Related Experiment Video

Updated: May 5, 2026

Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
04:32

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

7.6K

The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage

Daniel Bodmer1, Kerry A Vaughan, Brad E Zacharia

  • 1Department of Neurological Surgery, The Neurological Institute, Columbia University College of Physicians and Surgeons, New York, NY, 10032, USA.

Translational Stroke Research
|December 11, 2013
PubMed

Insights

Intracerebral hemorrhage (ICH) causes brain swelling and damage. Understanding key molecular pathways like coagulation, inflammation, and hemoglobin toxicity may lead to new treatments for this severe stroke.

Area of Science:

  • Neuroscience
  • Pathology
  • Pharmacology

Background:

  • Intracerebral hemorrhage (ICH) is a severe stroke with limited therapeutic options.
  • Cerebral edema significantly contributes to secondary brain injury and poor outcomes following ICH.
  • Molecular mechanisms driving edema formation after ICH are not fully understood.

Purpose of the Study:

  • To review the key signaling pathways implicated in edema formation after ICH.
  • To discuss the experimental evidence supporting the role of these pathways in ICH-induced edema.
  • To identify potential therapeutic targets for reducing edema in ICH patients.

Main Methods:

  • Review of existing literature on molecular pathways involved in ICH.
  • Analysis of experimental evidence linking specific pathways to edema formation.
  • Identification of potential pharmacological targets based on pathway mechanisms.

Main Results:

  • The coagulation cascade/thrombin, inflammatory response/matrix metalloproteinases, and complement cascade/hemoglobin toxicity are identified as major edema-promoting pathways in ICH.
  • Experimental data support the role of these pathways in exacerbating brain swelling and neuronal damage.
  • These pathways represent promising targets for novel therapeutic interventions.

Conclusions:

  • Targeting the coagulation cascade, inflammatory response, and hemoglobin toxicity pathways offers potential for developing new ICH therapies.
  • Further research into these molecular mechanisms is crucial for advancing ICH treatment.
  • Pharmaceutical targeting of these pathways could reduce cerebral edema and improve outcomes for ICH patients.

More Related Videos

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage09:41

Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage

Published on: July 3, 2014

14.5K
Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

717

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...
19
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
30
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...
20
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...
30
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
24
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins...
20