In this touchNEUROLOGY interview, editorial board member Prof Peter Goadsby (King’s college Hospital, London) highlights two presentations from the annual European Academy of Neurology (EAN), July 1–4, 2023, in the field of migraine; the first by Klein et al. looking at a new potential biomarker of visual snow syndrome, and the second a presentation that he worked on looking at clinical predictors of cranial autonomic symptoms in patients with chronic migraine.
Disclosures: Peter Goadsby has received consultant fees from: Aeon Biopharma, Abbvie, Amgen, CoolTech LLC, Epalex, Eli Lilly, GlaxoSmithKline, Gerson Lehrman Group, Guidepoint, Tremeau, Lundbeck, Novartis, Pfizer, Praxis, SAI Med Partners, Sanofi, Satsuma, Shiratronics, Teva Pharmaceuticals and Vector Metric. He has received royalties or licenses from Massachusetts Medical Society, Oxford University Press, UptoDate and Wolters Kluwer. He has received grant/research support from Celgene and honoraria/honorarium from CME Outfitters. He is a member of the advisory board for Aeon Biopharma, and discloses a leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid with: American Headache Society,
Migraine Trust and Organisation for Understanding Cluster Headache (UK).
Support: Interview and filming was supported by Touch Medical Media. The interview was conducted by Sophie Nickelson.
Filmed as highlight of EAN 2023.
Hi. Peter Goadsby. I’m at the European Academy of Neurology here in Budapest. And I’m going to talk about three areas that have caught my attention.
I thought that is a paper by Klein and Schankin and others looking at visual snow syndrome. What they did was EEG, they looked at the alpha-rhythm power using fast Fourier transformation, and showed that if they compared visual snow patients that didn’t have migraine with controls, there was a difference in the alpha power. That’s still early days, but it shows there may be a signature for visual snow that we could use as a biomarker moving forward for treatment, and that’s quite exciting because, really, that’s an area where there aren’t any useful treatments. And lastly, they studied pure physiology, physiology with a clinical translation.
Dr Villar Martinez and myself, we looked at more than 400 patients at the prevalence of cranial autonomic symptoms like lacrimation, conjunctival injection, nasal congestion, which actually occurs to some extent in about three quarters of migraine patients. Most of us think about it in terms of cluster, but it’s interesting that they’re in migraine patients. And what predicted their presence? What predicted their presence was aura. Now when you think about it physiologically, aura offers a threat to the brain, brain blood flow, and it’s probable that these systems in cranial autonomic outflow and indeed the whole trigeminal autonomic system is a protective system. So it’s perhaps unsurprising that aura would be more likely to trigger those symptoms than migraine without aura. And it tells us that the underlying pathophysiology of migraine involves disturbance of what are quite fundamental mechanisms in the brain. Of course, as we understand, and we understand migraine better, I think we understand many other aspects of neurology, including potential understanding for stroke.
So, an exciting meeting. I get a buzz for what’s happening in migraine, and I hope you enjoy looking at those questions.
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