JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Cortical activity after stimulation of the corticospinal tract in the spinal cord.

OBJECTIVE: Intraoperative electrical stimulation of the spinal cord evokes not only high amplitude cortical somatosensory evoked potentials (ScEPs: spinal cord-evoked potentials) recorded from the scalp but also early potentials. It has been postulated that the early potential recorded from the scalp could be generated by antidromic stimulation of the cortico-spinal tract (ACSP: Antidromic Corticospinal tract Potential or "anti D-wave"). In this study, we aimed to investigate the anti D-wave evoked by epidural stimulation in a population of neurologically uncompromised/compromised patients during spine and spinal cord surgery. To better define its origin, we examined its spatial distribution, response to stimulation modification and recording parameters, and finally, we correlated anti D-waves and corresponding epidural recorded D-waves after a transcranial electric stimulation at the same level of spinal cord stimulation.

METHODS: Tibial nerve somatosensory evoked potentials (SEPs), transcranially elicited muscle motor evoked potentials (m-MEPs), epidural motor evoked potentials (D-wave), and cortical spinal cord-evoked potentials (ScEPs) as well as Antidromic Cortico Spinal tract Potential (anti D-wave) were intraoperatively recorded in 30 subjects with different degrees of neurological involvement. ScEPs and anti D-wave were evoked by epidural stimulation of the spinal cord, both cranially and caudally to the surgery site and were recorded over the scalp at the midline. The effects of the stimulus rate and high pass filter were also tested.

RESULTS: The anti D-wave was recordable in all neurologically intact patients and was clearly isolated from the ScEPs by its very short latency; recordings of the anti D-wave were limited to the anterior midline, and its amplitude was only slightly reduced by increasing the stimulus rate or by changing the high pass filter, and its latency was slightly longer than that of the D-wave latency. In neurologically compromised patients, the anti D-wave and D-wave exhibit a similar behaviour, both of which were present in neurologically intact or moderately compromised patients and absent in patients with quadri/paraplegia. In a patient with paraplegia due to T8 meningioma and in neurologically intact patients in whom the cauda/conus stimulated the anti D-wave, cortical ScEPs were absent when the stimulation was performed caudally to the surgical site.

CONCLUSIONS: We provide evidence that the anti D-wave behaviour and its parameters have a close correlation with the behaviour of the D-wave; specifically, its distribution, response to filtering, stimulus rate, and absence in paraplegic patients.

SIGNIFICANCE: The presented data demonstrate that the anti D-wave is generated by the antidromic stimulation of fast neurons of the corticospinal tract, and consistent findings have been previously published in animals.

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