4.6 Article

Parallel spinal pathways generate the middle-latency N1 and the late P2 components of the laser evoked potentials

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CLINICAL NEUROPHYSIOLOGY
卷 118, 期 5, 页码 1097-1104

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ELSEVIER IRELAND LTD
DOI: 10.1016/j.clinph.2007.01.015

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laser evoked potentials; nociception; medial pain system; lateral pain system; spinal cord; parallel pathways

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Objective: To investigate the possible presence of multiple spino-thalamic pathways with different conduction velocities (CVs) in the human spinal cord. Methods: Laser evoked potentials (LEPs) were recorded in 10 healthy subjects after stimulation of the dorsal midline at four vertebral level: C5, T2, T6, and T10. This method allowed us to minimize the influence of the conduction in the peripheral fibers and to calculate the spinal CV in two different ways: (1) the reciprocal of the slope of the regression line was obtained from the latencies of the different LEP components, and (2) the distance between C5 and T10 was divided by the latency difference of the responses at the two sites. In particular, we considered the middle-latency NI potential (latencies of around 135, 150, 157, and 171 ms after stimulation at C5, T2, T6, and T10 levels, respectively), which is generated in the second somatosensory (SII) area, and the late P2 response (latencies of around 336, 344, 346, and 362 ms after stimulation at C5, T2, T6, and T10 levels, respectively), which is generated in the anterior cingulate cortex (ACC). Results: The calculated CV of the spinal fibers generating the N1 potential (around 9 m/s) was significantly different (P < 0.05) from the one of the pathway producing the P2 response (around 13 m/s). Conclusions: Our results suggest that the N1 and the P2 LEP components are generated by two parallel spinal pathways. Significance: Both the N1 and P2 potentials should be recorded in the clinical routine since a dissociated abnormality of either response may be found in lesions of the nociceptive system not only in the brain, but also at spinal cord level. (c) 2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

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