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10th European Congress on Epileptology

Posted in Courses & Conferences on 10th Dec 2012

Conference details: 30 September – 4 October 2012, ExCel International Conference Centre, London, UK.
Reviewed by:  Dr Mark Manford, Consultant Neurologist, Addenbrooke’s Hospital, Cambridge, UK.

I walked into the Excel Arena, amid thousands of smiling expectant faces, the familiar five rings and a friendly jostling for places – Oh no! Sorry, that was the Olympics. But there was the same warmth of hospitality even for 3500 European Congress of Epilepsy delegates, even if they did not even fill one small corner of this vast building. Simon Shorvon and Phil Smith, the British contingent leading the organising committee did what the Brits do best. They created a conference that was scientifically interesting, educational, well-organised and tinged with quirky eccentricity, starting with a video celebrating London including the brain surgery sketch from Monty Python’s Flying Circus. The theme continued through the conference with a quiz loosely based on University Challenge, with the winner’s trophy being taken by Ireland.

There were two major general interest lectures. The first, given by mathematician Timothy Gowers, grandson of Gowers of neurological fame, concerned the problems with the distribution of knowledge in modern science. He espoused the view that the age of the subscription journal was passing. He argued that journals act as a distorting filter and a brake on scientific publication and that science should be published online and reviewed online, which would allow a trail of review and arguably improve the peer review process. He argued that the journals had a vested interest in preventing this process which they exercised. Sir Peter Mansfield, to whom every neurologist should genuflect each morning on their way to work, gave a talk on some aspects of the development of MRI. As a physicist, I was impressed with his comprehensive knowledge of anatomy. I should have liked to hear a little more of his personal story, but it was enough to be in the presence of the great man himself.

However hard I tried to escape educating myself about epilepsy, there were inevitable moments when guilt struck and I found myself, for better or for worse, updating my knowledge.

A few years ago I was rather pessimistic about the future of epilepsy treatment, with an endless series of drugs that seemed to me to be a variation on a theme that had not really changed since the introduction of phenytoin in 1937. However, things are moving and with deeper understanding of the mechanisms of epileptogenesis, we are slowly but steadily moving towards treatments which address these mechanisms. Previous experimental models have required most of the treatments to be given either before the insult triggering epilepsy, or very soon afterwards. But most patients present with seizures and we may not necessarily know when the trigger occurred. But now we are starting to see some mechanisms which will act later in the process.  Histones which upregulate NSRF will block some of the effects of epileptogenesis, even if given after the insult which triggered seizures and similarly neuropeptide Y seems to have a powerful effect. Professor Dimitri Kullman described how the potassium channel Kv1.1 can be upregulated when introduced focally into the cerebral cortex by modified lentivirus and this will completely suppress seizures even after seizures have started. Of course, making every patient with refractory epilepsy have a minor neurosurgical procedure will cause eyebrows to be raised in the Treasury. However, Stephen Gray described how the adeno-associated virus, a tiny nonpathogenic human virus, enters the brain across the blood brain barrier.  Since seizures disrupt the blood brain barrier, there is the potential to concentrate the virus in the region of epilepsy activity. By repeated cycles of intravenous virus injection then purification from the brain, his group has selected a virus that when injected intravenously will appear in high concentrations in the region of seizure activity, with relatively little elsewhere. The potential of combining these techniques to introduce a gene by intravenous injection, which modulates epilepsy activity and is concentrated in the appropriate brain is a very exciting prospect.

We conventionally describe epilepsies as either focal or generalised, but the term generalised is really descriptive of a clinical syndrome rather than the basic mechanism. Indeed some patients with so-called absences of idiopathic generalised epilepsy have much greater alteration of awareness than others and functional neuroimaging in these patients shows that the degree of alteration of awareness correlates with the extent of cortical involvement in the process. We know that in Idiopathic Generalised Epilepsy, there is an interaction between the cerebral cortex and the thalamus, but which is the chicken and which the egg in the process. The conclusion seems to depend on the investigative technique used and remains a cause of debate.

There are some practical advances in the treatment of status epilepticus which are grounded in new revelations of the underlying science. It has been known for some time that GABA is depleted early during status epilepticus and that this explains the failure of the response to benzodiazepines, which occurs after about an hour of continuous seizure activity. But new research shows that drugs that regulate calcium entry by changing potassium channel properties such as flurtipine or retigabine can prevent the habituation to the action of benzodiazepines. As well as being of mechanistic interest, this has potential practical relevance, since retigabine is already available. The new drug perampanel which is the first drug to block glutamate transmission and not be unacceptably toxic, may also have a role in this regard. One thing is clear, that other than for benzodiazepines, clinical studies of drugs in status epilepticus are inadequate. I have previously written about a recent study demonstrating that the ease of use of intramuscular midazolam means that its effect is as rapid as more complex to administer intravenous preparations and it should be thought of as a first-line drug. In the UK, phenytoin remains sacrosanct as first-line treatment after benzodiazepines, despite the fact that it is clearly a nasty drug to give. Valproate, levetiracetam and lacosamide are effective and widely used but we need studies see if they work better, although they are generally cleaner. Other treatments for the desperate include the anaesthetic ketamine, which paradoxically also has some pro-convulsive effects and the ketogenic diet, which is relatively easy to administer in the intensive care setting.

As well as these highlights, there were large numbers of smaller studies discussing surgical treatment, imaging techniques, the inevitable league of new genes, which I shall never remember, and a session on infective and inflammatory causes of epilepsy.  There were also sessions on comorbidities of epilepsy and a debate on whether it is more important to treat them than the epilepsy itself. The result predictably. is that one should try to do both, without jeopardising the other.

Overall, there is the feeling that epilepsy is starting to emerge from the 20th century into the 21st with new vistas on basic mechanisms and treatment and a broader view of the importance of other aspects of quality of life than simply seizure number.

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