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Background The stapedial artery is an embryonic artery that transiently supplies the cranial vasculature of the human embryo. Postnatal persistence of the stapedial artery may cause conductive hearing loss and pulsatile tinnitus due to its course through the middle ear. We describe a patient with a persistent stapedial artery (PSA) managed by endovascular coil occlusion prior to stapedotomy. Methods A 48-year-old woman presented with left-sided conductive hearing loss and pulsatile tinnitus. Ten years earlier the patient had undergone explorative tympanoplasty, which was aborted due to a large PSA. Digital subtraction angiography was performed to confirm the anatomy and endovascular occlusion of the proximal PSA was achieved by deployment of coils. Results The pulsatile tinnitus improved immediately after the procedure. The size of the artery subsequently decreased and surgery could be performed with only a minor intraoperative bleeding. Successful stapedotomy resulted in postoperative normalization of her hearing with some minor residual tinnitus. Conclusion Endovascular coil occlusion of a PSA is feasible and safe in patients with favorable anatomy and facilitates middle ear surgery. It decreases the size of the artery and minimizes the risk of intraoperative bleeding in patients with a large PSA. The future role of this novel technique in the management of patients with PSA-related conductive hearing loss and pulsatile tinnitus remains to be determined., Background: The stapedial artery is an embryonic artery that transiently supplies the cranial vasculature of the human embryo. Postnatal persistence of the stapedial artery may cause conductive hearing loss and pulsatile tinnitus due to its course through the middle ear. We describe a patient with a persistent stapedial artery (PSA) managed by endovascular coil occlusion prior to stapedotomy. Methods: A 48-year-old woman presented with left-sided conductive hearing loss and pulsatile tinnitus. Ten years earlier the patient had undergone explorative tympanoplasty, which was aborted due to a large PSA. Digital subtraction angiography was performed to confirm the anatomy and endovascular occlusion of the proximal PSA was achieved by deployment of coils. Results: The pulsatile tinnitus improved immediately after the procedure. The size of the artery subsequently decreased and surgery could be performed with only a minor intraoperative bleeding. Successful stapedotomy resulted in postoperative normalization of her hearing with some minor residual tinnitus. Conclusion: Endovascular coil occlusion of a PSA is feasible and safe in patients with favorable anatomy and facilitates middle ear surgery. It decreases the size of the artery and minimizes the risk of intraoperative bleeding in patients with a large PSA. The future role of this novel technique in the management of patients with PSA-related conductive hearing loss and pulsatile tinnitus remains to be determined.

Objective: This 2-year observational study aimed to test the feasibility of implementing a pediatric stroke triage-setup that connected frontline providers with vascular neurologists and to examine final diagnoses in children triaged for suspected stroke. Methods: Prospective, consecutive registration of children with suspected stroke triaged by a team of vascular neurologists from Jan 1st, 2020 and through Dec 2021, Eastern Denmark (census 530,000 children). Based on the provided clinical information, the children were triaged to either assessment at the Comprehensive Stroke Center (CSC) in Copenhagen or to a pediatric department. All included children were retrospectively followed-up for clinical presentations and final diagnosis. Results: A total of 163 children with 166 suspected stroke events were triaged by the vascular neurologists. Cerebrovascular disease was present in 15 (9.0%) suspected stroke events; one child had intracerebral hemorrhage, one had subarachnoid hemorrhage, two children presented with three TIA events and nine children presented with 10 ischemic stroke events. Two children with ischemic stroke were eligible for acute revascularization treatment of which both were triaged to the CSC. The sensitivity of the triage by acute revascularization indication was 1.00 (95% confidence interval (95% CI): 0.15-1.00) and specificity 0.65 (95% CI: 0.57-0.73). Non-stroke neurological emergencies were present in 34 (20.5%) children, including seizures in 18 (10.8%) and acute demyelinating disorders in 7 (4.2%). Conclusion: Implementing regional triage-setup that connected frontline providers to vascular neurologists was feasible; this system was activated for the majority of children with ischemic stroke according to an expected incidence and led to identification of children eligible for revascularization treatments.

While intracranial aneurysms rarely develop after neurosurgical procedures, delayed pseudoaneurysm formation after foramen magnum decompression (FMD) has never been reported. A 52-year-old woman presented with an atypical subarachnoid hemorrhage in the posterior fossa 12 years after a FMD for symptomatic Chiari malformation type I was performed. A pseudoaneurysm on a dural-pial anastomosis was identified as the bleeding source and successfully occluded by endovascular means with full clinical recovery of the patient. Injury to the distal posterior inferior cerebellar artery related to surgery and postoperative infection likely caused formation of a dural-pial anastomosis. Additionally, hemodynamic stress or dissection may have contributed to delayed pseudoaneurysm formation and rupture.

Objective The aim of the study was to investigate (1) the 30-day, 3-month, and 12-month cumulative mortalities for patients who underwent aneurysm occlusion, and (2) the causes of death, and (3) the potential risk factors for death.Methods All patients who underwent surgical clipping or endovascular treatment of a ruptured aneurysm at Copenhagen University Hospital, during the period of January 1, 2017-December 31, 2019, were included and followed up for 12 months. Data regarding vital status, causes of death, comorbidities, treatment, and clinical presentations on admission was collected. The absolute mortality risk was estimated as a function of time with a 95% confidence interval. The associations between potential risk factors and death were estimated as odds ratios with 95% confidence intervals using logistic regression models.Results A total of 317 patients were included. The overall cumulative mortalities after 30 days, 3 months, and 12 months were 10.7%, 12.9%, and 16.1%, respectively. The most common cause of death was severe primary hemorrhage (52.9%), followed by infections (15.7%) and rebleeding (11.8%). WFNS score > 3 and Fisher score > 3 on admission, preprocedural hydrocephalus, and preprocedural rebleeding were found significantly associated with higher risk of death.Conclusions Considerable mortality was seen. Possible preventable causes accounted for approximately 22% of the deaths. The occurrence of both pre- and postprocedural rebleeding's indicates an opportunity of further improvement of the mortality by (1) further reduction of time from aSAH to aneurysm occlusion and (2) continuous efforts in improving methods of aneurysm occlusion.

Contains fulltext : 233536.pdf (Publisher’s version ) (Open Access)

Contains fulltext : 233536.pdf (Publisher’s version ) (Open Access)

BACKGROUND: Arteriovenous fistulas (AVFs) involving the cavernous sinus usually become clinically apparent due to eye symptoms. Although rare, the same symptoms can be associated with AVFs located remote from the cavernous sinus when the shunt drains into its tributaries. We report the unusual case of a dural AVF in which such communication was not immediately obvious from the diagnostic angiogram.CASE DESCRIPTION: A 61-year-old male presented with increasing lid swelling, proptosis, and redness of the right eye for 1 month. Digital subtraction angiography showed no evidence of a cavernous sinus fistula but revealed a dural AVF between the right middle meningeal artery and the vein of Trolard. The fistula had a minor drainage through a small superficial middle cerebral vein toward the middle cranial fossa. Late venous-phase images eventually revealed faint opacification of the right cavernous sinus and superior ophthalmic vein. Endovascular treatment was performed by transarterial embolization with complete occlusion of the AVF obtained after 2 sessions.CONCLUSIONS: Dural AVFs involving cortical veins may cause atypical symptoms suggesting a cavernous sinus fistula due to remote venous drainage. Understanding venous anatomy helps to correlate vascular pathology and clinical symptoms and thus allows efficient and safe treatment.

Accumulation of contrast medium in the subdural space after diagnostic intraarterial contrast administration is a rare observation. The authors report the case of a subdural contrast effusion (SCE) presenting during endovascular treatment of an intracranial dural arteriovenous fistula (DAVF) mimicking an acute subdural hematoma. Differentiation between the two by computed tomography (CT) or intraprocedural Dyna CT and early neurological examination can be crucial for patient management. We believe that repeated large-volume contrast injections via large-bore intermediate catheters into the territory of an (even partly) occluded DAVF may induce leakage of contrast medium into the extravascular subdural space thereby causing a SCE.

Accumulation of contrast medium in the subdural space after diagnostic intraarterial contrast administration is a rare observation. The authors report the case of a subdural contrast effusion (SCE) presenting during endovascular treatment of an intracranial dural arteriovenous fistula (DAVF) mimicking an acute subdural hematoma. Differentiation between the two by computed tomography (CT) or intraprocedural Dyna CT and early neurological examination can be crucial for patient management. We believe that repeated large-volume contrast injections via large-bore intermediate catheters into the territory of an (even partly) occluded DAVF may induce leakage of contrast medium into the extravascular subdural space thereby causing a SCE.