Beneficial effect of infiltration around the greater occipital nerve in cluster headache independent of modulation of the nociceptive blink reflex

Abstract

Objectives and Background: We aimed to explore the effect of greater occipital nerve (GON) infiltration on trigeminal transmission and its relation to clinical response. Infiltration of the GON with a local anesthetic and corticosteroids is effective in the treatment of both episodic (ECH) and chronic cluster headache (CCH). This effect is hypothesized to be due to delayed trigeminal transmission, resulting in a prolonged blink reflex with increased R2 latencies.MethodsIn this single-center, prospective cohort study, participants with either ECH or CCH were followed 12 weeks post-GON infiltration with daily e-diary monitoring and nociceptive blink reflex measurements at four timepoints: 30 min before infiltration; and 30 min, 1, and 4 weeks post-infiltration. The primary outcome was the R2 latency. Secondary outcomes were attack frequency and intensity. Data were collected between October 2020 and March 2023. Results: A total of 33 participants were included in the primary analysis. No increased R2 latencies after GON infiltration were observed. When compared to baseline, daily attack frequency was significantly reduced during Week 1 (ECH: Delta -2.17, 95% confidence interval [CI] -3.43 to -0.64; CCH: Delta -1.36, 95% CI -1.93 to -0.71) and Week 4 (ECH: Delta -2.90, 95% CI -3.86 to -1.36; CCH: Delta -1.57, 95% CI -2.43 to -0.57), as was the attack intensity in Week 1 (ECH Delta -2.1, 95% CI -3.4 to -0.9; CCH: Delta -1.5, 95% CI -2.3 to -0.7) and Week 4 (ECH Delta -3.6, 95% CI -6.4 to -0.8; CCH: Delta -1.7, 95% CI -2.6 to -0.7) after GON infiltration compared to baseline. In all, 76% (25/33) of participants experienced a >= 30% reduction of their CH attacks and 27% (9/33) were attack free in Week 4. Unexpectedly, the R2 latency slightly decreased, but only in a solitary measurement ipsilateral to the infiltration side 4 weeks post-infiltration. No correlation between R2 latencies and clinical response were observed. Conclusion: The observed neurophysiological alterations were minor and were not associated with any clinical outcome. Therefore, despite rigorous analysis of multiple neurophysiological parameters in a relatively large patient sample, we did not find any evidence that the clinical response of GON infiltration is caused by reduced-or modulated-transmission of the trigeminal nerve or the trigeminal cervical complex. Although effective, the mechanism of the GON infiltration thus remains enigmatic.