CSF metabolomics alterations after aneurysmal subarachnoid hemorrhage: what do we know?

Purpose: The purpose of this mini review is to describe metabolomics in cerebrospinal fluid (CSF) and its potential in aneurysmal subarachnoid hemorrhage (aSAH). In brain injury, patients' micro dialysis enables detecting biochemical change in brain tissue. Indicators for ischemia were detected such as lactate, pyruvate, glucose, and glutamate.

Link between both infratentorial and supratentorial intracranial pressure burdens and final outcome in patients with infratentorial brain injury.

Objective: Increased intracranial pressure (ICP) is most likely not being transmitted uniformly within the cranium. The ICP profiles in the supra- and infratentorial compartments remain largely unclear. Increased ICP in the cerebellum, however, is insufficiently captured by supratentorial ICP (ICPsup) monitoring due to compartmentalization through the tentorium.

Ultrasound-guided versus computed tomography-controlled periradicular injections of the first sacral nerve: a prospective randomized clinical trial.

Aim: To compare ultrasound (US)-guided versus computed tomography (CT)-controlled periradicular injections of the first sacral spinal (S1) nerve in a prospective randomized clinical trial.

Materials And Methods: Thirty-nine patients with S1-radiculopathy were consecutively enrolled for 40 periradicular injections and assigned to an US or CT guided group. Needle position after US-assisted placement was controlled by a low-dose CT-scan.

Cerebral Energy Status and Altered Metabolism in Early Brain Injury After Aneurysmal Subarachnoid Hemorrhage: A Prospective 31P-MRS Pilot Study.

Background: Acute changes of cerebral energy metabolism in early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (aSAH) may play a crucial role for overall neurological outcome. However, direct detection of these alterations is limited. Phosphorous magnetic resonance spectroscopy (31P-MRS) is a molecular-based advanced neuroimaging technique allowing measurements of pathophysiological processes and tissue metabolism based on various phosphorous compound metabolites.

Time Course of Metabolomic Alterations in Cerebrospinal Fluid After Aneurysmal Subarachnoid Hemorrhage.

The aim of this study was to investigate metabolite levels in cerebrospinal fluid (CSF) in their time-dependent course after aneurysmal subarachnoid hemorrhage (aSAH) comparing them to patients harboring unruptured intracranial aneurysms. Eighty CSF samples of 16 patients were analyzed. The study population included patients undergoing endovascular/microsurgical treatment of ruptured intracranial aneurysms ( = 8), which were assessed for 9 days after aSAH.

Transcallosal, transchoroidal clipping of a hypothalamic collateral vessel aneurysm in Moyamoya disease.

Peripheral collateral vessel aneurysms in Moyamoya disease (MMD) remain difficult to treat due to their deep location, small size, and vascular fragility. We report the case of an aneurysm localized in the hypothalamus, which was rapidly increasing in size with repeated hemorrhage despite revascularization surgery. Aneurysm clipping was performed to prevent further progress and rerupture with favorable outcome.

Autophagy after Subarachnoid Hemorrhage: Can Cell Death be Good?

Background: Autophagy is a prosurvival, reparative process that maintainsww cellular homeostasis through lysosomal degradation of selected cytoplasmic components and programmed death of old, dysfunctional, or unnecessary cytoplasmic entities. According to growing evidence, autophagy shows beneficial effects following subarachnoid hemorrhage (SAH). SAH is considered one of the most devastating forms of stroke.

IVIG activates FcγRIIB-SHIP1-PIP3 Pathway to stabilize mast cells and suppress inflammation after ICH in mice.

Following intracerebral hemorrhage (ICH), the activation of mast cell contributes to brain inflammation and brain injury. The mast cell activation is negatively regulated by an inhibitory IgG-receptor. It's signals are mediated by SHIP (Src homology 2-containing inositol 5' phosphatase), in particular SHIP1, which activation leads to hydrolyzation of PIP3 (Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P, leading to the inhibition of calcium mobilization and to the attenuation of mast cell activation.

"I am not afraid of death"-a survey on preferences concerning neurosurgical interventions among patients over 75 years.

Introduction: Treatment decisions in elderly patients with traumatic brain injury (TBI) are mainly determined by trauma severity and patient age. The aim of this study was to explore personal preferences of potential patients regarding life-prolonging neurosurgical interventions by interviewing ambulatory, autonomous elderly people.

Methods: One hundred consecutive patients older than 75 years frequenting the outpatient clinic of the Department of Neurosurgery were interviewed about their attitudes regarding the hypothetical case of an 81-year-old patient with TBI and a space-occupying acute subdural hematoma (aSDH) using a 21-point questionnaire.

Phase I and Phase II Therapies for Acute Ischemic Stroke: An Update on Currently Studied Drugs in Clinical Research.

Acute ischemic stroke is a devastating cause of death and disability, consequences of which depend on the time from ischemia onset to treatment, the affected brain region, and its size. The main targets of ischemic stroke therapy aim to restore tissue perfusion in the ischemic penumbra in order to decrease the total infarct area by maintaining blood flow. Advances in research of pathological process and pathways during acute ischemia have resulted in improvement of new treatment strategies apart from restoring perfusion.

Pharmacological Management Options to Prevent and Reduce Ischemic Hemorrhagic Transformation.

Background: Hemorrhagic transformation (HT) is a common and natural complication after acute ischemic stroke. The only FDA-approved treatment so far for acute ischemic stroke is rapid reperfusion with recombinant tissue plasminogen activator (rtPA). Although it has been shown to exaggerate the risk and severity of HT and to be associated with increased morbidity and mortality.

Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy.

Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating disease that primarily causes neuronal and white matter injury and is among the leading cause of death among infants. Currently there are no well-established treatments; thus, it is important to understand the pathophysiology of the disease and elucidate complications that are creating a gap between basic science and clinical translation. In the development of neuroprotective strategies and translation of experimental results in HIE, there are many limitations and challenges to master based on an appropriate study design, drug delivery properties, dosage, and use in neonates.

What's New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment.

Traumatic brain injury (TBI), defined as an alteration in brain functions caused by an external force, is responsible for high morbidity and mortality around the world. It is important to identify and treat TBI victims as early as possible. Tracking and monitoring TBI with neuroimaging technologies, including functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET), and high definition fiber tracking (HDFT) show increasing sensitivity and specificity.