Mayfield Brain & Spine

Vein of Galen malformation (VOGM) is the most common congenital cerebrovascular anomaly. Fetuses with VOGM and wide mediolateral falcine sinus diameters are at high risk for mortality, brain injury, and neurodevelopmental delay. In utero embolization may improve survival and outcomes. To report early results from this institutional review board-approved single-group intervention study of in utero embolization for VOGM. Single-center, single-group intervention study in the US. First enrollment was on September 30, 2022; the most recent follow-up was on April 10, 2025. Eligible fetuses had VOGM, no major brain injury on fetal magnetic resonance imaging, and falcine sinus width of 7 mm or greater. Fetal embolization was ultrasound guided, using transuterine, transcranial needle access and microcatheterization of the prosencephalic venous varix with detachable coils. In utero embolization of fetuses with VOGM. Neonatal mortality and neurodevelopmental outcomes. Pre- and postembolization fetal magnetic resonance imaging and echocardiography were performed. Seven patients were enrolled; 5 underwent successful embolization. The mean maternal age was 32.4 years (range, 22-36); the mean fetal gestational age was 35 6/7 weeks (range, 33 6/7 to 37 1/7); and the sex ratio was 3:4 (female to male). The mean falcine diameter (10.3 mm) corresponded to 90% expected mortality and 9% likelihood of reaching 6-month milestones with standard postnatal care. Overall mortality was 43%, and 43% were meeting milestones at 6 months. Three embolized patients (aged 8, 18, and 24 months) survived, all without neurodevelopmental delay. Four of the 7 patients underwent additional neonatal embolization. Fetal echocardiography showed a mean 33.4% reduction (range, 16%-46%) in cardiac output. Five of 7 patients (71.4%) had unscheduled deliveries and 3 of these 5 were preterm, at a mean of 3.2 days after intervention. Early results demonstrate the feasibility of fetal embolization. Any potential reduction in mortality, brain injury, and neurodevelopmental delays must be weighed against an increased risk of unscheduled, preterm delivery. ClinicalTrials.gov Identifier: NCT04434729.

Decades of experimental and clinical data revealed that spreading depolarizations (SDs) play a central causal role in the development of cortical lesions after acute brain injury. However, clinical documentation of events at the onset of focal ischemic stroke and during the initial phase of cortical injury development is lacking because electroencephalography monitoring of SD typically starts hours or days later. Here, we used nonhuman primates to map electrophysiological pathology through focal ischemic stroke's onset and acute stage. Craniotomies were performed over both hemispheres on 4 male and 1 female nemestrina and rhesus macaques aged 23 years to 32 years. Subdural electrode arrays were placed bilaterally over the middle cerebral artery territory, recording from 24 electrodes 1 cm apart on the left cortex and 7 on the right. After 30 minutes of baseline monitoring, the left middle cerebral artery and, in some cases, also the left internal carotid or anterior cerebral arteries were permanently occluded with aneurysmal clips. Repetitive SDs occurred during the next 3 hours, followed by terminal SD during euthanasia. No epileptiform activity was observed in any of the 5 animals. Nonspreading electrical silence developed in the ischemic core within seconds of ischemic onset, followed by terminal SD and SD-initiated negative ultraslow potential after several minutes. These events defined the ischemic core and led to histologically confirmed cell damage. Initial and subsequent transient SDs caused spreading depression of spontaneous activity in the normally perfused surrounding cortex without any signs of histological damage. Cardiocirculatory arrest at the end of experiments first induced nonspreading depression of activity followed by SD and, eventually, the SD-initiated negative ultraslow potential, which indicated brain death. Results in gyrencephalic nonhuman primates hold significant implications for understanding the role of SD in acute brain injury development and for the clinical translation and diagnosis of pathologies manifested in the SD continuum.

BackgroundThe optimal duration for dual antiplatelet therapy (DAPT) after stent-assisted coiling (SAC) of intracranial aneurysms is unclear. Longer-term therapy may reduce thrombotic complications but increase the risk of bleeding complications.MethodsA retrospective review of prospectively maintained data at 12 institutions was conducted on patients with unruptured intracranial aneurysms who underwent SAC between January 1, 2016 and December 31, 2020, and were followed ≥6 months postprocedure. The type and duration of DAPT, stent(s) used, outcome, length of follow-up, complication rates, and incidence of significant in-stent stenosis (ISS) were collected.ResultsOf 556 patients reviewed, 450 met all inclusion criteria. Nine patients treated with DAPT <29 days after SAC and 11 treated for 43–89 days were excluded from the final analysis as none completed their prescribed duration of treatment. Eighty patients received short-term DAPT. There were no significant differences in the rate of thrombotic complications during predefined periods of risk in the short, medium, or long-term treatment groups (1/80, 1.3%; 2/188, 1.1%; and 0/162, 0%, respectively). Similarly, no differences were found in the rate of hemorrhagic complications during period of risk in any group (0/80, 0%; 3/188, 1.6%; and 1/162, 0.6%, respectively). Longer duration DAPT did not reduce ISS risk in any group.ConclusionsContinuing DAPT >42 days after SAC did not reduce the risk of thrombotic complications or in-stent stenosis, although the risk of additional hemorrhagic complications remained low. It may be reasonable to discontinue DAPT after 42 days following non-flow diverting SAC of unruptured intracranial aneurysms.

In-stent stenosis has a reported prevalence of 14% to 19% at 1-yr follow-up after carotid stenting and is associated with an increased risk of acute ischemic stroke.1,2 Risk factors include female sex, diabetes, and dyslipidemia. Cutting balloon angioplasty is a safe and effective treatment modality for the treatment of carotid in-stent stenosis, and alternative treatment options include observation with medical management and placement of another stent.3,4 The authors present the case of a 61-yr-old man with carotid in-stent restenosis and progressive worsening on serial imaging with ultrasound. The patient had a history of carotid stenting for symptomatic stenosis 6 mo prior and was maintained on aspirin and clopidogrel. In light of the progressive worsening, the in-stent stenosis was confirmed on computed tomography (CT) angiogram. The options were discussed with the patient and he consented for treatment with cutting balloon angioplasty. Final angiogram showed improvement of the luminal diameter with a residual stenosis of 15%. The patient tolerated the procedure well and was discharged home on postoperative day 1. Follow-up ultrasound demonstrated moderate improvement in peak systolic velocities, and the plan is to continue observation with a clinical follow-up and repeat carotid Dopplers at 3 mo.

Management options for carotid stenosis include medical management, carotid endarterectomy, carotid stenting with distal filter protection, or stenting with either flow arrest or flow reversal techniques.1 Flow reversal with transcarotid artery revascularization (TCAR) technique represents a hybrid approach with surgical access to the common carotid for endovascular placement of a stent in the internal carotid artery. This direct access to the carotid artery avoids navigating the challenging anatomy of the aortic arch with endovascular devices.2 Compared to transfemoral stenting, TCAR possesses lower risk of transient ischemic attack and stroke, and compared to carotid endarterectomy, there is less risk of cranial neuropathy.3,4 We present the case of an 87-yr-old man with recurrent severe stenosis (85%) of the right internal carotid artery. The patient had a remote history of bilateral endarterectomies for asymptomatic stenosis and was found with recurrence and progression of right internal carotid artery stenosis. Options were discussed and decision was made to proceed with TCAR after he consented for the procedure. The patient tolerated the procedure well with satisfactory revascularization. Exam remained unremarkable prior to discharge on postoperative day 1 and during follow-up at 1 mo. Patient consented to the publication of their image.

Wide-necked bifurcation aneurysms pose technical and anatomical challenges to endovascular treatment, which make the simpler assisted (balloon or single stent) coiling techniques less effective.1 Consequently, unique endovascular solutions to treat such aneurysms have been devised.2,3 One such device is PulseRider (Cerenovus, New Brunswick, New Jersey), which is designed to provide neck support for a coil mass while protecting the bifurcation.3 The device comprises a body or stem that is deployed in the parent artery and a saddle component that sits at the aneurysm neck to keep the coil mass away from the bifurcation. There are several technical nuances involved in successful use of the device during positioning, deployment, and detachment.3 We present a surgical video detailing the steps of PulseRider-assisted coiling of unruptured basilar bifurcation (or basilar apex) aneurysms. The first case highlights index treatment at diagnosis and the second showcases treatment of a recurrent basilar apex aneurysm. Both patients provided informed consent to the procedure. We also briefly discuss the rationale for treating basilar apex aneurysms.4,5.