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  • Author or Editor: Johannes Schramm x
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Johannes Schramm, Rolf Krause, Taku Shigeno and Mario Brock

✓ Averaged somatosensory evoked potentials from the epidural space in response to sciatic nerve stimulation were recorded in bipolar and common reference mode in cats following various types of injury. An investigation was conducted on the development and properties of the spinal evoked response recorded from the center of the injury site, designated here as the “spinal cord evoked injury potential.” Typically it is a two-peak monophasic positive potential, approximately 40 msec in duration, with a slight negative afterwave. With increasing distance from the site of injury, its amplitude rapidly decreases, whereas latency remains constant. The common reference recording technique resulted in an earlier and better demonstration of the evoked injury potential, especially when it was transitory or incomplete. When impairment of conduction developed gradually, the evoked injury potential developed gradually too. In serial recordings along the spinal cord axis, the transition from a normal triphasic to a monophasic evoked injury potential allowed a precise localization of the lesion.

These data suggest that the diagnostic value of intraoperative spinal cord monitoring may be increased by adopting a technique that incorporates several epidural recordings with a common reference recording technique. The spinal cord evoked injury potential seems to be a more sensitive indicator of spinal cord injury than the cortical evoked potential. The findings are discussed in the light of the presently developing spinal cord monitoring techniques.

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Johannes Schramm, Taku Shigeno and Mario Brock

✓ Cortical and spinal evoked potentials were used to monitor the effect of experimental chronic cord compression in cats. An implantable compression screw made it possible to maintain the animals unrestrained. The mean compression period was 10 weeks (maximum 16.5 weeks). Compression was increased by stepwise tightening of the screw at intervals of 4 to 7 days under ketamine anesthesia. Evoked potentials were monitored before and after each compression step with repeated recordings, and were analyzed in terms of alterations in amplitude, latency, and waveform. Amplitude response curves were plotted where the amount of compression at each recording was expressed as a percentage of total compression. Changes in spinal evoked potentials occurred rather early (mean 36% of total compression), while obvious cortical evoked potential changes appeared rather late (mean 91% of total compression). Neurological alterations appeared later than alterations in spinal evoked response but prior to alterations in cortical evoked response. Thus, alterations in cortical somatosensory evoked potentials in the presence of chronic spinal compression indicate a severe degree of compression and do not seem to be of diagnostic value in the early detection of chronic spinal cord compression. It is suggested that the monitoring of spinal rather than cortical evoked responses would be more useful in locating and detecting chronic compression spinal cord damage.