Moving From Alteplase to Tenecteplase for Acute Ischemic Stroke: Mayo Clinic Experience.

OBJECTIVES: Tenecteplase is a fibrin-specific plasminogen activator that has shown promising results in the treatment of acute ischemic stroke. Tenecteplase has been suggested to reduce door-to-needle time and to increase the rate of spontaneous recanalization. In February 2021, Mayo Clinic Health System switched to Tenecteplase as the standard thrombolytic therapy for acute ischemic stroke. METHODS: In this center-based observational cohort study, we present clinical characteristics and outcomes of patients with acute ischemic stroke treated with tenecteplase between February 2021 and May 2022 compared with alteplase treatment between September 2019 and February 2021. We used descriptive and comparative statistics. RESULTS: Baseline characteristics were comparable between the groups. The incidence of symptomatic intracerebral hemorrhage was significantly less among the tenecteplase group (0.65% vs. 5%, P =0.027). Both groups had a similar door-to-needle time [55 (IQR 30.5) vs. 57 (IQR 38) in the tissue plasminogen activator group, P =0.395]. Spontaneous partial or complete recanalization was more commonly observed in the tenecteplase group (10.4% vs. 1.4%, P =0.038). Mechanical thrombectomy for large vessel occlusion was deferred due to marked clinical improvement more commonly in tenecteplase (6.3% vs. 1.4%); however, this difference was not statistically significant. Ninety-day modified Rankin Scale did not show a significant difference between the groups. CONCLUSION: Tenecteplase use as the thrombolytic agent in acute ischemic stroke was associated with lower rates of symptomatic intracranial hemorrhage, higher rates of spontaneous recanalization, but similar door-to-needle time and 90-day modified Rankin Scale as compared with tissue plasminogen activator.

Quantitative Analysis of Stress-Induced Hyperglycemia and Intracranial Blood Volumes for Predicting Mortality After Intracerebral Hemorrhage.

Stress-induced hyperglycemia (SIH) is a neuroendocrine response to acute illness. Although SIH has an adverse association with intracerebral hemorrhage (ICH), quantitative measures and determinants of SIH are not well delineated. In the present study, we objectively evaluated SIH using glycemic gap (GG) and identified its radiological and clinical determinants, with a 5-year retrospective review of charts of ICH patients. We calculated GG using the regression equation (GG = AG -28.7 × HbA1c + 46.7) and evaluated whether GG is an independent predictor of mortality using a multivariate regression model. Radiological volumes of different intracranial compartments were determined using image segmentation software. We correlated GG with different clinical and radiological parameters using Pearson correlation coefficient (PCC), Spearman's rank correlation (SRC), and Wilcoxon rank sum test. Then, we calculated the value of GG associated with mortality. Out of 328 patients, 238 (73%) survived hospitalization and 90 (27%) expired. GG was found to be an independent predictor of mortality (r=0.008, p=0.04). Additionally, GG was positively correlated with intraparenchymal hemorrhage (IPH) volume (PCC=0.185, p<0.01) and intraventricular hemorrhage (IVH) volume (PCC=0.233, p<0.01) and negatively correlated with cerebrospinal fluid (CSF) volume (PCC=-0.151, p<0.01) and brain tissue volume (PCC=-0.099, p=0.08). GG was positively correlated with patients' ICH score (SRC=0.377, p<0.01), Glasgow Coma Scale (GCS) (PCC=-0.356, p<0.01), hydrocephalus (p<0.01), and IVH in the third ventricle (p<0.01). The univariate logistic regression model identified 30.0 mg/dl as the value of GG (AUC=0.655, p<0.01) that predicted mortality with 52.2% sensitivity and 75.2% specificity and defined SIH. In conclusion, GG independently predicts mortality in ICH patients and positively correlates with IPH and IVH volumes. However, causality between the two is not established and would require specifically designed studies.

Cytotoxic Lesion in the Splenium of Corpus Callosum Secondary to Subacute Methotrexate Neurotoxicity.

Methotrexate neurotoxicity can present with a wide spectrum of neurologic symptoms and brain magnetic resonance imaging (MRI) typically demonstrates cerebral edema, demyelination, multifocal white matter necrosis, and atrophy relatively selective for the deep cerebral white matter. Here, we report a case of subacute methotrexate neurotoxicity in a 40-year-old man with B cell acute lymphoblastic leukemia. Brain MRI showed cytotoxic lesion in the splenium of corpus callosum and left middle cerebellar peduncle. Patient significantly improved 24 hours after receiving oral dextromethorphan. Methotrexate neurotoxicity should be suspected in any symptomatic patient receiving high dose of methotrexate or intrathecal methotrexate therapy. Dextromethorphan should be considered in these patients as it can modulate the excitatory responses to homocysteine and its metabolite which are usually elevated in such patients.