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There are some circumstances in which timing considerations are crucial In general, it is estimated that complete Wallerian degeneration requires 3 5 days to produce a noticeable decline in CMAP amplitudes, with the nadir occurring between days 7 and 9 In sensory nerves, there is a slight lag with amplitude loss becoming apparent between the 5th and 7th days, with the SNAP amplitude reaching its lowest point by the 10th or 11th day4 For this reason, an interval of 10 days to 2 weeks between injury and the performance of NCS is ideal in most instances There is a risk of false interpretation if NCS are preformed prematurely Normally, identi cation of a normal CMAP amplitude distal to a lesion and reduced amplitude above the lesion would imply the existence of a demyelinating conduction block If motor conductions are performed hyperacutely, an axon loss lesion may be falsely interpreted as demyelinating conduction block
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Historically, it was recommended that every laboratory establish their own normative data Improvements and standardization of commercially manufactured equip-
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APPROACH TO PATIENTS WITH NEUROMUSCULAR DISEASE
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Fibrillation potentials and positive waves, the most sensitive indicator of recent axon loss on EMG, may develop within days in muscles that are in close anatomic proximity to the injured nerve Three weeks may be required to develop a full density and distribution within all muscles at risk As many patients may be reluctant to undergo multiple examinations, the EDX should be postponed for 3 weeks after disease onset in most circumstances There are at least two circumstances in which it may be preferable to perform EDX earlier than the normal 3week recommendation One of these occurs when there is the suspicion or knowledge of a preexisting nerve injury It may be important for either legal or medical reasons to distinguish between new and old Performing two examinations, one as early as possible and then a second examination a month or more later, would be best suited to address this issue A second scenario would be a suspected Guillain Barr syndrome (GBS) e where rapid EDX support for the diagnosis is desired As in other neuromuscular disorders, it may require days or weeks for the EDX abnormalities characteristic of GBS to fully develop Nonetheless, the rapid evolution of NCS abnormalities, even if not diagnostic, in the absence of ndings characteristic of other potential causes of acute generalized weakness, can be reassuring to the clinician and guide management decisions in the critical rst week of the illness
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The routine EMG/NCS examination traditionally consists of motor NCS, sensory NCS, and the needle electromyographic examination F waves and H re exes are also commonly tested although in most cases provide complementary rather than novel information As mentioned previously, the nerves and muscles tested are selected on a case-by-case basis Initial selection is based on the diagnostic question posed and the clinical information available and is further modi ed as the test unfolds It is appropriate to emphasize that techniques used to detect disorders of neuromuscular transmission (DNMT) such as repetitive motor nerve stimulation (RNS) testing and single ber EMG (SFEMG) are not part of the routine evaluation in most laboratories Once again, the importance of clinical surveillance in test construction is emphasized
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NERVE CONDUCTION STUDIES Motor Nerve Conductions
Motor nerve conductions are performed by applying an active surface recording electrode overlying the midpor-
tion of a muscle belly This position is chosen to be in proximity to the motor point, ie, the con uence of neuromuscular junctions In addition, a reference electrode is used in proximity to but not on the muscle belly The response sought for, referred to as a compound muscle action potential (CMAP), is obtained by stimulating the nerve in question while recording from a muscle that it innervates To elicit the desired response, the intensity of the electrical stimuli applied to the nerve is increased until all involved axons and muscle bers are activated and the maximal CMAP response is obtained This is commonly referred to as the supramaximal stimulus and is the desired effect in all routine NCS Each nerve tested may be stimulated at one or more locations, limited primarily by anatomical considerations and patient tolerance Readily testable motor nerves are the median, ulnar, radial, accessory, facial, tibial, and common peroneal The phrenic, femoral, axillary, and musculocutaneous can be tested, although in each case technical issues may make reliable and reproducible information more dif cult to obtain The CMAP waveform that is obtained represents all of the individual single muscle ber action potentials (SFMAPs) within that muscle activated by the nerve stimulus Because different nerve bers within a nerve have different conduction velocities, the waveform is dome-like rather than spiked in its con guration The proximal or left-hand side of the waveform represents the action potentials of the bers innervated by the fastest conducting axons The trailing aspect of the dome represents the action potentials of the muscle bers innervated by the slowest conducting motor axons (Fig 2 1) As stimuli are delivered at increasing distances from the target muscle, the distance between the initial and terminal aspects of the CMAP waveform widens This results in an increasing duration of the CMAP waveform without a reduction in the area under the curve, as the number of activated nerve and muscle bers remain the same This is the basis of the normal physiological waveform dispersion described below Typically, three parameters are measured and one is more subjectively assessed The baseline to peak amplitude and the area under the curve of the CMAP waveform not only are re ections of the number of viable muscle bers but are indirectly a measure of the number of viable and excitable axons that innervate them Therefore, the CMAP amplitude provides an estimate of the number of functioning axons, neuromuscular junctions, and ultimately muscle bers In some instances, as will be subsequently described, the CMAP amplitude may be adversely affected by diseases that only affect the integrity of the myelin sheath The other two parameters measured are distal latency (time between stimulus delivery and initial activation of muscle) and conduction velocity These are
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