https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46793 Wed 30 Nov 2022 14:10:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54324 Wed 28 Feb 2024 15:22:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34583 Wed 23 Feb 2022 16:04:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31334 Wed 23 Feb 2022 16:02:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33102 15 mL, mismatch ratio > 1.8, baseline ischemic core < 70 mL, and volume of severely hypoperfused tissue < 100 mL). Patients meeting target mismatch criteria were analyzed as a subgroup to identify whether they had different treatment responses from the pooled group. Results: Of 146 pooled patients, 71 received alteplase and 75 received tenecteplase. Tenecteplase-Treated patients had greater early clinical improvement (median National Institutes of Health Stroke Scale score change: Tenecteplase, 7; alteplase, 2; P=0.018) and less parenchymal hematoma (2 of 75 versus 10 of 71; P=0.02). The pooled group did not show improved patient outcomes when treated with tenecteplase (modified Rankin scale score 0-1: odds ratio, 1.77; 95% confidence interval, 0.89-3.51; P=0.102) compared with alteplase therapy. However, in patients with target mismatch (33 tenecteplase, 35 alteplase), treatment with tenecteplase was associated with greater early clinical improvement (median National Institutes of Health Stroke Scale score change: Tenecteplase, 6; alteplase, 1; P < 0.001) and better late independent recovery (modified Rankin scale score 0-1: odds ratio, 2.33; 95% confidence interval, 1.13-5.94; P=0.032) than those treated with alteplase. Conclusions: Tenecteplase may offer an improved efficacy and safety profile compared with alteplase, benefits possibly exaggerated in patients with baseline computed tomography perfusion-defined target mismatch. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01472926. URL: https://www.anzctr.org.au. Unique identifier: ACTRN12608000466347.]]> Wed 19 Jan 2022 15:18:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38851  15 mL, mismatch ratio > 1.8 and ischemic core < 70 mL). We then investigated whether tenecteplase-treated patients had favorable odds of less disability (on modified Rankin scale, mRS) compared to those treated with alteplase, for clinical and imaging mismatch, respectively. Results: From 146 pooled patients, 71 received alteplase and 75 received tenecteplase. The overall pooled group did not show improved patient outcomes when treated with tenecteplase (mRS 0-1 OR 1.77, 95% CI 0.89–3.51, p = 0.102) compared with alteplase. A total of 39 (27%) patients met both clinical and imaging mismatch criteria, 25 (17%) patients met only imaging criteria, 36 (25%) met only clinical mismatch criteria and, finally, 46 (31%) did not meet either of imaging or mismatch criteria. Patients treated with tenecteplase had more favorable outcomes when they met either imaging mismatch (mRS 0–1, OR 2.33, 95% CI 1.13–5.94, p = 0.032) or clinical mismatch criteria (mRS 0–1, OR 2.15, 95% CI 1.142, 8.732, p = 0.027) but with differing proportions. Conclusion: Target mismatch selection was more inclusive and exhibited in a larger treatment effect between tenecteplase and alteplase.]]> Wed 16 Feb 2022 15:17:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47959 Wed 13 Mar 2024 07:52:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22216 Wed 11 Apr 2018 14:00:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34282 Tue 26 Feb 2019 12:16:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42433 Tue 23 Aug 2022 09:58:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47256 Tue 17 Jan 2023 12:30:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51192 150 mm Hg) after thrombolysis treatment for acute ischaemic stroke between March 3, 2012 and April 30, 2018. Methods: All available brain imaging were analysed centrally by expert readers. Log-linear regression was used to determine the effects of intensive blood pressure lowering on the size of cerebral infarction, with adjustment for potential confounders. The primary analysis pertained to follow-up computerised tomography (CT) scans done between 24 and 36 h. Sensitivity analysis were undertaken in patients with only a follow-up magnetic resonance imaging (MRI) and either MRI or CT at 24–36 h, and in patients with any brain imaging done at any time during follow-up. This trial is registered with ClinicalTrials.gov, number NCT01422616. Findings: There were 1477 (67.3%) patients (mean age 67.7 [12.1] y; male 60%, Asian 65%) with available follow-up brain imaging for analysis, including 635 patients with a CT done at 24–36 h. Mean achieved systolic blood pressures over 1–24 h were 141 mm Hg and 149 mm Hg in the intensive group and guideline group, respectively. There was no effect of intensive blood pressure lowering on the median size (ml) of cerebral infarction on follow-up CT at 24–36 h (0.3 [IQR 0.0–16.6] in the intensive group and 0.9 [0.0–12.5] in the guideline group; log Δmean −0.17, 95% CI −0.78 to 0.43). The results were consistent in sensitivity and subgroup analyses. Interpretation: Intensive blood pressure lowering treatment to a systolic target <140 mm Hg within several hours after the onset of symptoms may not increase the size of cerebral infarction in patients who receive thrombolysis treatment for acute ischaemic stroke of mild to moderate neurological severity. Funding: National Health and Medical Research Council of Australia; UK Stroke Association; UK Dementia Research Institute; Ministry of Health and the National Council for Scientific and Technological Development of Brazil; Ministry for Health, Welfare, and Family Affairs of South Korea; Takeda.]]> Thu 24 Aug 2023 14:38:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33105 Thu 17 Mar 2022 14:41:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31270 Thu 09 Dec 2021 11:04:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24016 Thu 04 Nov 2021 10:39:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7458 1.2 and perfusion deficit at least 10 mL>DWI volume) and CDM (NIHSS ≥8 and DWI volume ≤25 mL) was determined for each patient. We assessed lesion growth and neurological improvement (decrease in NIHSS ≥8 points between baseline and 90 days, or a 90-day NIHSS ≤1). Results: 86% of the patients had PDM, but only 41% had CDM. CDM detected PDM with a sensitivity of 46% and a specificity of 86%. We found statistically significant effects of reperfusion on the rate of neurological improvement (OR 9.92, 95% CI 1.91 to 51.64; P<0.01) and on absolute growth (difference: –59.60 mL, 95% CI –95.40 mL to –23.81 mL; P<0.01). Neither treatment with tPA nor reperfusion had a significantly different impact on lesion growth or clinical course in CDM patients compared to patients without CDM. Conclusions: There was no increased benefit from tPA in patients with CDM. The beneficial effects of reperfusion were similar in patients with and without CDM.]]> Sat 24 Mar 2018 10:46:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6925 Sat 24 Mar 2018 08:40:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8112 90% reduction in magnetic resonance perfusion-weighted imaging lesion volume and recanalization as improvement of MR angiographic Thrombolysis In Myocardial Infarction grading by ≥2 points from baseline to Day 3 to 5. At Day 3 to 5, reperfusion and recanalization with intravenous tissue plasminogen activator were strongly correlated. Reperfusion was associated with improved clinical outcome independent of whether recanalization occurred. In contrast, recanalization was not associated with clinical outcome when reperfusion was included as a covariate in regression analyses. Reperfusion is a surrogate marker of clinical outcomes independent of recanalization based on the criteria applied in EPITHET. The impact of recanalization on clinical outcomes was attributable to reperfusion.]]> Sat 24 Mar 2018 08:40:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9613 Sat 24 Mar 2018 08:39:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7888 Sat 24 Mar 2018 08:35:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9555 1.2, was independently scored by 1 expert and 2 inexperienced raters blinded to calculated volumes and clinical information. Visual mismatch was compared with region-of-interest-based volumetric calculation, which was used as the gold standard. Results: Volumetric calculation demonstrated perfusion-diffusion mismatch in 85/99 patients. Visual TTP-DWI mismatch was correctly classified by the experienced rater in 82% of the cases (sensitivity: 0.86; specificity: 0.54) compared to 73% for the inexperienced raters (sensitivity: 0.75; specificity: 0.57). The interrater reliability for TTP-DWI mismatch was moderate (к= 0.50). Visual T max -DWI mismatch performed better (agreement – 93 and 87%, sensitivity – 95 and 88%, specificity – 77 and 82% for the experienced and inexperienced raters, respectively). Conclusions: The assessment of visual TTP-DWI mismatch at the MRI console is insufficiently reliable for use in clinical trials. Differences in perfusion analysis technique and visual inaccuracies combine to make visual TTP-DWI mismatch substantially different to volumetric T max -DWI mismatch. Automated software that applies perfusion thresholds may improve the reproducibility of real-time mismatch assessment.]]> Sat 24 Mar 2018 08:34:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16030 Sat 24 Mar 2018 08:21:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10429 Sat 24 Mar 2018 08:13:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10901 190 mL). Excellent outcome from tPA treatment was substantially increased in patients with DWI lesions < 18mL (77% versus 18% placebo, OR= 15.0, P < 0.001). Benefit from tPA was also seen with DWI lesions up to 25mL (69% versus 29% placebo, OR= 5.5, P= 0.03), but not for DWI lesions > 25 mL. In contrast, increasing mismatch ratios did not influence the odds of excellent outcome with tPA. Clinical responsiveness to IV-tPA, and stroke outcome, depends more on baseline DWI and PWI lesion volumes than the extent of perfusion–diffusion mismatch.]]> Sat 24 Mar 2018 08:09:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10752 Sat 24 Mar 2018 08:08:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10746 Sat 24 Mar 2018 08:08:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10749 Sat 24 Mar 2018 08:08:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10907 Sat 24 Mar 2018 08:07:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21715 Sat 24 Mar 2018 08:06:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20950 Sat 24 Mar 2018 08:06:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21405 P=0·03) and a trend to lower absolute growth (-0·17ml versus 9·6ml, P=0·07). Reperfusion was increased in the tissue plasminogen activator group (58% versus 25%, P=0·03) and was associated with increased rates of good neurological (86% versus 28% P<0·001) and functional (modified Rankin scale 0-2 73% versus 34%, P=0·01) outcomes. Reperfusion was strongly associated with lower relative (80% versus 189%, P<0·001) and absolute (-2·5ml versus 40ml, P<0·001) infarct growth. Conclusions: Thrombolysis 4·5-6h after stroke onset reduced infarct growth and increased the rate of reperfusion, which was associated with good neurological and functional outcome.]]> Sat 24 Mar 2018 08:05:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18166 50% of neurons within the sample. To determine whether FMISO retention occurred after the tissue was already committed to infarction, FMISO was administered 4 to 6 hours after the onset of permanent vessel occlusion. Intense FMISO retention was consistently seen throughout the infarct core. In conclusion, FMISO retention occurs both within the ischaemic penumbra and within the early infarct core. Most penumbral tissues show evidence of selective cellular injury.]]> Sat 24 Mar 2018 08:04:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19908 max) with PH was examined using receiver operating characteristic analysis and multivariate logistic regression. Result: Of 132 patients, 70 were treated with thrombolysis, and 14 (10.6%) developed PH on follow-up imaging. Baseline National Institutes of Health Stroke Scale score (P=0.033) and thrombolysis (P=0.003) were both predictive of PH. Receiver operating characteristic analysis revealed that T_max>14 s (area under the curve=0.748; P=0.002) and relative cerebral blood flow <30% of contralateral mean (area under the curve=0.689, P=0.021) were the optimal thresholds, and the Bayesian information criterion (+2.6) indicated that T_max was more strongly associated with PH than relative cerebral blood flow. T_{max14 s volumes of >5 mL allowed prediction of PH with sensitivity of 79%, specificity of 68%, and negative likelihood ratio of 3.16. Tmax>14 s volume and thrombolysis were both independently predictive of PH in a multivariate logistic regression model (P<0.05). Conclusions: Tmax >14 s was the CTP parameter most strongly associated with PH. This outperformed relative cerebral blood flow <30%, which closely equates to CTP estimates of ischemic core volume. Although ischemic core volume on CTP is useful in the pretreatment prediction of PH, severe hypoperfusion on Tmax is more strongly associated and may allow better prediction of the likely anatomic location of hemorrhage.]]>} Sat 24 Mar 2018 08:03:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20340 6 seconds, ratio>1.2) in 3/119 (2.5%) patients. Diffusion lesion reversal between baseline and 3 to 6 hours DWI was also uncommon (7/65, 11%) and often transient. Clinically relevant DLR is uncommon and rarely alters perfusion-diffusion mismatch. The acute diffusion lesion is generally a reliable signature of the infarct core.]]> Sat 24 Mar 2018 08:02:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21179 4 seconds for lesion region of interest. The MR-Tmax >6 seconds perfusion lesion was automatically segmented and registered to CTP. Receiver-operating characteristic analysis determined the optimal CT-Tmax threshold to match MR-Tmax >6 seconds. Agreement of these CT parameters with MR perfusion-diffusion mismatch in coregistered slabs was assessed (mismatch ratio >1.2, absolute mismatch >10 mL, infarct core <70 mL). Results: In analysis of 49 patients (mean onset to CT, 213 minutes; mean CT to MR, 31 minutes), constraining relCBF <31% within the automated relTTP perfusion lesion region of interest reduced the median magnitude of volumetric error (vs diffusion-weighted imaging) from 47.5 mL to 15.8 mL (P<0.001). The optimal CT-Tmax threshold to match MR-Tmax >6 seconds was 6.2 seconds (95% confidence interval, 5.6–7.3 seconds; sensitivity, 91%; specificity, 70%; area under the curve, 0.87). Using CT-Tmax >6 seconds “penumbra” and relTTP-constrained relCBF “core,” CT-based and MRI-based mismatch status was concordant in 90% (kappa=0.80). Conclusions: Quantitative CTP mismatch classification using relCBF and Tmax is similar to perfusion-diffusion MRI. The greater accessibility of CTP may facilitate generalizability of mismatch-based selection in clinical practice and trials.]]> Sat 24 Mar 2018 07:58:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17780 1.2 and total coregistered mismatch volume was ≥10 mL. The primary outcome was a comparison of infarct growth in alteplase vs placebo patients with coregistered mismatch. Of 99 patients with baseline diffusion-weighted imaging and perfusion-weighted imaging, coregistration of both images was possible in 95 patients. Coregistered mismatch was present in 93% (88/95) compared to 85% (81/95) with standard volumetric mismatch. In the coregistered mismatch patients, of whom 45 received alteplase and 43 received placebo, the primary outcome measure of geometric mean infarct growth was significantly attenuated by a ratio of 0.58 with alteplase compared to placebo (1.02 vs 1.77; 95% CI, 0.33–0.99; P=0.0459). When using coregistration techniques to determine the presence of mismatch at study entry, alteplase significantly attenuated infarct growth. This highlights the necessity for a randomized, placebo-controlled, phase III clinical trial of alteplase using penumbral selection beyond 3 hours.]]> Sat 24 Mar 2018 07:57:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17758 Sat 24 Mar 2018 07:57:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16967 Sat 24 Mar 2018 07:55:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19971 Sat 24 Mar 2018 07:54:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19728 P<0.001) and smaller baseline diffusion lesion volume (Rho −0.70, P<0.001). In 30 patients without reperfusion at day 3 to 5, deterioration in collateral quality between baseline and subacute imaging was strongly associated with absolute (P=0.02) and relative (P<0.001) infarct growth. The deterioration in collateral grade correlated with increased mean Tmax hypoperfusion severity (Rho −0.68, P<0.001). Deterioration in Tmax hypoperfusion severity was also significantly associated with absolute (P=0.003) and relative (P=0.002) infarct growth. Collateral flow is dynamic and failure is associated with infarct growth.]]> Sat 24 Mar 2018 07:53:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19726 2 ml VLCBV threshold defined in EPITHET predicted PH with 100% sensitivity, 72% specificity, 35% positive predictive value, and 100% negative predictive value. Pooling EPITHET and DEFUSE (163 patients, including 23 with PH), regression models using VLCBV (p<0.001) and tPA (p=0.02) predicted PH independent of clinical factors better than models using diffusion or time to maximum>8 seconds lesion volumes. Excluding VLCBV in regions without reperfusion improved specificity from 61 to 78% in the pooled analysis. Interpretation: VLCBV predicts PH after stroke thrombolysis and appears to be a more powerful predictor than baseline diffusion or hypoperfusion lesion volumes. Reperfusion of regions of VLCBV is strongly associated with post-thrombolysis PH. VLCBV may be clinically useful to identify patients at significant risk of hemorrhage following reperfusion.]]> Sat 24 Mar 2018 07:53:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19328 Sat 24 Mar 2018 07:52:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21366 4 to >8 s. Hemorrhagic transformation was classified according to the European Cooperative Acute Stroke Studies criteria. Results: Of the 175 patients, 28 had definite atrial fibrillation, 30 probable atrial fibrillation, 111 no atrial fibrillation, and six were excluded due to insufficient imaging data. At baseline, patients with definite atrial fibrillation had more severe hypoperfusion (median time to maximum >8 s, volume 48 vs. 29 ml, P = 0·02) compared with patients with no atrial fibrillation. At outcome, patients with definite atrial fibrillation had greater infarct growth (median volume 47 vs. 8 ml, P = 0·001), larger infarcts (median volume 75 vs. 23 ml, P = 0·001), more frequent parenchymal hematoma grade hemorrhagic transformation (30% vs. 10%, P = 0·03), worse functional outcomes (median modified Rankin scale score 4 vs. 3, P = 0·03), and higher mortality (36% vs. 16%, P = 0·03) compared with patients with no atrial fibrillation. Definite atrial fibrillation was independently associated with increased parenchymal hematoma (odds ratio = 6·05, 95% confidence interval 1·60–22·83) but not poor functional outcome (modified Rankin scale 3–6, odds ratio = 0·99, 95% confidence interval 0·35–2·80) or mortality (odds ratio = 2·54, 95% confidence interval 0·86–7·49) three-months following stroke, after adjusting for other baseline imbalances. Conclusion: Atrial fibrillation is associated with greater volumes of more severe baseline hypoperfusion, leading to higher infarct growth, more frequent severe hemorrhagic transformation and worse stroke outcomes.]]> Sat 24 Mar 2018 07:51:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27117 Sat 24 Mar 2018 07:41:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27975 Sat 24 Mar 2018 07:38:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26463 1). Results: Overall, 152 patients (82 left hemisphere) were included. Median diffusion lesion volume was 37.0 ml, and median baseline National Institutes of Health Stroke Score was 13. In the left hemisphere, the strongest determinants of nonfavorable outcome were infarction of the uncinate fasciculus, followed by precuneus, angular gyrus and total diffusion lesion volume. In the right hemisphere, the strongest determinants of nonfavorable outcome were infarction of the parietal lobe followed by the putamen. Conclusions: Assessment of infarct location using CART demonstrates regional characteristics associated with poor outcome. Prognostically important locations include limbic, default-mode and language areas in the left hemisphere, and visuospatial and motor regions in the right hemisphere.]]> Sat 24 Mar 2018 07:27:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4663 Sat 24 Mar 2018 07:19:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4662 Sat 24 Mar 2018 07:19:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4830 Sat 24 Mar 2018 07:18:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23444 Sat 24 Mar 2018 07:13:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23824 1·2, and absolute mismatch >10 ml) will be randomized to either tissue plasminogen activator or placebo. Study outcome: The primary outcome measure will be modified Rankin Scale 0–1 at day 90. Clinical secondary outcomes include categorical shift in modified Rankin Scale at 90 days, reduction in the National Institutes of Health Stroke Score by 8 or more points or reaching 0–1 at day 90, recurrent stroke, or death. Imaging secondary outcomes will include symptomatic intracranial haemorrhage, reperfusion and or recanalization at 24 h and infarct growth at day 90.]]> Sat 24 Mar 2018 07:12:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44191 Mon 10 Oct 2022 12:19:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42211 P =.78). Patients managed in SUs more often received recommended management (e.g. swallowing screening). Conclusion: The benefits of SU care may extend to patients experiencing in-hospital stroke. Validation, including accounting for potential residual confounding factors, is required.]]> Fri 26 Aug 2022 09:25:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41084 Fri 22 Jul 2022 17:11:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40030 Fri 22 Jul 2022 13:07:48 AEST ]]>