TY - JOUR T1 - TRPV1, CGRP and SP in scalp arteries of patients suffering from chronic migraine JF - Journal of Neurology, Neurosurgery & Psychiatry JO - J Neurol Neurosurg Psychiatry SP - 393 LP - 397 DO - 10.1136/jnnp-2014-308813 VL - 86 IS - 4 AU - Marina Del Fiacco AU - Marina Quartu AU - Marianna Boi AU - M Pina Serra AU - Tiziana Melis AU - Riccardo Boccaletti AU - Elliot Shevel AU - Carlo Cianchetti Y1 - 2015/04/01 UR - http://jnnp.bmj.com/content/86/4/393.abstract N2 - Objective The transient receptor potential vanilloid type-1 receptor (TRPV1) and the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP) appear to be differently involved in migraine pain. A role of neurovascular scalp structures is also suggested by several data. We performed a quantitative study of TRPV1-like immunoreactive (LI), CGRP-LI and SP-LI innervation of scalp arterial samples from patients affected with chronic migraine (CM). Methods Short segments of scalp arteries were collected from 17 participants undergoing vascular surgery for treatment-resistant CM and from 6 controls who underwent neurosurgery for various indications. The immunoreactivity of the arterial innervation to TRPV1, CGRP, SP and to the pan-neuronal marker protein gene product 9.5 (PGP9.5) was examined. Immunoreactive nerve fibres in vessel cross-sections were quantified by computerised image analysis. Results A significant increase of TRPV1-LI nerve fibres was found in the arterial wall from CM compared with control patients (p<0.05), while no significant difference was found for CGRP and SP. Conclusions This study yields the first evidence for the existence of a TRPV1-LI innervation in human scalp arteries and provides the first quantitative assessment of the TRPV1-LI, CGRP-LI and SP-LI innervation of those vessels. The increase of TRPV1-LI periarterial nociceptive fibres of scalp arteries may represent, at least in some participants, a structural condition favouring CM (and possibly migraine), for example, by causing a higher sensitivity to algogenic agents. ER -