Cerebral Microbleeds May Be Less Detectable by Susceptibility Weighted Imaging MRI From 24 to 72 Hours After Traumatic Brain Injury.

Purpose: A former rodent study showed that cerebral traumatic microbleeds (TMBs) may temporarily become invisible shortly after injury when detected by susceptibility weighted imaging (SWI). The present study aims to validate this phenomenon in human SWI. Methods: In this retrospective study, 46 traumatic brain injury (TBI) patients in various forms of severity were included and willingly complied with our strict selection criteria. Clinical parameters potentially affecting TMB count, Rotterdam and Marshall CT score, Mayo Clinic Classification, contusion number, and total volume were registered. The precise time between trauma and MRI [5 h 19 min to 141 h 54 min, including SWI and fluid-attenuated inversion recovery (FLAIR)] was individually recorded; TMB and FLAIR lesion counts were assessed. Four groups were created based on elapsed time between the trauma and MRI: 0-24, 24-48, 48-72, and >72 h. Kruskal-Wallis, ANOVA, Chi-square, and Fisher's exact tests were used to reveal differences among the groups within clinical and imaging parameters; statistical power was calculated retrospectively for each comparison. Results: The Kruskal-Wallis ANOVA with Conover post hoc analysis showed significant (p = 0.01; 1-ß > 0.9) median TMB number differences in the subacute period: 0-24 h = 4.00 (n = 11); 24-48 h = 1 (n = 14); 48-72 h = 1 (n = 11); and 72 h ≤ 7.5 (n = 10). Neither clinical parameters nor FLAIR lesions depicted significant differences among the groups. Conclusion: Our results demonstrate that TMBs on SWI MRI may temporarily become less detectable at 24-72 h following TBI.

Microbleeds show a characteristic distribution in cerebral fat embolism.

This systematic review aims to test the hypothesis that microbleeds detected by MRI are common and show a characteristic pattern in cerebral fat embolism (CFE). Eighty-four papers involving 140 CFE patients were eligible for this review based on a systematic literature search up to 31 January 2020. An additional case was added from hospital records. Patient data were individually scrutinised to extract epidemiological, clinical and imaging variables. Characteristic CFE microbleed pattern resembling a "walnut kernel" was defined as punctuate hypointensities of monotonous size, diffusely located in the subcortical white matter, the internal capsule and the corpus callosum, with mostly spared corona radiata and non-subcortical centrum semiovale, detected by susceptibility- or T2* weighted imaging. The presence rate of this pattern and other, previously described MRI markers of CFE such as the starfield pattern and further diffusion abnormalities were recorded and statistically compared. The presence rate of microbleeds of any pattern, the "walnut kernel microbleed pattern", diffusion abnormality of any pattern, the starfield pattern, and cytotoxic edema in the corpus callosum was found to be 98.11%, 89.74%, 97.64%, 68.5%, and 77.27% respectively. The presence rate between the walnut kernel and the starfield pattern was significantly (p < 0.05) different. Microbleeds are common and mostly occur in a characteristic pattern resembling a "walnut kernel" in the CFE MRI literature. Microbleeds of this pattern in SWI or T2* MRI, along with the starfield pattern in diffusion imaging appear to be the most important imaging markers of CFE and may aid the diagnosis in clinically equivocal cases.

Cerebral Microbleeds Temporarily Become Less Visible or Invisible in Acute Susceptibility Weighted Magnetic Resonance Imaging: A Rat Study.

Previously, we reported human traumatic brain injury cases demonstrating acute to subacute microbleed appearance changes in susceptibility-weighted imaging (SWI-magnetic resonance imaging [MRI]). This study aims to confirm and characterize such temporal microbleed appearance alterations in an experimental model. To elicit microbleed formation, brains of male Sprague Dawley rats were pierced in a depth of 4 mm, in a parasagittal position bilaterally using 159 µm and 474 µm needles, without the injection of autologous blood or any agent. Rats underwent 4.7 T MRI immediately, then at multiple time points until 125 h. Volumes of hypointensities consistent with microbleeds in SWI were measured using an intensity threshold-based approach. Microbleed volumes across time points were compared using repeated measures analysis of variance. Microbleeds were assessed by Prussian blue histology at different time points. Hypointensity volumes referring to microbleeds were significantly decreased (corrected p < 0.05) at 24 h compared with the immediate or the 125 h time points. By visual inspection, microbleeds were similarly detectable at the immediate and 125 h imaging but were decreased in extent or completely absent at 24 h or 48 h. Histology confirmed the presence of microbleeds at all time points and in all animals. This study confirmed a general temporary reduction in visibility of microbleeds in the acute phase in SWI. Such short-term appearance dynamics of microbleeds should be considered when using SWI as a diagnostic tool for microbleeds in traumatic brain injury and various diseases.