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Vascular Spasm

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...

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Related Experiment Video

Updated: Jun 13, 2025

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

[Spreading Depolarization After Aneurysmal Subarachnoid Hemorrhage].

Fumiaki Oka¹, Hideyuki Ishihara

¹Department of Neurosurgery, Yamaguchi University School of Medicine.

No Shinkei Geka. Neurological Surgery

|September 17, 2024

Summary

Spreading depolarization (SD) contributes to brain injury after aneurysmal subarachnoid hemorrhage (aSAH). Targeting SD may offer new therapies to improve outcomes for aSAH patients.

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Last Updated: Jun 13, 2025

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Published on: August 30, 2020

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

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Published on: June 18, 2021

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Published on: October 4, 2024

Area of Science:

Neuroscience
Neurology
Critical Care Medicine

Background:

Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition leading to significant neurological deficits.
Spreading depolarization (SD) is increasingly recognized as a key factor in secondary brain injury following aSAH.
SD involves rapid alterations in neuronal and glial membrane potentials, impairing energy metabolism and causing neuronal dysfunction.

Purpose of the Study:

To review the mechanisms by which SD contributes to secondary brain injury in aSAH.
To evaluate the role of SD in both early brain injury (EBI) and delayed cerebral ischemia (DCI) after aSAH.
To identify potential therapeutic strategies targeting SD to improve aSAH patient prognosis.

Main Methods:

Literature review of studies investigating spreading depolarization in the context of aneurysmal subarachnoid hemorrhage.
Analysis of the pathophysiological impact of SD on neuronal and glial function.
Exploration of current and emerging therapeutic interventions aimed at modulating SD.

Main Results:

SD is implicated in the pathophysiology of both early brain injury and delayed cerebral ischemia following aSAH.
Disruption of energy metabolism and neuronal dysfunction are key consequences of SD.
Evidence suggests SD exacerbates poor clinical outcomes in aSAH patients.

Conclusions:

Spreading depolarization plays a critical role in the secondary brain injury cascade after aSAH.
Targeting SD represents a promising therapeutic avenue for improving neurological outcomes in aSAH.
Further research into SD-specific therapies is warranted to mitigate the devastating effects of aSAH.