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AAEM minimonograph 19: Somatosensory evoked potentials
Author(s) -
Aminoff Michael J.,
Eisen Andrew A.
Publication year - 1998
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199803)21:3<277::aid-mus1>3.0.co;2-7
Subject(s) - library science , citation , clinical neurology , gerontology , medicine , history , psychology , computer science , neuroscience
More than 40 years have elapsed since the first somatosensory evoked potential (SEP) was recorded from humans, and 15 years have passed since the clinical role of SEPs was reviewed as an American Association of Electrodiagnostic Medicine (AAEM) minimonograph. At that time, interest in SEPs was reaching its zenith, and a vast literature had already accumulated. The subsequent development of sophisticated imaging techniques has impacted on the role of SEPs in the clinical setting, making it timely to review this aspect as the end of the century is approached. This minimonograph considers current concepts of the physiologic basis of the SEP, discusses the different techniques available to elicit and record it, and critically analyzes its clinical utility. The peripheral electrical stimulus routinely used to elicit an SEP activates predominantly—if not entirely—the large-diameter, fast-conducting group Ia muscle and group II cutaneous afferent fibers. Selective intrafascicular stimulation has provided evidence for a direct muscle afferent fiber (Ia) projection to the human somatosensory cortex. However, when a mixed nerve is stimulated, both group Ia muscle afferents and cutaneous group II afferents contribute to the resulting SEP. Its amplitude is almost maximal when the peripheral nerve action potential is only 50% of its maximum. This translates into a requisite stimulus intensity of about twice sensory threshold. It is also possible to elicit SEPs using a variety of mechanical stimuli. This allows selective activation of specific sensory modalities, but the SEPs elicited are often of small amplitude and may require many hundreds of responses to be averaged. This limits the clinical utility of mechanically elicited SEPs. The SEP is greatly attenuated or abolished when the dorsal columns are selectively ablated in animals, indicating that within the spinal cord the SEP is mediated predominantly via these tracts. Conversely, cord lesions that do not interrupt the dorsal columns are associated with a relatively normal SEP. Loss of posterior column function in humans is almost invariably accompanied by a grossly abnormal SEP. Some SEP components may, however, reflect extralemniscal activity; they have been evoked in cats after selective dorsal column transection by stimuli that are sufficient to excite small-diameter peripheral fibers, and tourniquet-induced ischemia in humans abolishes short-latency before long-latency SEP components, suggesting that they are mediated by different centrally conducting tracts. Although in general the SEP is best recorded over the somatosensory cortex, topographic mapping indicates that several of its components are widely distributed over the scalp, and some are maximally recorded outside the somatosensory cortex. Because the SEP monitors more than just the somatosensory pathways, abnormalities recorded in certain primary diseases of the motor system (such as amyotrophic lateral sclerosis) should not cause concern. *Correspondence to: American Association of Electrodiagnostic Medicine, 421 First Avenue S.W., Suite 300 East, Rochester, MN 55902, USA