ObjectiveTo report clinical and laboratory characteristics, as well as treatment and clinical outcomes of patients admitted for neurologic diseases with and without COVID-19.MethodsIn this retrospective, single center cohort study, we included all adult inpatients with confirmed COVID-19, admitted to a Neuro-COVID Unit from February 21, 2020, who had been discharged or died by April 5, 2020. Demographic, clinical, treatment, and laboratory data were extracted from medical records and compared (FDR-corrected) to those of neurologic patients without COVID-19 admitted in the same period.ResultsOne hundred seventy-three patients were included in this study, of whom 56 were positive for COVID-19 while 117 were negative for COVID-19. Patients with COVID-19 were older (77.0, IQR 67.0–83.8 vs 70.1, IQR 52.9–78.6, p = 0.006), had a different distribution regarding admission diagnoses, including cerebrovascular disorders (n = 43, 76.8% vs n = 68, 58.1%), and had a higher quick Sequential Organ Failure Assessment (qSOFA) score on admission (0.5, IQR 0.4–0.6 vs 0.9, IQR 0.7–1.1, p = 0.006). In-hospital mortality rates (n = 21, 37.5% vs n = 5, 4.3%, p < 0.001) and incident delirium (n = 15, 26.8% vs n = 9, 7.7%, p = 0.003) were significantly higher in the COVID-19 group. COVID-19 and non-COVID patients with stroke had similar baseline characteristics but patients with COVID-19 had higher modified Rankin scale scores at discharge (5.0, IQR 2.0–6.0 vs 2.0, IQR 1.0–3.0, p < 0.001), with a significantly lower number of patients with a good outcome (n = 11, 25.6% vs n = 48, 70.6%, p < 0.001). In patients with COVID-19, multivariable regressions showed increasing odds of in-hospital death associated with higher qSOFA scores (OR 4.47, 95% CI 1.21–16.5; p = 0.025), lower platelet count (0.98, 0.97–0.99; p = 0.005) and higher lactate dehydrogenase (1.01, 1.00–1.03; p = 0.009) on admission.ConclusionsCOVID-19 patients admitted with neurologic disease, including stroke, have a significantly higher in-hospital mortality, incident delirium and higher disability than patients without COVID-19.

The antiangiogenic factor thrombospondin 1 (TSP-1) binds with high affinity to several heparin-binding angiogenic factors, including fibroblast growth factor 2 (FGF-2), vascular endothelial growth factor (VEGF), and hepatocyte growth factor/ scatter factor (HGF/SF). The aim of this study was to investigate whether TSP-1 affects FGF-2 association with the extracellular matrix (ECM) and its bioavailability. TSP-1 prevented the binding of free FGF-2 to endothelial cell ECM. It also IntroductionAngiogenesis, sprouting of new blood vessels from pre-existing ones, is a crucial event in physiologic and pathologic processes, including tumor growth and metastasis. 1 Angiogenesis is a complex process, regulated by pro-and antiangiogenic factors, that involves dynamic interaction between a variety of cells, growth factors, and the extracellular matrix (ECM). 2 As in other morphogenic processes, the ECM acts not just as a structural support, but also as a direct modulator of cellular functions. Matrix components and bioactive fragments released by limited proteolysis can directly regulate endothelial cell functions. 3 In addition, the matrix contributes to angiogenesis by acting as a reservoir for angiogenic factors. Growth factors are stored in the matrix through binding to heparansulfate proteoglycans (HSPGs). Binding to HSPGs is reversible, 4 and biologically active factors can be released from the matrix by different agents. 5,6 Fibroblast growth factor 2 (FGF-2, basic FGF) is the most extensively studied example of matrix-stored angiogenic factor. 5,7 As do other members of the FGF family, FGF-2 has a high affinity for the glycosaminoglycan heparin and for HSPGs. Cell-surface HSPGs are required for the formation of an active FGF/FGF receptor signaling complex, 8 for internalization, and hence for internalization-dependent activities such as endothelial cell proliferation. 7,9 Conversely, matrix-associated HSPGs allow the storage of FGF-2 within the ECM. 10 Matrix-associated FGF-2 can then act locally, or be released as a soluble, biologically active factor. 6 Mobilization of active FGF-2 from the matrix is an important mechanism of induction of angiogenesis. Biologically active FGF-2 is released by heparin, 11 matrix-degrading proteases, 12 heparanase, 13 and the FGF-binding protein (FGF-BP). 14 Conversely, other endogenous or pharmacologic agents that prevent FGF-2 interaction with HSPGs exert an antiangiogenic activity, as in the case of platelet factor 4 (PF-4), 15 a soluble syndecan ectodomain, 16 suramin, 17 chemically modified heparins, and heparin-mimicking polyanionic compounds. [18][19][20] Other important angiogenic factors, including vascular endothelial growth factor (VEGF) and hepatocyte growth factor/scatter factor (HGF/SF), bind to HSPGs that again contribute to growth factor binding to cell receptors and to the ECM. [21][22][23] Thrombospondin 1 (TSP-1) is the most studied member of a family of at least 5 related proteins. 24,25 TSP-1 is a matricellular molecule, a modular glycoprotein composed of mult...

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Futile recanalization occurs when successful recanalization fails to improve clinical outcome in acute ischemic stroke patients. Predictors of futile recanalization are still debated and may help in selecting patients for reperfusion strategies. We aim to determine whether leukoaraiosis may be useful in predicting futile recanalization in acute ischemic stroke patients treated by endovascular mechanical thrombectomy. We included in the analysis patients with acute ischemic stroke due to anterior circulation large vessel occlusion undergoing endovascular mechanical thrombectomy obtaining complete vessel recanalization. Demographics, vascular risk factors, baseline National Institutes of Health Stroke Scale score, time from symptoms onset to recanalization, Alberta Stroke Program Early CT Score, and leukoaraiosis graded on a 4-point van Swieten scale were collected. We dichotomized patients into those with moderate-severe leukoaraiosis (2-4) versus those with absent-slight leukoaraiosis (0, 1). Outcome measures were symptomatic intracranial hemorrhage, and modified Rankin scale score at 90 days. The relationships among radiological parameters and clinical data with outcome measures were studied with univariate and multivariable analyses. Sixty-eight patients were identified. Recanalization was futile in 32.4% of cases. On multivariable logistic regression analysis, the presence of moderate-severe LA was independent predictors of FR (P = 0.01). Furthermore, higher NIHSS score at baseline (P < 0.01) end endovascular mechanical thrombectomy alone treatment (P < 0.01) resulted associated with futile recanalization. Our results showed that the presence of moderate-severe leukoaraiosis is associated with poor outcome in recanalized patients.

COVID-19 impact on consecutive neurological patients admitted to the emergency department Letter copyright.

Transient Global Amnesia (TGA) is a common condition of unknown aetiology characterised by the abrupt onset of severe anterograde amnesia, which lasts less than 24 hours. Some authors have suggested that subclinical impairment of memory functions may persist for much longer, but neuropsychological assessment lasting years after TGA attack has not been performed so far. The aim of this study was to evaluate longterm cognitive functions in patients with a previous TGA episode. Fifty-five patients underwent a standardised neuropsychological assessment after at least one-year from the TGA attack, and were compared with 80 age-matched controls. TGA patients showed worse performances on tests evaluating verbal and nonverbal long-term memory and attention, with comparable global cognitive functions. By applying current criteria for amnestic Mild Cognitive Impairment (MCI-a) on TGA subjects, a group consisting of 18/55 (32.7%) MCI-a subjects was identified. There was no association between the presence of MCI-a and demographic variables, vascular risk factors, years since the TGA episode, or ApoE genotype. This study demonstrates that TGA appears to be a relatively benign syndrome although objective memory deficits fulfilling MCI-a criteria persist over time, as detected by multidimensional neuropsychological tasks performed at long-term follow-up.

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