• Lisa A van der Kleij, Jill B De Vis, Matthew C Restivo, L Christine Turtzo, Jeroen Hendrikse, and Lawrence L Latour.
• Department of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands.
• J. Neurotrauma. 2020 Feb 15; 37 (4): 600607600-607.

AbstractBiomarkers are needed to identify traumatic brain injury (TBI) patients at risk for accelerated brain volume loss and its associated functional impairment. Subarachnoid hemorrhage (SAH) has been shown to affect cerebral volume and perfusion, possibly by induction of inflammation and vasospasm. The purpose of this study was to assess the impact of SAH due to trauma on cerebral perfusion and brain volume. For this, magnetic resonance imaging (MRI) was performed 48 h and at 90 days after TBI. The 48-h scan was used to assess SAH presence and perfusion. Brain volume changes were assessed quantitatively over time. Differences in brain volume change and perfusion were compared between SAH and non-SAH patients. A linear regression analysis with clinical and imaging variables was used to identify predictors of brain volume change. All patients had a relatively good status on admission, and 83% presented with the maximum Glasgow Coma Scale (GCS) score. Brain volume decrease was greater in the 11 SAH patients (-3.2%, interquartile range [IQR] -4.8 to -1.3%) compared with the 46 non-SAH patients (-0.4%, IQR -1.8 to 0.9%; p  0.001). Brain perfusion was not affected by SAH, but it was correlated with brain volume change (ρ = 0.39; p  0.01). Forty-three percent of brain volume change was explained by SAH (β -0.40, p = 0.001), loss of consciousness (β -0.24, p = 0.035), and peak perfusion curve signal intensity height (0.27, p = 0.012). SAH and lower perfusion in the acute phase may identity TBI patients at increased risk for accelerated brain volume loss, in addition to loss of consciousness occurrence. Future studies should determine whether the findings apply to TBI patients with worse clinical status on admission. SAH predicts brain volume decrease independent of brain perfusion. This indicates the adverse effects of SAH extend beyond vasoconstriction, and that hypoperfusion also occurs separately from SAH.

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