Embolization of a cavernous carotid fistula through the vein of Labbé: a new alternative transvenous access route.

Endovascular treatment of carotid cavernous fistulas (CCFs) via a transvenous approach is standard, but in rare cases this approach is challenging due to absence or thrombosis of the commonly used venous routes. A 61-year-old woman presented with a symptomatic CCF with all but one of the venous access routes to the CCF thrombosed, leaving an engorged superficial middle cerebral vein (SMCV) as the only venous outflow from the cavernous sinus. Access to the CCF was made possible after careful navigation of the sigmoid sinus, the vein of Labbé and the SMCV, bypassing the need for surgical access to the SMCV or for a direct transorbital puncture.

Embolization of a cavernous carotid fistula through the vein of Labbé: a new alternative transvenous access route.

Endovascular treatment of carotid cavernous fistulas (CCFs) via a transvenous approach is standard, but in rare cases this approach is challenging due to absence or thrombosis of the commonly used venous routes. A 61-year-old woman presented with a symptomatic CCF with all but one of the venous access routes to the CCF thrombosed, leaving an engorged superficial middle cerebral vein (SMCV) as the only venous outflow from the cavernous sinus. Access to the CCF was made possible after careful navigation of the sigmoid sinus, the vein of Labbé and the SMCV, bypassing the need for surgical access to the SMCV or for a direct transorbital puncture.

Mechanical Thrombectomy in Wake-Up Strokes: A Case Series Using Alberta Stroke Program Early CT Score (ASPECTS) for Patient Selection.

Background: There is lack of published studies on mechanical thrombectomy with stent retrievers for wake-up stroke (WUS).

Objective: To report the outcomes of WUS patients with large vessel occlusions, selected for intervention based on Alberta Stroke Program Early CT Score (ASPECTS) and treated with stent retrievers or primary aspiration thrombectomy.

Methods: Data were collected retrospectively for each consecutive WUS patient undergoing mechanical thrombectomy with a stent retriever or primary aspiration catheter between February 2015 and September 2016.

Natural history, current concepts, classification, factors impacting endovascular therapy, and pathophysiology of cerebral and spinal dural arteriovenous fistulas.

Dural arteriovenous fistulas (DAVFs) may occur anywhere there is a dural or meningeal covering around the brain or spinal cord. Clinical manifestations are mostly related to venous hypertension, and may be protean, acute or chronic, ranging from minor to severe, from non-disabling tinnitus to focal neurological deficits, seizures, hydrocephalus, psychiatric disturbances, and developmental delay in pediatric patients. Although low-grade lesions may have a benign course and spontaneous involution may occasionally occur (i.

Brain temperature changes during selective cooling with endovascular intracarotid cold saline infusion: simulation using human data fitted with an integrated mathematical model.

The feasibility of rapid cerebral hypothermia induction in humans with intracarotid cold saline infusion (ICSI) was investigated using a hybrid approach of jugular venous bulb temperature (JVBT) sampling and mathematical modeling of transient and steady state brain temperature distribution. This study utilized both forward mathematical modeling, in which brain temperatures were predicted based on input saline temperatures, and inverse modeling, where brain temperatures were inferred based on JVBT. Changes in ipsilateral anterior circulation territory temperature (IACT) were estimated in eight patients as a result of 10 min of a cold saline infusion of 33 ml/min.

Brain cooling maintenance with cooling cap following induction with intracarotid cold saline infusion: a quantitative model.

Intracarotid cold saline infusion (ICSI) is potentially much faster than whole-body cooling and more effective than cooling caps in inducing therapeutic brain cooling. One drawback of ICSI is hemodilution and volume loading. We hypothesized that cooling caps could enhance brain cooling with ICSI and minimize hemodilution and volume loading.

Local control of temperature in a theoretical human model of selective brain cooling.

A method of feedback control of local brain temperature during therapeutic intracarotid cold saline infusion is presented and tested on a theoretical cerebral heat transfer model based on the Pennes bioheat equation. In this temperature control method, the infusion rate of cold saline is varied based on the rate of temperature change, and the deviation of temperature to a target, within a voxel in the treated region of brain. This control method is tested in cases where the head is exposed to ambient room temperature, and where the head is packed in ice.

The role of intracarotid cold saline infusion on a theoretical brain model incorporating the circle of willis and cerebral venous return.

This study describes a theoretical model of brain cooling by intracarotid cold saline infusion which takes into account redistribution of cold perfusate through the circle of Willis (CoW) and cold venous return (VR) from the head. This model is developed in spherical coordinates on a four tissue layer hemispherical geometrical configuration. Temperature evolution is modeled according to the Pennes bioheat transfer equation.

Heat transfer model of hyporthermic intracarotid infusion of cold saline for stroke therapy.

A 3-dimensional hemispheric computational brain model is developed to simulate infusion of cold saline in the carotid arteries in terms of brain cooling for stroke therapy. The model is based on the Pennes bioheat equation, with four tissue layers: white matter, gray matter, skull, and scalp. The stroke lesion is simulated by reducing blood flow to a selected volume of the brain by a factor of one-third, and brain metabolism by 50%.

Integration of jugular venous return and circle of Willis in a theoretical human model of selective brain cooling.

A three-dimensional mathematical model was developed to examine the induction of selective brain cooling (SBC) in the human brain by intracarotid cold (2.8 degrees C) saline infusion (ICSI) at 30 ml/min. The Pennes bioheat equation was used to propagate brain temperature.

Reperfusion injury following cerebral ischemia: pathophysiology, MR imaging, and potential therapies.

Introduction: Restoration of blood flow following ischemic stroke can be achieved by means of thrombolysis or mechanical recanalization. However, for some patients, reperfusion may exacerbate the injury initially caused by ischemia, producing a so-called "cerebral reperfusion injury". Multiple pathological processes are involved in this injury, including leukocyte infiltration, platelet and complement activation, postischemic hyperperfusion, and breakdown of the blood-brain barrier.

A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain.

A three-dimensional mathematical model was developed to examine the transient and steady-state temperature distribution in the human brain during selective brain cooling (SBC) by unilateral intracarotid freezing-cold saline infusion. To determine the combined effect of hemodilution and hypothermia from the cold saline infusion, data from studies investigating the effect of these two parameters on cerebral blood flow (CBF) were pooled, and an analytic expression describing the combined effect of the two factors was derived. The Pennes bioheat equation used the thermal properties of the different cranial layers and the effect of cold saline infusion on CBF to propagate the evolution of brain temperature.

Neuroprotection for ischemic stroke using hypothermia.

The development of animal models of acute stroke has allowed the evaluation of mild and moderate hypothermia as a therapeutic modality in this clinical setting. Studies have demonstrated that animals subjected to hypothermia up to 3 hours after the primary central nervous system insult have reduced mortality and neuronal injury, and improved neurological outcome. These results warranted the evaluation of hypothermia in clinical trials.

Extracellular Na+ removal attenuates rundown of the epithelial Na+-channel (ENaC) by reducing the rate of channel retrieval.

Regulation of the epithelial sodium channel (ENaC) is important for the long-term control of arterial blood pressure as evidenced by gain of function mutations of ENaC causing Liddle's syndrome, a rare form of hereditary arterial hypertension. In Xenopus laevis oocytes expressing ENaC a spontaneous decline of ENaC currents over time, so-called rundown, is commonly observed. Mechanisms involved in rundown may be physiologically relevant and may be related to feedback regulation of ENaC by intra- or extracellular Na+.

cAMP-dependent activation of CFTR inhibits the epithelial sodium channel (ENaC) without affecting its surface expression.

The cystic fibrosis transmembrane conductance regulator (CFTR) is thought to modulate epithelial sodium channel (ENaC) function in various preparations. However, the molecular nature and (patho-)physiological significance of the CFTR/ENaC interaction is still unclear and may vary in different tissues. Co-expression experiments in Xenopus laevis oocytes are a popular approach to investigate a possible functional interaction of CFTR and ENaC but have revealed controversial results.

The gamma-subunit of ENaC is more important for channel surface expression than the beta-subunit.

The amiloride-sensitive epithelial sodium channel (ENaC) plays a critical role in fluid and electrolyte homeostasis and is composed of three homologous subunits: alpha, beta, and gamma. Only heteromultimeric channels made of alphabetagammaENaC are efficiently expressed at the cell surface, resulting in maximally amiloride-sensitive currents. To study the relative importance of various regions of the beta- and gamma-subunits for the expression of functional ENaC channels at the cell surface, we constructed hemagglutinin (HA)-tagged beta-gamma-chimeric subunits composed of beta- and gamma-subunit regions and coexpressed them with HA-tagged alphabeta- and alphagamma-subunits in Xenopus laevis oocytes.

Identification of domains that control the heteromeric assembly of Kir5.1/Kir4.0 potassium channels.

Heteromultimerization between different inwardly rectifying (Kir) potassium channel subunits is an important mechanism for the generation of functional diversity. However, little is known about the mechanisms that control this process and that prevent promiscuous interactions in cells that express many different Kir subunits. In this study, we have examined the heteromeric assembly of Kir5.

Regulation of the epithelial sodium channel by N4WBP5A, a novel Nedd4/Nedd4-2-interacting protein.

The amiloride-sensitive epithelial sodium channel (ENaC) plays a critical role in fluid and electrolyte homeostasis and consists of alpha, beta, and gamma subunits. The carboxyl terminus of each ENaC subunit contains a PPXY motif that is believed to be important for interaction with the WW domains of the ubiquitin-protein ligases, Nedd4 and Nedd4-2. Disruption of this interaction, as in Liddle's syndrome where mutations delete or alter the PPXY motif of either the beta or gamma subunits, has been shown to result in increased ENaC activity and arterial hypertension.

Cystic fibrosis transmembrane conductance regulator-dependent up-regulation of Kir1.1 (ROMK) renal K+ channels by the epithelial sodium channel.

The epithelial sodium channel (ENaC) and the secretory potassium channel (Kir1.1/ROMK) are expressed in the apical membrane of renal collecting duct principal cells where they provide the rate-limiting steps for Na(+) absorption and K(+) secretion. The cystic fibrosis transmembrane conductance regulator (CFTR) is thought to regulate the function of both ENaC and Kir1.

Intrinsic sensitivity of Kir1.1 (ROMK) to glibenclamide in the absence of SUR2B. Implications for the identity of the renal ATP-regulated secretory K+ channel.

The precise molecular identity of the renal ATP-regulated secretory K+ channel is still a matter of some controversy. The inwardly rectifying K+ channel, Kir1.1 (ROMK) appears to form the pore of the channel, and mutations in Kir1.