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Ng, Wai-sang Poon , M.

Brain Edema:Part 2 ; Clinical picture

Disturbances in cerebrovascular regulation in the form of diminished cerebral vasoreactivity CVR to carbon dioxide and an altered pressure autoregulatory response PAR are common after traumatic brain injury TBI and correlate with clinical outcome. Daily assessment of the state of cerebrovascular regulation may assist in the clinical management of TBI patients. This study examined 20 ventilated TBI patients. We employed blood flow velocity BFV measurement using transcranial Doppler ultrasonography to assess the impact of injury type focal and diffuse on cerebral hemisphere asymmetry in cerebrovascular regulation and to examine whether impairment in CVR and PAR correlate with clinical outcomes.

Cerebral hemisphere asymmetry in cerebrovascular regulation in ventilated traumatic brain injury. T1 - Cerebral hemisphere asymmetry in cerebrovascular regulation in ventilated traumatic brain injury. N2 - Disturbances in cerebrovascular regulation in the form of diminished cerebral vasoreactivity CVR to carbon dioxide and an altered pressure autoregulatory response PAR are common after traumatic brain injury TBI and correlate with clinical outcome.

AB - Disturbances in cerebrovascular regulation in the form of diminished cerebral vasoreactivity CVR to carbon dioxide and an altered pressure autoregulatory response PAR are common after traumatic brain injury TBI and correlate with clinical outcome. Abstract Disturbances in cerebrovascular regulation in the form of diminished cerebral vasoreactivity CVR to carbon dioxide and an altered pressure autoregulatory response PAR are common after traumatic brain injury TBI and correlate with clinical outcome.

Fingerprint Cerebrum. Blood Flow Velocity. After cortical impact the craniotomy was closed with the initially removed bone and fixed with conventional tissue glue Histoacryl, Braun, Melsungen, Germany. The wounds were closed with filament sutures at the end of the surgery. The vehicle controls received vehicle solution 0.

The hemispheres were separated along the interhemispherical line and both hemispheres were weighted in order to obtain their wet weight ww. The amount of extravasated Evans Blue was expressed as optical density OD per g of the hemisphere. After drilling of a burr hole over the contralateral temporal bone, the probe was advanced 1.

The neuroscore consists of 10 different tasks evaluating motor ability, alertness, balancing, and general behavior. One point was awarded for failure to successfully perform a task. Healthy mice were successful in all tasks and received 0 points.

Table of contents

To determine the brain contusion volume, animals were killed after i. The area of both hemispheres and contused brain tissue, defined as region with lack of cresyl violet Nissl staining, were determined with a computerized image system Optimas 6. Contusion volume was analyzed by an investigator blinded towards to experimental group. Tissue segments were lysed in a buffer containing Statistical analysis was performed with Sigma Stat 3.

Body temperature and the systolic blood pressure during surgery were in all groups within physiological levels. Following head trauma brain water content increased significantly in vehicle treated animals. To further evaluate the BBB functionality, penetrability was assessed by quantification of extravasated Evans Blue dye. Increase in brain water content and increased permeability of the BBB resulted in elevated intracranial pressure.

Influence of MLCK inhibition on myosin light chain phosphorylation. Correspondingly, the primary lesion volume increased to Influence of MLCK inhibition on secondary brain damage, neurological function and cerebral inflammation. The influence of myosin light chain kinase MLCK inhibition was tested with 1.

Intracranial Pressure and Brain Monitoring XIII

Nissl stained coronal brain sections demonstrating the cortical contusion of 1. Although brain edema is considered to enhance secondary brain damage, MLCK inhibition did not ameliorate secondary brain damage, neurological function or cerebral inflammation. To investigate traumatic brain injury, multiple models have been developed to simulate focal head injury in rodents, ranging from e. One of the most frequently applied models is the controlled cortical impact CCI , which utilizes a piston to penetrate the brain at defined velocity, depth and impact duration.

This cerebral lesion triggers a pathophysiological cascade causing an expansion of brain damage into surrounding healthy parenchyma. Brain edema is considered to be one of the central pathophysiological events worsening outcome by raising intracranial pressure and impairing cerebral perfusion.

Several experimental approaches effectively limited brain edema formation by use of, e. These strategies intervene at different upstream cascades, but result all in an increased stability and integrity of the BBB. The BBB separates the blood content from the brain and plays therefore a crucial role in vasogenic brain edema formation. The exact mechanisms of BBB disruption are still in debate. The BBB is formed by cerebral microvascular endothelial cells, pericytes and astrocytes Rubin and Staddon and regulates the trafficking of ions, molecules and leukocytes in and out of the brain Hawkins and Davis Endothelial cells are linked by tight junctions, which ensure the structural integrity of the BBB and are connected to the contractile apparatus of the cell.

Brain Edema XIII | Julian T. Hoff | Springer

Increased brain edema possibly initiates a vicious cycle with elevated intracranial pressure ICP and impaired pericontusional perfusion. Increased intracranial pressure is considered to enhance secondary lesion expansion. It was therefore speculated that reduction of brain edema and consecutive decrease of ICP may result in reduced expansion of brain damage.

co.organiccrap.com/196668.php To rule out the possibility that 1. Independent of lesion size, stabilization of BBB by selective MLCK inhibition reduced brain edema formation, but did not influence secondary expansion of brain damage or neurological function. The results indicate that opening of tight junctions may be rather a result not the cause of pathophysiological events following brain trauma. The results of the present study are in accordance with data demonstrating a key role of inflammation as a trigger of brain edema formation.

Inflammation increases BBB permeability and brain edema formation following cerebral insults Abbott Inhibition of brain edema formation itself did not translate into reduced lesion volume. Therefore, prevention of brain edema formation at the endothelial level alone has to be combined with pharmacological interventions to reduce e. The results suggest, that myosin light chain kinase inhibitors could be a relevant target of novel drugs intended to stabilize BBB function after brain trauma. The authors want to thank Dana Pieter for her excellent technical assistance.

The authors have no conflicting financial interest to declare. This work was financially supported by departmental funding. Volume , Issue 4. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account.

If the address matches an existing account you will receive an email with instructions to retrieve your username. Journal of Neurochemistry Volume , Issue 4.


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