Related Experiment Video

Updated: Jul 3, 2026

Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
10:41

Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound

Published on: June 3, 2021

Pathophysiological basis of cerebral vasospasm following aneurysmal subarachnoid haemorrhage

V G Khurana1, M Besser

  • 1Department of Neurosurgery, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Australia.

Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia
|April 1, 1997
PubMed

Subarachnoid haemorrhage (SAH) following rupture of an intracranial aneurysm is associated with a greater than 35% mortality within the first 3 months. Delayed ischaemia due to cerebral vasospasm (CVSP) occurs in approximately one-third of all patients with this disease and accounts for over 20% of its overall morbidity and mortality. Although the clinical and experimental features of CVSP have been widely documented, the pathophysiology remains controversial. Its basis, however, is almost certainly multifactorial. The cerebrovascular microenvironment is significantly altered as a consequence of haemorrhage into the subarachnoid space. Important putative factors implicated in this change include oxyhaemoglobin, endothelin, oxygen- derived free radicals, and neurovascular nitric oxide, arachidonic acid and carbon monoxide systems. In addition, distinct histological changes related to the overall physiological response occur in cerebral vessels undergoing spasm. The present work aims to detail and unify our current understanding of the biological mechanisms underlying this devastating condition.

More Related Videos

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage10:34

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

Published on: August 30, 2020

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...
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...
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...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
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...