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Related Concept Videos

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...
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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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...
Hepatic Encephalopathy01:29

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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

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Related Experiment Video

Updated: Jul 20, 2026

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
09:35

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

Perihematomal mitochondrial dysfunction after intracerebral hemorrhage.

Jeong Sook Kim-Han1, Sarah J Kopp, Laura L Dugan

  • 1Department of Neurology, Washington University, St. Louis, MO, USA.

Stroke
|September 9, 2006
PubMed
Summary

Mitochondrial dysfunction, not ischemia, causes reduced brain metabolism in intracerebral hemorrhage (ICH) patients. This finding suggests new therapeutic targets for ICH treatment.

Related Experiment Videos

Last Updated: Jul 20, 2026

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
09:35

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Pathophysiology

Background:

  • Intracerebral hemorrhage (ICH) is associated with reduced cerebral blood flow and oxygen extraction.
  • A primary reduction in brain metabolism is suspected to cause these changes.

Purpose of the Study:

  • To investigate whether reduced mitochondrial respiratory function contributes to decreased metabolic demand in ICH patients.
  • To differentiate between mitochondrial dysfunction and ischemia as the cause of metabolic changes in ICH.

Main Methods:

  • Brain tissue samples were obtained from 6 acute spontaneous ICH patients and 6 control patients.
  • Mitochondrial oxygen consumption was measured using pyruvate, malate, ADP, oligomycin, and carbonylcyanide.
  • Studies were initiated within 1 hour of tissue collection.

Main Results:

  • Mitochondria from ICH patients exhibited approximately 40% lower State 3 (active) oxygen consumption compared to controls.
  • A progressive decline in State 3 respiration was observed with increasing time from hemorrhage.
  • Significantly reduced respiration was evident as early as 6 hours post-ICH.

Conclusions:

  • Data support mitochondrial dysfunction as the cause of reduced oxygen metabolism in ICH.
  • Findings suggest a novel therapeutic avenue for ICH, focusing on mitochondrial function.