#62. Epilepsy Explained - Professor Tony Marson

Professor Tony Marson of the University of Liverpool talks to Beth and Sahir about Epilepsy, a neurological disorder characterized by recurrent seizures, which are sudden, abnormal electrical activity in the brain. We discuss the types of epilepsy, what are its causes and how it manifests across time, what the current treatments for epilepsy are and what the future of epilepsy research looks like. 

This episode is part of our ongoing collaboration with the British Neuroscience Association, Liverpool Neuroscience Group and The Brain Charity.

https://www.liverpool.ac.uk/people/anthony-marson

Public Events run by LNG: https://meetings.bna.org.uk/BYOBLiverpool/

BNA Festival of Neuroscience: https://meetings.bna.org.uk/bna2025/ 

Chapters

• 0:00 Introduction
• 4:39 Understanding Epilepsy
• 17:14 Genetics in Epilepsy
• 24:12 Stigma around Epilepsy
• 28:15 SANAD Trial and Treatment Approaches
• 40:36 Detecting Epileptic seizures
• 45:39 Highlighting impact of Epilepsy

Transcript

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Ladies and gentlemen, boys, girls, and NBs, welcome back to the Smooth Brain Society.

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This is another episode where we'll be going over some of the great work being done

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at the British Neuroscience Festival,

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or some of the great work which is being showcased at the British Neuroscience Festival.

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And in the first episode, we spoke a little bit about...

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the BNA so the British Neuroscience Association and a little bit about the outreach

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work the Liverpool Neuroscience Group is doing but we had a third organization

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which we did not actually talk about in great detail although we did mention them

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and that was the Brain Charity and we needed to start off this episode by giving

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them their flowers so I'll let Beth go ahead and sort of go and talk a little bit

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about what they do who they are and yeah

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So the Brain Charity is a national UK charity that supports anyone affected by

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neurological conditions,

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whether it's something well known like dementia or epilepsy,

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or one of the 600 plus rare conditions like trigeminal neuralgia or Alice in

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Wonderland syndrome.

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They help people through practical support,

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emotional counselling and social activities,

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making sure no one feels alone after a diagnosis.

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What makes them particularly special is around 40% of the staff are neurodivergent

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or have neurological conditions themselves.

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So everything they do is rooted in lived experiences.

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They're based in Liverpool since 1993.

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They've grown into a vital service that helps thousands of people across the UK every year.

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And the need for what they do has only grown since the pandemic.

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And as part of the British Neuroscience Association Festival of Neuroscience,

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the guest speakers from Liverpool Neuroscience Group will run interactive sessions

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on a variety of topics relevant to brain health during April,

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May and June coffee mornings.

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So get yourself on the website and have a little look and see if you want to get

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yourself down there.

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And our Neuro Nights,

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first Neuro Nights comedy night last week was all,

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all the funds was raised to us to go to the Brain Charity.

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So thank you everyone who turned up.

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And we've got another one on the 24th of April.

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If you're free to go, it's Leaf, Bold Street.

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Tickets are a fiver.

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Everything goes to the Pain Relief Foundation.

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Awesome.

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Brilliant.

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All right.

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And without further ado, we'll introduce our guest.

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So today's guest, we're talking to Professor Tony Marson.

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He is Professor of Neurology and Executive Dean of the Institute of Systems,

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Molecular and Integrative Biology at the University of Liverpool.

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He leads the Liverpool Epilepsy Research Group and is an honorary consultant

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neurologist at the Walton Centre NHS Foundation Trust in Liverpool.

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So welcome, Tony.

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Pleasure to have you.

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It's a pleasure to join you.

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So I guess the first question which I ask,

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which I ask most of my guests,

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is sort of what was your journey into getting into your field of epilepsy research?

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What sort of made you take this path?

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Yeah, so I'm a clinician at heart.

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And pretty early on in my training, probably in medical school, actually, I...

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I discovered that neurology was probably what I wanted to do.

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Uh,

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so I was kind of fascinated by the neuroanatomy and the kind of the kind of logical

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approach to trying to work out where,

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whereabouts in the nervous system is the problem.

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What is it?

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And, uh, what is it that we can, uh, we can, uh, do to help, uh,

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Just to stop you,

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could I quickly clarify what's the difference between sort of like a neurologist,

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a neurosurgeon,

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and a neuroclinician,

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all these things?

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Are there like sort of differences between them?

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Yeah, good question.

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Because people often think I'm a neurosurgeon, which I'm not.

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So in medicine, we kind of have two main routes.

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One is to be a physician and the other is to be a surgeon.

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So I'm a physician,

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and I've gone on a track where I see people with a whole range of neurological conditions,

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and my main focus is on epilepsy.

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So my main job is seeing people in my clinics and giving them kind of diagnoses and

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advice about their management.

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So because you said epilepsy was sort of like your specialty,

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could you give me an idea of what all comes under epilepsy?

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Yes.

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So having decided I wanted to do neurology,

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I got some junior doctor's jobs and was exposed to epilepsy at a time when they

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were quite important.

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There was a lot of interest in developing new treatments and new approaches and for

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a lot of neurological diseases.

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So this is back in the very early 1990s.

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We didn't have much in the way of treatments,

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much in the way of treatments which altered the disease process.

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So we didn't have disease-modifying treatments for things like multiple sclerosis,

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which are now common-day treatments.

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And we were developing

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developing an epilepsy surgery program, so brain surgery for people with epilepsy.

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So there was a lot going on.

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There was a kind of an inspirational leader,

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David Chadwick,

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who turned out to be my mentor for a long time.

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And I think your career path is often very influenced by what you're interested in,

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but also the people around you and how they motivate you and stimulate you and

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mentor you.

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And I had

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really good exposure to epilepsy as a young clinician and then as a junior researcher.

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And I've spent most of my clinical and my research career in epilepsy.

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And you asked me a bit, you asked me earlier a bit about what epilepsy contains and one of the

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The fascinating things about epilepsy is that it is so kind of heterogeneous and

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there's a lot going on and a lot of questions that we've got to answer and a lot of

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things that we need to consider in clinical practice.

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So we say that people have got epilepsy when they are susceptible to having epileptic seizures.

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And one thing to say is that seizures are really a symptom of something going on in the brain.

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So whilst you might think about epilepsy being one condition,

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it's actually thousands of different conditions that manifest as seizures.

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And we're on a journey to try and understand the biology of those conditions.

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And the other area of heterogeneity is that there are lots of different types of

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epileptic seizures,

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ranging from episodes where people might get just a strange feeling,

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maybe a feeling of deja vu,

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a fertilized feeling in their tummy,

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to episodes where people might go blank,

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stare,

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lose awareness and behave automatically through to episodes that everyone would

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recognize as an epileptic seizure where somebody will collapse and be stiff and

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shaking on the floor for a few minutes.

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And the other area of complexity is that it happens,

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it can start at absolutely any age and it can be something that starts shortly

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after somebody's born and it can start later on in people's lives.

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And because our population is changing, we've got more older people in our population now.

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It's actually more common to diagnose epilepsy in older people than it is in children.

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So I think often we think of epilepsy as being a disease of children, but it's not.

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is something that can start at any age,

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a bit more common in children than that kind of middle life.

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But actually,

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it's much more common now in older people as we're accumulating damage to our

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brains from strokes and circulation disease and head injuries and brain tumors and

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so on.

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So whilst you might think epilepsy is just one condition, why is that so interesting?

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Well, actually, it's really fascinating.

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It happens at any age.

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There's lots of biological processes going on that we need to understand.

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And there is also

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Massive impact on human life.

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So it's a really stigmatizing condition.

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There's still a lot of myths around epilepsy.

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So people with epilepsy still feel stigmatized to some extent,

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even in what we might think of a more modern society,

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a more progressive age.

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And it impacts on employment.

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education um fertility it's you know it has massive ramification so it's it's a

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really broad and fascinating area to be involved in that's amazing tony said the

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absolute yeah you say heterogeneity of epilepsy is there a specific uh subtype of

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epilepsy you particularly research or is it all epilepsy or that is not possible

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Yes.

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So I'm an adult neurologist.

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So again,

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the way we kind of carve things up in health services is you're someone that sees

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children up to the age of 16 or you're someone that sees adults from the age of 16

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or 18 onwards.

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So I'm an adult neurologist.

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So I tend to see people over the age of 16.

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So people may have had a diagnosis in childhood and then they get transferred to me

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as an adult neurologist.

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Yeah.

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I've lost the track of the question there, sorry.

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No,

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no,

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I know you said about different types of FLC,

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so I think you've got like myoclonic seizures and other types of seizures.

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Is there any that you particularly like to research more?

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I know as a neurologist,

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I'm sure you'll see all sorts,

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but in terms of research,

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is there a specific one that you think you like to research more or requires more

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research or you just find particularly interesting?

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So the kind of questions we've focused on

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in our research program is thinking about early epilepsy.

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So not necessarily thinking about types of epilepsy,

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but thinking about where people are in their journey.

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And that point of diagnosis and the treatment choice at the diagnosis is really

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mission critical because you've really got to get it right at the start because

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that's your best opportunity to get people back to education,

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back into work,

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back driving and functioning in society.

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And sometimes the eye is drawn to the complex, and we'll probably talk about that later.

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But I think from a kind of a public health point of view,

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we do the best thing for society when we get it right at the start of someone's

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journey and make sure that they're not disadvantaged by not having their condition

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as well controlled as it might be.

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And practically, we think about

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Two main types of epilepsy,

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particularly in adulthood,

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when we think about epilepsy where seizures start in one place in the brain,

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we call that focal epilepsy.

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And it's probably about two thirds of people in adulthood have got a focal epilepsy,

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seizure starting in one place.

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And we have kind of paradigms and treatment approaches for that.

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And then there's about a third of people that have got what we might think about as

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being a generalized epilepsy.

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And for those people, seizures start on both sides of the brain at the same time.

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And the cause of that is probably mainly genetic.

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although we're still on the journey to really unpick the genetic architecture of

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the epilepsies.

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And then there's a much rarer group of epilepsies which will tend to present in childhood,

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some of which are really severe and associated with learning difficulties and other

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significant health problems.

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Again, that's a group of conditions that we think of as largely being genetic.

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These are the conditions that you may see on the news, conditions, for example, that we're

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there's a condition called Lennox-Gastaut syndrome and a condition called Dravet syndrome.

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They're the conditions that we might use cannabis for.

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And that,

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and that,

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and that's something that's been on the news,

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on the news quite a bit,

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but they're,

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they're really quite rare types of types of epilepsy.

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Yeah.

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I think last week we briefly spoke about HM and off on the after side of the memory side,

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but he had epilepsy,

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didn't he,

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where they had to cut part of his temporal lobe,

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I was believe,

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or his entire temporal lobes.

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Um,

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Is that usually where the epilepsy starts in the temporal lobes or can it be

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anywhere in the brain?

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Yeah.

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So epilepsy tends to start at the front of the brain.

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So either in the frontal lobe or the temporal lobe.

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And I think we readily recognize temporal lobe epilepsy as a condition.

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Most people think about, well, do I have an aura before my seizures?

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Yeah.

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I think it's pretty common parlance, isn't it?

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People understand this notion of an aura.

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And with temporal obel epilepsy,

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the sort of auras that people might get is kind of deja vu,

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strange taste,

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strange smell,

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butterflies feeling in their tummy.

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And those symptoms are actually coming from...

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mainly from the inside bit of the temporal lobe, something that we call the hippocampus.

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And in front of that, there's something called the amygdala.

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And we recognize that that bit of the brain is susceptible to scarring.

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So one of the most readily recognized types of epilepsy is temporal lobe epilepsy.

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So seizures that are coming from the temporal lobe.

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And it is generally coming from that inside bit of the temporal lobe.

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And for a long time,

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We've been aware that that sort of epilepsy often doesn't respond well to medication.

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We can't stop the seizures with medication.

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And so surgery might be the best option for that person.

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So can we cure their epilepsy or reduce the severity of their epilepsy by cutting

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out their temporal lobe?

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and most of that surgery is actually focused on this hippocampus inside bit of the

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temporal lobe and some units do an operation whereby they only take the inside bit

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out and others do an operation where they take the whole of the temporal lobe out

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on one side and interestingly people can function really well without

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one of their temporal lobes,

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and often you're taking out a temporal lobe that wasn't functioning very well.

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So we often worry about memory,

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but actually if you're taking out a damaged temporal lobe that wasn't really

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functioning very well from a memory point of view,

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then the other side's taken over anyway.

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Yeah, but just not both of them.

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Yeah, take both out.

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It's a disaster.

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You end up with somebody with zero memory.

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Yeah, yeah.

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This comes into the question of brain plasticity, right?

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So are these surgeries performed in sort of younger kids as well?

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And do they seem to recover better than if such a surgery where you had to take out

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half your temporal lobe was performed in an adult?

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Yeah, so the surgery is better performed younger.

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So a lot of the surgery used to be done in adults when it could have been done in children.

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Increasingly, much more epilepsy surgery is done in children now than it's done in adults.

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And brain plasticity is a really good reason for that because we're worried about memory.

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So we want the other side to take over in terms of memory function,

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but we might also be worried about speech,

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particularly if we're operating on a dominant hemisphere.

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So if we're operating on the left-hand side of the brain and you're right-handed,

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then we need to be very careful not to damage the speech center.

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But if there is any damage to the speech center,

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if the damage is done as a child,

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then there's much greater opportunity for brain plasticity to do its thing and for

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speech to develop in other bits of the brain,

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either in a slightly different bit of the temporal lobe or on the other side.

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And we will see

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People in adulthood who have kind of had damage to their left temporal lobe,

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they're right-handed,

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but the speech has moved over to the other side because the epilepsy was causing a

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lot of disruption or there was damage to the left temporal lobe,

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which meant that speech moved over to the right.

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That's really interesting.

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I had a question from a part which you said earlier, which has been burning.

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You had said that in adults,

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the adult case you see,

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about a third seemed to have a genetic component to it.

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That was the one where Caesars can start at any region in the brain.

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It's not a focal point one.

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That's right.

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Is that the one which is more common in children because it's genetic?

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Yeah,

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so generally focal epilepsies are all more common in general,

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but the generalized epilepsies,

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they start in childhood and adolescence mainly.

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So once somebody's over the age of 25,

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it's pretty unlikely that their epilepsy,

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if it's starting then,

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is a generalized epilepsy.

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So in adulthood,

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we will more commonly diagnose focal epilepsy than generalized epilepsy,

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but in pediatrics,

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they will diagnose a lot of generalized epilepsy.

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And the generalized epilepsies have a number of different patterns.

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So most people will have probably heard of kind of absence epilepsy or sometimes

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gets historically was called petty mal epilepsy where children just have brief

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blank spells.

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And that's a common type of epilepsy to present in childhood.

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And then we have

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generalized epilepsy can cause tonic-clonic seizures.

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So tonic means stiff and clonic means shaking.

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So again, something that we'd all recognize as a seizure.

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And then one of the particular types of epilepsy that starts in teenagers is

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something that we call juvenile myoclonic epilepsy.

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And that includes jerks,

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so jumps and jerks,

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which have myoclonic seizures as well as tonic-clonic seizures.

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So we

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we label the epilepsies or we give them a name based on the age that it starts and

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the type of seizures that people are having and we have to do that because at the

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moment we still don't understand the biology so if we could say this is a this is

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epilepsy caused by gene x then we'd say it's epilepsy caused by gene x because we

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don't have that we still have this quite complicated classification which which is

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which is much more based on kind of clinical clinical features rather than what we

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know about the biology hopefully in

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In a number of years' time,

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we will really understand the biology much better so that we can label it better,

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but also hopefully have better treatments because our treatments aren't as good as

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we would like them to be at the moment.

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So as it stands, there's no such thing as one epilepsy gene which you have, kind of?

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No.

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So we've all been working together around the world for about 20-odd years now

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trying to unpick the genetic architecture.

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So through our research projects,

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we've collected information and DNA from patients,

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and that DNA can be sequenced to look at their genetic makeup.

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And then we can pool all of that information because we need information on

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thousands and thousands of people to answer these sorts of questions.

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And I think what we thought when we started this was, well, we'll probably find a few genes.

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And it turns out that we're not going to find a few genes.

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And for a very small number of people, it's just one gene that's at fault.

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For most people, it's multiple genes and it's polygenic condition.

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So it means that you've got a number of gene problems added together and they cause

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the epilepsy.

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So everyone's working hard on unpicking the different genes that go wrong to cause

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the epilepsy and working on what are called polygenic risk models to help us work

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out who's at risk of epilepsy.

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And so it's a...

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we're on a journey and it's a much more complicated journey.

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The problem with complicated journeys is it takes you a long time to get the answer,

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but it also costs millions and millions and millions of pounds or dollars or

(00:21:12):
whatever to answer the questions and trying to get that money out of funders to

(00:21:15):
answer these questions is really quite challenging and tricky.

(00:21:21):
Yeah, but it affects so many people.

(00:21:24):
I don't even know the percentages it affects,

(00:21:26):
but I think is it...

(00:21:28):
Yeah,

(00:21:28):
it's about 1% of the population have got epilepsy.

(00:21:31):
So it's a common condition.

(00:21:33):
People don't often talk about it.

(00:21:34):
So you may know people that have got epilepsy that haven't told you they've got epilepsy.

(00:21:38):
But it's a huge problem, huge burden to individuals and society.

(00:21:44):
And we don't spend enough money on it at the moment to try and answer the questions.

(00:21:49):
So quick question, very back to the genetics.

(00:21:52):
So is it more likely you'll have generalized epilepsy if your parents have it?

(00:21:56):
Or is it because the genetics are just so, you know, there's not one gene, it's so mixed?

(00:22:03):
Yeah, there is an increased risk.

(00:22:06):
And for most people, yeah, what am I trying to say?

(00:22:13):
So there are some families where the generalized epilepsy is

(00:22:16):
run strongly in that family and some of the focal epilepsies actually but so having

(00:22:22):
a parent with epilepsy increases your risk but it only increases your risk by a

(00:22:27):
small amount unless you're someone in one of these families where there's a really

(00:22:30):
strong history of it and it

(00:22:34):
you know,

(00:22:35):
one way of trying to explain it is,

(00:22:36):
you know,

(00:22:36):
some genes from mom,

(00:22:37):
some from dad and added together,

(00:22:39):
they cause the epilepsy,

(00:22:40):
which,

(00:22:40):
which is probably why we don't,

(00:22:42):
why we don't see it as strong,

(00:22:44):
um,

(00:22:45):
inherited path,

(00:22:46):
uh,

(00:22:46):
uh,

(00:22:47):
pattern.

(00:22:47):
So,

(00:22:48):
so,

(00:22:48):
so whilst the genetic study,

(00:22:50):
the epidemiology tells us,

(00:22:51):
yep,

(00:22:52):
these are genetic conditions,

(00:22:54):
um,

(00:22:55):
It's rarely one gene.

(00:22:58):
There was a study,

(00:22:59):
I believe it was done at King's,

(00:23:00):
I think it was with Mark Richardson,

(00:23:02):
where he looked at imaging in family members and I think it was EEG and he found

(00:23:08):
very similar patterns,

(00:23:09):
but some people did have epilepsy and some of the relatives had very similar patterns.

(00:23:15):
had the exact same brain signals.

(00:23:17):
And that to me is like, okay, so they've got similar brain signals.

(00:23:20):
What is it that's almost pushing it over?

(00:23:21):
I don't know if you can shed any light on that because I found that fascinating

(00:23:24):
when I read that.

(00:23:26):
Yeah, so exactly.

(00:23:28):
And again,

(00:23:30):
that highlights what we were saying earlier,

(00:23:32):
that seizures are a symptom of a brain disorder and what is that brain disorder?

(00:23:37):
So that research was telling us that the brains of these people were

(00:23:41):
these families that are built differently.

(00:23:42):
They look a bit different to the general population, but not all of them are having seizures.

(00:23:46):
So what is that underlying brain problem?

(00:23:50):
And what is it, as you say, that

(00:23:52):
that tips them over the edge to also have seizures as part of that.

(00:23:56):
And we're on the journey to unpick that.

(00:24:00):
And it might not all be genetic either.

(00:24:01):
There may be that genetic environment interaction,

(00:24:05):
which is putting some people over the edge and making them have seizures.

(00:24:07):
So there's a lot of unanswered questions, I'm afraid.

(00:24:12):
A lot of layers just to warn you.

(00:24:16):
And I can feel like not borderline frustration that it's 1% of the population are affected.

(00:24:22):
And it's, you know, some people just don't even, I wouldn't even know that it was that high.

(00:24:26):
And,

(00:24:26):
you know,

(00:24:26):
briefly because I'm a neuroscientist and my supervisor,

(00:24:29):
Simon Keller also works in epilepsy.

(00:24:32):
Um,

(00:24:33):
Do you think it's, and you said recently before, like it's to do with stigmatization.

(00:24:36):
What is the stigma that people feel like they can't share it?

(00:24:39):
Are they worried?

(00:24:40):
What's the biggest fear?

(00:24:41):
Is it the fact that they can't, might not be able to drive, might lose their job?

(00:24:45):
What scares them so much?

(00:24:47):
And how can we overcome that as well?

(00:24:49):
Yeah, it's a good question.

(00:24:51):
I mean, people are frightened by epilepsy.

(00:24:55):
It's only if somebody has a seizure in the street.

(00:24:58):
Some people will rush and help, others will run away because it's a very frightening thing.

(00:25:05):
And there is... People can jump to conclusions.

(00:25:14):
This is somebody that's on drugs or something like that.

(00:25:18):
There's the kind of the historical...

(00:25:24):
perception of demon possession and lots of cultural history there,

(00:25:32):
isn't there,

(00:25:32):
around seizures and epilepsy which we need to break through.

(00:25:40):
And a lot of this is about education, isn't it?

(00:25:45):
Yes.

(00:25:47):
Education is what we need more of.

(00:25:52):
It's a bit of a catch-22, isn't it?

(00:25:54):
Because if people with epilepsy were able to declare their epilepsy and be more

(00:26:00):
open and discuss it,

(00:26:03):
then that would break taboos as well because people would realize,

(00:26:06):
actually,

(00:26:07):
I know somebody with epilepsy and they're a very sensible,

(00:26:15):
rational human being that's got a medical condition just like many others.

(00:26:20):
And I think that there is a challenge here with a kind of an episodic condition

(00:26:28):
because it means that it's hidden.

(00:26:29):
You know, if you've had a stroke and you've got a weak arm and leg, everybody can see that.

(00:26:34):
And it's a fixed disability.

(00:26:36):
But for something like epilepsy,

(00:26:38):
people look completely fine and then they're not fine for a few minutes having a seizure.

(00:26:42):
So it's a very hidden disability that people are frightened of.

(00:26:49):
Do these seizures then get worse over time?

(00:26:51):
That's the other thing for epilepsy, which I wanted to ask.

(00:26:54):
Because like you said, they happen and then...

(00:26:57):
they could potentially be people could be performing normally again and then they

(00:27:00):
can happen again so yeah so what what used what often happens is kind of the

(00:27:07):
epilepsy will declare itself with a seizure and then you go through kind of a

(00:27:14):
period of time working out how bad is it you know some because some people will

(00:27:18):
then have very infrequent seizures some people then go on to have quite quite

(00:27:23):
frequent seizures and once you've gone through that period of

(00:27:26):
epilepsy kind of declaring itself and its pattern often it it doesn't deteriorate

(00:27:32):
but there are a small number of people where where where the epilepsy gets worse

(00:27:37):
over the course of time and and the million dollar question is what is that process

(00:27:42):
what is going on in those brains that um that we can actually interfere with and

(00:27:47):
stop so that you know

(00:27:51):
We can stop people from developing a severe and treatment refractory epilepsy.

(00:27:56):
And that's probably a really important question for the people that might end up

(00:28:01):
requiring epilepsy surgery or the people that have got really bad epilepsy where we

(00:28:04):
just can't do an operation.

(00:28:05):
What is that process?

(00:28:07):
What can we do to stop people getting into that state of having a severe drug

(00:28:13):
refractory epilepsy?

(00:28:15):
Yeah.

(00:28:16):
I know that the SANAD trial, you were looking at some of these drugs as well.

(00:28:22):
Could you talk us through that a little bit, a little bit about the SANAD trial?

(00:28:25):
I think that's a good example of it.

(00:28:27):
Yeah, so the SANAD stands for standard in new anti-epileptic drugs.

(00:28:32):
So we've been through a period of developing a whole new generation,

(00:28:38):
possibly two generations of what we now call anti-seizure medications and have

(00:28:43):
previously been called anti-epileptic drugs.

(00:28:47):
And we've got some really kind of practical questions like,

(00:28:51):
OK,

(00:28:51):
which of these drugs should we be using first line and for which patients?

(00:28:57):
And if you're the NHS or National Health Service or a funder of health care,

(00:29:02):
you don't only want to know which one's best,

(00:29:04):
but you want to know which one gives you the best bang for your buck.

(00:29:06):
So you want to know which one's cost effective.

(00:29:10):
So we've tried to answer these questions in our conversation.

(00:29:14):
So what we've done is we've run a big randomized control trials within the UK health system.

(00:29:24):
And we've recruited people with newly diagnosed epilepsy and they've been randomly

(00:29:29):
allocated to one of a number of treatments.

(00:29:35):
And we then follow people up for a number of years and find out, you know, what

(00:29:41):
what happened to them what happened to their treatments what what happens to their

(00:29:45):
to their epilepsy and when we're when we're treating a long-term condition like

(00:29:49):
epilepsy we do need to follow people up for a few years to answer that question we

(00:29:52):
can't answer that question in just a few weeks and so and and our treatment

(00:29:59):
paradigms in epilepsy are one level of pretty simple so we think about have people

(00:30:03):
got a focal epilepsy if they've got a focal epilepsy

(00:30:06):
Then we use drugs like carbamazepine historically and then lamotrigine as

(00:30:10):
first-line treatments.

(00:30:12):
So the CENAD trials were comparing carbamazepine in the first set of trials and

(00:30:15):
then lamotrigine in the second set of trials with other treatments.

(00:30:21):
And what we find is that at the moment,

(00:30:25):
the best drug to start for most people with focal epilepsy is lamotrigine because

(00:30:29):
it's controlled seizures,

(00:30:31):
it's really well tolerated,

(00:30:33):
and it's cheap.

(00:30:35):
And so focal epilepsy from a new diagnosis point of view is fairly simple.

(00:30:43):
For the generalized epilepsies,

(00:30:45):
for a long time,

(00:30:46):
we've known that valproate is an effective treatment.

(00:30:49):
And the question then is, OK, how does valproate compare with the newer treatments?

(00:30:54):
Or perhaps the other way around, how do the newer treatments compare with valproate?

(00:31:00):
And in the most recent trial, we compared valproate with medicine called levotiracetam.

(00:31:05):
And again, we find that valproate is the most effective treatment.

(00:31:13):
So we've got really good information from randomized controlled trials as to what

(00:31:17):
should be the first line treatments if we're just thinking about how well does the

(00:31:21):
drug work and how is it from a side effect point of view.

(00:31:26):
But of course, because we're

(00:31:28):
But we also need to take a step back and think about what else is going on in people's lives.

(00:31:36):
And half the people that we're treating here are female.

(00:31:41):
And what's really important to be thinking about is the impact on contraception and

(00:31:47):
fertility and the outcome of children.

(00:31:52):
And what we know about sodium valparate is that if

(00:31:57):
babies are exposed to it in the womb,

(00:32:00):
there's about a 10% chance that they'll have a major malformation,

(00:32:04):
maybe a problem with their spine or an arm or a leg or something.

(00:32:08):
And also about a 30% chance that they're going to have a significant reduction in their IQ.

(00:32:14):
So it's really important that women don't take sodium valparate whilst they're pregnant.

(00:32:20):
So I've got this really, really challenging scenario for women

(00:32:26):
whereby we know what the most effective treatment is,

(00:32:30):
but we want to avoid that treatment in pregnancy.

(00:32:33):
And of course,

(00:32:34):
most women,

(00:32:34):
when we make a diagnosis of epilepsy,

(00:32:36):
they're not thinking about starting a family at the same time.

(00:32:39):
But that decision we make when we start treatments will potentially influence what

(00:32:44):
treatment people are on when they become pregnant.

(00:32:47):
So at the moment,

(00:32:48):
we've got this really difficult position whereby we almost effectively deny women

(00:32:53):
the access to the most effective treatment.

(00:32:55):
because of our fears about it in pregnancy and does that have longitudinal effects

(00:33:03):
if you stop it two years before would you still have those percentages or is it

(00:33:07):
still unknown yeah so so we think that it's safe to stop if we stop it it's safe

(00:33:17):
once women have been off it for three months there is a caveat to that so

(00:33:23):
It's all got a bit more complicated in the past two years because there is some

(00:33:28):
information from animal data in particular that there might be an effect for men

(00:33:38):
taking sodium valparate.

(00:33:40):
So if men are taking sodium valparate and their partner gets pregnant whilst

(00:33:44):
they're taking it,

(00:33:45):
there's a possibility that their children will be affected.

(00:33:51):
And on top of that,

(00:33:53):
there's a problem that...

(00:33:54):
So sodium valparate has what we call an epigenetic effect.

(00:33:58):
So it has an impact on the DNA.

(00:34:03):
And there's a risk that there's concern that men or women could take sodium

(00:34:11):
valparate and have children.

(00:34:13):
And those children could be affected by the sodium valparate because of an epigenetic effect.

(00:34:17):
And then their children...

(00:34:19):
even if they're not exposed to valparate in utero in the womb,

(00:34:24):
might be carrying this genetic,

(00:34:27):
epigenetic effect down the generation.

(00:34:29):
So there's a concern in the background that sodium valparate might be causing,

(00:34:34):
changing the genetics,

(00:34:36):
which is then passed down the generations.

(00:34:38):
We don't know whether that's a real thing or not, but it's a worry in the background.

(00:34:43):
And so we've got some really urgent questions to answer.

(00:34:49):
Is there really an effect on children born to men taking sodium valproate?

(00:34:54):
And is there a transgenerational effect caused by epigenetics?

(00:35:00):
And it's really difficult in consultations at the moment because we have to have a

(00:35:06):
conversation with men and women about these things.

(00:35:08):
But we've also got to tell them we don't really know whether some of these things

(00:35:11):
are true or not.

(00:35:12):
But we've got to warn them about the risk.

(00:35:14):
Yeah.

(00:35:15):
consultations and conversations with people are really easy when you know what the

(00:35:18):
risks are when you're saying there's a possible risk but yeah we've got to manage

(00:35:21):
this possible risk that's really frustrating and really difficult so we've got to

(00:35:25):
answer these questions crack on and do the research to sort this out yeah and

(00:35:31):
because most of the epigenetic stuff in terms of men is relatively recent because

(00:35:38):
Yeah,

(00:35:38):
because I've done work in my lab about alcohol and the transgenerational effects of

(00:35:43):
alcohol if men are drinking before conception.

(00:35:48):
And yeah,

(00:35:48):
you see these sort of effects,

(00:35:51):
but there's no large studies,

(00:35:55):
not enough studies to sort of confirm and be like,

(00:35:58):
yes,

(00:35:58):
this is a problem.

(00:35:59):
It's more like this could likely be a problem.

(00:36:01):
And I understand that level of frustration as someone who has to talk to

(00:36:06):
patients or anybody who comes in,

(00:36:08):
I feel like there's evidence for it,

(00:36:11):
but...

(00:36:14):
I mean,

(00:36:14):
one of the models for autism is to give mice...

(00:36:19):
high-dose valproate exposure during development in the womb.

(00:36:26):
And then offspring of those mice will also have these autistic traits.

(00:36:31):
So there is this kind of animal model,

(00:36:34):
but the doses used to create that autistic model are much,

(00:36:38):
much higher than we use in human practice.

(00:36:42):
So we're...

(00:36:45):
We've got this kind of alarming possibility in the background,

(00:36:48):
but we don't know whether it's true or not.

(00:36:52):
Can I ask with regards to Valparate,

(00:36:54):
because you said it's for generalized epilepsy was the one which you said it's

(00:37:00):
really good for.

(00:37:01):
Valparate's been around for ages.

(00:37:05):
How come no new drugs have been developed, which sort of have been better over the time?

(00:37:11):
Yeah, that's interesting.

(00:37:13):
One of the really frustrating things.

(00:37:15):
So we're working hard around the world to develop new treatments,

(00:37:19):
but we've not been able to develop any treatments that are better than what we had

(00:37:22):
already in terms of controlling seizures.

(00:37:24):
So Valparate remains the drug that is best at controlling seizures.

(00:37:30):
And it's probably worth just taking a...

(00:37:35):
going down an alley if it's like just talking about sodium valparate and drug

(00:37:39):
development in epilepsy.

(00:37:40):
So one of the challenges in epilepsy is that we still don't understand the

(00:37:44):
mechanisms properly in the brain.

(00:37:48):
We got very excited in the 1990s when we learned a lot about hyper excitability in the brain.

(00:37:55):
but we realized we've got so much more to learn about mechanisms.

(00:37:59):
And there was a period of time when we didn't really understand how Valbrate worked anyway.

(00:38:03):
We knew it worked, but we didn't understand how it worked.

(00:38:07):
And I don't know whether you know, but it was actually discovered by accident.

(00:38:11):
So people were doing, I think some French, I think they were in France, they were doing

(00:38:17):
Experiments on cats that they made epileptic.

(00:38:20):
And they were trying different drugs.

(00:38:22):
And they found out that all the drugs seemed to be working.

(00:38:24):
And they scratched their heads and thought,

(00:38:26):
oh,

(00:38:26):
gosh,

(00:38:26):
it must be the solvent that we're using to deliver the drugs.

(00:38:30):
And so they said they were using Valparais as a solvent.

(00:38:32):
So Valparais discovered completely by accident as a highly effective treatment.

(00:38:39):
And despite our advances in science,

(00:38:41):
understanding of mechanisms,

(00:38:43):
we've still not been able to develop a drug that is better than sodium valparate at

(00:38:47):
treating seizures for people with generalized epilepsy.

(00:38:50):
And we've got similar stories for focal epilepsy.

(00:38:53):
And I think one of the really important things to highlight is that all of our

(00:38:58):
medicines at the moment are really treating the symptom,

(00:39:02):
a bit like taking an aspirin for a headache.

(00:39:04):
They treat the seizures, but they don't treat the disease.

(00:39:08):
So what we desperately need in epilepsy is treatments that alter the basic biology,

(00:39:12):
treatments that are actually disease-modifying in epilepsy.

(00:39:15):
We've achieved that in multiple sclerosis to an extent.

(00:39:21):
And I guess we've got some rare instances where we're treating genetic diseases

(00:39:31):
through new technologies that are coming through.

(00:39:35):
We need to be able to do this for common diseases like epilepsy.

(00:39:38):
What is what are the common mechanisms despite this heterogeneity?

(00:39:42):
What are the common mechanisms that we can attack to modify the disease, reduce its severity?

(00:39:52):
I thought I would spend this like last sort of part talking about something which

(00:39:56):
you mentioned earlier and what your work is generally around is around the early

(00:40:02):
sort of detection or early epilepsy early epileptic detection and some of the

(00:40:08):
things which you said made me think how hard it actually is because you said

(00:40:12):
anything from staring off into blank space for a little bit could be someone having

(00:40:16):
a seizure so

(00:40:19):
how does it work how what would someone need to know in terms of being able to like

(00:40:25):
i guess someone needs to self-identify that it's potentially a seizure before they

(00:40:28):
even come see you so yeah how how does all this work how difficult is it because it

(00:40:32):
sounds really really hard yeah so um it it's it's complicated and i guess one thing

(00:40:42):
says it requires experience but but we but we recognize patterns and i'd

(00:40:48):
And one of the things that the medics are trained to do,

(00:40:52):
and they might not realize that they're being trained to do it,

(00:40:54):
but they recognize patterns.

(00:40:56):
So when you've seen things lots and lots of times before,

(00:40:59):
you recognize it very quickly and you also work out

(00:41:03):
what doesn't fit the pattern and, and probably isn't a seizure.

(00:41:06):
So if you,

(00:41:07):
if you've only seen this once or twice,

(00:41:09):
then you're going to be struggled to be certain.

(00:41:11):
Whereas if you've seen it hundreds of times,

(00:41:13):
then of course you're going to be more confident in,

(00:41:15):
in,

(00:41:16):
in,

(00:41:16):
in what you're dealing with.

(00:41:17):
And if somebody has just had one episode,

(00:41:20):
it can be really difficult to know whether it was a seizure or not.

(00:41:25):
And, and just, just think about our job as a clinician, what,

(00:41:32):
There are two really important things.

(00:41:35):
One is getting an eyewitness.

(00:41:36):
So we need eyewitness descriptions of events.

(00:41:41):
And that's important because for most seizures, people lose awareness.

(00:41:47):
So they've got no knowledge of what happened.

(00:41:49):
So the only way to get a good story is to have an eyewitness.

(00:41:57):
The other thing is that seizures are stereotyped.

(00:41:59):
So while seizures can be really quite varied,

(00:42:02):
When an individual is having seizures,

(00:42:05):
their seizures will tend to be the same thing every time.

(00:42:08):
So clearly you can't make a judgment about things being stereotyped if you've only

(00:42:13):
heard a story of one thing.

(00:42:15):
But often you hear a story of somebody that's had a number of episodes.

(00:42:19):
And if the story is of stereotyped events,

(00:42:22):
then you're increasingly confident that they are seizures,

(00:42:24):
particularly if they are a pattern that is consistent with seizures.

(00:42:32):
But one of our jobs as a clinician is to work out what is a seizure and what's not

(00:42:36):
a seizure because there is that uncertainty.

(00:42:39):
So people go to see their GP,

(00:42:40):
they go to the emergency department,

(00:42:42):
somebody raises the question,

(00:42:43):
what was it a seizure?

(00:42:44):
And then they get referred to our services to answer that question.

(00:42:48):
And on average,

(00:42:49):
we need to see about three people in those clinics to see one person that has

(00:42:53):
actually had a seizure.

(00:42:55):
So there is a lot of uncertainty about that and it's our role as

(00:42:58):
clinicians in this space to kind of resolve the uncertainty and we will be able to

(00:43:03):
relatively confidently say it wasn't a seizure,

(00:43:06):
it was a seizure,

(00:43:07):
or I'm not sure,

(00:43:08):
let's wait and see.

(00:43:09):
And if there are more seizures,

(00:43:10):
we'll get a description and then we'll become more confident about it.

(00:43:14):
But the other thing to say, I guess, is that there's an error rate.

(00:43:19):
So clinicians get into trouble when they make a decision and they're not prepared

(00:43:23):
to reevaluate that decision.

(00:43:25):
And in this space, there is an error rate.

(00:43:27):
So

(00:43:28):
We need to continually reassess and consider, is the diagnosis right here?

(00:43:33):
Are we on the right track?

(00:43:34):
Are we doing the right things?

(00:43:40):
Yeah, it makes sense.

(00:43:42):
And good the fact that you can say,

(00:43:43):
yes,

(00:43:43):
basically is it you saying like,

(00:43:45):
yep,

(00:43:45):
we've got it wrong,

(00:43:45):
but that's all part of the process.

(00:43:48):
And some people aren't happy to say that, I guess.

(00:43:52):
Next,

(00:43:52):
could we maybe move on to the,

(00:43:54):
you were a plenary speaker at the British Inner Science Association.

(00:43:57):
festival.

(00:43:58):
Could you maybe give us a little bit of a taster or preview of what you're going to

(00:44:03):
be talking about there?

(00:44:05):
Yeah, and I think we've already talked on some of that already.

(00:44:08):
So I'm going to be talking about treatment choice in newly diagnosed epilepsy,

(00:44:13):
how we design trials or clinical trials or experiments to answer

(00:44:18):
those questions and talk about the evidence that we've got so far that drives

(00:44:22):
clinical practice around the world in terms of treatment choice in focal epilepsy

(00:44:26):
and treatment choice in generalized epilepsy and some of those trade-offs that we

(00:44:29):
might make about benefits and harm when we come to make decisions.

(00:44:37):
Yeah.

(00:44:38):
Now, that sounds super exciting.

(00:44:41):
I look forward to hearing you talk about it way more.

(00:44:45):
And yeah.

(00:44:47):
Could you just,

(00:44:48):
I guess,

(00:44:50):
because we're coming to the end,

(00:44:52):
would you have any final thoughts,

(00:44:53):
anything that we did not cover which you think we should cover?

(00:44:56):
I think we covered a lot of ground, actually.

(00:45:02):
I think what's really important to highlight,

(00:45:06):
again,

(00:45:07):
is that we need to be all working together to understand mechanisms so that we can

(00:45:15):
develop some treatments which

(00:45:19):
modify disease.

(00:45:20):
And one of the things we didn't talk about was the fact that about a third of

(00:45:26):
people with epilepsy,

(00:45:27):
we can't control the seizures.

(00:45:29):
I don't think we made that clear enough during the presentation actually on reflection.

(00:45:33):
So we say we've got a disease affecting 1% of the population,

(00:45:38):
which is a lot of people,

(00:45:39):
and a third of those people,

(00:45:40):
which is still a lot of people,

(00:45:42):
are having seizures that we can't control.

(00:45:44):
So we desperately need to understand how we stop that happening.

(00:45:49):
That's a lot.

(00:45:51):
So just 30%,

(00:45:52):
so like 0.3%,

(00:45:54):
3% of the population are just wandering around with uncontrolled seizures.

(00:45:58):
Yep.

(00:45:59):
That's a wild number.

(00:46:00):
Just put that in perspective.

(00:46:02):
Gosh, I don't even, it's growing so quickly.

(00:46:04):
But how many people are in the UK now?

(00:46:06):
Is it 70 million?

(00:46:08):
About 70 million, isn't it?

(00:46:09):
About 70 million.

(00:46:10):
So that's about 3 million,

(00:46:12):
maybe just under 2.5 million,

(00:46:15):
possibly wandering around with uncontrolled seizures.

(00:46:17):
Yeah, so it's less... No, no, no, no, no.

(00:46:20):
It's less 250,000.

(00:46:20):
250,000.

(00:46:20):
That was so embarrassingly off.

(00:46:21):
Sorry, 250,000.

(00:46:22):
I haven't got a coffee yet.

(00:46:23):
Please ignore.

(00:46:24):
250,000 people.

(00:46:24):
So I got past this morning, apparently, is it?

(00:46:26):
Don't let me do that again.

(00:46:29):
Yeah, we estimate there are about 600,000 people, just over 600,000 people in the UK with

(00:46:43):
with epilepsy at the moment.

(00:46:44):
So it'll be about 200,000 people, probably a bit more with uncontrolled seizures.

(00:46:49):
But it's a lot of people.

(00:46:51):
So that's a city size.

(00:46:53):
It's actually a size of a big city.

(00:46:55):
I was about to say, Glasgow is about 600,000 people.

(00:46:58):
So yeah, that's like the entire city of Glasgow having seizures.

(00:47:04):
Yeah,

(00:47:05):
sometimes when you put things in percentages,

(00:47:07):
they seem a lot smaller than what they actually are.

(00:47:09):
Do you think doctors should use big numbers instead?

(00:47:12):
Just to...

(00:47:13):
Yeah, it depends on the message you're trying to give.

(00:47:15):
I mean,

(00:47:15):
you don't want to scare the life out of people,

(00:47:18):
but absolutely right,

(00:47:20):
we need to get the message over.

(00:47:24):
And I think there's a lot of kind of neuroscience where,

(00:47:30):
looking at this from a clinical point of view,

(00:47:32):
where we haven't made the arguments well enough about getting the funding in.

(00:47:36):
I think dementia have done really well.

(00:47:39):
This recently, motor neurone disease are on trajectory.

(00:47:45):
But there's a lot of burden from neurological diseases.

(00:47:53):
we need to address.

(00:47:56):
And I guess this chimes in with the kind of brain health message.

(00:48:02):
And we realize that kind of cancer and other areas of kind of

(00:48:08):
done really well with their messaging,

(00:48:11):
but actually brain health and poor brain health is a much bigger problem for society,

(00:48:16):
particularly in a post-industrial society like ours where the capital is in the

(00:48:20):
brain health of our population.

(00:48:22):
So we need to be much better with our communication from a neuroscience point of

(00:48:27):
view and flying the flag for more resources into

(00:48:33):
not only research,

(00:48:35):
but also into the care that we provide for people with brain and neurological conditions.

(00:48:39):
Yeah, yeah.

(00:48:41):
So we need more salesmen.

(00:48:42):
That's what we need.

(00:48:43):
We need more marketing.

(00:48:44):
We need better marketing.

(00:48:51):
But we need to be more effective in the way that we come together and the way that

(00:48:54):
we do things as well,

(00:48:55):
don't we?

(00:48:56):
Of course,

(00:48:57):
the British Festival of Neuroscience is a great place for us all to come together

(00:49:00):
and discuss how we want to change the world.

(00:49:05):
Awesome.

(00:49:05):
I think that's a great note to end on.

(00:49:07):
So yeah, thank you, Tony, for coming on.

(00:49:11):
Thanks, Beth, again.

(00:49:14):
And do you have any final message for our listeners as well, Beth?

(00:49:18):
Get yourself to the British Neuroscience Association.

(00:49:20):
And if not, get yourself to all the public engagement events happening around Liverpool.

(00:49:24):
There are tens of events going on.

(00:49:27):
If you go on the BNA, bring your own brain, then you can have a little look.

(00:49:31):
So we've got something for everyone.

(00:49:33):
Of course.

(00:49:33):
And like we said at the start, the Brain Charity keeps doing things throughout the year.

(00:49:37):
So there's events and things going on throughout the year.

(00:49:41):
And we're going to keep everything up online as well,

(00:49:43):
too,

(00:49:44):
so that people who can't make it also have access to as much information as we can give.

(00:49:49):
So awesome.

(00:49:50):
Take care, everybody.

(00:49:51):
And yeah, thank you.

(00:49:52):
Bye.