By William S. Pease MD, Henry L. Lew MD, Ernest W. Johnson MD
Now in its Fourth version, this article offers physiatry and neurology citizens a finished, useful creation to electromyography. part I studies the anatomy and body structure of nerve difficulties on the subject of the making plans and function of electrodiagnostic tactics. part II presents technical info on electrophysiology, instrumentation, and particular concepts, with electronic images exhibiting vital floor anatomy. part III publications physicians via a variety of medical EMG difficulties, starting with the patient's indicators and continuing via electrodiagnostic review and analysis. This variation comprises over 500 new illustrations.
A bound-in CD-ROM comprises electronic videoclips of EMG recordings and try questions that may be submitted for CME credit.
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Extra info for Johnson's practical electromyography
Example text
Naϩ rapidly flows through the membrane, and this ion flux creates an electrical field that can be recorded with proper instrumentation. This is the all-or-none aspect of nerve action first described by Cajal. The free flow of Naϩ into the cell alters the membrane charge, creating a further positive change to ϩ35 mV, a total increase of ϩ105 mV. This large spike will be useful later as we review the propagation of the depolarization wave. If left to flow to equilibrium, the Nernst equation predicts an even higher membrane voltage, but two factors blunt this response.
It’s worth noting that pioneer electrodiagnostic investigators would easily recognize current studies despite a half-century of rapid advances in medical technology. While much is similar, our understanding is far deeper and new challenges are always at hand. This chapter reviews the clinical challenges and physiologic principals of adult and pediatric NCVs. Understanding nerve structure and function at the molecular level is essential to incorporating the growing knowledge base of genetic and molecular-level pathology into daily electrodiagnostic practice.
3-4 and 3-5). During this period, responses of the separated distal axon segment to an adequate stimulation will remain essentially normal. This makes it impossible to distinguish Figure 3-4 ● Axonotmetic lesion with axon changes demonstrated (A) immediately after injury and (B) 10 days after injury. The evoked responses obtained by stimulation proximal (left) and distal (right) to the lesion of the corresponding times (A1 and B1) are demonstrated at the bottom. In contrast to Figure 3-3B, the response is absent at 7 to 10 days.
