Glucose Control and Risk of Symptomatic Intracerebral Hemorrhage Following Thrombolysis for Acute Ischemic Stroke: A SHINE Trial Analysis.

Background And Objectives: Baseline hyperglycemia is associated with worse outcomes in acute ischemic stroke (AIS), including higher risk of symptomatic intracerebral hemorrhage (sICH) following treatment with thrombolysis. Prospective data are lacking to inform management of post-thrombolysis hyperglycemia. In a prespecified analysis from the Stroke Hyperglycemia Insulin Network Effort (SHINE) trial of hyperglycemic stroke management, we hypothesized that post-thrombolysis hyperglycemia is associated with a higher risk of sICH.

Intensive Versus Standard Treatment of Hyperglycemia in Acute Ischemic Stroke Patient: A Randomized Clinical Trial Subgroups Analysis.

Background: Benefit from blood glucose (BG) control during acute ischemic stroke may depend on glycemic parameters. We evaluated for associations between the SHINE (Stroke Hyperglycemia Insulin Network Effort) randomized treatment group and the SHINE predefined 90-day functional outcome, within-patient subgroups defined by various glycemic parameters.

Methods: The SHINE Trial randomized 1151 patients within 12 hours with acute ischemic stroke and hyperglycemia to standard (target BG 80-179 mg/dL) or intensive (target BG 80-130 mg/dL) BG control for 72 hours.

Paradoxical Cerebral Air Embolism after Cardiac Ablation in Williams-Beuren Syndrome: A Clinico-Pathological Correlation.

Non-traumatic neurological deterioration is a medical emergency that may arise from diverse causes, to include cerebral infarction or intracranial hemorrhage, meningoencephalitis, seizure, hypoxic-ischemic or toxic/metabolic encephalopathy, poisoning, or drug intoxication. We describe the abrupt onset of neurological deterioration in a 53-year-old man with Williams-Beuren syndrome, a sporadically occurring genetic disorder caused by chromosomal microdeletion at 7q11.23.

Thrombectomy for Treatment of Acute Stroke in the COVID-19 Pandemic.

This commentary will focus on the role of thrombectomy for the treatment of embolic stroke during the 2019 novel coronavirus disease (COVID-19). We will begin with review of recently promulgated guidelines for use of thrombectomy in COVID-19-associated stroke. We will then survey the reported experience of thrombectomy applied to treatment of large-vessel occlusion (LVO) stroke in COVID-19.

Can a diagnosis of multiple sclerosis be made without ruling out neuromyelitis optica spectrum disorder ?

Background: The symptoms of multiple sclerosis (MS) can overlap with neuromyelitis optica spectrum disorder (NMOSD). Although testing is available for aquaporin 4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies, screening for NMOSD is recommended but not mandatory to establish a diagnosis of MS.

Methods And Results: We queried 319,994 individuals who filed claims for MS and NMOSD in a Truven Health Analytics (THA) database and had at least one year of uninterrupted health insurance coverage.

Nerve Stimulation Enhances Task-Oriented Training for Moderate-to-Severe Hemiparesis 3-12 Months After Stroke: A Randomized Trial.

Objective: The aim of the study was to determine whether somatosensory stimulation affects outcomes of motor training for moderate-to-severe upper limb hemiparesis less than 12 mos before stroke.

Design: Fifty-five adults participated in 18 intervention sessions pairing 2 hours of active (n = 33) or sham (n = 22) somatosensory stimulation with 4 hours of intensive task-oriented motor training. Wolf Motor Function Test, Action Research Arm Test, Fugl-Meyer Assessment, and Stroke Impact Scale were administered at baseline, postintervention, and 1- and 4-mo follow-up.

The TNFα-Transgenic Rat: Hippocampal Synaptic Integrity, Cognition, Function, and Post-Ischemic Cell Loss.

The cytokine, tumor necrosis factor α (TNFα), is a key regulator of neuroinflammation linked to numerous neurodegenerative conditions and diseases. The present study used transgenic rats that overexpress a murine TNFα gene, under the control of its own promoter, to investigate the impact of chronically elevated TNFα on hippocampal synaptic function. Neuronal viability and cognitive recovery in TNFα Tg rats were also determined following an ischemic insult arising from reversible middle cerebral artery occlusion (MCAO).

Albumin Administration in Acute Ischemic Stroke: Safety Analysis of the ALIAS Part 2 Multicenter Trial.

Background: Albumin treatment of ischemic stroke was associated with cardiopulmonary adverse events in previous studies and a low incidence of intracranial hemorrhage. We sought to describe the neurological and cardiopulmonary adverse events in the ALIAS Part 2 Multicenter Trial.

Methods: Ischemic stroke patients, aged 18-83 and a baseline NIHSS ≥ 6, were randomized to treatment with ALB or saline control within 5 hours of stroke onset.

C-reactive protein as a prognostic marker after lacunar stroke: levels of inflammatory markers in the treatment of stroke study.

Background And Purpose: Inflammatory biomarkers predict incident and recurrent cardiac events, but their relationship to stroke prognosis is uncertain. We hypothesized that high-sensitivity C-reactive protein (hsCRP) predicts recurrent ischemic stroke after recent lacunar stroke.

Methods: Levels of Inflammatory Markers in the Treatment of Stroke (LIMITS) was an international, multicenter, prospective ancillary biomarker study nested within Secondary Prevention of Small Subcortical Strokes (SPS3), a phase III trial in patients with recent lacunar stroke.

Calpain cleaves methionine aminopeptidase-2 in a rat model of ischemia/reperfusion.

Ischemic stroke results in multiple injurious signals within a cell including dysregulation of calcium homeostasis. Consequently, there is an increase in the enzymatic activity of the calpains, calcium dependent proteases that are thought to contribute to neuronal injury. In addition, cellular stress due to ischemia/reperfusion also triggers a decrease in protein translation through activation of the unfolded protein response (UPR).

Emotion recognition and marital satisfaction in stroke.

Deficits in the comprehension of facial and prosodic expressions are commonly associated with right hemisphere stroke. However, little is known regarding the impact of these disorders on social relations. We examined facial and prosodic processing, mood, and marital satisfaction in 12 right hemisphere damaged (RHD) stroke patients and nine controls.

Matrix metalloproteinase-9 in an exploratory trial of intravenous minocycline for acute ischemic stroke.

Background And Purpose: Plasma matrix metalloproteinase-9 levels predict posttissue plasminogen activator (tPA) hemorrhage.

Methods: The authors investigated the effect of minocycline on plasma matrix metalloproteinase-9 in acute ischemic stroke in the Minocycline to Improve Neurological Outcome in Stroke (MINOS) trial and a comparison group.

Results: Matrix metalloproteinase-9 level decreased at 72 hours compared with baseline in MINOS (tPA, P=0.

Focal cerebral ischemia and mitochondrial dysfunction in the TNFα-transgenic rat.

Post-ischemic neurodegeneration may be accelerated by a cytokine-receptor mediated apoptotic pathway, as shown in a transgenic rat overexpressing tumor necrosis factor-alpha (TNFα) in brain. To further investigate the mechanism of ischemic cellular injury in this animal, we tested the hypothesis that increased synthesis of TNFα augments neuronal death by promoting mitochondrial dysfunction, calcium dysregulation, and oxidative stress. Adult male TNFα-transgenic (TNFα-Tg) and non-transgenic (non-Tg) littermates underwent reversible middle cerebral artery occlusion (MCAO) for 1 hour followed by 1 hour of reperfusion.

Minocycline to improve neurologic outcome in stroke (MINOS): a dose-finding study.

Background And Purpose: Minocycline is a promising anti-inflammatory and protease inhibitor that is effective in multiple preclinical stroke models. We conducted an early phase trial of intravenous minocycline in acute ischemic stroke.

Methods: Following an open-label, dose-escalation design, minocycline was administered intravenously within 6 hours of stroke symptom onset in preset dose tiers of 3, 4.

Focal cerebral ischemia in the TNFalpha-transgenic rat.

Background: To determine if chronic elevation of the inflammatory cytokine, tumor necrosis factor-alpha (TNFalpha), will affect infarct volume or cortical perfusion after focal cerebral ischemia.

Methods: Transgenic (TNFalpha-Tg) rats overexpressing the murine TNFalpha gene in brain were prepared by injection of mouse DNA into rat oocytes. Brain levels of TNFalpha mRNA and protein were measured and compared between TNFalpha-Tg and non-transgenic (non-Tg) littermates.

Telephonic guidance of systemic thrombolysis in acute ischemic stroke: safety outcome in rural hospitals.

Objectives: To determine the safety of telephonic guidance for use of intravenous recombinant tissue plasminogen activator (IV rtPA) in rural hospitals.

Patients And Methods: We performed a retrospective survey of 123 consecutive patients treated with IV rtPA for acute ischemic stroke (AIS) in rural hospitals between November 2003 and September 2006 and subsequently transferred to a tertiary medical center. Selection for treatment was performed by a stroke neurologist who conducted a structured telephone interview of the requesting physician.

Hereditary hemorrhagic telangectasia and spinal cord infarct: case report with a review of the neurological complications of HHT.

Hereditary hemorrhagic telangectasia (HHT), also known as Osler-Weber-Rendu disease, is an autosomal dominant vascular dysplasia with high penetrance and variable expressivity. A wide variety of neurological complications have been reported in association with this condition. We report the first case of spinal cord infarction likely due to paradoxical embolization with HHT and review the literature on the neurological complications of this disorder.

The effects of stroke disability on spousal caregivers.

Objective: To examine the effects of unilateral stroke patients' neurobehavioral characteristics on spousal psychosocial function.

Participants: The sample consisted of twenty unilateral stroke patients and their spousal caregivers.

Methods: Patient assessments included mood, affect perception, sensorimotor and cognitive function, marital satisfaction, and activities of daily living.

Protective effects of NIM811 in transient focal cerebral ischemia suggest involvement of the mitochondrial permeability transition.

Cerebral ischemia followed by reperfusion activates numerous pathways that lead to cell death. One such pathway involves the release of large quantities of the excitatory amino acid glutamate into the synapse and activation of N-methyl-D-aspartate receptors. This causes an increase in mitochondrial calcium levels ([Ca(2+)](m)) and a production of reactive oxygen species (ROS), both of which may induce the mitochondrial permeability transition (MPT).

Pharmacokinetics of arundic acid, an astrocyte modulating agent, in acute ischemic stroke.

Arundic acid is an astrocyte modulating agent that improves neurological outcome in experimental acute stroke models. The pharmacokinetics of arundic acid in patients with acute ischemic stroke was investigated in a randomized, double-blind study. Six groups of 8 to 9 patients each received 2, 4, 6, 8, 10, or 12 mg/kg/h of arundic acid for a daily 1-hour infusion until completion of 7 doses.

A phase 2 study of tramiprosate for cerebral amyloid angiopathy.

Background And Purpose: No treatments have been identified to lower the risk of intracerebral hemorrhage due to cerebral amyloid angiopathy (CAA). A potential approach to prevention is the use of agents that interfere with the pathogenic cascade initiated by the beta-amyloid peptide (Abeta). Tramiprosate (3-amino-1-propanesulfonic acid) is a candidate molecule shown in preclinical studies to reduce CAA in a transgenic mouse model.

Safety and tolerability of arundic acid in acute ischemic stroke.

Arundic acid (AA; ONO-2506), a novel modulator of astrocyte activation, may improve neuronal survival after stroke. We conducted a multicenter, dose-escalating, randomized, double-blind Phase I trial of AA in acute ischemic stroke. Subjects were randomized to treatment with AA or placebo in sequential dose tiers of 2-12 mg/kg/h (10-16 patients/group) within 24 h of stroke onset.

Effect of arundic acid on serum S-100beta in ischemic stroke.

We prospectively examined the effect of arundic acid (AA; ONO-2506) on S-100beta, an astrocyte-derived protein, in a phase I acute stroke study. Subjects with acute ischemic stroke were randomized to daily infusion of AA or placebo for 7 days. Serum S-100beta levels were assayed pre-infusion on Days 1-7 and post-infusion on Days 1, 3, and 7, and correlated with National Institutes of Health Stroke Scale (NIHSS).

The mitochondrial uncoupler 2,4-dinitrophenol attenuates tissue damage and improves mitochondrial homeostasis following transient focal cerebral ischemia.

Ischemic stroke is caused by acute neuronal degeneration provoked by interruption of cerebral blood flow. Although the mechanisms contributing to ischemic neuronal degeneration are myriad, mitochondrial dysfunction is now recognized as a pivotal event that can lead to either necrotic or apoptotic neuronal death. Lack of suitable 'upstream' targets to prevent loss of mitochondrial homeostasis has, so far, restricted the development of mechanistically based interventions to promote neuronal survival.