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.

The Effect of Mild Traumatic Brain Injury on Cerebral Microbleeds in Aging.

A traumatic brain injury (TBI) induces the formation of cerebral microbleeds (CMBs), which are associated with cognitive impairments, psychiatric disorders, and gait dysfunctions in patients. Elderly people frequently suffer TBIs, especially mild brain trauma (mTBI). Interestingly, aging is also an independent risk factor for the development of CMBs. However, how TBI and aging may interact to promote the development of CMBs is not well established. In order to test the hypothesis that an mTBI exacerbates the development of CMBs in the elderly, we compared the number and cerebral distribution of CMBs and assessed them by analysing susceptibility weighted (SW) MRI in young (25 ± 10 years old, n = 18) and elder (72 ± 7 years old, n = 17) patients after an mTBI and in age-matched healthy subjects (young: 25 ± 6 years old, n = 20; aged: 68 ± 5 years old, n = 23). We found significantly more CMBs in elder patients after an mTBI compared with young patients; however, we did not observe a significant difference in the number of cerebral microhemorrhages between aged and aged patients with mTBI. The majority of CMBs were found supratentorially (lobar and basal ganglion). The lobar distribution of supratentorial CMBs showed that aging enhances the formation of parietal and occipital CMBs after mTBIs. This suggests that aging and mTBIs do not synergize in the induction of the development of CMBs, and that the different distribution of mTBI-induced CMBs in aged patients may lead to specific age-related clinical characteristics of mTBIs.

Traumatic brain injury-induced cerebral microbleeds in the elderly.

Traumatic brain injury (TBI) was shown to lead to the development of cerebral microbleeds (CMBs), which are associated with long term cognitive decline and gait disturbances in patients. The elderly is one of the most vulnerable parts of the population to suffer TBI. Importantly, ageing is known to exacerbate microvascular fragility and to promote the formation of CMBs. In this overview, the effect of ageing is discussed on the development and characteristics of TBI-related CMBs, with special emphasis on CMBs associated with mild TBI. Four cases of TBI-related CMBs are described to illustrate the concept that ageing exacerbates the deleterious microvascular effects of TBI and that similar brain trauma may induce more CMBs in old patients than in young ones. Recommendations are made for future prospective studies to establish the mechanistic effects of ageing on the formation of CMBs after TBI, and to determine long-term consequences of CMBs on clinically relevant outcome measures including cognitive performance, gait and balance function.

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.

Both hemorrhagic and non-hemorrhagic traumatic MRI lesions are associated with the microstructural damage of the normal appearing white matter.

Traumatic microbleeds (TMBs) and non-hemorrhagic lesions (NHLs) on MRI are regarded as surrogate markers of diffuse axonal injury. However, the actual relation between lesional and diffuse pathology remained unclear, since lesions were related to clinical parameters, largely influenced by extracranial factors. The aim of this study is to directly compare TMBs, NHLs and their regional features with the co-existing diffuse injury of the normal appearing white matter (NAWM) as measured by diffusion tensor imaging (DTI). Thirty-eight adults with a closed traumatic brain injury (12 mild, 4 moderate and 22 severe) who underwent susceptibility weighted imaging (SWI), T1-, T2 weighted and FLAIR MRI and routine CT were included in the study. TMB (on SWI) and NHL (on T1-, T2 weighted and FLAIR images) features and Rotterdam scores were evaluated. DTI metrics such as fractional anisotropy (FA) and mean diffusivity (MD) were measured over different NAWM regions. Clinical parameters including age; Glasgow Coma Scale; Rotterdam score; TMB and NHL features were correlated to regional NAWM diffusivity using multiple regression. Overall NHL presence and basal ganglia area TMB load were significantly, negatively correlated with the subcortical NAWM FA values (partial r=-0.37 and -0.36; p=0.006 and 0.025, respectively). The presence of any NHL, or TMBs located in the basal ganglia area indicates diffuse NAWM damage even after adjusting for clinical and CT parameters. To estimate DAI, a conventional lesional MRI pathology evaluation might at least in part substitute the use of quantitative DTI, which is yet not widely feasible in a clinical setting.

Microbleeds may expand acutely after traumatic brain injury.

BACKGROUND AND PURPOSE: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury. MATERIALS AND METHODS: We present here five closed moderate/severe (Glasgow coma scale≤13) TBI patients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points. RESULTS: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time. CONCLUSION: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.