Yes.

I'm going to talk about the use of electro biography 

in understanding neuro muscular disease,

histone chemistry,

tissue culture,

electron micah scruffy muscle 

biochemistry,

these may seem like arcane arts an 

electro biography or E.M.G.

May be the most mysterious of all with 

his differential amplifiers,

common mode rejection ratios and band pass 

filters.

I don't intend to cover these technical aspects 

in our brief time here,

but I do hope to cover some clinical points of 

electrophysiology.

So the electro biographers in the audience 

can make the reports a bit more understandable 

and non electro biographers no longer 

blinded by flashing lights and cathode ray 

tubes can make better use 

of data from E.

M.

G.

The MG is quite useful in studying neuro 

muscular disorders.

It's helpful in localizing neurogenesis 

lesions and studying the phenomena at the neuro 

muscular junction in studying nerve 

conduction and I don't intend to cover these 

topics today,

I want to concentrate on the findings on the 

E.

M.

G.

Needle examination.

Let's go to our first slide which 

shows a 23 year old patient who was seen in 

NIH with weakness 

localized to the gastronomy is 

muscle on physical examination.

As we see on the next slide 

there is wasting,

quite localized in the gas rock.

And examination of muscle strength 

showed no weakness elsewhere.

E.

M.

G.

Needle examination showed brief,

small,

abundant the recruited polyphasic 

potentials in many muscles,

both in the arms and the legs.

Only with the MG.

Were we able to document the extent 

of the patient's neuro muscular disease.

However,

having documented the extent of the 

disease,

we were very we were unable to 

say much space specifically about its 

ideology.

Now I'm going to run the risk of 

over overemphasizing this non 

specificity today and concentrate 

on the view.

E.

M.

G.

Can give us of electrophysiology.

Let's start with the spontaneous activity,

spontaneous activity refers to 

action potentials recorded from the 

muscle after insertion activity has 

subsided and when there is no voluntary 

activity,

we'll go first on the next slide to the 

fibrillation.

The fibrillation potential is the action potential 

of a single muscle fiber or in some instances 

a few muscle fibers not elicited by 

nerve impulses but occurring repetitive 

li these 

definitions by the way are those of the committee on 

terminology of electro biography.

The fibrillation potential has a duration less than five 

milliseconds can vary greatly 

in amplitude and his try 

physic inform with an 

initial downward deflection,

2nd phase,

upward and a third phase 

downward.

Now as we talk,

I'm going to use the E.

M.

G.

Convention that negative deflections 

are up and positive deflections are 

down and we'll stick with that Throughout the talk.

The next slide shows the model 

of the muscle fiber as a cylinder,

positive on the outside,

negative inside if we 

imagine a stimulating electrode 

right here and a recording 

electrode at the surface of the muscle fiber 

extra singularly somewhat down the 

fiber,

we see that when the fiber is 

stimulated,

there's a current flow into the 

cell which makes the 

point of stimulation 

positive.

Excuse me,

negative with with respect to 

the recorder.

Thus we get an initial downward or positive 

deflection recorded at the recording 

electrode.

As the action potential is propagated 

along the muscle fiber and approaches the recording 

electrode.

The recording electrode becomes progressively more 

negative and a up going 

phase of the action 

potential is recorded.

Then as the action potential continues to 

propagate on down the muscle fiber 

past the recording electrode,

the negativity decreases 

and we get a final small 

positive deflection for the 

third phase of the fibrillation.

Going on to the next slide,

we can see this same 

fibrillation recorded in vivo 

with the single fiber E.

M.

G.

Technique.

This is the technique of extension Stalberg 

and they record a try 

facing potential for the fibrillation just 

as predicted by the the cylindrical 

model.

Now this picture actually represents the 

superposition of about 90 consecutive fibrillation.

And the constancy of the form of the fibrillation 

is further is further proof that the 

fibrillation represents the action 

of only a single fire fiber.

Following firing.

Excuse me.

Now,

there have been theoretical arguments that some 

fib relations might represent more than one 

fiber firing,

but I think that for general purposes we can assume that 

fibrillation are single fibers 

action potential.

Let's go on to the next slide where we can 

look at the form of the fibrillation 

on the reach on the routine E.

M.

G.

Often the third phase which is so 

small is lost and we get a 

biphasic potential down 

first and then up second.

Now it's very important in 

using your criteria for identifying fibrillation is to 

concentrate on the initial downward 

deflection because action 

potentials recorded at the motor inn plate 

as in this illustration can 

be upward first 

or in some cases up first and 

down second.

So the initial downward deflection is a key 

criteria for identifying a 

fibrillation.

Now the fibrillation can be recorded 

with a subcutaneous electrode so it is 

not related to needle injury of the muscle 

fiber.

A single fibrillation found in a single 

muscle should not be considered abnormal.

And to consider fibrillation as an 

abnormal finding,

one must demand that they be found at more than one 

site 

Classically fibrillation are associated with the 

innovation.

And I think this is well shown on the next slide 

where we've superimposed a muscle 

muscle muscle biopsy findings 

which show small angular fibers.

Classical findings and innovation 

with an with MG from the same muscle 

showing repetitive 

fibrillation.

Now we're not sure that the fibrillation is 

actually come from the angle from the angular 

fibers but evidence that fib 

relations do occur with the innovation 

are that fibrillation will occur 

2 to 4 weeks after 

nerve section.

That they can occur earlier if the 

nerve is shorter or if there's a distal 

lesion.

If the lesion is more distal,

that disease is associated with peripheral 

neuropathy have fibrillation more commonly 

than diseases associated with the anterior horn cell.

They're of course,

very valuable for localizing 

root lesions and other uh 

localized neurogenesis disease.

And I don't want to go into the practical 

aspects of that right now.

What I want to talk about instead is the 

fact that a number of other diseases,

not all of which are clearly dinner vein diseases 

can cause fibrillation.

The next slide lists some of the other 

causes of fibrillation,

botulism can have fibrillation here.

The mechanism is probably related 

to the action of botulinum toxin in preventing 

acetylcholine release from the neuro muscular junction.

Thus,

the the one can imagine that the muscle 

fiber becomes functionally dina vacated cannot 

fire in the absence of acetylcholine 

and the fibrillation scene and botulism may 

represent a functional d innovation.

Fibrillation are also common in polymorphous 

itis being reported in about 50% of the 

cases.

And here there's evidence 

on muscle biopsy in terms of numerous angular 

fibers that suggests that there might 

be d innovating aspects as well 

as my empathic aspects to this 

disease.

However,

when one goes to the next topic on the 

list Duchenne dystrophy,

the same argument cannot apply in Duchenne 

dystrophy.

There is not evidence of the innovation on the 

muscle biopsy and 

the cause of the fibrillation and this disorder is not 

clear.

Some people have suggested that 

necrosis of fibers and splitting of fibers 

might separate part of a fiber 

from its muscle from its in plate and make it 

functional and innovated.

And I think that this point has to simply be regarded as 

as yet unproven 

the other diseases on the list.

My atomic atrophy,

late onset rod disease,

type one hypertrophy with central nuclei 

acid malt,

taste efficiency all 

have elements of 

myopathy in them.

Excuse me,

all have 

elements of neuro muscular disease in them that are not 

clearly understood and why these should 

have.

Fibrillation is really yet 

unclear.

Going to the last category 

a promoter neuron disease.

I purposely put a question mark after 

that because I'm 

not absolutely sure that fibrillation can be 

seen with an upper motor neuron lesion alone.

There have been reports in the literature of patients 

with strokes,

patients with uh spinal cord 

injury,

uh having 

fibrillation that should not be explained 

by lower motor neuron disease,

but these are as yet scattered reports.

And I think the topic is still one of much 

debate.

Let's move on from the fibrillation to another 

form of spontaneous activity.

The positive sharp wave.

The positive sharp wave is a slow wave 

with a rapid onset which occurs repetitive li 

usually associated with needle insertion or movement 

injury.

When recorded at um unipolar needle exploring 

electrode,

the initial potential changes in a positive direction,

followed by a slower exponential change in the negative 

direction,

which may continue into a prolonged negative phase of 

low amplitude.

The total duration usually exceeds 10 milliseconds 

and maybe 100 milliseconds or more 

positive sharp waves can be 

seen in every situation in which 

fibrillation are seen and I think should be 

treated identically defib relations.

In discussions of neuro muscular path of 

physiology,

let's now move on to the articulation.

The physical ation is an action potential,

having the dimensions of a motor unit action 

potential of either normal or abnormal 

size and form,

which occurs spontaneously and sporadically.

The associated twitch of the bundle of muscle fibers 

may be visible.

The source of the relation 

has been the matter of some uh 

discussion and 

there are two schools of thought.

I think the predominant evidence is that the 

relation arises peripherally in 

the motor neuron.

The evidence for this is that relations can 

persist after peripheral nerve block and can 

persist 2 to 5 days after nerve section.

Furthermore,

anti colonist race medications,

which act predominantly at the neuro muscular junction,

can increase the frequency of circulations.

The arguments for a central mechanism are based on the 

fact that articulations occur more commonly in 

anterior horn cell disease than in peripheral nerve 

disease.

And in an isolated reports 

of synchronicity of 

articulations recorded in muscles in 

different muscles supplied by different peripheral nerves,

but in the same Maya tome 

the next slide illustrates 

of articulation and I think that the 

important points are the 

changes in form from from one physical ation 

to the next and the 

presence of and they're sporadic 

firing nature.

Now let's go on to the next 

slide which lists some of the causes of 

relations.

I think that I've already pretty much covered the 

causes.

Uh It's always good to remember that fire a toxic 

oh sis among the endocrine diseases can be associated with 

circulations.

But one of the thorniest diagnostic questions is that a 

so called benign facil relations?

The patient who presents with the stipulations 

alone without weakness 

on E.

M.

G.

The facil relations 

usually have the similar 

characteristics in terms of number of 

phases,

amplitude,

duration as the voluntarily recruited 

motor units and 

if and are.

And the configuration of the physical ation 

itself is not helpful in 

determining whether a 

uh whether a neuropathy or anterior 

horn cell is causing the relation or whether their so called 

benign.

This distinction has to be made on clinical 

grounds or on basis of other AMG 

findings.

We'll now move on to the next type of spontaneous 

activity.

The maya tonic response.

My antonia is a high frequency repetitive 

discharge of either biphasic 

spikes or positive waves induced by 

different means.

The amplitude and frequency of the potentials wax and 

wane.

And this is associated with a characteristic musical 

sound which increases and then decreases in 

twitch.

This sound is the so called dive bomber.

Our next slide shows 

some examples of my Antonio 

and the characteristic findings 

are the variation in amplitude,

the variation and frequency so that the interval 

between potentials is much greater here than it is 

here and the gradual 

stop rather than an abrupt stop.

My antonia seems to arise from the muscle 

fiber itself.

The evidence for this is its persistence,

after cure ization 

and it can be seen in a number of different 

conditions.

My tonic atrophy.

Maya Tonia congenital to Parramatta,

Tonia congenital to in this complex with hypoglycemic 

periodic paralysis.

Condo,

destroy my antonia.

These diseases,

the electrical,

my antonia is often associated with 

clinical my antonia either on on grip 

or with percussion.

In de innovation,

acid maltese deficiency,

polymorphous itis.

The presence of the Maya Tonia may 

be listed only electrically and not be present 

clinically.

It said that in acid malt taste 

efficiency,

the maya Tonia is predominantly in 

axial muscles,

whereas in my atomic 

atrophy,

it's often easiest to elicit the maya Tonia in the 

most distant muscles.

However,

I do not think that this is a hard and fast rule that 

one can rely upon in making 

diagnoses.

It's one form of spontaneous 

activity which is sometimes confused with my 

antonia is the bizarre high frequency potential.

This is illustrated This is defined on the next slide,

Bizarre high frequency potentials are action 

potentials which are usually polyphasic,

repeating 10-150 times a second 

with very uniform frequency shape and amplitude.

They generally start and stop abruptly.

We'll go on to the next slide,

which gives an illustration of a bizarre high 

frequency potential and shows these characteristics that 

I'm speaking of.

You can distinguish it from the Maya 

Tonia by the fairly constant 

amplitude,

the fairly constant frequency,

the abrupt start and stop.

I speak of constant.

I'm willing to allow a 10 or 20% variation in the 

amplitude or in the inter spike interval.

But compared to the Maya Tony,

I think you can see the difference 

now.

It's very important in talking about bizarre high 

frequency potentials.

Not to use the term pseudo my antonia.

It's always an error to introduce a word that you want 

people to forget.

But let me say that pseudo my antonia means different things 

to different people to some people.

It is bizarre.

High frequency potentials to some people with electrical 

my antonia without clinical my antonia.

To some people with clinical my antonia without 

electric.

Clinical stiffness without electrical Maya Tonia.

I think the term is best discarded.

Well,

I think we've pretty much covered the 

forms of spontaneous activity and let's now 

turn to the voluntary action potential.

The motor unit potential is an action 

potential,

expressing the activity of that part of a 

single motor unit,

which is within the recording range of an electrode.

It is recorded by is recognized by its consistent 

relation to contraction of the muscle 

terms implying diagnostic significance 

such as myopathy unit potential are 

not recommended in in describing motor 

unit potentials.

Now the concentration 

on the 

term an atomic 

versus physiologic motor unit I think is very important.

I'd like to turn now to a slide,

illustrating an experiment done by cougar burke 

and Enstrom,

in which they stimulated a single alpha motor 

neuron in an attempt to exhaust the 

muscle fibers supplied by that alpha motor neuron.

They then biopsied the muscle 

and stained it with PS.

For glycogen.

Here,

you can see that the muscle fibers 

belonging to the stimulated motor unit were depleted with 

glycogen of depleted of glycogen and did 

not stay in with P.

A.

S.

So that the distribution 

of a motor unit throughout a muscle is really quite 

diffuse around each 

fiber that belongs to the motor unit.

There are a number of fibers that don't belong.

Now let's let's 

imagine that we have an 

electrode sitting near this motor 

unit.

It's been demonstrated with multi electrode 

techniques that 

as we move away from the muscle 

fiber,

there's a fall off of the height of the action 

potential that we will record from it,

so that if we are 

More than .4 

mm from the muscle fiber 

will only record 10% of its amplitude.

Now,

the average average diameter of a muscle fiber is 

about 50 micro.

So if we move eight fiber diameters 

away from this muscle fiber,

it will really be contributing very little 

to the action potential that we recorded the electrode,

we can guess that any 

place we put the electrode in this muscle.

Only a couple handful,

maybe a dozen uh muscle fibers 

will make making a major contribution to the 

amplitude of the action potential that 

we record from any single motor unit.

This,

despite the fact that there may be 100 or 

200 muscle fibers in that motor 

units scattered throughout the muscle.

The normal motor unit potential 

is shown in the next slide.

I don't want to talk about its 

characteristics in terms of 

normal amplitude,

normal duration.

Since these will vary quite a bit with the type of needle 

use the techniques that the electron biographer is 

using in making his recording and the care with which he 

measures.

However,

I can point out that it has less 

than has only three phases and if it 

has five or more we call it polyphasic,

that its duration in this case is around 10 

milliseconds and its amplitude is 

somewhat less than a million volt.

Now,

as I say,

I'm not going to talk about the range of normal values,

since this is quite large in the background,

I have a example of a normal muscle 

biopsy stained with the A.

T.

P.

A stain which chains type two fibers dark and 

type one fibers light and you can see that there's a mosaic 

pattern here,

which spreads out,

which suggests that the muscle 

fibers of this particular motor unit are 

diffuse the spread throughout the muscle.

Now,

if there's an anatomical rearrangement of 

the muscle fibers,

the the 

configuration of the motor unit will also 

change.

Going to the next slide.

We can see an illustration of a normal motor 

of a set of normal motor units where we have four 

anterior horn cells each innovating 

a number of muscle fibers.

The ash potential 

is of normal size and duration.

Now if disease attacks one or 

2 anterior horn cells,

the muscle fibers 

innovated by that those anterior horn cells become 

temporarily de innovated and then collateral 

sprouts come from the surviving anterior horn 

cells to re innovate 

those fibers and gain control over 

them.

The result is that we have more 

muscle fibers per motor 

unit and we get a larger action potential.

Actual histology of this situation is illustrated over 

here where a normal biopsy 

shows a mosaic pattern of type one and type two 

fibers.

Whereas after D.

Innovation and collateral re innovation.

There's a there's type grouping with 

large patches of type two fibers and 

type one fibers.

The E.

M.

G.

Findings of innovation are 

listed on the next slide.

These are increased 

amplitude of motor units,

increased duration of motor units,

increased incidence of long duration 

polyphasic motor units and decreased recruitment.

I'll come to the problem of recruitment later.

But I think you can see 

why increased 

number of fibers per motor unit will yield 

increased amplitude and increased duration 

increased pol.

If asia excuse me,

let's go to the next slide.

And I want to give an example of this where 

we have a area of 

type grouping or type predominance where all 

the fibers in the field are of 

one type and the result is larger motor 

units longer in duration,

with extra phases.

Now I think we can see 

some learn something from the single fiber recording techniques 

about why there's an increased incidence of pol if 

asia with the innovating diseases 

here this work is 

that of Bornstein and just met.

On the next slide,

we can see Single 

fiber potentials recorded from two 

different electrodes.

The recording is triggered by the first 

electron elect by the spike of the first action 

potential from one fiber and then the spike of 

the action potential from the second fiber is recorded.

You can see that there's a variation interval between 

spikes.

This is what's known as the jitter.

Now with collateral re 

innovation.

The re innovating axons are 

decreased in diameter and are often less 

reliable than the usual axon twigs.

The result is that this jitter 

increases and 

late potentials can 

can add a single fibers,

can add on to the action potential at a later 

time than usual.

Now we can see this illustrated in terms of 

action potentials in the next slide 

where we record repetitive lee 

a very long action potential 

with a number of spikes that are 

part of the action potential occurring quite a few 

milliseconds afterwards,

in addition to which at times 

one spike or another is 

absent,

probably because of complete failure 

transmission of the new axon twig.

Now,

just as a motor unit 

can increase in size increase 

in the number of fibers per 

anterior horn cell,

it can also decrease in size 

and we refer to this as fraction ation of the motor 

unit.

The fraction nation can occur on either 

physiologic or an an atomic basis.

The result is decreased 

motor unit duration,

brief action potentials,

decreased motor unit amplitude,

small action potentials,

increased recruitment of motor units,

abundant extra potentials and increased 

incidence of short polyphasic potentials,

polyphasic potentials.

This has given rise to the acronym B.

S.

A P.

Or B.

S.

A P P E M.

G.

Now the this 

the findings of A B.

S.

A.

P E.

M.

G were first noted back in the 19 

forties to occur in Duchenne 

dystrophy and polymorphous itis 

and were quickly associated with 

myopathy.

However,

they can be seen in a number of other conditions.

And I've taken a historical example from a paper 

by Kugel Berg in 1947.

This E.

M.

G.

Is a typical Bs ap pattern.

You note that the that the 

potential is quite brief that at 

times it can be quite polyphasic that the 

recruitment is abundant.

Now this E.

M.

G.

Was not taken from a patient who had a myopathy 

or who had polymorphous itis,

but rather from patient who had a localized kuraitis of the 

shoulder girdle.

Now,

of course,

on clinical examination,

the distinction between 

a local neuropathy 

and a 

myopathy can usually be made,

but the E.

M.

G.

Cannot make that distinction 

as if one looks at a variety of neuro muscular 

diseases.

One can imagine a different 

mechanisms of vaccination of the motor unit.

I already I've already mentioned Duchenne dystrophy in which the 

fractious nation presumably occurs because muscle 

fibers themselves are degenerating.

Patients with periodic paralysis may have 

normally mg between 

week periods and then have brief motor units at 

time when they're weak.

Thus just functional 

muscle fiber impairment can cause B.

S.

A.

P types of findings without having 

anatomical disease.

The B.

S.

A.

P.

E.

M.

G.

Can also be found in myasthenia gravis in some patients 

in in which case we associate with blockade of the 

neuro muscular junction.

As as in the example I just gave you from kugel 

berg neuropathy in terms of Exxon 

twig disease can give A B.

S.

A.

P.

M.

G.

And the disease of type one hypertrophy with central 

nuclei where other people,

what people have also called maya jupiter 

myopathy or central nuclear myopathy can have A B.

S.

A.

P.

E.

M.

G.

And has been hypothesized.

This is a disease of congenital motor unit 

hyperplasia.

Now there are a number of neuro muscular diseases of 

whose ideology is far from clear which also have 

A B.

S.

A.

P.

E.

M.

G.

Examples would be my atomic atrophy.

Please excuse the extra End rod 

disease.

Central core disease.

Some of the neuro muscular diseases associated with 

abnormal thyroid function or neuro muscular diseases 

associated with abnormal calcium metabolism.

Now,

when we don't know the ideology of these diseases 

and when the E.

M.

G.

Is A B.

S.

A.

P.

Pattern,

it would be an error to stultified.

Are thinking by thinking on the 

basis of the E.

M.

G.

Findings.

Thus I'd like to go back to the definition of 

a motor unit potential in which we started this section of the 

discussion and emphasize what the 

committee on terminology emphasized.

If we can go to the next slide,

that terms implying diagnostic significance in 

discussing the motor unit potential are not recommended.

Now in talking about both B.

S.

A.

P.

E.

M.

G.

S and about neuropathy.

I've talked about interference patterns.

I'd like to now go to the problem of recruitment.

An interference pattern is a pattern of electrical 

activity produced when numerous motor units are 

active so that their action potentials can no longer be 

identified individually.

When a when one 

first starts voluntary activity in a 

muscle a single motor unit is active.

Fied is activated and starts to fire.

Thus we see a single motor unit 

firing now as forces as 

as contraction increases the 

frequency of firing of the single motor unit will increase 

as we see here and a second motor unit 

will also start to fire eventually 

with increasing effort.

The a number of more motor units will be 

recruited and the result will be 

that the 

individual motor units are no longer identifiable.

Now we can 

have decreased recruitment on a number 

of on the basis of a number of causes 

going to the next slide.

We can see that in the presence of 

innovation when there are less active motor,

fewer active motor units,

there will be decreased recruitment 

in the end stage muscle.

When there are fewer available muscle fibers 

there will be,

there will often be decreased recruitment,

decreased recruitment can also occur 

episodically in diseases with neuromuscular 

neuromuscular junction blockade.

In my in Parramatta Tony agenda 

where transient dysfunction 

of muscle fibers can cause decreased 

recruitment in central nervous system 

disease and with decreased effort on the 

patient's part.

Now we can say something about 

distinguishing the latter two causes central nervous system disease and 

decreased effort from the other causes of decreased 

recruitment.

As I said,

normally when one 

recruits,

the frequency of firing increases 

before the extra motor units are brought 

in.

Now in lower motor neuron disease,

a patient making a good effort even though he 

has very few lower motor neurons available,

will increase the frequency of firing of those motor neurons,

which he does have the patient who is making a 

decreased effort for whatever reason,

will not show that increased frequency of 

firing and will have a rather uneven 

pattern.

Now,

I'm somewhat embarrassed to have this line in 

because this is a slide that was made before the B.

S.

A.

P.

Era in any event,

when there are fewer motor units available 

for the opportunity when the motor units available are 

smaller as in B.

S.

A.

P.

Pattern more and more units have to 

be recruited to give an equivalent amount of effort.

The result is abundant recruitment and an 

increased density of interference pattern.

Now there's one other factor which 

which affects the way motor units fire 

and that is whether they're type one or type two motor units.

It's it's been shown as the next 

slide shows that type one motor 

units tend to fire in sustained 

rhythmic fashion with low frequency of 

discharge on mild contraction.

Type two motor units on the other hand 

give brief bursts of firing fire with a high 

frequency of discharge and require a vigorous 

contraction to be recruited.

This is this has been discovered 

through the open biopsy MG.

Work that was done by 

wormholes and Engel,

and I suppose one has to qualify it by saying 

that that so far has only been established in 

pathological muscle.

The next slide shows an example of an open 

biopsy E.

M.

G.

Taken from a patient in which there is predominance of type 

one motor unit,

type one muscle fibers.

The Type two muscle fibers single one.

The open biopsy MG.

From this muscle showed 

a regularly firing easily recruit herbal motor 

unit.

A type one motor unit.

Now on the other hand,

if one looks at an area where 

type two fibers predominate as the next slide shows 

the open biopsy.

E.

M.

G.

Shows an irregularly firing motor unit that 

fires with a high frequency and requires increased 

effort to recruit it.

Now the this 

suggests that in routine 

clinical E.

M.

G.

We're only looking at type one 

fibers because these are the ones that are most 

easily recruited and it may well be that certain 

diseases of type two fibers.

For example those diseases which cause type two 

atrophy such as uh predniSONE therapy or 

disuse will have a normally MG.

Despite clearly defined pathology 

with history with history chemistry,

I've emphasized some of the shortcomings of the 

MG.

Some of the questions that AMG cannot answer.

I don't want to end with the impression that E.

M.

G.

Is not a value.

We consider it an indispensable part of a patient's neuro muscular 

evaluation.

It's very helpful in demonstrating the extent of neuro 

muscular disease.

It can establish the presence of neuro muscular 

disease in a patient with with equivocal 

clinical findings.

It can raise interesting research questions 

what do all the diseases in which electrical maya 

Tony is seen have in common.

Perhaps other speakers in this series will discuss 

more specific examples of the MG usefulness.

Remember M.

G.

Is most valuable when we can precisely report what 

information the MG renders and then integrate 

that information into the total clinical picture 

of the patient.

Thank you