Use of GABAergic sedatives after subarachnoid hemorrhage is associated with worse outcome-preliminary findings.

Study Objective: Recent experimental evidence identified GABAergic sedation as a possible cause for deprived neuroregeneration and poor outcome after acute brain injury. Patients with aneurysmal subarachnoid hemorrhage are often sedated, and GABAergic sedation, such as midazolam and propofol, is commonly used.

Design: Retrospective cohort study based on a prospectively established database.

Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group.

Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes.

Changes in electrocorticographic beta frequency components precede spreading depolarization in patients with acute brain injury.

Objective: Spreading depolarization (SD) occurs after traumatic brain injury, subarachnoid hemorrhage, malignant hemispheric stroke and intracranial hemorrhage. SD has been associated with secondary brain injury, which can be reduced by ketamine. In this present study frequency bands of electrocorticographic (ECoG) recordings were investigated with regards to SDs.

Cerebral Glucose Metabolism and Sedation in Brain-injured Patients: A Microdialysis Study.

Background: Disturbed brain metabolism is a signature of primary damage and/or precipitates secondary injury processes after severe brain injury. Sedatives and analgesics target electrophysiological functioning and are as such well-known modulators of brain energy metabolism. Still unclear, however, is how sedatives impact glucose metabolism and whether they differentially influence brain metabolism in normally active, healthy brain and critically impaired, injured brain.

Endogenous nitric-oxide synthase inhibitor ADMA after acute brain injury.

Previous results on nitric oxide (NO) metabolism after traumatic brain injury (TBI) show variations in NO availability and controversial effects of exogenous nitric oxide synthase (NOS)-inhibitors. Furthermore, elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) were reported in cerebro-spinal fluid (CSF) after traumatic subarachnoid hemorrhage (SAH). Therefore, we examined whether ADMA and the enzymes involved in NO- and ADMA-metabolism are expressed in brain tissue after TBI and if time-dependent changes occur.

Clusters of spreading depolarizations are associated with disturbed cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage.

Background And Purpose: We studied the dynamics of extracellular brain tissue concentrations of glucose, lactate, pyruvate, and glutamate during the occurrence of spreading depolarizations (SDs) in patients with aneurysmal subarachnoid hemorrhage.

Methods: In this prospective observational study, patients with aneurysmal subarachnoid hemorrhage received multimodal cerebral monitoring, including intracranial pressure, cerebral microdialysis, and subdural electrocorticography.

Results: Seven of the 17 recruited patients had intracerebral hemorrhage, acute ischemia and severe brain oedema leading to acute ischemic neurological deficits associated with early disturbance of metabolism at the recording site.

Clinical review: Traumatic brain injury in patients receiving antiplatelet medication.

As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality.

Effect of analgesics and sedatives on the occurrence of spreading depolarizations accompanying acute brain injury.

Spreading depolarizations are waves of mass neuronal and glial depolarization that propagate across the injured human cortex. They can occur with depression of neuronal activity as spreading depressions or isoelectric spreading depolarizations on a background of absent or minimal electroencephalogram activity. Spreading depolarizations are characterized by the loss of neuronal ion homeostasis and are believed to damage functional neurons, leading to neuronal necrosis or neurological degeneration and poor outcome.

Influence of isoflurane on neuronal death and outcome in a rat model of traumatic brain injury.

In the developing brain agents clinically used for the purpose of analgosedation can cause severe neurodegeneration. In patients with TBI analgosedation is a first-line treatment for intracranial hypertension. At the same time, damaged neuronal networks undergo conformational changes and use developmental mechanisms to restore brain function.

Spreading depolarizations in a case of migraine-related stroke.

Background: Cortical spreading depolarization (CSD) has been implicated in the pathophysiology of migraine with aura. Patients that suffer from this type of migraine have shown a higher risk of developing an ischaemic stroke.

Case: A 42-year-old female exhibited reoccurring migraine attacks for the first time 1 month before suffering an ischaemic infarction.

Cerebral metabolism after early decompression craniotomy following controlled cortical impact injury in rats.

After traumatic brain injury, a cascade of metabolic changes promotes the development of secondary brain damage. In this study, we examined metabolic changes in rats in the acute stage after trauma. Furthermore, we investigated the effect of a very early decompression craniotomy on intracranial pressure (ICP) and on metabolic parameters.

Reversible occlusion (on-off) valves in shunted tumor patients.

The first commercially produced adjustable valve for shunted hydrocephalus patients was introduced by H. Portnoy and R. Schulte in 1973.

The use of danaparoid to manage coagulopathy in a neurosurgical patient with heparin-induced thrombocytopenia type II and intracerebral haemorrhage.

This study presents a case of bifrontal intracerebral haemorrhage in a patient with heparin-induced thrombocytopenia type II (HIT II). HIT II was induced by treatment with low-molecular-weight heparin for recurrent deep vein thrombosis caused by essential thrombocytosis and accompanied by hepatic thromboembolism. This patient was treated with platelet substitution and neurosurgical haematoma evacuation.

Inositol-1,4,5-trisphosphate receptor-mediated Ca2+ waves in pyramidal neuron dendrites propagate through hot spots and cold spots.

We studied inositol-1,4,5-trisphosphate (IP(3)) receptor-dependent intracellular Ca(2+) waves in CA1 hippocampal and layer V medial prefrontal cortical pyramidal neurons using whole-cell patch-clamp recordings and Ca(2+) fluorescence imaging. We observed that Ca(2+) waves propagate in a saltatory manner through dendritic regions where increases in the intracellular concentration of Ca(2+) ([Ca(2+)](i)) were large and fast ('hot spots') separated by regions where increases in [Ca(2+)](i) were comparatively small and slow ('cold spots'). We also observed that Ca(2+) waves typically initiate in hot spots and terminate in cold spots, and that most hot spots, but few cold spots, are located at dendritic branch points.

Regulation of cytokine signaling components in developing rat retina correlates with transient inhibition of rod differentiation by CNTF.

Ciliary neurotrophic factor (CNTF) is known to inhibit the differentiation of rod photoreceptors from postmitotic precursor cells. During early postnatal development, photoreceptor precursors lose their responsiveness to CNTF. The underlying events causing this change in responsiveness are unknown.

Inositol 1,4,5 trisphosphate receptor and chromogranin B are concentrated in different regions of the hippocampus.

Calcium (Ca(2+)) release from intracellular stores plays a crucial role in many cellular functions in the brain. These intracellular signals have been shown to be transmitted within and between cells. We report a non-uniform distribution of proteins essential for Ca(2+) signaling in acutely prepared brain slice preparations and organotypic slice cultures, both made from rat hippocampus.