A Pilot Study of Facial Nerve Stimulation on Cerebral Artery Vasospasm in Subarachnoid Hemorrhage Patients.

Background: The objective of this pilot study was to assess the safety and efficacy of VitalFlow stimulation in aneurysmal subarachnoid hemorrhage (aSAH) patients with vasospasm for the purpose of guiding the design of larger, controlled studies in vasospasm patients, a largely untreated condition [1].

Methods: Six patients with angiographic vasospasm developing post-aSAH were treated with VitalFlow stimulation. Digital subtraction angiograms were obtained at the time of diagnosis (baseline) and then 30 minutes post-stimulation.

Haptoglobin genotype and aneurysmal subarachnoid hemorrhage: Individual patient data analysis.

Objective: To perform an individual patient-level data (IPLD) analysis and to determine the relationship between haptoglobin () genotype and outcomes after aneurysmal subarachnoid hemorrhage (aSAH).

Methods: The primary outcome was favorable outcome on the modified Rankin Scale or Glasgow Outcome Scale up to 12 months after ictus. The secondary outcomes were occurrence of delayed ischemic neurologic deficit, radiologic infarction, angiographic vasospasm, and transcranial Doppler evidence of vasospasm.

Haemoglobin scavenging in intracranial bleeding: biology and clinical implications.

Haemoglobin is released into the CNS during the breakdown of red blood cells after intracranial bleeding. Extracellular free haemoglobin is directly neurotoxic. Haemoglobin scavenging mechanisms clear haemoglobin and reduce toxicity; these mechanisms include erythrophagocytosis, haptoglobin binding of haemoglobin, haemopexin binding of haem and haem oxygenase breakdown of haem.

Facial nerve stimulation in normal pigs and healthy human volunteers: transitional development of a medical device for the emergency treatment of ischemic stroke.

Background: Magnetic stimulation of the facial nerve has been tested in preclinical studies as a new, non-invasive emergency treatment of ischemic stroke that acts by increasing cerebral blood flow (CBF). The objective of the studies reported herein was to identify minimal stimulation parameters that increase CBF in large animals and then test those stimulation parameters in healthy volunteers for safety, tolerability, and effectiveness at increasing CBF. This translational research is necessary preparation for clinical studies in ischemic stroke patients.

Magnetic facial nerve stimulation in animal models of active seizure.

Purpose: As part of our efforts to develop a non-invasive facial nerve stimulator as an emergency treatment for ischemic stroke, we considered possible safety consequences if the technology was misapplied to stroke mimics, e.g., seizure.

Facial nerve stimulation as a future treatment for ischemic stroke.

Stimulation of the autonomic parasympathetic fibers of the facial nerve system (hereafter simply "facial nerve") rapidly dilates the cerebral arteries and increases cerebral blood flow whether that stimulation is delivered at the facial nerve trunk or at distal points such as the sphenopalatine ganglion. Facial nerve stimulation thus could be used as an emergency treatment of conditions of brain ischemia such as ischemic stroke. A rich history of scientific research has examined this property of the facial nerve, and various means of activating the facial nerve can be employed including noninvasive means.

Effects of noninvasive facial nerve stimulation in the dog middle cerebral artery occlusion model of ischemic stroke.

Background And Purpose: Facial nerve stimulation has been proposed as a new treatment of ischemic stroke because autonomic components of the nerve dilate cerebral arteries and increase cerebral blood flow when activated. A noninvasive facial nerve stimulator device based on pulsed magnetic stimulation was tested in a dog middle cerebral artery occlusion model.

Methods: We used an ischemic stroke dog model involving injection of autologous blood clot into the internal carotid artery that reliably embolizes to the middle cerebral artery.

Restored brain perfusion after non-invasive stimulation of the facial nerve in a canine stroke model.

Ischemic stroke affects over 15 million patients per year and is a leading cause of death worldwide. Currently available treatments are indicated for less than 5% of patients. Stimulation of the facial nerve has been proposed as a possible new treatment of ischemic stroke that acts by increasing blood flow to the brain and thereby restoring perfusion through collateral vessels.

Effect of pulsed magnetic stimulation of the facial nerve on cerebral blood flow.

In these experiments we define an effective means of pulsed magnetic stimulation of the facial nerve for the purpose of increasing cerebral blood flow (CBF). In normal anesthetized dog and sheep, a focal magnetic field was directed toward the facial nerve within the temporal bone by placing a 6.5 cm figure-8 stimulation coil over the ear.

Infarction involving the insula and risk of mortality after stroke.

Background: Cerebral infarction involving the insula has been associated with decreased survival following stroke. We hypothesized that infarct volume may reduce this association.

Methods: The subjects were acute stroke patients who had consented to 2-year follow-up after stroke as part of the Michigan Acute Stroke Care Overview and Treatment Surveillance System registry.

The relation of brain ouabain-like compounds and idiopathic intracranial hypertension.

Objectives: To determine the relationship between levels of ouabain-like compounds (OLC) in the cerebrospinal fluid (CSF) and the occurence of idiopathic intracranial hypertension (IIH).

Background: OLC are naturally occurring inhibitors of the sodium-potassium ATPase that are found in the CSF of mammals. Since the production of CSF is dependent upon sodium-potassium ATPase activity, and since there is evidence that the increased intracranial pressure found in the condition of IIH may be the result of increased CSF production, we hypothesized that the level of endogenous OLC would be reduced in the CSF of patients with IIH.

Focal neurological injury caused by West Nile virus infection may occur independent of patient age and premorbid health.

Introduction: Limited evidence suggests that focal neurological injury (e.g., acute flaccid paralysis) caused by infection with the West Nile virus (WNV) is more common in older patients.

Effects of the search technique on the measurement of the change in quality of randomized controlled trials over time in the field of brain injury.

Background: To determine if the search technique that is used to sample randomized controlled trial (RCT) manuscripts from a field of medical science can influence the measurement of the change in quality over time in that field.

Methods: RCT manuscripts in the field of brain injury were identified using two readily-available search techniques: (1) a PubMed MEDLINE search, and (2) the Cochrane Injuries Group (CIG) trials registry. Seven criteria of quality were assessed in each manuscript and related to the year-of-publication of the RCT manuscripts by regression analysis.

The effects of endogenous interleukin-1 bioactivity on locus coeruleus neurons in response to bacterial and viral substances.

In a previous study, we found that microinjection of the cytokine interleukin-1 (IL-1) into the locus coeruleus (LC) increased the electrophysiological activity of LC neurons. To determine if endogenous IL-1 similarly affects the LC, brain IL-1 was induced with lipopolysaccharide (LPS), a substance derived from Gram-negative bacteria. LPS microinjected directly into the LC increased the activity of LC neurons in anesthetized rats, and this effect was blocked by microinfusion of the IL-1 receptor antagonist (IL-1RA) protein into the LC indicating the involvement of IL-1 receptors.

Peripheral endotoxin causes long-lasting changes in locus coeruleus activity via IL-1 in the brain.

Activity of locus coeruleus (LC) neurons, the major noradrenergic cell-body group in the brain whose axons give rise to approximately 70% of norepinephrine (NE) in the brain, is believed to play an important role in attention/vigilance, cognitive functions and behavioral disorders, particularly depression. Results described here show that in the rat, intraperitoneal (i.p.

Alteration of locus coeruleus neuronal activity by interleukin-1 and the involvement of endogenous corticotropin-releasing hormone.

Activity of the locus coeruleus (LC), which is the source of most of the norepinephrine in the brain, may participate in effects of the cytokine interleukin (IL)-1. This report describes the influence of IL-1 beta on the electrophysiological single-unit activity of LC neurons. When microinjected into the LC, human recombinant IL-1 beta (50 pg to 5 ng) increased the activity of LC neurons, predominantly by increasing 'burst' firing, which occurs in response to a sensory stimulus.