By Richard

I am a clinician/scientist, interested in the dynamics of large-scale neuronal networks during human development. Currently I am working with Karl Friston and Torsten Baldeweg on experimentally deriving an effective connectivity account of developmental changes of sensory processing using dynamic causal modeling on EEG. I am combining this work with investigations into specific epilepsy patient cohorts and computational models, probing the links between neuronal pathophysiology and network-wide abnormalities.

New England vs Montreal: Data Sharing in 2016

Research parasites are all the rage these days.

This last week, two stories about data sharing caught my eyes. And even thought they have emerged from just about 350 miles apart, the attitudes involved could not be further from each other.

The first story that caught my eye was the editors of the New England Journal of Medicine summarising what they think about data sharing. They talk about it like self-assured conscientious capitalists describe their idea of communism:

“The aerial view of the concept of data sharing is beautiful. […] The moral imperative to honor their collective sacrifice is the trump card that takes this trick. However, many of us who have actually conducted clinical research […] have concerns about the details.”

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It’s not what it looks like: High Frequency Oscillations

Following on from the last post on baseline shifts, this is the second post on a few things we don’t normally consider when talking about standard EEG measurements. I had the idea for this one after a few excellent talks by Liset Menendez de la Prida at ISWP7 earlier this year.

Fast and furious (or is it)

Fast stuff on the EEG is difficult to see for a number of reasons: i) We usually filter raw EEG signal to make it look neater and often exclude high-gamma range signal. ii) The signal we measure on the scalp itself is already attenuated by passing through different tissues, making fast activity appear less sharp and prominent. This is true even for ECOG when compared to direct LFP recordings (which is becoming more relevant now that microelectrodes are being used more and more in patients with epilepsy). iii) Higher frequencies have a lower power – usually fast fluctuations are a lot smaller than bigger shifts on the EEG and seem to pale in comparison, when visually analysing the EEG.

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It’s not what it looks like: Baseline Shifts

Cook et al. 2013
The implantable device from Cook et al. 2013

I’ve just come back from the fantastic IWSP7: Epilepsy Mechanisms, Prediction and Control conference in Melbourne. Having apparently outgrown the initial meetings’ focus on seizure prediction, this year covered all aspects from computational models, intracranial devices, to imaging in epilepsy. For those who don’t know – Melbourne is a great place for such a conference, since Mark Cook and colleagues have managed a couple of years ago to pull off a clinical trial of implantable intracranial recording devices designed for long-term ambulatory recordings, in addition to the potential for responsive neuromodulation. The set-up can be seen on the right (an image the conference conveners seemed to love), and was a first in the world of seizure prediction. [1]

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A Wolf in Sheep’s Clothing


I spent the day yesterday in clinic, seeing a few fantastic kids, all with a rare epilepsy syndrome that is known to cause a lot of cognitive and learning problems. This is exactly what I worry about most in childhood epilepsies – the effect of the seizures and the epilepsy on learning and development.

So as odd as it may sound, making a diagnosis of one of the more ‘benign’ epilepsy syndromes can be reassuring for me as a clinician. If I have a child with typical childhood absence epilepsy in clinic, I know that there is a good chance we will get the seizures under control, and that after puberty many patients will become seizure free. Yet ‘benign’ in medicine is always a double edged sword: Whilst all the above may be true, it turns out childhood absence epilepsy in some ways is not a harmless condition without any lasting effects. 
It’s Purple Day – aka Epilepsy Awareness Day. So yes – let’s get talking about Epilepsy! It’s great to see so many people, differently affected by epilepsy join the discussion on twitter and give a public face to the condition.

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Moving on from the Seizure Reservoir

One of the most challenging and puzzling issues for both patients and clinicians is the apparent unpredictability of seizures. Beyond a few general statements of things that increase your chance of having a seizure, it is difficult (impossible) to pinpoint, why a seizure happens at exactly the time that it does. The issue becomes even more intriguing when there is not even a focal ‘epileptogenic’ zone – as for children with idiopathic generalised epilepsy, whose brains will look completely normal on brain scans, but will suffer apparently unprovoked seizures again and again. 

Richardson (2011)
Drawing from Richardson MP (2011) J Progr Biophys Mol Biol, 105:5-13, originally from Lennox (1941) Science and Seizures, New Light on epilepsy and Migraine. Harper Bros, NY

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Let’s talk about death

When making a new diagnosis of epilepsy, I often encounter fear – I speak to parents who have seen their child having a seizure in front of them, becoming unresponsive and shaking uncontrollably. And from their faces I can see that they were worried about one thing above all: Is my child going to die?

In the majority of cases the answer is clearly no. Seizures themselves very rarely cause mortality, and other than the rare sudden unexplained death in epilepsy (SUDEP), or patients with significant neurodevelopmental disabilities and life-limiting comorbidities, we rarely see deaths in our paediatric patients with epilepsy.

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Is it, or isn’t it? EFHC1 mutations in epilepsy

Back at the European Neurological Society I went to a session on “What every young neurologist should know”. And apart from a few general career comments, it was clear that the crucial skill a 21st century neurologist needs to learn, according to the organisers, was a thorough appreciation of genetics. 

And we can see why. Modern genetic investigations have completely revolutionised neurological subspecialties: More than 40 single-gene causes of movement disorders have been described, many of which are now tested for routinely in the clinical setting and can transform the diagnosis and management of affected patients. 
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