Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section
Waveform analysis of spinal somatosensory evoked potential: paradoxically enhanced negative peaks immediately caudal to the site of conduction block
Introduction
In peripheral nerve entrapment syndromes, localization of the precise site of compression is best achieved by serial short incremental stimulation searching for focal conduction abnormalities (Kimura, 1979). Similarly, in compression myelopathies, the vertebral level responsible for the symptoms can be disclosed by recording the ascending axonal volley at multiple sites along the spinal cord (Kimura and Kaji, 1991; Waxman et al., 1995). For this purpose, pickup electrodes must be placed in the structures adjacent to the spinal cord itself. In this case, an abrupt reduction in size of the negative wave over a short segment is the strong evidence of a conduction block (McDonald and Sears, 1970; Cornblath et al., 1991). In practice, the change is often rendered steeper, and thereby more easily recognized by the presence of an enhanced negative wave in the lead immediately caudal to the lesion. Were it not for an enlargement of this kind, it might be more difficult to distinguish conduction block from physiologic temporal dispersion in mild cases. Despite its clinical advantage, little attention has been given to the mechanisms underlying this enhancement except in a work using bipolar epidural leads (Ohmi et al., 1991). We have therefore conducted waveform analysis to elucidate the phenomenon based on our data of spinal somatosensory evoked potentials (SSEPs) recorded during posterior operations for compression myelopathies.
Section snippets
Patients
From July 1991 to July 1996, 33 patients with compression myelopathies underwent intraoperative SSEP studies. Informed consent was obtained. We analyzed the recordings in 26 patients selected on the basis of an unequivocal focal conduction block with reduction in amplitude of the negative peak to 50% or less compared to the immediately caudal level. Myelopathy resulted from cervical spondylosis (16), ossified posterior longitudinal ligament (OPLL) (7), rheumatoid arthritis of the cervical spine
Results
Incremental studies uncovered a single site of focal conduction block designated as 0 in all patients, one each at Cl/2 and C2/3, 10 each at C3/4 and C4/5, 3 at C5/6 and one at T3/4. At this level, the amplitude of the negative component was reduced (P<0.0001) to 32±22% (mean±SD) and the area to 31±22% compared to the −4 level, which was taken as the baseline (Table 1). In contrast, the initial positivity was increased (P<0.0001) to 170±78% in amplitude and 296±201% in area (Table 2). In
Discussion
The present study was designed to document an apparent enhancement of the SSEPs recorded at the sites preceding a conduction block in chronic compression myelopathies. This is apparently paradoxical because, had it not been for the conduction block at the 0 level, the negative components would have been progressively smaller in size from −4 to −1, as predicted from physiological temporal dispersion with phase cancellation (Kimura et al., 1988). An enlargement of this kind cannot simply be
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Cited by (16)
Descending spinal cord evoked potentials in cervical spondylotic myelopathy: Characteristic waveform changes seen at the lesion site
2014, Clinical NeurophysiologyCitation Excerpt :Electrophysiologic techniques used to localize the site of the spinal cord lesion have made steady progress since earlier studies conducted under the term “electrospinogram” in animal models (Morrison et al., 1975; Rossini et al., 1980) and humans (Shimoji et al., 1971). As previously reported in cervical spondylotic myelopathy (CSM) (Tani et al., 1998, 1999, 2002), multisegmental recording of ascending spinal cord evoked potentials (A-SCEPs) can precisely localize the site of conduction abnormalities before decompression procedures. This method utilizes monopolar recording electrodes placed in the structures adjacent to the spinal cord and bipolar stimulating electrodes inserted in the lumbar epidural space.
Effects of experimental focal compression on excitability of human median motor axons
2009, Clinical NeurophysiologyCitation Excerpt :Metabolic products of ischemia may interfere with the recovery of Na+ channels from inactivation, inducing a rapidly reversible conduction block seen in our previous experiments (Tani et al., 2001; Tsuboya et al., 2007). All these findings considered together imply that the sharply-localized conduction abnormalities demonstrated electrophysiologically in peripheral nerve entrapment syndromes (Kimura, 1979, 2001) and compression myelopathies (Tani et al., 1998, 1999, 2002, 2006) may, in part, result from focal nerve ischemia (Kiernan et al., 1999). We conclude that compressing the nerve by a small probe causes focal ischemia, which in turn induces a very localized, reversible axonal depolarization directly under the compression followed by hyperpolarization upon release of compression.
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