Abstract 46: Leukoaraiosis Evolves Through Discrete Acute Ischemic Injuries: Weekly Diffusion Tensor Imaging and T2 Relaxometry at 16 Time Points
Bibliographic record
Abstract
INTRODUCTION: Leukoaraiosis, the presence of “incidental” white matter lesions in the aging brain, is increasingly recognized as a predictor for dementia, ischemic stroke, intracerebral hemorrhage and vascular death. The pathogenesis of leukoaraiosis remains controversial, with abnormalities of small arterioles hypothesized to play an important role. To investigate this hypothesis, we sought to characterize the temporal evolution of the individual lesions making up leukoaraiosis. HYPOTHESIS: Discrete occlusive events at the level of small arterioles play a key role in the pathogenesis of leukoaraiosis. METHODS: Participants were prospectively recruited through an outpatient neurology clinic (inclusion criteria: age > 60 years, Fazekas grade 3 leukoaraiosis burden; exclusion criteria: cortical infarct, cardioembolic disease, dissection, carotid stenosis > 50%). Subjects underwent an identical MRI protocol in each of 16 consecutive weeks, including diffusion tensor imaging (DTI) and multi-echo T2-weighted imaging. Parametric maps of the apparent diffusion coefficient (ADC), fractional anisotropy (FA) and T2 relaxation time were constructed and coregistered (Analysis of Functional NeuroImages, NIH; 3D Slicer, www.slicer.org; Matlab, The MathWorks). Images were reviewed for new diffusion restricting lesions, and such lesions were manually segmented. Plots of lesion ADC, FA and T2 were generated and temporally aligned to the onset of acute diffusion restriction. RESULTS: Five subjects (mean age 69 ± 8 years) met criteria and completed all 16 MRI scans. There were no lacunar or large artery infarcts during the study period. A total of 9 new diffusion restricting white matter lesions were identified (mean volume 0.06 ± 0.03 cc). Evolution of these lesions showed striking similarity to that of cerebral infarction, with acute reduction in ADC, followed by gradual rise in ADC and T2, and corresponding decline in FA. At 8 weeks, new lesions were indistinguishable from pre-existing white matter disease. CONCLUSION: Leukoaraiosis evolves through temporally and spatially discrete acute ischemic injuries. This supports the hypothesized role of small vessel arteriolar pathology as a key pathogenetic mechanism.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".