Detour ahead: possible causes of corticospinal tract truncation in upper motor neuron–predominant amyotrophic lateral sclerosis
Bibliographic record
Abstract
Clinical diagnosis of amyotrophic lateral sclerosis (ALS) depends on finding evidence of combined of upper motor neuron (UMN) and lower motor neuron degeneration. T2- and proton density (PD)-weighted images reveal intracranial corticospinal tract (CST) hyperintensity in some UMN-predominant ALS patients who also exhibit faster disease progression compared to those without CST hyperintensity. Our previous study identified CST fibre tract truncation in a subset of UMN-predominant ALS patients, both with and without CST hyperintensity. In this study, we investigated the underlying cause(s) of CST fibre tract truncation in such ALS patients. Routine clinical diffusion tensor imaging (DTI) scans were acquired in 14 neurologic controls and 45 ALS patients using a 1.5 T magnetic resonance imaging (MRI) scanner. UMN-predominant ALS patients were categorized into two subgroups based on their clinically-acquired conventional MRI findings. DTI reconstruction was performed using both single-exponential and bi-exponential fitting approaches (the latter for free water [FW] estimation). DTI along the perivascular space (ALPS) index was also measured. CST fibres were reconstructed using tractography in both control and ALS subgroups. In CST-truncated ALS patients, the fibres deviated from their normal trajectory and entered the superior longitudinal fasciculus (SLF) at the level of the centrum semiovale, resulting in apparent truncation and overlap with the SLF. Axial diffusivity, radial diffusivity, FW content, and mean diffusivity values were normal along the expected CST pathway in cases of truncation, suggesting that axonal or myelin degeneration, inflammation, or oedema were unlikely to be responsible for CST truncation. ALPS index was significantly increased in CST-truncated patients compared to those without CST truncation. Based on these results, we hypothesize that impaired axonal guidance mechanisms or dysfunction of the glymphatic system may contribute to CST fibre tract truncation in ALS.
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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 | 0.001 | 0.003 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.000 | 0.001 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
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".