Altered structure and function of astrocytes following status epilepticus.

Temporal lobe epilepsy (TLE) is a devastating seizure disorder that is often caused by status epilepticus (SE). Temporal lobe epilepsy can be very difficult to control with currently available antiseizure drugs, and there are currently no disease-modifying therapies that can prevent the development of TLE in those patients who are at risk. While the functional changes that occur in neurons following SE and leading to TLE have been well studied, only recently has research attention turned to the role in epileptogenesis of astrocytes, the other major cell type of the brain. Given that epilepsy is a neural circuit disorder, innovative ways to evaluate the contributions that both neurons and astrocytes make to aberrant circuit activity will be critical for the understanding of the emergent network properties that result in seizures. Recently described approaches using genetically encoded calcium-indicating proteins can be used to image dynamic calcium transients, a marker of activity in both neurons and glial cells. It is anticipated that this work will lead to novel insights into the process of epileptogenesis at the network level and may identify disease-modifying therapeutic targets that have been missed because of a largely neurocentric view of seizure generation following SE. This article is part of a Special Issue entitled "Status Epilepticus".

Ruptured Persistent Trigeminal Artery Causing Direct Cavernous Sinus Fistula Treated with Pipeline Embolization and Minimal Coiling.

BACKGROUND: Rupture of a persistent trigeminal artery associated with development of a cavernous sinus fistula in a traumatic setting is rare. These arteries are typically treated with coil embolization of the cavernous sinus. CASE DESCRIPTION: We present the case of a 42-year-old woman who developed a direct cavernous carotid fistula after a motor vehicle accident. Angiographic imaging revealed a rupture point of a persistent trigeminal artery as it connected with the cavernous segment of the internal carotid artery, causing a cavernous sinus fistula. Coiling of the cavernous sinus was abandoned after placement of 1 coil because of coil herniation into the internal carotid artery. A Pipeline embolization device was placed to oppose the coil against the intima and keep the lumen open. The combination of coil embolization and flow diversion acutely decreased the fistulous flow. Surprisingly, an angiographic follow-up at 6 months showed complete fistula occlusion despite placement of only 1 coil into the cavernous sinus. CONCLUSIONS: We report a rare case where undercoiling of the cavernous sinus occluded a cavernous sinus fistula because of the adjunct use of a Pipeline embolization device in the presence of a traumatic rupture of a persistent trigeminal artery.