LAUSR

Introduction/Hypothesis: Therapeutic temperature modulation (TTM) can protect against secondary brain injury and its clinical benefit was demonstrated in post-cardiac arrest survivor. Ischemic penumbra in stroke patients is the most vulnerable tissue that progresses into irreversible infarct in the end. We aimed to examine the effects of TTM on infarct growth in penumbral tissue. Methods: We included ischemic stroke patients <24h after onset from Oct 2010 to Mar 2018 with the following criteria; initial NIHSS score ≥ 10-point, internal carotid or middle cerebral artery occlusion, no recanalization treatment, baseline Tmax >6s volume >100 mL in perfusion MRI, and initial infarct volume > 50 mL. Perfusion quantification, 3D voxel-registration and image segmentation were done by Olea 3.0 and Analyze 12.0. The implementation of TTM was determined after discussing with caregiver who initially refused early decompressive craniectomy. Under the standardized institutional protocol, TTM was achieved with cold saline infusion and a surface cooling device with a target temperature of 33.5°C. Penumbral tissue loss was defined as infarct volume in the follow-up image. Hypoperfusion intensity ratio was defined by the proportion of Tmax >10s over Tmax >6s. Results: Among 26 patients included (age 74.2±14.9; male, 38.5%), median baseline NIHSS score was 18 (interquartile range [IQR], 13–22). The median volume of initial infarct was 109 mL (IQR, 86–165), Tmax>6s was 230 mL (IQR, 170–273), hypoperfusion intensity ratio was 0.66 (IQR, 0.59–0.75), and penumbral tissue loss was 54 ± 19%. A total of 9 patients (34%) received TTM and the median duration of TTM was 132 hours [IQR, 112–150]. Baseline characteristics between the TTM group and the usual-care group were not statistically different. In a generalized linear model adjusted age, sex, Tmax>6s and hypoperfusion intensity ratio, TTM showed inverse correlation with penumbral tissue loss (beta ± SE; 20.2 ± 8.4 %, P=0.025). Conclusions: Therapeutic temperature modulation may have protective effects against penumbral tissue loss in patients with acute non-recanalized large vessel occlusion. Further studies are needed to investigate the beneficial effects of TTM on functional outcome of this population.