The impact of intravenous thrombolysis on outcome of patients with acute ischemic stroke after 90 years old

BACKGROUND: Age increases the risk of mortality and poor prognosis following stroke. The benefit of intravenous thrombolysis in very old patients remains uncertain. The purpose of the study was to evaluate the efficacy and safety of thrombolysis in very old patients considering their perfusion-imaging profile. METHODS: We conducted a retrospective study including patients older than 90 y.o. admitted for an acute ischemic stroke. A computed tomography perfusion-imaging (CTP) was performed in patients who received thrombolysis. Primary outcome was the functional status at 3 months, assessed by the modified Rankin scale (mRS). Secondary outcomes were the rate of hemorrhagic transformations, duration of hospitalization and the rate of death in the first 7 days. Patients receiving thrombolysis were compared with an age-matched group of non-thrombolysed patients. RESULTS: 78 patients were included (31 % male, aged 92 ± 1.7 y.o). 37 patients received thrombolysis and among them, 30 had CTP with a mismatch. The three months mRS was not significantly different in the two groups (mRS 0–2: 5 % and 7 % in the thrombolysed and non-thrombolysed group, respectively). Hemorrhagic transformations were more frequent in the thrombolysed group (54 % versus 12 %, p = 0.002) and symptomatic intracranial hemorrhage tended to be associated with mRS at three months and death in the first 7 days. Duration of hospitalization was longer in the thrombolysed group (10 days ± 12 versus 7 days ± 9, p = 0.046). CONCLUSIONS: Patients who received thrombolysis did not have a better functional prognosis than non-thrombolysed patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12877-016-0331-1) contains supplementary material, which is available to authorized users

The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients

The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis

Atraumatic Nonaneurysmal Sulcal Subarachnoid Hemorrhages: A Diagnostic Workup Based on a Case Series

&lt;b&gt;&lt;i&gt;Introduction:&lt;/i&gt;&lt;/b&gt; Atraumatic and nonaneurysmal sulcal subarachnoid hemorrhage (sSAH) is a rare type of cerebrovascular disease with various etiologies previously reported in small case reports. In this study, we propose to analyze clinical presentations, imaging patterns and etiologies in a large case series of such patients in order to propose a diagnostic workup. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; We retrospectively analyzed clinical and radiological data of consecutive patients with a diagnosis of atraumatic and nonaneurysmal sSAH, admitted to our institution between 2008 and 2011. All patients had both computed tomography (CT) and magnetic resonance imaging (MRI) as a part of their initial evaluation. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; 30 patients (18 women and 12 men, mean age: 60 years) were identified. The main clinical symptoms at presentation were focal and transient neurological deficit (n = 22) and thunderclap headache (n = 10). Four patients had progressive headache and 4 other had partial or generalized epileptic seizures. MRI abnormalities associated with sSAH were prior hemorrhages, microbleeds, severe leukoencephalopathy and hemosiderosis suggesting cerebral amyloid angiopathy (CAA; n = 9), vasogenic edema in parieto-occipital areas compatible with a posterior reversible encephalopathy syndrome (PRES; n = 3), cortical venous thrombosis (n = 2) and concomitant acute cortical stroke (n = 3). Other underlying causes of sSAH, not diagnosed on MRI, were reversible cerebral vasoconstriction syndrome (RCVS) based on clinical criteria and conventional angiography (n = 4), angiitis diagnosed by skin biopsy (n = 1), vascular malformation diagnosed on CT and digital subtraction angiographies (n = 3), and overanticoagulation (n = 1). Four cases remained unresolved. &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; This study confirmed that sSAH is a rare condition related to a wide spectrum of etiologies. Combination of brain MRI and magnetic resonance angiography and eventually digital subtraction angiography allowed the identification of an underlying etiology for 87% of patients. CAA, RCVS and PRES represented more than 50% of the etiological mechanisms. Among older patients, sSAH was mainly related to CAA while in younger patients, RCVS represented the most frequent etiology.</jats:p