Abstract
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.
Highlights
The N13 component of somatosensory evoked potential (N13 SEP) represents the segmental response of dorsal horn neurons
Capsaicin application to the ulnar nerve territory of the right-hand dorsum induced an area of primary hyperalgesia with flare, with a surrounding area of secondary hyperalgesia (10.6 ± 14.5 cm2) characterised by increased sensitivity to mechanical pinprick stimulation relative to the baseline assessment
Post hoc analysis showed a significant increase of the N13 SEP amplitude after treatment on the capsaicin-treated side (p < 0.005; Cohen’s d effect size 1.8)
Summary
The N13 component of somatosensory evoked potential (N13 SEP) represents the segmental response of dorsal horn neurons. Our neurophysiological study showed that capsaicin application modulates N13 SEP and that this modulation is prevented by pregabalin, suggesting that N13 SEP may reflect changes in dorsal horn excitability and represent a useful biomarker of central sensitization in human studies. Capsaicin and other experimental pain models are commonly used to investigate the mechanisms underlying central sensitization and its association with chronic pain[12], how to reliably quantify central sensitization within the dorsal horn of the human spinal cord is still an issue of controversy. The N13 component of somatosensory evoked potentials (N13 SEP) recorded in anterior–posterior direction from the lower neck (Cv6) after upper limb stimulation is mediated by non-nociceptive Aβ fibres This component, generated at the cervical dorsal h orn[16], probably reflects the segmental postsynaptic response of dorsal horn neurons in the lower cervical grey matter[17], presumably neurons in laminae IV–V18,19. We tested whether pregabalin, a first-line treatment for neuropathic pain[20] targeting voltage-gated calcium channels expressed in the dorsal horn and the brain[21], is able to modulate capsaicin-induced N13 SEP sensitization
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