Eating the Mediterranean Style: A Tasty Way for Stroke Prevention☆

Abstract Stroke is a leading cause of death and disability, with high individual, social and economic costs. Diet has been identified as a modifiable risk factor for cardiovascular diseases and stroke in several large epidemiological studies. The evaluation of foods groups and dietary patterns provides a more realistic representation of actual dietary intake, and gives clues to developing guidelines aimed at general population. We review the role of Mediterranean diet, fruit and vegetables, and olive oil consumption, on the risk of stroke and other vascular outcomes. Findings from major studies indicate that, together with a healthy lifestyle, the traditional Mediterranean way of eating, including social and cultural components, and inscribed on the Representative List of the Intangible Cultural Heritage of Humanity by UNESCO, may be considered a cost-effective intervention to reduce the human, social and economic burden of stroke and cardiovascular disease

Intracerebral haemorrhage pathophysiology: time is brain

Intracerebral haemorrhage is associated with high mortality and morbidity. Cerebral small vessel disease, either due to hypertensive small vessel disease or to amyloid angiopathy, is the common substrate for primary spontaneous intracerebral haemorrhage.The current understanding of brain injury induced by intracerebral haemorrhage is based on both clinical and experimental studies. The initial injury immediately after its onset is from the direct mechanical force of the expanding hematoma, resulting in cytotoxic edema and cellular necrosis. After this, the degrading hematoma releases its breakdown products, which lead to the activation of oxygen free radicals, matrix metalloproteinases, complement proteins and inflammatory markers, thus determining an increase of the BBB permeability, the recruitment of inflammatory cells, apoptosis, and ultimately the exacerbation of cerebral edema and neuronal death.Evidence suggests that early and aggressive medical management and specialist care can improve the overall outcome in patients with intracerebral haemorrhage. The growing insight into the molecular pathophysiological mechanisms may contribute to the development of neuroprotective strategies

Intravenous Tirofiban With Intra-Arterial Urokinase and Mechanical Thrombolysis in Stroke

Background and Purpose— To evaluate preliminarily efficacy and safety of intravenous tirofiban combined with mechanical clot disruption and urokinase in patients with stroke attributable to major cerebral artery occlusion. Methods— Eleven consecutive patients with stroke attributable to acute occlusion of a major cerebral artery were treated with an intravenous bolus injection of the platelet glycoprotein IIb/IIIa antagonist tirofiban combined with heparin and by endovascular procedures including mechanical thrombolysis and locally delivered urokinase. Of the 11 cases, 9 involved angioplasty and 2 only microcatheter and microguidewire manipulation. Results— There were 7 patients with internal carotid or middle cerebral artery occlusion treated within 6 hours and 4 patients with basilar artery occlusion treated within 12 hours of symptom onset. Median National Institutes of Health Stroke Scale (NIHSS) score on admission was 20. After the interventional procedure, vessel recanalization was partial (thrombolysis in myocardial infarction grade flow 2 [TIMI 2]) in 7 patients and absent or insufficient in 4 patients. Twenty-four hours after the procedure, all the patients but 1 improved substantially, and on control angiography, the occluded vessel was totally patent (TIMI 3) in 10 of the 11 patients. One patient with partial recanalization did not improve and died 3 months later from pulmonary embolism. Neither a symptomatic intracerebral hemorrhage nor systemic bleedings requiring blood transfusion occurred in any patient. At discharge, median NIHSS score was 2. The 3-month outcome was excellent in 8 patients (modified Rankin Scale [mRS] 0 to 1), good in 2 patients (mRS 2), and poor in 1 patient (mRS 6). Conclusions— The combination of intravenous tirofiban with intra-arterial mechanical clot disruption and urokinase may be successful in reopening an occluded major cerebral vessel without increasing the hemorrhagic risk and with good functional outcome. This strategy cannot be recommended as the systematic treatment of stroke attributable to major cerebral artery occlusion until tested in a controlled study design

Urgent Carotid Endarterectomy in Patients with Recent/Crescendo Transient Ischaemic Attacks or Acute Stroke.

Objective of this study was to review the results of urgent carotid endarterectomy (CEA) performed in patients with recent (< 24 h) or crescendo (at least 2 episodes in 24 h) transient ischaemic attack (TIA) or with acute stroke in a single centre experience

Lacunar infarcts, depression and anxiety symptoms one year after stroke

Background: Mood disorders are frequent after stroke and are associated with poorer quality of life. Previous studies have reported conflicting results as to stroke subtype in the incidence of poststroke mood disorders. We explored the relationship between subcortical ischemic stroke subtype (lacunar) and presence of such symptoms at 1 year after stroke. Methods: Anonymized data were accessed from the Virtual International Stroke Trials Archive. Stroke subtypes were classified according to the Trial of Org 10172 in Acute Stroke Treatment classification. Depression and anxiety symptoms were assessed using Hospital Anxiety and Depression Scale. We investigated independent predictors of depression and anxiety symptoms using a logistic regression model. Results: Data were available for 2160 patients. Almost one fifth of the patients developed both anxiety and depression at 1-year follow-up. After adjusting for confounders, the lacunar subtype was least associated with both anxiety (odds ratio [OR] = .61; 95% confidence interval [CI] = .46-.80) and depression symptoms (OR = .71; CI = .55-.93) versus other stroke subtypes. Conclusions: Lacunar strokes have a weaker association with presence of anxiety and depression symptoms compared with other subtypes

Prediction of Impaired Performance in Trail Making Test in MCI Patients With Small Vessel Disease Using DTI Data

Mild cognitive impairment (MCI) is a common condition in patients with diffuse hyperintensities of cerebral white matter (WM) in T2-weighted magnetic resonance images and cerebral small vessel disease (SVD). In MCI due to SVD, the most prominent feature of cognitive impairment lies in degradation of executive functions, i.e., of processes that supervise the organization and execution of complex behavior. The trail making test is a widely employed test sensitive to cognitive processing speed and executive functioning. MCI due to SVD has been hypothesized to be the effect of WM damage, and diffusion tensor imaging (DTI) is a well-established technique for in vivo characterization of WM. We propose a machine learning scheme tailored to 1) predicting the impairment in executive functions in patients with MCI and SVD, and 2) examining the brain substrates of this impairment. We employed data from 40 MCI patients with SVD and created feature vectors by averaging mean diffusivity (MD) and fractional anisotropy maps within 50 WM regions of interest. We trained support vector machines (SVMs) with polynomial as well as radial basis function kernels using different DTI-derived features while simultaneously optimizing parameters in leave-one-out nested cross validation. The best performance was obtained using MD features only and linear kernel SVMs, which were able to distinguish an impaired performance with high sensitivity (72.7%-89.5%), specificity (71.4%-83.3%), and accuracy (77.5%-80.0%). While brain substrates of executive functions are still debated, feature ranking confirm that MD in several WM regions, not limited to the frontal lobes, are truly predictive of executive functions

Variation in risk factors for recent small subcortical infarcts with infarct size, shape and location

BACKGROUND AND PURPOSE: Lacunar infarction is due to a perforating arteriolar abnormality. Possible causes include embolism, atheromatosis or intrinsic disease. We examined whether the size, shape or location of the lacunar infarct varied with embolic sources, systemic atheroma or vascular risk factors. METHODS: We examined data from three prospective studies of patients with clinical and diffusion-weighted imaging (DWI) positive symptomatic lacunar infarction who underwent full clinical assessment and investigation for stroke risk factors. Lacunar infarct size (maximum diameter; shape, oval/tubular; location, basal ganglia/centrum semiovale/brainstem) were coded blind to clinical details. RESULTS: Amongst 195 patients, 48 infarcts were tubular, 50 were 15-20mm diameter, 97 were in the basal ganglia and 74 in the centrum semiovale. There was no association between infarct size or shape and any risk factors. Centrum semiovale infarcts were less likely to have a potential relevant embolic source (4% v 11%, OR 0.16 95% confidence interval (CI) 0.03-0.83) and caused a lower National Institute of Health Stroke Scale (NIHSS) (2 v 3, OR 0.78 95% CI 0.62-0.98) than basal ganglia infarcts. There were no other differences by infarct location. CONCLUSIONS: Lacunar infarcts in the basal ganglia caused marginally more severe strokes and were three times as likely to have a potential embolic source than those in the centrum semiovale but the overall rate of carotid or known cardiac embolic sources (11%) was low. We found no evidence that other risk factors differed with location, size or shape suggesting that most lacunar infarcts share a common intrinsic arteriolar pathology

Is the Oxidant/Antioxidant Status Altered in CADASIL Patients?

The altered aggregation of proteins in non-native conformation is associated with endoplasmic reticulum derangements, mitochondrial dysfunction and excessive production of reactive oxygen species. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare hereditary systemic vasculopathy, caused by NOTCH3 mutations within the receptor extracellular domain, that lead to abnormal accumulation of the mutated protein in the vascular wall. NOTCH3 misfolding could cause free radicals increase also in CADASIL. Aim of the study was to verify whether CADASIL patients have increased oxidative stress compared to unrelated healthy controls. We enrolled 15 CADASIL patients and 16 gender- and age-matched healthy controls with comparable cardiovascular risk factor. Blood and plasma reduced and total aminothiols (homocysteine, cysteine, glutathione, cysteinylglycine) were measured by HPLC and plasma 3- nitrotyrosine by ELISA. Only plasma reduced cysteine (Pr-Cys) and blood reduced glutathione (Br-GSH) concentrations differed between groups: in CADASIL patients Br-GSH levels were higher (p = 0.019) and Pr-Cys lower (p = 0.010) than in controls. No correlation was found between Br-GSH and Pr-Cys either in CADASIL patients (rho 0.25, P=0.36) or in controls (rho -0.15, P=0.44). Conversely, 3- nitrotyrosine values were similar in CADASIL and healthy subjects (p = 0.82). The high levels of antioxidant molecules and low levels of oxidant mediators found in our CADASIL population might either be expression of an effective protective action against free radical formation at an early stage of clinical symptoms or they could suggest that oxidative stress is not directly involved in the pathogenesis of CADASIL