bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract Number ‐ 210: Curative Embolization of Ruptured Pediatric Cerebral Arteriovenous Malformations
Authors: Saal‐Zapata Giancarlo , Rodriguez‐Calienes Aaron , Vivanco‐Suarez Juan , Galecio‐Castillo Milagros , Farooqui Mudassir , Zevallos Cynthia , Ortega‐Gutierrez Santiago 
Published: April 2023

Introduction
The incidence of ruptured cerebral arteriovenous malformations (AVMs) has increased as a consequence of the publication of the ARUBA trial. In the setting of ruptured AVMs, target embolization of high‐risk features can be considered to decrease the risk for recurrent hemorrhage. However, embolization with the intention to cure has not been well studied in ruptured AVMs. Furthermore, the role of primary curative embolization of pediatric AVMs is uncertain. Hence, we aimed to characterize the safety and efficacy of curative embolization for ruptured AVMs in pediatric patients.

Methods
Between 2010 and 2022, a retrospective analysis of all pediatric (≤18 years) patients who underwent curative embolization for ruptured AVMs was conducted in two institutions. Demographic data, clinical presentation, Spetzler‐Martin (SM) grade, associated high‐risk vascular structures, and procedural characteristics were retrieved. The safety (intraprocedural complications and mortality) and efficacy (complete angiographic obliteration after the last embolization session) were evaluated.

Results
Sixty‐eight patients (38 females; mean age 12.4 ± 3.4 years) underwent a total of 109 embolization sessions. The most frequent clinical presentation was headache (79%). There were 15 (22%) SM grade I lesions, 34 (51%) grade II, 14 (21%) grade III, and 4 (6%) grade IV. In 21 patients, twenty‐three high‐risk structures were observed (3 prenidal aneurysms, 12 intranidal aneurysms, 3 venous aneurysms, 2 varicose veins, 3 arteriovenous fistulae). Decompressive craniectomy with intracerebral hemorrhage evacuation was performed in 15 patients (22%). The mean number of sessions per patient was 1.6 (range 1 to 6) and n‐butyl cyanoacrylate was the most used embolic agent (30%). The transarterial approach was the most common (91%). The mean volume of embolic agents in each patient was 2.1 ml (range 0.1 to 6 ml). Seventeen intraprocedural complications (16% of procedures) were observed and no deaths were reported. In patients with high‐risk structures the rate of intraprocedural complications was 24%. The most common complication was microcatheter‐related vessel perforation (7%). Complete angiographic obliteration was achieved in 42 patients (62%). In 30 patients (44%) the AVM was occluded with a single embolization session. The rate of complete obliteration in patients with high‐risk structures was 62%.

Conclusions
Curative embolization of ruptured pediatric AVMs shows a high rate of intraprocedural complications, especially when high‐risk associated vascular structures are present. In addition, acceptable complete obliteration rates were found. Appropriate long‐term follow‐up in prospective studies tailored to the pediatric population are required to determine the best therapeutic approach.
Abstract Number ‐ 212: Endovascular vs. Open Surgery for Craniocervical Junction Dural Arteriovenous Fistulas: Assessing Safety and Efficacy
Authors: Brown Nolan , Singh Rohin , Bocanegra‐Becerra Jhon , Bui Nicholas , Hallak Hana , Koester Stefan , Shahrestani Shane , Stonnington Henry , Gendreau Julian 
Published: April 2023

Introduction
Arteriovenous fistulas at the craniocervical junction (CCAVFs) are challenging to treat due to variation in angioarchitecture and shunting sites. No consensus exists as to whether open surgery or endovascular approaches are better in regards to outcomes, complications, and need for reintervention. As such, weexplore the efficacy, outcomes, and complications of endovascular versus open surgery for dural arteriovenous fistulas at the craniocervical junction.

Methods
A systematic review was performed using the EMBASE, PubMed,and Cochrane databases in April 2022. MeSH search terms included (craniocervical) AND (arteriovenous OR fistula OR AVF). Inclusion criteria were defined as patients with CCAVFs who were treated with open surgery or endovascular therapy with reported clinical outcomes at 6 months or later.

Results
A total of 357 studies were screened; of which 75 were included. A total of 416 patients (309 males, 91 females) were included with an average age of 61.9 years. A total of 236 patients underwent surgery (mean age: 61.5), 71 patients underwent embolization (mean age: 62.6), and 25 patients underwent a combination (mean age: 54.7). Outcomes were reported in 39 surgery cases (mean follow up time: 31.4 months), and 54 endovascular cases (mean follow up time: 24.2 months). Within the open surgery group 47 (57.3%) had complete symptom resolution, 23 (28%) had symptom improvement or stabilization, 11 (13.4%) permanent deficit, and 1 (1.2%) resulted in death. Within the endovascular group 26 (56.5%) had complete symptom resolution, 5 (10.9%) had symptom improvement or stabilization, 15 (32.6%) permanent deficit, and 0 (0%) resulted in death.

Conclusions
Open surgery and embolization yield comparable symptomatic improvement and stabilization. However, the rate of permanent deficits is higher withembolization, while mortality is higher with open surgery. Further studies are required to better associate these outcomes to baseline parameters including treatment decision making, size of the lesion, patient age, and co‐morbidities.
Abstract Number ‐ 214: Woven EndoBridge in Conjunction with Coiling: Novel Technique for Treatment of a Large Basilar‐tip Aneurysm
Authors: Kiaei Benjamin , Miremadi Brian , Edgell Randall 
Published: April 2023

Introduction
Basilar tip aneurysmscan bechallenging to treatgiven their location andoftencomplex geometryand size.Endovascular coilinghas historically been the standardoftreatmentfor less complex aneurysms, proving to bebothsuccessfulandsafe.However, recanalization ratesfor large and giant aneurysmshave beenunacceptably high.More recently, devicessuch asthe Woven EndoBridge (WEB) have been developed toreduce the rate of recanalization.Here we describea uniquecase of alarge basilar tip aneurysm that was treated withcombination oftheWEBdeviceandcoilembolizationsimultaneously.

Methods
Case report.

Results
A woman in her fifties presented with several days of headache, nausea and vomiting, vision changes, and unsteady gait. MRA of the brain visualized a large unruptured basilar tip saccular aneurysm which was confirmed via a diagnostic cerebral angiogram (size: 12.9×11.2×14.0 mm, neck: 4.5 mm) [Figure 2A]. Given the sizeand locationof the aneurysm,we attempted embolization with the largest available WEBSLdevice. This device was undersized for the aneurysm.We therefore utilized a novel combinationcoiling,to partially fill the dome and posterior aneurysm sac,and the largest WEB SL available (11×9 mm). Using a radial system, the WEB device was partly unsheathed at the base of the aneurysm. Then, using a femoral system three coils (18 Hydroframe 28cm 7mm, 18 Hydroframe 15cm 7mm 10, 10 Hydroframe 23cm 7mm) were introduced into the remaining space of the aneurysm, filling the void between the aneurysm dome and the partly deployed WEB SL device. Once all coils were appropriately placed and stable, the WEB device was fully deployed, which lead to successful embolization and occlusion of the aneurysm [Figure 2B].

Conclusions
The challenge of treatinglargebasilar tip aneurysmshasencouragedthedevelopment of innovative devices and novel interventional techniques.Here we demonstratethepossibility ofcombiningaWEBdevicewith standard coilingto treatlarge, wide‐necked basilar tip saccularaneurysms that are not ideal candidates for standard therapy.
Abstract Number ‐ 215: Distinct presentation of RCVS and PRES co‐existence and overlap of their pathophysiology
Authors: Patel Priyadarshee , Garg Aayushi , Rocha Marcelo 
Published: April 2023

Introduction
Reversible cerebral vasoconstriction syndrome (RCVS), is characterized by reversible segmental and multifocal vasoconstrictionof cerebral arteries leading to infarcts and cytotoxic edema. Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic edema predominantly in the parieto‐occipital regions associated with acute onset encephalopathy, seizures, headache, and visual disturbances.Whether PRES and RCVS are independent syndromes and sometimes overlapped or part of a continuum process, these theories are still debated. We report a case of a patient with distinct overlapping of RCVS and PRES.

Methods
Case Report

Results
52‐year‐old woman with past medical Hx of Hypertension, Diabetes, Migraines and cocaine use, initially presented with hypertensive emergency andsubacute headaches with worsening confusion. Initial CT head was negative for bleed but showed evolving subcortical hypodensities in the right parietal and left frontal lobes. CTA head and neck showed multifocal intracranial irregularities of bilateral ACAs and MCAs with paucity of left anterior M2 branch, left V3/V4 steno‐occlusion. This vasculopathy and clinical presentation is very consistent with RCVS.MRI of brain showed multiple acute / subacute punctate infarcts in the left corona radiata, bilateral basal ganglia, right greater than left thalami, right dorsal pons, right mesial temporal lobe, bilateral occipital regions. Vasogenic edema was noted in the bilateral border zone regions, right parietal being most prominent with some contrast enhancement. The MRI showed vasogenic edema and cytotoxic edema with multiple infarcts which is consistent with PRES and RCVS vasculopathy. CSF analysis was negative for pleocytosis and showed mildly elevated protein. The patient was started on Verapamil and Aspirin and Atorvastatin for secondary stroke prevention. With improvement in mental status was discharged to Rehab.

Conclusions
The pathophysiological mechanisms of PRES and RCVS are still unknown. Theories whether RCVS and PRES are independent syndromes and sometimes overlap or part of spectrum, are still debated. However, some common characteristics make conceivable a common origin linked with impaired cerebral autoregulation, endothelial dysfunction, and BBB breakdown. Increased clinical awareness of their co‐existence may help in quickerdiagnosis and treatment.
Abstract Number ‐ 216: Limb‐Shaking Transient Ischemic Attack in the Setting of Moyamoya Disease
Authors: Xie Sophie J , Xie Sophie J , Rodriguez Wilson , Miremadi Brian B 
Published: April 2023

Introduction
Moyamoya disease (MMD) is a cerebrovascular disorder characterized by progressive narrowing of the large intracranial arteries, primarily the internal carotid artery (ICA) and its branches, with secondary development of prominent small‐vessel collaterals. Limb shaking is a rare manifestation of transient ischemic attack (TIA) that is characterized by brief, irregular, involuntary jerking of the arms or legs and momentary disorientation without complete loss of consciousness. It is mainly associated with high grade carotid stenosis. In rare cases, limb‐shaking TIA can occur in the setting of MMD.

Methods
The patient was identified in routine clinical practice.

Results
A woman in her 50s presented with a six‐year history of progressive weakness below the neck when standing and initiating movement. These episodes were followed by violent shaking of her arms and legs that lasted several seconds to minutes. She reported transient confusion after the events, but no seizure activity was seen on multiple EEGs, and anti‐epileptic drugs (AEDs) failed to alleviate her symptoms. Further neurological workup included a MR angiogram of the brain that was suggestive of MMD. Catheter angiography confirmed bilateral occlusion of the M1 segments of the middle cerebral arteries (MCAs) and the A1 segment of the left anterior cerebral artery (ACA). There was neovascularization in the same territories with significant collateral flow from the posterior circulation. She was diagnosed with bilateral limb‐shaking TIA in the setting of MMD. She recently underwent two revascularization procedures, a left superficial temporal artery (STA) to middle cerebral artery (MCA) bypass and a right sided encephaloduroarteriosynangiosis (EDAS).

Conclusions
Limb‐shaking TIA is predominantly associated with severe atherosclerotic extracranial carotid artery stenosis. In rare cases, the limb‐shaking episodes are caused by cerebral hypoperfusion secondary to severe stenosis of the ICAs, and their branches, in the setting of moyamoya disease. Treatment of limb‐shaking TIA to prevent further brain ischemia includes adjustment of fluid intake, careful blood pressure management to avoid episodes of relative brain hypoperfusion, and revascularization procedures. Revascularization is also the most effective method of treating MMD and patients will often experience improvement of their symptoms within one year. Early recognition of limb‐shaking TIA in MMD is critical to avoid unnecessary and potentially harmful treatments (e.g. AEDs), provide patients with accurate explanations of their symptoms, and ensure timely administration of the appropriate treatments.
Abstract Number ‐ 217: Case Study: Snowball strokes
Authors: Pirahanchi Yasaman , Wagner Jeffrey 
Published: April 2023

Introduction
55 year old RH female, PMH of hypothyroidism and gastric bypass who presented with complaints of 1–2 weeks of “feeling foggy in the head”, dizziness, and unsteady gait. The patient’s husband said she had delayed responses. She denied headache, vision change, or hearing loss. Exam was without focal neurologic deficit, NIHSS of 0.Though CTA head and neck were unremarkable, MRI Brain showed multiple scattered small acute or subacute infarcts involving the corpus callosum. This distribution was thought to suggest a central embolic source. The patient was admitted for stroke workup which was unrevealing including: Normal echocardiogram including bubble study. Her symptoms progressed and she was unable to find outpatient follow up. Two weeks later, she presented again but this time with progressive generalized weakness. At the time of her initial discharge, the patient was ambulatory with her walker, however upon re‐admission the patient required a wheelchair. Exam showed flaccid bilateral lower extremities, brisk reflexes, bilateral Hoffman’s and Babinski signs.Repeat MRI Brain was concerning for Susac syndrome with new lesions in the corpus callosum. CSF showed pleocytosis with markedly elevated protein (WBC 8, protein 153, glucose 55). Treatment with Solu‐Medrol 1000 mg q12h IV, then IVIG 0.4 kg/mg/day both for 5 days, Rituximab 1000mg for 2 days, then transition to prednisone 80 mg /day and CellCept 1000mg BID. She returned 14 days after with confusion, regression of prior gait improvement, and repeat MRI Brain showed additional new multifocal strokes. She repeated 3 days of 1000mg IV Solu‐Medrol, then was treated with cyclophosphamide due to clinical progression. Fluorescein angiography showed evidence of branch retinal artery occlusions bilaterally. She was placed on a prednisone taper from 80mg/day to 40mg/day over the course of the 2 months, with the plan to continue Cellcept 1000mg BID for 2 years.

Methods
NA‐ Single case study

Results
NA‐Single case study

Conclusions
Susac syndrome is an autoimmune disorder, affecting microvasculature of the brain, retina and cochlea. A triad of symptoms: encephalopathy, branch retinal artery occlusions, and hearing loss is classic, though only 13% have the complete triad at onset. It is often associated with headaches, psychiatric features (paranoia), bilateral cochlear hearing loss, and vertigo. It typically occurs in women 20–40 years of age. Brain MRI WO shows white‐matter disturbance, frequently mistaken for Multiple Sclerosis, however the main difference is that the corpus callosum is always affected with lesions that resemble “snowballs”, or “holes”. Treatment for Susac syndrome is immunosuppression, with high‐dose corticosteroids, also with IVIG, Mycophenolate mofetil, and Cyclophosphamide.
Abstract Number ‐ 220: Internal Carotid Artery Hypoplasia of Unique Anatomical Variance
Authors: Mahmoud Noor A , Alshaqi Ola , Almeida Nyle C , Cornwell Benjamin , Alawwad Ahmad 
Published: April 2023

Introduction
Hypoplasia of the internal carotid artery (ICA) is incomplete development of the ICA with the presence of empty carotid canal. Despite anecdotal data reporting less than a 0.01% of developmental anomalies of ICA, the true incidence remains unknown. Many cases are asymptomatic and thus escape diagnostic detection or appropriate intervention. In 1968, Lie and Hage described collateral circulation in ICA developmental anomalies through the Circle of Willis, persistent embryonic vessels, or skull base arteries/anastomosis or rete mirabile. While collateral systems exist, subsequent cerebrovascular insufficiency and vascular malformations may occur as a result. To our knowledge, there is an incomplete body of literature surrounding the implications of ICA hypoplasia of varying anatomy.

Methods
We present a case report of left ICA hypoplasia and a comprehensive literature review.

Results
A 70‐year‐old woman with hypertension, nicotine dependence, and chronic obstructive pulmonary disease (COPD) presented with COPD exacerbation and disorientation. Computed tomography (CT) head angiography showing left cervical/petrous ICA aplasia with presence of a small carotid canal. The left external carotid and vertebral artery originate at the aortic arch. Majority of the blood supply to the left anterior cerebral artery (ACA) and middle cerebral artery (MCA) is suppliedby the right anterior communicating artery (AComA), posterior communicating artery (PComA). There is also a small left supraclinoid and carotid terminus that reconstitute predominantly by right A1 segment and PComA (Figure 1).

Conclusions
Although ICA hypoplasia may be an incidental finding, accurate and promptrecognition is essential for the consideration of endovascular implications, screening for vascular malformations, understanding cerebral vascular flow, managing cerebrovascular risk, and avoiding misinterpretation of clinical and imaging patterns.
Abstract Number ‐ 226: Pontine Stroke Presenting as 1.5 Syndrome Evolving to 9 Syndrome over 72 Hours.
Authors: Nene Yash , Reddy Aravind , Kaur Navreet , Masoud Hesham 
Published: April 2023

Introduction
A 75 year old woman with a past medical history of hypertension developed sudden‐onset vertigo, nausea and vomiting. She did not immediately seek medical care, thinking she was suffering from food poisoning. The following day her symptoms improved however she developed new right sided weakness and gait imbalance, prompting her presentation to the ED. Her neurologic exam noted complete loss of adduction of the right eye and loss of horizontal extraocular movements of the left eye. She also displayed right upper extremity paresis, right upper extremity dysmetria and mild dysarthria. MRI of the brain disclosed acute pontine infarcts in the ventral and dorsal left paramedian regions. Over the next three days, her horizontal gaze palsy improved with some return of adduction of the right eye and horizontal movements of the left eye. However right sided paresis worsened, and in addition, progressed to include complete left facial palsy (lower motor neuron lesion). She was able to be discharged to rehab, placed on Aspirin 81 mg daily and Ezetimibe (due to elevated liver function enzymes) and 30 day Cardiac Event Monitor follow up.

Methods
Case report and review of literature.

Results
Due to the combination of multiple cranial nuclei and white matter tracts in the brainstem, ischemia can lead to several clinical manifestations. There are various presenting clinical syndromes, named numerically by structures involved and/or the clinical deficit. One‐and‐a‐half (1.5) syndrome, first reported by Fischer in 1967, is an uncommon entity caused by a lesion (most commonly infarction) in the pontine tegmentum [1]. It consists of complete ipsilateral horizontal gaze palsy (due to involvement of ipsilateral Paramedian Pontine Reticular Formation/Abducens Nucleus and Medial Longitudinal Fasciculus) and loss of adduction of the contralateral eye (due to involvement of the contralateral Medial Longitudinal Fasciculus). Extension of the lesion to the facial nucleus can produce ipsilateral lower motor neuron type facial palsy, leading to an even more uncommon 8.5 syndrome (7 + 1.5), described by Eggenberger in 1998 [2]. When the lesion involves the corticospinal tracts and/or the medial lemniscus, it can lead to contralateral hemiparesis and/or hemisensory deficits; the so called “9 syndrome” first proposed by Rosini et al in 2013 [3]. This rare entity has been reported in only a handful of cases.

Conclusions
The awareness of complex brainstem neuroanatomy enables precise localization of the clinical deficits. The noted slow progression of the clinical syndrome from 1.5 to 8.5 and finally 9 syndrome over 72 hours in this case highlights the complexity of small vessel brainstem ischemia.
Abstract Number ‐ 229: Combined Open and Endovascular Treatment of a Ruptured Aneurysm with Excellent Clinical and Angiographic Outcome
Authors: Browne Declan , Simms Neil 
Published: April 2023

Introduction
A 49‐year‐old lady presented to hospital with a WFNS 3 aneurysmal subarachnoid haemorrhage. Her symptomatology included sudden onset headache, vomiting, neck stiffness and mild left‐sided weakness. Her past medical history comprised discoid lupus, scleroderma and hypertension. Plain CT imaging demonstrated a significant blood load distributed primarily around the right Sylvian fissure. CT angiography confirmed two right‐sided middle cerebral artery (MCA) aneurysms. The proximal aneurysm appeared smooth and unruptured. The distal aneurysm appeared irregular and was therefore believed to be the ruptured lesion. The anatomy of this aneurysm precluded endovascular coiling as it was fully incorporated into the inferior MCA M2 branch.

Methods
Following interdisciplinary discussion, the patient proceeded to open surgical clipping of both aneurysms. A clip was placed across the rupture point of the distal aneurysm but a significant neck was left to permit filling of the distal branches. Post‐operative angiography accordingly showed a small residual component to the aneurysm. On follow‐up angiography one week later, this remnant appeared to have increased in size. The decision was therefore made to endovascularly place a contour device to reduce flow to the persistent portion of the aneurysm. This combined treatment approach resulted in excellent clinical and angiographic outcome.

Results
The patient was eventually discharged home with a modified Rankin scale score of 1 and had no residual neurological deficit at 1‐year outpatient follow‐up. Similarly, follow‐up catheter angiography at 1‐year demonstrated continued satisfactory appearances with the combination of clip and contour device.

Conclusions
This case highlights the successful clinical and radiological outcomes of a combined surgical and endovascular approach in aneurysmal subarachnoid haemorrhage ‐ despite an anatomically difficult vascular abnormality ‐ due to good interdisciplinary cooperation and careful patient follow‐up. It furthermore demonstrates the effective use of a relatively novel endovascular device following acute haemorrhage and open surgery which avoided the need for long‐term antiplatelet medication.