Nerve Conduction Study

Transcription

1 Speaker Nerve Conduction Study John lourde, hd, A-C, EEG/E Sandi Jo Viers, electrodiagnostic technician Sensory Median Ulnar adial Sural S. eroneal Non routine Saphenous Medial/Lat. Antebrachial Cutaneous Motor Median Ulnar adial eroneal ibial Non routine Axillary Suprascapular Femoral Nerve Conduction Interpretation; a case based approach objective cont. BJECIVES erform portions of an NCV/EMG as well as experience a NCS/EMG. Discuss and identify the basic components of the EMG table (graphical data), as well as denervation both acute and chronic. Discuss and identify the nerve conduction values from standard NCS/EMG reports, identify the main components such as latencies, amplitudes and conduction velocities. Discuss focal entrapment neuropathies on standard reports and correlate electrophysiologic measurements (demyelination, axonopathy) with reported velocity and amplitude measurements. Discuss radiculopathy and correlated EMG raw data to identify root (myotomal) level, severity or chronicity, including denervative potentials and the morphologic features as well as reinnervative discharges. Sensory Nerve Conductions Sensory conduction velocity is an easier measure to compute, but is more technically difficult to record.his test can be done in either an orthodromic (i.e. distal stimulation and proximal recording) or antidromic (i.e. proximal stimulation and distal recording) direction. Sensory nerves that can be recorded are: radial, median, ulnar, sural nerve and superficial peroneal nerve. he recording is made directly from the sensory nerve (the evoked response is called the sensory nerve action potential SNA) and therefore is quite small. he distance between the site of stimulation and recording is divided by the latency (i.e., the amount of time from the electrical stimulus to the SNA) to determine the sensory nerve conduction velocity over the segment. If the extremity is too cold the SNA may not be recordable. Motor Conduction Studies Motor conduction studies are performed by stimulating a motor nerve while recording the response from its target muscles. It is important to note that the electrical signal that is being recorded following motor nerve stimulation (called the compound muscle action potential CMA) is actually generated by the muscle, and therefore it is quite large. When motor nerve fibers are stimulated close to the muscle, the amount of time before the muscle starts depolarizing is called the terminal latency. Latency is used to define the time between a stimulus and the appearance of a response. erminal latency includes the amount of time it takes the nerve to conduct from the point of stimulation to the motor end plate area and the amount of time for the neuromuscular junction transmission to activate the muscle. he terminal latency does not directly measure nerve conduction (because it includes the neuromuscular junction activation phase also) but it is a reasonable reflection of nerve conduction over this segment of the nerve in the absence of uncommon neuromuscular diseases. here are tables of normal for the terminal latencies of defined lengths for each of the major motor nerves of the limb. Abnormal prolongation of this value is often of benefit in the detection of distal entrapment neuropathies. nce a terminal latency has been recorded, the motor conduction velocity can be determined by stimulation of another, more proximal site along the motor nerve. EMG/NCS Workshop 1

2 he computation of motor nerve conduction velocity requires knowing the distance between the two simulation sites and the difference in the terminal latencies recorded from the more distal and more proximal sites. Dividing the distance by the time gives the nerve conduction velocity over the segment in between the stimuli Median nerve Nerve conduction studies can be used 3 different ways A nerve may be a "nerve of interest", for example median nerve studies where carpal tunnel syndrome is suspected. A nerve may be a useful comparison, for example bilateral ulnar nerve studies where cubital tunnel syndrome is suspected. A nerve may be tested as a sense of general nerve health, eg, some diffuse polyneuropathy, such as we might do when we suspect diabetic polyneuropathy, or some kind of demyelinating polyneuropathy. Even when the clinical syndrome suggests a focal neuropathy, there is value in seeing whether there is general nerve sensitivity to pressure or whether this is clearly just a focal phenomenon. M o t Median Nerve rolonged DML 9.45 ms Left ) Normal Median al Motor Latency nset ight ) Abnormal Median al Motor latency nset Site N nset Norm nset Amp (mv) Norm Amp (mv) Neg Dur Segment Name Delta Vel (m/s) Norm Vel (m/s) ight Median (Abd oll Brev) *9.45 < > Axilla ight Ulnar (Abd Dig Min) 3.13 < > B Elbow >53.0 B Elbow A Elbow B Elbow >53.0 A Elbow Left Median (Abd oll Brev) *4.92 < > Elbow >50.0 Elbow Median Sensory Nerve Action otential (absent) AIEN C/ BILAEAL HAND AIN AND INGLING IN A MEDIAN NEVE DISIBUIN, IGH > LEF. HE AIN AWAKENS HE. IGH HAND AIN ADIAES U HE FEAM. SHE HAS BEEN A HAIDESSE F 30 YEAS. Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment Sensory Nerves Site N eak Norm eak Amp Norm Amp Segment Name Delta Vel Norm Vel (m/s) (m/s) Left Abd oll Brev Median C8 1 Incr Nml 1+ Nml >12ms 0 Nml Nml Left ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml ight 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml ight Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml Left Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml ight C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml ight C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml Left C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml Left C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml Left C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml Left 1 arasp ami 1 Nml Nml Nml Nml Nml 0 Nml Nml ight Abd oll Brev Median C8 1 Incr Nml >12ms 0 educed Nml Left Median Anti (2nd Digit) 5.34 < >10.0 2nd Digit 5.34 >39.0 2nd Digit 5.34 >48.0 2nd Digit 5.34 ight Median Anti (2nd Digit) *0 <3.6 0 >10.0 2nd Digit 5.59 >39.0 2nd Digit 5.59 >48.0 2nd Digit 5.59 ight Ulnar Anti (5th Digit) 3.53 < >15.0 5th Digit 3.53 >50.0 Left Ulnar Anti (5th Digit) 3.47 < >15.0 5th Digit 3.47 >50.0 EMG/NCS Workshop 2

3 Summary: NCV 1. MAKEDLY LNGED IGH MEDIAN DISAL M LAENCY. 2. LNGED LEF MEDIAN DISAL M LAENCY. 3. ABSEN IGH MEDIAN SENSY SUDY A HE WIS. 4. SLWING F HE LEF MEDIAN SENSY SUDY A HE WIS. EMG a) MILD DENEVAIN AND A DECEASE IN M UNI ECUIMEN A HE IGH ABDUC LLICIS BEVIS. b) EVIDENCE F CHNIC DENEVAIVE FINDINGS A HE LEF ABDUC LLICIS BEVIS. Impression: 1. SEVEE IGH MEDIAN NEUAHY A HE WIS, CMAIBLE WIH CAAL UNNEL SYNDME. HE INCEASE IN SNANEUS ACIVIY AND FIBILLAIN ACIVIY SUGGES NGING AXNAL LSS, CNSIDEED AN INDICAIN F SUGICAL INEVENIN. 2. MDEAELY SEVEE LEF MEDIAN NEUAHY A HE WIS, CMAIBLE WIH CAAL UNNEL SYNDME AND MANIFESED BY SEGMENAL DEMYELINAIN AND AXNAL LSS. 3. N EVIDENCE F A ME XIMAL LESIN, LEXAHY CEVICAL ADICULAHY Normal appearing analog waveform An Idealized Sensory Waveform ULNA NEUAHY A HE ELBW (CUBIAL UNNEL). Demyelination at entrapment site causes loss of myelin and slowing of conduction velocities. Further damage into the axonal body causes loss of wave form amplitude. S = Stimulus point, = akeoff point, = eak he time (latency) from S to is typically about 3 milliseconds. he amplitude would be measured in microvolts (μv). Ulnar neuropathy at the elbow (cubital tunnel) he clinical syndrome is one of weakness in the hand, perhaps atrophy of hand muscles, and numbness in the ulnar aspect of the hand. Although possible, it is not likely a patient with a pure ulnar neuropathy will complain of numbness in the entire hand, in contrast to those with pure CS. While there can often seem to be an abrupt onset from the patient's perspective, the findings usually suggest a chronic situation NSE F HE DISAL M LAENCY IS HE IN F HE WAVE NSE BASE IN A MEASUEMEN F IME FM HE SIMULAIN IN WHICH IS XIMAL HE CAAL UNNEL ACSS HE CAAL UNNEL & HE ECDING ELECDES LACED N HE M IN F HE ABDUC LLICIS BEVIS. HIS IS HE DELAIZED ACIN ENIAL AGAED BY ELECNIC ACIVAIN A HE SIMULAIN SIE AND AVELING ALNG HE NEVE AND CAUSING AN ACIN ENIAL AND CNACIN F HE ABDUC LLICIS BEVIS. NMAL LAENCY IS BELW 4.0ms Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name Delta Vel Norm Vel (mv) (mv) (m/s) (m/s) ight Median (Abd oll Brev) 4.22 < > Elbow >50.0 Elbow ight Ulnar (Abd Dig Min) > < B Elbow >50.0 B Elbow A Elbow B Elbow >50.0 A Elbow Left Median (Abd oll Brev) 4.06 < > Elbow >50.0 Elbow EMG/NCS Workshop 3

4 Low amplitude right ulnar sensory nerve action potential CS Worksheet Waves Site N eak Norm eak Amp Norm Amp Segment Name Delta Left Median Motor Left Median Anti (2nd Digit) 3.52 < >10.0 2nd Digit 2nd Digit 2nd Digit Left Ulnar Anti (5th Digit) 3.22 < >15.0 5th Digit Elbow ight Ulnar Anti (5th Digit) 2.66 < >15.0 ight Median Anti (2nd Digit) 3.44 < >10.0 2nd Digit NCV Worksheet CS motor ight Median Motor Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name (mv) (mv) Delta Vel Norm Vel (m/s) (m/s) ight Median (Abd oll Brev) 7.11 < > Elbow >50.0 Elbow ight Ulnar (Abd Dig Min) 2.81 < > B Elbow >53.0 B Elbow A Elbow B Elbow >53.0 Elbow A Elbow Left Median (Abd oll Brev) 7.19 < > Elbow >50.0 Elbow NCV Worksheet Questions Motors CS Sensory Worksheet CS Site N eak Norm eak Amp Norm Amp Segment Name Delta he left median motor distal motor latency onset is ms, with the normal onset latency of < ms. he right median conduction velocity is m/sec_, with the normal velocity of > m/sec. Left Median Anti (2nd Digit) 6.6 < >10.0 ight Median Anti (2nd Digit) 6.8 <3. > nd Digit nd Digit 2nd Digit he right median distal motor latency onset is ms, with the normal onset latency of < ms. he left median conduction velocity is m/sec, with the normal velocity of > m/sec ight Ulnar Anti (5th Digit) 3.3 < >15 5th Digit 14 Left Ulnar Anti (5th Digit) 3.3 < >15 5th Digit 14 EMG/NCS Workshop 4

5 Sensory Worksheet CS Questions cts worksheet wave raw data Left Median Anti Sensory he left median sensory peak latency is ms, with the normal peak latency of < ms. he right median sensory peak latency is ms, with the normal peak latency of < ms 20 2 cts worksheet wave raw data Ulnar Neuropathy Worksheet ight Median Anti Sensory Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name (mv) (mv) Delta Vel Norm Vel (m/s) (m/s) ight Median (Abd oll Brev) 5.08 < > Elbow >50.0 Elbow ight Ulnar (Abd Dig Min) 2.27 < > B Elbow >50.0 B Elbow A Elbow B Elbow >50.0 A Elbow Left Median (Abd oll Brev) 5.31 < > Elbow > Sensory Worksheet Ulnar Ulnar Neuropathy Worksheet Questions Site N eak Norm eak Amp Norm Amp Segment Name Delta Vel (m/s) he left median motor distal motor latency onset is ms, with the normal onset latency of < ms. Left Median Anti (2nd Digit) 4.50 < >10. he right ulnar conduction velocity across the elbow is m/sec, with the normal conduction velocity of > 50 m/sec. ight Median Anti (2nd Digit) 5.47 < >10. 2nd Digit 14 he right median distal motor latency onset is ms, with the normal onset latency of < ms. ight Ulnar Anti (5th Digit) 3.64 < >15. 5th Digit 14 Left Ulnar Anti (5th Digit) he left median conduction velocity is m/sec, with the normal velocity of > m/sec. he right ulnar sensory nerve action potential amplitude is uv, with a normal amplitude of > uv < >15. EMG/NCS Workshop 5

6 1) ULNA NEVE FM WIS ADM. 2) ULNA FM BELW ELBW ADM. 3) ULNA FM ABVE ELBW ADM (ACSS HE CUBIAL UNNEL). Ulnar nerve and branches CLAW DEFMIY ULNA LESIN arts of an EMG here is some understandable confusion about this since the examination as a whole is called an EMG yet the individual parts are NCS or Nerve Conduction Study and EMG or needle electromyography. Most patients should have both parts since they do not substitute for each other but are complementary. Although a referring physician will indicate what should be done, typically in terms of an area or areas of the body, it is up to the electromyographer to decide precisely which nerves and muscles to test. ften, a report Summary or Impression will indicate that there are "neuropathic changes" in one or more muscles. Here I will try to explain how nerve damage in its various phases, hyperacute, acute, subacute, and chronic connect to a conceptualization of what has happened or is happening to the nerve. It will be easier to explain and discuss this from the point of view of a focal nerve injury, acute such as with a peripheral nerve laceration or perhaps a root neuropathy related to a disk herniation, or chronic from severe carpal tunnel syndrome or the chronic effects of a root neuropathy. Hyperacute/Acute A classic hyperacute situation might arise in a severe laceration of an extremity in which a nerve is completely severed. bviously, immediately there is a complete interruption of motor nerve signals traveling down the nerve from the anterior horn cell, and sensory signals from the periphery finding their way to the dorsal root ganglion, and thus the acute motor and sensory findings of the clinical exam. he role of an EMG in this setting could be to attempt to identify the precise point of injury, as well as find information about whether this might be a complete or partial nerve interruption. his is especially important when there is no obvious laceration. NEEDLE EMG First, let's consider what the needle is reading or measuring. In order to understand what the EMG needle is reading, you need to understand the concept of the "motor unit." he motor unit is the smallest subdivision that can be made of the nerve muscle connection. It starts physiologically with a single anterior horn cell in the spinal cord, electrically silent at rest, then sending repetitive electrical impulses down its single axon to the muscle. It remains a single axon until it is very near its end destination inside the muscle, where the axon then sends out branches to individual muscle fibers. Each of these branches only connects to a single muscle fiber at the neuromuscular junction, and each muscle fiber only has one neuromuscular junction his anterior horn cell, its axon, and the collection of muscle fibers it innervates is called the motor unit. In the schematic diagram above, we see a very simplified representation of the number of muscle fibers a typical motor neuron innervates. For most limb muscles, one would expect tens to a 1000 or so muscle fibers innervated by a motor neuron. Smaller muscles used for fine motor activities, such as the intrinsic hand muscles, will have fewer, while a large muscle such as the quadriceps will have more. Furthermore, within an individual muscle, there will be a range in the number of fibers innervated. Initially, at low levels of muscle contraction, smaller motor neurons with fewer associated muscle fibers will activate first, then as more force needs to be made, more and larger motor neurons, each with more muscle fibers per neuron, are activated (or recruited). In addition, one can also generate more force in the muscle by having an individual motor neuron fire more frequently, so what we see in the EMG is a combination of more motor unit potentials (MUs), each firing more rapidly with greater force. So, to summarize, when we put a needle in a normal muscle, we expect no electrical activity at rest, then as the patient contracts the muscle, we see MUs repetitively firing, and as the strength of contraction increases, we see more different MUs, each firing more rapidly. Much of the training of learning to perform and interpret an EMG comes from developing a sense of what this normal activation looks and sounds like not only do we see these MUs on a screen, but also the signals are amplified and put through a speaker, so we not only see these potentials, but also get auditory information about size and frequency content of these complex MU waveforms. EMG/NCS Workshop 6

7 Does EMG Hurt? he Motor Unit Spinal Cord to Muscle How Much Does an EMG Hurt? Now we're getting to a more pertinent question. Unfortunately, I don't have any good answer. o be more clear, I have done EMGs on myself, not for the entertainment value or to "understand the pain" my patients are going through, but typically to evaluate a new EMG machine, or maybe make sure it was working. And this includes sticking a needle in a muscle, always an interesting experience, since it seems I usually use a hand muscle to more easily relax it while I fiddle with the equipment. So on a personal level I have an understanding about how much it hurts, but that doesn't really help much. he problem is, the reactions that one person has versus another are quite unpredictable and I have to say hard to make sense out of. Some tears are common; occasionally, not often, someone will bail out in the middle, saying, "hat's enough, I'm done." But you can have a grown man crying, saying how awful the test is, and next do a child who hardly complains at all what does that mean? Needle EMG and Axonal Degeneration In a situation of complete axonal disruption, initially muscle will continue to show normal reactions to needle insertion (in essence, noise sounds like static on the radio), but otherwise the muscle is silent. Within 1 2 weeks, there should gradually develop some increase in the insertional activity (the static lasts longer), and slightly later denervation potentials, positive sharp waves and fibrillation potentials. Generally, it may take 3 to 4 weeks for these signs of denervation to fully develop, so needle exam will be most useful in judging severity of nerve injury at or after 3 to 4 weeks post injury. In short, the denervation gives a sense of the degree of disconnection of nerve from muscle. ecovery at the Site of Injury Shortly after axonal degeneration is complete, there will be regeneration of the proximal axonal stump, and these growing axons will try to follow the connective tissue pathways down to the original nerve connection point. his will be severely impaired when a nerve has been severed, thus the benefit of reconnecting a lacerated nerve when possible. In the best of circumstances this axonal growth can occur at 1 3mm per day what I usually suggest to patients is an inch per month. hus, the recovery time for a proximal nerve injury can be quite prolonged. ecovery ally his is most evident in nerve muscle connections, where there will be additional branches sent out from remaining axons in the muscle to reinnervate muscle fibers. here is a limitation on how many muscle fibers an individual nerve can innervate, however Wallerian Degeneration Let's take a side trip for a moment and talk about the pathological sequence of events when axons are interrupted in some way. Later we'll connect that to what we see on EMGs. Whether or not there is a total physical severing of the axon, any time that there is sufficient interruption of fast axoplasmic transport, which has to do with the travel of components inside the axon to maintain the nerve structure, there will be Wallerian degeneration. his happens in a predictable pattern, with a predictable timing of events. Immediately after a severe injury or severing of a nerve, there is of course complete conduction block at the point of injury. At this time, though, both segments of nerve remain neurophysiologically functional, which means that the distal segment is still able to be stimulated and should record reasonably normal responses. he potential use is to differentiate a complete conduction block from a severe but incomplete one. As long as some axons remain connected through the point of injury, you may be able to see some transmission of signals through the injured site. If there is a reason to consider a surgical exploration, locating the site can be very useful, and conversely, if conduction block is incomplete there may be no reason for surgical exploration. Wallerian degeneration proceeds very rapidly, with some changes beginning within hours of injury, and fully developed degeneration in 3 to 5 days. here is simultaneous degeneration of axon and its contents, and of the myelin sheath, so in very short amount of time total inexcitability of the nerve occurs. In most clinical situations, this degeneration only involves some of the nerve fibers, others developing focal conduction block and perhaps demyelination, and others remaining intact. he relative degrees of these outcomes should be reflection in EMG changes athophysiologic basis of the denervative process and the corresponding electrophysiologic findings. Denervation As this term indicates part or all of a muscle has lost it s nerve supply. In fact only in severe trauma does total denervation occur, and the more common scenario is the loss of a small percentage of the hundreds of nerve fibers supplying a muscle. (see M UNIS). his occurs for example when a bulging disc presses on the nerve root radiculopathy causing pain from the compression of the sensory fibers and weakness sometimes imperceptible to the patient in the limb. Unlike the damage to the nerve sheath, demyelination, when there is a conduction block, here we are considering the more severe problems that follow when the central core of the nerve the axon is damaged. A series of events take place in the individual, denervated muscle fibers that can be detected as abnormal electrical signals. First of all, over the period of a week or two, the denervated muscle fiber becomes progressively more mechanically irritable. herefore, electrical discharges provoked by movement of the needle can outlast the actual movement by more than a second. his is termed increased insertional activity. Although this finding is not particularly specific, it does indicate that the muscle is excessively irritable. Muscle fibers also become chemically sensitive to their microenvironment and their membranes can also become unstable enough to produce spontaneously activity. his is recorded as depolarization of individual muscle fibers. he spontaneous depolarizations of the individual fibers appear as fibrillation potentials and positive sharp waves.hese do not occur in normal muscles since the normal muscle fibers are only responsive to the activation of their motor unit by neuromuscular transmission. ypically, it takes more than a week for such potentials to develop and they will disappear with complete degeneration of the denervated muscle fiber.. Needle EMG is very sensitive for the detection of these signals and they most often reflect denervation, although they may also occur in severe muscle disease or injury. he finding of fibrillations and positive sharp waves is the most reliable and objective test that there is for damage to motor axons to the muscle after one week at least up to 12 months after the damage. If there is ongoing damage such as in Amyotrophic Lateral Sclerosis one can see ongoing denervation. Unfortunately, the finding of fibrillations and positive sharp waves is often termed acute denervation, although acute in this case refers to weeks and months. EMG/NCS Workshop 7

8 einnervation einnervation takes place over several weeks and can continue for up to three years. he result is that long and finally large motor units are observed on the EMG and from knowledge of anatomy an accurate assessment of the site of previous nerve damage can be made. Moreover these EMG changes usually remain fixed for life, so even years after damage and repair have occurred the EDX physician can report on past nerve involvement. I have observed that at the time of reinnervation, when the axons are thinly myelinated or insulated, the nerve is very susceptible to the effects of alcohol so while reinnervation is being established it is wise to reduce alcohol consumption to a minimum. In addition to the large, long units there is frequently a reduction in the number of units firing, so clearly although strength may have been restored by the reinnervation the remaining axons are supplying a much greater territory of muscle than they were designed for, and this can, over years lead to fatigue. he way to counter this is to consistently undertake an exercise program of ten minutes twice a day to help these "stressed" nerves maintain their function athophysiologic basis of reinnervation and the associated EMG findings einnervation of muscle is an ongoing process, occurring whenever a muscle is partially denervated. his process typically involves the development of sprouts from adjacent, unaffected motor nerve fibers that ultimately contact at least some of the denervated muscle fibers. hese reinnervated muscle fibers cluster right in the area of other, normally innervated muscle fibers. his process results in the development of clumps of reinnervated muscle fibers attached to individual motor neurons (remember, the normal motor unit innervates muscle fibers scattered throughout the muscle). ypically these motor units become significantly larger both in amplitude and duration, since the needle is likely to be recording from more muscle fibers in this clump. Also, the MUs often become more irregular (termed polyphasic ). his process takes months to develop and indicates the presence of chronic denervation. It should be noted that the needle study is much less sensitive to the process of reinnervation than it is to the findings of fibrillations and positive sharp waves that are seen with recent denervation. he typical needle EMG examination requires sampling several muscles. Its ability to localize a lesion depends on sampling muscles innervated by the same nerve but different nerve roots, muscles innervated by the same nerve root but different nerves and muscles innervated at different locations along the course of the nerves. araspinal muscles can be very useful in this regard because nerve root damage will tend to produce abnormalities in these muscles as well as within the muscles of the limbs (helping to distinguish a radiculopathy from a plexopathy or peripheral neuropathy, for example). Sometimes precise localization can be difficult due to the overlap in innervation of the various nerve root levels. Usually MUs and recruitment patterns are not assessed in the paraspinal muscles EMG ABLE Left side of the table represents acute column ight side represents chronic or reinnervative changes Dorsal root ganglion Sensory studies in cervical radiculopathy very useful in c8/t1 re ganglionic & ost ganglionic diagram Multiple sensory NCS allow the investigator to locate sensory neuropathies that involve single or multiple digital nerves distally (for example, vasculitis or hand arm vibration syndrome) right up to the major trunks, cords, and divisions of the brachial plexus proximally. In proximal nerve trauma, maintenance of the sensory potential depends on the intact cell bodies in the dorsal root ganglia. hus sensory NCS are extremely useful in localising a NS lesion as either pre and/or post ganglionic. In a patient with a clinically suspected C8, 1 root lesion and with appropriate anaesthesia in that dermatome, the absence of the ulnar and medial antebrachial cutaneous sensory potential places the lesion distal to the dorsal root ganglion (DG) in the lower trunk of the brachial plexus and not at root level (fig 6). Needle EMG can then be used to define this further. Sensory responses are normal in pre ganglionic lesions even though sensation may be abnormal clinically. ost ganglionic lesions result in abnormal sensory responses. EMG/NCS Workshop 8

9 Cervical adiculopathy Cervical adiculopathy EMG atient History: AIEN C/ LEF AM AIN F SEVEAL YEAS. HE AIN IS DESCIBED AS NEUALGIC AND INDEED AFE DISCUSSIN SHE EVIUSLY HAD A DEMAL MANIFESAIN (HEEIC) FLLWED BY S HEEIC NEUALGIA. HE NEUALGIC AIN IS CMLEE IN HE DEMAMAL EESENAIN A C6 INCLUDING HE SHULDE, FEAM, WIS AND HUMB. N EXAM SHE HAS C7 MUSCLE LSS AND WEAKNESS, WHICH SEEMS UNELAED. Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment ight Abd oll Brev Median C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml Left Abd oll Brev Median C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left ronatoreres Median C6 7 Incr Nml >12ms 1+ educed Nml Left Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Anconeus adial C7 8 Incr Nml 1+ Nml Nml 2+ Nml Nml Left Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left riceps adial C6 7 8 Incr Nml 1+ Nml Nml 1+ educed Nml ight Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Biceps Musculocut C5 6 Nml Nml Nml incr Nml 0 educed Nml ight riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Deltoid Axillary C5 6 Nml Nml Nml inc Nml 0 educed Nml Left C6 arasp ami C6 inc Nml Nml Nml Nml 2+ Nml Nml Left C7 arasp ami C7 Incr Nml Nml 0 Nml Nml Left C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml ight C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml ight C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml ight C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml ight C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml he electrodiagnostic criteria required for diagnosis of radiculopathy is the demonstration of denervation in 2 or more muscles from separate nerves that share common roots. EMG discharges as seen with root lesions, upper motor neuron disease & myotonic (complex repetitive discharge) Name the nerves and roots seen in the above EMG table that meet this criteria. Muscles: Nerves: oot: adial nerve with amplitude loss across the spiral groove and temporal dispersion. eroneal Neuropathy at the Fibular Head Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name (mv) (mv) Delta Vel Norm Vel (m/s) (m/s) ight ibial (AHB) Ankle 4.69 < > Knee Ankle >41.0 Knee Left eroneal (EDB) Ankle 4.45 < > B Fib Ankle >40.0 B Fib oplt B Fib >40.0 oplt Left ibial (AHB) Ankle 4.45 < > Knee Ankle >41.0 EMG/NCS Workshop 9

10 atient History: IGH F D ENEAL ALSY SSIBLY FLLWING F SUGEY VS L5 ADICULAHY. AIEN'S INIIAL F D SEEMED FLLW A EID F SENUUS EXECISE FLLWING F SUGEY. Superficial eroneal Sensory EMG Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment ight ostibiailis ibial L5, S1 Nml Nml Nml Nml Nml 0 Nml Nml ight eroneuslong Sup Br eron L5 S1 Nml Nml Nml Nml Inc 0 Nml Nml ight MedGastroc ibial S1 2 Nml Nml Nml Nml Nml 0 Nml Nml ight Antibialis Dp Br eron L4 5 Inc Nml Nml 0 Nml Nml ight ExtHallLong Dp Br eron L5, S1 inc Nml 1+ Nml Nml 2+ dec Nml ight BicepsFemL Sciatic L5 S2 Nml Nml Nml Nml Nml 0 Nml Nml Left ostibiailis ibial L5, S1 Nml Nml Nml Nml Nml 0 Nml Nml Left Antibialis Dp Br eron L4 5 Nml Nml Nml Nml Nml 0 Nml Nml Left MedGastroc ibial S1 2 Nml Nml Nml Nml Nml 0 Nml Nml ight Ext Dig Long Dp Br eron L5 S1 Inc Nml 2+ Nml inc 0 dec Nml Left BicepsFemL Sciatic L5 S2 Nml Nml Nml Nml Nml 0 Nml Nml Left VastusMed Femoral L2 4 Nml Nml Nml Nml Nml 0 Nml Nml ight VastusMed Femoral L2 4 Nml Nml Nml Nml Nml 0 Nml Nml ight L3 arasp ami L3 Nml Nml Nml Nml Nml 0 Nml Nml ight L4 arasp ami L4 Nml Nml Nml Nml Nml 0 Nml Nml ight L5 arasp ami L5 Nml Nml Nml Nml Nml 0 Nml Nml ight S1 arasp ami S1 Nml Nml Nml Nml Nml 0 Nml Nml Left L3 arasp ami L3 Nml Nml Nml Nml Nml 0 Nml Nml Left L4 arasp ami L4 Nml Nml Nml Nml Nml 0 Nml Nml Left L5 arasp ami L5 Nml Nml Nml Nml Nml 0 Nml Nml Left S1 arasp ami S1 Nml Nml Nml Nml Nml 0 Nml Nml Site N eak Norm eak Amp Norm Amp Segment Name Delta Vel Norm Vel (m/s) (m/s) Left Sural (Lat Mall) 14 cm 4.47 < > cm Lat Mall 4.47 ight Sural (Lat Mall) 14 cm 3.31 < > cm Lat Mall 3.31 Left Sup eron (Ant Lat Mall) 14 cm 2.34 < > cm Ant Lat Mall 2.34 ight Sup eron (Ant Lat Mall) 14 cm 3.53 < > cm Ant Lat Mall 2.53 Lumbar adiculopathy (l5) Conus and roots Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment ight eroneuslong Sup Br eron L5 S1 Nml Nml Nml Nml Nml 0 Nml Nml ight ExtHallLong Dp Br eron L5, S1 Nml Nml Nml Nml Nml 0 Nml Nml Left eroneuslong Sup Br eron L5 S1 Incr Nml Nml 0 Nml Nml Left MedGastroc ibial S1 2 Nml Nml Nml Nml Nml 0 Nml Nml Left BicepsFemL Sciatic L5 S2 Nml Nml Nml Nml Nml 0 Nml Nml ight BicepsFemL Sciatic L5 S2 Nml Nml Nml Nml Nml 0 Nml Nml ight VastusMed Femoral L2 4 Nml Nml Nml Nml Nml 0 Nml Nml Left VastusMed Femoral L2 4 Nml Nml Nml Nml Nml 0 Nml Nml Left L3 arasp ami L3 Nml Nml Nml Nml Nml 0 Nml Nml Left L5 arasp ami L5 Incr Nml Nml 0 Nml Nml ight L3 arasp ami L3 Nml Nml Nml Nml Nml 0 Nml Nml ight L4 arasp ami L4 Nml Nml Nml Nml Nml 0 Nml Nml ight L5 arasp ami L5 Incr Nml 1+ Nml Nml 0 Nml Nml ight S1 arasp ami S1 Nml Nml Nml Nml Nml 0 Nml Nml Left L4 arasp ami L4 Nml Nml Nml Nml Nml 0 Nml Nml Left S1 arasp ami S1 Incr Nml 1+ Nml Nml 0 Nml Nml Left ostibiailis ibial L5, S1 Incr Nml >12ms 0 educed Nml Left Antibialis Dp Br eron L4 5 Incr Nml >12ms 0 educed Nml Left ExtHallLong Dp Br eron L5, S1 Incr Nml >12ms 1+ Nml Nml EMG c8 t1 radiculopathy 2011 study atient History: AIEN C/ LEF HAND WEAKNESS WIH MAKED AHY F HE MUSCULAUE INCLUDING HE AB, FDI, ADM. SHE HAS NUMBNESS IN HE DISIBUIN F HE HYHENA EMINENCE AND HE ING & LILE FINGES. E: UE EXEMIIES DIFFUSE D'S ASYMMEIES, AELLA 3+/ 4 BILA. ANKLES 4 BILA. os. plantar reflexes with sustained clonus bilat. Hoffmann s bilat. Fine finger hypermetria, GAI SASIC EMG/NCS Workshop 10

11 C8 t1 radiculopathy values Left ulnar motor 2011 Left Ulnar Motor B Elbow A Elbow C8/t1 radic 2012 study motor nerves Left ulnar motor 2012 Left Ulnar Motor Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name (mv) (mv) Delta Vel (m/s) Norm Vel (m/s) Left Median (Abd oll Brev) 3.83 < > Elbow >50.0 Elbow Left Ulnar (Abd Dig Min) 3.52 < > B Elbow >53.0 B Elbow A Elbow B Elbow >53.0 B Elbow A Elbow A Elbow Ulnar sensory c8/t1 radicu 2012 EMG c8/t1 radiculopathy 2011 Left Ulnar Anti Sensory Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Left Abd oll Median C8 1 Nml Nml Nml Nml >12ms 1+ educed Nml Brev Left ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml >12ms 1+ educed Nml Left 1stDorInt Ulnar C8 1 Nml Nml Nml Nml >12ms 1+ educed Nml ight Abd oll Brev Median C8 1 Nml Nml Nml Incr >12ms 0 educed Nml ight ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 1+ educed Nml ight 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 educed Nml ight ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 apid Nml Left ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 educed Nml Left Anconeus adial C7 8 Nml Nml Nml Incr Nml 1+ educed Nml Left riceps adial C6 7 8 Nml Nml Nml Nml >12ms 0 educed Nml ight Brachioad adial C5 6 Nml Nml Nml Nml Nml 1+ Nml Nml ight Anconeus adial C7 8 Incr 1+ Nml Incr >12ms 1+ educed Nml ight Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight riceps adial C6 7 8 Nml Nml Nml Nml >12ms 1+ educed Nml ight Deltoid Axillary C5 6 Nml Nml Nml Nml >12ms 0 Nml Nml Left Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 1+ educed Nml Left C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml Left C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml Left C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml Left C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml ight C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml ight C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml 20 2 ight C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml ight C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml EMG/NCS Workshop 11

12 C8/t1 radic 2012 study C8/t1 radic 2012 impression Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment Left Abd oll Brev Median C8 1 Incr Nml 1+ Nml >12ms 0 educed Nml Left 1stDorInt Ulnar C8 1 Incr 1+ Nml Nml Nml 0 educed Nml Left FlexolLong Median (Ant Int) C7 8 Incr Nml Nml 2+ educed Nml Left ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml Left Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight Abd oll Brev Median C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml ight Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml Left Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml Left Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml Left Deltoid Axillary C5 6 Incr Nml Nml 1+ Nml Nml ight Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml ight C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml ight C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml ight C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml ight 1 arasp ami 1 Nml Nml Nml Nml Nml 0 Nml Nml Left C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml Left C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml Left C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml Left C8 arasp ami C8 Incr Nml Nml 0 Nml Nml Left ABD DigMinimi Ulnar C8 1 Incr Nml >12ms 0 educed Nml Left Supraspinatus SupraScap C5 6 Incr Nml 1+ Nml >12ms 1+ Nml Nml Findings: NCV 1. UNIFMLY LW AMLIUDE LEF ULNA M SUDY INDICAIVE F AXNAL LSS A ALL SIMULAIN SIES. HIS SUDY IS UNCHANGED FM HE EVIUS NCV/EMG (09/15/2011). 2. NMAL ULNA SENSY SUDIES BILAEALLY. ALS UNCHANGED FM EVIUS SUDIES. 3. UNIFMLY LW AMLIUDE LEF MEDIAN M SUDY A HE XIMAL AND DISAL SIES. ALS UNCHANGED FM SUDY N (09/15/2011). 4. NMAL MEDIAN SENSY SUDIES BILAEALLY. 5. HEE IS N EVIDENCE F A MEDIAN ULNA ENAMEN NEUAHY F HE HE LEF IGH UE EXEMIY. HE NMAL SENSY SUDIES SEEN DAY AND N I SUDY(09/15/2011) SUGGES A EGANGLINIC LESIN (). HE SYMMEICAL AND DIFFUSE AMLIUDE CHANGES SEEN N BH SUDIES AE CNSISEN WIH DIFFUSE AXNAL LSS AND IN VIEW F HESE NMAL SENSY SUDIES, EXCLUDES A EIHEAL LESIN. EMG MILD MDEAELY SEVEE DENEVAIN WIH LNG SANDING AXNAL LSS IDENIFIED A HE LEF C8/1 SEGMENAL MYMAL LEVLES. IMESSIN: 1. FINDINGS CMAIBLE WIH CEVICAL SNDYLSIS AND MDEAELY SEVEE LEF C8/1 ADICULAHY WIH MYELAHY. 2. N EVIDENCE F A MEDIAN ULNA ENAMEN NEUAHY F HE UE EXEMIIES (see ncv #5). Myelopathy Findings: NCV 1. LW AMLIUDE SENSY SUDIES WIH SLWING F HE EAK LAENCIES BILAEALLY IN HE UE EXEMIIES. EMG DIFFUSE AXNAL LSS F HE UE EXEMIIES BILAEALLY AS NED IN HE ABVE ABLE. IMESSIN: 1. FINDINGS CMAIBLE WIH CEVICAL SNDYLSIS, DIFFUSE LNG SANDING AXNAL LSS SEEN BILAEALLY IN HE UE EXEMIIES, AND CEVICAL MYELAHY, LIKELY DUE CANAL SENSIS. 2. MILD MDEAE DISAL SYMMEICAL AND EDMINANLY SENSY EIHEAL LYNEUAHY. 3. FINDINGS INCLUDE BILAEAL S1 WEAKNESS (not addressed on this study) CNSISEN WIH LESINS. AN MI F HE L SINE MAY BE INDICAED A SME IN eroneal and tibial motor Motor Nerves Site N nset Norm nset Amp Norm Amp Neg Dur Segment Name Delta Vel Norm Vel (mv) (mv) (m/s) (m/s) ight eroneal (EDB) Ankle 8.13 < > B Fib Ankle >40.0 B Fib oplt B Fib >40.0 oplt ight ibial (AHB) Ankle 4.38 < > Knee Ankle >40.0 Knee Left ibial (AHB) Ankle 3.67 < > Knee Ankle >40.0 Knee Left eroneal (EDB) Ankle 6.02 < > B Fib Ankle >40.0 B Fib oplt B Fib >40.0 oplt EMG Worksheet esults Side Muscle Nerve oot Ins Act Fibs sw Amp Dur oly ecrt Int at Comment ight Abd oll Brev Median C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml ight ronatoreres Median C6 7 Nml Nml Nml Nml Nml 0 Nml Nml ight Brachioad adial C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Abd oll Brev Median C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left ABD DigMinimi Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left 1stDorInt Ulnar C8 1 Nml Nml Nml Nml Nml 0 Nml Nml Left ronatoreres Median C6 7 Incr Nml 1+ Nml >12ms 1+ educed Nml Left Brachioad adial C5 6 Incr Incr >12ms 1+ educed Nml Left Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml Left Biceps Musculocut C5 6 Incr Incr >12ms 0 educed Nml Left riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Anconeus adial C7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Biceps Musculocut C5 6 Nml Nml Nml Nml Nml 0 Nml Nml ight riceps adial C6 7 8 Nml Nml Nml Nml Nml 0 Nml Nml ight Deltoid Axillary C5 6 Nml Nml Nml Nml Nml 0 Nml Nml Left Deltoid Axillary C5 6 Incr Incr >12ms 1+ educed Nml Left C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml Left C6 arasp ami C6 Incr Nml Nml 0 Nml Nml Left C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml Left C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml Left 1 arasp ami 1 Nml Nml Nml Nml Nml 0 Nml Nml ight C5 arasp ami C5 Nml Nml Nml Nml Nml 0 Nml Nml ight C6 arasp ami C6 Nml Nml Nml Nml Nml 0 Nml Nml ight C7 arasp ami C7 Nml Nml Nml Nml Nml 0 Nml Nml ight C8 arasp ami C8 Nml Nml Nml Nml Nml 0 Nml Nml ight 1 arasp ami 1 Nml Nml Nml Nml Nml 0 Nml Nml Summary and Findings: NCV 1. ABSEN SENSY SUDIES BILAEALLY IN HE LWE EXEMIIES. 2. ABSEN/LW LAE ESNSES BILAEALLY IN HE LWE EXEMIIES. 3. LW AMLIUDE IBIAL & ENEAL CMUND M ACIN ENIALS A BH XIMAL AND DISAL SIMULAIN SIES. EMG a) MDEAELY SEVEE DENEVAIVE CHANGES IDENIFIED A HE LEF L5 SEGMENAL MYMAL LEVEL. Impression: 1. FINDINGS CNSISEN WIH LUMBA SNDYLSIS, MDEAELY SEVEE LEF SUBACUE L5 ADICULAHY. HWEVE, EVIDENCE F AXNAL LSS A HE L5 AND S1 LEVELS BILAEALLY SUGGES SSIBLE CANAL SENSIS. 2. MDEAELY SEVEE UNDELYING DISAL SYMMEICAL SENSIM EIHEAL LYNEUAHY (AXNAL). HESE FINDINGS AE LIKELY DUE HIS DIABEES EMG/NCS Workshop 12

13 Myopathy In myopathy, a disease of the muscle rather than the nerves, there is usually a great variation in the size of the muscle fibers. As a consequence the rate at which the individual muscle fibers conduct their signal varies considerably and the electrical signal picked up by the EMG needle is fragmented and reduced in size. he body tries to compensate for the weakness by firing the nerve signals faster and consequently the hallmark of myopathy is small, short, fast firing motor units Contraindication to NCV/EMG No real complications exist as a result of performing NCV/EMG. Many labs will say can not perform if.pacemakers, internal defibrillators or pt on Coumadin. A pacemaker is looking for a select pause or change in frequency structure of the overall electrophysiologic cycle of the heart. A stray current (as in the NCV) is unlikely to cause morphologic waveform characteristics that would cause the pace maker to erroneously discharge. Internal defibrillators record & require arrhythmias segments to be greater than 12 seconds of continuous abnormal discharge with select frequencies or asynchrony windows of non artifact cardiac electrophysiology, before discharge. he longest duration waveform we use is onetenth of a second. Again the overall malfunction rate of the defibrillator is higher than the statistical possibility of the NCV causing a discharge of the defibrillator. Further by chance the patient has an arrhythmia in office they have an internal defibrillator and statistically stand a better chance of survival than the occult sudden death patient that has no known history of cardiac arrhythmias that is in the office for NCV/EMG. eferences Electromyography in clinical practice A case study approach 1998, Mosby: Bashar Katirji, M.D. F.A.C.. Journal of Neurology, Neurosurgery & sychiatry; Nerve conduction studies: Essentials and itfalls in ractice 2005; 76:ii23 ii31: Arup Mallik, M.D.; A.I. Weir, M.D. Journal of Neurology, Neurosurgery & sychiatry; he Basics of Electromyography 2005,76:ii32 ii35: K.. Mills, hd Informationisfree.com; Gary ittman, M.D. EMG/NCS Workshop 13