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Brain Infarction (brain + infarction)
Selected AbstractsLiposome-Encapsulated Hemoglobin Alleviates Brain Edema After Permanent Occlusion of the Middle Cerebral Artery in RatsARTIFICIAL ORGANS, Issue 2 2009Akira T. Kawaguchi Abstract Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH. [source] SCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in ratsJOURNAL OF PINEAL RESEARCH, Issue 3 2007Ming-Yang Lee Abstract:, We have previously shown that exogenous melatonin improves the preservation of the blood,brain barrier (BBB) and neurovascular unit following cerebral ischemia,reperfusion. Recent evidence indicates that postischemic microglial activation exaggerates the damage to the BBB. Herein, we explored whether melatonin mitigates the cellular inflammatory response after transient focal cerebral ischemia for 90 min in rats. Melatonin (5 mg/kg) or vehicle was given intravenously at reperfusion onset. Immunohistochemistry and flow cytometric analysis were used to evaluate the cellular inflammatory response at 48 hr after reperfusion. Relative to controls, melatonin-treated animals did not have significantly changed systemic cellular inflammatory responses in the bloodstream (P > 0.05). Melatonin, however, significantly decreased the cellular inflammatory response by 41% (P < 0.001) in the ischemic hemisphere. Specifically, melatonin effectively decreased the extent of neutrophil emigration (Ly6G-positive/CD45-positive) and macrophage/activated microglial infiltration (CD11b-positive/CD45-positive) by 51% (P < 0.01) and 66% (P < 0.01), respectively, but did not significantly alter the population composition of T lymphocyte (CD3-positive/CD45-positive; P > 0.05). This melatonin-mediated decrease in the cellular inflammatory response was accompanied by both reduced brain infarction and improved neurobehavioral outcome by 43% (P < 0.001) and 50% (P < 0.001), respectively. Thus, intravenous administration of melatonin upon reperfusion effectively decreased the emigration of circulatory neutrophils and macrophages/monocytes into the injured brain and inhibited focal microglial activation following cerebral ischemia,reperfusion. The finding demonstrates melatonin's inhibitory ability against the cellular inflammatory response after cerebral ischemia,reperfusion, and further supports its pleuripotent neuroprotective actions suited either as a monotherapy or an add-on to the thrombolytic therapy for ischemic stroke patients. [source] Defense mechanism to oxidative DNA damage in glial cellsNEUROPATHOLOGY, Issue 2 2004Takashi Iida Astrocytosis is a sequential morphological change of astrocytic reaction to tissue damage, and is associated with regulation of antioxidant defense mechanisms to reduce oxidative damage. The repair enzymes to oxidative DNA damage, oxidized purine-nucleoside triphosphatase (hMTH1) and a mitochondrial type of 8-oxoguanine DNA glycosylase (hOGG1,2a) in brain tumors and neurons of Alzheimer's disease, were previously reported. In the present study, glial expression of these repair enzymes under such pathological conditions as cerebrovascular diseases and metastatic brain tumors, were investigated. Furthermore, an in-vitro experiment using a glioma cell-line under oxidative stress was performed to verify the immunohistochemical results of post-mortem materials. As a result, hOGG1,2a immunoreactivities in reactive astrocytes were more intense than those to hMTH1. Oligodendrocytes of acute or subacute stage of brain infarction were strongly immunoreactive to both repair enzymes. In-vitro study revealed that, hOGG1,2a is constitutively expressed in both untreated glioma cells and the glioma cells under oxidative stress. However, although no immunoreactivity to hMTH1 was found in the control cells, accumulation of hMTH1 was rapidly induced by oxidative stress. These results indicate that the two repair enzymes to oxidative DNA damage are differentially regulated in glial cells, and that there is a difference in the expression of the repair enzymes between reactive astrocytes and oligodendrocytes. [source] Evaluating Patients with Acute Ischemic Stroke with Special Reference to Newly Developed Atrial Fibrillation in Cerebral EmbolismPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2007MINORU TAGAWA M.D. Background:Cardioembolic strokes are extensive and have a poor prognosis. To identify the cardiovascular risk factors of cardioembolic stroke, we evaluated the cardiovascular status with special reference to persistent atrial fibrillation (AF) and paroxysmal atrial fibrillation (PAF) combined with the type of acute ischemic stroke. Methods:We divided 315 consecutive patients admitted to our Department of Neurosurgery with an acute ischemic stroke into four types of brain infarction using clinical history, onset pattern of stroke, and brain imaging: cardioembolic (group E, n = 105), lacunar (group L, n = 92), atherothrombotic (group T, n = 111), and unclassified (n = 7). All patients underwent standard electrocardiography (ECG), a 24-hour ECG recording (Holter ECG) and transthoracic echocardiography (UCG). Results:Persistent AF or PAF was detected in 97 patients (31.5%) using Holter ECG: more frequently in group E (67.6%) than in groups L (15.2%) or T (9.2%). Persistent AF or PAF was first diagnosed on admission using a standard ECG in 16 patients (5.2%) with no previous history and 14 of these patients belonged to group E (13.3%). PAF was newly detected on Holter ECG in another 26 patients (8.4%) and 13 of these patients (12.4%) belonged to group E. Concerning UCG, left atrial enlargement and mitral regurgitation were more frequent in group E than in group L or T. Conclusion:Holter ECG in addition to ECG on admission is important for detecting persistent AF or PAF in patients with ischemic stroke, especially with cardioembolism as diagnosed by neuroimaging. [source] Heparin-induced thrombocytopenia with multiple organized thrombi accompanied by unusual cholesterin deposition: Autopsy case after long-term follow upPATHOLOGY INTERNATIONAL, Issue 10 2009Masaaki Ichinoe Heparin-induced thrombocytopenia (HIT) is characterized by a reduction in the platelet count and systemic thromboembolism during heparin therapy. Herein is reported a case of HIT with characteristic thrombus formation. A 68-year-old man who had been treated for hypertension for 27 years suffered a brain infarction and was treated with heparin. After this treatment, other new infarctions occurred in multiple organs. Because serum antibodies against heparin/PF4 complex were detected, he was diagnosed as having HIT, and warfarin and argatroban were administered instead of heparin. He died, however, 119 days after the first onset. At autopsy infarction due to organized thrombi with cholesterin deposition in multiple organs were found, similar to usual atherosclerotic emboli, but different to them with regard to clinical course and distribution of thrombi. This case in which organization and frequent cholesterin deposition were found in thromboembolized lesions of multiple organs after relatively long-term follow up, is unusual. The findings suggest that HIT accompanied by marked hypercholesterolemia of long duration contributes to a characteristic form of thromboembolism that needs careful management. [source] Neuroprotective effect of HT008-1, a prescription of traditional Korean medicine, on transient focal cerebral ischemia model in ratsPHYTOTHERAPY RESEARCH, Issue 8 2010Youngmin Bu Abstract HT008-1 is one of the prescriptions used in Traditional Korean Medicine for the treatment of mental and physical weakness. It is composed of Panax ginseng, Acanthopanax senticosus, Angelica sinensis and Scutellaria baicalensis, which have been reported to have various pharmacological effects on the central nervous system. The study investigated whether HT008-1 has neuroprotective effects in a focal cerebral ischemia rat model. Stroke was induced in rats by 2,h of middle cerebral artery occlusion (MCAo) followed by 22,h of reperfusion. HT008-1 (30, 100 and 300,mg/kg) and the component herbs (300,mg/kg) were administered orally twice at 0 and 2,h after ischemia. Oral administration of 300,mg/kg HT008-1 reduced brain infarction by 45.7%, prolonged the latency time by 24.8% in the rotarod test, and enhanced the score by 17.0% in the balance beam test. Only P. ginseng and S. baicalensis showed protective effects, and HT008-1 showed a greater effect than its component herbs. HT008-1 down-regulated the COX-2 and OX-42 expression in the penumbra region. In conclusion, the results show that HT008-1 may be effective in a rat stroke model by an antiinflammatory mechanism and may improve sensory-motor function by reducing damage in the cortex and caudoputamen. Copyright © 2010 John Wiley & Sons, Ltd. [source] Matrix metalloproteinase-3 and intracranial arterial dolichoectasiaANNALS OF NEUROLOGY, Issue 4 2010Fernando Pico MD Objective Intracranial arterial dolichoectasia (IADE), also called dilatative arteriopathy of the brain, is defined as an increase in length and diameter of intracranial arteries. Abdominal aortic aneurysm and ectasia of coronary arteries have been reported in association with IADE. In both conditions, a dysfunction of matrix metalloproteinases (MMP)-2, -3, and -9 have been found. Our aim was to investigate these MMP pathways in stroke patients with IADE. Methods Five hundred ten Caucasians patients with brain infarction were consecutively recruited at 12 centers. The diagnosis of IADE was made by consensus between 2 neurologists based on magnetic resonance imaging scans. Determination of MMP-2, -3, and -9 plasma levels was centralized in 1 laboratory. Because we found a threshold effect of MMP-3 plasma levels with the risk of IADE, determination of the MMP-3 5A/6A polymorphism was carried out. Results IADE was identified in 12% of stroke patients. There was no association of IADE with mean MMP-2, -3, and -9 plasma levels. After categorization of MMP plasma levels into tertiles, we found a higher risk of IADE with the lowest MMP-3 tertile (adjusted odds ratio [OR], 2.48; 95% confidence interval [CI], 1.17,5.23). In genotype analysis, there was a significant additive effect of the 5A allele on the risk of IADE, with an adjusted OR of 1.62 (95% CI, 1.03,2.55). Interpretation In this cohort of stroke patients of Caucasian ancestry, IADE was associated with low MMP-3 plasma levels and with the 5A/6A polymorphism of the promoter region of MMP-3. These results suggest that MMP-3 may play a role in IADE. ANN NEUROL 2010;67:508,515 [source] New England medical center posterior circulation registryANNALS OF NEUROLOGY, Issue 3 2004Louis R. Caplan MD Among 407 New England Medical Center Posterior Circulation registry patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs then strokes, and 16% had only TIAs. Embolism was the commonest stroke mechanism (40% of patients including 24% cardiac origin, 14% intraarterial, 2% cardiac and arterial sources). In 32% large artery occlusive lesions caused hemodynamic brain ischemia. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes); the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Severe occlusive lesions (>50% stenosis) involved more than one large artery in 148 patients; 134 had one artery site involved unilaterally or bilaterally. The commonest occlusive sites were: extracranial vertebral artery (52 patients, 15 bilateral) intracranial vertebral artery (40 patients, 12 bilateral), basilar artery (46 patients). Intraarterial embolism was the commonest mechanism of brain infarction in patients with vertebral artery occlusive disease. Thirty-day mortality was 3.6%. Embolic mechanism, distal territory location, and basilar artery occlusive disease carried the poorest prognosis. The best outcome was in patients who had multiple arterial occlusive sites; they had position-sensitive TIAs during months to years. Ann Neurol 2004;56:389,398 [source] Post-stroke depression: can we predict its development from the acute stroke phase?ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009B. Fuentes Objectives,,, To identify possible predictive factors for post-stroke depression (PSD) in the acute phase of stroke. Methods,,, The study design was prospective, observational cohort study of patients with acute cerebral infarction (CI). Neurological and neuropsychological evaluations were conducted within the first 10 days from the onset of stroke and repeated at the 3-month follow-up. DSM-IV criteria were used to define PSD. Results,,, From a total of 85 patients with CI, 59 patients completed the 3-month follow-up and 17 of them (28.8 %) fulfilled PSD criteria at the 3-month follow-up. Melancholy index of the Hamilton Depression Rankin Scale (HDRS) was associated with a risk three times greater than that of PSD at the 3-month follow-up in the univariate analysis (OR 3.07; 95% CI 1.53,6.16; P = 0.002) with no significant influence of stroke severity or the location of brain infarction (right or left side). The receiver operating characteristic curves pointed to a melancholy index ,1.5 as the optimal cut-off level associated with the development of PSD at the 3-month follow-up. Conclusions,,, Melancholy index of the HDRS ,1.5 could be a useful clinical tool to detect patients with acute stroke at high risk of developing PSD. [source] Early diagnosis of rhinocerebral mucormycosis by cerebrospinal fluid analysis and determination of 16s rRNA gene sequenceEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2007D. Bengel A 40-year-old diabetic woman was diagnosed with rhinocerebral mucormycosis. Cerebral mucormycosis is an acute life-threatening disease, which is caused by fungi of the class Phycomycetae. Clinical suspicion and detection of the fungal hyphae in cerebrospinal fluid (CSF) led to early diagnosis, subsequently confirmed by immunohistochemistry and molecular analysis of fungal RNA. Early infiltration of the infectious agent into the central nervous system resulted in septic thrombosis of the cavernous sinus, mycotic meningoencephalitis, brain infarctions as well as intracerebral and subarachnoidal hemorrhages. Despite immediate high-dose antimycotic treatment, surgical debridement of necrotic tissue, and control of diabetes as a predisposing factor, the woman died 2 weeks after admission. Although fungal organisms are rarely detectable in CSF specimens from patients with mycotic infections of the central nervous system, comprehensive CSF examination is beneficial in the diagnosis of rhinocerebral mucormycosis. Furthermore, a concerted team approach, systemic antifungal agents and early surgical intervention seem to be crucial for preventing rapid disease progression. [source] | ||||||||||||||||||||||