bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract Number ‐ 190: Acute Ischemic Stroke patients post Endovascular Thrombectomy complicated by gastrointestinal bleeding have worst clinical outcomes
Authors: Ali Syed F , Dominguez Jose , Osman Masha , Meadows Sarah , Das Ankita , Al‐Mufti Fawas 
Published: April 2023

Introduction
The objective of this study was to scrutinize the stroke severity markers, complications, and clinical outcomes in patients with AIS who underwent EVT complicated by gastrointestinal bleeding (GIB). It is known that anemia is associated with poor functional outcomes in patients with mechanical thrombectomy (Nisar, 2021). Anemia also predicts poor clinical outcomes despite fair or good collateral circulation (Pienimäki, 2020). With the increasing use of EVT for acute management of AIS, it is prudent to investigate the relationship between gastrointestinal bleeding in acute ischemic stroke patients who have underwent mechanical thrombectomy.

Methods
The 2016–2019 National Inpatient Sample (NIS) database was queried for patients with the diagnosis of acute ischemic stroke (AIS) by using International Classification of Disease, 10threvision (ICD10) diagnosis codes. From this cohort of AIS patients, those that underwent endovascular thrombectomy (EVT) were then identified using ICD 10 procedure codes. A subpopulation of AIS‐EVT patients was created for patients with a diagnosis of GI bleeds. Baseline demographic, stroke severity, complication, and outcome variables were evaluated between GI bleed and no‐GI bleed patients who underwent EVT.

Results
Of 132,210 patients hospitalized for AIS who had underwent EVT, there were 130,970 cases of no GIB (99.1% %) and 1,240 cases of GIB (0.9%) complications. Mean age greater than 65 was 980 (79%) in GI bleed group versus 82,945 (63.3%) in no GI bleed group (p‐value < 0.001, CI 95%: 1.903 ‐ 2.5, OR 2.2). Interestingly, the no GI bleed group had more use of Aspirin 31,790 (24.3%) versus GI bleed group 200 (16.1%) (p‐value < 0.001, CI 95%: 0.515 ‐ 0.698, OR 0.6). Furthermore, the GI bleed group had the following risk factors that were statistically significant: history of atrial fibrillation and chronic renal failure (46% vs 37.2% and 21.8% vs 15.1%, respectively). In fact, this study failed to show increased risk of GI bleed due to being on aspirin, AC, having a history of DM, HTN, HLD, and CHF. Stroke severity was worst in GI bleed group with average NIHSS score 15.92 vs 14.05 (P‐value < 0.001) and worst hemiplegia (75% vs 70.2%, P‐value < 0.001, 1.3 CI 1.118‐1.447). The GI bleed group had statistically worst complications including sepsis, DVT, PE, AKI, and aspiration pneumonia. Lastly, the GI bleed patients were most likely to be discharged to SNF versus routine discharge to home (68.5% vs 49.6%, p‐value < 0.001, CI 1,962 ‐ 2.496, OR 2.2).

Conclusions
GIB occurrence in patients with AIS status post EVT is relatively rare but is associated with poor in‐hospital outcomes, including mortality. We identified risk factors associated with GIB in AIS post EVT, which allows physicians to monitor patient populations at the highest risk.
Abstract Number ‐ 196: The Impact of Pre‐existing Depression on Functional Outcomes After Endovascular Treatment of Ischemic Stroke
Authors: Christopher Kara M , Gao Xiaoyi , Kiaei Benjamin , Chen Yongzhen , Hwee Brenton , Rodriguez Wilson , Scott Jordan , Miremadi Brian , Linares Guillermo 
Published: April 2023

Introduction
Stroke is a leading cause of morbidity and mortality, and many factors predict a poor outcome, including age, NIH Stroke Scale (NIHSS), ambulatory status, and ability to swallow1. Mood disorders have previously been associated with an increased risk of cardiovascular disease2. The association between pre‐existing mood disorders and stroke outcome, however, has not been well studied. The objective of the current study was to explore the impact of pre‐existing depression on functional outcomes post‐endovascular treatment.

Methods
We reviewed the records of 178 patients who received mechanical thrombectomy (MT) at our institution[BH1][BM2] from 2019–2022. We collected data on baseline characteristics and demographics, including functional outcome at 90 days as measured by modified Rankin Scale (mRS), which was categorized as favorable (mRS 0–2) or unfavorable (mRS 3–6).

Results
Of patients who received MT, 54 (30.3%) had a prior medical history of depression. On univariate analysis, patients with a history of depression had 2.5 times higher odds of an mRS score of 3–6 (cOR = 2.47, 95% CI = 1.11‐5.48). Multivariate analysis included history of smoking, hypertension, obesity, Alberta Stroke Program Early CT Score (ASPECTS)[YC1][KC2], time to recanalization, and discharge NIHSS score, along with history of depression. We found that the odds of having an unfavorable mRS were 5 times higher in those with a history of depression than those with no history (aOR = 5.15, 95% CI = 1.09‐23.31). Additionally, discharge NIHSS was associated with 1.5 times higher odds of unfavorable mRS for each point increase in NIHSS score (aOR = 1.47, 95%CI = 1.25‐1.74). While pre‐existing depression was associated with poorer functional outcomes, it was not associated with mortality, cOR = 1.12, 95%CI = 0.55‐2.27.

Conclusions
In this study, we found that a prior medical history of depression is associated with unfavorable functional outcomes at 90 days in patients who received MT. Future studies should investigate the association between the severity of depression and stroke outcomes and explore methods to mitigate the impact of depression on stroke outcomes.
Abstract Number ‐ 198: Management of poor grade aneurysmal subarachnoid hemorrhage: illustrative case and literature review
Authors: Brown Nolan , Bamimore Michael , Lee Seung , Perez‐Vega Carlos , Singh Rohin , Gendreau Julian , Ravindran Krishnan , Al‐Shaikh Rana , Jeevaratnam Suren , Freeman William 
Published: April 2023

Introduction
Poor‐grade aneurysmal subarachnoid hemorrhage (aSAH) is associated with high mortality. Overall, 20–30% of aSAH are described as poor grade. Despite recent advances in management strategies, prognosis of poor‐grade aSAH remains dismal. As such, we review the most current literature regarding management strategies that can be used to decrease the risk of the four most common causes of secondary brain injury: 1) aneurysm re‐rupture, 2) hydrocephalus, 3) cerebral salt wasting, and 4) delayed cerebral ischemia/vasospasm.

Methods
We present a 46‐year‐old female patient with poor‐grade aSAH after a loss of consciousness following thunderclap headache. Examination showed a dilated left pupil and Glasgow Coma Scale (GCS) of 4. Imaging revealed a ruptured anterior communicating artery aneurysm, and she was subsequently taken to the neuro‐interventional radiology suite for EVD placement. On POD 7 Transcranial Doppler (TCD) suggested moderate vasospam of left MCA. Two successful balloon angioplasties of the basilar, ACA‐A1, and MCA‐M1 were successfully performed on separate consecutive days. By POD 10, intermittent severe ICP spikes required targeted temperature management (TTM) with hypothermia. On POD 24, her ICP normalized, she was no longer comatose, and her EVD was clamped and removed. She was rapidly weaned off ventilator and transitioned to rehabilitation. 3‐months postoperatively, Modified Rankin Scale score was 0.

Results
Based upon the result of our literature review, we propose maintaining blood pressure below 160 mmHg prior to intervention, after which it can be increased to 160–240 mmHg to prevent vasospasm. Transcranial Doppler is essential to detect vasospasm as the aSAH symptoms subtle; once identified, vasospasm can be successfully treated with balloon angioplasty. Finally, targeted temperature management, mannitol, hypertonic saline, and neuromuscular paralysis are essential for postoperative management of ICP levels.

Conclusions
The multimodal approach should be considered when managing poor grade aSAH. Further research in aSAH management would benefit the patients who present with poor prognosis, thereby improving patient care and leading to a standard, effective approach for aSAH management.
Abstract Number ‐ 218: Mechanical Thrombectomy in a HIV Patient with Staphylococcus Lugdunensis Bacteremia: A Case Report.
Authors: Collins Braylee W , Collins Braylee , Sadeghpour Shirin , Patel Sunay , Neal Jason 
Published: April 2023

Introduction
Occlusion of cerebral arteries account for 40–50% of neurological complications of infective endocarditis with the emboli most commonly lodging in the middle cerebral artery. The management of these occlusions with the use of thrombolytic therapies are associated with intracranial hemorrhage whereas outcomes with endovascular thrombectomy, while still under investigation, appear to be more favorable. In this case report, we present a HIV patient with persistent staphylococcus lugdunenesis bacteremia of unknown origin and acute left middle cerebral artery occlusion, who underwent endovascular thrombectomy.

Methods
Case Report

Results
A 66‐year‐old male past medical history of HIV on Elvitegravir/Cobicistat/Emtricitabine/ Tenofovir, pancytopenia and treated hepatitis C who presented for malaise, back pain, and urinary symptoms for 1 week. Initial labs remarkable for pancytopenia, CD4 count 44 and positive urinalysis. Ceftriaxone was started for UTI and Trimethoprim/Sulfamethoxazole for PJP prophylaxis. Urine and multiple blood cultures were positive for staphylococcus lugdunensis. Vancomycin was added to antibiotic therapy. On day two of hospitalization, patient developed new onset aphasia, right facial droop, and right hemiparesis. Upon evaluation, NIHSS was 14. CT head was negative. CTA head and neck showed left M1 occlusion. CT perfusion showed an infarct core of 20cc and 144cc of penumbra. Due to concern for possible infective endocarditis, thrombolytics were not administered but he was taken for thrombectomy. Emboli retrieval was successful with mTICI‐2c reperfusion. During thrombectomy, clot noted to have septic emboli appearance. Post thrombectomy, patient had complete resolution of neurological deficits. MRI brain showed multiple punctate foci of restricted diffusion in the left middle cerebral artery distribution consistent with embolic process. TTE was inconclusive. Intraoperative cultures of the clot resulted positive for staphylococcus lugdunensis and pathology examination detailed clot with bacterial colonization. TEE was performed and negative for valvular vegetations, mass, thrombus, or endocarditis but there was an intrapulmonary shunt. Patient later developed a small acute left parietal lobe parenchymal hematoma and basal ganglia infarct. His neurological status remained unchanged. He completed 6 weeks of IV antibiotic therapy upon discharge.

Conclusions
This case illustrates the importance of timely endovascular thrombectomy in suspected cerebral septic emboli as outcomes are favorable. It supports prompt recognition of septic emboli bacterial species for targeted antibiotic therapy along with further investigation into staphylococcus lugdunensis and its relation with cerebral septic emboli. This case urges additional exploration into the relationship between HIV patients and cerebrovascular disease including cerebral septic emboli.
Abstract Number ‐ 219: Spinal cord infarct in young: Fibrocartilaginous Embolism with Occlusion of Anterior Spinal Artery
Authors: Tran Thanh Lam N , AlHashim Hayder , Harrigan Mark 
Published: April 2023

Introduction
Spinal cord infarctions are rare and account for fewer than 1% of all strokes. Diagnosis is usually established by clinical symptoms of sudden onset paraplegia and sensory dysfunction along with radiographic evidence of a non‐enhancing, diffusion‐restricted T2 hyperintense lesion on spinal cord MRI. We describe an interesting case of anterior spinal artery infarct from suspected fibrocartilaginous embolus from intervertebral disc.

Methods
Case report. Demographics and clinical history were obtained by chart review. MRI and cerebral angiogram images were reviewed and compared to radiology reports.

Results
21‐year‐old female with no prior medical history presented with sudden onset headache, bilateral arm tingling, and neck stiffness that rapidly progressed within the hour to quadriplegia with numbness below the T2 sensory level. She continued to worsen, developed respiratory failure and required intubation. MRI of the cervical cord revealed a longitudinally extensive, non‐enhancing, diffusion‐restricted lesion extending from the bilateral medial medulla to the ventral spinal cord at C5/6 vertebral level. Cerebral and spinal digital subtraction angiography was notable for non‐opacification of the cervical anterior spinal artery. She had extensive work up for dissection, vasculitis, hypercoagulable state, autoimmune conditions that were all negative. However, there was a diminished T2 signal in her C5‐6 intervertebral disc with subtle loss of intervertebral disc space concerning for disc compression, likely related to her job requiring intensive heavy lifting. It was surmised that she developed a ventral cervical cord infarct secondary to fibrocartilaginous embolization and occlusion of anterior spinal artery, from recent mechanical compression of her C5‐6 disc. Cases of spinal cord infarcts following mechanical trigger, such as heavy lifting or falls, with histopathological confirmation of fibrocartilaginous material in the vasculature postmortem are well reported. It is postulated as a mechanism of spinal cord infarct in young patients that compressive forces on the intra‐vertebral body trigger embolization of nucleus pulposus material through persistent nuclear anastomoses to the spinal circulation.

Conclusions
Ischemic infarct should be considered in the differential diagnosis for sudden onset of symptoms localizable to spinal cord, especially when spinal MRI shows restricted diffusion in a vascular distribution. Demonstrating non‐opacification of the anterior spinal artery on digital subtraction angiography confirms the diagnosis. In case of negative work up for spinal cord infarct, the presence of an abnormal signal in the intervertebral disc on MRI may suggest fibrocartilaginous embolism as a mechanism of infarction in young patients.
Abstract Number ‐ 221: Lower Thoracic Spinal Dural Arteriovenous Fistula Presenting With Progressive Paraplegia: A Case Report
Authors: Mehta Amit , Lightfoot Nathan , Khan Fahad , Sur Samir , Barry Brian 
Published: April 2023

Introduction
We present a 72‐year‐old male with osteoarthritis, lumbar stenosis, coronary artery disease with a 4‐vessel bypass graft in February 2020, hypertension, hyperlipidemia, and obesity who presented with subacute progressive lower extremity weakness. He began having lower back pain following his cardiac surgery in February 2020. He was evaluated by a rehabilitation doctor in September 2020 who diagnosed him with lumbar radiculopathy and treated him with one round of steroid injections that helped a bit. Six months later he returned for follow‐up with the aid of a wheelchair which he started using in the last two weeks due to progressive lower extremity weakness. He was sent to the ED for neurologic evaluation. He denied radicular pain, saddle anesthesia, and urinary or bowel incontinence.

Methods
On neurologic exam, he had 2/5 bilateral hip flexion strength, 4/5 bilateral distal lower extremity strength, intact sensation to all modalities, and diffuse bilateral hyporeflexia (1+) with flexor plantar responses. An MRI brain was unremarkable. An MRI cervical, thoracic and lumbar spine with contrast showed extensive confluent cord edema with enhancement from T9 to the conus medullaris. He was started on high‐dose IV methylprednisolone for concern of transverse myelitis. Serum metabolic, hematologic, autoimmune, and infectious workup were negative. Due to a lack of improvement, his spinal imaging was reviewed with neuroradiology who recognized previously unidentified posterior T2 flow voids in the subarachnoid space at T1. A spinal angiogram for suspicion of a spinal dural arteriovenous fistula (dAVF) was subsequently scheduled.

Results
Angiography confirmed a type I spinal dAVF which was treated with posterior laminectomy and surgical ligation. The patient’s lower extremity strength improved and he was discharged to acute rehab. At his 1‐month neurology follow‐up appointment, he was ambulating with minimal assistance from a cane with near full lower extremity strength.

Conclusions
With an initial presentation of subacute progressive lower extremity weakness and imaging findings concerning for longitudinally extensive transverse myelitis, our initial suspicion was highest for an underlying autoimmune or infectious disease. However, this case teaches us to not presume all transverse myelitis or enhancing spinal cord lesions must be from an inflammatory, neoplastic, or infectious condition. A wide differential for this presentation including spinal dAVF is necessary as this is one of the most commonly missed neurovascular diagnoses. T2 flow voids are highly suggestive of this condition, but a spinal angiogram is the gold standard for diagnosis.
Abstract Number ‐ 223: Spontaneous Revascularization of Completely Occluded Internal Carotid Artery: Case Report
Authors: Ghani Mohammad , Kemper Nicholas , Coghlan Meghan A , Yousaf Muhammad I , Ander Tracy M , Remmel Kerri , Liu Wei 
Published: April 2023

Introduction
Occlusion of the internal carotid artery (ICA), caused by atherosclerotic thrombosis, arterial embolism, or dissection, is associated with high morbidity and mortality of acute stroke. Commonly, these lesions are managed with aggressive medical treatment due to their chronic and usually irreversible nature. Spontaneous recanalization of the occluded ICA has been described in rare instances.

Methods
We present a report here on three cases with spontaneous recanalization of complete occluded carotid arteries.

Results
Our first patient was a 62‐year‐old male with a history of hypertension, who presented with transient left eye vision loss. CT angiography of the head and neck (CTA HN) demonstrated left ICA complete occlusion while the left middle cerebral artery (MCA) and anterior cerebral arteries (ACA) were patent. He was treated with apixaban. At the two‐month follow‐up, the repeat CTA HN demonstrated complete recanalization of the left ICA. The etiology of the occlusion remained cryptogenic. Our second patient was a 71‐year‐old male with a prior history of right carotid endarterectomy, peripheral vascular disease, coronary artery disease, hypertension, and dyslipidemia, who presented with acute right MCA stroke. Work‐up with CTA HN demonstrated right ICA complete occlusion. He was treated medically with aspirin and clopidogrel. Six months later, he presented with a two‐week history of intermittent confusion and left‐sided weakness. His MRI brain was negative foracute stroke. Interestingly, CTA HN demonstrated that the right ICA had complete recanalization. The cause of carotid thrombosis remained cryptogenic. Our third patient was a 46‐year‐old female with a history of hypertension, hyperlipidemia, remote low‐speed vehicle collision, and cervical spine chiropractic treatment (the last neck manipulation was about two years prior), presenting with sudden onset dizziness, right‐sided neck pain, and left homonymous hemianopia. Brain MRI showed acute right posterior cerebral artery (PCA) stroke. CTA HN revealed occlusion of the right ICA with a flare‐up appearance suggestive of a carotid dissection. She also had a right fetal PCA. She was treated medically with rivaroxaban. Four months later, a follow‐up MR angiogramof the neck showed a fully revascularized right ICA. Her hypercoagulable workup revealed that she had a rare form of breast cancer.

Conclusions
Although ICA occlusion is generally considered chronic and irreversible, our case series suggests that the lesion can have spontaneous recanalization with medical treatment. Further studies of characterizing carotid occlusion to predict recanalization are warranted.
Abstract Number ‐ 224: Stroke Mimic—Patient with Symptomatic Amyloid‐Related Imaging Abnormalities Presenting with Stroke‐like Symptoms.
Authors: Kmeid Michael , Blanden Adam R , Kaur Navreet , Clos Siara , Masoud Hesham 
Published: April 2023

Introduction
Amyloid‐related imaging abnormalities (ARIA) are rare phenomena in patients taking monoclonal antibodies directed against amyloid beta in Alzheimer’s disease clinical trials. The pathogenesis is unclear, but may be due to an induced inflammatory microangiopathy. While the majority of cases are asymptomatic and resolve without intervention, a small subset can experience symptoms of sudden or uncertain onset. Given the relative rarity of this phenomena and the striking imaging findings, ARIA can be misdiagnosed as ischemic stroke or primary microangiopathy when presenting with acute‐subacute symptoms. Following diagnosis there is no clinical consensus on the optimal management and approaches range from withdrawal of the study drug to pulse‐dose steroids.

Methods
We present a case study of a patient admitted to our inpatient stroke service after 4 days of rapidly progressive confusion and sudden vision loss with MRI workup reporting subacute stroke. The findings were ultimately determined to be secondary to ARIA.

Results
A 67‐year‐old man with early onset Alzheimer’s disease enrolled in a clinical trial for donamemab presented with four days of marked cognitive decline including increased forgetfulness, confusion, and episodic hallucinations following an episode of abrupt vision loss. An outpatient MRI brain demonstrated subcortical hyperintensity that was initially reported as a subacute left occipital stroke. Notably, an MRI performed 3 months prior showed no abnormality. Neurological exam was remarkable for right superior quadrantanopia, memory impairment, and mild confabulation. Repeat MRI demonstrated FLAIR white matter hyperintensities and extensive susceptibility artifact in the left parieto‐occipital lobe, consistent with an inflammatory cerebral amyloid angiopathy (or ARIA). Spot EEG demonstrated no associated epileptiform discharges. Patient was treated with 7‐day course of IV Solumedrol and had improvement in visual symptoms. He was discharged on a prednisone taper and a followup MRI brain 4 weeks later showed near‐ complete resolution of the previously noted subcortical white matter changes.

Conclusions
ARIA can be seen in patients receiving anti‐amyloid monoclonal antibody treatments. Surveillance MRIs have been implemented to screen for such cases as a minority of patients with ARIA present with symptoms. As noted with this case study, a relatively acute presentation and imaging characteristics can lead to an initial misdiagnosis as subacute ischemic stroke. Vascular neurologists should be aware of this clinical entity, noting the natural history and treatment are not well established. This patient was treated aggressively as an inflammatory cerebral amyloid angiopathy with IV steroids and noted positive outcome. More research is required to establish the optimal acute medical management of patients with ARIA.