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Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
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Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
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Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans

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Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans
Journal Article

Modulation of the N13 component of the somatosensory evoked potentials in an experimental model of central sensitization in humans

2021
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Overview
The N13 component of somatosensory evoked potential (N13 SEP) represents the segmental response of dorsal horn neurons. In this neurophysiological study, we aimed to verify whether N13 SEP might reflect excitability changes of dorsal horn neurons during central sensitization. In 22 healthy participants, we investigated how central sensitization induced by application of topical capsaicin to the ulnar nerve territory of the hand dorsum modulated N13 SEP elicited by ulnar nerve stimulation. Using a double-blind placebo-controlled crossover design, we also tested whether pregabalin, an analgesic drug with proven efficacy on the dorsal horn, influenced capsaicin-induced N13 SEP modulation. Topical application of capsaicin produced an area of secondary mechanical hyperalgesia, a sign of central sensitization, and increased the N13 SEP amplitude but not the peripheral N9 nor the cortical N20-P25 amplitude. This increase in N13 SEP amplitude paralleled the mechanical hyperalgesia and persisted for 120 min. Pregabalin prevented the N13 SEP modulation associated with capsaicin-induced central sensitization, whereas capsaicin application still increased N13 SEP amplitude in the placebo treatment session. Our neurophysiological study showed that capsaicin application specifically modulates N13 SEP and that this modulation is prevented by pregabalin, thus suggesting that N13 SEP may reflect changes in dorsal horn excitability and represent a useful biomarker of central sensitization in human studies.