Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective study of 100 newborns and young babies suffering from purulent meningitis was carried out over a period of 11 months in the radiology department of CHU in Treichville. All the children included in the study were hospitalised in the pediatric department of the CHU. We found cerebral complications in 76% of cases. The most frequent complication was ventricular dilation which occurred in 82.6% of cases. Pericerebral bleeding occurred in 9.3%, cerebral ischemia in 3.5%, brain abscesses in 2.3% and ventriculitis in 2.3% of cases. Our study demonstrated the two important uses of trans-fontanelle ultrasound scans in the study of meningitis: (i) in diagnosis, for the detection of cerebral complications; (ii) in treatment, interventional use of ultrasound makes it possible to evacuate intra-cranial septic fluids.
 ...
PMID:[Fontanel ultrasonography of purulent meningitis in children in Abidjan (Ivory Coast)]. 929 7

This study explored the role of inducible nitric oxide (NO) synthase (iNOS) in an infant rat model of group B streptococcal meningitis. Brain iNOS activity increased during meningitis (P < .001), and iNOS was detected by immunocytochemistry in the walls of meningeal vessels and cells of the cerebrospinal fluid (CSF) inflammation. Animals treated with iNOS inhibitor aminoguanidine (AG; 130 mg/kg every 8 h) had reduced NO production (P < .05), higher CSF bacterial titers (P < .05), and increased incidence of seizures (P < .01) compared with untreated infected animals. AG also increased areas of severe hypoperfusion in the cortex (31% +/- 14% in controls vs. 56% +/- 16% in AG; P < .01) and the extent of cortical neuronal injury, both when administered at the time of infection (P < .05) and in established meningitis (P < .02). Thus, NO produced by iNOS may be beneficial in this model of experimental meningitis by reducing cerebral ischemia.
 ...
PMID:Inducible nitric oxide synthase and the effect of aminoguanidine in experimental neonatal meningitis. 949 49

Symptomatic vasospasms or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction is currently the most important cause of morbidity after acute subarachnoid hemorrhage. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. There is typically a gradual deterioration of the level of consciousness accompanied by focal neurological deficits. 30% of patients who survived aneurysmal SAH develop delayed cerebral ischemia secondary to vasospasm. Vasospasm produces cerebral ischemia and infarction by hemodynamic mechanisms. Vasospasm is an important independent predictor of poor outcome after aneurysmal SAH. Other conditions than aneurysmal subarachnoid hemorrhage such as trauma, tumors, unruptured aneurysms, meningitis and ruptured AVM may be associated with vasospasm.
 ...
PMID:[Epidemiology, clinical study and pathology of vasospasm]. 1036 47

Cerebrospinal fluid (CSF) has anti-infectious defense abilities similar to those of the serum of a neutropenic patient. A septic inoculation as in case of nosocomial meningitis (NM), results rapidly in microbial proliferation with major alterations to the blood brain barrier, cerebral oedema and loss of autoregulation of the cerebral blood flow. Arterial hypotension during NM may induce focal or global cerebral ischaemia. The incidence of NM is increasing, staphylococci and Gram negative bacilli being the most frequent pathological agents. Clinical symptoms are not specific in this postoperative and post-traumatic context. In this context, the analysis of pleocytosis and the increased protein content of CSF is disturbing. Numerous clinical conditions may cause NM. Among them, NM from spinal puncture is an important issue for anaesthetists, while combined epidural and spinal anaesthesia carry the highest risks. Cutaneous contamination plays a major role. Half of the post-operative infections after neurosurgery are due to NM, and CSF leakage, iterative operations and surgery in contaminated conditions are the main risk factors. Antibioprophylaxis for postoperative NM is validated for clean and clean-contaminated surgery. Some consider that only procedures of more than two hours require this prophylaxis. Prophylaxis is targeted on staphylococci. Other preventive measures (drainage of less than 24 h, head shaving and prevention of CSF leakage) are of major importance. Antibiotherapy should be guided by the same considerations as for community acquired meningitis, associated with specific issues in the surgical context (presence of foreign material and CSF blockage).
 ...
PMID:[Nosocomial meningitis in the adult]. 1061 53

By using an infant rat model of pneumococcal meningitis, we determined whether endothelins contribute to neuronal damage in this disease. Cerebrospinal fluid analysis demonstrated a significant increase of endothelin-1 in infected animals compared with uninfected controls. Histopathological examination 24 hours after infection showed brain damage in animals treated with ceftriaxone alone (median, 9.2% of cortex; range, 0-49.1%). In infected animals treated intraperitoneally with the endothelin antagonist bosentan (30 mg/kg, every 12 hours) also, injury was reduced to 0.5% (range, 0-8.6%) of cortex. Cerebral blood flow was reduced in infected animals (6.5 +/- 4.0 ml/min/100 g of brain vs 14.9 +/- 9.1 ml/min/100 g in controls. Treatment with bosentan restored cerebral blood flow to levels similar to controls (12.8 +/- 5.3 ml/min/100 g). Improved blood flow was not mediated by nitric oxide production, because bosentan had no effect on cerebrospinal fluid or plasma nitrite/nitrate concentrations at 6, 12, or 18 hours. These data indicate that endothelins contribute to neuronal injury in this model of pneumococcal meningitis by causing cerebral ischemia.
 ...
PMID:Endothelin inhibition improves cerebral blood flow and is neuroprotective in pneumococcal meningitis. 1071 52

In this study, we tested the hypothesis that decreased cerebral perfusion pressure (CPP) induces cerebral ischemia and worsen brain damage in neonatal bacterial meningitis. Meningitis was induced by intracisternal injection of 10(9) colony forming units of Escherichia coli in 21 newborn piglets. Although CPP decreased significantly at 8 hr after bacterial inoculation, deduced hemoglobin (HbD), measured as an index of changes in cerebral blood flow by near infrared spectroscopy, did not decrease significantly. In correlation analyses, CPP showed significant positive correlation with brain ATP and inverse correlation with brain lactate levels. CPP also correlated positively with HbD and oxidized cytochrome aa3 (Cyt aa3) by near infrared spectroscopy. However, CPP did not show significant correlation with cerebral cortical cell membrane Na+,K+-ATPase activity, nor with levels of lipid peroxidation products. In summary, decreased CPP observed in this study failed to induce cerebral ischemia and further brain injury, indicating that cerebrovascular autoregulation is intact during the early phase of experimental neonatal bacterial meningitis.
 ...
PMID:Effects of decreased cerebral perfusion pressure on cerebral hemodynamics, brain cell membrane function and energy metabolism during the early phase of experimental Escherichia coli meningitis in the newborn piglet. 1080 99

Gp91-phox is an integral component of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex that generates reactive oxygen species (ROS) in activated circulating phagocytes. The authors previously demonstrated that gp91-phox knockout (KO) mice show significant protection from neuronal injury after cerebral ischemia--reperfusion injury, suggesting a pivotal role for this enzyme. Moreover, results from chimeric mice suggested that elimination of gp91-phox from both circulating phagocytes and a putative central nervous system (CNS) source were required to confer neuroprotection. In the current study, the authors demonstrated gp91-phox-specific immunostaining of perivascular cells in the CNS of control rats. However, after transient cerebral ischemia, gp91-phox-positive phagocytes were observed within the core ischemic region and activated microglial cells were positive in the penumbra. Such activated microglial cells were also gp91-phox-positive in the CNS of a chimpanzee with mild meningitis. Finally, in humans, both normal adult CNS tissues and isolated fetal microglial cells expressed gp91-phox mRNA. These microglia also expressed mRNA for the five other known components that comprise the NADPH oxidase complex. These data strongly suggest that microglial cells may contain a functionally active NADPH oxidase capable of generating ROS during CNS inflammation.
 ...
PMID:Induction of gp91-phox, a component of the phagocyte NADPH oxidase, in microglial cells during central nervous system inflammation. 1132 23

Twenty-eight patients with cerebral infarction secondary to chronic meningitis were retrospectively identified at our institution over a period of 5 years. They accounted for 47% (17/36) of tuberculous meningitis (TBM) and 32% (11/34) of cryptococcal meningitis cases. Single infarctions were found in 15 patients and multiple infarctions in 13. The distribution of single infarctions was: basal ganglia 7; internal capsule 3; thalamus 1; cerebellum 1; and cortical infarct 3. Therapeutic outcomes at 3 months were determined using a modified Barthel INDEX: At follow-up of 3 months or more, 10 had good outcomes while the other 18 had poor outcomes. The 18 with poor outcomes included six who died, and 12 who had severe neurological sequelae. TBM and cryptococcal meningitis shared similar clinical features, both being frequently associated with other neurological complications, including hydrocephalus, cranial nerve palsy, and seizures in our patients. However, extracranial involvement, such as spinal and pulmonary involvement, was more commonly found in TBM patients. Cerebral infarction can occur in both the acute stage and later stages of treatment. Mortality and morbidity are high, and early diagnosis and appropriate antimicrobial treatment are essential. If hydrocephalus is demonstrated, early ventricular decompression is needed to prevent further cerebral ischaemia.
 ...
PMID:Cerebral infarction in chronic meningitis: a comparison of tuberculous meningitis and cryptococcal meningitis. 1135 98

Adrenomedullin is a recently discovered 52-amino acid peptide that is a potent vasodilator and is produced in the brain in experimental models of cerebral ischemia. Infusion of adrenomedullin increases regional cerebral blood flow and reduces infarct volume after vascular occlusion in rats, and thus may represent an endogenous neuroprotectant. Disturbances in cerebral blood flow (CBF), including hypoperfusion and hyperemia, frequently occur after severe traumatic brain injury (TBI) in infants and children. We hypothesized that cerebrospinal fluid (CSF) adrenomedullin concentration would be increased after severe TBI in infants and children, and that increases in adrenomedullin would be associated with alterations in CBF. We also investigated whether posttraumatic CSF adrenomedullin concentration was associated with relevant clinical variables (CBF, age, Glasgow Coma Scale [GCS] score, mechanism of injury, and outcome). Total adrenomedullin concentration was measured using a radioimmunometric assay. Sixty-six samples of ventricular CSF from 21 pediatric patients were collected during the first 10 days after severe TBI (GCS score < 8). Control CSF was obtained from children (n = 10) undergoing lumbar puncture without TBI or meningitis. Patients received standard neurointensive care, including CSF drainage. CBF was measured using Xenon computed tomography (CT) in 11 of 21 patients. Adrenomedullin concentration was markedly increased in CSF of infants and children after severe TBI vs control (median 4.5 versus 1.0 fmol/mL, p < 0.05). Sixty-two of 66 CSF samples (93.9%) from head-injured infants and children had a total adrenomedullin concentration that was greater than the median value for controls. Increases in CSF adrenomedullin were most commonly observed early after TBI. CBF was positively correlated with CSF adrenomedullin concentration (p < 0.001), but this relationship was not significant when controlling for the effect of time. CSF adrenomedullin was not significantly associated with other selected clinical variables. We conclude adrenomedullin is markedly increased in the CSF of infants and children early after severe TBI. We speculate that adrenomedullin participates in the regulation of CBF after severe TBI.
 ...
PMID:Increased adrenomedullin in cerebrospinal fluid after traumatic brain injury in infants and children. 1156 98

Severe complications such as spinal epidural haematoma and an array of adverse neurological events leading to temporary or permanent disability have been ascribed to central neuraxial blocks. Infections (meningitis, abscesses), chemical injuries and very rarely cerebral ischaemia or haemorrhage, or both, have also been ascribed directly or indirectly to spinal and/or epidural anaesthesia. Some case reports, and very few retrospective studies, have focused their attention on the fact that central nerve blocks can cause, albeit rarely, permanent damage to the spinal cord or nerve roots, or both. The cause of this damage in many cases remains unclear. The attention of investigators and practitioners is focused both on understanding the causative mechanisms of such accidents and in identifying 'alarm events' that can arise during the administration of a central block, if any. We reviewed the international literature for the neurological complications of central neuraxial blocks to identify some events that, if they occurred during the block procedure, could be perceived as dangerous.
 ...
PMID:Neurological complications following central neuraxial blocks: are there predictive factors? 1246 82


<< Previous 1 2 3 4 Next >>