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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

More than 60% of newborns with severe congenital cardiac disease develop perioperative brain injuries. Known risk factors include: pre-operative hypoxemia, cardiopulmonary bypass characteristics, and post-operative hypotension. Infection is an established risk factor for white matter injury in premature newborns. In this study, we examined term infants with congenital cardiac disease requiring surgical repair to determine whether infection is associated with white matter injury. Acquired infection was specified by site - bloodstream, pneumonia, or surgical site infection - according to strict definitions. Infection was present in 23 of 127 infants. Pre- and post-operative imaging was evaluated for acquired injury by a paediatric neuroradiologist. Overall, there was no difference in newly acquired post-operative white matter injury in infants with infection (30%), compared to those without (31%). When stratified by anatomy, infants with transposition of the great arteries, and bloodstream infection had an estimated doubling of risk of white matter injury that was not significant, whereas those with single ventricle anatomy had no apparent added risk. When considering only infants without stroke, the estimated association was higher, and became significant after adjusting for duration of inotrope therapy. In this study, nosocomial infection was not associated with white matter injury. Nonetheless, when controlling for risk factors, there was an association between bloodstream infection and white matter injury in selected sub-populations. Infection prevention may have the potential to mitigate long-term neurologic impairment as a consequence of white matter injury, which underscores the importance of attention to infection control for these patients.
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PMID:Infection and white matter injury in infants with congenital cardiac disease. 2155 28

Understanding the vascular injury pathway is crucial to developing rational strategies for secondary stroke prevention in children. The multicenter Vascular Effects of Infection in Pediatric Stroke (VIPS) cohort study will test the hypotheses that (1) infection can lead to childhood arterial ischemic stroke by causing vascular injury and (2) resultant arteriopathy and inflammatory markers predict recurrent stroke. The authors are prospectively enrolling 480 children (aged 1 month through 18 years) with arterial ischemic stroke and collecting extensive infectious histories, blood and serum samples (and cerebrospinal fluid, when clinically obtained), and standardized brain and cerebrovascular imaging studies. Laboratory assays include serologies (acute and convalescent) and molecular assays for herpesviruses and levels of inflammatory markers. Participants are followed prospectively for recurrent ischemic events (minimum of 1 year). The analyses will measure association between markers of infection and cerebral arteriopathy and will assess whether cerebral arteriopathy and inflammatory markers predict recurrent stroke.
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PMID:The vascular effects of infection in Pediatric Stroke (VIPS) Study. 2161 22

Background. Infections increase the risk of ischemic stroke (IS) and may worsen IS prognosis. Adverse effects of in-hospital infections on stroke outcome were also reported. We aimed to study the prevalence of pre- and poststroke infections and their impact on IS outcome. Methods. We analysed clinical data of 2066 IS patients to assess the effect of pre-stroke and post-stroke infections on IS severity, as well as short-term (up to 30 days) and long-term (90 days) outcome. The independent impact of infections on poor outcome (death, death/dependency) was investigated by use of logistic regression analysis. The effect of antibiotic therapy during hospitalization on the outcome was also assessed. Results. Pre-stroke infections independently predicted worse short-term outcome. In-hospital infections were associated with worse short-term and long-term IS prognosis. Antibacterial treatment during hospitalization did not improve patients' outcome. Conclusions. Prevention of infections may improve IS prognosis. The role of antibiotic therapy after IS requires further investigations.
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PMID:Infections and ischemic stroke outcome. 2176 26

Background. The activation of inflammatory cascades triggered by ischemic stroke may play a key role in the development of infections. Methods. Patients admitted with ischemic stroke within 24 hours were prospectively enrolled. Biomarkers of infection were measured on days 1, 3, and 5. The patients were continuously monitored for predefined infections. Results. Patients with infection were older (OR 1.06 per year, 95% CI 1.01-1.11) and had a higher National Institute of Health Stroke Scale Score (NIHSS, OR 1.21, 95% CI 1.10-1.34), localization in the insula, and higher stroke volumes on diffusion-weighted imaging. The maximum temperature on days 1 and 3, leukocytes, interleukin-6, lipopolysaccharide-binding protein on days 1, 3, and 5, C-reactive protein on days 3 and 5, and procalcitonin on day 5 were higher and HLA-DR-expression on monocytes on days 1, 3, and 5 lower in patients with infection. Age and NIHSS predicted the development of infections. Infection was an independent predictor of poor functional outcome. Conclusions. Severe stroke and increasing age were shown to be early predictors for infections after stroke.
Stroke Res Treat 2011
PMID:Infection after acute ischemic stroke: risk factors, biomarkers, and outcome. 2178 73

Although several risk factors for stroke have been identified, one-third remain unexplained. Here we show that infection with Streptococcus mutans expressing collagen-binding protein (CBP) is a potential risk factor for haemorrhagic stroke. Infection with serotype k S. mutans, but not a standard strain, aggravates cerebral haemorrhage in mice. Serotype k S. mutans accumulates in the damaged, but not the contralateral hemisphere, indicating an interaction of bacteria with injured blood vessels. The most important factor for high-virulence is expression of CBP, which is a common property of most serotype k strains. The detection frequency of CBP-expressing S. mutans in haemorrhagic stroke patients is significantly higher than in control subjects. Strains isolated from haemorrhagic stroke patients aggravate haemorrhage in a mouse model, indicating that they are haemorrhagic stroke-associated. Administration of recombinant CBP causes aggravation of haemorrhage. Our data suggest that CBP of S. mutans is directly involved in haemorrhagic stroke.
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PMID:The collagen-binding protein of Streptococcus mutans is involved in haemorrhagic stroke. 2195 19

Cerebrovascular disease is a complication of a variety of infections affecting the central nervous system (CNS). Infection may cause vasculitis affecting primarily the vessels at the base of the brain in the setting of meningitis; an immune-mediated parainfectious process leading to vasospasm or thrombosis; or a hypercoagulable state in combination with endothelial dysfunction resulting from activation of inflammatory and procoagulant cascades. Although systemic signs and symptoms may be present to aid in the diagnosis, cerebral infarction secondary to infection may be indistinguishable from more typical causes of stroke. Confirmation of an infectious vasculitis may also be challenging, as brain biopsy, the gold standard for diagnosis, is rarely pursued. In many CNS infections, vascular complications portend a poor prognosis as they are often associated with devastating neurologic outcomes, including death, underscoring the importance of early recognition and appropriate therapy. In this review, we address bacterial, viral, fungal, and parasitic causes of cerebrovascular disease.
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PMID:Cerebrovascular disease in central nervous system infections. 2196 46

Infection with the tick-borne spirochete, BORRELIA BURGDORFERI, affects the nervous system in well-defined ways. Accurate diagnostic tools and effective therapeutic regimens are now well established. Persistent misconceptions about (1) the role and interpretation of laboratory tests, (2) what is and is not evidence of nervous system infection, and (3) what constitutes an expected response to treatment have fostered widespread perceptions that this disease is highly controversial. Infection causes the classically described triad of meningitis, radiculoneuritis, and cranial neuritis; however, virtually every known neurologic disorder has been blamed on this infection. For most (multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer disease, Parkinson disease), evidence is scant, nonexistent, or coincidental. For some (cerebral vasculitis with stroke, optic neuritis) a few case reports suggest a rare possible causal link.
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PMID:Nervous system lyme disease: is there a controversy? 2196 48

Autoimmune encephalitis related to voltage-gated potassium channel (VGKC) antibodies can occur as a complication of cancer but, more frequently, as a non-paraneoplastic disorder. The prompt recognition and treatment could mitigate the morbidity associated with this entity, but the broad-spectrum of neurological manifestations often makes the diagnosis a challenge. The authors describe, here, a unique case of autoimmune encephalitis related to VGKC antibodies preceded by an ischaemic stroke. Conditions associated with the stroke (infection, seizures, metabolic disturbances) had delayed the diagnosis. The authors suggest that autoimmune encephalitis needs to be taken into consideration as part of a differential diagnosis in patients with prolonged encephalopathy following an ischaemic stroke. Infection may trigger an inflammatory response. In addition, the rupture of blood brain barrier that occurs in stroke may have a pathogenic role by allowing antibodies to gain access to the central nervous system.
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PMID:Stroke preceding autoimmune encephalitis with neuronal potassium channel antibody. 2260 45

Infection in the acute phase of stroke has been identified as an independent predictor of poor outcome, both in the short and intermediate term. Various factors raising the risk of developing an infection (exposure to multiple pathogens, disruption of the protective function of the mucous membranes and a state of relative immunosuppression) coexist during the acute phase of stroke. Several risk factors have been identified for their development (especially increasing age and stroke severity). It has been proposed that infection contributes to a worse prognosis through different mechanisms, notably the development of an inflammatory response to brain tissue (with a potential to add secondary damage to that caused by the ischemic insult). Clinical trials evaluating the prophylactic and early administration of antibiotics to reduce the incidence of infection in the acute phase of stroke have yielded inconsistent results. Immunomodulating strategies, which may provide therapeutic alternatives in the future, are currently being evaluated.
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PMID:[Advances in the pathophysiology and management of infections in the acute phase of stroke]. 2265 18

Infections are a major cause of death and morbidity after acute injury of the central nervous system (CNS). Acute lesions of the CNS alter immune homeostasis contributing to the development of immunosuppression (IS), and making the bed of the infection. IS results in a decreased phagocytic functions of neutrophils and macrophages as well as monocyte deactivation (decreased capacity of antigen presentation to lymphocytes). The immune abnormalities occur very quickly and may last for weeks. The neurovegetative system is closely connected to the secondary lymphoid organs where cells of innate immunity receive information from injured organs inducing the long lasting adaptive immune response (immune synapse). The sympathetic system is critically involved in the IS through production of anti-inflammatory mediators like interleukin-10. This may prove important as all types of acute injury of the CNS can lead to direct damage to sympathetic centers. Specialized units of care for ischemic stroke, taking into account the risk of infection related to the IS, have improved the prognosis until 18th month after the initial damage of the SNC. It is now well recognized that the improved long-term prognosis is related with the secondary prevention of recurrent ischaemia as well as aggressive management of pulmonary infections. A better understanding of the pathophysiology of IS can be considered in the near future, opening the door to immunomodulatory therapeutic trials.
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PMID:[Brain injury, immunity and infections]. 2268 65


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