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Title: The role of spike synchrony in tactile perception revealed by kilohertz-frequency spinal cord stimulation

Abstract:Spinal cord stimulation (SCS) is an effective treatment for chronic pain, including phantom limb pain. Conventional SCS (40-60 Hz) reduces pain by engaging inhibitory mechanisms in the spinal dorsal horn via activation of A-beta axons in the dorsal columns. But activating those axons also produces a buzzing sensation, or paresthesia, that can limit the intensity (“dose”) of SCS and its analgesic efficacy. Recently developed kilohertz-frequency SCS (kfSCS) produces paresthesia-free analgesia. The absence of paresthesia has been inferred to mean that A-beta axons are not activated, raising questions about how analgesia is produced. Based on electrophysiological studies in rats, we found that A-beta axons are activated by kfSCS but that action potentials (spikes) are not synchronized across axons, unlike conventional SCS, which evokes synchronous spiking. Our experimental data and computational modeling demonstrate that when electrical pulses are delivered at intervals shorter than an axon’s refractory period, spikes occur intermittently, in response to only a subset of stimulus pulses; because different axons respond to different pulses, spikes become desynchronized. We speculate that asynchronous spiking in A-beta axons is sufficient to activate inhibitory neurons mediating analgesia whereas synchronous spiking is necessary to activate projection neurons mediating paresthesia. Consistent with this model, cortical recordings show that brain oscillations are altered by conventional SCS but not by kfSCS, though somatosensory evoked potentials are equally attenuated by both forms of SCS. These results have important implications for understanding the neural basis for paresthesia but also have practical implications for choosing SCS parameters to optimize clinical outcomes.

Biography: Dr. Prescott studies how somatosensory information is normally encoded and how disruption of that coding leads to neuropathic pain. His lab combines computational simulations with experimental techniques including in vitro and in vivo electrophysiology, calcium imaging, and optogenetics. Lines of research include how biophysical properties impact neuron coding properties and, in turn, how neuron properties impact network-level phenomena like synchrony. His lab applies information about these fundamental issues to uncover how different forms of spinal cord stimulation (SCS) act to reduce pain, and why some forms of SCS cause paresthesia whereas others do not.

Full video can be watched on our Vimeo... :

00:00:00 Introduction
00:02:08 Thermal illusions
00:03:26 Gate control theory
00:04:28 Gate control theory and spinal cord stimulation (SCS)
00:05:43 Spinal cord stimulation paradigms
00:07:37 Spinal cord stimulation in rats
00:09:10 SCS-mediated modulation
00:10:26 SCS-induced cortical activity
00:11:24 Both types of SCS activate dorsal column axons
00:13:18 Non-electrophysiological evidence for activation of dorsal column axons
00:15:40 Difference between 50 Hz SCS and 1 kHz SCS
00:18:14 Spike patterns can be reproduced in a simple model
00:19:36 Impact of differentially synchronized inputs on postsynaptic neurons
00:24:54 Perception as Bayesian Interface
00:27:05 Impact of expectations on perception
00:29:42 Questions