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PubMed2003

Pleuropulmonary blastoma with a large embolic cerebral infarct.

We report on a 3-year-old girl who developed a large embolic cerebral infarct 1 day after an uneventful thoracotomy to remove a large pleuropulmonary blastoma. The tumour had encased the heart and great vessels and ruptured into the left hemithorax. Pleuropulmonary blastoma is a rare, but unique, primary thoracic neoplasm in young children and, to our knowledge, the development of a secondary large embolic cerebral infarct is also uncommon and has not been reported in this tumour.

Cerebral Infarction↗
PubMed1996

Lipoprotein(a) is an independent risk factor for multiple cerebral infarctions.

In an attempt to ascertain whether Lp(a) is a risk factor for multiple cerebral infarctions (MCI), we have studied 83 patients with proven MCI and 39 subjects without MCI by computed tomography (CT). Seventy-one patients with non-insulin-dependent diabetes mellitus (NIDDM) were included: 52 with and 19 without MCI. Serum Lp(a) levels were significantly higher in patients with MCI than in subjects without MCI. There were no differences in serum Lp(a) levels between NIDDM and non-diabetic patients with MCI. The logistic regression analysis revealed that Lp(a) and hypertension were independent risk factors for the cerebral event. The current study demonstrated that Lp(a) and hypertension are significant risk factors for multiple cerebral infarctions.

Aged↗
PubMedDate not supplied

Cerebral infarction of the basal ganglia due to embolism from the heart.

We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be considered when CT scan demonstrates a deep cerebral infarct.

Adult↗
PubMed1994

Pretreatment with a competitive NMDA antagonist D-CPPene attenuates focal cerebral infarction and brain swelling in awake rats.

The purpose of the study was to assess effects of the competitive N-methyl-D-aspartate (NMDA) receptor antagonist D-(E)-4-(3-phosphonoprop-2-enyl)piperazine-2-carboxylic acid (D-CPPene) upon focal cerebral infarction and brain oedema in the rat. Focal cerebral ischaemia was produced by permanent occlusion of the middle cerebral artery under halothane anaesthesia. The anaesthetic gas was discontinued immediately after the occlusion and the rats were killed 24 hours later. Cerebral infarction and brain swelling were each assessed on the frozen brain sections at 8 predetermined coronal planes. Pretreatment with D-CPPene (4.5 mg/kg i.v. followed by continuous infusion at 3 mg/kg/h until sacrifice) 15 minutes prior to MCA occlusion, significantly reduced the volume of infarction in the cerebral hemisphere by 29% (p < 0.05). Brain swelling, obtained by subtracting the nonischaemic hemispheric volume from the ischaemic hemispheric volume, was significantly reduced with D-CPPene treatment and the mean reduction in swelling (34% less than the controls: p < 0.001) proportionately similar to the decrease in infarct volume in the same animals. These data indicate that systemic administration of the competitive NMDA receptor antagonist D-CPPene has neuroprotective effects against ischaemic brain damage, and the reduction in brain swelling occurs in parallel with the reduction in ischaemic damage.

Animals↗
PubMed2006

Geranylgeranylacetone, a noninvasive heat shock protein inducer, induces protein kinase C and leads to neuroprotection against cerebral infarction in rats.

Previous studies demonstrated the cytoprotective effect of geranylgeranylacetone (GGA), a heat shock protein (HSP) inducer, against ischemic insult. Protein kinase C (PKC) is thought to be an important factor that mediates the expression of heat shock protein 70 (HSP70) in vitro. However, the signaling pathways in the brain in vivo after oral GGA administration remain unclear. We measured and compared infarction volumes to investigate the effect of GGA on cerebral infarction induced by permanent middle cerebral artery (MCA) occlusion in rats. To clarify the relationship between PKC induction and HSP70 expression, we determined the amounts of HSP70 and PKC proteins after GGA administration by immunoblotting. We evaluated the effects of pretreatment with chelerythrine (CHE), a specific PKC inhibitor, on expressions of PKC and HSP70 proteins with immunoblotting. Neuroprotective effects of GGA (pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia) were prevented by CHE pretreatment, which indicates that PKC may mediate the GGA-dependent protection. Oral GGA-induced HSP70 expression induced PKC delta, and GGA pretreatment enhanced ischemia-induced HSP70, both of which were prevented by CHE pretreatment. These results suggest that a single oral dose of GGA induces PKC delta and promotes HSP70 expression in the brain and that GGA plays an important role in neuroprotection against cerebral ischemia.

Alkaloids↗
PubMedDate not supplied

Echocardiographic evaluation of young adults with nonhemorrhagic cerebral infarction.

We reviewed echocardiographic findings in patients aged 15 to 45 years with acute nonhemorrhagic cerebral infarction (NHCI). Among 132 patients with NHCI, 96 (72.7%) had M-mode and two-dimensional echocardiography, including contrast echocardiography with intravenous saline injection when clinically indicated. Echocardiograms were abnormal in 33 patients. Of these, 7 had other conditions that could cause NHCI. Echocardiography corroborated the clinical diagnosis of a cardiogenic source for cerebral infarction in 17 others. The other 9 had no other clues for cardiovascular disease. Potential etiologies of NHCI diagnosed by echocardiography in these 9 cases included: paradoxical embolism, 5 patients; right atrial myxoma, 1; rheumatic mitral valve vegetation, 1; myxomatous mitral valve (marantic endocarditis at postmortem), 1; and left atrial enlargement associated with decreased left ventricular function, 1. Routine echocardiography frequently conveys useful information in patients under age 45 with NHCI. In young patients with cerebral embolism of unknown etiology if routine M-mode and two dimensional echocardiographic studies are normal, contrast echocardiographic studies should be performed to rule out intracardiac shunts and the possibility of paradoxical cerebral embolism.

Adolescent↗
PubMed1986

Lp(a) lipoprotein as a risk factor for coronary heart disease and cerebral infarction.

Attempts were made to prepare antisera monospecific for Lp(a) lipoprotein and to investigate the distribution of subjects according to plasma levels of Lp(a) in Japanese controls and patients with coronary heart disease or cerebral infarction. Positive plasma reactions to the double diffusion test for Lp(a) (Ouchterlony) were observed in 32.3% of the healthy Japanese subjects, which is similar to results previously reported in western countries. The plasma threshold level of 17 mg/dl was considered an appropriate point for dividing subjects into positive and negative groups depending on reactions to the double diffusion test. When subjects were divided into two groups at 17 mg/dl, a significant association was found between a high plasma level of Lp(a) and either coronary heart disease or cerebral infarction in the distribution of the cortical artery. These results suggest that Lp(a) may play an important part as a risk factor for coronary heart disease and cerebral infarction.

Aged↗
PubMed2003

Coagulation and fibrinolytic activity in patients with acute cerebral infarction.

OBJECTIVE: To measure the concentration of D-dimer (DD), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen (PLG) activity in plasma and cerebrospinal fluid in patients with acute cerebral infarction and to investigate their clinical significance. METHODS: The concentrations of D-dimer, t-PA, and PAI-1 in plasma and cerebrospinal fluid in patients were measured by enzyme-linked immunosorbent assay (ELISA). The PLG biological activity was detected using the chromophore method. The results were compared with those of the controls. RESULTS: The concentrations of D-dimer, t-PA and PAI-1 in cerebrospinal fluid and plasma in patients with acute cerebral infarction were much higher than those of normal subjects (P < 0.01). Conversely, the level of PLG activity was significantly lower in the patients than in the controls (P < 0.01). CONCLUSION: Hypercoagulability and secondary hyperfibrinolysis exist in patients with acute cerebral infarction.

Acute Disease↗
PubMed2007

Development of cerebral infarction shortly after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Cerebral infarction (CI) occurring soon after intracerebral hemorrhage (ICH) has been rarely reported. The purpose of the present study was to characterize this condition and discuss the possible pathophysiology. METHOD: We retrospectively studied 6 patients who developed CI within 10 days after the onset of ICH. RESULTS: The initial ICHs were located in the putamen (n=3), thalamus (n=2) and cerebellum (n=1), and were considered to be caused by hypertension in all of the patients. They showed sudden worsening (n=4) or change in neurologic symptoms (n=2) within 10 days after the initial ICH. Follow-up imaging revealed corresponding lacunar (n=2) and territorial (n=4) infarcts. Possible factors related to the development of new CIs included mechanical compression of cerebral vessels (n=2), dehydration (n=4), hypotension (n=2), infection (n=2) and concomitant small-vessel pathology (n=2). CONCLUSIONS: ICH may predispose certain patients to the development of infarcts through a combination of mechanisms, including mechanical compression of cerebral vessels, hemodynamic instability, inflammation and concomitant small-vessel pathology.

Adult↗
PubMed1985

[NMR and CT studies in acute and late-stage cerebral infarct].

MR offers an additional non-invasive means for the investigation of cerebro-vascular disease. This new digital imaging method competes with CT. Twenty-four patients with cerebral infarcts were examined by CT and MR; of these, 12 were in the acute stage of necrosis and resorption, and 12 were examined after six weeks following the formation of cysts and glial scars. Because of the increased relaxation time of T1 and T2, there is a large signal difference between infarcted and normal brain. Consequently, cerebral infarcts can be clearly recognised during the first 24 hours. MR also has advantages in demonstrating infarcts in the pons and medulla and if one wishes to avoid contrast enhancement during CT. Problems may arise in differentiating fresh infarcts from haemorrhage and from gliomas. At the present time, the length of the procedure and its high cost justify MR in exceptional circumstances only.

Cerebral Infarction↗
PubMed2002

Cerebral infarctions in the fetus and neonate: maternal-placental-fetal considerations.

Historical data, clinical examination findings, and laboratory information must be integrated along a variable timeline that includes antepartum, intrapartum, and postnatal time periods when cerebral infarction can occur, in the context of the neonates genetic endowment. Genetic susceptibility or prenatal acquired vulnerabilities regarding stroke syndromes may set in motion a cascade of molecular pathways that ultimately cause or exacerbate brain injury when the vulnerable child experiences adverse medical conditions. The clinician must consider maternal, placental, and fetal conditions on which a stroke syndrome may be superimposed, with or without additional brain injury from other pathogenic mechanisms. Evaluation of fetal and neonatal cerebral infarction requires knowledge of mechanisms of brain injury that cross medical disciplines and may involve consultation with maternal/fetal specialists, placental and pediatric pathologists, neonatologists, geneticists, and other pediatric subspecialties. Comprehensive evaluations of survivors of cerebral infarction are needed to better understand structural and functional plasticity of the developing brain after a cerebrovascular event in the fetal and neonatal periods.

Algorithms↗
PubMed1986

Lectin (UEA-1) reaction of capillary endothelium with reference to permeability in autopsied cases of cerebral infarction.

The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-1) and the permeability of the vascular wall in human autopsied cases of cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface membrane of endothelial cells. Albumin in the neuropil of sections was demonstrated for the estimation of increased vascular permeability. The results showed that endothelial reactivity to UEA-1 was reduced in cases where death had occurred 3 to 5 days after onset of cerebral infarction. Reactivity was also diminished in cases where death had occurred after 13 and 25 days; these cases showed fresh ischemic lesions caused by re-attacks of infarction. Albumin extravasation into the neuropil was demonstrated in these intermediate cases. Chronic cases, dying after more than 52 days, showed no reduction of endothelial reactivity to UEA-1 and no albumin extravasation was proved. It was concluded that UEA-1 can be employed as a useful morphological marker for evaluation of endothelial function and vascular permeability.

Aged↗
PubMed1983

Disturbance of oxidative metabolism of glucose in recent human cerebral infarcts.

Eight patients with recent cerebral hemispheric infarction were studied with positron emission tomography and the oxygen-15 steady-state inhalation and [18F]deoxyglucose techniques to obtain values of regional cerebral blood flow, oxygen consumption, and glucose metabolism. The Sokoloff equation, used to calculate glucose metabolism, was simplified to exclude the exponential terms containing the rate constants. A value of the lumped constant quoted for normal brain (0.42) was used for infarcted regions and contralateral hemisphere. Mean regional cerebral blood flow, oxygen consumption, and glucose metabolism were all significantly depressed within the infarcts compared with the mirror regions in the contralateral cerebral hemisphere. The mean fractional extraction of oxygen was low, indicating an adequate supply of oxygen for residual oxidative metabolism. Regional oxygen consumption and glucose metabolism were significantly correlated within the infarcts, but with a relationship of 2 moles of oxygen per mole of glucose--one-third that in the contralateral hemisphere and in normal brain. Although these results suggest that the metabolizing tissue of a recent cerebral infarct utilizes aerobic glycolysis, caution about the validity of this pathophysiological observation is dictated by limitations in current positron emission tomographic tracer methodology.

Adult↗
PubMed1998

[Effects of monocyte-derived endothelin on acute cerebral infarction].

To investigate the mechanism that monocytes participate in ischemic brain injury, endothelin (ET) levels in plasma, supernatants of cultured monocytes in vitro and those pretreated by dexamethason (DXM) were assayed by radioimmunoassay in 31 patients with acute cerebral infarction and 16 patients with hypertension (served as control). Compared with the control group, the ET levels in supernatants of cultured monocytes increased and positively related with those in plasma and degree of neurological damage in the acute cerebral infarction group, while the ET levels in supernatants of cultured monocytes pretreated by DXM decreased. This suggests that intensifying the synthesis and release ET may be one of the mechanisms for the involvement of monocytes in the pathologic process of ischemic brain injury during acute cerebral infarction. DXM can improve this process by inhibition of producing monocyte-derived ET.

Adult↗
PubMed2000

Prevalence and risk factors of silent cerebral infarction in apparently normal adults.

Cerebrovascular disease is a major cause of death and disability in adults. Silent cerebral infarction (SCI) portends more severe cerebral infarctions or may lead to insidious progressive brain damage resulting in vascular dementia. This study was designed to evaluate the prevalence and risk factors of SCI in an apparently normal adult population. Nine hundred ninety-four consecutive symptom-free adults (mean age 49.0+/-7.7; men:women 830:164) who underwent brain magnetic resonance imaging at the Center for Health Promotion at Samsung Medical Center were assessed. All were neurologically normal in history and physical examination. A total of 121 SCI lesions was observed in 58 subjects. The lesion prevalence adjusted for patient age was 5.1%. There was no gender difference in prevalence. Ninety-nine lesions were <1 cm in diameter, 15 were between 1 and 2 cm, 3 were between 2 and 3 cm, and 4 were >3 cm in diameter. The most frequent site of the SCI lesion was basal ganglia, after which the periventricular white matter, cerebral cortex, and thalamus were the most frequent sites. Old age, hypertension, a history of coronary artery disease, evidence of cardiomegaly in chest radiographs, and high fasting glucose/hemoglobin A1c levels were associated with SCI on univariate analysis. Multivariate analysis demonstrated old age and hypertension to be independent risk factors for SCI, and mild alcohol consumption was revealed as an independent protective factor against SCI.

Adult↗
PubMed1980

Cerebral infarction secondary to sickle cell disease: arteriographic findings.

Cerebral angiograms were performed in 14 children with sickle cell disease and clinical findings of cerebral infarction. The angiogram was normal in four patients. Ten patients had abnormalities in the carotid artery or its branches. The internal carotid artery was stenosed or occluded usually with bilateral disease. The anterior and middle cerebral arteries were involved in nine patients and branch occlusion was frequent. The posterior fossa arteries were not involved in these patients. The risk of angiography is low if appropriate precautions are taken. In these patients the indications for arteriography were to evaluate the effects of hypertransfusion therapy on cerebrovascular disease.

Adolescent↗
PubMed2004

Cerebral infarction related to cryptococcal meningitis in an HIV-infected patient: case report and literature review.

Neurological dysfunction as the first manifestation of AIDS has been found in 10 to 20% of symptomatic human immunodeficiency virus infections. However, stroke has rarely been reported in AIDS patients. The most common causes of cerebral infarction in AIDS are central nervous system infections: toxoplasmosis, cryptococcal meningitis and tuberculosis. Potential vascular mechanisms for cerebral infarction and transient neurological deficits among AIDS patients include deposition of antigen-antibody complexes with vasculitis and infarction, and a direct toxic effect of a viral antigen or infectious agent on vascular endothelium. The role of cryptococcal meningitis in vasculopathy is still not clear. We report a case of cerebral infarction in an HIV-infected patient, with cryptococcal meningitis as the first manifestation of AIDS.

AIDS-Related Opportunistic Infections↗