Dr Francine Chassoux graduated from the University of Paris V, Faculty of Medicine Cochin Port-Royal, Paris, France.  Certified in Neurology in 1989. Neurological training: Pitié-Salpétrière Hospital (Paris) 1985-89.
Epileptological training at Sainte-Anne Hospital with Jean Bancaud and Jean Talairach in 1983 and between 1989 and 1993, focusing on pre-operative evaluation of patients with drug-resistant partial epilepsy, based on electro-clinical and anatomical correlations and intracranial recordings (SEEG).
Collaborator with the Nuclear Medicine Department (SHFJ-CEA, Orsay, France) since 1999.
Main publications and research topics related to focal cortical dysplasias and other malformations of cortical development, hippocampal sclerosis and epilepsy surgery; correlations between invasive techniques (SEEG, Wada test) and new imaging techniques (functional MRI, PET-scan, PET-MR).

Focal cortical dysplasias (FCD) represent a group of developmental brain lesions found in cortical specimen of patients operated on for intractable focal epilepsy.  FCD type 2, characterised by dysmorphic cytomegalic neurons, has an intrinsic epileptogenicity demonstrated by intracranial recordings, especially by SEEG.
Intralesional electrical pattern consists in continuous rhythmic or pseudo-rhythmic spikes, which frequency varies between 0.5 to 10 Hz (usually 1-3 Hz) without identifiable background activity, or pseudo-periodic bursts of spikes interrupted by suppression of activity for few seconds. These rhythmic spike discharges (RSD) have proven to be a marker of the dysplastic tissue. RSD are not suppressed by Diazepam IV injection whereas fast rhythms are recorded on non-dysplastic areas. They are recorded on areas larger than FCD during NREM sleep and after ictal discharges. RSD can be recorded on scalp EEG in 30-50% of the cases during waking, and up to 65% during sleep.
Ictal onset pattern is typically characterized by a brief acceleration of spikes preceding a low voltage fast discharge. In the post-ictal phase, a focal depression combined with an early reappearance of rhythmic spikes corresponds to the epileptogenic zone (EZ) and the FCD localisation. Low frequency stimulation (1Hz) can elicit seizures when performed within the FCD, consistent with a low epileptogenic threshold. All these interictal and ictal neurophysiological criteria obtained with SEEG allow to delineate accurately the dysplastic tissue and the EZ.
On scalp EEG, the typical interictal and ictal pattern can be observed similarly to intracranial recordings in about half of the cases. However, it can be missed in some locations, especially in mesial extratemporal areas and in the insula.
In this presentation, we will discuss the correspondence between intracranial and scalp EEG and the role of sleep recordings for FCD localisation. Overall, we will interpret the scalp EEG features in light of neurophysiological information provided by SEEG in FCD type 2. The final goal of this comparison is to recognize the typical FCD signature on scalp EEG without invasive monitoring, whenever possible.