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EMG
“Number of insertions”
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I
realize this is a bit of an overworked subject but I am
a bit confused. In reading some of the previous posts
here on the forum regarding needle EMG, you stated: "The
needle EMG part of the test consists of inserting needle
probes in the muscles, usually, 4-5 such insertions per
extremity." What I am confused about is that the online
EMG manual you talk about studying 20-25 MU per muscle,
calculating average amplitude, phasing etc. Since I assume
by your post listed above you are referring to studying
4-5 muscles per extremity. Even with testing in multiple
directions after insertion, is it possible to study 20-25
units with one insertion (stick) per muscle? Also is doing
one needle insertion per muscle, again testing in multiple
directions, enough to detect spontaneous activity in even
mild involvement or early in a disease process? Thank
you very much.
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Answer |
What
I should have said is "usually, 4-5 such muscles
(not insertions) per extremity". In each muscle I
usually do one insertion but sample the muscle in 4-5
different directions from that same insertion. Most of
the time this is sufficient to detect denervation, but
as you know, nothing is ever foolproof in this business,
that's why it is called an art, and an EMGer's experience
and familiarity with the various presentations of disease
play a great role as well. |
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Comment |
Thanks
for the clarification. Do you normally test for minimal,
moderate and maximal effort in each direction after insertion?
Or do you just test for spontaneous activity in the 5
directions and only test (as seems to be very common)
for voluntary in one.
Finally do you test for both spontaneous and voluntary
activity in the paraspinals? My doctor had a hard time
finding a position (he had me on my side) where I could
totally relaxed. He rocked me back and forth and got short
moments of total relaxation and no activity. He said he
could see there was no spontaneous activity in the half
second or so long relaxed moments. Is this a valid test?
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Answer |
In
routine everyday work, I check the activation (mild, moderate,
full) in one or two insertion points only. When I am doing
a quantitative study and locking for abnormalities, I
look in more places.
Paraspinals are indeed hard to relax and I usually
check only the insertional activity in them. So you
catch what you can get when they are difficult to relax
and frequently that is sufficient.
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Worried
about having NCV study |
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I'm
going in to have a nerve conduction test on Monday. I
have extensive damage to my left hand due to a weight-training
accident 2 years ago. My muscles have atrophied and I've
been in constant pain since mid-January of this year.
I've lost almost all use of my hand. I can barely type
or write with it. I know I have to have this test done,
but I'm worried because I hate needles. Is there anything
I could be told to ease my fears? I already read the FAQ.
But that made things worse. |
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Answer |
Of
course I cannot stop all your worries but allow me to
tell that I had such test before, it is not that bad at
all, you may feel little discomfort. It is a sort of probe
to examine the muscles. I am sure you will find it much
easier that what it looks like. It will help you not to
hurt you. Think positively that way. I am certainly sure
you would find the test very much tolerable as I know
not only in myself but also for thousands of patients
I have seen. All the best.
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Comment |
I
had my test completed. What was I supposed to expect?
My hand barely twitched on the shocks. My fingers twitched
and my hand raised off the bed once. That’s it. My
mother had one a few years ago and she said she almost
smacked him as a reflex. On the sticks, they hurt like
hell and I bled. 3 were silent and 2 made a lot of noise
and he had me move my elbow or thumb. The pad by my thumb
hurts really badly right now. After my test, my hand was
paralyzed. When I’d try to move my fingers I’d
get no response and eventually I got them to twitch a
slight bit. . They’re back to normal now. But hurt
so badly. I’m about o take some painkillers and go
to bed. So, is this normal? or is it all a bad sign? |
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Answer |
Yes,
post EMG local pain or soreness (due to local tissue irritation)
does not last long. Usually will disappear in the same
day, rarely to next day. Your symptoms could be related
to your primary illness. I think you should consult your
neurologist to check your EMG results and accordingly
management is offered. |
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Comment |
The
muscle by my thumb hurt really bad last night. Now it
hurts and is more swollen. the muscle is atrophied.. But
it's swollen to twice the size of my other hand. I can’t
use my fingers. But that’s probably just due to aggravation
of the condition. I had to call in 'sick' to school because
my left hand is the one w/the problems and I’m left
handed. |
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Answer |
I
share your feelings and pain. It seems that the pain is
out of proportion. Although, I must say and should be
very clear that it is difficult to decide from your symptoms,
but it is perhaps a kind of/or part of it related to sympathetic
nervous system dysfunction. Again, further consultation
with neurologist is worthwhile. |
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Effect
of hand Squeezing on LL NCV |
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When
Having my conduction velocities study, It seemed that
the neuro could not get what he wanted when giving me
the electric stimulation to my legs (peroneal, tibial
nerves), he then told me to squeeze tightly my hand and
only then did he got what he wanted to get and said all
was fine. Dear doctors! What do you think he could not
get (I think I recall he said It was the Amplitude)? Was
it "legal" - I mean I am just curious whether getting
"the wanted NCV result" that way is all right and not
"cheating"? THANK YOU FOR READING THIS AND RESPONDING! |
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Answer
1 |
That's
is usually to get the F-wave (http://www.teleEMG.com/jbr070.htm)
in the lower extremity, and it is a "legal"
maneuver. |
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Answer
2 |
Squeezing
the hand during EMG helps to get better amplitude fro
the evoked response: F-wave, H-reflex or a motor evoked
response. Squeezing the hand is also asked to at times,
by physicians during a clinical examination to obtain
better deep tendon reflexes. |
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Hand
contraction with EMG of LL |
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In
read in previous post that it is quite common to ask the
patient squeeze his hand in an EMG. A month ago I had
my EMG and the neuro said he was not getting good CAMP
amplitude as He had wished to, so told me to squeeze my
hand. He also "hit" me with tremendous currents, and then
he got normal CMAP. (Also read posts in this forum about
it) About the nature of CMAP amplitude - A. How far can
it change with higher currents, can it get from 2 to 15
MV (in supramaximal stimulation+25%)? in MU - How much
can it change in low and high currents? B. In which current
does he have to stop? Is there a "limit current" in which
more current would not produce higher amp or "the sky
is the limit"? C. And about the "squeezing the hand" thing
- IN MV- HOW higher can it get? I mean, how much additional
MU can squeezing the hand yield? (2,5,10,15)? And MOST
importantly for me why some people get the right CMAP
amplitude without squeezing the hand while others should
do so - Does it depend on the physical condition of one's
nerves or not - I mean if he asked me to do so - Is there
a problem (even minor) with my nerves? Hope to get your
insights on these "CMAP THINGS" |
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Answer |
Thank
you Rob. As pointed out in previous posts that squeezing
increases the motor response, it works by enhancing the
response. Of course it will work to certain limits. To
answer your point, it may increase from 2 mV to 15 mV.
Once the maximum level or value is reached, then any further
increase of current will lead to stimulation of the nearby
nerves giving a false result. Therefore, only a 25% increase
of stimulus is added after obtaining the maximal CMAP
response to avoid such stimulation of other nearby nerves.
All commercial EMG machines have limit of stimulation,
which cannot be exceeded for patient safety. This squeezing
method does not reflect any pathology of the nerves but
just a physiological variation between individuals. |
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Comment |
What
Do you mean by maximal response? How can the examiner
know when is the maximal response for a certain nerve?
Because as you said, the higher current you give the higher
amplitude you get! So how Does the examiner know when
he had reached the point where he gets false increase
from nearby nerves? How does he know what is the real
"maximal CMAP response for a nerve”?? (And that
from now on he crosses the limit of stimulating neraby
nerves)
* What would be the range of normal CMAP for the peroneal?
, Tibial? And ulnar? |
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Answer |
The
following should help to get the best response. First
of all the examiner should be familiar with the anatomy
of the peripheral nerves. A surface electrode is used
for stimulation; it is easier and less uncomfortable for
the patient. The cathode of the stimulating electrode
should be placed over the nerve closet to the recording
electrode. The anode is placed parallel to the nerve,
away from recording electrode, you may rotate it to minimize
stimulus artifact. The nerve should be stimulated with
stepwise increasing strengths. Enough current must be
applied to activate all of the axons of the nerve. This
amount, called supramaximal response can be obtained with
an electrical stimulation of 10-75 mA and pulse duration
of 0.1-0.5 ms. Over stimulation would produce latency
artifactually short or a conduction velocity too fast
for that nerve. Also, stimulation of adjacent nerves could
produce CMAP larger than expected and has initial positive
deflection (except tibial nerve). That how I would make
sure it is a response from that particular nerve and no
contribution from other nerves. This problem is encountered
commonly between unlar and median nerves at thr wrist.
Normal values from Liverson and Ma 1992: ulnar CMAP between
4-22 mV. Tibial CMAP 5.8-32 mV. Peroneal CMAP 2.6-20 mV.
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How
does medication affect EMG test? |
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I've
been taking Toprol, Wellbutrin and Lipator for about three
years..I recently took an EMG and I wasn't asked about
any of the medication I was taking..how would this affect
the results of the EMG? |
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Answer |
None
of these medications would affect your EMG results |
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Meaning
of increased muscle irritability |
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I
would appreciate your relation to the following point:
The issue of the so-called irritability is mentioned in
the EMG manual and also in the forum. Yet some of the
features are not clear: 1. Prolonged insertional activity=irritability???
2.does irritability look like the spikes of fibs and PSW
- does it look like spikes at all? Does it have a typical
sound - what is it like and how long does it persist?
3.The relation to denervation - in the manual It is said
that irritably is seen in early denervation - How early
Do you see it in denervation? I know that for fibrillations
it takes 2 months - Is it the same for irritability or
does it appear earlier? |
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Answer |
Thank
you for these basic but actually interesting questions;
my comment will be divided into 2 parts, first quick As
to your Qs and second is a general description. First:
1. Yes, increased insertional activity (IA) does indicate
irritability. 2. IA looks as spikes but they are not fibs
or PSW, sound like perhaps "crack"!!. 3. Increased
IA occurs before fibs and PSWs. Second: The IA is considered
as "injury" potentials due to needle movements
in the muscle, this is causing irritation of the cell
membrane. They come in bursts each usually lasts 75-400
msec. following each needle movement, each burst formed
of several muscle fibers (normal phenomenon). Hyperexcitability
of the muscle membrane leads to prolonged IA, for instance,
in early denervation before appearance of fibs and PSW.
Practically I find the increased IA develops several days
before fibs and PSWs, I think related to the affected
nerve length. Regarding the appearance of fibs and PSWs,
it is axon length dependent (not 2 months). The shorter
the distal part to the lesion or stump the faster the
fibs to appear. Some practical lesions; about 7-10 days
seen in paraspinal muscles after disc lesions, but about
4 weeks in distal muscles. Longer in the lower limb muscles
compared to upper limb muscles. After facial nerve lesion,
fibs could be seen by 8 days. Also, practically, I usually
suggest an early lesion or nerve "irritation"
with prolonged IA, but do not make (or attempt) conclusive
evidence out of it. A follow up is usually needed if those
patients are seen that early. I hope this will answer
all your questions. Thank you |
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Comment |
HI!
Thank you so much for your answer about irritability!
My question refers mainly to ALS (mnd): - I did not read
irritability in connection to ALS (but fibs and PSW) so
my question to you is: according to your experience how
common irritability is with ALS -Did The majority of your
ALS patients come with irritability or fibs and PSW????
(From what I understand irritability is seen mainly with
"simple" nerve injury not als?? and due to the
rapid progression of ALS fibs and PSW are always seen
the first EMG- you never "catch" an ALS patient
that early to see irritability??? Thank you again! |
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Answer |
Right,
this is important point, in patients with ALS; I have
never considered increased insertional activity as evidence
for muscle involvement, but look for the definite denervation
activity. I believe that increased insertional activity
has no practical significance in ALS. |
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Comment |
Thank
you for the previous reply. So according to your experience,
Do you find irritability (in ALS) prior to denervation
in the ALS patient's FIRST EMG (such as in simple nerve
injury) and if so what is the time for fibs to appear
in that case? or by the time there is irritability there
are always signs of active denervation as well (fibs,PSW)
in ALS - never irritability alone.. in ALS even if very
early. |
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Answer |
I
do not know the answer to your points. Practically, I
look just for signs of denervation in ALS and do not actually
considered looking into increased insertional activity
per se. |
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Comment |
The
diagnosis of amyotrophic lateral sclerosis (ALS) being
so dramatic for the patient, we need to have strong evidence
of peripheral neurogenic involvement we are looking for
signs of denervation such as fibrillations, positive sharp
waves not only insertional activity.
Fasciculations and reduced recruitment pattern of large
motor units are also important EMG sings in ALS? |
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Answer |
Absolutely
correct, I agree with you. Stringent criteria always needed
to be fulfilled. |
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Identical
sounds of motor units in unrelaxed muscle vs. fasciculations.
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Dear
Doctors! I know that motor unit firing at rest in an EMG
test (due to poorly relaxed muscles) is quite common.
However they produce popping sounds ("like pop corn machine"),
which is the same sound (popping) of fasciculation potentials
so how do you distinguish fasciculations from firing of
normal healthy motor units (of poorly relaxed muscle)?
As they both produce the same popping (popcorn machine
like) sound? (By their rhythm, regularity or something
else)? |
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Answer |
Practically
speaking the patient should always be relaxed, otherwise
I cannot tell whether the potential is fasciculation or
voluntary firing MUP.
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What
can EMG tell? Relation of tingling to level of B12 |
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Have
had these symptoms for following month. FATIGUE, kinda
dizzy/lightheaded like in a fog, or had 1 alcoholic drink,
legs, mostly left shaky like jello inside and weak, Cold
feet, twitching, and slight numbness along anterior aspect
of left shin. Doc referred me to Neuro who is doing an
EMG. What will this tell me? Also, I insisted on a B12
level (which he thought I was reading too much about)
and the level was 148 pmol/L. The range said anything
>150, NOT deficient. 110-150, POSSIBLY deficient, and
<110 PROBABLE deficiency. Could this, even though only
slightly under the "normal" range, be the root of my problem??? |
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Answer |
Yes,
peripheral neuropathy is quite possible from your symptoms;
therefore EMG should be useful to decide about neuropathy.
Of course the history and clinical examination of your
neurologist is equally important. The examination should
help to suspect if you have B12 deficiency as a cause.
He should decide if you need other investigations if needed.
However, the B12 level seems to be within normal limits.
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Explanation
for NCV report |
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Dear
doctor! I hope you will be able to help me understand
my NCV results. It is said. MOTOR NERVES: dAMP is. (For
each nerve) and later AMP% is. For each nerve which is
the actual amplitude of the nerves: AMP% or dAMP - what
is the meaning I wonder because for the sensory nerves
it is just AMP. *the dAMP are positive . AMP% - some are
positive and some are negative. (-10,-20,5,-17) For example
left ulnaris (motor) dAMP is 7 while AMP% is 5. |
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Answer |
The
dAMP stands for motor response at distal site. Another
stimulation at proximal site will produce a response.
This proximal response is either higher, similar or lower
(-) amplitude expressing as AMP% compared to distal response
(dAMP). While the sensory response is only done at one
site, so no comparison with proximal response. |
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Response
of latency and amplitude of CMAP to increasing stimulus
intensity |
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Dear
doctors! In previous posts the issue of the connection
between the amount of electricity and the CMAP was discussed.
However, one thing remains unclear: We know that the more
current you give, the higher the CMAP is and (also the
latency get shorter and we get better conduction velocity)
However which of these two factors is FIRST influenced
by the amount of current? As far as I know the latency
and conduction velocities reach their "best scores" before
the CMAP, I mean by the time you reached the optimal results
for velocity and latency, you have not reached yet the
maximal CMAP amplitude and there for more current is needed?
In other words, in order to reach optimal results of velocity
and latency, less current is needed than for the maximal
CMAP amplitude CORRECT? Looking for your insight on that
matter |
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Answer |
I
disagree with that concept for the following reason; when
you use a submaximal stimulation it might happen that
the most rapidly conducting fibers were not stimulated
so the latency is too long (those fibers are responsible
for shortest latencies and fastest conduction velocities),
therefore, it is custom to increase the stimulus intensity
until you get highest CMAP. Then we know practically,
that the fastest conducting nerve fibers are stimulated
and latency is the shortest and CV is the fastest.
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Is
it neuropathy or not? |
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In
letters to my G.P. my neurologist has noted that I have
"decreased pin sensation, temperature distally in the
lower extremities. Position sense and vibration sense
are normal. Deep tendon reflexes are absent in the lower
extremities and +1 in the upper extremities..Babinski's
sign is absent." He recommended EMG/NCS. After testing,
he reported ". Normal sensory nerve conduction in the
left superficial peroneal nerve with distal latency of
3.68mS..motor nerve conduction in the right peroneal nerve
is within normal limits with a velocity of 40 meters per
second and distal latency of 6.40 mS and left peroneal
nerve with a velocity of 44 meters per second and distal
latency of 5.20 mS. The H-reflex in the right and left
tibial nerves is abnormal in that there are no responses.
He concluded ". Not enough findings to really indicate
definite neuropathy since the sensory and motor nerve
conduction are normal." Entering the left superficial
peroneal nerve distal latency of 3.68mS and the appropriate
age, sex, and height (41, M, 190cm) into the appropriate
boxes on your lower extremity sensory/H-Ref teleEMG calculator
(thank you very much) produced an MRV of -4.2. I wasn't
sure how to use the lower extremity motor calculator,
but it may have produced negative MRVs of -1.1 or closer
to zero. Three questions: 1) Neuropathy or not? , and
2) Can you recommend an unrelated source for normal values
of EMG/NCS (I'm looking for corroboration) including books,
and 3) recommend additional means of investigation and/or
wait for progression. Based solely on reported findings
(no foot problems, though arches somewhat high, thanks
for asking), and slow progression over perhaps eight years
or longer (just detected this, though deep tendon reflexes
gone for at least six years), I am inclined to suspect
some sort of very mild hereditary sensory neuropathy?
Please reply. Thank You. |
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Answer |
Looking
at your history and NCS data; you have some symptoms and
signs to suggest neuropathy, and some data in NCS to support
that (absent H reflex, right peroneal latency of 6.4 ms
and CV of 40 m/s). Absent H reflex is definite abnormality
(neuropathy is one cause but not the only one), and peroneal
nerve, to me, it is slightly slow but it varies according
to laboratory normal limits, but anyhow, not enough by
itself to say peripheral neuropathy even if abnormal.
However, additional information would be useful and important
for instance, sural nerve, amplitudes of motor and sensory
responses, F wave and needle EMG examination and perhaps
additional test for small fibers (sympathetic skin response).
Looking at the duration of symptoms seems to be very slowly
progressive if any. I think a follow up study is worthwhile
after several months. About the last point being hereditary
or not, I would say, this study cannot tell you that,
you need more information in the history and further genetic
study that could be discussed with your neurologist. I
hope this is helpful. |
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Comment |
Isn't
a conduction velocity of 40 completely normal for the
preoneal nerve?
If not what are the limits for this nerve in your laboratory? |
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Answer |
MCV
for peroneal nerve is 41 m/s or faster. |
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Why
CMAP amplitude changes with change in stimulation current? |
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Dear
Doctor! Is it true that according to the laws of electrophysiology
the amplitude of the activated motor potential (CMAP)
SHOULD NOT change theoretically with current changes?
And if so how come clinically there is so many differences
in CMAP due the amount of current? (In my test It went
from 4(lower current was given) to 15 (higher current
was given)-in 2 different tests? THANKS IN ADVANCE? |
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Answer |
This
is important point, but a little complicated. I will try
to explain it. The CMAP (also called M wave) is compound
muscle action potential therefore it represents action
potential recorded from muscle when a motor nerve is stimulated
activating some or all muscle fibers in that muscle. The
nerve composed of axons, when each axon is stimulated
by electrical current at threshold, following the role
of all or none (all or nothing), the muscle fibers innervated
by that stimulated motor axon will generate activity or
share in the formation of CMAP. But not all axons are
stimulated or reaching threshold at the same stimulus
intensity, as they are (relatively) at variable distances
from the stimulus electrode. That is why we use supramaximal
stimulation with proper stimulus position to make sure
that all axons in the nerve are stimulated, so maximum
CMAP is obtained.
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What
is Interference Pattern in EMG recording? Muscle contraction
& spontaneous discharges |
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What
does 60%FF Effort Mean? On EMG reports, there is a column
for Interference Patterns with the following Options:
%Full Pattern Discrete Single Recruit. Ratio Effort I
have read your manual, but have not found anything that
gives those kinds of values. Is this the decreased rate
of recruitment? What does this "Effort" mean and what
are the normal values for it? My other question is, I
see that things like mild effort, etc. is mentioned. Should
the examiner be asking a person to contract muscles while
they are doing the EMG? |
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Answer |
The
interference pattern is part of the EMG study to see in
simple terms how much the patient can contract his muscle.
The examiner or electromyographer will ask the patient
to contract the muscle in 2 steps first mild contraction
to study the motor unit potentials and then maximum contraction
for the interference pattern. 60 % effort, for instance,
would mean generally that the patient did not produce
full contraction. However, this does not mean always a
”pathology".
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Comment |
My
next question would be, why would I not be asked to contract
my muscles? Is it or is it not normal procedure to have
the person contract muscles? If I had been asked to contract
muscles, would this have given a better response?
This FF percentage ranges from 30 to 70 % (1 muscle).
I had leg and arm tested. The gastrocnemius was on 30%,
biceps 40%, Abductor digiti 40%, rt. extensor 50% interrupted,
anterior tibialis 50%, vastus medialis 60% and abductor
pollicis brevis 70%. I was not asked to contract any
muscles.
What pathological conditions cause this? Is ALS one
of the conditions? (My aunt died from ALS so this is
always in the back of my mind)
Can plates and screws in my neck cause it? Can these
plates and screws be causing a severe spinal stenosis
of some type? Can it be some kind of demyelinating disorder?
My report said that there is no neuropathy, no radiculopathy
and NO something else. According to the report, there
was nothing wrong, yet I walk with an abduction and
am quite weak and spastic. In fact, they operated on
a Thoracic Disc thinking it could be contributing to
the problem, wrong. Surgery didn't help and left a few
more secondary problems.
I have lots of bulges, and spondylosis. I am quite
myelopathic. I had bi-lateral positive Babinski, clonus
etc. Recently my toes did nothing, no up no down. Nothing.
I am assuming that this is now indicative of lower motor
neuron damage. I really would like to know what could
be done, if anything. I would also like to know if those
kinds of readings could indicate ALS as I would then
go to the appropriate MDA Clinic for testing instead
of beating my head against the wall trying to surgically
correct the uncorrectable.
If it is radiculopathies, why don't they show up? The
doctor said, central nervous stuff doesn't show up,
so now I am quite confused. If it is radiculopathies,
they don't show, if it is central it doesn't show so
what was the purpose of the EMG's.
What pathological conditions cause that kind of patterns?
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Comment
2 |
One
other question. Does contraction of the muscles have any
bearing on whether or not one would see any spontaneous
activity such as fibrillations, positive sharp waves,
fasciculations, myotonia or repetitive discharges?
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Answer |
First
asking the patient to contract the muscle during EMG is
a normal procedure, if the patient can contract voluntarily.
Otherwise, if the patient cannot contract his muscle for
any reason, I just examine or do EMG to see if there are
any spontaneous discharges. Contracting the muscle has
nothing to do with production of Fib, PSW, etc. On the
contrary, we ask the patient to relax his muscles, because
such spontaneous discharges are seen at rest. Contracting
the muscle would simply obscure such discharges. |
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Relation
of interference pattern with upper or lower motor neuron
diseases |
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Concerning
spinal stenosis. Could severe spinal stenosis cause reduced
interference pattern, or is it just upper motor neuron
diseases? |
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Answer |
The
reduction in the interference pattern (IP) is not specific
for any particular lesion. A lower motor neuron disorder
could be a cause, as in your case severe spinal stenosis.
As I said in previous post that reduced IP may be variable
and changes with the patient's cooperation, the strength
of the muscle, pain and the presence or absence of disease
of upper motor neuron such as spasticity. A combination
of factors is quite possible as cause for IP in your case.
However, we cannot take it as a solid parameter by itself,
but always other EMG parameters are required to support
it. Final word, I must say that IP is not specific but
it has diagnostic value by doing quantitative analysis
of IP (and concept of cloud) in lower motor neurone diseases
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