Search results for "Cerebral edema"
showing 10 items of 18 documents
Tissue elastance and fluid conduction in normotensive and hypertensive intracerebral mass haematomas.
1988
This is an investigation into the prognostic factors of 117 patients with spontaneous normo- and hypertensive intracerebral haematomas, supported by animal experiments. Preserved tissue elastance and fluid conduction enables the drainage of intrinsic haematoma serum into the CSF spaces in normotensive patients, who showed an increased extension of a perifocal hypodensity in the CT. Arterial hypertension decreased the possibility of fluid resolution. Our experimental studies showed that in hypertensive cases the serum remained trapped in the haematoma, which explains the small hypodense area around the haematoma in most of the hypertensive cases. If as an exception in hypertensives of perifo…
Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke.
2008
Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels o…
Experimental investigations on a model of cryogenic edema.
1987
The role of mechanisms underlying formation and progression of vasogenic brain edema is investigated. On this purpose, cerebral edema was produced by cortical freezing in two different brain situations in rabbits (with or without replacement of bone flap). BBB (Blood-Brain Barrier) breakdown was evaluated by observation of Evans blue extravation, while a histopathological evaluation was carried out by light and transmission electron microscopy. Water content of brain tissue was determined by the wet/dry weight ratio method. Comparison of extension and intensity of cerebral edema between these two groups of animals shows a statistically significant difference: there was evidence of higher wa…
Plasma Hyperosmolality Prolongs QTc Interval and Increases Risk for Atrial Fibrillation in Traumatic Brain Injury Patients
2020
Introduction: Hyperosmotic therapy with mannitol is frequently used for treatment cerebral edema, and 320 mOsm/kg H2O has been recommended as a high limit for therapeutic plasma osmolality. However, plasma hyperosmolality may impair cardiac function, increasing the risk of cardiac events. The aim of this study was to analyze the relation between changes in plasma osmolality and electrocardiographic variables and cardiac arrhythmia in patients treated for isolated traumatic brain injury (iTBI). Methods: Adult iTBI patients requiring mannitol infusion following cerebral edema, and with a Glasgow Coma Score below 8, were included. Plasma osmolality was measured with Osmometr 800 CLG. Spatial Q…
Battered child syndrome: cerebral ultrasound and CT findings after vigorous shaking.
1992
Child abuse by whiplash-shaking can lead to severe cerebral damage, neurological defects and mental retardation. Cerebral damage has been found with and without external evidence of head injury. We report the sonographic findings in two children after traumatization due to repetitive vigorous whiplash shaking. Cerebral sonography revealed cerebral edema at admission or within 48 hours thereafter. Follow-up studies demonstrated development of marked brain atrophy in both cases. The sonographic findings were confirmed by cranial computerized tomography. Doppler sonography was used to monitor cerebral perfusion by measuring intracranial blood flow. The clinical history of the patients demonstr…
Blood constituents trigger brain swelling, tissue death, and reduction of glucose metabolism early after acute subdural hematoma in rats
2009
Outcome from acute subdural hematoma is often worse than would be expected from the pure increase of intracranial volume by bleeding. The aim was to test whether volume-independent pathomechanisms aggravate damage by comparing the effects of blood infusion with those of an inert fluid, paraffin oil, on intracranial pressure (ICP), cerebral perfusion pressure (CPP), local cerebral blood flow (CBF), edema formation, glucose metabolism ([18F]-deoxyglucose, MicroPET), and histological outcome. Rats were injured by subdural infusion of 300 μL venous blood or paraffin. ICP, CPP, and CBF changes, assessed during the first 30 mins after injury, were not different between the injury groups at most …
Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury
2012
Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortality after traumatic brain injury (TBI). As anesthetic care is mandatory in patients suffering from severe TBI it may be important to elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ) such as zonula occludens-1 (ZO-1) and claudin-5 (cl5) play a central role for BBB stability. First, the influence of the volatile anesthetics sevoflurane and isoflurane on in-vitro BBB integrity was investigated by quantification of the electrical resistance (TEER) in murine brain endothelial monolayers and neurovascular co-cultures of the B…
Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.
2010
The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…
Glutamate-containing parenteral nutrition doubles plasma glutamate: A risk factor in neurosurgical patients with blood-brain barrier damage?
1999
OBJECTIVES: Animal studies have shown that the elevation of plasma glutamate levels increase cerebral edema formation whenever the blood-brain barrier is disturbed. Therefore, changes in plasma glutamate levels as influenced by the administration of a glutamate-containing amino acid solution were investigated in neurosurgical patients. DESIGN: Prospective, descriptive study. SETTING: Eight-bed neurosurgical intensive care unit in a university hospital. PATIENTS: Twenty-three neurosurgical patients requiring parenteral nutrition. INTERVENTIONS: Parenteral nutrition was begun 24 hrs after craniotomy. Patients receiving a glutamate-containing amino acid solution (3.75 g/L glutamate) were compa…
Brain Edema and Intracerebral Necrosis Caused by Transcranial Low-Frequency 20-kHz Ultrasound
2006
Background and Purpose— Ultrasound-accelerated thrombolysis is a promising approach toward acute stroke treatment. In previous in vitro studies, we demonstrated enhanced thrombus destruction induced by 20-kHz ultrasound. However, little is known about biological interactions of low-frequency ultrasound with brain tissue. The aim of this in vivo MRI study was to assess safety aspects of transcranial low-frequency ultrasound in rats. Methods— The cranium of 33 male Wistar rats was sonificated for 20 minutes (20-kHz continuous wave). Power output was varied between 0 and 2.6 W/cm 2 . Tympanal and rectal temperature was monitored. Diffusion-weighted imaging and T2-weighted imaging was performe…