Systemic inflammatory markers of persistent cerebral edema after aneurysmal subarachnoid hemorrhage.

Background: Cerebral edema (CE) at admission is a surrogate marker of 'early brain injury' (EBI) after subarachnoid hemorrhage (SAH). Only recently has the focus on the changes in CE after SAH such as delayed resolution or newly developed CE been examined. Among several factors, an early systemic inflammatory response has been shown to be associated with CE.

The Spot Sign and Intraventricular Hemorrhage are Associated with Baseline Coagulopathy and Outcome in Intracerebral Hemorrhage.

Background: Spontaneous intracerebral hemorrhage (ICH) is the second most prevalent subtype of stroke and has high mortality and morbidity. The utility of radiographic features to predict secondary brain injury related to hematoma expansion (HE) or increased intracranial pressure has been highlighted in patients with ICH, including the computed tomographic angiography (CTA) spot sign and intraventricular hemorrhage (IVH). Understanding the pathophysiology of spot sign and IVH may help identify optimal therapeutic strategies.

Representation Learning of 3D Brain Angiograms, an Application for Cerebral Vasospasm Prediction.

Stroke is the fifth leading cause of death in the United States. Subarachnoid hemorrhage (SAH) is a type of stroke often caused by the spontaneous rupture of a cerebral aneurysm. About 30% of the SAH patients develop delayed cerebral ischemia (DCI) a serious secondary complication with devastating impact.

Early glioma is associated with abnormal electrical events in cortical cultures.

The prodromal stages of some neurological diseases have a distinct electrical profile which can potentially be leveraged for early diagnosis, predicting disease recurrence, monitoring of disease progression, and better understanding of the disease pathology. Gliomas are tumors that originate from glial cells present in the brain and spinal cord. Healthy glial cells support normal neuronal function and play an important role in modulating the regular electrical activity of neurons.

Disruption of thrombo-inflammatory response and activation of a distinct cytokine cluster after subarachnoid hemorrhage.

Background: Unregulated inflammatory and thrombotic responses have been proposed to be important causes of early brain injury and worse clinical outcomes after subarachnoid hemorrhage (SAH).

Objective: We hypothesize that SAH is characterized by an increased inflammatory and thrombotic state and disruption of associations between these states.

Methods: This is a retrospective cohort study of 60 patients with SAH.

The Subarachnoid Hemorrhage Early Brain Edema Score Predicts Delayed Cerebral Ischemia and Clinical Outcomes.

Background: Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is an important determinant of clinical outcomes. However, a major hindrance to studies of EBI is the lack of radiographic surrogate marker.

Objective: To propose a scoring system based on early changes in clinically obtained computed tomography (CT), called the Subarachnoid hemorrhage Early Brain Edema Score (SEBES).

Assessment of the Relationship between Body Mass Index and Incidence of Venous Thromboembolism in Hospitalized Overweight and Obese Patients.

Study Objective: To assess whether a positive linear association exists between body mass index (BMI) and incidence of venous thromboembolism (VTE) in overweight and obese hospitalized patients.

Design: Single-center retrospective observational cohort study.

Setting: Large academic tertiary care medical center.

Impact of practice change in reducing venous thromboembolism in neurocritical overweight patients: 2008-2014.

Publications regarding early initiating venous thromboembolism (VTE) prophylaxis have been available since the early 1990s. These recommendations became available in current guidelines on and after 2012. The purpose of this study is to review the practice change in reducing the incidence of VTE in brain injury patients from 2008 to 2014.

Quantification of Cerebral Edema After Subarachnoid Hemorrhage.

Background: Global cerebral edema (GCE) is a manifestation of early brain injury (EBI) after subarachnoid hemorrhage (SAH) and is an independent risk factor for poor outcome. The lack of a quantitative method to measure GCE limits the study of its pathophysiology. The goal of this study is to develop a quantitative surrogate marker that represents GCE after SAH.