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Updated: Jul 7, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

Vasomotion in multiple spontaneous cervical artery dissections.

Claudio Baracchini¹, Simone Tonello, Roberta Vitaliani

¹Department of Neurology, Ospedale Ca' Foncello, Treviso, Italy.

|February 23, 2008

Summary

Patients with multiple spontaneous cervical artery dissections (sCAD) exhibit impaired arterial vasomotion. This suggests an underlying arteriopathy may predispose individuals to dissection events.

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A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

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

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

Published on: June 3, 2021

Area of Science:

Vascular Biology
Neurology
Cardiology

Background:

The causes of spontaneous cervical artery dissection (sCAD) remain unclear.
An underlying arteriopathy affecting vasomotion is suspected but not proven.

Purpose of the Study:

To investigate spontaneous, endothelial-dependent, and endothelial-independent vasodilation in patients with multiple sCAD.
To compare vasodilation parameters between sCAD patients and healthy controls.

Main Methods:

High-resolution ultrasound assessed arterial dilation in common carotid, vertebral, and brachial arteries.
Spontaneous and isosorbide dinitrate-mediated (endothelial-independent) dilations were measured.
Flow-mediated (endothelial-dependent) dilation was assessed in brachial arteries.

Main Results:

Impaired spontaneous and endothelial-independent dilations were observed in carotid and vertebral arteries of sCAD patients.
No significant difference in spontaneous or endothelial-independent dilation was found in brachial arteries.
Endothelial-dependent dilation of brachial arteries was significantly lower in sCAD patients compared to controls.

Conclusions:

Multiple sCAD patients demonstrate significantly impaired arterial vasomotion.
This vasomotion deficit may represent a predisposing factor for dissection.