Retrosigmoid Craniectomy for Clip Ligation of Flow-Diverted Posterior Inferior Cerebellar Artery Aneurysm.

Flow diversion (FD) has revolutionized the treatment of cerebral aneurysms. Since the introduction of the Pipeline Embolization Device, there has been a significant shift in the management of cerebral aneurysms, with increasing emphasis being placed on use of endoluminal reconstruction as a means of long-term, durable treatment of aneurysms. Increasingly, FD stents are being used as primary treatment for aneurysms, including those that present with subarachnoid hemorrhage.1 Improper use of FD stents, however, may create havoc, as access to the aneurysm sac is blocked with the placement of these devices. Aneurysms that are incompletely treated with FD may continue to grow and rupture. The inability to use coils or endosaccular devices for treatment of these aneurysms means the only options for treatment are placement of additional FD devices, deconstructive strategies with or without bypass, or microsurgical clipping,2 thereby making an aneurysm that may have been straightforward to treat with another strategy a complex lesion to treat with the presence of the FD stent. Although deconstructive techniques can be used for treatment of failed aneurysm occlusion with flow diversion, where possible, surgical clipping can result in the simplest, most durable solution. Herein we present (Video 1) a case of a patient with a posterior inferior cerebellar artery aneurysm treated previously with FD using a single pipeline embolization device without aneurysm occlusion over 1 year of follow-up who was treated with retrosigmoid craniotomy and clipping of aneurysm. Nuances of the approach selection, clipping of the aneurysm, and preservation of the stent are discussed.

Contralateral Interhemispheric Transfalcine Approach to the Basal Ganglia.

The contralateral interhemispheric approach provides a robust path into the mesial frontal lobe and basal ganglia structures.1 The use of gravity to retract the dominant frontal lobe allows the surgeon to avoid injury caused by exposure of the dominant hemisphere. The transfalcine corridor, however, is long and often not well illuminated, necessitating the use of lighted instruments. Within the path of approach lie the anterior cerebral arteries, which must be carefully dissected and preserved. Upon opening the falx, the entire mesial frontal lobe and deep basal ganglia structures can be readily accessed. Herein, we present a patient with familial cerebral cavernous malformation-1 syndrome who presented after an acute hemorrhage from a deep basal ganglia cerebral cavernous malformation (Video 1). The patient consented to the procedure. The patient was hemiparetic and aphasic, likely secondary to mass effect from the bleed. The lesion was approached from a contralateral interhemispheric approach and removed completely. The patient's examination improved with removal of the mass lesion. This case demonstrates the utility of this approach for accessing deep corridors within the cerebral cortices.

Transcervical Vertebral Artery Origin Endarterectomy for Vertebrobasilar Insufficiency.

Vertebral artery (VA) stenosis is a cause of vertebrobasilar insufficiency (VBI) and disabling posterior circulation stroke,1 accounting for up to 30% of all strokes.2 Although the natural history of VBI is not as well delineated as that of carotid stenosis, strokes in the basilar circulation can be more disabling than their anterior circulation counterparts. Stenosis exceeding 30% at the origin of the vertebral artery is associated with increased risk of stroke.3 The authors present a case of a female patient with significant peripheral vascular disease who presented with concerns for VBI. The patient was on antiplatelet and anticoagulative medications and a statin at the time of her presentation. Angiography demonstrated bilateral vertebral artery origin stenosis. The left VA was diminutive and arose directly from the arch (Video 1). The right VA demonstrated critical stenosis at its origin. Attempts at endovascular access of the right VA for placement of a balloon-mounted stent were unsuccessful. The patient underwent a transcervical approach for endarterectomy of the VA origin. The VA can be readily accessed using a small supraclavicular incision to isolate the V1 segment of the vessel. The procedure was performed with the patient heparinized and on antiplatelet medications. Alternatives to this strategy include patch grafting in addition to the endarterectomy or use of a short vein graft to bypass the stenosis of the VA beyond the stenotic segment.

Keyhole Retrosigmoid Craniotomy for Lateral Pontine Cavernous Malformation.

With improvements in anesthesia, monitoring, and peroperative care, the surgical removal of intrinsic brainstem pathology has become a possibility.1 Although surgical removal of deep-seated lesions continues to have significant morbidity, at least temporarily, associated with it, removal of exophytic lesions can be accomplished with little disability for the patient. The key to a good outcome, when removing cerebral cavernous malformation, is preservation of adjacent neurovascular bundles, use of sharp dissection over blunt pulling, judicious use of cautery in and around the brainstem, and preservation of the developmental venous anomaly, when present. The authors present a case of a lateral pontine cerebral cavernous malformation that was exophytic at the lateral and peritrigeminal safe entry zones.2 Neuromonitoring was used an adjunct to ensure safety of the procedure. The lesion is accessed using a keyhole retrosigmoid craniotomy (Video 1). We do not routinely use lumbar drains for these procedures as careful arachnoid dissection can result in adequate cerebrospinal fluid release. The window of access to this area is between CN 5 and the CN 7/8 complex. The arachnoid over the nerves is preserved, but the layer between the nerves is exposed to gain access to the lateral pons. The lesion is sharply dissected from the lateral pons, taking care to save the developmental venous anomaly, from which this lesion arises.

Exploring the dynamics of adult Axin2 cell lineage integration into dentate gyrus granule neurons.

The Wnt pathway plays critical roles in neurogenesis. The expression of Axin2 is induced by Wnt/ß-catenin signaling, making this gene a reliable indicator of canonical Wnt activity. We employed pulse-chase genetic lineage tracing with the Axin2-CreERT2 allele to follow the fate of Axin2+ lineage in the adult hippocampal formation. We found Axin2 expressed in astrocytes, neurons and endothelial cells, as well as in the choroid plexus epithelia. Simultaneously with the induction of Axin2 fate mapping by tamoxifen, we marked the dividing cells with 5-ethynyl-2'-deoxyuridine (EdU). Tamoxifen induction led to a significant increase in labeled dentate gyrus granule cells three months later. However, none of these neurons showed any EdU signal. Conversely, six months after the pulse-chase labeling with tamoxifen/EdU, we identified granule neurons that were positive for both EdU and tdTomato lineage tracer in each animal. Our data indicates that Axin2 is expressed at multiple stages of adult granule neuron differentiation. Furthermore, these findings suggest that the integration process of adult-born neurons from specific cell lineages may require more time than previously thought.

Dynamics of Adult Axin2 Cell Lineage Integration in Granule Neurons of the Dentate Gyrus.

The Wnt pathway plays critical roles in neurogenesis. The expression of Axin2 is induced by Wnt/ß-catenin signaling, making this gene a sensitive indicator of canonical Wnt activity. We employed pulse-chase genetic lineage tracing with the Axin2-CreERT2 allele to follow the fate of Axin2 -positive cells in the adult hippocampal formation. We found Axin2 expressed in astrocytes, neurons and endothelial cells, as well as in the choroid plexus epithelia. Simultaneously with tamoxifen induction of Axin2 fate mapping, the dividing cells were marked with 5-ethynyl-2'-deoxyuridine (EdU). Tamoxifen induction resulted in significant increase of dentate gyrus granule cells three months later; however, none of these neurons contained EdU signal. Conversely, six months after the tamoxifen/EdU pulse-chase labeling, EdU-positive granule neurons were identified in each animal. Our data imply that Axin2 is expressed at several different stages of adult granule neuron differentiation and suggest that the process of integration of the adult-born neurons from certain cell lineages may take longer than previously thought.