BACKGROUND: There is emerging evidence that COVID-19 can trigger thrombosis because of a hypercoagulable state, including large-vessel occlusion ischemic strokes. Bihemispheric ischemic stroke is uncommon and is thought to indicate an embolic source. Here, we examine the findings and outcomes of patients with bihemispheric stroke in the setting of COVID-19. METHODS: We performed a retrospective cohort study at a quaternary academic medical center between March 1, 2020, and April 30, 2020. We identified all patients with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection who presented with simultaneous bihemispheric ischemic strokes. RESULTS: Of 637 COVID-19 admissions during the 2-month period, 13 had a diagnosis of acute ischemic stroke, including 5 who developed bihemispheric cerebral infarction. Three of those 5 (60%) were female, median age was 54 (range 41–67), and all five were being managed for severe COVID-19-related pneumonia complicated by acute kidney injury and liver failure before the diagnosis of cerebral infarction was established. Five presented with elevated ferritin, lactate dehydrogenase, and interleukin-6 (IL-6) levels, and four had lymphopenia and elevated D-dimer levels. All patients underwent neuroimaging with computed tomography for persistent depressed mentation, with or without a focal neurologic deficit, demonstrating multifocal ischemic strokes with bihemispheric involvement. Outcome was poor in all patients: two were discharged to a rehabilitation facility with moderate-to-severe disability and three (60%) patients died. CONCLUSIONS: Stroke is implicated in SARS-CoV-2 infection. Although causality cannot be established, we present the imaging and clinical findings of patients with COVID-19 and simultaneous bihemispheric ischemic strokes. Multifocal ischemic strokes with bihemispheric involvement should be considered in COVID-19 patients with severe infection and poor neurologic status and may be associated with poor outcomes.

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Alzheimer's disease is a neurological condition that causes the disruption of neuronal connections in the human brain. It is progressive and targets about 10% of the United States population over the age of 65.3 to date, there is no cure to the disease. Physicians can treat symptoms but lack the ability to stop the progression of the disease. However, promising research has come to the surface in recent years. A collection of these therapeutic targets, which have yielded positive results in mice models, are presented in this article. They include targets such as meningeal lymphatics, mitochondrial homeostasis, genomic instability, calcium homeostasis, and cold-shock proteins such as RNA-binding motif protein 3 and reticulon-3, high-density lipoprotein, and antibodies.

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INTRODUCTION: While endovascular coiling has been shown to be a safe treatment option for intracranial aneurysms, there remains concern regarding increased recurrence and retreatment rates. Preliminary studies evaluating hydrogel coated coils have demonstrated decreased recurrence rates compared to bare metal coils. METHODS: A retrospective chart review was done on all patients with anterior communicating artery aneurysms (ACoAAs) treated with endovascular coiling between 2014 and 2018. Treatment groups were divided into hydrogel coated coils or bare metal coils. Patients were categorized into the hydrogel group when ≥ 70% of the coil length was hydrogel coated. RESULTS : Eighty-four ACoAAs were treated with coil embolization between 2014 and 2018. Postoperative imaging was available for 68 patients. Twenty-six patients were categorized into the hydrogel treatment group. Aneurysm recurrence was seen in 7.7% (2/26) of patients treated with hydrogel coated coils compared to 33.3% (14/42) of those treated with bare metal coils (P = 0.03). Subanalysis of patients with ruptured aneurysms revealed decreased recurrence rates in patients treated with hydrogel coated coils at 5.9% (1/17) compared to patients treated with bare metal coils at 39.4% (13/33) (P = 0.01). CONCLUSIONS: Hydrogel-coated coils may reduce recurrence rates in the treatment of both ruptured and unruptured ACoAAs.

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BACKGROUND: Recurrent strokes cause greater complications and worse outcomes by adding to the existing neurological deficit. There is the paucity of data on serum markers of inflammation as predictors of recurrent stroke. This study was planned to analyze the clinico-etiological profile of recurrent noncardioembolic ischemic stroke, estimate aspirin resistance among regular aspirin users and evaluate blood biomarkers high-sensitivity C-reactive protein (hsCRP), Tumor necrosis factor-alpha (TNF-α), Lipoprotein-associated phospholipase A₂ (Lp-PLA2) as probable predictors of stroke recurrence. METHODS: Patients of recurrent noncardioembolic ischemic stroke fulfilling the inclusion criteria were enrolled. Detailed history, clinical examination, and investigations were obtained as per protocol. Aspirin resistance was determined by light transmission aggregometry. Serum hsCRP, TNF-α, and Lp-PLA2 levels were estimated. RESULTS: This study included 34 males and 16 females. Majority of the patients were > 60 years (n = 30, 60%). Thirty (60%) cases had a repeat stroke after 1 year of primary event. Thirty-nine (78%) study participants had hypertension, while 15 (30%) had diabetes. Middle cerebral artery (n = 40, 80%) was the most common vascular territory. Thirty-one (62%) cases belonged to TOAST subtype 1 (large artery atherosclerosis). Seventy two percent cases were prescribed aspirin after index stroke, but only 36% were compliant. Median (range) hsCRP level was 7.5 (0.3–155) mg/L with 72% of patients having high hsCRP level (>3 mg/L). Median (range) serum PLA2 level was 11.98 (3.31–87.24) ng/ml in patients and 6.96 (0.15–61.42) ng/ml in controls (P = 0.029). Median (range) serum TNF-α level in patients was significantly higher than controls (68.22 [1.3–287] pg/ml versus 0.098 [0.002–36.31] pg/ml, P < 0.001). Aspirin resistance was found in 41.7% patients while 16.7% were semi-resistant. Mean % platelet aggregation was 34.75 ± 21.58 in patients and 64.75 ± 16.98 for controls (P < 0.001). CONCLUSIONS: Majority of patients with recurrent stroke were elderly (>60 years), hypertensive, and non-compliant with aspirin. Aspirin resistance was an important factor in patients with antiplatelet compliance. Inflammatory biomarkers hsCRP, PLA2, and TNF-α were found to be significantly elevated in patients compared to controls.

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Detecting the stroke etiology in young patients can be challenging. Among others, determining causality between ischemic stroke and patent foramen ovale (PFO) remains a complicated task for stroke neurologists, given the relatively high prevalence of PFOs. Thorough diagnostic workup to identify incidental vascular risk factors and rare embolic sources is crucial to avoid premature PFO closure suggesting successful secondary stroke prevention. In this paper, we report on a 38-year-old patient with recurrent vertebrobasilar territory, especially right posterior inferior cerebellar artery (PICA) territory strokes. After the initial suspicion of a left vertebral artery (VA) dissection was not confirmed by ultrasound and magnetic resonance imaging (MRI) and other major risk factors were excluded, a PFO was detected and closed. Successful PFO closure was confirmed by transesophageal echocardiography, yet recurrent transient-ischemic attacks and vertebrobasilar strokes, especially during nighttime and in the early morning, occurred despite various antiplatelet and antithrombotic regimes and a persistent right-to-left shunt was detected by bubble transcranial Doppler. Finally, MRI after another vertebrobasilar infarction detected a transient left VA occlusion that finally led to the diagnosis of a left VA pseudoaneurysm from an incident emboligenic dissection in the atlas segment. This pseudoaneurysm together with an anatomical variant of the right PICA originating with the right anterior inferior cerebellar artery from the basilar artery finally explained the recurrent ischemic events of the patient. After successful treatment with coil occlusion, the patient suffered no further stroke and recovered completely. In summary, stroke in the young remains a diagnostic challenge. The incidental finding of a PFO should not deter from thorough stroke workup and the follow-up of these patients including PFO closure verification should be performed under the guidance of vascular neurologists.

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OBJECTIVES: Lacunar strokes can have fluctuations and progression in the acute period leading to poor outcomes. Our study sought to evaluate if, in lacunar strokes, neurological deterioration (ND) was associated with blood pressure (BP) variations, stroke size, or increased time to peak (TTP) on admission computed tomography perfusion (CTP). METHODS: Patients with lacunar stroke who had magnetic resonance imaging and CTP performed were enrolled in the study. ND was defined as ≥1-point worsening on a modified National Institutes of Health Stroke Scale (NIHSS) score or the Medical Research Council scale compared to baseline assessment. The difference in BP between the day of admission and the day of ND was calculated. Multivariate logistic regression analysis, adjusted for pertinent clinical and imaging covariates, was performed to determine predictors of ND. RESULTS: Among 409 patients screened, 49 were eligible for the study. There was no difference in age, gender, race, medical history, admission BP, and the modified NIHSS score between patients with and without ND. In unadjusted analysis, patients with ND tended to have increased TTP in the stroke area compared to the control (12 [63%] vs. 11 [37%], P = 0.07). On multivariate analysis adjusted for covariates, presence of an increased TTP on CTP was a predictor of ND (odds ratio [95% confidence interval] = 4.80 [1.15–20.10], P = 0.03). CONCLUSION: The presence of an increased TTP on CTP corresponding to the stroke lesion on diffusion-weighted imaging is a predictor of ND in patients with lacunar stroke. Larger studies are needed to confirm our findings.

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Current guidelines do not include radiologic assessment of the carotid arteries before catheter ablation procedures. There are multiple studies describing the risks of periprocedural cardioembolic strokes during cardiac ablation procedure but none describing the risks of periprocedural watershed strokes due to hypoperfusion during cardiac ablation. It is critically important for neurologists, cardiologists, and all other associated health-care workers to recognize the risks of neurologic complications, such as watershed strokes, before cardiac procedures are performed. We are presenting an 84-year-old male who presented to the emergency room with complaints of vision changes after a cardiac ablation procedure for atrial fibrillation. He described spotty vision with decreased visual acuity in both eyes. Magnetic resonance imaging of the brain showed multiple strokes bilaterally. Based on the radiologic features, all the strokes happened at approximately the same time. Of note, subsequent computed tomography angiography of the head and neck showed 65%–70% bilateral stenosis of the internal carotid arteries.

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OBJECTIVES: Since the beneficial effect attained by mechanical thrombectomy (MT) seems to be worse in older than in the younger population, the establishment of an ideal and distinctive patient selection protocol in older is warranted. Herein, we modified our patient selection protocol based on age and premorbid independence in older adult patients. MATERIALS AND METHODS: We retrospectively reviewed 141 consecutive patients with acute ischemic stroke who were treated with MT between 2015 and 2020. We started to restrict the indication of MT in very old patients (≥85-year-old) with severe premorbid functional independence (≥modified Rankin Scale [mRS] 3) in 2018. Clinical outcomes before the modification of protocol (period 1) were compared to after (period 2). RESULTS: Although there were no significant differences in median mRS at 90 days and the rates of favorable outcomes (mRS 0–2) between both periods, rates of poor outcomes (mRS 5, 6) significantly decreased (37.3% vs. 19.7%, P = 0.021) during period 2 compared with period 1. For older adults (≥80-year-old), median mRS was significantly better (P = 0.012) during period 2 than period 1. During period 1, rates of favorable outcomes were significantly lower (P = 0.004) in older than in younger. However, this significant difference was diminished (P = 0.28) during period 2. CONCLUSION: Our modified patient selection protocol in older adults, not only limited by age but also premorbid function, improved the therapeutic outcome of MT. In rapidly aging society, further investigations facilitating a better understanding are necessary to establish an optimal patient selection protocol.

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Pulmonary arteriovenous malformations (PAVMs) encompass congenital and genetic vascular anomalies characterized by complex interlacing of arteries and veins connected by fistulas, which allow rapid and continuous extracardiac right-to-left shunting (RLS). Presenting neurologic manifestations of PAVM include brain abscess and stroke, as the consequence of paradoxical embolism. Although rare, PAVM represents an overlooked cause of cryptogenic ischemic stroke in young adults, being misdiagnosed as patent foramen ovale and a preventable trigger of silent cerebral ischemic changes.In the emergency clinical setting, the recommended ischemic stroke workup in patients with RLS should include the influence of postural changes and the effect of Valsalva maneuver on the entity of the RLS on contrast-enhanced transcranial color Doppler ultrasound and the delay in the right inferior pulmonary vein and left heart opacification on contrast-enhanced transthoracic echocardiography. This is in addition to the evaluation of chest X-rays or thoracic computed tomography. We here describe two patients with ischemic stroke due to sporadic and genetic PAVM-associated paradoxical embolism.

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OBJECTIVE: Proper blood flow is essential for the maintenance of homeostasis for the human cerebrum. The dural venous sinuses comprise the dominant cerebral venous outflow path. Understanding the spatial configuration of the dural venous sinuses can provide valuable insight into several pathological conditions. Previously, only two-dimensional or cadaveric data have been used to understand cerebral outflow. For the first time, we applied three-dimensional rotational venography (3D-RV) to study and provide detailed quantitative morphological measurements of the terminal cerebral venous sinus system in several pathological states. SUBJECTS AND METHODS: Patients who underwent a 3D-RV procedure were identified by reviewing our local institution's endovascular database. Patients with high-quality angiographic images were selected. Eighteen patients were included (37.1 ± 3.8 years). Sinuses were divided into four segments, starting at the torcula and ending at the internal jugular vein. Segment length, 3D displacement, and cross-sectional area were measured. RESULTS: The transverse sinus (60.2 mm) was the longest segment, followed by the sigmoid sinus (55.1 mm). Cross-sectional areas were smallest at the middle of the transverse sinus (21.3 mm²) but increased at the sigmoid sinus (33.5 mm²) and at the jugular bulb (49.7 mm²). The only variation in displacements of venous flow was at the sigmoid-jugular junction, where 55% of cases had lateral displacements versus 45% medial, and 78% superior versus 22% inferior. CONCLUSIONS: We describe the terminal venous sinus system of patients with a variety of diagnoses, detailing segment length, cross-sectional area, and 3D path.

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Patients with left ventricular assist devices (LVADs) provide a unique challenge with regard to the management of subdural hematomas (SDH), due to preexisting comorbidities and induced coagulopathy. We report on the case of a 63-year-old female with a preexisting LVAD who developed an acute on chronic SDH with 15 mm of midline shift. She was successfully treated with middle meningeal artery (MMA) embolization and placement of a bedside subdural evacuating port system without hematoma recurrence at 1-year follow-up. Both operative and nonoperative management of SDHs in patients with LVAD is associated with high risk of mortality and morbidity. Chronic SDHs in this patient population can be successfully managed with a minimally invasive approach that includes MMA embolization and bedside subdural drain placement.

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Coexisting arteriovenous malformations (AVMs) and cavernous malformations (CMs) are rare. Here, we present our dilemmas in managing a patient with a cerebral AVM and a pontine CM. A 47-year-old patient suffered from headaches, vomiting, and transient swallowing difficulties. The cerebral computed tomography showed a pontine hyperintense lesion, while the axial magnetic resonance imaging of the head disclosed a frontal interhemispheric AVM and a CM located in the rostral and ventral aspect of the pons. Despite a pontine hemorrhage, the patient underwent microsurgical excision of the frontal lesion in the first place, due to the increased bleeding risk, followed by stereotactic radiosurgery of the pontine CM. On the 6 months follow-up, the patient's clinical status was stable. A reasonable treatment strategy based on risk stratification is paramount in managing patients with coexisting AVMs and CMs. The optimal outcome frequently requires a staged multidisciplinary approach.

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