and occasionally moved up to her elbow and shoulder. Occasional paresthesiae but more dense numbness which was progressive. One year ago she began noticing similar sxs in her left hand but not as severe. 6 mnths ago she began noticing tingling in her toes bilat. Denies any weakness.

PMHx:
Asthma
Chronic Hep C Dx in 2001

Meds:
Qvar
Albuterol
Vicodin 1-2 per day


Social:
Drug use: PCP (smoke), Heroin (IV) until 1998
Was in prison from 1998-2000 for heroin posession
Now only occasional alcohol
No smoking

Surgeries:
CTR right in 2002
CESIs x2 in 2006

Exam:
Motor: 5/5 throughout
Sensory: 0/2 right index and thumb, 1/2 other fingers, palm, dursum hand
1/2 left hand, 2/2 feet
Reflexes 2+
No atrophy

Labs: ALT/AST normal, INR normal, glucose tol normal, HGBA1C normal

(She has not had treatment for Hep C as her labs have been normal except for pos Hep C abs and viral load)

A/P

1. I am thinking this could be a pure sensory axonal polyneuropathy secondary to Hep C and cryoglobulinemia?

- I sent her to the Hepatitis clinic for possible treatment as I read some studies where the neuropathy improved if the virus was treated. I also read that Interferon can exacerbate the neuropathy so I thought I should get a Hepatologist's opinion

Has anyone ever seen this? Am I way off track here?