Migraine often co-occurs with epilepsy, displaying a bi-directional association. Although the neurological symptoms associated with attacks of migraine are quite distinct from those of attacks of epilepsy, in both cases hyperexcitability appears to underlie disease susceptibility. Also, in both cases attacks may be provoked by trigger factors such as bright light, hyperventilation or stress. It is intriguing that genes associated with migraine are also related to epilepsy, whereby the pathogenic mutations are often related to dysfunction of ion transport. Familial hemiplegic migraine type 1 (FHM1) mutant mice that carry a missense mutation in the Cacna1a gene, which had been previously identified in patients, display enhanced glutamatergic neuronal excitability and increased susceptibility to cortical spreading depression, the most likely mechanism of the migraine aura.

In my talk, I will show findings from functional studies on CSD and seizure activity in FHM1 migraine mice that underscore the overlap in mechanisms between migraine and epilepsy. Longitudinal in vivo DC-EEG recordings and visual evoked potential studies in freely behaving and anesthetized mice, paralleled by EEG studies migraine patients, are used to identify predictive biomarkers for attacks. Recent implementation of optogenetic technology allowed us to induce CSD, and investigate effects of cortical excitability changes in relation to migraine and epilepsy, in a non-invasive manner in freely behaving mice. Additional development of biosensors for monitoring brain K+ and pH changes in relation to CSD and seizures help to provide insight in the role of metabolic changes related to neuronal excitability and attacks.

Wednesday 17 June 2015, 16:30 - 17:30 h

Building Carré - room CR 3.022