Since their introduction into clinical medicine almost 50 years ago. The techniques of Electro biography have added immeasurably to the recognition, understanding and direction of therapy of neuro muscular disease in man. What I shall attempt this afternoon is a definition of some of the techniques that are useful in vivo. I shall review their application limitations and value in disorders of the motor unit, and I shall attempt a prophecy of some of the innovative developments of recent years. Therefore this is by no means a compendium of a field that has already nurtured five International Congress is one in which several standard texts are extended. I shall try to give you some of the field for the fact that E. M. G. Must be clearly tailored to the clinical problem of the patient as a fishing expedition. It is rarely fruitful as an exercise in clinical physiology. It is often exciting if we can go to the first slide on this are depicted the various levels of the nervous system pathology at any level of which may lead to a complaint of weakness. The techniques of electro biography have their most application, their highest application in the motor unit, which is all you all of you recall, is the anterior horn cell. It's peripheral extension, the motor nerve fiber, the neuro muscular junction and all of the muscle fibers supplied by a given anterior horn cell. We go to the next slide, we can see that at the level of peripheral nerve. There are several techniques which are useful for studying the health of nerve. Basically these have to do with the measurement of conduction velocity of nerve in motor mixed and sensory nerve fibers and the excitability of peripheral nerve. The next slide, please this slide attempts a schematic representation of the techniques of nerve conduction velocity. Perhaps it is a bit simplistic, but I believe if one understands the simple factors behind the measurement of motor nerve conduction velocity, then some of the difficulties in the application of this technique become apparent. Under ordinary circumstances, a nerve is selected that may be stimulated distantly and proximately in order to give rise after a latent period to a muscle action potential. Now one would think that if velocity is distance per unit time, that all that needed to be done would be to measure the time from the stimulus to the response, divide that into the distance between stimulating point and recording point and come up with a velocity. However, the basic tenants of physiology have us to understand that nerve conduction velocity, in which we are interested is a phenomenon which in normal individuals occurs at a magnitude of 40 to 60 m per second, whereas muscle conduction velocity occurs in the range of 4 to 6 m per second. Thus one doesn't know where the nerve impulse leaves off and the muscle impulse starts. For this reason one must subtract the latency from a distal stimulus from the total latency from a proximal stimulus to come up with a latency difference that can be divided into the distance between stimulating electrodes and a velocity derived two other points should be evident from this slide that not only velocity can be calculated in this fashion, but also one can look at the distal latency itself, and one can as well look at the amplitude or size of the muscle action potential. Since velocity is distance per unit time, one would think that one could draw a plot between distal distance and distal latency And have a straight line relationship between the two. This is not true for distal distances rather over a wide range of distances. Distal latency occurs within a fairly narrow band. The absolute value of distal latency, therefore is quite important, irrespective of the distance over which the stimulus occurs. That absolute value may be the only indication of disease in nerves which is much more prominent distantly. Likewise, the amplitude of the muscle action potential itself may be a measure of the number of nerve fibers that are stimulus bill, or the number of muscle fibers which respond to that stimulus. In ordinary circumstances, that amplitude is expressed as a million volt phenomenon of the negative peak of the action potential on occasion as a peak to peak amplitude. Later, I think we shall see that with certain conditions of stimulation, the amplitude may appear to increase while the duration of the response decreases the total area, therefore not changing Edward Montgomery about two years ago introduced a technique for the automatic analysis of evoke muscle action potential area in the hopes that this would be a better measure of neuromuscular disease. Unfortunately, in normal subjects, the range of area is as great or greater than the range of amplitude itself. With that as a background. Let us go on to some of the applications of nerve conduction velocity in the next slide, which are a series of data obtained from a patient with the G. In barre syndrome of idiopathic pollen iritis. One can see that in the early stages of this illness on occasion with proximal stimulation, the response is often quite small and broken up, whereas with distal stimulation it is fairly large. This difference becomes apparent as the disease progresses but then is repaired so that in health at time d hear the response to a to a distal stimulus was about the same size and shape is that to a proximal stimulus. You will note that the latency two onset of distal stimulus at the height of the disease when the patient was first studied was quite prolonged compared to the latency in recovery. Thus, distal latency in this instance was an indication of neuropathy. These data are graphed out in the next slide with conduction velocity, showing at the top of the graph versus time distal latency in the middle graph and evoked muscle action potential amplitude. With distal stimulation shown with the crosses and proximal stimulation shown with the open circles In this particular patient changes in all three Parameters occurred. The initial study showed a very small action potential that improved as the patient improved with a prolonged distal latency that even got worse during the course of his illness, only to return to normal values and with the conduction velocity that at least for onset muscle uh latency differences was close to normal range but dipped down to clearly abnormal range is only to return as the patient's strength improved. This pattern of change in velocity, latency and amplitude in the next slide can be plotted against the months that it takes to recover and although the data are kind of scattered, a fairly straight line relationship With a correlation value that is not unrestricted ble can be seen from a series of 40 patients studied the University of Kentucky Medical Center over the past nine years. In this instance, it was of interest that the patients with the slowest velocities have the shortest kind of illness. The summary of this application of motor nerve, conduction velocity would be that it has great role, a great role to play in certain kinds of neuropathy. But in the next slide, The problems faced with this technique in other kinds of neuropathy should be evident. These data are taken from a paper by PK Thomas that appeared in the Lancet in 1959. At the top are shown data from patients in chronic renal failure and at the bottom. Normal controls on the left hand side and upper extremity nerve, the median nerve and on the right hand side, a lower extremity nerve. The lateral pop little nerve. Although the patients with chronic renal failure show a general skew of their velocities towards slower velocities. I think it is readily evident that many your E. Mc patients with obvious clinical neuropathy had velocities within normal range in the next slide, this problem of overlap cannot be gotten away from with serial measurements in this slide at the top are taken data from a paper that appeared in the new England Journal about five years ago. The patient whose data are reported here was quite seriously ill in renal failure with neuropathy at the time the initial media nerve conduction velocity was taken. Renal transplantation was performed then and over the next several months improvement occurred and improvement in his velocity occurred. The authors who published this data offered this as evidence for a technique to document changes in a condition known to be associated with neuropathy. The data at the bottom of the slide are taken from a paper that a medical student at the University of Kentucky published About seven years ago. These particular data are serial observations on a classmate of his who was no weaker at the beginning of the study than he was at the end of the study. The point of this slide is that even serial observations may show a random change that is as great as or perhaps even more than the observations from subjects with neuropathy. Therefore, there are limitations to the measurement of motor nerve conduction velocity in identifying patients with clear and unequivocal neuropathy, and how do we overcome these limitations? Let us look at the next slide. It has been suggested that one way to overcome the limitations is to look not only at the direct or M, or muscle response to nerve stimulation in this instance distantly and here approximately, but to look at a late wave as well, a wave which takes longer to occur the further away from the spinal cord one stimulates and a wave therefore which is reflex in character. Richard Meier showed very nicely about 10 years ago that this waveform occurred in the upper extremities of patients whose dorsal nerve roots had been sectioned for the control of pain in carcinoma and therefore that this small muscle, small muscle or F wave was a axon axon reflex occurring with anti drama, traveling up the motor nerve through the motor nerve root and back out again Ortho dramatically from that initial stimulus. The latency over this much longer distance is a fairly regular phenomenon and disorders which selectively affect the nerve root may prolong that latency. And so just as distal latency may may may be a measure of distal neuropathy. So, to F wave latency, in the presence of normal velocities may give a clue to the presence of neuropathic weakness. If this sort of technique is normal, what else can be done in the next slide? A schematic representation of a nerve action potential, which is multiphasic. As one can see here with nerve stimulation can be seen look tall and Rosenfeld. Using averaging techniques with multiple sensory nerve stimuli have shown that one can in the intact human subject record a compound nerve action potential whose various components can be measured in terms of their velocity and in terms of the amplitude of the envelope conducting at that velocity. And they have shown very nicely in a paper reported in brain in 1972, a strong correlation between the changes either in velocity of one or another of these components or in the amplitude of the envelope and the histological appearance of that neuropathy. Since many Europa these are purely sensory. This technique of compound nerve action potential study is a very useful adjuvant to the analysis of peripheral nerve disease. Other techniques are shown in the ensuing slides. The next slide, please Here is graft the thesis behind the measurement of nerve excitability, which Wilson described in the journal of neurology neurosurgery and psychiatry more than 10 years ago. If one relates the intensity of a stimulus required to elicit a threshold nerve action potential, giving paired stimuli at various intervals and relating the intensity of the second or test stimulus. Following a super maximal conditioning first stimulus, one is able to define the absolute refractory period as the time during which a second stimulus, no matter how intense will not elicit a second response, the relative refractory period with the two stimuli or equal intensity and a following period called super normal period where the second stimulus needs to be even less than it is without the conditioning stimulus. I think you can tell or deduce from the description of this technique that it is a very meticulous one requiring a great deal of time. And so in the next slide James Heckman, then a medical student at the University of Kentucky decided to re approach the old concept of a strength duration curve. He noted that with the standard stimulator available for measuring strength duration curves uh in the normal fashion that any fizzy interest will use that stimulator while it could give a square wave that very brief stimulus durations had to have a superimposed R. F. Wave to give a pseudo square wave at longer durations. Thus, using this stimulator, one doesn't know really at what level the stimulus is at any moment during this long stimulus. Using a different light isolated stimulator. Even at the long intervals, a quite square wave was elicited and in the next slide, if one compared stimuli of varying strengths from this light isolated constant current stimulator over varying durations, one was able to depict a so called excitability curve. The response in the instance of the excitability curve was the nerve action potential elicited by per cutaneous nerve stimuli When Heckman compared these data In the same patients, or at least five out of the six of the same patients with a standard strength duration curve. He noted that this excitability curve was significantly more sensitive to this parameter of nerve function than the standard strength duration curve in the next slide. Elizabeth right, extending his technique even further has shown that there is a range of normal values depicted in the crosshatched area here against which can be compared a group of patients who have normal nerve conduction velocities but obvious clinical neuropathy, their conduction velocities did not pick out the neuropathy. This excitability curve clearly did, especially at the long duration stimuli. This technique has been of a special use in the next slide in the analysis of peripheral nerve function in patients and chronic renal failure, where it can be seen That of a group of 19 patients who had clinical neuropathy. Their upper extremity ulnar nerve conduction velocity was outside normal range only seven out of 19 times the perennial nerve conduction velocity was rather more sensitive. But ulnar nerve excitability identified every patient with neuropathy, there is a problem. Clearly in the excess sensitivity of both of these techniques. Since certain numbers of patients without clinical neuropathy in your E mia will have slow conduction velocities or decreased excitability. I think it should be recalled that nerve biopsy of all patients in your E. Mia in some studies will show clear cut changes. Histological E what Hickman's technique was after was a clinically useful way of approaching and identifying the patient who will have neuropathy or who may go on to develop it. And in the next slide, this question was looked at. Eight patients having serial studies showed a slow peroneal nerve conduction velocity before the onset of their neuropathy only in 25% or two out of eight of the times. Whereas six out of the eight patients had decreased excitability. This technique is in its infancy as a clinical tool, but may, together with the book tall way of looking at compound nerve action potential, be an extension of nerve function with electro maya graphic techniques. Let us go on to the next slide. Another extension has been developed by McComas and his colleagues initially in London and subsequently in Ontario. They have noted that if a peripheral nerve is stimulated and recording made from a muscle supplied from that nerve with a reference electrode in this instance, on the foot and a ground strap between the two. In the next slide that with increasing strength of stimuli, increasing size of surface recorded muscle action potentials can be had. If one looks at a reference electrode placed elsewhere on the foot. This particular extension digitally umbrellas muscle is the only muscle responding to perennial nerve stimulation and that perhaps is why they have chosen this preparation for most of their approach. Using threshold stimuli, one can define a minimal motor unit size and in McCormack's technique. this is referred to as the size of a single motor unit. One can therefore divide into the maximal response this single size to come up with a measure of the number of motor units in that particular patients extensive digital and bravest muscle. And what does this technique show us in the next slide? If one looks at control subjects, the amplitude of their motor unit, the size of the motor unit with the McComas technique is about the same as it is with limb girdle muscular dystrophy, and in fact, there may be some skew toward increasing amplitude of potentials in spinal muscular atrophy. There are many potentials which are of significantly larger amplitude, so that in McComas hands, the individual amplitude is perhaps of help in clearly neuropathic disorders, but not of much help in the limb girdle, muscular dystrophy, and other dis trophic disorders. But what is more amazing in the next slide, if one looks at the number of units from the extensive digital and bravest muscle in control subjects compared to a series of disorders which are at least traditionally held to be my opa thick one is struck that the McComas technique shows a drop out in the number of motor units. Now that's supposed to happen only with neuropathic disease. And so in the next slide, McComas has hypothesized that neuro muscular or motor unit disease may derive from a change in the motor unit, which ultimately occurs because the motor neuron itself becomes sick. And as that sickness progresses, single fibers drop out until generalized atrophy occurs and whole motor units are lost. It is this hypothesis which electrically gives support to the concept that much, if not all, of motor unit disease is ultimately neural in character. In the next slide, there are some who take issue with this particular way of looking at things and if they compare their control data in terms of motor unit potential amplitude with a variety of muscular dystrophy ease. And in this particular instance most of them were classic Duchenne dystrophy ease. I think it is fairly evident that the size the individual units with the McComas technique is here clearly shifted towards smaller units, looking at the total number of units, and I do not have a slide to show you from this author showed a a similar number of motor units. And so the McComas technique supported what standard electro media graphic techniques had suggested in the past. I would simply summarize my discussion of this technique by saying that there are many questions. It raises questions which are not yet answered. In the next slide, we go to the next level of the motor unit, the neuro muscular junction and at this level the response to repetitive nerve stimulation is the hallmark of a change of a sickness that may be productive of weakness. The next slide shows us the basic principle on which clinical E. M. G. Analysis of neuro muscular transmission is based. In this instance, a nerve stimulus is applied to the whole nerve supplying many motor units and a muscle action potential recorded with surface electrodes. In this instance it is of eight million volts theoretical amplitude as far as the negative wave is concerned if during the course of repetitive super maximal nerve stimulation, motor units drop out as indicated by the black marks. Here the evoked action potential amplitude will decrease and one can express The change during repetitive stimulation as a proportion in this instance, a 50% block in the next slide, this change is nowhere more clear than in the illness. Myasthenia gravis, in which paired stimuli At intervals less than 1/2. In this instance, 100 and 60 milliseconds show a fall off in the amplitude of the second stimulus. In all instances the stimuli are super maximal for nerve you have heard earlier and I'm sure recall that the classic hallmark of Myasthenia gravis is a fall off during repetitive stimulation that repairs itself early on in the course of repetitive stimulation. In this instance, at 10 impulses per second. This so called early dip is seen classically in myasthenia gravis and only in one other setting in individuals who have been given a small amount of your r if the stimulation is continued for a long time, the fall off with a late exhaustion is observed and both of these phenomena can be ameliorated if colonist arrays inhibitors are given in the next slide, it is important to be certain that the response in muscle to nerve stimulation does not arrive at other levels. One way of looking at this is to apply a stimulus through a needle electrode in the distal portions of muscle away from the zone of innovation. The motor point and to record with needle recording electrodes at two points are one here and our two here. In this instance, the same repetitive stimulation was given and the response, aside from a little baseline artifact, was the same to the initial response as it was during the course of stimulation. There was a little change in conduction velocity during repetitive stimulation, but the amplitude, the size of the evoked response response in muscle to muscle stimulation stayed the same even though, as we saw in the former slide, it changed with nerve stimulation so much for the theory behind the analysis of neuro muscular disease. Let us go on into the next slide. This kind of technique can be applied to the study of Children born of my aesthetic mothers and I think in the case of the data on the right hand side, from a child who had transient neonatal myasthenia, one can see it fast rates of stimulation and its lower rates the early dip phenomenon once again, and in the case of a child born to a another mother with myasthenia, but a child not manifesting clinical weakness. No such early dip was observed. This is therefore a useful technique for the uncovering of myasthenia gravis. In the next slide There are a certain proportion of patients, however, who will not show any change with repetitive stimulation. Dr. Young and his associates have estimated that if one looks at a single nerve muscle junction preparation in Vivo, that the incidence of abnormalities even in the presence of defined Myasthenia is of the order of 60%. If you look at two or three or more neuromuscular junctions, that incidents can be increased to 85, perhaps 90%. But the remaining portion of patients who have classic myasthenia in whom repetitive stimulation will give no abnormality for this reason Colin Brown reintroduced a technique of Regional Cure Ization, in which the same stimulus and recording parameters with an intervening uh ground strap are observed and under tourniquet conditions, an intravenous infusion of a small amount of Harare is given after a latent period. The tourniquet is released and after four minutes or so permitting restoration of normal function. Then studies of neuro muscular transmission are had in the next slide data from his paper in the Journal of neurology neurosurgery and psychiatry this year show what happens in three normal subjects. The response to repetitive stimulation before the administration of cure are at rates of two stimuli per second show no change afterwards. There is a minor fall off in the total amplitude of the response, but repetitive stimulation really doesn't do very much. But if we look at this in my aesthetic subjects in the next slide one can see that although ocular my aesthetics may not show very much change. Patients with generalized weakness, even though it may be mild without any evidence of change with repetitive stimulation to start with may show a complete and total block with very small doses of cure our regional cure Ization therefore may help to identify the 10 or 15% of patients with classic myasthenia who do not show a defect on repetitive stimulation. The next slide not only is the detrimental response occasionally seen, But there are conditions in which very slow stimulation. In this instance, one per second will show a fall off, but very rapid stimulation. In this instance, 20 per second will show a marked increase in the amplitude of the response. The next slide shows that this increase may in part be due to the narrowing of duration and increase in amplitude. The so called bunching phenomenon, but that if one looks at the response at the end of this stimulus train at 10 cycles per second and compares it to the beginning. Not only is it shorter, but also it is significantly larger in area I. E. The increase in amplitude is even more than one would expect from the bunching phenomenon. That's important to realize because a certain amount of facilitation, perhaps up to as much as 20% can be seen in normal subjects because of bunching. This phenomenon of increase with fast repetitive stimulation is what one would expect theoretically with a defect in acetylcholine release. And these two slides have been taken from the classic defect in acetylcholine release that associated on occasion with a small cell carcinoma of the bronchus, the Eaton lambert syndrome. In the next slide, a similar defect can be seen particularly with fast repetitive stimulation and in this instance the enhanced potentially ation or facilitation and muscle action potential amplitude is expressed as a percentage of baseline stimulation during and after a train of repetitive stimuli. The marked increase to 2.5 to 4 times the amplitude occurred in this young man seen in the next slide, who, when he was admitted to hospital, had a very blank face with immobile eyes and dilated, fixed pupils that would not respond to light seen in his hometown of Stinking Creek Kentucky. Two months after this, he was a tasseled haired little boy with quite evident open eyes, fully mobile, not only in his ocular and bulb our muscles, but also elsewhere. It is likely, although not proven beyond the shadow of a doubt that this child's pre synaptic defect in acetylcholine release was caused by the presence of botulinum toxin in some of the food found near of his home. In the next slide, a response halfway between myasthenia and the pre synaptic defects we've been considering can be seen on occasion in this instance an individual who became weak after the administration of a polyp peptide and an amino black aside antibiotic was studied not only was nerve stimulation given and muscle action potential recorded, but also the anti drama nerve action potential was recorded during repetitive stimulation. Thus in this instance the change which is occurring in muscle action potential was not seen in the nerve action potential and hence must be at the neuro muscular junction. This patient's response started off quite small and got seriously smaller with repetitive stimulation at slow rates with faster rates. The rate of decline was not so great. It wasn't a full potential ation But at least faster rates of stimulation overcame some of the block present in this instance when stimuli were given one every 10 seconds. This defect has been shown with single fiber E. M. G. Studies in vitro to be associated with disordered pre synaptic acetylcholine metabolism. The next slide, please. I think it's important to call to mind the character of the defect once again with the early dip and late fall off during repetitive stimulation at varying frequencies. Because this hallmark of myasthenia gravis in the next slide Was what was clearly shown by Patrick and Lindstrom in their classic paper in science in 1973, in which they showed that Myasthenia gravis could be induced in laboratory animals by the administration of purified receptor protein. In the next slide, the MG defect in such an animal is seen much more clearly during and after repetitive stimulation, where an immediate post titanic facilitation sometimes occurs with a later post titanic fall off. This defect can be seen to be changed by the administration of a colonist arrays inhibitor in the rabbit. The point I'm trying to get across is that this E. M. G technique is the way in which we recognize and affirm that the animal model is truly an animal model of myasthenia gravis. In the next slide, the same defect was seen by Dr Druckman during immediately after and the post titanic exhaustion observed in a rat exposed to cobra venom in order that one could show that blocking of the N plate receptor protein could produce a neuro muscular disorder, a neuro muscular disorder recognized by the AMG hallmark of an early dip. And finally in the next slide Dr Jackman's delineation that such a defect occurs in mice who are given chronic administration of immunoglobulin from patients with myasthenia is one of the real breakthroughs and the understanding of myasthenia gravis, a breakthrough that supports the concept that it is a disorder associated with circulating antibodies to receptor protein. That this is clinically and electrically true is seen once again by the early dip phenomenon. So much for neuro muscular transmission. Let us move on to the next slide at the last level of the motor unit in muscle itself. Various needle electrode biographic techniques measuring conduction velocity and excitability of of muscle fibers directly as well are used to analyze disease. If we can see the theory behind these in the next slide. Under ordinary circumstances, two kinds of needles are used either a concentric needle or else a very fine multi electrode on occasion as well. Single mono polar electrodes are used and these techniques give different kinds of information. Let us explore that now in the next slide, schematically represented. Here is something that anyone who has ever listened to a radio realizes a multi electrode placed inside of a muscle In which only one motor unit in the center of the muscle at level two is being activated, will record a muscle action potential of a given amplitude and duration above and below. That active motor unit the same duration, the same frequency, the same tune if you were, is heard but at much lower amplitude. So that using concentric needles, the duration of the motor unit is the thing that counts book tall and his co workers have correlated motor unit duration with the size or the number of muscle fibers supplied by each anterior horn cell. And has shown that with very small motor units, such as occur in the extra ocular muscles, very brief motor units are recorded and with large ones and the large muscles of the thigh. Long motor units are recorded. He and his colleagues have established normal motor unit duration values for different subjects at different ages and in different muscles and has shown that if one can observe increased duration units, then one must postulate an increase in motor units size and again, that can only occur when there has been degeneration due to neuropathy with re innovation and increase in the size of the motor unit, decreased motor unit duration can be seen with decreased motor unit size and is often referred to as my opa thicken character. The next slide. Such brief motor units can be seen with weak effort when there is spotty drop out of muscle fibers, whereas with whole muscle fiber drop out and perhaps re innovation, the motor units are larger. There is some activity at rest in the next slide that has a particular and peculiar fashion. That sounds like a motorcycle revving up for those who remember the days of funds and his friends on Happy Days, the dive bomber of World War Two. A potential which increases in amplitude and frequency and later decreases in both. In this instance, the muscle was per cust with the needle in place and this phenomenon is the electrical concomitant of maya Tonia, a phenomenon missing from a normal muscle and a very clear and classic hallmark of the maya tonic disorders in the next slide, other sorts of abnormalities can be seen at rest. The slide was taken from dr lambert's article in the clinical examinations in neurology textbook from the Mayo clinic. Normally with insertion, a brief bursts of potentials occurs with no activity persisting at rest. If one gets right into the zone of innovation, miniature end plate potentials may be recorded with the Innovation. There are lots of different six simple waves and occasionally positive sharp waves as well. The Maya tonic phenomenon we've commented on, and a bizarre high frequency discharge can be seen in a variety of non specified neuro muscular disorders. In the next slide I will review for you motor units, which, if each box here represents, 10 milliseconds are seen to be quite brief and therefore deriving from motor units whose size whose number of muscle fibers is reduced in the next slide at rest from the same muscle from which the prior slide was recorded are seeing positive sharp waves and fibrillation potentials. The hallmarks largely of D innovation. Thus it can be seen that brief motor units can arise when leaves, drop off a sick rooted tree and are not necessarily myopathy in a path, a demonic sense. With that. As a background, one can simply relate motor unit, size two must to motor unit uh duration and derive some physiologic thoughts about the character of the problem facing you. In the next slide is depicted. Another way of looking at E. M. G. With increasing effort, increased numbers of motor units are recruited such that at maximal effort and interference pattern is observed. If there has been a neuropathy with drop out of motor units, the recruitment must perforce be less such that at maximal effort. Single motor units are observed with a myopathy. On the other hand, since each motor unit is reduced in size, increased numbers must be recorded per unit effort and a more dense, lower amplitude interference pattern and maximal effort is seen. There have been a variety of electronic averaging techniques that have been used to define the differences between these kinds of activity and between various points on this curve. Suffice it to say that when one compares these techniques to the analysis of motor unit duration, the motor unit duration techniques show a much higher correlation with the ultimate clinical diagnosis of the patient. In the next slide, different kinds of activity with maximal effort are observed, I believe these were shown schematically in the last slide. In the next slide, one must recall when doing AMG studies something which King angle showed us quite elegantly several years ago that inflammatory change in muscle may occur as it did in this guinea pig muscle within days after Needling the muscle for electro maya graphic study. And so the studies of E. M. G. Must be done in conjunction with examination of the whole patient and biopsy must not be taken from an area previously needled the next slide because of the limitations of standard needle E. M. G. Techniques, Stalberg and his associates over the past 10 and now almost 13 years have introduced a new way of looking at the motor unit. That new way involves very small multi electrodes and the recording is made from one or another point on the multi electrode in response to voluntary stimulation or in this instance, repetitive threshold nerve stimulation. In normal subjects 12 and often three fibers from that region can be recorded. And if the response to subsequent stimuli is measured, Each of these responses bear the same time relationship to each other within less than 40 milliseconds. If we compare this in the next slide, however, to similar observations made in patients with myasthenia gravis, two things are observed in the first instance, the 2nd, 3rd and 4th units drop out with repetitive stimulation and in the second instance the timing of the second one gets much later. A so called jitter response and increased duration between the 1st and 2nd responses is observed. This jitter phenomenon is the hallmark of disordered neuro muscular transmission. It is seen preeminently with Stalberg single fiber AMG technique in the illness Myasthenia gravis, but obviously and logically can be seen in any other disorder of peripheral nerve or muscle in which delay in conduction in nerve fibers or at the neuro muscular junction or muscle fibers themselves can occur? I believe that's all the slides. Is there any way we can have the slides off at this stage of the game and simply summarize by saying that we have attempted to review the theoretical basis behind the various standard clinically MG techniques, we have indicated some of their limitations and their application in diseases at various levels of the motor unit, and indicated, I hope that if these techniques are applied with reference to the patient's clinical problem, the experience will be an enjoyable one for you, as well as for the patient. Thank you.