- High-frequency spinal cord stimulation at the cervicomedullary junction can address intractable facial pain.1
- This extends neuromodulation approaches to craniofacial pain at the brainstem level.1 1
Weekly enrichment (2026-07-20)
- A 2026 Frontiers in Neuroscience case report documents 6-year follow-up of 10 kHz high-frequency spinal cord stimulation (HFSCS) at the cervicomedullary junction (CMJ) in a 67-year-old woman with refractory right-sided trigeminal neuropathic pain following petroclival meningioma surgery (removed in 2006).2
- Prior therapies had all failed, including carbamazepine/gabapentin, tooth extractions, thermorhizotomy, intrathecal morphine then ziconotide, radiosurgery, and a 2013 cervical tonic SCS (Medtronic Model 37702 at C2–C4, 300 μs pulse width, 40–60 Hz) that was discontinued due to bothersome paresthesia and no relief.2
- The definitive HFSCS system was implanted in December 2018: an 8-contact epidural lead (Nevro Senza, Nevro Corp., Redwood City, CA) at the C1–C2 level under fluoroscopy, connected to a rechargeable pulse generator in the right abdomen.2
- Stimulation parameters were 10 kHz, 30 μs pulse width, amplitude 1.2–1.8 mA (mean ~1.5 mA), subperception/bipolar — complete relief of paroxysmal electric-shock pain was achieved within 15 days, restoring chewing and oral hygiene.2
- Neuromodulatory effect was objectively confirmed by nociceptive blink reflex testing (supraorbital V1 stimulation at 1.2× pain threshold, ~8–12 mA, 0.2 ms, 0.2–0.3 Hz, 20 stimuli): HFSCS activation reduced R2 amplitude by 27% (from ~320 μV to ~235 μV) and partially restored habituation (~45%), while the non-nociceptive blink reflex stayed intact.2
- Complete pain relief (Numerical Rating Scale = 0) was maintained at 3-month, 2-year, and 4-year follow-ups with SF-36, HADS, and BDI-II gains; a residual dull background pain was managed adjunctively with pregabalin.2
- At the 6-year mark pain recurred to NRS = 10 due to complete IPG battery depletion from irregular charging; recharging restored immediate complete relief without changing pregabalin, and sustained relief was confirmed at the June 2024 visit with no lead migration, infection, or hardware failure.2
- The tight temporal coupling between stimulation status and pain provides causal evidence that continuous HFSCS — not pregabalin — drives the analgesia, targeting the spinal trigeminal nucleus caudalis at the brainstem level.2
- The original 2020 index case (Floridia et al., Medicine 99:e22304) was the first report of HFSCS at the CMJ for trigeminal neuropathy unresponsive to tonic SCS and conventional management, showing reshaped trigeminal-facial reflex responses consistent with brainstem-level inhibition of nociceptive input.3
- Authors caution the evidence is a single case and call for larger prospective and randomized studies of CMJ-targeted HFSCS for refractory craniofacial pain.2
Footnotes
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https://www.sciencedirect.com/science/article/pii/S1935861X26000433?dgcid=rss_sd_all ↩ ↩2 ↩3
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https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2026.1665633/full ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9
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https://journals.lww.com/md-journal/fulltext/2020/10020/effectiveness_of_high_frequency_cervical_spinal.27.aspx ↩