A5042883211- Traumatic Brain Injury and Neurovascular Disturbances
- Neuroscience and Neuropharmacology Research
- Intracranial Aneurysms: Treatment and Complications
- Traumatic Brain Injury Research
- Migraine and Headache Studies
- EEG and Brain-Computer Interfaces
- Trauma and Emergency Care Studies
- Epilepsy research and treatment
- Advanced MRI Techniques and Applications
- Nitric Oxide and Endothelin Effects
- Optical Imaging and Spectroscopy Techniques
- Functional Brain Connectivity Studies
- Ion channel regulation and function
- Cerebrospinal fluid and hydrocephalus
- Cardiac Arrest and Resuscitation
- Neural dynamics and brain function
- Neurosurgical Procedures and Complications
- Acute Ischemic Stroke Management
- Cerebrovascular and Carotid Artery Diseases
- Neuroscience and Neural Engineering
- Neuroscience of respiration and sleep
- Anesthesia and Sedative Agents
- Anesthesia and Neurotoxicity Research
- Neonatal and fetal brain pathology
- Neurological Disorders and Treatments
Humboldt-Universität zu Berlin
2011-2025
Charité - Universitätsmedizin Berlin
2016-2025
Freie Universität Berlin
2011-2025
Einstein Center for Neurosciences Berlin
2018-2025
Bernstein Center for Computational Neuroscience Berlin
2011-2025
Berlin Institute of Health at Charité - Universitätsmedizin Berlin
2024
Medical University of Vienna
2021-2023
University of Groningen
2022
Karolinska Institutet
2022
Centre Hospitalier Régional et Universitaire de Nancy
2021
In clinical trials and observational studies there is considerable inconsistency in the use of definitions to describe delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage. A major cause for this combining radiographic evidence vasospasm with features ischemia, although multiple factors may contribute DCI. The second issue variability overlap terms used each phenomenon. This makes comparisons among difficult.An international ad hoc panel experts involved hemorrhage...
Progressive ischaemic damage in animals is associated with spreading mass depolarizations of neurons and astrocytes, detected as negative slow voltage variations. Speculation on whether occur human stroke has continued for the past 60 years. Therefore, we performed a prospective multicentre study assessing incidence timing delayed neurological deficit (DIND) patients major subarachnoid haemorrhage (SAH) requiring aneurysm surgery. Spreading were recorded by electrocorticography subdural...
The term cortical spreading depolarization (CSD) describes a wave of mass neuronal associated with net influx cations and water. Clusters prolonged CSDs were measured time-locked to progressive ischaemic damage in human cortex. CSD induces tone alterations resistance vessels, causing either transient hyperperfusion (physiological haemodynamic response) healthy tissue; or hypoperfusion [inverse response = ischaemia (CSI)] tissue at risk for damage, which has so far only been shown...
Perturbations in the integrity of blood-brain barrier have been reported both humans and animals under numerous pathological conditions. Although prevents penetration many blood constituents into brain extracellular space, effect such perturbations on function their roles pathogenesis cortical diseases are unknown. In this study we established a model for focal disruption rat cortex by direct application bile salts. Exposure cerebral vivo to salts resulted long-lasting extravasation serum...
Abstract Objective Cortical spreading depression (CSD) and periinfarct depolarization (PID) have been shown in various experimental models of stroke to cause secondary neuronal damage infarct expansion. For decades it has questioned whether CSD or PID occur human ischemic stroke. Here, we describe patients with malignant middle cerebral artery infarction detected by subdural electrocorticography (ECoG). Methods Centres the Co‐operative Study Brain Injury Depolarisations (COSBID) recruited 16...
Spreading depolarization of cells in cerebral grey matter is characterized by massive ion translocation, neuronal swelling and large changes direct current-coupled voltage recording. The near-complete sustained above the inactivation threshold for action potential generating channels initiates spreading depression brain activity. In contrast, epileptic seizures show modest translocation below channels. Such allows synchronous, highly frequent firing; ictal field potentials being its...
In barbiturate-anesthetized rats, we induced 3 hours of permanent middle cerebral artery occlusion (MCAO) by an intraluminal thread (n = 6), or 1 hour MCAO followed 2 reperfusion 6). Through a closed cranial window over the parietal cortex, production reactive oxygen species (ROS) was measured in infarct border using online vivo chemiluminescence (CL) while monitoring appearance peri-infarct depolarizations (PID). The borderzone localization ROS and direct current (DC) potential measurements...
We investigated the combined effect of increased brain topical K + concentration and reduction nitric oxide(NO . ) level caused by oxide scavenging or synthase (NOS) inhibition on regional cerebral blood flow subarachnoid direct current (DC) potential. Using thiopental-anesthetized male Wistar rats with a closed cranial window preparation, superfusion combination NO scavenger hemoglobin(Hb; 2 mmol/L) in artificial cerebrospinal fluid ([K ] ACSF at 35 mmol/L led to sudden spontaneous...
Object. The pathogenesis of delayed ischemic neurological deficits after subarachnoid hemorrhage has been related to products hemolysis. Topical brain superfusion artificial cerebrospinal fluid (ACSF) containing the hemolysis K + and hemoglobin (Hb) was previously shown induce ischemia in rats. Superimposed on a slow vasospastic reaction, events represent spreading depolarizations neuronal—glial network that trigger acute vasoconstriction. purpose present study investigate whether such...
Spreading depolarizations are waves of mass neuronal and glial depolarization that propagate across the injured human cortex. They can occur with depression activity as spreading depressions or isoelectric on a background absent minimal electroencephalogram activity. characterized by loss ion homeostasis believed to damage functional neurons, leading necrosis neurological degeneration poor outcome. Analgesics sedatives influence activity-dependent therefore represent potential modulators...
How does infarction in victims of stroke and other types acute brain injury expand to its definitive size subsequent days? Spontaneous depolarizations that repeatedly spread across the cerebral cortex, sometimes at remarkably regular intervals, occur patients with all injury. Here, we show experimentally vivo real-time imaging similar, spontaneous cycle around ischaemic lesions enlarge lesion step each cycle. This behaviour results periodicity depolarization when monitored a single point...