Edema progression in proximity to traumatic microbleeds: evolution of cytotoxic and vasogenic edema on serial MRI

Jacquie Lee1,2, Emily Baniewicz1, Nicole L Peterkin1

  • 1Acute Cerebrovascular Diagnostics Unit, National Institute of Neurological Disorders and Stroke, Bethesda (MD), United States.

Neuroimage. Reports
|April 1, 2024
PubMed
Abstract

Insights

This study tracked cerebral edema progression in mild traumatic brain injury (TBI) patients using MRI. Edema evolved from cytotoxic to vasogenic, offering insights into traumatic microbleeds as biomarkers.

Area of Science:

  • Neuroimaging
  • Neurology
  • Radiology

Background:

  • Cerebral edema after traumatic brain injury (TBI) is common but poorly understood, especially in mild TBI cases.
  • Magnetic resonance imaging (MRI) is crucial for detecting subtle changes not visible on CT scans in the early days post-injury.

Purpose of the Study:

  • To visually classify and quantitatively measure edema progression in relation to traumatic microbleeds (TMBs) in mild TBI patients up to 30 days post-injury.
  • To investigate the hypothesis that hypointense lesions on Apparent Diffusion Coefficient (ADC) MRI would evolve into hyperintense Fluid Attenuated Inversion Recovery (FLAIR) lesions.

Main Methods:

  • Utilized multimodal MRI (ADC and FLAIR) to classify edema at three timepoints: ≤48 hours, ~1 week, and 30 days post-injury.
  • Identified cytotoxic edema via hypointense ADC lesions (ADC+) and vasogenic edema via hyperintense FLAIR lesions (FLAIR+).
  • Quantitatively assessed edema progression using Signal Intensity Ratio (SIR) calculations from ADC and FLAIR.

Main Results:

  • ADC+ lesions within 48 hours and at ~1 week correlated with FLAIR+ lesions at ~1 week and 30 days, respectively, suggesting cytotoxic to vasogenic edema transition.
  • A significant proportion (67%) of FLAIR+ lesions at 30 days were initially ADC+ within 48 hours.
  • Quantitative analysis confirmed lesion progression, with significantly higher FLAIR SIRs at ~1 week when lesions were initially ADC+ within 48 hours (p=0.002).

Conclusions:

  • Cerebral edema can progress from cytotoxic to vasogenic in TBI patients, with TMBs potentially serving as early indicators.
  • Understanding edema evolution near TMBs can aid in monitoring patients and developing new therapeutic strategies for traumatic cerebrovascular injury.