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Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images
Published on: November 20, 2015
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.
Introduction:
Although cerebral edema is common following traumatic brain injury (TBI), its formation and progression are poorly understood. This is especially true for the mild TBI population, who rarely undergo magnetic resonance imaging (MRI) studies, which can pick up subtle structural details not visualized on computed tomography, in the first few days after injury. This study aimed to visually classify and quantitatively measure edema progression in relation to traumatic microbleeds (TMBs) in a cohort of primarily mild TBI patients up to 30 days after injury. Researchers hypothesized that hypointense lesions on Apparent Diffusion Coefficient (ADC) detected acutely after injury would evolve into hyperintense Fluid Attenuated Inversion Recover (FLAIR) lesions.
Methods:
This study analyzed the progression of cerebral edema after acute injury using multimodal MRI to classify TMBs as potential edema-related biomarkers. ADC and FLAIR MRI were utilized for edema classification at three different timepoints: ≤48 hours, ~1 week, and 30 days after injury. Hypointense lesions on ADC (ADC+) suggested the presence of cytotoxic edema while hyperintense lesions on FLAIR (FLAIR+) suggested vasogenic edema. Signal intensity Ratio (SIR) calculations were made using ADC and FLAIR to quantitatively confirm edema progression.
Results:
Our results indicated the presence of ADC+ lesions ≤48 hours and ~1 week were associated with FLAIR+ lesions at ~1 week and 30 days, respectively, suggesting some progression of cytotoxic edema to vasogenic edema over time. Ten out of 15 FLAIR+ lesions at 30 days (67%) were ADC+ ≤48 hours. However, ADC+ lesions ≤48 hours were not associated with FLAIR+ lesions at 30 days; 10 out of 25 (40%) ADC+ lesions ≤48 hours were FLAIR+ at 30 days, which could indicate that some lesions resolved or were not visualized due to associated atrophy or tissue necrosis. Quantitative analysis confirmed the visual progression of some TMB lesions from ADC+ to FLAIR+. FLAIR SIRs at ~1 week were significantly higher when lesions were ADC+ ≤48 hours (1.22 [1.08-1.32] vs 1.03 [0.97-1.11], p=0.002).
Conclusion:
Awareness of how cerebral edema can evolve in proximity to TMBs acutely after injury may facilitate identification and monitoring of patients with traumatic cerebrovascular injury and assist in development of novel therapeutic strategies.
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.
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