2018 AANS Annual Scientific Meeting-713. Compensation for Neuropathic Hyperexcitability in Peripheral Nerves Ultimately Fails

713. Compensation for Neuropathic Hyperexcitability in Peripheral Nerves Ultimately Fails

Video Transcription

Video Summary

In this video, presented by Hussain Shaquille, the topic of compensation for neuropathic hyperexcitability in peripheral nerves is discussed. Neuropathic pain is associated with over-responsiveness of pain processing neurons to innocuous or no stimulation. Studies have shown that changes in potassium and sodium ion channels in peripheral neurons can switch them from onset-only spiking to repetitive spiking, leading to neuropathic hyperexcitability. Compensation between potassium and sodium channels can offset changes in excitability, but ultimately fails to maintain stability and other measures of excitability. Computational simulations were used to study the effects of ion channel expression on excitability. The speaker speculates that reaching a critical point, such as high ATP use per spike, may lead to decompensation and the development of neuropathic pain. The possibility of neuromodulation pushing the system back to physiological spiking patterns is also mentioned.

Asset Caption

Husain Shakil (Canada)

Keywords

compensation

neuropathic hyperexcitability

peripheral nerves

potassium ion channels

sodium ion channels