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Updated: Dec 21, 2025
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
Published on: July 28, 2018
Correlation between gray matter volume loss followed by aneurysmal subarachnoid hemorrhage and subarachnoid
Geon Yang Lee1, Chang-Woo Ryu2,3, Hak Cheol Ko4
1Department of Radiology, Kyung Hee University Medical Center, Seoul, South Korea.
Purpose:
Aneurysmal subarachnoid hemorrhage (SAH) can chronically affect cognitive function, and SAH has been suggested to result in regional brain damage. This study aimed to assess regional structural damage according to initial clinical status including SAH volume.
Methods:
A total of 63 consecutive patients treated with coil embolization for intracranial aneurysms for more than 6 months were enrolled. Of these, 35 patients had SAH and 28 patients who were treated for unruptured aneurysms served as controls. Volumetric T1-weighted images were acquired with 1 mm isotropic voxel. The SAH volume was measured semi-automatically from the initial brain CT scan. Voxel-based group comparison was conducted to assess regional gray matter volume (GMV) changes. Voxel-based multiple regression was conducted to analyze regional GMV change and SAH volume. The clinical factors (Glasgow Coma Scale (GCS), SAH volume, systolic blood pressure, and serum laboratory findings) associated with regional GMV were also analyzed by using multiple regression.
Results:
The SAH group had significantly lower GMV in the left hippocampus and higher GMV in the visual cortex than controls (Alphasim-corrected p < 0.05, voxel level of p < 0.001). The GMV of the bilateral hippocampi, thalami, and left medial orbital gyrus was negatively correlated with the initial SAH volume (FDR-corrected p < 0.05). SAH volume and GCS were associated with the hippocampal GMV in multiple regression (p < 0.05).
Conclusions:
Chronic regional GMV change after SAH was related to the severity of initial clinical status including SAH volume. This finding supports the pathophysiological hypothesis of SAH-induced microstructural brain injury.
