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This study aims to compare the incidences of neurological deterioration (ND) and poor outcome (a modified Ranking scale > 2 points at discharge) among patients with different atherosclerotic stroke patterns. A total of 688 participants were categorized into 4 groups according to atherosclerotic stroke pattern: multiple small infarcts (MSI), single subcortical infarction (SSI), borderzone infarct (BZI) and large infarct groups. Among the 4 groups, MSI group had the lowest incidences of ND and poor outcome (13.5% and 16.2%, respectively). In multivariable analyses, for BZI patients, the risks of ND [odds ratio (OR) = 3.90, 95% confidence interval (CI) = 2.10–7.22, p  < 0.001] and poor outcome (OR = 3.45, 95% CI = 1.67–7.14, p  = 0.001) both significantly increased compared to MSI, both of which were the highest among the 4 stroke patterns. The neutrophil to lymphocyte ratio in BZI and large infarct groups were higher than in MSI and SSI groups [3.35 (2.28, 5.04) and 3.36 (2.53, 4.94) vs. 2.64 (1.89, 4.06) and 2.71 (1.93, 3.91), p  < 0.001]. BZI group had the highest risks of ND and poor outcome among atherosclerotic stroke patients. BZI and large infarct patients had stronger poststroke inflammation than MSI and SSI patients.

Background: The anatomical location of white matter hyperintense lesions in small vessel disease are apparently similar to those of borderzone infarction. The objective of this study is to find clinical and radiological points of differentiation between the two vascular disorders in a sample of Egyptian patients which might have an impact on primary and secondary prevention. Methods: Ischemic stroke patients with white matter lesions were categorized into two groups: small vessel disease and borderzone infarctions. NIHSS was done on admission. Risk factor profile was reported, and investigations done including: HbA1C, lipid profile, CRP, ECG, echocardiography, carotid duplex, brain MRI, MRA and MR perfusion study. Results: 46 patients completed the study, 29 with SVD and 17 with BZI. Smoking, hypertension and recurrent stroke were more common in borderzone infarctions, but only diabetes was significantly higher (p = 0.047). Limb shaking was more observed in borderzone infarctions (p = 0.049). Radiologically: lacunar pattern was observed more in small vessel disease, while rosary pattern was more in borderzone infarctions (p = 0.04). FLAIR symmetrical lesions and microbleeds were more significant in small vessel disease (p = <0.001; 0.048, respectively). Perfusion study time to peak denoted evidence of significant hypoperfusion in all regions of interest in borderzone infarctions. Conclusion: Limb shaking, retinal claudication or syncope, with MRI showing rosary pattern of white matter hyperintensity, few microbleeds and markedly impaired perfusion favor the diagnosis of borderzone infarctions. On the other hand, presence of lacunae, FLAIR showing symmetrical WMH and microbleeds with minimal or no perfusion deficit suggests the diagnosis of small vessel disease.

Traditionally hypoperfusion and embolism are considered separate important causes of stroke in patients with arterial occlusive disease. However, although hypoperfusion and embolism differ in mechanisms and location, they generally coincide in severe obstructive lesions and cause washout disturbances of embolism in low perfusion territories distal to stenosis. Unless the collateral blood supply is sufficient to prevent ischemia, multiple remote spot-like infarctions occur within the hypoperfused brain territory. In border-zone distributed infarction – long suspected to result from hemodynamic compromise alone – complementary interaction of embolisation and hypoperfusion territories has to be considered. Thus hypoperfusion with embolism or embolism alone are the most common explanations for stroke, the former often associated with less severe clinical deficits than the latter.

The EU's internal borders have become mostly invisible. Today, external borders are at the centre of controversy about an alleged 'fortress Europe'. Using different theoretical and methodological perspectives this book examines the challenges facing the EU's external borders, including Neighborhood Policy, migration issues and the diffusion of norms and values to other countries. Divided into two parts, the book first presents different theoretical approaches and empirical studies of the EU's external borders, mobility and security issues. It is an invaluable guide to border research within a framework of European Integration and Globalization Studies. The second part of this volume focuses on the analyses of the EU's Neighbourhood Policy, the approach to Eastern Europe and EU energy policy. Expert contributors collaborate to explore debates about migration, the EU as a normative, 'civil' power, energy security and the securitization of borders. Highly relevant and insightful, the text provides a timely assessment of EU borders in an increasingly globalized and integrated European neighbourhood. The EU's Shifting Borders will be of interest to students and scholars of European Union Politics and International Relations.

Borderzone infarcts (BZIs) are anatomically defined as ischemic lesions occurring at the junction between two arterial territories, accounting for 2% to 10% of strokes. Three types of hemispheric BZIs are described according to topography (ie, superficial anterior, posterior, and deep). Although published series on related aphasia are rare in the setting of BZI, aphasia is of transcortical (TCA) type, characterized by the preservation of repetition. TCA can be of motor, sensory, or mixed type depending on whether expression, understanding, or both are impaired. Recent studies have reported specific aphasic patterns. BZI patients initially presented with mixed TCA. Aphasia specifically evolved according to the stroke location, toward motor or sensory TCA in patients with respectively anterior or posterior BZI. TCA was associated with good long-term prognosis. This specific aphasic pattern is interesting in clinical practice because it prompts the suspicion of a BZI before the MRI is done, and it helps in the planning of rehabilitation and in providing adapted information to the patient and family concerning the likelihood of language recovery.

A 41-year-old male presented with acute onset weakness of the left hand. Magnetic resonance imaging (MRI) of the brain showed hyperacute infarct in the right middle cerebral artery (MCA)-posterior cerebral artery (PCA) watershed territory. Magnetic resonance angiography (MRA), Doppler ultrasonography, and digital subtraction angiography revealed severe right internal carotid artery (ICA) stenosis. The patient underwent carotid endarterectomy. The second patient was a 48-year-old male with acute onset right wrist drop. MRI of brain showed acute infarct in the left MCA-PCA watershed territory. MRA of brain and neck, Doppler ultrasonography of the neck vessels, and echocardiography were normal. Both the cases were not initially considered strokes by the referring physicians. Isolated hand palsy is a rare presentation of stroke, often mistaken for peripheral lesion. Fractional limb weakness as a presentation of acute ischemic stroke due to borderzone infarction involving parietal lobe is a rarely reported entity.

Background and Purpose: Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD). Methods: Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts. Results: Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each. Conclusion: The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.

Background: Borderzone as well as territorial infarcts can occur in severe atherosclerotic carotid artery disease. It remains controversial whether the borderzone distribution of infarcts is due to hypoperfusion or due to artery-to-artery embolism. Purpose: The present study investigates whether cobalt-55 ( 55Co) positron emission tomography (PET) shows a different pattern of ischaemia according to the topography of the infarct in severe atherosclerotic carotid artery disease. Patients and methods: Five patients with a cortical borderzone and seven with a territorial infarct, due to symptomatic carotid artery disease, were investigated with 55Co PET 3–6 months after stroke. Average 55Co counts in the infarct area, the adjacent cortical zone, the deep white matter and, contralateral cerebral cortex and white matter, were compared to the values in the cerebellum used as reference. Results: No differences in 55Co ratio were observed in the different regions of interest (ROIs) between patients with cortical borderzone and those with territorial infarcts. The 55Co uptake was similar or lower than the reference value for all ROIs in all individual patients. Conclusion: In patients with borderzone as well as with territorial infarcts no evidence was found for subclinical ischaemic injury in or around the infarcts. These data do support the conclusion that cortical borderzone infarcts may not be due to ongoing chronic haemodynamic impairment, but by no means is this conclusive evidence.

From an ongoing stroke registry, including all patients with a first cerebral infarct, we studied 41 borderzone small deep infarcts: (SDIs) in comparison with 123 remaining SDIs. We noted vascular risk factors, presence of a carotid occlusion or Stenosis > 50%, and the presence of asymptomatic lesions on CT. By univariate analysis and subsequent multivariate logistic regression analysis, we found that carotid stenosis/occlusion was more frequent among the borderzone group, but this difference was not statistically significant. The vascular risk factor profile was similar in both groups. Asymptomatic lesions, but especially asymptomatic borderzone small deep lesions were significantly more frequent among the symptomatic borderzone group. We conclude that carotid stenosis is not a numerically important contributor to the occurrence of borderzone SDI; generalised small-vessel disease may be more important in this respect. Therefore borderzone SDIs are most likely due to haemodynamic compromise in the distal supply areas of the perforating arteries.

Objective: The mechanism underlying cerebral infarction in the borderzone between the territories of deep and superficial perforating arteries has not yet been clarified. This study was performed to investigate the prevalence, volume, site, and etiology of this type of subcortical infarction in a large unselected group of stroke patients. Methods and Patients: We analyzed a continuous series of 383 patients with recent cerebral infarction observed in our Stroke Unit. Patients underwent a complete clinical and instrumental workup. The subgroup of subjects with internal borderzone infarct alone were compared with the subgroups of patients with other types of cerebral infarcts by uni- and multivariate statistical tests. Results: There were 90 internal borderzone infarcts of 725 ischemic lesions (12% of the total), with a median volume of 0.32 ml (95% confidence interval 0.24–0.44; range: 0.012–20.2 ml). Internal borderzone infarcts alone occurred in only 13 of 383 (3.4%) patients. A comparison between patients with ‘pure’ internal borderzone infarction and patients with other types of cerebral infarcts by multiple logistic regression analysis demonstrated a significant independent causal role of carotid stenosis or occlusion. Conclusion: Our study suggests that ‘pure’ internal borderzone infarctions are quite rare findings in patients with ischemic stroke, and that the hemodynamic impairment due to atherosclerotic occlusion or stenosis of the carotid system could be the cause in the large majority of cases.