ArticleNeurobiology of aging2022
White matter degradation near cerebral microbleeds is associated with cognitive change after mild traumatic brain injury.
Article in Neurobiology of aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- From microbleeds to axonal damage: current evidence and future directions.Frontiers in radiology · 2026Review
- Neurobiology of Chronic Pain, Posttraumatic Stress Disorder, and Mild Traumatic Brain Injury.Biology · 2025Review
- Concussion and the Autonomic, Immune, and Endocrine Systems: An Introduction to the Field and a Treatment Framework for Persisting Symptoms.Journal of personalized medicine · 2025Review
- Anatomic Interpretability in Neuroimage Deep Learning: Saliency Approaches for Typical Aging and Traumatic Brain Injury.Neuroinformatics · 2024Article
- Prediction of cognitive outcome after mild traumatic brain injury from acute measures of communication within brain networks.Cortex; a journal devoted to the study of the nervous system and behavior · 2024Article
- Cerebral microhaemorrhage count is related to processing speed, but not level of symptom reporting, independently of age, psychological status and premorbid functioning, after first-ever mild traumatic brain injury.Brain imaging and behavior · 2023Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
To explore how cerebral microbleeds (CMBs) accompanying mild traumatic brain injury (mTBI) reflect white matter (WM) degradation and cognitive decline, magnetic resonance images were acquired from 62 mTBI adults (imaged ∼7 days and ∼6 months post-injury) and 203 matched healthy controls. On average, mTBI participants had a count of 2.7 ± 2.6 traumatic CMBs in WM, located 6.1 ± 4.4 mm from cortex. At ∼6-month follow-up, 97% of CMBs were associated with significant reductions (34% ± 11%, q < 0.05) in the fractional anisotropy of WM streamlines within ∼1 cm of CMB locations. Male sex and older age were significant risk factors for larger reductions (q < 0.05). For CMBs in the corpus callosum, cingulum bundle, inferior and middle longitudinal fasciculi, fractional anisotropy changes were significantly and positively associated with changes in cognitive functions mediated by these structures (q < 0.05). Our findings distinguish traumatic from non-traumatic CMBs by virtue of surrounding WM alterations and challenge the assumption that traumatic CMBs are neurocognitively silent. Thus, mTBI with CMB findings can be described as a clinical endophenotype warranting longitudinal cognitive assessment.
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