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

Review of the neurological complications encountered in 83 patients who received cardiac homografts over a seven-year period leads to the following conclusions: (1) Neurological disorders are common in transplant recipients, occurring in over 50 per cent of patients. (2) Infection was the single most frequent cause of the neurological dysfunction, being responsible for one-third of all CNS complications. (3) The infective organisms were typically those considered to be usually of low pathogenicity: fungi, viruses, protozoa and an uncommon bacterial strain. (4) Other clinical neurological syndromes were related to vascular lesions, often apparently from cerebral ischaemia or infarction occurring during the surgical procedure, metabolic encephalopathies, cerebral microglioma, acute psychotic episodes and back pain from vertebral compression fractures. (5) The infectious complications and probably the development of neoplasms de novo, are related to immunosuppressive therapy which impairs virtually all host defence mechanisms and alters the nature of the host's response to infective agents or other foreign antigens. (6) Because neurological symptoms and signs were usually those of behavioural changes or deterioration in intellectual performance, the neurological examination was often of little value in diagnosing the nature or even the anatomical site of the neuropathological process. (7) The possibility of an infectious origin of the neurological manifestations must be aggressively pursued even in the absence of fever and a significantly abnormal spinal fluid examination. The diagnostic error made most frequently was to ascribe neurological symptoms erroneously to metabolic disturbances or to "intensive care unit psychosis" when they were in fact due to unrecognized CNS infection. (8) Maintenance of mean cardiopulmonary bypass pressures above 70 mmHg, particularly in patients with known arteriosclerosis, may reduce operative morbidity. (9) Though increased diagnostic accuracy is possible with routine use of a variety of radiological and laboratory techniques, two further requirements probably must be met before a significant reduction in the frequency of neurological complications will occur: the advent of greater immunospecificity in suppressing rejection of the grafted organ while preserving defences against infection; and a more effective armamentarium of antiviral and antifungal drugs.
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PMID:The neurological complications of cardiac transplantation. 19 13

Acute liver failure is a multiorgan syndrome with dramatic clinical features and, often, a fatal outcome. It is characterized by the onset of coma and coagulopathy within 6 months, and usually in < 6 weeks, from onset of illness. Viral hepatitis, drug-related liver injury, and the alcohol-acetaminophen syndrome are the most common etiologies. Altered mental status accompanied by jaundice is a hallmark of acute liver failure. A unique feature is the evolution of increased intracranial pressure due to cerebral edema. The resulting cerebral ischemia and brainstem herniation account for approximately 50% of deaths in patients with acute liver failure. Mannitol therapy may successfully treat most patients with high intracerebral pressure. Most patients demonstrate features of the multiple organ failure syndrome, including a shock-like state, renal failure, and occasionally respiratory distress syndrome. Close monitoring of volume status is necessary, since administration of large quantities of fluid may be required. Infection is also common; most pathogens are gram-positive, and fungal infections are also seen. Because an optimum therapy for acute liver failure does not yet exist, liver transplantation should be considered early, before advanced levels of coma develop. Alternative, experimental treatment modalities include heterotopic liver grafting, administration of hepatocyte growth factor, use of an extracorporeal liver-assist device, and liver cell transplantation, but none of these has attained widespread use.
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PMID:Acute liver failure. 810 86

The established risk factors for ischemic stroke do not sufficiently explain all clinical and epidemiological features of the disease, such as the winter peak of stroke incidence, the decline of stroke during this century and the time point of cerebral ischemia. A role of infectious disease as stroke risk factor may partly explain above features. Several case-control studies with both hospital and population control groups showed that acute infection within the preceding week and mainly respiratory infection of both viral and bacterial origin increase the risk of cerebral ischemia independent from other risk factors (odds ratio 2.9-14.5). Infection as a risk factor appears to be most important in young age groups. Infection may cause a procoagulant state and thus, trigger thrombosis and cerebral ischemia. There is increasing evidence for chronic infection as stroke risk factor. A case-control study indicated chronic and recurrent bronchitis to increase stroke risk. Two case-control and one cohort study showed that chronic dental infection, mainly parodontitis, is a risk factor for stroke. There are conflicting results on chronic infection with cytomegalovirus and insufficient evidence for a role of Helicobacter pylorii infection in pathogenesis of stroke. Seroepidemiological studies and analyses of carotid plaques indicate a role of Chlamydia pneumoniae in ischemic stroke. However, causality can not yet be inferred from present results. Acute and chronic infectious diseases are treatable and partly preventable conditions. Their recognition as stroke risk factors could therefore be important for stroke prevention.
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PMID:[Infection, atherosclerosis and acute ischemic cerebrovascular disease]. 1069 60

Previous infection has been shown to be a risk factor for acute cerebral ischemia. We tested the hypothesis that recent infection is also a risk factor for intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). We performed a case-control study with 56 consecutive patients with ICH, 44 consecutive patients with SAH, and 56 and 44 neurological control patients, respectively. Infection within 4 weeks was associated with SAH independently of hypertension and smoking (p = 0.049). There was no significant association between infection and ICH. Recent infection, primarily upper respiratory tract infection, may be a risk factor for SAH by contributing to the formation and rupture of aneurysms.
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PMID:Recent infection as a risk factor for intracerebral and subarachnoid hemorrhages. 1097 Oct 20

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.
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PMID:Neurological complications following central neuraxial blocks: are there predictive factors? 1246 82

Infections are a leading cause of death in stroke patients. In a mouse model of focal cerebral ischemia, we tested the hypothesis that a stroke-induced immunodeficiency increases the susceptibility to bacterial infections. 3 d after ischemia, all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss of lymphocytes and a shift from T helper cell (Th)1 to Th2 cytokine production. Adoptive transfer of T and natural killer cells from wild-type mice, but not from interferon (IFN)-gamma-deficient mice, or administration of IFN-gamma at day 1 after stroke greatly decreased the bacterial burden. Importantly, the defective IFN-gamma response and the occurrence of bacterial infections were prevented by blocking the sympathetic nervous system but not the hypothalamo-pituitary-adrenal axis. Furthermore, administration of the beta-adrenoreceptor blocker propranolol drastically reduced mortality after stroke. These data suggest that a catecholamine-mediated defect in early lymphocyte activation is the key factor in the impaired antibacterial immune response after stroke.
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PMID:Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1-like immunostimulation. 3162 20

Infection following endovascular therapy for cerebrovascular disease is a potential but rare complication. A 70-year-old lady in whom an intracranial abscess formed secondary to GDC embolisation of a giant right internal carotid artery aneurysm is reported. Computed tomography (CT) showed the abscess and staphylococcus aureus was cultured from the cerebrospinal fluid and blood. The abscess was successfully treated by antibiotic therapy. Infected Guglielmi detachable coils (GDC) may result in abscess formation in the presence of underlying cerebral ischaemia.
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PMID:Intracerebral abscess formation following embolisation of an internal carotid artery aneurysm using Guglielmi detachable coils. 1452 May 52

Infection, inflammation, and hyperthermia associated with cerebral ischaemia are known to contribute to enhanced neuronal cell loss and more severe behavioural deficits. Because neonatal exposure to an immune challenge has been shown to alter the severity of inflammatory and febrile responses to a further immune challenge experienced in adulthood, we hypothesised that this could also alter temperature responses and neuronal survival after ischaemia. Thus, male Sprague-Dawley rats were treated at postnatal day 14 with a single injection of the bacterial endotoxin lipopolysaccharide (LPS) and were examined as adults for temperature changes, behavioural deficits, and neuronal cell loss associated with global cerebral ischaemia after a two-vessel occlusion (2VO). Neonatally LPS-treated rats showed behavioural differences in a novel object exploration paradigm, as well as altered temperature responses to the 2VO compared with neonatally saline-treated controls. Interestingly, these neonatally LPS-treated rats also showed increased cell loss in the central nucleus of the amygdala, a region that is important in the processing of emotional responses, but that is not usually examined in animal models of cerebral ischaemia. No differences were seen in the CA1, CA3, or dentate gyrus regions of the hippocampus. This work shows the importance of examining brain regions other than the hippocampus in association with global ischaemia. We also highlight the importance of the early period of development in programming an animal's ability to deal with injury such as cerebral ischaemia in adulthood.
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PMID:Rat neonatal immune challenge alters adult responses to cerebral ischaemia. 1609 15

Cyclooxygenase-2 (COX-2) activity has been implicated in the pathogenesis of cerebral ischemia. To determine whether COX-2 activity within the neuron itself exacerbates hypoxic neuronal injury, neuron-enriched cultures were subjected to anoxia. Treatment with COX-2 selective antagonists decreased cell death. Neurons cultured from homozygous COX-2 gene disrupted mice were resistant to hypoxia compared to those of heterozygotes. Infection of primary neurons with AAV expressing COX-2 exacerbated cell death compared to neurons infected with enhanced green fluorescent protein (EGFP) control vector. Addition of PGE2, PGD2 or PGF2 alpha to the medium exacerbated injury, suggesting that the deleterious effects of COX-2 overexpression in hypoxia could be mediated by direct receptor mediated effects of prostaglandins. Overexpression of COX-2 did not increase expression of cyclin D1 or phosphoretinoblastoma protein (pRb), or cleavage of caspase 3 suggesting that this cell cycle mechanism does not mediate COX-2 toxicity in this model.
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PMID:Neuronal cyclooxygenase-2 activity and prostaglandins PGE2, PGD2, and PGF2 alpha exacerbate hypoxic neuronal injury in neuron-enriched primary culture. 1776 46

Infectious diseases are the most common medical complication after cerebral ischemia, inpairing both the neurological and the general medical outcome. The most frequent infectious complications are bacterial pneumonia and urinary tract infections. There is a growing body of evidence that a secondary immunosuppressive state accounts for the increased risk of infection following stroke. Infections do not only have an important impact on outcome after stroke but also are known risk factors for stroke. Thus, suitable models for investigating the relation between infections and stroke are urgently needed. Elucidating the underlying mechanisms might facilitate the development of new therapeutic strategies and improve patient outcome. Here we present recent insights into the relationship between infections and stroke, based on experimental models of post-stroke infection. In addition we give a brief overview of models that explore the impact on stroke of preceding infections.
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PMID:Models of infection before and after stroke: investigating new targets. 2016 71


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