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Cerebral Infarction (cerebral + infarction)
Selected AbstractsCerebral Infarction in Conjunction With Patent Foramen Ovale and May-Thurner SyndromeJOURNAL OF NEUROIMAGING, Issue 4 2001David M. Greer MD ABSTRACT Stroke patients with paradoxical embolus mandate a search for deep venous thrombosis (DVT) in the lower extremities. Iliac vein compression, or May-Thurner syndrome, places certain patients at risk for development of DVT. The authors present 3 stroke patients with patent foramen ovale and paradoxical cerebral embolism, with demonstrated iliac vein compression as the presumed source of their embolus. May-Thurner syndrome should be considered a potential source of clot, as definitive therapy of this disorder can be curative. [source] Animal Model with Detrusor Overactivity Caused by Cerebral Infarction as a Useful Tool for Pharmacological Therapeutic ApproachesLUTS, Issue 2009Osamu YOKOYAMA Supra-pontine lesions resulting from neurological disorders, such as vascular disease or Parkinson's disease, cause a sense of urgency, frequency, and/or urge incontinence, all of which constitute an overactive bladder. This phenomenon is due in part to the elimination of cortical inhibitory control of the micturition center in the pontine and in part to facilitation of excitatory control. These controls consist of several neurotransmitter systems that include acetylcholine, dopamine, and glutamate. The development of detrusor overactivity following cerebral infarction is mediated by upregulation and downregulation of excitatory and inhibitory inputs of these neurotransmitter systems to the micturition center in the brain, respectively. [source] Liposome-Encapsulated Hemoglobin Reduces the Size of Cerebral Infarction in Rats: Effect of Oxygen AffinityARTIFICIAL ORGANS, Issue 2 2009Dai Fukumoto Abstract Liposome-encapsulated hemoglobin (LEH) with a low oxygen affinity (l-LEH, P50 = 45 mm Hg) was found to be protective in the rodent and primate models of ischemic stroke. This study investigated the role of LEH with a high O2 affinity (h-LEH, P50 = 10 mm Hg) in its protective effect on brain ischemia. The extent of cerebral infarction was determined 24 h after photochemically induced thrombosis of the middle cerebral artery from the integrated area of infarction detected by triphenyltetrazolium chloride staining in rats receiving various doses of h-LEH as well as l-LEH. Both h-LEH and l-LEH significantly reduced the extent of cortical infarction. h-LEH remained protective at a lower concentration (minimal effective dose [MED]: 0.08 mL/kg) than l-LEH (MED: 2 mL/kg) in the cortex. h-LEH reduced the infarction extent in basal ganglia as well (MED: 0.4 mL/kg), whereas l-LEH provided no significant protection. h-LEH provided better protection than l-LEH. The protective effect of both high- and low-affinity LEH may suggest the importance of its small particle size (230 nm) as compared to red blood cells. The superiority of h-LEH over l-LEH supports an optimal O2 delivery to the ischemic penumbra as the mechanism of action in protecting against brain ischemia and reperfusion. [source] S -Nitrosylated Pegylated Hemoglobin Reduces the Size of Cerebral Infarction in RatsARTIFICIAL ORGANS, Issue 2 2009Akira T. Kawaguchi Abstract Cell-free hemoglobin-based oxygen carriers have well-documented safety and efficacy problems such as nitric oxide (NO) scavenging and extravasation that preclude clinical use. To counteract these effects, we developed S -nitrosylated pegylated hemoglobin (SNO-PEG-Hb, P50 = 12 mm Hg) and tested it in a brain ischemia and reperfusion model. Neurological function and extent of cerebral infarction was determined 24 h after photochemically induced thrombosis of the middle cerebral artery in the rat. Infarction extent was determined from the integrated area in the cortex and basal ganglia detected by triphenyltetrazolium chloride staining in rats receiving various doses of SNO-PEG-Hb (2, 0.4, and 0.08 mL/kg) and compared with rats receiving pegylated hemoglobin without S -nitrosylation (PEG-Hb) or saline of the same dosage. Results indicated that successive dilution revealed SNO-PEG-Hb but not PEG-Hb to be effective in reducing the size of cortical infarction but not neurological function at a dose of 0.4 mL/kg. In conclusion, SNO-PEG-Hb in a dose of 0.4 mL/kg (Hb 24 mg/kg) showed to be most effective in reducing the size of cortical infarction, however, without functional improvement. [source] Accuracy of transcranial Doppler sonography for predicting cerebral infarction in aneurysmal subarachnoid hemorrhageJOURNAL OF CLINICAL ULTRASOUND, Issue 8 2006Ji-Yong Lee MD Abstract Purpose. To evaluate the accuracy of transcranial Doppler (TCD) sonography using different criteria for predicting cerebral infarction due to symptomatic vasospasm. Methods. We retrospectively evaluated the clinical and radiologic data of consecutive patients admitted with acute aneurysmal subarachnoid hemorrhage (SAH) in the anterior cerebral circulation between January 2001 and June 2002. TCD sonographic examinations were performed on alternate days up to 20 days after admission. Cerebral infarction was defined on CT as a new hypodensity in the vascular distribution with corresponding clinical symptoms. Vasospasm was diagnosed as mild or severe when TCD sonography revealed a mean blood flow velocity (MBFV) greater than 120 and 180 cm/s in the middle or anterior cerebral artery and in the intracranial part of the internal carotid artery, respectively. Results. A total of 93 patients with aneurysmal SAH in the anterior cerebral circulation were included. Vasospasm was demonstrated by TCD sonography in 60 patients (64.5%) and was shown via multivariable logistic regression analysis to be predictive of cerebral infarction (OR 3.11, 95% CI 1.46,6.59), with an 82.6% and 69.6% sensitivity, a 41.4% and 77.1% specificity, a 31.7% and 50.0% positive predictive value, and an 87.9% and 88.5% negative predictive value when the MBFV was greater than 120 and 180 cm/s, respectively. Conclusions. Vasospasm on TCD was found to be predictive of symptomatic cerebral infarction on CT, but its positive predictive value remained low despite the adoption of restrictive TCD criteria for vasospasm. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:380,384, 2006 [source] Racial disparity in stroke risk factors: the Berlin,Ibadan experience; a retrospective studyACTA NEUROLOGICA SCANDINAVICA, Issue 2 2009M. O. Owolabi Background,,, Different workers have reported racial disparities in the distribution of risk factors for stroke and stroke subtype (ischemic vs hemorrhagic). No transcultural transnational studies have been conducted to confirm and relate these disparities to one another. Our objective was to identify differences in the distribution of risk factors for stroke and stroke subtypes among urban-dwelling stroke patients in Nigeria, a developing country, and Germany, an industrialized country. Methods,,, Consecutive stroke patients in Ibadan (100) and Berlin (103) were studied. Their hospital records were screened to identify documented vascular risk factors and stroke subtype. Results,,, The stroke patients in Ibadan were younger than those in Berlin (t = 4.940, P = 0.000). Hypertension was significantly more common in Ibadan while cigarette smoking, dyslipidemia, atherosclerosis, and cardiac factors were significantly more frequent in Berlin. Cerebral infarction was more common in Berlin (80%) than in Ibadan (63%). Conclusion,,, The risk factors associated with cerebral infarction were more frequent in Berlin. We suspect that racial disparity in risk factors for stroke may account for the difference in proportions of stroke subtype in black and white populations. Larger prospective community-based multinational multiracial studies are required to confirm these disparities and identify possible underlying genetic, dietary, and socio-economic factors. [source] Enterobacter sakazakii infection in the newbornACTA PAEDIATRICA, Issue 3 2001B Bar-Oz Enterobacter sakazakii, a Gram-negative bacillus, previously known as "yellow pigmented Enterobacter cloacae," is a rare cause of neonatal infection. We describe the detailed clinical presentation of two cases in whom E. sakazakii was isolated in our neonatal service during the course of 1 mo. These include one case of sepsis and meningitis complicated by cerebral infarction, and one case of sepsis. In addition, three cases of intestinal colonization were identified. The source of the organism was thoroughly sought and was found to be a blender in the milk kitchen that was used for preparation of the reconstituted powdered milk formula. Conclusion: Our paper adds clinical and laboratory information about the disease spectrum caused by this relatively rare organism and emphasizes the importance of a thorough search for the source of the infection. [source] Etiology of strokes in children with sickle cell anemiaDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 3 2006Michael R. DeBaun Abstract The most devastating complication of sickle cell anemia is cerebral infarction, affecting ,30% of all individuals with sickle cell anemia. Despite being one of the most common causes of stroke in infants and children, the mechanism of cerebral infarction in this population has not been extensively studied and is poorly understood. Multiple, synergistic factors are important in the pathogenesis of stroke including the hemodynamic effects of cerebral arterial occlusive disease, viscosity, chronic and acute anemia and acute medical events. This review focuses on the relationship between these factors in order to provide a foundation for further study of the etiology of strokes in this high-risk population. MRDD Research Reviews 2006;12:192,199. © 2006 Wiley-Liss, Inc. [source] Vertebral artery fibromuscular dysplasia: an unusual cause of stroke in a 3-year-old childDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2003Ana Camacho MD Fibromuscular dysplasia (FMD) is a systemic arteriopathy which tends to affect renal arteries followed by cervicocranial vessels. It can lead to cerebral infarction if cephalic arteries are involved. FMD is an unusual cause of stroke in childhood that generally affects the carotid area. Only four cases of vertebral FMD and subsequent stroke have been reported previously and we present the youngest patient of all. A healthy 3-year-old female was admitted to Hospital Doce de Octubre in Madrid, Spain with cerebellar infarction. Angiography disclosed basilar artery thrombosis and typical signs of FMD in both vertebral arteries. No other angiographic alteration was noted in the other vessels studied. Her phenotype and other investigations were unremarkable. The patient was treated with anti-aggregation therapy (aspirin) and the outcome was excellent. Investigation of the occurrence in childhood of this kind of arteriopathy may lead to clarification of its natural history and speculation about its unclear pathogenesis. [source] Arterial dissection complicating tonsillectomyDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 9 2003E Wraige MRCPCH Tonsillectomy is a frequently performed surgical procedure. Surgical complications can be serious. We report the case of a 7,year-old female who experienced an arterial ischaemic cerebral infarction following elective adenotonsillectomy. [source] Bilateral cerebral hemispheric infarction associated with sildenafil citrate (Viagra®) useEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2008K.-K. Kim Sildenafil citrate (Viagra®) is one of the frequently prescribed drugs for men with erectile dysfunction. We describe a 52-year-old man with bilateral middle cerebral artery (MCA) territory infarction after sildenafil use. He ingested 100 mg of sildenafil and about 1 h later, he complained of chest discomfort, palpitation and dizziness followed by mental obtundation, global aphasia and left hemiparesis. Brain magnetic resonance imaging documented acute bilateral hemispheric infarction, and cerebral angiography showed occluded bilateral MCA. Despite significant bilateral MCA stenosis and cerebral infarction, systemic hypotension persisted for a day. We presume that cerebral infarction was caused by cardioembolism with sildenafil use. [source] Etiology of and risk factors for cerebral infarction in young adults in western Norway: a population-based case-control studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2004H. Naess We sought to study the etiology of and risk factors for cerebral infarction in young adults in Hordaland County, Norway. All patients aged 15,49 years living in Hordaland County with a first-ever cerebral infarction during 1988,97 were included. Etiology was analyzed in subgroups defined by sex, age (<40 years versus 40 years), circulation territory (anterior versus posterior circulation) and short-term functional outcome [modified Rankin score (mRS) 2 versus mRS > 2]. A questionnaire was used to evaluate possible risk factors amongst the patients compared with an age- and sex-matched control group. The distribution of etiology was significantly different in all subgroups. Atherosclerosis was frequent amongst men (22.8% vs. 4.2%) and patients 40 years (20.8% vs. 2.7%). All patients with microangiopathy had favorable short-term outcome. Significant risk factors were smoking more than 15 cigarettes per day (P < 0.001), hypertension (P = 0.001), and myocardial infarction (P = 0.035). Modifiable risk factors were frequent. [source] LPL polymorphism predicts stroke risk in menGENETIC EPIDEMIOLOGY, Issue 3 2002Alanna C. Morrison Abstract Variation in lipid levels has been associated with atherosclerotic vascular disease, including stroke. Genes contributing to interindividual variation in lipid levels may play a role in the etiology of stroke, either through their effects on lipid synthesis and metabolism or through separate pathways. For this reason, we sought to examine the association between polymorphisms in the lipoprotein lipase (LPL) and apolipoprotein E (APOE) genes and subclinical and clinical stroke in the Atherosclerosis Risk in Communities (ARIC) Study. Subclinical stroke was determined by cerebral magnetic resonance imaging (MRI). Subclinical cerebral infarct cases (n = 197) were compared to a stratified random sample identified from individuals participating in the MRI examination (n = 200). Incidence of clinical ischemic stroke was determined by following the ARIC cohort for an average of 7.5 years for potential cerebrovascular events; 218 validated clinical ischemic strokes were identified. A stratified random sample of the ARIC cohort (CRS, n = 964) was used as the comparison group for clinical cases. The LPL S291-carrying genotypes and APOE ,2- and ,4-carrying genotypes were not significantly associated with subclinical or clinical stroke. The LPL X447-containing genotypes were significantly associated with subclinical (odds ratio [OR], 4.32; 95% confidence interval [CI], 1.23,15.15; P = 0.020) and clinical stroke (hazard rate ratio [HRR], 2.57; 95% CI, 1.24,5.34; P = 0.01) in men, both by themselves and after adjustment for multiple stroke risk factors. The LPL S447X polymorphism is significantly associated with subclinical cerebral infarction and incident clinical ischemic stroke in men from a middle-aged American population. This association does not appear to be mediated by triglyceride, high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol levels, or additional stroke risk factors. Genet. Epidemiol. 22:233,242, 2002. © 2002 Wiley-Liss, Inc. [source] Elucidation of the molecular mechanism of platelet activation: Dense granule secretion is regulated by small guanosine triphosphate-binding protein Rab27 and its effector Munc13-4GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2006Hisanori Horiuchi Cardiovascular diseases such as myocardial and cerebral infarction are common critical diseases occurring more frequently in the elderly. The trigger of the diseases is platelet activation following plaque rupture or erosion. Investigation of the molecular mechanism in platelet activation has been exclusively performed pharmacologically. We have succeeded in establishing the granule secretion and aggregation assays using permeabilized platelets. These systems enabled us to examine the molecular mechanism in platelet activation with molecular biological and biochemical methods. Using these assay systems, we have been investigating the molecular mechanism of platelet activation. With a support grant from the Novartis Foundation for Gerontological Research, we found several molecules involved in the regulation. In this report, I present the progress in the research of the granule secretion mechanism in activated platelets, which was reported in the Japanese Geriatric Society Meeting in 2005. [source] Pulse wave velocity and cerebral infarctionINTERNAL MEDICINE JOURNAL, Issue 8 2007W. Liang No abstract is available for this article. [source] Patent foramen ovale and cryptogenic cerebral infarctionINTERNAL MEDICINE JOURNAL, Issue 1 2001D. McGaw Abstract The patent foramen ovale (PFO) has been increasingly implicated in the aetiology of stroke, particularly in young patients with no other identifiable cause (cryptogenic stroke). The mechanism is by the passage of venous clots through the patent foramen into the arterial circulation, enabling cerebral embolism. Such patients with cryptogenic stroke and PFO are often treated with life-long anticoagulants or antiplatelet agents in an attempt to decrease the risk of a recurrence. Less commonly, surgical closure of the PFO has been undertaken in these patients. However, the recent evolution of closure devices that are delivered percutaneously by standard cardiac catheter techniques now offer an alternative non-surgical option. These alternative therapies are yet to be compared adequately. Two issues remain to be resolved. First, in determining appropriate therapy, patients with cryptogenic stroke may be divided into three groups: those with no PFO but an alternative unrecognized aetiology, those with an ,innocent' PFO and an alternative unrecognized aetiology and those with a causative PFO. The distinction between these groups clearly has important treatment implications. Second, the risk versus benefit of each available treatment modality must be determined for these different patient subgroups. These two issues require resolution before rational evidence-based treatment can be prescribed for patients with PFO and cryptogenic stroke. (Intern Med J 2001; 31: 42,47) [source] Intravascular lymphoma associated with systemic lupus erythematosusINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 1 2004Masanao Naya Abstract We report a case of systemic lupus erythematosus (SLE) associated with intravascular (angiotropic) lymphoma. A 27-year-old woman had been suffering from uncontrolled severe eruptions for a long time and was admitted because of high fever due to hemophagocytic syndrome (HPS). As her SLE had not been well-controlled by moderate doses of steroids and azathioprine, autoimmune associated HPS was first considered. She was initially treated with steroid pulses and ,-globulin for HPS. However, chromosomal analysis of bone marrow cells revealed severe abnormalities. After malignant lymphoma-associated HPS was diagnosed, chemotherapy was commenced in the intensive care unit with artificial respiration and continuous hemodiafiltration. The patient died of cerebral infarction at day 45. It is suggested that the SLE itself was associated with the development of the intravascular lymphoma rather than due to the azathioprine. [source] Estimating nurses' workload using the Diagnosis Procedure Combination in JapanINTERNATIONAL NURSING REVIEW, Issue 3 2008Y. Kamijo rn Aim:, To examine the methods used to estimate nurse staffing levels in acute care settings with Diagnosis Related Groups, which in Japan are called the Diagnosis Procedure Combination (DPC). Methods:, For estimating staffing requirements, the study used four DPC groups: (1) acute or recurrent myocardial infarction (AMI) with stenting, (2) angina pectoris with coronary artery bypass grafting (CABG), (3) sub-arachnoid haemorrhage (SAH) with clipping surgery, and (4) cerebral infarction with carotid endarterectomy (CEA). Registered nurses with more than 3-year nursing experience in nine university hospitals in the Tokyo metropolitan area completed self-report questionnaires in order to obtain nursing care time and care intensity per each DPC. The concordance rate was measured by Kendall's coefficient of concordance. The relationship between the care time and the care intensity was examined by a time series graph per DPC. Care intensity consisted of professional judgement, mental effort for helping patients, professional skill, physical effort for providing activities of daily living support, and nurse stress, based on the Hsiao and colleagues' model of resource-based relative value scale. Results:, Twenty-five nurses in nine university hospitals answered for a hypothetical typical patient with AMI and with CABG, and 28 nurses in nine university hospitals answered for a hypothetical typical patient with SAH and with CEA. Kendall's coefficient of concordance was 0.896 for AMI, 0.855 for CABG, 0.848 for SAH, 0.854 for CEA. The time series data of the care time and the care intensity items showed different patterns for each DPC. Conclusion:, The DPC for cardiovascular and cerebral surgical procedures can be used for estimating nurses' workload. [source] Sleep Apnea, Delirium, Depressed Mood, Cognition, and ADL Ability After StrokeJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001Olov Sandberg MD OBJECTIVES: The incidence of sleep apnea and stroke increases with age. The aim of this study was to investigate the presence of sleep apnea after stroke and its relationship to delirium, depressed mood, cognitive functioning, ability to perform activities of daily living (ADLs), and psychiatric and behavior symptoms. DESIGN:Cross-sectional study. SETTING:Geriatric stroke rehabilitation unit. PARTICIPANTS:133 patients (78 women and 55 men, mean age 77.1 ± 7.7 years) consecutively admitted to a geriatric stroke rehabilitation unit. MEASUREMENTS: All patients underwent overnight respiratory sleep recordings at 23 ± 7 days (range 11 to 41 days) after suffering a stroke. The patients were assessed using the Organic Brain Syndrome Scale, Montgomery-Åsberg-Depression-Rating Scale, Mini-Mental State Examination (MMSE), and Barthel-ADL Index. Sleep apnea was defined as an apnea-hypopnea index (AHI) of 10 or more. RESULTS: The median of the AHI for the studied sample (N = 133) was 13 (range 0,79; interquartile range 6,28). Fifty-nine percent fulfilled the criteria for sleep apnea; 52% with first-ever stroke had sleep apnea. More patients with sleep apnea than without were delirious, depressed, or more ADL-dependent. Sleep apnea patients also had a higher frequency of ischemic heart disease and had more often suffered from an earlier cerebral infarction. Multivariate analysis showed that obesity, low ADL scores, ischemic heart disease, and depressed mood were independently associated with sleep apnea. Low ADL scores, apnea-related hypoxemia, body mass index ,27, and impaired vision were independently associated with delirium. The presence of sleep apnea was not associated with any specific type of stroke or location of the brain lesion. CONCLUSIONS:Sleep apnea is common in stroke patients and is associated with delirium, depressed mood, latency in reaction and in response to verbal stimuli, and impaired ADL ability. We suggest a trial investigating whether delirium, depressed mood, and ADL ability improve with nasal continuous positive airway pressure treatment of sleep apnea in stroke patients. [source] Variable number of tandem repeats polymorphism of platelet glycoprotein Ib , in Chinese people and CC genotype with aspirin sensitivity in patients with cerebral infarctionJOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 2 2009Y.-Y. Jin MM Summary Background and objective:, To study the prevalence of variable number of tandem repeats (VNTR) polymorphism in platelet membrane glycoprotein (GP) Ib , in a Chinese Han population and to determine the relationship between VNTR polymorphisms and aspirin resistance. Methods:, Three hundred healthy individuals and 110 patients with cerebral infarction volunteered to participate in this study. The genotype status of all participants was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. Platelet aggregation in patients with cerebral infarction receiving aspirin (100 mg/day) for at least 7 days, was measured by optical transmission aggregometry. Results and discussion:, Only three alleles of GP Ib ,, namely, B, C and D, were found. Type A was not found in the Chinese Han participants. Aspirin-sensitive patients were significantly more often of CC genotype than aspirin-semi-responders. Conclusions:, Only three types of alleles B, C and D were detected in the north-eastern region of China. The CC genotype of the VTNR polymorphism in GPIb appears to be more sensitive to the inhibitory action of low-dose aspirin. [source] Accuracy of transcranial Doppler sonography for predicting cerebral infarction in aneurysmal subarachnoid hemorrhageJOURNAL OF CLINICAL ULTRASOUND, Issue 8 2006Ji-Yong Lee MD Abstract Purpose. To evaluate the accuracy of transcranial Doppler (TCD) sonography using different criteria for predicting cerebral infarction due to symptomatic vasospasm. Methods. We retrospectively evaluated the clinical and radiologic data of consecutive patients admitted with acute aneurysmal subarachnoid hemorrhage (SAH) in the anterior cerebral circulation between January 2001 and June 2002. TCD sonographic examinations were performed on alternate days up to 20 days after admission. Cerebral infarction was defined on CT as a new hypodensity in the vascular distribution with corresponding clinical symptoms. Vasospasm was diagnosed as mild or severe when TCD sonography revealed a mean blood flow velocity (MBFV) greater than 120 and 180 cm/s in the middle or anterior cerebral artery and in the intracranial part of the internal carotid artery, respectively. Results. A total of 93 patients with aneurysmal SAH in the anterior cerebral circulation were included. Vasospasm was demonstrated by TCD sonography in 60 patients (64.5%) and was shown via multivariable logistic regression analysis to be predictive of cerebral infarction (OR 3.11, 95% CI 1.46,6.59), with an 82.6% and 69.6% sensitivity, a 41.4% and 77.1% specificity, a 31.7% and 50.0% positive predictive value, and an 87.9% and 88.5% negative predictive value when the MBFV was greater than 120 and 180 cm/s, respectively. Conclusions. Vasospasm on TCD was found to be predictive of symptomatic cerebral infarction on CT, but its positive predictive value remained low despite the adoption of restrictive TCD criteria for vasospasm. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:380,384, 2006 [source] 9-Cis-retinoic acid reduces ischemic brain injury in rodents via bone morphogenetic proteinJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2009Hui Shen Abstract Retinoic acid (RA), a biologically active derivative of vitamin A, has protective effects against damage caused by H2O2 or oxygen-glucose deprivation in mesangial and PC12 cells. In cultured human osteosarcoma cells, RA enhances the expression of bone morphogenetic protein-7 (BMP7), a trophic factor that reduces ischemia- or neurotoxin-mediated neurodegeneration in vivo. The purpose of this study is to examine whether RA reduces ischemic brain injury through a BMP7 mechanism. We found that intracerebroventricular administration of 9-cis-retinoic acid (9cRA) enhanced BMP7 mRNA expression, detected by RT-PCR, in rat cerebral cortex at 24 hr after injection. Rats were also subjected to transient focal ischemia induced by ligation of the middle cerebral artery (MCA) at 1 day after 9cRA injection. Pretreatment with 9cRA increased locomotor activity and attenuated neurological deficits 2 days after MCA ligation. 9cRA also reduced cerebral infarction and TUNEL labeling. These protective responses were antagonized by the BMP antagonist noggin given 1 day after 9cRA injection. Taken together, our data suggest that 9cRA has protective effects against ischemia-induced injury, and these effects involve BMPs. © 2008 Wiley-Liss, Inc. [source] Melatonin influences the proliferative and differentiative activity of neural stem cellsJOURNAL OF PINEAL RESEARCH, Issue 4 2007Takahiro Moriya Abstract:, Though melatonin has a wide variety of biological functions, its effects on the neural stem cells (NSCs) is still unknown. In this study, we examined the effects of melatonin at either physiological (0.01,10 nm) or pharmacological concentrations (1,100 ,m) on the proliferation and neural and astroglial differentiation of NSCs derived from the mouse embryo striatum using an in vitro culture system. We found that melatonin at pharmacological concentrations, but not at physiological concentrations, suppressed epidermal growth factor (EGF)-stimulated NSC proliferation (increment of viable cells, DNA synthesis and neurosphere formation) in a concentration-dependent manner. Furthermore, treatment with melatonin at a pharmacological concentration during the proliferation period facilitated 1% FBS-induced neural differentiation of NSCs without affecting the astroglial differentiation. In contrast, the treatment with melatonin at pharmacological concentrations during the differentiation period decreased the neural differentiation of the NSCs. As with melatonin, MCI-186, an antioxidant, suppressed EGF-stimulated NSC proliferation and facilitated the subsequent neural differentiation of NSCs. These results suggest that melatonin exerts potent modulatory effects on NSC functions including the suppression of the proliferation and facilitation of neuronal differentiation, likely via its antioxidant activity. As neurogenesis is thought to play an important role in ameliorating the deficit in neurodegenerative diseases, melatonin might be beneficially used for the treatment diseases such as cerebral infarction. [source] Animal Model with Detrusor Overactivity Caused by Cerebral Infarction as a Useful Tool for Pharmacological Therapeutic ApproachesLUTS, Issue 2009Osamu YOKOYAMA Supra-pontine lesions resulting from neurological disorders, such as vascular disease or Parkinson's disease, cause a sense of urgency, frequency, and/or urge incontinence, all of which constitute an overactive bladder. This phenomenon is due in part to the elimination of cortical inhibitory control of the micturition center in the pontine and in part to facilitation of excitatory control. These controls consist of several neurotransmitter systems that include acetylcholine, dopamine, and glutamate. The development of detrusor overactivity following cerebral infarction is mediated by upregulation and downregulation of excitatory and inhibitory inputs of these neurotransmitter systems to the micturition center in the brain, respectively. [source] Pathological changes in the cerebral medullary arteries of five autopsy cases of malignant nephrosclerosis: Observation by morphometry and reconstruction of serial sectionsNEUROPATHOLOGY, Issue 3 2003Riki Okeda Hypertension (HT) is a serious risk factor of not only cerebral infarction and bleeding, but also Binswanger's encephalopathy (BE). In BE especially, severe stiffening of the cerebral medullary arteries because of hypertensive changes with loss of medial smooth muscle cells (SMC) occurs, which induces diffuse atrophy of the cerebral white matter. But, it is not yet ascertained whether HT is particularly severe in BE. Therefore, a spectrum of the pathological changes of the cerebral arteries were investigated by reconstruction of serial sections and morphometry of the medial thickness in five autopsied patients with malignant nephrosclerosis (MN) of exacerbated form. Each presented clinically acute progression of long-standing HT at the terminal stage and pathologically typical renal changes. The heartweight was 380,900 g. Morphometry of the medial thickness of the arachnoid arteries presented significant medial hypertrophy in four cases of MN, but in the medullary arteries it presented in only two cases with marked cardiomegaly of 700 g and 900 g. In four cases of MN, only a few medullary arteries showed slight pathological changes. However, in another case with cardiomegaly of 900 g, all 10 medullary arteries showed multiple segments of atheroma, medial SMC loss, and prominent dilatation; edematous concentric intimal fibrosis with luminal obstruction and atrophy of the white matter were absent. In conclusion, only one case of MN showing marked cardiomegaly of 900 g presented severe pathological changes of the cerebral medullary arteries comparable with those of BE, although other MN-cases showing severe cardiac hypertrophy presented only trivial arterial changes. Therefore, the cerebral medullary artery seems to be protected from HT, yet it is involved in a case of severe and long-standing HT inducing an extreme cardiomegaly. [source] Overactive bladder in diabetes: A peripheral or central mechanism?,NEUROUROLOGY AND URODYNAMICS, Issue 6 2007Chiharu Yamaguchi Abstract Aims To study diabetic cystopathy with reference to overactive bladder (OAB). Methods We retrospectively analyzed diabetic cystopathy in our digitized database that comprised 2300 case records, including data from a lower urinary tract symptoms questionnaire, data from a urodynamic study, and data from neurological examinations. Results Diabetic cystopathy was seen in 4% of cases (84 cases): 58 males, 26 females; mean age, 60.8 years; duration of diabetes, 143.5 months; HbA1C, 7.7 %. In addition to large post-void residual and decreased sensation, OAB, detrusor overactivity (DO), and increased bladder sensation were seen in 55%, 42%, and 14%, respectively. The frequency of DO in patients with increased bladder sensation was 58%. DO increased with age, but not with the duration of diabetes. A brain MRI was performed in 32 cases. The frequency of multiple cerebral infarction (MCI) in patients with DO was 76.5%. The remaining 23.5% of patients with DO had no MCI, and the remaining 42% with increased bladder sensation had no DO. Conclusions OAB commonly occurs in diabetic cystopathy. Both central and peripheral mechanisms are involved, e.g., MCI due to diabetic cerebral vasculopathy for the DO, and, to a lesser extent, peripheral nerve irritation for the DO and increased bladder sensation. Neurourol. Urodynam. 26:807,813, 2007. © 2007 Wiley-Liss, Inc. [source] Improvement of bladder storage function by ,1-blocker depends on the suppression of C-fiber afferent activity in rats,NEUROUROLOGY AND URODYNAMICS, Issue 5 2006Osamu Yokoyama Abstract Aims ,1-blockers improve voiding symptoms through the reduction of prostatic and urethral smooth muscle tone; however, the underlying mechanism of improvement of storage symptoms is not known. Using a rat model of detrusor overactivity caused by cerebral infarction (CI), we undertook the present study to determine whether the effect of an ,1-blocker, naftopidil, is dependent on the suppression of C-fiber afferents. Methods To induce desensitization of C-fiber bladder afferents, we injected resiniferatoxin (0.3 mg/kg, RTX) sub-cutaneously to female Sprague-Dawley rats 2 days prior to left middle cerebral artery occlusion (MCAO) (RTX-CI rats). As controls we used rats without RTX treatment (CI rats). MCAO and insertion of a polyethylene catheter through the bladder dome were performed under halothane anesthesia. We investigated the effects on cystometrography (CMG) of intravenous (i.v.), intracerebroventricular (i.c.v.), or intrathecal (i.t.) administration of naftopidil in conscious CI rats. Results Bladder capacity (BC) was markedly reduced after MCAO in both RTX-CI and CI rats. I.v. administration of naftopidil significantly increased BC in CI rats without an increase in residual volume, but it had no effects on BC in RTX-CI rats. I.t. administration of naftopidil significantly increased BC in CI but not in RTX-CI rats. Conclusions These results suggest that naftopidil has an inhibitory effect on C-fiber afferents in the lumbosacral spinal cord, improving BC during the storage phase. Neurourol. Urodynam. © 2006 Wiley-Liss, Inc. [source] Metabolites from cerebrospinal fluid in aneurysmal subarachnoid haemorrhage correlate with vasospasm and clinical outcome: a pattern-recognition 1H NMR studyNMR IN BIOMEDICINE, Issue 1 2005Victoria G. Dunne Abstract Following subarachnoid haemorrhage the most significant complication is sustained cerebral vascular contraction (vasospasm), which may result in terminal brain damage from cerebral infarction. Despite this, the biochemical cause of vasospasm remains poorly understood. In this study, the global high-concentration metabolite composition of CSF has been correlated with patient outcome after subarachnoid haemorrhage using multivariate statistics and 1H NMR spectroscopy. In total, 16 patients with aneurysmal subarachnoid haemorrhage (aSAH) were compared with 16 control patients who required a procedure where CSF was obtained but did not have aSAH. Multivariate statistics readily distinguished the aSAH group from the heterogeneous control group, even when only those controls with blood contamination in the CSF were used. Using principal components analysis and orthogonal signal correction, vasospasm was correlated to the concentrations of lactate, glucose and glutamine. These pattern recognition models of the NMR data also predicted Glasgow Coma Score (54% within ±,1 of the actual score on a scale of 1,15 for the whole patient group), Hunt and Hess SAH severity score (88% within ±,1 of the actual score on a scale of 1,5 for the aSAH group) and cognitive outcome scores (78% within ±,3 of the actual score on a 100% scale for the whole patient group). Thus, the approach allowed the prediction of outcome as well as confirming the presence of aSAH. Copyright © 2004 John Wiley & Sons, Ltd. [source] In-vivo visualization of phagocytotic cells in rat brains after transient ischemia by USPIONMR IN BIOMEDICINE, Issue 4 2002M. Rausch Abstract Cerebral ischemia provokes tissue damage by two major patho-physiological mechanisms. Direct cell necrosis is induced by diminished access of neurons and glia to essential nutrients such as glucose and oxygen leading to energy failure. A second factor of cellular loss is related to the activation of immune-competent cells within and around the primary infarct. While granulocytes and presumably monocytes are linked to the no-reflow phenomenon, activated microglia cells and monocytes can release cytotoxic substrates, which cause delayed cell death. As a consequence the infarct volume will increase, despite restoration of cerebral perfusion. In the past, visualization of immune competent cells was only possible by histological analysis of post-mortem tissue. However, contrast agents based on small particles of iron oxide are known to accumulate in organs rich in cells with phagocytotic function. These particles can be tracked in vivo by MRI methods based on their relaxation properties. In the present study, the spatio-temporal distribution of USPIO particles was monitored in a rat model of transient cerebral infarction using T1 - and T2 -weighted MRI sequences. USPIO were detected in vessels at 24,h after administration. At later time points specific accumulation of USPIO was observed within the infarcted hemisphere, with maximal signal enhancement on day 2. Their detectability based on T1 -contrast disappeared between day 4 and day 7. Immuno-histochemically (IHC) stains confirmed the presence of macrophages, presumably blood-derived monocytes within areas of T1 signal enhancement. Direct visualization of iron-burdened macrophages by IHC was only possible later than day 3 after occlusion. Copyright © 2002 John Wiley & Sons, Ltd. [source] Catastrophic multiple organ ischemia due to an anti-Pr cold agglutinin developing in a patient with mixed cryoglobulinemia after treatment with rituximab,AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2009Joshua Ruch Cold agglutinin disease occurring with cryoglobulinemia is a rare occurrence. Here, we report a patient with mixed cryoglobulinemia that was treated with rituximab and, after response, developed an anti-Pr cold agglutinin that manifested with hemolysis and microvascular occlusion causing mesenteric ischemia and cerebral infarction. Unlike previous reports of patients with cryoglobulinemia and cold agglutinin disease, our patient did not have a detectable cryoprecipitate when his cold agglutinin manifested. Am. J. Hematol, 2009. © 2008 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||||||||||||||