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Introduction: Tissue at risk, as estimated by CT perfusion utilizing Tmax+6, correlates with final infarct volume (FIV) in acute ischaemic stroke (AIS) without reperfusion. Tmax thresholds are derived from Western ethnic populations but not from ethnic Asian populations. We aimed to investigate the influence of ethnicity on Tmax thresholds. Methods: From a clinical-imaging registry of Australian and Indonesian stroke patients, we selected a participant subgroup with the following inclusion criteria: AIS under 24 h and absence of reperfusion therapy. Clinical data included demographics, time metrics, stroke severity, pre-morbid, and 3-month Modified Rankin Score. Baseline computed tomography perfusion and MRI <72 h were performed. Volumes of Tmax utilizing different thresholds and FIVs were calculated. Spearman correlation was used to evaluate relationship involving ordinal variables and calculate the optimal Tmax threshold against FIV in both populations. Results: Two hundred patients were included in the study sample, 100 in Jakarta and 100 in Geelong. The median National Institutes of Health Stroke Scale (IQR) were 6 (3–11) and 3 (1–5), respectively. The median Tmax+6 (IQR) was 0 (0–46.5) in Jakarta group and 0 (0–7.5) in Geelong group. The median FIV (IQR) was 0 (0–30.5) and 0 (0–5.5). Tmax+8 s in Jakarta population against FIV showed Spearman's coefficient ρ = 0.72, representing the optimal Tmax threshold. Tmax+6 s showed Spearman's coefficient ρ = 0.51 against FIV in the Geelong population. Conclusion: Tmax thresholds approximating FIV were possibly different in the Asian when compared with the non-Asian populations. Future studies are required to extend and confirm the validity of our findings. [ABSTRACT FROM AUTHOR]

Background and purpose Methods Results Discussion Given the accepted multistep process of disease causation in amyotrophic lateral sclerosis (ALS), the present study was undertaken to determine the number of steps required for disease onset across each of the ALS phenotypes.Clinical and demographic data were prospectively accumulated using the Australian Motor Neurone Disease Registry (2005–2016), and age‐specific incidence rates were calculated. Poisson regression was utilized to assess the relationship between log age‐specific incidence and log age of onset, with McFadden's R2 used to assess the goodness of fit of the model.In total, 2647 ALS patients were included, with mean disease‐onset age being 62.2 ± 12.1 years. A linear relationship between log incidence and log age was established across ALS phenotypes, with variable slope estimates: bulbar 5.1 (95% confidence interval [CI] 4.6–5.6); cervical 2.7 (95% CI 2.3–3.0); lumbar 3.5 (95% CI 3.2–3.9); flail arm 4.7 (95% CI 3.9–5.5); flail leg 3.6 (95% CI 2.6–4.5); primary lateral sclerosis 2.7 (95% CI 1.8–3.7). Slope estimates were significantly higher in the bulbar compared to the cervical, lumbar and primary lateral sclerosis phenotypes. McFadden's R2 values were >0.4 for all phenotypes indicating excellent model fit.A multistep process has been established across all ALS phenotypes with variable slope estimates, suggesting that the number of steps to develop disease is different across clinical presentations. Identification of mechanisms underlying slope estimate variability could exert pathophysiological significance. [ABSTRACT FROM AUTHOR]