Migraine Sessions at CONy 2019

As part of our CONy 2019 highlight series, the second of two Teva-supported debates revealed fascinating insights into the importance of aura as a prodrome of migraine.

The debate hosted by Dr. Dimos Mitsikostas (National & Kapodiistrian University of Athens, Greece), opposed Drs. Isabel Pavão Martins (University of Lisbon, Portugal) and Margarita Sánchez del Río (Clínica Universidad de Navarra, Madrid, Spain), and examined whether migraine with aura (MA) and migraine without aura (MoA) are the same disease. Dr. Mitsikostas opened the session by reminding the audience that 1–2 out of 5 patients with migraine have auras and that this prevalence is identical in both genders.1 He further described that the likely basis of migraine aura symptoms lies in the phenomenon of cortical spreading depression (CSD), a wave of increased electrocortical activity and vasodilation (hyper-perfusion), followed by sustained decreased activity and prolonged vasoconstriction (hypo-perfusion).2

As a proponent of the position that MA and MoA are the same disease, Dr. Martins argued that human neuroimaging studies have shown that CSD play a role in migraine, regardless of the presence of aura. She also presented findings of a study by Vincent MB and Hadjikhani N3 that would suggest that MoA could simply be a migraine with subclinical aura. Dr. Martins further provided evidence of the presence of transient visual disturbances (TVD) during migraine attacks in patients with MoA.4 As a last argument in support of her position, Dr. Martins also reminded the audience that most prophylactic agents improve patients with migraine regardless of the presence of aura.

On the other side of the debate, Dr. Sánchez del Río presented her case for a clear distinction between MA and MoA. She even proposed to reclassify MA as “headache attributed to aura.” In support of her position, Dr. Sánchez del Río emphasized differences between MA and MoA in terms of: clinical aspects (e.g. aura sometimes occurs without headaches); treatment (MA not responsive to acute or preventive drugs used in MoA); pathophysiology (e.g. CGRP triggers MoA but not MA); and cardiovascular risk (increased in MA).5-6

At the end of the debate, the audience voted with a narrow majority that MA and MoA were manifestations of the same disease. The questions from the audience and rebuttals from the debaters left us with one certainty: this debate is far from over.


  1. Stewart WF, et al. Development and testing of the Migraine Disability Assessment (MIDAS) Questionnaire to assess headache-related disability. Neurology. 2001;56(6 Suppl 1):S20-8.
  2. Hadjikhani N, et al. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci USA. 2001;98:4687-92.
  3. Vincent MB, et al. Migraine aura and related phenomena: beyond scotomata and scintillations. Cephalalgia. 2007;27:1368-77.
  4. Mattsson P, et al. Characteristics and prevalence of transient visual disturbances indicative of migraine visual aura. Cephalgia. 1999;19:479-84.
  5. Pascual J, et al. Preventing disturbing migraine aura with lamotrigine: an open study. Headache. 2004;44:1024-8.
  6. Vgontzas A, et al. Episodic migraine with and without aura: key differences and implications for pathophysiology, management, and assessing risks. Curr Pain Headache Rep. 2018;22:78. doi: 10.1007/s11916-018-0735-z.