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5 ms and rarely exceeding 300 mV in amplitude When brief spontaneous brillation potentials of this sort are observed ring regularly at two or three different locations (outside the end-plate zone) of a resting muscle, one may conclude that the bers are denervated Usually, brillation potentials discharge at an almost regular rate In some early lesions (less than 6 to 8 weeks), irregularly ring brillation potentials may be observed Diseases such as poliomyelitis, which damage spinal motor neurons, or injuries of peripheral nerves or anterior spinal roots frequently produce only partial denervation of the involved muscles In such muscles, one electrode placement may record brillation potentials at rest from denervated bers and normal potentials during voluntary contraction from nearby healthy bers Fibrillation potentials continue until the muscle ber is reinnervated by progressive proximal-distal regeneration of the interrupted nerve ber or by the outgrowth of new axons from nearby healthy nerve bers (collateral sprouting), or until the atrophied bers degenerate and are replaced by connective tissue, a process that may take many years In addition, brillation potentials may take the form of positive sharp waves, ie, spontaneous, initially positive diphasic potentials of longer duration and slightly greater amplitude than the spikes of brillation potentials (see Fig 45-7A) Fibrillation potentials, while characteristic of neurogenic denervation, are not altogether speci c; for example, they are seen in muscle diseases such as polymyositis and inclusion body myositis, which presumably damage the neural innervation to small regions of muscle or isolate segments of a muscle ber from its end plate Fasciculation Potentials As stated earlier, a fasciculation is the spontaneous or involuntary contraction of a motor unit or part of a motor unit Such contractions may cause a visible dimpling or twitching under the skin, though ordinarily they are of insuf cient force to move a joint Large distal fasciculations, however, can brie y displace a nger or toe; they occur irregularly and infrequently, and prolonged inspection of the skin overlying a muscle may be necessary to detect them The accompanying electrical form of an individual fasciculation potential is relatively constant Typically, a fasciculation potential will have three to ve phases (ie, they are polyphasic as described later, in contrast to normal biphasic muscle activity), a duration of 5 to 15 ms (longer than normal but somewhat less in the facial muscles), and an amplitude of several millivolts (see Fig 45-7B) Fasciculation potentials are evidence of motor nerve ber irritability, most often the result of reinnervation following nerve or motor neuron damage Thus, the combination of brillations and fasciculations indicates active denervation combined with more chronic reinnervation of muscle; ie, a long-standing but still ongoing process The precise source of fasciculation is still contested Forster and colleagues, in the 1940s, challenged the original belief that the discharge originated in anterior horn cells by demonstrating that fasciculations persisted after nerve block in ALS and ceased only with the appearance of brillation potentials, signifying wallerian (axonal) degeneration These observations favored a distal site of generation Other physiologic and pharmacologic evidence pointed to the rst segment of the motor axon, or to the distal axon, or even to the motor point (the site of insertion of the nerve into muscle), involving elements of the postsynaptic muscle membrane (particularly in the case of benign fasciculations) as the source of the spontaneous electrical activity It seems that several regions of the axon are capable of spontaneous impulse generation, depending on the underlying disease Most of the diseases that produce fasciculations involve the anterior horn cell or the motor root, but more. asp.net pdf 417 ASP . NET PDF-417 Barcode Generator - Generate 2D PDF417 in ...
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