Acute Infarction Research Articles

Abstract 093: Carotid Stump Syndrome: an Insidious Source of Recurrent Ischemic Strokes

Introduction Carotid stump syndrome (CSS) is a paradoxical phenomenon that occurs when there are repeated ischemic events in the carotid vascular territory despite demonstrated occlusion of the ipsilateral internal carotid artery (ICA). It is thought to be caused by turbulent blood flow in the patent stump of the occluded ICA creating microemboli which reach the brain through anastomotic channels and retrograde flow. We present a case of recurrent infarctions in setting of known ipsilateral ICA occlusion, who was diagnosed with carotid stump syndrome. Methods A male veteran in his 60s with a medical history of DVTs on apixaban, PVD, and ischemic stroke with residual right‐sided weakness, presented with worsening right‐sided weakness and difficulty with ambulation. Two months prior to the presentation he was diagnosed with acute infarcts in left frontal, parietal, and temporal lobes due to thromboembolism from left ICA occlusion. On presentation his neurological exam revealed right‐sided hemiparesis. MRI brain showed multiple acute and chronic cortical and subcortical infarcts in the left frontotemporoparietal lobes and lack of flow void in the left distal ICA. To further evaluate the dynamics of blood flow patient underwent a cerebral angiogram which confirmed the diagnosis of complete occlusion of left ICA and demonstrated reconstitution of the intracranial ICA through retrograde filling via the ophthalmic artery and anastomotic branches with the internal maxillary artery (IMax). For secondary prevention he was started on statin and aspirin while his home Apixaban was continued. Surgical and endovascular treatment approaches were discussed but the patient declined any intervention. In his four months follow up clinic visit he had no further concerns of recurrent strokes or new symptoms. Results Carotid stump syndrome is a rare cause of cerebral and retinal ischemia; however, it must be considered in patients with recurrent ischemic strokes and chronic ipsilateral ICA occlusion. Due to the patent proximal, or perhaps in some cases distal, carotid stump, there’s turbulent flow and hence the thrombus formation can occur. Hemodynamic and embolic factors attribute towards the microembolization from the proximal carotid stump through the external carotid artery (ECA), into the facial artery and IMax and their distal branches which anastomose with the ophthalmic artery, causing the emboli to end up in the major branches of the carotid terminus. If a distal stump is symptomatic, then the microemboli can readily end up in the distal ICA branches. In addition to medical management with DAPT or anticoagulation and high intensity statin, our literature review supports endovascular or surgical interventions due to reportedly good outcomes. Interventional approaches may include ECA‐ICA stenting with a covered stent or stent‐assisted coil embolization of the proximal stump. Surgical procedures include an endarterectomy on the ipsilateral ECA or contralateral ICA to increase collateral circulation. ECA‐ICA bypass is another option. Conclusion Carotid stump syndrome is a rare and underrecognized cause of recurrent ischemic strokes, though it is a potentially treatable entity. The therapeutic goals include medical management along with endovascular or surgical treatment whenever possible.

Abstract 094: Sudden Onset Dysphagia: A Symptom To Be Aware of During Code Strokes

Introduction Lateral medullary infarction (LMI) can present with dysphagia, dysphonia, dysarthria, vertigo, nausea, skew deviation, and ipsipulsion. Patients may also exhibit sensory loss and ipsilateral Horner’s syndrome. LMS often develops because of an acute infarct from the vertebral arteries or posterior inferior cerebellar arteries (PICA). The most common mechanism of stroke usually is atherothrombosis, followed by cardioembolic, dissection and embolic source of undetermined source (ESUS). While dysphagia often accompanies the constellation of LMS symptoms, it is rarely the first symptom and has only been reported in a few cases in the literature. In this report we describe the case of a man in his 40s with acute onset dysphagia as the presenting finding ahead of an LMS diagnosis. Methods The patient was identified in routine clinical practice. Results A man in his 40s with medical history of HTN, type 2 DM and polycystic kidney disease, presented with sudden‐onset dysphagia which started while he was drinking alcohol. Later he noticed that he was unable to keep his balance. His National Health Institute Stroke Scale was 4. Neurologic exam was pertinent for left‐sided miosis, ptosis, and dysmetria. Pinprick and temperature sensation were decreased on the right arm and leg. Facial sensation to light touch was diminished on the left. Brain MRI showed an acute infarct in the left lateral medulla (Figure A). CTA showed calcified atherosclerosis of the V4 segment of left vertebral artery (Figure B). Mechanism of ischemic stroke was artery to artery thromboembolism from the left V4 segment of vertebral artery. For secondary prevention, dual antiplatelet therapy, high intensity statin, and optimization of his risk factors were initiated. Conclusion This case report demonstrates that dysphagia can be the initial symptom of an acute ischemic stroke. Diagnosis and recognition of an atypical presentation of lateral medullary syndrome can pose a particular challenge especially in this era of “time is brain” but is of the utmost importance to facilitate good outcomes. Patients presenting with dysphagia who have risk factors for stroke and no other obvious etiology for their symptoms should be worked up for possible cerebrovascular etiology.

Abstract 110: Autoangiogenesis Secondary to Chronic Cocaine Use Mimicking Moya‐Moya

Introduction We present the case of a young male presenting with syncope who was found to have incidental hypodensities on computed tomography (CT) of his head, with magnetic resonance imaging (MRI) concerning for Moya‐Moya related occlusion of the right internal carotid artery, but with digital subtraction angiography (DSA) showing extensive autoangiogenesis and collateralization from all other intracranial vascular territories, without Moya‐Moya related changes. This presumably developed as reactive changes to severe chronic cocaine use. Methods We present a case from a tertiary care center in the borough of Manhattan, New York City, USA. All information is deidentified and exempt from IRB approval. Results A 36‐year‐old man with history significant for asthma, active smoker status, and active cocaine use, presented for loss of consciousness. The patient reported 3 days of upper respiratory symptoms and decreased oral intake with subsequent loss of consciousness immediately preceded by lightheadedness and nausea, and without any post‐event confusion, lacerations, or incontinence. Neurologic history is significant for right upper extremity weakness from 9/2022‐12/2022 that self‐resolved and was believed to be a peripheral nerve pathology. Admission exam without focal deficits. Admission CT of his head showed multifocal confluent hypodensities in the subcortical right frontal lobe. CT Angiogram of head and neck showed severe narrowing at right Internal Carotid Artery (ICA) terminus and right M1 segment with lenticulostriate arterial collateralization, severe bilateral A1 stenosis with distal Anterior Cerebral Artery (ACA) flow suggestive of chronic collateralization, and significant right Posterior Cerebral Artery (PCA) collateralization. Given concern for Moya‐Moya disease, MRI of the brain was obtained and despite no acute infarct, MRI was significant for multifocal white matter T2/FLAIR hyperintensities with the largest in the right frontal lobe. The patient subsequently underwent digital subtraction angiography (DSA) to assess collaterals and stratify for possible need for future encephaloduroarteriosynangiosis (EDAS). DSA showed significant auto‐angiogenesis between numerous vascular territories, including recruitment of right Posterior Cerebral Artery and External Carotid Artery branches to perfuse the territory of the severe right ICA terminus steno‐occlusive disease. With minimal anterograde flow into the right Anterior Choroidal Artery and none to the right Middle Cerebral Artery (MCA), the characteristic Moya‐Moya appearance was not appreciated on DSA given minimal anigogenesis around the right ICA occlusion site. Rather, distal perfusion of the R ICA territory was dependent on collaterals from the right PCA, right ACA via the Anterior Communicating Artery, angiogenesis between the right Anterior Falcine Artery and R ACA, and angiogenesis between the right MCA and ACA/MCA cortical branches. These proliferative changes involved all cranial vascular territories, including those without steno‐occlusive disease. Conclusion Acute cocaine use is associated with increased risk of acute ischemic stroke[1], due in part to its sympathomimetic effects causing vasospasm and to its arrhythmic properties[2]. Neuroadaptation after chronic cocaine use is less well understood though rat models suggest that as cerebral ischemia develops from chronic cocaine use, the HIF‐VEGF pathway is activated to promote angiogenesis to restore local blood flow[3]. We present this case as evidence of a similar angiogenic physiologic response in humans to minimize the microvascular ischemic injury from chronic cocaine use.

Abstract 213: Successful Mechanical Thrombectomy in Acute Stroke With Pre‐interventional Thrombolysis‐Induced Intracerebral Hemorrhage: Case Report

Introduction Intravenous thrombolytics (IVT) and mechanical thrombectomy (MT) have become the standards of care for treating patients with large vessel occlusion (LVO) acute ischemic strokes (AIS) [1‐4}. Intracerebral hemorrhage (ICH) is a main complication of IVT, with prevalence reported around 3.2% in a large multicentered meta‐analysis [2,6]. However, limited data remains about the safety and efficacy for patients to undergo MT with IVT associated pre‐interventional ICH as no randomized control trials or standard of care guidelines are available [2,4,5,7]. Methods NA Results 56‐yo male with history of alcohol abuse presented via EMS as a stroke alert with acute onset right hemiplegia, global aphasia, right facial droop, and leftward gaze preference two hours prior to arrival. RACE 10+ with NIHSS 24. No known history antiplatelet or anticoagulation use. Computerized Tomography (CT) Brain scan showed left middle cerebral artery (MCA) hyperdense sign with left insular cortical ribboning. CT angiography (CTA) showed near occlusive stenosis of the left carotid bulb with an acute thrombus within Supraclinoid Internal Carotid Artery (ICA) extending into the Left MCA and origin of Left Anterior Cerebral Artery (ACA). Patient was emergently administered IV‐tissue Plasminogen Activator (IV‐tPA) and taken for endovascular thrombectomy. During initial angiogram, after crossing the stenotic cervical bulb, the left Supraclinoid ICA and MCA occlusions were visualized. There was longitudinal partially occlusive thrombus extending from the M1 into the M2 divisions. No opacification of the inferior M2 branch was visualized, with perfusion deficit over the temporal, parietal and frontal regions. Additionally, extravasation of contrast was seen within the left basal ganglia region, concerning for hemorrhagic transformation from IV‐tPA. Reversal of IV‐tPA was initiated, and patient was given cryoprecipitate, platelets, and tranexamic acid. Decision to undergo MT was made secondary to severity of debilitating neurologic symptoms, age, and large perfusion deficit observed. He underwent single pass complete recanalization, TICI 2C using Stent retriever and aspiration. Left ICA stenting was not completed secondary to hemorrhagic transformation. Repeat CT Brain confirmed moderate left frontal lobe hemorrhage with vasogenic edema and 3mm left‐to‐right midline shift. No neurosurgical intervention required. Magnetic resonance imaging (MRI) Brain showed left cerebral hematoma with mass effect, acute infarct within left caudate nucleus, and minimal posterior cortical restricted diffusion without hemorrhagic conversion. Patient was monitored for 1 week with serial brain imaging. Patient was discharged on Aspirin 81 mg daily to inpatient rehabilitation with NIHSS 21, mRS 4 (0 prestroke). Today, in rehab he ambulates with walker with moderate expressive aphasia and right upper extremity weakness. Plan to follow‐up 2‐month post‐hospitalization for left ICA stenting. Conclusion While pre‐interventional IVT‐associated ICH in AIS with LVO are rare, few cases have been shown to have positive neurological outcomes [2,5,7]. We demonstrate a unique case of early identification of reperfusion hemorrhage on fluoroscopy with prompt reversal initiated. The decision to continue with MT based on downstream occlusion of basal ganglia hemorrhage not at further risk of expansion from reperfusion. The patient did well on follow‐up imaging despite the hemorrhage. Further randomized control clinical trials are required to establish best care guidelines, safety, and efficacy.

Abstract 161: Repeated administration of thrombolytic therapy in the setting of stuttering lacunar infarct

Introduction Tissue plasminogen activator (tPA) is the standard of care for the treatment of acute ischemic stroke with symptom onset within 4.5 hours. One exclusion criterion for tPA administration is stroke within 3 months due to the presumed increased risk of hemorrhage. While the rate of early recurrent stroke (ERS) within 3 months is as high as 14.5‐18.3%, the safety and effectiveness of repeated tPA administration remain unclear. An increasing number of studies pose a challenge to this recommendation. One study identified 19 patients who received tPA for ERS and found no symptomatic intracranial hemorrhage. Fifteen other studies with a cohort of 57 patients (including one patient receiving repeated tPA within 90 minutes) reached the same conclusion that repeated tPA is safe in ERS. We present a patient with stuttering motor weakness who received intravenous (IV) tPA twice, 3 days apart with discharged modified Rankin scale (mRS) of 3. Methods The patient was identified in routine clinical practice. Results Our patient is a 61‐year‐old right‐handed Caucasian woman with a medical history of untreated hypertension presented with sudden onset of left arm and leg weakness. IV tPA was given at the local emergency department (ED) and she was then transferred to our comprehensive stroke center. Upon arrival, her National Institutes of Health Stroke Scale (NIHSS) was 0. Her symptoms were completely resolved. Computed tomography (CT) head was unremarkable and CT angiography (CTA) did not show significant stenosis or occlusion. Magnetic resonance imaging (MRI) of the brain was negative for an acute infarct. She was diagnosed with a transient ischemic attack and was discharged home with aspirin and a high‐intensity statin for secondary stroke prevention. She presented to the ED the next day with identical left‐sided weakness again. Her NIHSS was 5 this time and IV tPA was given again. MRI showed an acute infarct in the right posterior limb of the internal capsule. Transthoracic echo did not reveal an intracardiac shunting or thrombus. The stroke mechanism was small vessel disease, and anti‐hypertensive medications were added to the treatment. She was discharged to an acute rehabilitation center with an mRS of 3 and her 90‐day mRS was 1 on follow up. Conclusion Management of ERS is a challenging issue in stroke care. Our case adds value to the current limited literature demonstrating the safety and effectiveness of repeated tPA in ERS, especially in patients with MR negative stuttering lacunar infarct and subsequent improvement following tPA. Further research with larger registries is needed to identify appropriate selection criteria for repeated tPA use in this patient population.

Abstract 092: Vasospasm as a Consequence of IVIg Usage for GBS.

Introduction The relationship between Intravenous Immunoglobulin (IVIg) and cerebrovascular vasospasm is poorly and incompletely understood. Some case reports have identified IVIg as potential therapy for vasospasm, while others have implicated it as a causative agent in primarily coronary artery vasospasm and the development of atypical angina. This case illustrates a situation in which a patient with Guillain‐Barre Syndrome (GBS) was started on IVIg and developed subsequent vasospasm with cerebral infarcts requiring intra‐arterial therapy. Methods Case Report Results Our patient is a 62 year old female with a history of cervicothoracic subdural hematoma status postevacuation with left leg weakness, hypertension, known right ICA aneurysm, and chronic left ICA occlusion who presented as a transfer from an outside facility where she initially presented with progressive back pain, lower extremity weakness, areflexia and dysautonomia. MRI brain initially demonstrated posterior‐predominant T2 hyperintensities affecting subcortial white tracts suggestive of PRES. Lumbar puncture demonstrated cytoalbuminologic dissociation supporting a superimposed GBS. IVIg was initiated, however the patient's mentation and examination declined. Repeat MRI demonstrates bilateral, posterior‐predominant acute multifocal ischemic infarcts. Vessel imaging demonstrated vasospasm of the basilar and bilateral anterior Circle of Willis. Oral Verapamil was initiated. Digital Subtraction Angiography confirmed these findings; intra‐arterial verapamil was utilized with significant improvement in the patient's examination. Conclusion IVIg has only a weak association with coronary artery vasospasm, however is heavily implicated in the onset of this patient's diffuse vasospastic ischemic disease. Prompt identification and aggressive initiation of treatment is essential in minimizing the burden of ischemic stroke and optimizing outcomes for these complex patients.

Abstract 006: Glenzocimab Is Associated With Less Haemorrhagic Transformation Using Artificial Intelligence Imaging In Mechanical Thrombectomy Patients

Introduction Lesion volume measurement provides an objective and quantitative assessment of stroke severity and it is often used as a surrogate endpoint of clinical outcome in therapeutic trials. ACTIMIS (NCT03803007) was a randomized phase 1b/2a clinical trial evaluating glenzocimab, a monoclonal antibody fragment targeting platelet receptor glycoprotein VI, versus placebo in patients with acute ischemic stroke treated by thrombolysis alone or associated with mechanical thrombectomy (MT), both subgroups being well balanced. Primary analysis demonstrated a significant reduction in intracranial hemorrhage occurrence stroke‐related mortality and a trend towards reduction in severe disability. In this sub‐analysis, Artificial Intelligence (AI) imaging biomarkers were used to assess efficacy of glenzocimab in the subgroup undergoing MT in the pooled phase 1b (dose escalation) and phase 2a (dose confirmation) studies. Methods In the phase 1b study, patients were randomized to an escalating dose of glenzocimab or placebo (4:1, n=12 per group, 125mg, 250mg, 500mg, 1000mg). In the phase 2 dose confirmation study, patients were randomized (1:1) with 1000mg glenzocimab or placebo. CT scan or MRI was acquired at baseline with CT at 24 hours and MRI at 7 days (CT if MRI not available) for safety and efficacy analysis, respectively. Baseline and follow up imaging were processed using Brainomix software (Oxford, UK). AI output was reviewed for accuracy by an expert clinician (DC) blinded to treatment allocation. Results Of 166 patients in the trial, 81 patients underwent MT and had follow up non‐contrast CT imaging available at 24 hours (48 glenzocimab, 33 placebo) and 72 had Day‐7 imaging (47 glenzocimab, 25 placebo). Day‐7 imaging was available for 8 fewer placebo patients and 1 glenzocimab patient than at 24 hours. All except 2 patients (1 placebo, 1 glenzocimab) with missing data at Day‐7 died during the study. Multivariate regression modelling showed a significant interaction between patients undergoing MT and receiving glenzocimab. Glenzocimab had a greater effect on reducing the risk of haemorrhagic transformation in the MT subgroup (exploratory p=0.001). Presenting acute infarct volume was similar between glenzocimab and placebo arms (mean [SD]; 16.27mL [30.2] vs. 19.62mL [28.98], non‐significant). There was a significantly smaller volume of haemorrhagic transformation in the glenzocimab group at 24 hours compared to placebo (1.83mL [6.59] vs 33.46mL [75.07], exploratory p<0.01) and a trend towards smaller volume of ischemic injury in the glenzocimab group (52.32mL [82.07] vs 62.93mL [79.4]). Similar significant trend at Day‐7 for haemorrhagic transformation was seen but less marked due to the unbalanced loss to follow up at Day‐7 (2.99mL [12.35] vs 4.19mL [10.83], exploratory p<0.05). Conclusion Glenzocimab reduces likelihood of haemorrhagic transformation in patients undergoing MT. Haemorrhage volumes were smaller in the glenzocimab group and encouragingly there was a trend to smaller volumes of ischemic injury. There was a greater drop‐out rate in the placebo group between 24 hours and Day‐7, which resulted in a smaller difference in haemorrhagic volumes at Day‐7. Those results, which are to be further analysed in ACTIMIS overall population of AIS patients, could highlight glenzocimab mechanism in the reperfusion injury mitigation.

"Uncrossed Central Facial Paralysis" Caused by Pontine Infarction: A Case Report.

We report a patient with extraordinary pontine infarction-induced contralateral central facial palsy and weakened limb strength. This is a 66-year-old man with left arm movement difficulty for 10 days and worsening over the last 1 day. His left nasolabial fold flattening and left arm strength and sensory were decreased. He could not complete the finger-nose test well with his right hand. Magnetic resonance and magnetic resonance angiography tests confirmed his right pontine acute infarction but without large vessel stenosis or occlusion. "Uncrossed paralysis" patients may present with contralateral face and body weakness with pontine infarcts, if the infarct occurs above the level of the facial nucleus head, and may be simmilar with the higher level pontine lesions or cerebrum semisphere infarction, which need particular attention during clinical practice.

Abstract 108: Artery Of Percheron Infarctions (AOP): A Tale of Two Outcomes

Introduction The AOP is a rare anatomic variant in which a solitary arterial trunk arises from the proximal segment of the posterior cerebral artery (PCA) and supplies the bilateral paramedian thalami and rostral midbrain. Occlusion may result in variable bilateral thalamic and midbrain infarcts. The clinical presentation is most commonly lethargy and somnolence thought to lack other localizing features. Often the diagnosis and treatment of stroke is delayed. Methods Here we present two cases of likely AOP infarcts which highlight the importance of considering this diagnosis on the differential of acute lethargy as timely treatment can lead to a significant difference in morbidity and mortality. Results Case 1: A 68‐year‐old male was initially admitted to an outside hospital with acute lethargy. He was transferred to our institution where he was found to be somnolent and required repeated stimulation to participate with interview. On further exam he was noted to have left ptosis, anisocoria, restricted left supra‐ and add‐ duction, and dysarthria. CT angiogram (CTA) showed no large vessel occlusion (LVO) or significant stenosis. Magnetic resonance imaging (MRI) demonstrated acute infarcts in the medial thalami and subthalamic nuclei bilaterally and uppermost portion of the midbrain. He was out of the window for IV thrombolytic. He was ultimately discharged to inpatient rehab with a persistent CN III palsy. Case 2: A 71‐year‐old female was evaluated emergently via telestroke for acute lethargy and was found to additionally have vertical diplopia, right facial palsy, and subsequent bilateral numbness of the face, arms, and legs. NIHSS 10 for LOC questions (1), facial palsy (2), motor drift (1 pt for each limb), sensory loss (1), aphasia (1), and dysarthria (1). She was treated with IV tenecteplase 179 minutes after the last known well and ultimately had complete symptom resolution. CTA was negative for LVO or significant stenosis. MRI brain demonstrated acute infarcts in the medial thalami bilaterally. Conclusion Here we present two cases of acute onset lethargy. MRI Brain revealed relatively symmetric restricted diffusion in the bilateral thalami of both patients suggesting the presence of an AOP variant. In contrast to the first case, signs of a posterior circulation infarct were quickly recognized in the second patient and IV thrombolytic administration resulted in return to baseline. In both cases there were subtle neurologic findings that suggested midbrain involvement – ptosis, restricted ductions, anisocoria. A high level of suspicion for bilateral thalamic infarct and potential AOP variant should be maintained in cases of acute lethargy. Careful neurologic exam often reveals other signs suggestive of posterior circulation infarct and timely therapeutics can significantly improve morbidity and mortality.

Abstract 105: Limb Shaking Transient Ischemic Attack: A Rare Presentation of Internal Carotid Artery Occlusion

Introduction Limb‐shaking transient ischemic attack (LS‐TIA) is a rare disorder characterized by brief, irregular, involuntary movements of the extremities with or without loss of consciousness. Associated paroxysmal hyperkinetic extremity movements often described by patients as “shaking,” “tremors,” or “twitching” are an uncommon and under‐reported presentation of cerebral hypoperfusion. Vascular etiology must remain on the differential as these transient but hemodynamically significant episodes are associated with severe carotid steno‐occlusive disease and carry an elevated risk for stroke. Methods The patient was evaluated in routine clinical practice. Results A man in his 50s with medical history of chronic right internal carotid artery (ICA) occlusion, coronary artery disease and tobacco use disorder presented with two months of intermittent, progressive worsening of left extremity tremors associated with ipsilateral weakness and mild confusion during the spells. These involuntary paroxysmal spells—precipitated by standing up, exertion and neck hyperextension—initially occurred 4 to 5 times per week in left upper extremity but progressed to 4 to 5 times per day with prolonged durations reaching 20 minutes and involving the left lower extremity. The initial event involved loss of consciousness, but no further syncopal episodes were noted. While ipsilateral hemiparesis and mild confusion occurred during the spells, spontaneous resolution and immediate return to baseline were reported afterward. On presentation, the National Institutes of Health Stroke Scale (NIHSS) was zero. Computed tomography (CT) head did not show acute intracranial process. CT angiography (CTA) re‐demonstrated right ICA occlusion at its origin. A load of Clopidogrel 300 mg and Aspirin 325 mg was administered. Orthostatic blood pressure measurements were normal. CT perfusion of brain demonstrated a perfusion decrease within the right frontoparietal lobes in the right middle cerebral artery (MCA) region. Routine EEG was performed, and it did not show interictal discharges. Brain MRI did not show acute infarcts. Catheter cerebral angiogram was then pursued, confirming right ICA occlusion at its origin and additionally showed mild atherosclerosis of the left ICA without flow‐limiting stenosis. After thorough evaluation, these events of unilateral extremity shaking and hemiparesis were deemed to be LS‐TIA. Neurosurgery was consulted and offered extracranial‐intracranial (EC‐IC)/ superficial temporal artery‐MCA bypass surgery. He was discharged in stable condition to continue DAPT and high‐dose statin while pending surgical intervention. Conclusion This case not only provides a descriptive narration of the presentation of LS‐TIA along with the steps in management undertaken but also encourages the consideration of vascular etiology as a potential cause for acute onset paroxysmal hyperkinetic movements. Early diagnosis and appropriate treatment are crucial to reduce burden of poor outcomes and prevention of stroke.

Abstract 112: When Cell Blood Count Matter, Hypereosinophilic Syndrome a Rare Cause of Ischemic Strokes

Introduction Hypereosinophilic syndrome (HES) is a rare hematological disorder defined by persistently elevated blood eosinophil count (>1500/μL), associated with evidence of organ damage. It can occasionally present primarily with neurological conditions such as ischemic strokes, encephalopathy, or sensory neuropathy. Driving hypothesized mechanisms are hypercoagulability owing to eosinophil‐related endothelial damage or cardioembolism. We present an unusual case of ischemic strokes due to HES in the setting of Fip1‐like 1‐platelet‐derived growth factor receptor alpha (FIP1L1‐PDGFRA) mutation. Methods The patient was identified in routine clinical practice. Results 38 year‐old‐male with no significant medical history who was transferred to our institution for blurred vision, and dizziness. His initial National Institutes of Health Stroke Scale was 3 for bilateral leg weakness. The neurological exam was pertinent for paresis in his left arm and legs. Magnetic resonance imaging (MRI) of the brain demonstrated multiple acute infarcts in bilateral cortical and subcortical structures as shown in Figure 1. Computed tomography angiography (CTA) of the brain and neck did not show significant stenosis or occlusion. During admission, transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) did not reveal any source for cardioembolism. Subsequently, he developed hyperactive delirium requiring anti‐psychotics. He was worked up for any infectious etiology because he continued to have a leukocytosis with an eosinophil count as high as 49%. Doppler of lower extremities showed deep vein thrombosis in the left femoral vein. Hematology evaluated the patient and, after performing a bone marrow biopsy, he was diagnosed with primary Hypereosinophilic syndrome (HES) in the setting of FIP1L1‐PDGFRA mutation. He was started on high‐dose methylprednisolone, hydroxyurea and later switched to Imatinib. A cardiac MRI was performed which was negative for eosinophilic myocarditis. The patient's mental status improved significantly after starting Imatinib and his anti‐psychotics were discontinued. In regards to secondary prevention, vascular neurology wanted antiplatelet monotherapy, however, the patient was started on Apixaban to treat his DVT. He was followed up in the stroke clinic 2 months after discharge, his modified Rankin score (mRS) was 1. Aspirin was recommended for secondary stroke prevention once hematology considers it safe to discontinue apixaban. Conclusion This case encourages the consideration of HES in patients with low cardiovascular risk factors who have infarcts following a cardioembolic or watershed pattern in brain imaging. Going back to the basics and reviewing simple laboratory tests like cell blood count can be the initial clue for diagnosis. Early recognition is crucial as immunosuppression is the most important treatment in the acute phase. While imatinib is the treatment of choice for FIP1L1‐PDGFRA mutation HES, patients continued to be at risk of stroke recurrence despite having normal eosinophil count as described by Rohmer et al.

Abstract 088: Treatment of a Ruptured AVM with Inflow Aneurysms: Mixed approach using coil and liquid embolization

Introduction Arteriovenous malformations(AVMs) are high‐flow vascular abnormalities characterized by direct communications between arteries and veins of various complexities. Cerebral AVMs may manifest with new‐onset seizures or intraparenchymal (IPH) or subarachnoid hemorrhages (SAH). Life‐threatening bleeds may occur from the AVM nidus or associated aneurysms. We report a patient with hemorrhage from a complex AVM that included a prominent nidus and large inflow aneurysms requiring several endovascular techniques for treatment. Methods N/A Results A 35 year old male patient newly arrived from the Philippines with a history of hypertension presented to the hospital after being found unresponsive at home with frothing from the mouth and incontinence. The patient regained consciousness in the ER, complaining of a posterior headache which he had been experiencing for a week. NIHSS of 0 was noted with no neurological deficits. CT‐head revealed extensive SAH in interhemispheric falx anterior to and outlining the entire corpus callosum with intraventricular extension. CT‐ angiogram demonstrated a prominent AVM with a well‐developed nidus situated to the left of midline about the posterior corpus callosum. Two large inflow aneurysms, felt to be the rupture site, projecting from the proximal left pericallosal artery were also demonstrated. An incidental ACA aneurysm was also noted. Cerebral angiography redemonstrated these findings as well as the drainage of the AVM primarily through the straight sinus. Graded as Spetzler Martin 4. Common femoral approach was used. An access catheter was passed into the left ICA. The pericallosal artery was accessed with a detachable tip microcatheter which was further advanced past the inflow aneurysms into the main pedicle feeding the AVM nidus. The inflow aneurysms were accessed and embolized with coils using a second microcatheter prior to AVM embolization. This sealed off access to the aneurysms and parent vessel against liquid agent backflow. Onyx‐18 was then injected into the main AVM pedicle under a blank roadmap. Extensive but partial filling of the AVM was noted anteriorly but full embolization of the posterior aspect of the nidus was not achieved. Finally coiling of the ACA aneurysm was performed after accessing the right ICA. An MRI with and without contrast was performed and an expected acute infarction in the left ACA territory was observed. A repeat angiogram was performed a week later revealing posterior cerebral artery and posterior choroidal branches feeding the posterior 1/3 of the AVM. Embolization of three posterior feeding pedicles was subsequently performed utilizing dilute NBCA. Because of coil impaction the proximal pericallosal inflow aneurysm required re‐treatment with further coil placement 8 months after initial treatment. The patient has regular angiograms to monitor the AVM, which appears stable without significant residual shunting. Conclusion Ruptured AVMs are fatal events requiring careful treatment to prevent further bleeding while preserving viable brain tissue. AVMs are fragile formations of vessels which can receive collaterals from multiple targets and often have associated high risk features like inflow aneurysms. Accordingly endovascular treatment may require a mixture of techniques to ensure adequate and safe embolization. Regular monitoring of these structures and adjacent vessels is required to prevent any poor outcomes.

Abstract 188: Rescue Left Middle Cerebral Artery Stenting With Xience Skypoint Everolimus‐Eluting Stent: Technical Report

Introduction Drug‐eluting stent (DES) use in symptomatic intracranial atherosclerosis disease (ICAD) has been described in the literature using different guiding and distal access catheters. We describe a case of deployment of a Xience Skypoint everolimus‐eluting stent (EES) (Abbott Vascular, Abbott Park, Illinois) into a symptomatic stenosed left M1 segment using Armadillo catheter (Q'Apel, Fremont, CA) with a successful result. Methods Case report and review of literature Results 67‐year‐old woman with type II diabetes mellitus, hypertension, hyperlipidemia, and recent admission for transient ischemic attack (resolving right hemiparesis and mild dysnomia in the setting of severe left M1 segment stenosis with discharge on Aspirin, Clopidogrel and Atorvastatin), presented with recurrence of symptoms, and MRI brain showing left basal ganglia acute infarction. No tPA was given low NIHSS and resolution of symptoms. Patient’s aphasia and hemiparesis worsened with segmental hypoperfusion which resolved by maintaining high blood pressures with norepinephrine drip. Decision was made to deploy a drug eluting stent into the stenosed M1 segment. Through femoral access, a 7F long destination sheath was inserted to the left common carotid origin. A 7F Armadillo catheter was then inserted into the left internal carotid artery (ICA) terminus. ASAHI Prowater coronary guidewire was inserted over which Xience Skypoint EES deployment was attempted but was unsuccessful given difficulty traversing the ICA ophthalmic segment. Ultimately, Armadillo catheter was advanced over a Phenom catheter (Medtronic) with good access into the distal M1 segment. The Phenom intermediate catheter was then removed, and the 2.25 mm x 12 mm stent was introduced through the Prowater guidewire into the segment and inflated to a pressure of 8 atm, with restoration of blood flow. Postoperatively, SBP was lowered to prevent reperfusion injury. Patient’s exam stabilized with mild dysnomia and right hemiparesis without any elevated blood pressure requirements. At 5‐months follow‐up, patient’s exam was non‐focal with NIHSS 0 and repeat DSA showed no evidence of stent occlusion and patent M1 segment. Conclusion Xience Skypoint EES can be successful in treating symptomatic MCA stenosis refractory to maximal medical therapy with good long term results.

A rare case report: isolated midbrain lacunar infarct affecting the ipsilateral medial longitudinal fasciculus causing internuclear ophthalmoplegia effect

Isolated medial longitudinal fasciculus infarct is rare and can also be associated with cranial nerve nuclei or extra-nuclear regions leading to respective neurological deficit. We report a case of 73-year-old woman presenting with a 24 hour of confusion, abnormal eye movement and unsteady gait on a background history of uncontrolled diabetes mellitus (DM), hypertension and Alzheimer’s disease. Her examination found to have dysdiadokinesia in left upper limb and inability to adduct right eyeball on left lateral gaze, without affecting the pupil. She was not oriented to time and place while before this event she could. Her examination found to have normal power in limbs and sensation. Her computed tomography (CT) brain showed no evidence of acute infarction or intracranial bleed. Magnetic resonance imaging (MRI) brain demonstrated acute lacunar infarct involving the ipsilateral medial longitudinal fasciculus. This case demonstrates rare brainstem infarct affecting medial longitudinal fasciculus region below the IIIrd cranial nerve nucleus giving features of internuclear ophthalmoplegia affecting medial rectus muscle without affecting autonomic fibres of IIIrd cranial nerve due to which the pupil is not affected. We recommend strict control of predisposing conditions, mainly diabetes and hypertension to reduce the incidence of brainstem stroke.

Different patterns of multiple acute infarctions and long-term prognosis in minor posterior circulation stroke

ObjectivesDifferent classification of multiple acute infarctions (MAIs) existed in minor posterior circulation stroke (PCS). We aimed to explore the association between different patterns of MAIs and long-term prognosis in minor PCS. Materials and methodsWe derived data from Chinese Intracranial Atherosclerosis (CICAS) study. We analyzed the clinical features and outcomes in MAIs among anterior circulation stroke (ACS) and PCS. The patterns of MAIs in PCS were further classified into multiple infarcts, multilevel infarcts, or multiterritorial infarcts. The long-term prognosis included ischemic events recurrence and poor functional outcome (modified Rankin Scale, mRS=2–6) in 1 year. Multivariable Cox and logistic regression were adopted respectively to evaluate the correlation of different patterns of MAIs with recurrence and poor functional outcome. ResultsWe totally enrolled 802 patients with minor stroke in CICAS study, including 484 ACS and 318 PCS. In univariate analysis, MAIs were significantly associated with recurrence in ACS (P<0.01), but were significantly correlated with poor functional outcome in PCS (P=0.044). Among the PCS patients, there were 90 patients with multiple infarcts, 32 patients with multilevel infarcts and 36 patients with multiterritorial infarcts. Multivariable Cox regression showed that multiterritorial infarcts were independently associated with ischemic events recurrence (HR, 3.083; 95 % CI, 1.078–8.813). In multivariable logistic regression, significant correlation with poor functional outcome in 1 year was revealed in multilevel infarcts (OR, 2.788; 95 % CI, 1.144–6.797). ConclusionsDifferent patterns of MAIs provide different predictive performances for PCS prognosis. It is imperative to perform more detailed image interpretation of MAIs in PCS.

A Case Report on Right Hemiparesis after Left Thalamus Infarction Treated with &lt;italic&gt;Boyanghwanoh-tang-gagam&lt;/italic&gt; and Complex Korean Medicine Treatment

Objectives: This study reports the case of a patient with right hemiparesis after a left thalamic infarction, in which the patient experienced improved clinical symptoms (hemiparesis, constipation) after treatment with a complex Korean medicine treatment.Methods: A 81-year-old male patient diagnosed with acute left thalamic infarction was treated with daily acupuncture and herbal medicine (&lt;i&gt;Boyanghwanoh-tang-gagam&lt;/i&gt;) three times a day. &lt;i&gt;Jowiseunggi-tang&lt;/i&gt; extract granules were administered to treat constipation by adjusting the dosage according to the reported symptoms. The patient’s clinical course was assessed using changes in Modified Barthel Index (MBI) score, Manual Muscle Testing (MMT) grade, and defecation frequency .Results: The patient’s MBI score improved from 35 to 69 and was discharged with the ability to walk under supervision. The MMT grade also improved from 3/4 to 5/5 in the upper/lower extremities. Other clinical symptoms, including constipation, also improved, leading to the discontinuation of magnesium medication.Conclusion: These findings suggest that complex Korean medicine treatments, including herbal medicine and acupuncture, may be an effective treatment for post-stroke hemiplegic patients.

White Matter Hyperintensity Volume and Poststroke Cognition: An Individual Patient Data Pooled Analysis of 9 Ischemic Stroke Cohort Studies.

White matter hyperintensities (WMH) are associated with cognitive dysfunction after ischemic stroke. Yet, uncertainty remains about affected domains, the role of other preexisting brain injury, and infarct types in the relation between WMH burden and poststroke cognition. We aimed to disentangle these factors in a large sample of patients with ischemic stroke from different cohorts. We pooled and harmonized individual patient data (n=1568) from 9 cohorts, through the Meta VCI Map consortium (www.metavcimap.org). Included cohorts comprised patients with available magnetic resonance imaging and multidomain cognitive assessment <15 months poststroke. In this individual patient data meta-analysis, linear mixed models were used to determine the association between WMH volume and domain-specific cognitive functioning (Z scores; attention and executive functioning, processing speed, language and verbal memory) for the total sample and stratified by infarct type. Preexisting brain injury was accounted for in the multivariable models and all analyses were corrected for the study site as a random effect. In the total sample (67 years [SD, 11.5], 40% female), we found a dose-dependent inverse relationship between WMH volume and poststroke cognitive functioning across all 4 cognitive domains (coefficients ranging from -0.09 [SE, 0.04, P=0.01] for verbal memory to -0.19 [SE, 0.03, P<0.001] for attention and executive functioning). This relation was independent of acute infarct volume and the presence of lacunes and old infarcts. In stratified analyses, the relation between WMH volume and domain-specific functioning was also largely independent of infarct type. In patients with ischemic stroke, increasing WMH volume is independently associated with worse cognitive functioning across all major domains, regardless of old ischemic lesions and infarct type.

Cerebral hemodynamics and stroke risks in symptomatic intracranial atherosclerotic stenosis with internal versus cortical borderzone infarcts: A computational fluid dynamics study

There may be different mechanisms underlying internal (IBZ) and cortical (CBZ) borderzone infarcts in intracranial atherosclerotic stenosis. In 84 patients with symptomatic, 50-99% atherosclerotic stenosis of M1 middle cerebral artery (MCA-M1) with acute borderzone infarcts in diffusion-weighted imaging, we classified the infarct patterns as isolated IBZ (n = 37), isolated CBZ (n = 31), and IBZ+CBZ (n = 16) infarcts. CT angiography-based computational fluid dynamics models were constructed to quantify translesional, post-stenotic to pre-stenotic pressure ratio (PR) in the MCA-M1 lesion. Those with IBZ infarcts were more likely to have a low PR (indicating impaired antegrade flow across the lesion) than those without (p = 0.012), and those with CBZ infarcts were more likely to have coexisting small cortical infarcts (indicating possible embolism) than those without (p = 0.004). In those with isolated IBZ or CBZ infarcts, low PR was independently associated with isolated IBZ infarcts (adjusted odds ratio = 4.223; p = 0.026). These two groups may also have different trajectories in the stroke risks under current medical treatment regimen, with a higher risk of same-territory ischemic stroke recurrence within 3 months in patients with isolated IBZ infarcts than isolated CBZ infarcts (17.9% versus 0.0%; log-rank p = 0.023), but similar risks later in 1 year.

Cholecystitis in older patients following hip fracture: a case series and literature review

ObjectiveThis study’s aim is to describe the characteristics of perioperative acute cholecystitis in older patients with hip fracture.MethodsFrom January 1, 2018, to April 30, 2023, 7,746 medical records were retrospectively collected for patients aged ≥ 65 years who were hospitalised for hip fracture in Beijing Jishuitan Hospital, Capital Medical University. We reviewed 10 cases with confirmed diagnoses of acute cholecystitis.ResultsOf these 10 cases, five femoral neck fractures and five intertrochanteric fractures received orthopaedic surgery. The ratio of males to females was 2:8, the median age was 83.1 years (71–91 years), and there was a median BMI of 25.35 (15.56–35.16). 50% of cases had a poor functional capacity before fracture of below four metabolic equivalents. The median onset time of acute cholecystitis was five days (2–14 days) after fracture, including five cases before orthopaedic surgery and five cases after orthopaedic surgery. All patients had anorexia and fever during the course of the disease. In seven cases of calculous cholecystitis, two underwent percutaneous transhepatic biliary drainage, and one underwent percutaneous cholecystostomy. Two cases of calculous cholecystitis had poor prognosis; one died 49 days after fracture operation, and the reason for death was multiple organ failure caused by severe infection. The other one developed acute cerebellar infarction after gallbladder surgery through treatment in an intensive care unit and neurology department. The case was discharged with dysphasia, and the duration from fracture to discharge was 92 days.ConclusionThis is the first study on the characteristics of acute cholecystitis in older patients with hip fracture in China. The incidence of acute cholecystitis in our study was 0.13%, with a high risk of in-hospital mortality and elevated hospitalisation costs. Our 10 cases with hip fractures accompanied by acute cholecystitis have common characteristics of poor-to-moderate functional capacity before fracture, increased blood glucose levels and enhanced protein metabolism after fracture. The death and the severe case have similar characteristics of low BMI, multiple underlying diseases, high plasma osmotic pressure and calculous cholecystitis, which occurred after orthopaedic surgery. These issues require attention and prompt, active intervention. Related issues require further research.

Safe and time-saving treatment method for acute cerebellar infarction: Navigation-guided burr-hole aspiration - 6-years single center experience.

While patients with medically intractable acute cerebellar infarction typically undergo suboccipital craniectomy and removal of the infarcted tissue, this procedure is associated with long operating times and postoperative complications. This study aimed to investigate the effectiveness of minimally invasive navigationguided burr hole aspiration surgery for the treatment of acute cerebellar infarction. Between January 2015 and December 2021, 14 patients with acute cerebellar infarction, who underwent navigation-guided burr hole aspiration surgery, were enrolled in this study. The preoperative mean Glasgow Coma Scale (GCS) score was 12.7, and the postoperative mean GCS score was 14.3. The mean infarction volume was 34.3 cc at admission and 23.5 cc immediately following surgery. Seven days after surgery, the mean infarction volume was 15.6 cc. There were no surgery-related complications during the 6-month follow-up period and no evidence of clinical deterioration. The mean operation time from skin incision to catheter insertion was 28 min, with approximately an additional 13 min for extra-ventricular drainage. The mean Glasgow Outcome Scale score after 6 months was 4.8. Navigation-guided burr hole aspiration surgery is less time-consuming and invasive than conventional craniectomy, and is a safe and effective treatment option for acute cerebellar infarction in selected cases, with no surgery-related complication.