Neuroscience Letters 384 (2005) 150–155 Capsaicin failed in suppressing cortical processing of CO 2 laser pain in migraine patients Marina de Tommaso , Luciana Losito, Olimpia Difruscolo, Michele Sardaro, Giuseppe Libro, Marco Guido, Paolo Lamberti, Paolo Livrea Neuroscience Department, University of Bari, Bari, Italy Received 26 January 2005; received in revised form 7 April 2005; accepted 22 April 2005 Abstract The aim of this study was to compare the properties of the nociceptive system in eight migraine without aura patients in the pain-free phase with 10 healthy controls, by evaluating the topography and the source of the CO 2 laser-evoked potentials (LEPs) obtained by the right supraorbital skin, during and after capsaicin topical application. In healthy subjects the acute cutaneous pain induced by capsaicin reduced the amplitude of the vertex LEPs and induced a posterior shifting of the P2 wave dipolar source within the anterior cingulate cortex. These functional changes seemed significantly reduced in migraine patients, for a disturbed pattern of pain modulation at the cortical level, which may subtend the onset and persistence of migraine. © 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Migraine; Pain; Central nervous system; Dipolar modelling Previous studies showed that in normal adults acute cuta- neous pain induced by capsaicin lead to functional changes of the nociceptive system [16]. Capsaicin applied on the skin causes pain by stimulation of C nociceptors: in previous studies it was shown to cause attenuation of cortical poten- tials obtained by the CO 2 laser stimulation of the painful cutaneous territory (LEPs) [11,16] and the cutaneous areas represented adjacently [16]. The dipolar source analysis of LEPs revealed that the inhibition of laser-induced pain during capsaicin might be due to functional changes of the anterior cingulate cortex (ACC), which, during capsaicin, appeared mostly activated in the posterior portion, probably for the reduced activity of the rostral region [16]. Changes of cortical processing of pain were previously observed in migraine. In a recent study of LEPs in patients with chronic or episodic migraine, an abnormal pattern of modulation of pain-related cortical potentials was found in both migraine groups. This abnormal pattern consisted of a reduced inhibitory effect of distraction on the elaboration of Correspondence at: Clinica Neurologica, Policlinico, Piazza G. Cesare 11, 70124 Bari, Italy. Tel.: +39 080 5478546 538; fax: +39 080 5478532. E-mail address: m.detommaso@neurol.uniba.it (M. de Tommaso). the experimental painful stimulus [7]; it might suggest a basic dysfunction of cortical areas that modulate pain during the in- terictal phase in migraine. Basing on the most recent hypoth- esis about migraine pathogenesis, it is likely that a network of cortical and subcortical structures with modulatory no- ciceptive and antinociceptive function becomes abnormally activated in a migraine attack or even between attack [18]. The aim of this study was to detect the properties of the no- ciceptive system in migraine patients in the pain-free phase, by evaluating the topography and the source of the P2 wave obtained by the CO 2 laser stimulation of the trigeminal in- nervated skin, during and after capsaicin application. Ten patients were selected for the study: they were all affected by migraine without aura, according to the Interna- tional Headache Society Criteria [9]. Patients with general medical, neurological, or psychiatric diseases were excluded from the study. All patients were evaluated at least 72h af- ter the end of the critical migraine phase (mean 74 ± 3.1 h) and well before the next attack (mean 72 ± 4.2 h), verified by the headache diary during a following clinical examination. Two patients were excluded for the poor quality of the LEPs tracks, and the final group included 8 patients, 6 women and 2 men, mean age 32.3 ± 4.4 (range 21–44), with 12 ± 6.6 years 0304-3940/$ – see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.neulet.2005.04.086