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Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in patients with refractory epilepsy. The pathophysiology of SUDEP is unknown. Postictal phenomena such as postconvulsive immobility (PI), postictal generalized electroencephalography (EEG) suppression (PGES), arousal deficits, cardiac arrhythmias, central apneas, and obstructive apneas due to laryngospasms have been suggested to contribute to SUDEP. We present, to our knowledge, the first case of a near-SUDEP event in a patient undergoing intracranial, stereotactic EEG (sEEG) monitoring. This case spotlights potential mediators of SUDEP, most notably the striking PGES and postictal apnea. The nature of the sEEG investigation illustrates the extent of cortical and subcortical postictal EEG suppression and showcases a transient return of cerebral activity likely to be missed on scalp-EEG recording. Critically, this case emphasizes the importance of continuous cardiorespiratory monitoring and underscores the importance of postictal arousal as a pathophysiological mechanism in SUDEP.

Occipital epilepsy is the least common among surgical series because: (1) the location makes it hard to asses by EEG; (2) the seizure semiology often reflects propagation; and (3) surgery entails a high risk of neurological deficits. In children, subjective symptoms are harder to assess, adding to the difficulty of a proper diagnosis. We aimed to determine electroclinical characteristics of occipital lobe epilepsy in a paediatric population by reviewing 20 children between one and 16 years, who had undergone intracranial recordings with depth electrodes. Eight patients had pure occipital epilepsies and 12 had "occipital plus" epilepsies. We identified four different seizure spreading patterns: (1) pure occipital (40%) with oculomotor symptoms; (2) temporal (30%) with hypomotor behaviour and automatisms; (3) frontal (20%) with movements of the limbs; and (4) spasms (10%). Two thirds of the children above 11 years reported visual aura, but this was probably underestimated in younger children as some seizures began with non-specific motion arrest. Automatisms were only observed when the lateral temporal lobe was involved. Patients with a pure occipital form had a seizure onset zone strictly in the occipital lobe. Lingual and cuneus gyri were the most epileptogenic structures. Scalp EEG showed diffuse EEG abnormalities in two thirds of the patients and 25% of these led to false lateralization of the SOZ. Although MRI lesions were always visible, imaging and scalp EEG could be misleading and often not sufficient to guide surgery. After surgery, 68% of the patients were classified as Engel Class I, and surgical outcome was even better for patients in whom the supracalcarine area was affected, with 87.5% reaching seizure freedom. Seizure spread patterns in occipital epilepsy are similar in paediatric and adult populations, even though it is often impossible to obtain subjective symptoms in children. Postsurgical outcome is better than in adults, especially in patients in whom the supracalcarine area is affected.

Presurgical monitoring with intracerebral electrodes in patients with drug-resistant focal epilepsy represents a standard invasive procedure to localize the sites of seizures origin, defined as the epileptogenic zone (EZ). During presurgical evaluation, intracerebral single-pulse electrical stimulation (SPES) is performed to define the boundaries of eloquent areas and to evoke seizure- associated symptoms. Extensive intracranial exploration and stimulation generate a large dataset on brain connectivity that can be used to improve EZ detection and to understand the organization of the human epileptic brain. We developed a protocol to analyse field responses evoked by intra- cranial stimulation. Intracerebral recordings were performed with 105-162 recording sites posi- tioned in fronto-temporal regions in 12 patients with pharmacoresistant focal epilepsy. Recording sites were used for bipolar SPES at 1 Hz. Reproducible early and late phases (

Communication between regions of the brain, both normal interactions and pathologic traffic, is manifest by electromagnetic activity. Magnetoencephalography (MEG)--with high resolution in both the temporal and spatial domains, as well as a comprehensive, whole-head view--offers ready noninvasive access to this ongoing communication. The waveforms are amenable to a variety of signal processing techniques that can elucidate connectivity between brain areas. In conjunction with the other modalities acquired during the evaluation of a patient with epilepsy, MEG can provide information that is important for determining therapeutic strategy.

Summary: Pyramidal cell densities in various regions of the anterior and posterior hippocampal formation were measured from en bloc temporal lobe resections and compared with presurgical stereoelectroencephalography (SEEG) data derived from depth electrodes in 12 patients with temporal lobe epilepsy. These data were compared with cell densities observed in four nonepileptic control patients. Patients who consistently exhibited anterior focal changes in the SEEG accompanying onset of ictus had cell densities that were selectively reduced in the anterior hippocampal formation but normal with respect to controls in the posterior hippocampal formation. Patients who exhibited more regional changes in the SEEG at onset of ictus had reduced cell densities in both the anterior and posterior hippocampal formation. Patients who exhibited focal spike activity in the anterior hippocampal formation as their predominant interictal SEEG pattern also had selectively reduced cell densities in the anterior hippocampal formation, while patients with widespread spiking throughout the hippocampal formation had reduced cell densities both anteriorly and posteriorly. These data support the concept that epileptogen-esis occurs in or near those areas of epileptic hippocampus that are most damaged. Hippocampal sclerosis must be viewed as related to adjacent hyperexcitable or epileptogenic neurons and not solely as a passive result of repeated anoxia or ischemia. RESUMEN En 12 pacientes con epilepsia del lobulo temporal se midieron las densidades de las celulas piramidales en varias regiones del hipocampo anterior y posterior, obtenidas mediante resecciones en bloque del lobulo temporal, y se compararon con la information de los SEEG prequirurgicos registrados con electrodos profundos. Estos datos se compararon con las densidades celulares observadas en 4 enfermos control, no epilepticos. Los enfermos que le modo persistente mostraron cambios focales anteriores en el SEEG, simultaneos con el comienzo los ataques, mostraron densidades celulares que estaban reducidas selecti-vamente en la formation hipocampica anterior pero que eran normales con respecto a los controles en la formacion hipocampica posterior. Los enfermos que mostraron mas cambios regionales en el SEEG durante el comienzo del ataque mostraron una reduction de la densidad celular en ambas formaciones hi-pocampicas anterior y posterior. Los enfermos que mostraron una actividad de puntas en la formacion hipocampica anterior como patron predominante del SEEG interictal, tambien mostraron selectivamente densidades celulares reducidas en la formacion hipocampica anterior mientras que los pacientes con puntas diseminadas por la formacion hipocampica tenian densidades celulares reducidas tanto en zonas anteriores como post-eriores. Estos datos apoyan el concepto de que la epileptogen-esis ocurre en aquellas areas del hipocampo epileptico que esta mas lesionado o en su vecindad. La esclerosis hipocampica debe ser considerada en relacion con neuronas adyacentes epilepto-genicas o hiperexcitables y no solamente como un resultado pa-sivo de isquemia o anoxia repetidas. ZUSAMMENFASSUNG Die Dichte der Pyramidenzellen wurde in verschiedenen Ge-genden des vorderen und hinteren Hippokampus gemessen. Dazu diente en bloc resezierter Temporallappen. Die Ergebnisse wurden mit SEEG-Daten verglichen, die vor der Operation durch Tiefenelektrodenableitungen bei 12 Patienten mith Tem-porallappenepilepsie gewonnen wurden. Die Ergebnisse wurden mit der Zelldichte verglichen, die bei 4 nicht-epileptischen Kon-trollpatienten ermittelt wurden. Patienten, die bestandig fokale Veranderungen im SEEG der vorderen Gegend zeigten, die den Anfallsbeginn begleiteten, zeigten eine selektive reduzierte Zelldichte in der vorderen Hippokampusformation; gegenuber Kontrollen war die hintere Hippokampusformation normal. Bei Patienten, die eher regionale Veranderungen beim Anfallsbeginn im SEEG zeigten, fand man sowohl in der vorderen wie in der hinteren Hippokampusformation eine reduzierte Zelldichte. Bei Patienten, die als ihr vorherrschendes interiktales SEEG-Muster eine fokale spike-Aktivitat in der vorderen Hippokapusformation boten, fand man auch eine selektiv reduzierte Zelldichte in der vorderen Hippokampusformation. Bei Patienten mit ausgedehn-teren spikes im Gebiet der gesamten Hippokampusformation war die Zelldichte sowohl in den vorderen wie in den hinteren Abschnitten reduziert. Diese Ergebnisse unterstutzen das Konzept, das die epileptische Erregung ihren Ursprung in oder in der Nahe der am starksten geschadigten Gegenden des Hippb-kampus hat. Eine Hippokampussklerose mus zur Hyperexcita-bilitat oder Epileptogenitat benachbarter Neurone in Beziehung gesetze werden; sie stellte nicht lediglich das Ergebnis einer wiederholten Anoxie oder Ischamie dar.

A patient was studied who had posttraumatic epilepsy with adversive, psychomotor, and grand mal seizures. During tele-EEG recording from depth electrodes, 4 psychomotor seizures were accompanied by discharge originating in the frontal lobe. The patient sometimes could recall his behavior and believed it to be voluntary. Amnesia was more apt to be total after the seizure than during it.