Galcanezumab modulates Capsaicin-induced C-fiber reactivity

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Galcanezumab modulates Capsaicin-induced C-fiber reactivity. / Basedau, Hauke; Oppermann, Thalea; Gundelwein Silva, Elisa; Peng, Kuan-Po; May, Arne.

In: CEPHALALGIA, Vol. 42, No. 13, 11.2022, p. 1331-1338.

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@article{9f8d8760bb824d5ea261b50dae09178d,
title = "Galcanezumab modulates Capsaicin-induced C-fiber reactivity",
abstract = "BACKGROUND: The vasodilatory calcitonin-gene related peptide (CGRP) is understood as pivotal mediator in migraine pathophysiology. Blocking CGRP with small molecules or monoclonal antibodies (CGRP-mAb) reduces migraine frequency. However, prescription of CGRP-mAbs is still regulated and possible predictive measures of therapeutic success would be useful.METHODS: Using standardized capsaicin-induced dermal blood flow model, 29 migraine patients underwent a laser speckle imaging measurement before and after administration of galcanezumab. At both sessions dermal blood flow before and after capsaicin stimulation as well as flare size were analyzed over all three trigeminal branches and the volar forearm for extracranial control. Long-term measures were repeated in 14 patients after continuous treatment ranging from 6 to 12 months.RESULTS: Resting dermal blood flow remained unchanged after administration of galcanezumab. Capsaicin-induced dermal blood flow decreased significantly after CGRP-mAb in all tested areas compared to baseline and this was consistent even after 12 months of treatment. However, following galcanezumab administration, the flare size decreased only in the three trigeminal dermatomes, not the arm and was therefore specific for the trigemino-vascular system. None of these two markers distinguished between responders and non-responders.CONCLUSION: CGRP-mAb changed blood flow response to capsaicin stimulation profoundly and this effect did not change over a 12-month application. Neither capsaicin-induced flare nor dermal blood flow can be used as a predictor for treatment efficacy. These data suggest that the mechanism of headache development in migraine is not entirely CGRP-mediated.",
author = "Hauke Basedau and Thalea Oppermann and {Gundelwein Silva}, Elisa and Kuan-Po Peng and Arne May",
year = "2022",
month = nov,
doi = "10.1177/03331024221112906",
language = "English",
volume = "42",
pages = "1331--1338",
journal = "CEPHALALGIA",
issn = "0333-1024",
publisher = "SAGE Publications",
number = "13",

}

RIS

TY - JOUR

T1 - Galcanezumab modulates Capsaicin-induced C-fiber reactivity

AU - Basedau, Hauke

AU - Oppermann, Thalea

AU - Gundelwein Silva, Elisa

AU - Peng, Kuan-Po

AU - May, Arne

PY - 2022/11

Y1 - 2022/11

N2 - BACKGROUND: The vasodilatory calcitonin-gene related peptide (CGRP) is understood as pivotal mediator in migraine pathophysiology. Blocking CGRP with small molecules or monoclonal antibodies (CGRP-mAb) reduces migraine frequency. However, prescription of CGRP-mAbs is still regulated and possible predictive measures of therapeutic success would be useful.METHODS: Using standardized capsaicin-induced dermal blood flow model, 29 migraine patients underwent a laser speckle imaging measurement before and after administration of galcanezumab. At both sessions dermal blood flow before and after capsaicin stimulation as well as flare size were analyzed over all three trigeminal branches and the volar forearm for extracranial control. Long-term measures were repeated in 14 patients after continuous treatment ranging from 6 to 12 months.RESULTS: Resting dermal blood flow remained unchanged after administration of galcanezumab. Capsaicin-induced dermal blood flow decreased significantly after CGRP-mAb in all tested areas compared to baseline and this was consistent even after 12 months of treatment. However, following galcanezumab administration, the flare size decreased only in the three trigeminal dermatomes, not the arm and was therefore specific for the trigemino-vascular system. None of these two markers distinguished between responders and non-responders.CONCLUSION: CGRP-mAb changed blood flow response to capsaicin stimulation profoundly and this effect did not change over a 12-month application. Neither capsaicin-induced flare nor dermal blood flow can be used as a predictor for treatment efficacy. These data suggest that the mechanism of headache development in migraine is not entirely CGRP-mediated.

AB - BACKGROUND: The vasodilatory calcitonin-gene related peptide (CGRP) is understood as pivotal mediator in migraine pathophysiology. Blocking CGRP with small molecules or monoclonal antibodies (CGRP-mAb) reduces migraine frequency. However, prescription of CGRP-mAbs is still regulated and possible predictive measures of therapeutic success would be useful.METHODS: Using standardized capsaicin-induced dermal blood flow model, 29 migraine patients underwent a laser speckle imaging measurement before and after administration of galcanezumab. At both sessions dermal blood flow before and after capsaicin stimulation as well as flare size were analyzed over all three trigeminal branches and the volar forearm for extracranial control. Long-term measures were repeated in 14 patients after continuous treatment ranging from 6 to 12 months.RESULTS: Resting dermal blood flow remained unchanged after administration of galcanezumab. Capsaicin-induced dermal blood flow decreased significantly after CGRP-mAb in all tested areas compared to baseline and this was consistent even after 12 months of treatment. However, following galcanezumab administration, the flare size decreased only in the three trigeminal dermatomes, not the arm and was therefore specific for the trigemino-vascular system. None of these two markers distinguished between responders and non-responders.CONCLUSION: CGRP-mAb changed blood flow response to capsaicin stimulation profoundly and this effect did not change over a 12-month application. Neither capsaicin-induced flare nor dermal blood flow can be used as a predictor for treatment efficacy. These data suggest that the mechanism of headache development in migraine is not entirely CGRP-mediated.

U2 - 10.1177/03331024221112906

DO - 10.1177/03331024221112906

M3 - SCORING: Journal article

C2 - 35796521

VL - 42

SP - 1331

EP - 1338

JO - CEPHALALGIA

JF - CEPHALALGIA

SN - 0333-1024

IS - 13

ER -