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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...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
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 with...
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...
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...

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Related Experiment Video

Updated: May 12, 2026

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Hydrocephalus following decompressive craniectomy for ischemic stroke.

Satoru Takeuchi1, Yoshio Takasato, Hiroyuki Masaoka

  • 1Department of Neurosurgery, National Defense Medical College, Saitama, Japan. s.takeuchi@room.ocn.ne.jp

Acta Neurochirurgica. Supplement
|April 9, 2013
PubMed
Summary

Decompressive craniectomy for hemispheric cerebral infarction can lead to hydrocephalus in nearly half of patients. This study details hydrocephalus incidence and outcomes following the procedure, highlighting potential discrepancies with prior research.

Related Experiment Videos

Last Updated: May 12, 2026

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Area of Science:

  • Neurosurgery
  • Neurology
  • Critical Care Medicine

Background:

  • Decompressive craniectomy (DC) is established for severe traumatic brain injury.
  • Limited data exists on DC for hemispheric cerebral infarction, particularly regarding hydrocephalus.
  • Previous reports on DC-associated hydrocephalus are scarce.

Purpose of the Study:

  • To investigate the incidence of hydrocephalus after DC for hemispheric cerebral infarction.
  • To present clinical details of patients undergoing DC for this condition.
  • To analyze hydrocephalus development before and after cranioplasty.

Main Methods:

  • Retrospective analysis of 23 patients undergoing DC for hemispheric cerebral infarction.
  • Documentation of patient demographics, infarction location, and Glasgow Coma Scale (GCS) scores.
  • Assessment of hydrocephalus incidence pre- and post-cranioplasty.

Main Results:

  • Hydrocephalus was observed in 11 (47.8%) patients pre-cranioplasty.
  • Post-cranioplasty hydrocephalus occurred in 7 (36.8%) of those who underwent the procedure.
  • Only one patient required a shunt procedure after cranioplasty.

Conclusions:

  • Hydrocephalus is a significant complication following DC for hemispheric cerebral infarction.
  • Discrepancies with prior studies may stem from differing definitions of hydrocephalus and shunting indications.
  • Further research is needed to clarify hydrocephalus management in this patient population.