MICHAEL-Prize – Award Winner 1999

The Michael-Prize 1999

The 1999 Michael-Prize was awarded to

 

Klinik für Epileptologie, University Bonn, Germany

Bonn (Germany)

 

Dr. Heinz Beck

Dipartimento di Neurofisiologia, Istituto Nazionale Neurologico, Milano, Italy

Milan (Italy)

 

Dr. Marco de Curtis

Department of Neurology, University of California, School of Medicine, Los Angeles, USA

Los Angeles (USA)

 

Prof. Dr. Istvan Mody

The Michael Prize 1997/98 is granted - in alphabetical order - to:

Dr. Heinz Beck, Klinik für Epileptologie, University Bonn, Germany,
Dr. Marco de Curtis, Dipartimento di Neurofisiologia, Istituto Nazionale Neurologico, Milano, Italy,
Dr. Istvan Mody, Department of Neurology, University of California, School of Medicine, Los Angeles, USA

By that the merits of these scientists in the field of experimental and clinical epileptology are honoured.

As a whole, the scientific developments initiated and the results elaborated by the honoured scientists represent an outstanding progress in epileptology. They will be trend-setting in the next years.

Laudatio

The scientific interest of Dr. Beck is focussed on function and regulation of voltage dependent calcium channels in human temporal lobe epilepsy. The data obtained in humans are compared with those from epilepsy models in animals. Electrophysiological studies are combined with molecular ones aiming to further understand the mechanisms leading to the initiation of seizures in temporal lobe epilepsies.

 

In the center of scientific interest of Dr. de Curtis are cellular mechanisms underlying interictal spikes including the role played by gap junctions and their modulations by activity dependent pH-changes, propagation of epileptiform activity, induction of secondary epileptogenesis, and, last not least, interactions of neuronal activity and cerebrovascular activity.

 

The scientific effort of Dr. Mody is primarily devoted to the role of synaptic inhibition in epileptogenesis. Using a combined anatomical and electrophysiological approach, it was demonstrated, for the first time, that the number of synaptic GABA A receptors is significantly increased in an experimental model of temporal lobe epilepsy. This finding is in favour of a much more complex scenario of epileptogenesis than previously thought from animal studies with blockers of inhibition. There are already some strong hints about how neuronal synchrony can be generated by more GABA A receptors at synapses.