Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Hemorrhagic Stroke l: Introduction

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...

Hemorrhagic Stroke ll: Pathophysiology

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...

Bacterial Meningitis II: Pathophysiology

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...

Increased Intracranial Pressure l: Introduction

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: Pathophysiology

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 ll: Pathophysiology

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...

You might also read

Related Articles

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

Sort by

Same author

From spreading depression to the trigeminovascular system.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology·2006

Same author

Surgical management of middle cerebral artery aneurysms.

Neurosurgery·2001

Same author

[Endarterectomy and carotid angioplasty: surgical perspective].

Revista de neurologia·2001

Same author

Cerebrovascular surgery: past, present, and future.

Neurosurgery·2000

Same author

Contralateral subdural hematoma resulting from intraoperative aneurysm rupture. Case illustration.

Journal of neurosurgery·2000

Same author

Vascularized pedicle graft.

Journal of neurosurgery·1999

Search research articles

Related Experiment Video

Updated: May 8, 2026

A Murine Model of Subarachnoid Hemorrhage

A Murine Model of Subarachnoid Hemorrhage

Published on: November 21, 2013

Subarachnoid hemorrhage.

R C Heros, N T Zervas

Annual Review of Medicine

|January 1, 1983

Summary

Subarachnoid hemorrhage (SAH) is a major cause of stroke-related death and disability. Early detection of SAH warning signs is crucial for effective treatment and reducing patient morbidity.

Area of Science:

Neurology
Neurosurgery
Public Health

Background:

Subarachnoid hemorrhage (SAH) accounts for approximately 10% of all stroke cases, leading to significant mortality and morbidity.
Despite advances in surgical interventions for aneurysms and arteriovenous malformations (AVMs), the overall morbidity associated with SAH has remained largely unchanged.
A critical need exists to improve medical community awareness of SAH warning signs.

Purpose of the Study:

To emphasize the importance of recognizing SAH warning signs.
To highlight the potential for improved outcomes with early detection and intervention.
To underscore the role of timely diagnosis in mitigating SAH-related morbidity.

Main Methods:

Review of current understanding of SAH pathophysiology and treatment.

More Related Videos

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

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

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

Published on: June 18, 2021

Related Experiment Videos

Last Updated: May 8, 2026

A Murine Model of Subarachnoid Hemorrhage

A Murine Model of Subarachnoid Hemorrhage

Published on: November 21, 2013

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

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

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

Published on: June 18, 2021

Analysis of the impact of delayed diagnosis on patient outcomes.

Emphasis on clinical recognition of SAH symptoms.

Main Results:

SAH remains a significant cause of death and disability.
Current surgical techniques offer effective treatment for aneurysms and AVMs when detected early.
Morbidity rates associated with SAH have not substantially decreased, indicating a gap in timely diagnosis or intervention.

Conclusions:

Increased medical awareness of SAH warning signs is essential for reducing morbidity.
Early detection and prompt treatment of aneurysms and AVMs can significantly improve patient outcomes.
Effective management of SAH hinges on early identification and intervention before major hemorrhage occurs.