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Updated: Jul 24, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
08:12

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

Published on: July 28, 2018

Acute Cytotoxic and Vasogenic Edema after Subarachnoid Hemorrhage: A Quantitative MRI Study

J M Weimer1, S E Jones2, J A Frontera3

  • 1From the Cerebrovascular Center of the Neurological Institute (J.M.W., J.A.F.).

AJNR. American Journal of Neuroradiology
|April 2, 2017
PubMed
Abstract

Insights

Subarachnoid hemorrhage (SAH) causes early brain injury, with both vasogenic and cytotoxic edema contributing. Increased apparent diffusion coefficient (ADC) values suggest diffuse vasogenic edema, while cytotoxic edema correlates with injury severity.

Area of Science:

  • Neurology
  • Radiology
  • Neuroscience

Background:

  • Early brain injury mechanisms post-subarachnoid hemorrhage (SAH) remain incompletely understood.
  • Investigating cytotoxic and vasogenic edema as potential contributors to early brain injury in SAH patients.

Purpose of the Study:

  • To evaluate the role of cytotoxic and vasogenic edema in early brain injury following subarachnoid hemorrhage.
  • To compare apparent diffusion coefficient (ADC) values in SAH patients and controls.

Main Methods:

  • Retrospective analysis of diffusion-weighted MR imaging in 33 SAH patients and 66 controls within 72 hours of onset.
  • Evaluation of whole-brain histograms and 19 ROIs for ADC values, assessing cytotoxic edema outside ROIs.
  • Comparison of ADC values between SAH patients and controls, and between mild (Hunt and Hess 1-3) and severe (Hunt and Hess 4-5) early brain injury groups.

Main Results:

  • Globally increased average median ADC values in SAH patients (808 × 10-6 mm2/s) compared to controls (788 × 10-6 mm2/s, P < .001).
  • Higher ADC values observed in SAH patients across various brain regions (gray matter, white matter, tracts) after age adjustment.
  • Early cytotoxic edema detected in 39% of SAH patients, significantly more prevalent in severe early brain injury (87.5% in Hunt and Hess 4-5 vs. 24.0% in Hunt and Hess 1-3, P = .001).

Conclusions:

  • Age-adjusted ADC values are globally increased in SAH patients, indicating diffuse vasogenic edema even in normal-appearing regions.
  • Cytotoxic edema is present in SAH patients and its prevalence correlates with the severity of early brain injury.
  • Findings suggest both vasogenic and cytotoxic edema are significant factors in early brain injury following subarachnoid hemorrhage.

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