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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...
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...
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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
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...
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...

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Related Experiment Video

Updated: Jun 12, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
09:14

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

[Spinal hematomas: the spinal apoplexy].

P Varela Rois1, J González García, M Regueira Portas

  • 1Servicio de Neurocirugía, Complejo Hospitalario Universitario de Vigo (CHUVI), Vigo, Pontevedra, España. pilirois@hotmail.com

Neurologia (Barcelona, Spain)
|May 22, 2010
PubMed
Summary
This summary is machine-generated.

Spinal haematomas (SH) are rare but can cause rapid neurological decline. Prompt diagnosis and surgical intervention are crucial for patients with neurological symptoms, with preoperative status being the key prognostic factor.

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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
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The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects
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The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects

Published on: October 2, 2014

Area of Science:

  • Neurology
  • Neurosurgery
  • Pathology

Context:

  • Spinal haematomas (SH) are uncommon and can lead to severe, irreversible neurological deficits.
  • Understanding the factors contributing to SH is essential for timely management.

Purpose:

  • This study retrospectively analyzes 8 cases of spinal haematomas treated over five years.
  • To evaluate the clinical presentation, radiological findings, treatment strategies, and outcomes of spinal haematoma patients.

Summary:

  • The study reviewed 8 SH cases (5 female, 3 male; age 13-81). Predisposing factors included hypertension, coagulation disorders, physical exertion, lumbar puncture, and cavernous angioma.
  • All patients experienced pain followed by neurological symptoms. Surgical intervention for progressive deterioration yielded limited improvement, whereas non-operative management led to spontaneous recovery in some cases.
  • The physiopathology and triggering mechanisms of SH remain debated, with uncertainty regarding the involved vessels and anatomical compartments.

Impact:

  • Highlights the critical role of preoperative neurological status in predicting outcomes for spinal haematomas.
  • Emphasizes the need for prompt diagnosis and urgent surgical treatment in cases with neurological compromise.
  • Suggests that non-operative management may be beneficial for certain spinal haematoma presentations.