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HCN channels: novel therapeutic targets for peripheral neuropathic pain
  1. Paul Howard1,2
  1. 1Earl Mountbatten Hospice, Newport, UK
  2. 2Palliative Care Team, Isle of Wight NHS Trust, Newport, UK
  1. Correspondence to Dr Paul Howard; paul.howard1{at}nhs.net

Abstract

Hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels control neuronal firing thresholds. Together with sodium channels, they accumulate at sites of nerve injury, creating ectopic foci of action potential generation (EFAPG) that result in neuropathic pain.

Their presence may explain why EFAPG do not always respond to sodium channel blockers (eg, lacosamide). Further, several current analgesics (clonidine, dexmedetomidine, ketamine and systemic lidocaine) block HCN channels in addition to their better-known actions. Future research could explore the use of ivabradine (an HCN blocker) and multichannel blockade for refractory EFAPG and develop tools to distinguish EFAPG from secondary ‘upstream’ pain mechanisms (eg, central sensitisation).

  • Drug administration
  • Palliative Care
  • Pharmacology

Data availability statement

There are no data in this work.

https://doi.org/10.1136/spcare-2025-005509

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    Data availability statement

    There are no data in this work.

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    Footnotes

    • Contributors PH conceived and wrote the manuscript and serves as the guarantor.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests PH is an editor for the neuropharmacology sections of the Palliative Care Formulary; has contributed to updating the adjuvant analgesic, clonidine, oxcarbazepine, lacosamide and systemic lidocaine monographs and has delivered invited lectures on the palliative uses of antiepileptics, clonidine and sodium channel blockers.

    • Provenance and peer review Not commissioned; internally peer reviewed.