Abstracts Cephalalgia 2015, Vol. 35(6S) 1–296 ! International Headache Society 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0333102415581304 cep.sagepub.com International Headache Society abstracts ScS1-1 IS02 Special Session I – Headache Trainees Excellence Tournament Special Session I – Headache Trainees Excellence Tournament Propagation of cortical spreading depression reduced by 5HT1 receptors alternation Altered white matter tract integrity in patients with prolonged post-concussion symptoms A. Karimi Goudarzi1, M. Ahmadi2, B. Khodaie2, 1 1 A. Lotfinia2, M. Lotfinia2 C. Chong , T.J. Schwedt 1 1Basic Sciences, Islamic Azad University Karaj Branch, Neurology, Mayo Clinic, Phoenix, USA KARAJ, Iran Introduction: Routine structural neuroimaging is typic- 2 Neurophysiology, Shefa Neuroscience Research Center, ally normal following concussion, even in patients who Tehran, Iran have a multitude of post-concussion symptoms. The migraine attack has been observed to be associated with cortical spreading depression (CSD) associated with Diffusion Tensor Imaging (DTI), which allows for the inter- low level of serotonin (5-HT). However, the mechanism rogation of white matter tract integrity, has been useful in underlying this phenomenon is still unclear. The develop- determining brain alterations in acutely concussed ment of serotonin receptor agonists in alleviation of patients, yet the existence of white matter alterations in migraine pain in clinical trials, further implicates the role patients with prolonged post-concussion symptoms (>1 of serotonin as a key molecule in migraine. In this regard, month) remains controversial. present study evaluated the role of 5-HT1 receptor on electrophysiological parameter of the cortical spreading Methods: Using global probabilistic DTI tractography, we depression (CSD). Wistar rats (n ¼ 28) were injected examined the integrity of several major fiber tracts in 12 interventricular with fluoxetine (5, 10, 20 mg/kg) and/or concussed patients (age ¼ 36.0; SD ¼ 15.9) who continued saline. CSD was recorded immediately after KCl (3 mM; to be symptomatic at least 1 month post-concussion but 10–15 ml) injection. In addition, all groups were CSD- had normal routine T1 and T2 imaging and in 12 healthy, recorded for 60–70 min. The interventricular fluoxetine age-matched control subjects (age ¼ 38.9 SD ¼ 13.0). injection effect was reverted after flushing the treated region with saline. Fluoxetine applied during the CSD- Results: Concussed patients showed higher axial diffusiv- induction period. CSD-velocities reduced significantly in ity (AD) but unchanged fractional anisotropy (FA) in the 10 and 20 mg/kg (P < 0.05). Also amplitude and duration right (AD: p ¼ .043; FA: p ¼ .545) and left (AD: p ¼ .022; of CSD waves were significantly decreased in 5, 10, and FA; p ¼ .066) superior longitudinal fasciculi and higher AD 20 mg/kg of fluoxetine (P < 0.05). The present effect of (p ¼ .035) and lower FA (p ¼ .044) in the forceps major fluoxetine, supports the hypothesis of a serotoninergic relative to controls. No significant group differences in influence on CSD, as previously suggested in experiments tract FA and AD were found for the left (AD: p ¼ .706; using other serotoninergic drugs. FA: p ¼ .485) and right (AD: p ¼ .673; FA: p ¼ .904) uncin- ate fasciculus. Exploratory post-hoc analyses indicated that Keywords: Serotonin, Migraine, Electrophysiology, patients with multiple concussions (n ¼ 6) had higher FA in Spreading Depolarization the left superior longitudinal fasciculus (p ¼ .02) relative to ! International Headache Society 2015 2 Cephalalgia 35(6S) Figure. Fmajor ¼ forceps major; Unc ¼ uncinate fasciculusl; Slft ¼ superior longitudinal fasciculus. patients with one concussion (n ¼ 6). No other tract antimigraine drug, sumatriptan, in different components metric differences were identified. of the trigeminovascular system in FHM1 mice with the R192Q missense mutation. Conclusion: In patients with persistent symptoms, white matter tract integrity is altered beyond 1 month following Method: Dura mater, trigeminal ganglion (TG) and tri- concussion. Tract damage might be more extensive in geminal nucleus caudalis (TNC) were isolated from adult patients with multiple concussions. R192Q mice. Tissues were triggered with 60 mM KCl in the absence or presence of sumatriptan (30 mM). Supernatant was collected for CGRP measurements. IS03 Data are expressed as relative stimulated CGRP release (mean Æ s.e.m). This study is approved by the ethics com- Special Session I – Headache Trainees Excellence mittee of the Erasmus Medical Center in Rotterdam Tournament Results: We found no difference in KCl-induced CGRP Trigeminovascular cgrp release in familial release in different components of the trigeminovascular hemiplegic migraine type 1 knockin mice system between R192Q (dura mater: 5.8 Æ 2.0, TG: 5.0 Æ K. Chan1, S. Labruijere1, I. Garrelds1, K. Ibrahimi1, 1.9, TNC:4.9 Æ 1.1) and wildtype (dura mater: 16.1 Æ 5.7, A. Danser1, A. van den Maagdenberg2, TG:5.9 Æ 1.7, TNC:6.4 Æ 1.2) mice. Sumatriptan only A. MaassenVanDenBrink1 inhibited the CGRP release in the TNC (control: 4.7 Æ 1.1, sumatriptan: 2.6 Æ 1.0) and dura mater (control: 1Internal Medicine. Div of Vascular Medicine and 5.7 Æ 3.3, sumatriptan: 0.8 Æ 0.1) of wildtype but not in Pharmacology, Erasmus Medical Center, Rotterdam, R192Q (TNC; control: 5.3 Æ 1.3, sumatriptan: 3.4 Æ 1.0 Netherlands and dura mater; control: 4.8 Æ 2.2, sumatriptan: 5.6 Æ 2Neurology and Human Genetics, Leiden University Medical 3.2) mice. Center, Leiden, Netherlands Background: Neuronal hyperexcitability has been shown Conclusion: KCl-induced CGRP release seems unaf- in transgenic knockin mice carrying the familial hemiplegic fected by the R192Q mutation, in contrast with earlier migraine type 1 (FHM1) mutations in the Cacna1a gene. findings in TG of younger R192Q mice (Fioretti et al. However, the effects of FHM1 mutations on the trigemi- (2011), J. Physiol, 589.23). Interestingly, sumatriptan novascular system and the release of neuropeptides are reduced trigeminovascular activation in the wildtype but largely unknown. not in the R192Q mice, suggesting a disinhibition of the trigeminovascular system. Aim: To investigate the release of calcitonin gene-related peptide (CGRP) in the absence and presence of the ! International Headache Society 2015 Abstracts 3 IS04 83.3%, specificity 85.7%) was reached when separating patients with from those without aura. Special Session I – Headache Trainees Excellence Tournament Conclusion: The data support the view that migraine is a brain disorder with distinctive cortical/ subcortical ana- Feasibility of using structural brain data for tomical features. Although the diagnostic accuracy cur- diagnosing migraine rently remains too low for clinical practice, it is a good L. Gaetano1, S. Magon1,A.May2, A. Stankewitz2, starting point for a future supplementary diagnostic tool. P.J. Goadsby3, A.R. Tso3, M. Ashina4, F.M. Amin4, C.L. Seifert5, M. Chakravarty6, T. Sprenger7 IS05 1Department of Neurology, University Hospital Basel, Basel, Switzerland Special Session I – Headache Trainees Excellence 2Department of Systems Neuroscience, University Medical Tournament Center Hamburg-Eppendorf, Hamburg, Germany 3Headache Group-Department of Neurology, University of Pain related cortical and subcortical grey California San Francisco, San Francisco, USA matter changes in cluster headache 4 Danish Headache Center and Department of Neurology, 1,2 1 1 1 1 N. Szabo´ , A. Kira´ly , P. Farago´ , G. Csete ,E.To´th , University of Copenhagen, Copenhagen, Denmark 1 1 1 1,3 A. Pa´rdutz , D. Szok , J. Tajti ,L.Ve´csei , 5Department of Neurology, Technische Universitaet Z.T. Kincses1,2 Muenchen, Munich, Germany 6Department of Psychiatry, McGill University, Montreal, 1Department of Neurology, Albert Szent-Gyo¨rgyi Clinical Canada Center University of Szeged, Szeged, Hungary 7Department of Neurology, DKD Helios Klinik, Wiesbaden, 2International Clinical Research Center, St. Anne’s University Germany Hospital Brno, Brno, Czech Republic 3MTA-SZTE Neuroscience Research Group, Szeged, Background: Migraine is diagnosed using operational cri- Hungary teria according to ICHD II/III-beta. Changes in brain struc- ture or function, or other biomarkers are not currently Background: Subcortical structures, like the basal gang- considered in the diagnostic process. lia, thought to have a crucial role in pain processing, which was underlined by neuroimaging studies detected activa- Aim: Using multicenter high-resolution structural MRI tion in these areas in acute and chronic pain. data, we tested the ability of a machine learning technique to distinguish migraineurs from healthy subjects on the Aim: In the current study we investigated the cortical and basis of cortical thickness and subcortical morphology. subcortical grey matter volume in cluster headache patients. Methods: T1-weighted MPRAGE data of 131 migraineurs (40 with aura; 31 Æ 9yo; 109 women; monthly attack fre- Method: High-resolution T1 weighted images were quency: 3.2 Æ 2.5; disease duration: 14 Æ 8.4y) and 115 acquired from seventeen CH patients and thirty-one age- matched healthy subjects (29 Æ 7yo; 81 women) acquired matched healthy controls. Voxel based morphometry with at four different centers at 3 Tesla were pooled. Cortical threshold-free cluster enhancement statistic and surface thickness and subcortical morphology were assessed using based subcortical segmentation analysis were