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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

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Updated: May 15, 2026

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
07:19

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Published on: October 26, 2013

Association between endothelial dysfunction and acute brain dysfunction during critical illness.

Christopher G Hughes1, Alessandro Morandi, Timothy D Girard

  • 1Department of Anesthesiology, Division of Critical Care, Vanderbilt University School of Medicine, 1211 21st Ave. South, 526 MAB, Nashville, Tennessee 37212, USA. christopher.hughes@vanderbilt.edu

Anesthesiology
|December 25, 2012
PubMed
Summary
This summary is machine-generated.

Systemic endothelial dysfunction, indicated by lower vascular reactivity, is linked to prolonged acute brain dysfunction in critically ill patients. This finding highlights the importance of vascular health in critical care outcomes.

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Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples

Published on: October 23, 2020

Area of Science:

  • Critical care medicine
  • Neuroscience
  • Vascular biology

Background:

  • Acute brain dysfunction (delirium and coma) is common in critical illness, impacting patient outcomes and healthcare costs.
  • The underlying pathophysiology of acute brain dysfunction remains poorly understood.
  • Endothelial dysfunction, prevalent in critical illness, may affect cerebral blood flow and blood-brain barrier integrity, but its direct link to acute brain dysfunction is unstudied.

Purpose of the Study:

  • To investigate the association between systemic endothelial dysfunction and the occurrence and duration of acute brain dysfunction in critically ill patients.
  • To determine if impaired vascular reactivity correlates with increased delirium and coma in the intensive care unit (ICU) setting.

Main Methods:

  • Prospective cohort study of adult ICU patients with shock or respiratory failure.
  • Systemic endothelial function assessed using peripheral artery tonometry to calculate the reactive hyperemia index (RHI).
  • Acute brain dysfunction evaluated using the Richmond Agitation-Sedation Scale and Confusion Assessment Method for the ICU; multivariable regression analyzed RHI association with delirium/coma-free days and delirium duration.

Main Results:

  • Lower reactive hyperemia index (indicating worse endothelial function) was significantly associated with fewer delirium/coma-free days (P=0.02).
  • Worse endothelial function also correlated with a longer duration of delirium (P=0.05) after adjusting for multiple clinical factors.
  • The study included 147 patients with a median age of 57 and APACHE II score of 26.

Conclusions:

  • Critically ill patients exhibiting poorer systemic endothelial function experience a greater duration of acute brain dysfunction.
  • These findings suggest that endothelial function is a relevant factor in the development and persistence of delirium and coma in critical illness.
  • Targeting endothelial dysfunction may represent a potential therapeutic strategy to mitigate acute brain dysfunction in the ICU.