Definition, prediction, prevention and management of patients with severe ischemic stroke and large infarction / 中华医学杂志(英文版)

Severe ischemic stroke carries a high rate of disability and death. The severity of stroke is often assessed by the degree of neurological deficits or the extent of brain infarct, defined as severe stroke and large infarction, respectively. Critically severe stroke is a life-threatening condition that requires neurocritical care or neurosurgical intervention, which includes stroke with malignant brain edema, a leading cause of death during the acute phase, and stroke with severe complications of other vital systems. Early prediction of high-risk patients with critically severe stroke would inform early prevention and treatment to interrupt the malignant course to fatal status. Selected patients with severe stroke could benefit from intravenous thrombolysis and endovascular treatment in improving functional outcome. There is insufficient evidence to inform dual antiplatelet therapy and the timing of anticoagulation initiation after severe stroke. Decompressive hemicraniectomy (DHC) <48 h improves survival in patients aged <60 years with large hemispheric infarction. Studies are ongoing to provide evidence to inform more precise prediction of malignant brain edema, optimal indications for acute reperfusion therapies and neurosurgery, and the individualized management of complications and secondary prevention. We present an evidence-based review for severe ischemic stroke, with the aims of proposing operational definitions, emphasizing the importance of early prediction and prevention of the evolution to critically severe status, summarizing specialized treatment for severe stroke, and proposing directions for future research.

Multidetector computed tomography angiography in clinically suspected hyperacute ischemic stroke in the anterior circulation: an etiological workup in a cohort of Brazilian patients / Angiotomografia computadorizada multidetectores na avaliação da suspeita clínica de acidente vascular encefálico isquêmico hiperagudo da circulação anterior: determinação etiológica precoce em um grupo de pacientes brasileiros

Objective The potential of computed tomography angiography (CTA) was assessed for early determination of stroke subtypes in a Brazilian cohort of patients with stroke. Method From July 2011 to July 2013, we selected patients with suspected hyperacute stroke (< 6 hours). Intracranial and cervical arteries were scrutinized on CTA and their imaging features were correlated with concurrent subtype of stroke. Results Stroke was documented in 50/106 selected patients (47.2%) based on both clinical grounds and imaging follow-up (stroke group), with statistically significant arterial stenosis and vulnerable plaques on CTA. Intracranial large artery disease was demonstrated in 34% of patients in the stroke group. Partial territorial infarct prevailed (86%) while artery-to-artery embolization was the most common stroke mechanism (52%). Conclusion Multidetector CTA was useful for the etiologic work-up of hyperacute ischemic stroke and facilitated the knowledge about the topographic pattern of brain infarct in accordance with its causative mechanism. .

Objetivo Avaliar o potencial da angiotomografia computadorizada multidetectores (ATCM) na determinação etiológica precoce do acidente vascular encefálico (AVE) e correlacionar o mecanismo causal com o padrão de infarto. Método De Julho de 2011 a Julho de 2013, foram selecionados os pacientes com suspeita clínica de AVE hiperagudo. Os achados da ATCM dos vasos intracranianos e cervicais foram correlacionados com a etiologia final do evento. Resultados AVE foi confirmado em 50/106 pacientes (47,2%). Estes apresentaram alterações angiográficas estatisticamente mais relevantes. Aterosclerose dos grandes vasos intracranianos esteve presente em 34% destes pacientes. O padrão radiológico topográfico de infarto mais comum foi o infarto territorial parcial (86%). A embolização arterio-arterial foi o mecanismo mais prevalente (52%). Conclusão A utilização da ATCM traz benefícios na detecção etiológica precoce dos pacientes com suspeita de AVE hiperagudo, além de possibilitar o entendimento do padrão radiológico topográfico de acordo com o mecanismo causal do evento isquêmico. .

The 'silence' of silent brain infarctions may be related to chronic ischemic preconditioning and nonstrategic locations rather than to a small infarction size

OBJECTIVE: Silent brain infarctions are the silent cerebrovascular events that are distinguished from symptomatic lacunar infarctions by their 'silence'; the origin of these infarctions is still unclear. This study analyzed the characteristics of silent and symptomatic lacunar infarctions and sought to explore the mechanism of this 'silence'. METHODS: In total, 156 patients with only silent brain infarctions, 90 with only symptomatic lacunar infarctions, 160 with both silent and symptomatic lacunar infarctions, and 115 without any infarctions were recruited. Vascular risk factors, leukoaraiosis, and vascular assessment results were compared. The National Institutes of Health Stroke Scale scores were compared between patients with only symptomatic lacunar infarctions and patients with two types of infarctions. The locations of all of the infarctions were evaluated. The evolution of the two types of infarctions was retrospectively studied by comparing the infarcts on the magnetic resonance images of 63 patients obtained at different times. RESULTS: The main risk factors for silent brain infarctions were hypertension, age, and advanced leukoaraiosis; the main factors for symptomatic lacunar infarctions were hypertension, atrial fibrillation, and atherosclerosis of relevant arteries. The neurological deficits of patients with only symptomatic lacunar infarctions were more severe than those of patients with both types of infarctions. More silent brain infarctions were located in the corona radiata and basal ganglia; these locations were different from those of the symptomatic lacunar infarctions. The initial sizes of the symptomatic lacunar infarctions were larger than the silent brain infarctions, whereas the final sizes were almost equal between the two groups. CONCLUSIONS: Chronic ischemic preconditioning and nonstrategic locations may be the main reasons for the 'silence' of silent brain infarctions.

Linfoma intravascular de células B grandes: hallazgos clínicos y morfológicos en un caso con desenlace fatal / Intravascular large B cell lymphoma: Report of one case

Intravascular large B cell lymphoma is a rare subtype of large cell lymphoma that is characterized by the proliferation of lymphoid cells within the lumina of small blood vessels. We report a 61-year-old male presenting paresis of both lower limbs, confusion and a history of weight loss. Magnetic resonance and CAT imaging studies showed multiple images of brain and cerebellar infarctions. Twenty days after admission, the patient died and the postmortem study demonstrated a multisystem intravascular large B cell lymphoma.

The Effect of Treadmill Exercise on Ischemic Neuronal Injury in the Stroke Animal Model: Potentiation of Cerebral Vascular Integrity

PURPOSE: This study was done to identify whether pre-conditioning exercise has neuroprotective effects against cerebral ischemia, through enhance brain microvascular integrity. METHODS: Adult male Sprague-Dawley rats were randomly divided into four groups: 1) Normal (n=10); 2) Exercise (n=10); 3) Middle cerebral artery occlusion (MCAo), n=10); 4) Exercise+MCAo (n=10). Both exercise groups ran on a treadmill at a speed of 15 m/min, 30 min/day for 4 weeks, then, MCAo was performed for 90 min. Brain infarction was measured by Nissl staining. Examination of the remaining neuronal cell after MCAo, and microvascular protein expression on the motor cortex, showed the expression of Neuronal Nuclei (NeuN), Vascular endothelial growth factor (VEGF) & laminin. RESULTS: After 48 hr of MCAo, the infarct volume was significantly reduced in the Ex+MCAo group (15.6+/-2.7%) compared to the MCAo group (44.9+/-3.8%) (p<.05), and many neuronal cells were detected in the Ex+MCAo group (70.8+/-3.9%) compared to the MCAo group (43.4+/-5.1%) (p<.05). The immunoreactivity of laminin, as a marker of microvessels and Vascular endothelial growth factor (VEGF) were intensively increased in the Ex+MCAo group compared to the MCAo group. CONCLUSION: These findings suggest that the neuroprotective effects of exercise pre-conditioning reduce ischemic brain injury through strengthening the microvascular integrity after cerebral ischemia.

Migrainous infarct: an update

Migraine and stroke have been linked in a complex bi-directional association, though there are quite a few pathophysiological pieces to be found to complete the puzzle. International Classification of Headache Disorders-11 [ICHD-II] has defined a specific term 'migrainous infarct' that can be the crucial link between the two disorders. The authors review the latest developments related to migrainous infarct and present a compilation of case reports from 1988 to 2006

Neuroprotective Effect of Cycloheximide on Hypoxic-Ischemic Brain Injury in Neonatal Rats

This study was done to determine the neuroprotective effect of cycloheximide on neonatal hypoxic-ischemic brain injury. Seven day-old newborn rat pups were subjected to 90 min of 8% oxygen following a unilateral carotid artery ligation. The extent of cerebral infarction was evaluated at 1 and 4 week of recovery. Apoptosis was identified by performing terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and flow cytometry with a combination of fluoresceinated annexin V and propidium iodide. Brain infarction area was significantly increased at 4 week compared to 1 week after hypoxia-ischemia in the control group. With cycloheximide treatment, the number of TUNEL positive cells in the ipsilateral cerebral cortex at 48 hr and peri-infarct area at 1 and 4 week of recovery was significantly reduced, both apoptotic and necrotic cells by flow cytometry 48 hr after the injury were significantly reduced, and the extent of cerebral infarction at 1 and 4 week of recovery was also significantly attenuated compared to the hypoxia-ischemia control group. In summary, our data suggest that apoptosis plays an important role in the development of delayed infarction, and inhibition of apoptosis with cycloheximide significantly reduces the ensuing cerebral infarction in a newborn rat pup model of cerebral hypoxia-ischemia.

Brain MRI Findings of Carbon Disulfide Poisoning

OBJECTIVE: To evaluate the findings of brain MRI in patients with carbon disulfide poisoning. MATERIALS AND METHODS: Ninety-one patients who had suffered carbon disulfide poisoning [male:female=87:4; age, 32-74 (mean 53.3) years] were included in this study. To determine the extent of white matter hyperintensity (Grade 0-V) and lacunar infarction, T2-weighted MR imaging of the brain was performed. RESULTS: T2-weighted images depicted white matter hyperintensity in 70 patients (76.9%) and lacunar infarcts in 27 (29.7%). CONCLUSION: In these patients, the prevalent findings at T2-weighted MR imaging of the brain were white matter hyperintensity and lacunar infarcts. Disturbance of the cardiovascular system by carbon disulfide might account for these results.