Practice Patterns for Acute Ischemic Stroke Workup: A Longitudinal Population-Based Study.

Background: We examined practice patterns of inpatient testing to identify stroke etiologies and treatable risk factors for acute ischemic stroke recurrence.

Methods And Results: We identified stroke cases and related diagnostic testing from four 1-year study periods (July 1993 to June 1994, 1999, 2005, and 2010) of the Greater Cincinnati/Northern Kentucky Stroke Study. Patients aged ≥18 years were included.

GABAB Encephalitis: A Fifty-Two-Year-Old Man with Seizures, Dysautonomia, and Acute Heart Failure.

Autoantibodies to the γ-aminobutyric acid receptor, subtype B (GABAB), are a known cause of limbic encephalitis. The spectrum of clinical manifestations attributable to this antibody is not well defined at the present time. Here we present a case of GABAB encephalitis presenting with encephalopathy, status epilepticus, dysautonomia, and acute heart failure.

Depletion of GR-1-Positive Cells Is Associated with Reduced Neutrophil Inflammation and Astrocyte Reactivity after Experimental Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is the stroke subtype with the highest mortality and morbidity with 25% of patients dying within the first 48 h and a high incidence of poor outcomes. Because of high early mortality rates, an understanding of acute brain injury mechanisms is essential. In this study, we have investigated the putative role of acute inflammation in brain injury after experimental ICH.

Unconjugated bilirubin contributes to early inflammation and edema after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a stroke subtype with significant mortality and morbidity. The role of unconjugated bilirubin (UBR) in ICH brain injury is not well understood. Therefore, we studied the effects of UBR on brain injury markers and inflammation, as well as mechanisms involved therein.

Iron and early brain injury after subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage (SAH) affects approximately 27,000 Americans per year. Although delayed cerebral vasospasm is of high clinical significance, mortality within the first 2 days may approach 30%. In this issue of the Journal of Cerebral Blood Flow and Metabolism, Lee et al have studied the role of iron in early brain injury after experimental SAH.

A novel brain injury mechanism after intracerebral hemorrhage: the interaction between heme products and the immune system.

In this paper we hypothesize a novel mechanism by which brain injury occurs after intracerebral hemorrhage. We propose the following mechanism: (1) heme that is derived from extravasated erythrocytes is degraded into bilirubin and bilirubin oxidation products (BOXes). (2) Bilirubin and BOXes activate microglia and astrocytes, which are cells with immune functions in the brain.

Intracerebral hemorrhage leads to infiltration of several leukocyte populations with concomitant pathophysiological changes.

Intracerebral hemorrhage (ICH) is a stroke subtype with high rates of mortality and morbidity. The immune system, particularly complement and cytokine signaling, has been implicated in brain injury after ICH. However, the cellular immunology associated with ICH has been understudied.

A novel duplex ELISA method for quantitation of plasma proteins in areas of brain edema.

We have developed a novel type of duplex enzyme-linked immunosorbent assay (ELISA) for the quantitation of the major plasma proteins, IgG and albumin, in edematous brain tissue. We test this duplex ELISA on our porcine intracerebral hemorrhage (ICH) model and show that it is as accurate and sensitive as independent single ELISAs. This method is useful as a marker of edema in brain tissue and the same design can be applied to other proteins and sample types.

An in vitro model of aneurysmal subarachnoid hemorrhage: oxidation of unconjugated bilirubin by cytochrome oxidase.

Aneurysmal subarachnoid hemorrhage is a stroke subtype with high rates of mortality and morbidity. Cerebral vasospasm can lead to ischemic injury or death and is a common complication of aneurysmal subarachnoid hemorrhage, usually occurring 3-9 days afterwards. The cause of vasospasm is not known.

Plasma proteins in edematous white matter after intracerebral hemorrhage confound immunoblots: an ELISA to quantify contamination.

Intracerebral hemorrhage (ICH) and traumatic brain injury can induce brain tissue edema (i.e., interstitial and/or vasogenic), containing high concentrations of plasma proteins.