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Tony292

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Learn about ALS
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I cant make sense of most of this, I am NOT of any sort of medical background whatsoever, I would appreciate any translation or thoughts on what it means in laymans terms:

Electromyography:
Left tibialis anterior (L4,5,deep peroneal n.): Normal insertional activity, no spontaneous activity.
50% complex, mildly unstable, mildly increased duration motor unit potentials. Normal recruitment, full
interference pattern.
Left medial gastrocnemius (S1,2,tibial n.): Increased insertional activity, no spontaneous activity.
Normal motor unit potentials. Normal recruitment, full interference pattern.
Left vastus lateralis (L2,3,4,femoral n.): Normal insertional activity, no spontaneous activity.
Normal motor unit potentials. Normal recruitment, full interference pattern.
Left lumbosacral paraspinals (L3/4, L5/S1): Normal insertional activity, no spontaneous activity.
Left thoracic paraspinals (T7/8): Increased insertional activity, no spontaneous activity.
Left thoracic paraspinals (T6/7): Normal insertional activity, no spontaneous activity.
Left first dorsal interosseous (C8,T1,ulnar n.): Normal insertional activity, 2+ complex
fasciculation potentials. 25% complex, mildly unstable, mildly increased duration motor unit potentials.
Normal recruitment, full interference pattern.
Left deltoid (C5,6,axillary n.): Normal insertional activity, no spontaneous activity. 25% complex,
stable motor unit potentials. Normal recruitment, full interference pattern.
Left trapezius (accessory,C3,4), left genioglossus (hypoglossal n.): Normal insertional activity, no
spontaneous activity. Normal motor unit potentials. Normal recruitment, full interference pattern.

Summary:
NCS: All studies were performed at a limb temperature of greater than 32 degrees Celsius. The
left peroneal motor response and F-waves were normal. The left tibial motor response and F-waves were
normal with A-waves noted at 25.0 and 39.6 msec. The left sural and superficial peroneal sensory
responses were normal.
RNS: The cramp protocol was used with supramaximal stimulation of the left tibial nerve
recording over the left abductor hallucis. A train of 5 stimulations at 1Hz was administered followed by 5
at 5Hz and 10 at 10Hz. No afterdischarges, electrophysiologic cramps, or clinical cramps were noted.
EMG: Concentric needle EMG was performed of selected muscles in the left lower extremity, left
lumbosacral paraspinal musculature, left thoracic paraspinal musculature, left upper extremity, and left
cranial musculature. The study was remarkable for evidence of a very mild though widespread motor
axonopathy affecting the left upper and lower extremities, sparing the cranial musculature, with evidence
of only mild muscle membrane instability in the thoracic paraspinal musculature.

SFEMG: Jitter analysis was performed of the left frontalis using a 25mm 30g concentric needle
electrode. 20 fiber pairs were examined in the left frontalis with a mean MCD of 29.0msec (age-matched
single fiber normal < 35.5msec1). 5% of fiber pairs examined demonstrated abnormal jitter; the
remaining 95% were normal (age-matched single fiber normal < 53.5msec1). Of note, the fiber pain
demonstrating abnormal jitter was contained within a triplet; jitter was normal between the other two fiber
pairs in the triplet.
1. Bromberg MB, Scott DM, et al. Single fiber EMG reference values: reformatted in tabular form. Muscle Nerve
1994;17:820-1.
Conclusion:
This is an abnormal study. There is electrophysiologic evidence of a mild though widespread motor
axonopathy with involvement of the cervical and lumbosacral regions on the left. Evidence of muscle
membrane instability was noted in the left thoracic paraspinal musculature without overt denervation.
Given the waveform characteristics, the borderline abnormal single fiber EMG was likely a false positive
secondary to the noted motor axonopathy; as such, though findings on concentric needle
electromyography of the cranial musculature (trapezius, genioglossus) were normal, the findings are
suggestive of a subtle motor axonopathy affecting the cranial musculature as well.
As such, the constellation of findings approaches though does not clearly meet the lower motor neuron
portion of the El Escorial criteria for motor neuron disease. Clinical correlation is recommended;
recommended repeat electrodiagnostic testing in 3 to 6 months.
 
To put it into context, the first post was written by my EMG Doctor. this, the second post was written by my neurologist who discussed the abnormal findings and told me I had MND and possibly ALS:


System: Mental status: The patient is awake, alert and oriented, speech fluent and language intact. Conversational discourse
is normal.
Cranial nerves: The face is symmetric, moving well bilaterally. Extraocular movements are intact, no nystagmus is noted today.
Tongue is midline speech, no furrowing or fasciculation is noted is clear there is no indication of facial weakness.
Motor: There is no indication of weakness either upper or lower extremities bilaterally. Rapid alternating movements fair.
Questionable fasciculations noted in the thighs bilaterally evident visually and by palpation (seems most evident during
extension of the knee however).
DTRs: Mild pos jaw jerk, positive Hoffmann's 3/4 bilaterally with plantar response mute or upgoing. No clonus however.
Station and gait: Station is normal, gait appears loose at the hips with some spasticity noted distally

Abnormal electromyogram: Discuss the results of the EMG/NCV with the patient. The results subtly indicate the process of a
widespread motor axonopathy although not meeting all the criteria to define the process, concerning for lower motor neuron
disorder. Discussed this at that the patient in some detail. This may be indicative of an early presentation of ALS although by no
means is the diagnosis established. We'll look for other issues within the differential however we did discuss that whatever this is,
this test should be repeated in about 3-6 months as recommended by the neuromuscular consult. In addition, discussed that what
ever this is, the progression of this would not be consistent with the performance of unlimited military duty particularly required by
the Army.

Released w/o Limitations
Follow up: as needed in 3 to 6 month(s) in the NEUROLOGY clinic or sooner if there are problems. - Comments: Will follow up as
discussed, we'll keep in contact with the patient
Discussed: Diagnosis, Alternatives with Patient who indicated understanding. - Comments: 20-30 minutes used to discuss the
results of the testing and possible implications which can be quite serious with the patient. Emphasized the importance of followup
as recommended in 3-6 months per the consultant. Patient should feel free to contact us here for any difficulties.
 
although he states no weakness, I do have weakness in my left hand, grip strength and foot drop. we discussed both but he failed to put it in his report.
 
More notes from the EMG/Neuromuscular Doc, I forgot to add these in the first post and cannot figure out how to edit the post, so here they are:

Focused neurological examination revealed normal facial strength to include eye closure, cheek puff,
tongue protrusion, and jaw closure. No ptosis was noted. Mild bilateral medial rectus paresis was noted
via red lens testing; prominent horizontal nystagmus was provoked with convergent gaze. Muscle bulk
and tone were normal in the upper extremities. Fasciculations were noted in the left posterior leg as well
as the left FDI. Motor impersistence was noted with strength testing; focal weakness was appreciated
only with FDP-4,5 on the left (MRC 4+/5) with otherwise full strength including neck flexion, neck
extension, deltoid, triceps, biceps, wrist extension, wrist flexion, finger extension, left FDP-4,5, FDP 2,3,
FDI, ADM, hip flexion, knee extension, knee flexion, ankle dorsiflexion, and ankle plantarflexion. Deep
tendon reflexes were diffusely brisk including brisk jaw jerk; reflexes were as follows (R/L): triceps 2+/4
(2-3 beats), biceps 2+/3+, brachioradialis 2/3+, knee 3/3, ankle 3/3, downgoing plantar responses
bilaterally. Fisher’s and finger-to-nose were normal bilaterally. Sensory examination of the lower
extremities was unremarkable with intact sensation to pinprick.


what do all the numbers mean above? how about FDI, FDP, ADM? I admit I am clueless about medical terminology.
 
I am worried that u think it appropriate to post you medical reports here and then ask non-doctors what they mean. CALL YOUR DOC.
 
I am worried that u think it appropriate to post you medical reports here and then ask non-doctors what they mean. CALL YOUR DOC.


I DID SPEAK TO MY DOC. He explained the upper and motor neuron signs and the summaries. If my doc had printed this report and showed it to me I would have asked him what each thing meant, it didn't turn out that was, what he told me about the EMG was all verbal. I did not get the report until later when I requested a copy of my medical records. I understand most here aren't docs, but there is a lot of experience here and I thought that sites like this were about helping each other when and where we can? I have figured out some of the acronyms, such as fDI First Dorsal Interrosseous. And the strength and reflex numbers

What I didn't figure out is why you would go through the effort to make the statement you did. I learned nothing from it and neither did anyone else on the forum. The forum here would have been better off without your input. I bet you reply a lot on caps with "CALL YOUR DOC"

The. On doctors you speak of are intelligent and have read several of their own Emgs, some area CALS with medical terminology being something they understand. Why should I not ask about an EMG report on a site like this, I could get a lot of great insight from people here.
 
Because Tony, for every expert on here there are as many "not an expert" and your chances of receiving an incorrect commentary on a highly technical question is significant.

Second, Tony, I stand by my statement. CALL YOUR DOC. He must know you requested copies of the exam and it is his duty to explain them.

Last, it is true there are docs on here as members. However, you are asking for a free medical consultation on a lengthy set of data, some of which you already understand and some of which you don't. Your docs have given you a summary - a bottom line. What we are seeing is the chart and notes. We have no idea of the conversation that surrounded it.

As your questions are purely technical, I'm not be cute when I say "go buy a good book" as that is what I did and others do. (Andrew Michell's "Understanding EMG" for instance).
 
Fair enough, I may just have to buy a book. I am slowly piecing it together. Axonopathy is bad, but I don't find much about it other than the definition of the word. I figured out the reflex and strength scales they are using as well.

What still confuses me is the 25% complex, 50% complex. That and it showed no fibs or positive sharp waves.

The sad part is my doc didn't show me any charts or notes, he just told me that the EMG had found widespread lower motor neuron damage and that when combined with my upper motor signs on exam meant that I had MND and that he thought I was in the beginning stage of ALS. I could call him, but he doesn't take calls, he has a secretary that will get back with patients.... Or not.... Depending on if he wishes to get back with them. I requested my records because I am about to do another military move and figured I would need to give them to my next neurologist.
 
I would suggest that you ask your neurologist these question. None of here are neurologists. Surely you will see some one in your process that should be able to answer these questions.

Rick
 
Tony, is the EMG doctor and your Neurologist the same doctor? The reason asking is the following in your post, "Discussed: Diagnosis, Alternatives with Patient who indicated understanding. - Comments: 20-30 minutes used to discuss the results of the testing and possible implications which can be quite serious with the patient. Emphasized the importance of followup as recommended in 3-6 months per the consultant. Patient should feel free to contact us here for any difficulties."
 
Tony, I am not a doctor but I will give you my thoughts…
Quick anatomy for what we deal with most on this site—upper motor neurons (UMN) are in the brain and they give a command (like, move your finger); that command goes to the lower motor neurons (LMN, or anterior horn cells, AHC) in the spinal column; each lower motor neuron has an axon that carries the command all the way out to the muscle; the axon is covered with myelin (the axon is like a sold copper strand in a wire and the myelin is like the insulation; at the muscle the axon branches off and goes to hundreds of nerve fibers; at the nerve-muscle-junction the command, which started in the upper motor neurons, is transmitted to the muscle fibers chemically.

Weakness, which is the predominant symptom of ALS, can be caused by a breakdown anywhere along that chain of command. And remember that clinical weakness (your muscles don’t work) and perceived weakness (it seems harder for my muscles to do things than it should) are different. My guess is that when your neuro said you had no weakness, he meant “your muscles still work”… and that’s good.

A nerve conduction test can readily differentiate between problems in the myelin or problems in the axon. Demyelinated nerves have a markedly slowed velocity with normal amplitude. Axonal problems show up with normal velocity but reduced amplitude.

An EMG will show or not show signs of acute (current) denervation by showing insertional activity and spontaneous fibrillations (spontaneous activity on your report). It will show chronic (long term) denervation by examining MUPs (Motor Unit Potentials) and finding increased duration, amplitude, polyphasicity, decreased recruitment and MUP instability.

Currently, there is no lab test to positively prove UMN problems. This is a clinical determination by a neurologist (and is much more “art” than science).

Having a “mild though widespread motor axonopathy” is a long way from ALS, so first thing try to relax. Remember that the axon is an offshoot of the lower motor neuron, so determining whether the problem is in the axon or the LMN is very difficult, but it sounds like your doctors think your tests show an axonopathy, not a lower motor neuronopathy. (Those two are very similar in most tests except that LMN is wide ranging across many muscles and body parts where axonopathy may be localized. And generally, denervation in the thoracic paraspinals seems to be more indicative of an LMN. But sometimes you just have to wait for the disease to progress enough that a determination can be made. But if it’s an axonopathy, you do not have ALS. (The half-empty folks can say “Yet”, but then I haven’t been hit by a bus… yet… and anything can happen in the future.)

I would say go back and study your results, keeping in context that some of us on this site have insertional activity and spontaneous activity in nearly every muscle tested. Pick another neuro if you want—you don’t sound thrilled with this guy’s “no calls” policy—and a second opinion never hurts. And it seems, some neuros seem to want to warn patients about the possibility of ALS right off the bat, while others wait until you’ve marched up the El Escorial criteria.

Also, I sympathize with your failure to ask all the questions as I think it can 3, 4 or 5 visits to a neuro before you even learn enough of the language to be able to converse with him and ask the questions. (Really, guys who asked all the right questions on their first visit?) Finally, an axonopathy is not the end of the world… and that’s all they seem to be saying at this point. You have lots of options—a second opinion, a follow up in 3-6 months—but keep living your life and don’t let the possibility of an illness stop you from living. Good luck!
 
Dusty7, would Demyelinated Nerves explain Carpal Tunnel with no symptoms? Thank you for your plain English thoughts of UMN disorder. I hope Tony292 replies to your post. Please follow mine so he sees your user name.
 
Al, I once suffered from carpal tunnel syndrome—truly a self-induced repetitive stress injury. I had moved to Florida and was building docks and decks and walkways at my new home. After days of pounding nails, my wrists let me know that was enough. And what I remember most about it was pain. So, carpal tunnel with no symptoms sounded strange to me. I checked at
Carpal tunnel syndrome | University of Maryland Medical Center
and found that “Initial symptoms include pain in the wrist and palm side of the hand… Early on, the patient also usually reports numbness, tingling, burning, or some combination of symptoms… Over time, the hand may become numb, and patients may lose the ability to feel heat and cold. Patients may experience a sense of weakness and a tendency to drop things… Patients may feel that their hands are swollen even though there is no visible swelling.”

That site also went on to say: “Any disease or abnormality that affects the muscles and nerves, including those in the spine, may produce symptoms in the hand that mimic carpal tunnel syndrome.”

So, yes, I am not a doctor, but I agree with your theory that symptom-less carpal tunnel syndrome could actually be demyelination slowing the nerve velocity, and not slowing from compression of the median nerve. I believe there are other tests for CTS that could prove the earlier diagnosis correct, but the diagnosis would be critical because the treatment would be completely different. CTS treatment can range from rest to surgery, while those would do nothing for a person with ALS.
 
Thank you for the reply. (I am very familiar with your Avatar.) I have been diagnosed with more than moderate CTS but no symptoms. I do have the indentation between my thumb and first fingers, no strength in either and wondered if it was just from the CTS. Also familiar with building docks in Florida... my parents lived on one of the salt water canals just north of Clearwater. It was a hinged floater and during one of the hurricanes it broke loose, took some of the deck with it. No CTS but I mashed my thumb with a 20oz framing hammer. :)
 
The muscle between thumb and index finger on the back of the hand is the First Dorsal Interosseus. Mine on my left hand is atrophying. The muscle at the base of the thumb on the palm side is the Abductor Pollicis Minimis. My left hand APB is also atrophying, creating a depression in the palm. (And yes, I have weakness in the "pincer" grip.) These are very important muscles because there is a lot of research on the "Split Hand Index (SI)" going on in (at least) Australia, Canada and India. Teams there believe that the SI "robustly differentiates ALS from mimic disorders", "is a useful diagnostic sign in early ALS," and "this study demonstrated conclusively that the split hand sign was fairly specific for ALS." So the studies indicate the SI is a positive sign of ALS--the first positive laboratory test for absolutely determining ALS. (A positive is positive for ALS; a negative would be inconclusive.) But my thought for you is that an atrophied FDI seems to be very much consistent with ALS. I don't mean to be challenging your CTS diagnosis, but you sort of asked if CTS without symptoms could be something else and these are my thoughts. Good luck!
 
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