Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Ischemic brain edema.

G A Rosenberg1

  • 1Department of Neurology, University of New Mexico, Albuquerque 87131, USA. grosen@salud.unm.edu

Progress in Cardiovascular Diseases
|December 22, 1999
PubMed
Summary

Brain edema following stroke involves cell swelling and membrane damage. Understanding these molecular events is key to developing new treatments for this life-threatening complication.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Editorial: WHO Guidelines on Community-Level Interventions to Manage Declines in Intrinsic Capacity: The Road for Preventing Cognitive Declines in Older Age?

The journal of prevention of Alzheimer's disease·2018
Same author

Blood-Brain Barrier Permeability in Aging and Alzheimer's Disease.

The journal of prevention of Alzheimer's disease·2015
Same author

Intranuclear matrix metalloproteinases promote DNA damage and apoptosis induced by oxygen-glucose deprivation in neurons.

Neuroscience·2012
Same author

Tissue inhibitor of matrix metalloproteinases-3 (TIMP-3) lacks involvement in bacterial collagenase-induced intracerebral hemorrhage in mouse.

Acta neurochirurgica. Supplement·2008
Same author

Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia.

Neuroscience·2008
Same author

Tissue inhibitor of metalloproteinases-3 facilitates Fas-mediated neuronal cell death following mild ischemia.

Cell death and differentiation·2007

Area of Science:

  • Neurology
  • Pathophysiology
  • Biochemistry

Background:

  • Brain edema is a severe complication of cerebral infarction (stroke).
  • Cerebral ischemia triggers a molecular cascade involving ionic pump failure, cell swelling, and membrane damage from free radicals and proteases.
  • This process can lead to irreversible brain injury.

Purpose of the Study:

  • To review the pathophysiology of brain edema after ischemic stroke.
  • To discuss current diagnostic and therapeutic strategies.
  • To highlight the potential for novel treatments targeting the injury cascade.

Main Methods:

  • Review of molecular mechanisms of ischemic brain edema.
  • Discussion of diagnostic advancements, particularly magnetic resonance imaging (MRI).
  • Analysis of therapeutic interventions, including thrombolytics and osmotherapy.

Main Results:

  • Brain edema, both cytotoxic and vasogenic, peaks 24-72 hours post-ischemia.
  • Magnetic resonance imaging (MRI) has improved diagnostic accuracy.
  • Thrombolytics can improve outcomes by reperfusing tissue but may worsen edema if delayed.
  • Osmotherapy's efficacy in treating ischemic edema is not definitively proven.

Conclusions:

  • Further understanding of the molecular events in ischemic brain edema is crucial.
  • Novel therapeutic strategies targeting specific stages of the injury cascade are anticipated.
  • Improved diagnostics and targeted treatments hold promise for managing this critical condition.

Related Experiment Videos