Abnormalities of cerebral blood flow in the acute phase of bacterial meningitis in adults

Förderreuther, S.; Tatsch, Klaus; Km, Einhäupl; Hw, Pfister

doi:10.1007/bf00856807

Cited by 38 publications

(22 citation statements)

References 39 publications

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“…Cerebral blood flow reduction during meningitis can be global, as a result of reduced cerebral perfusion pressure (49), or focal. Vasculitis of cerebral arteries and veins caused by the surrounding subarachnoid space inflammation may lead to temporary vasospasm or to permanent thrombosis, resulting in focal cerebral ischemia (10,47,53). The pronounced ROI production associated with the cerebral vasculature and the marked restitution of cerebral cortical perfusion by PBN in our model indicate that ROI play a critical role in the vascular events during meningitis that lead to cerebral hypoperfusion.…”

Section: Discussionmentioning

confidence: 81%

“…During cerebral inflammatory states, endothelial cells and vascular smooth muscle cells have been identified as cellular sites of ROI production in the rat brain microvasculature (1). The colocalization of ROI production with cerebral blood vessels suggests that ROI may contribute to the changes of cerebral blood flow observed during bacterial meningitis (10,47). In a study in rats using a cranial window preparation, exposure of pial arterioles to live and killed GBS produced a marked and progressive vasodilatation which was prevented by ROI scavengers (11).…”

Section: Discussionmentioning

confidence: 99%

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Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Leib¹,

Kim²,

Chow³

et al. 1996

J. Clin. Invest.

219

159

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Leib¹,

Kim²,

Chow³

et al. 1996

J. Clin. Invest.

219

159

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“…A decrease in cerebral blood flow has been observed in patients with this infection [62][63][64][65]. The data on cerebral blood flow in animals with experimental meningitis are extensive and sometimes conflicting.…”

Section: Cerebral Blood Flow and Metabolism During Bacterial Meningitismentioning

confidence: 99%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

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Morbidity and mortality associated with bacterial meningitis remain high, although antibiotic therapy has improved during recent decades. The major intracranial complications of bacterial meningitis are cerebrovascular arterial and venous involvement, brain edema, and hydrocephalus with a subsequent increase of intracranial pressure. Experiments in animal models and cell culture systems have focused on the pathogenesis and pathophysiology of bacterial meningitis in an attempt to identify the bacterial and/or host factors responsible for brain injury during the course of infection. An international workshop entitled "Bacterial Meningitis: Mechanisms of Brain Injury" was organized by the Department of Neurology at the University of Munich and was held in Eibsee, Germany, in June 1993. This conference provided a forum for the exchange of current information on bacterial meningitis, including data on the clinical spectrum of complications, the associated morphological alterations, the role of soluble inflammatory mediators (in particular cytokines) and of leukocyte-endothelial cell interactions in tissue injury, and the molecular mechanisms of neuronal injury, with potential mediators such as reactive oxygen species, reactive nitrogen species, and excitatory amino acids. It is hoped that a better understanding of the pathophysiological events that take place during bacterial meningitis will lead to the development of new therapeutic regimens.Although the recent licensure of Haeniophilus influenzae type b (Hib) polysaccharide conjugate protein vaccines has had a marked impact on the incidence of invasive Hib disease in the United States and Western Europe. bacterial meningitis overall remains a significant problem worldwide. In addition, despite the introduction of new antimicrobial agents and improved diagnostic techniques, the mortality and morbidity associated with bacterial meningitis remain unacceptably high. This discrepancy between a rapid bacteriologic response at the site of infection (i.e .. eradication of viable bacteria from the CSF due to treatment with potent bactericidal agents) and the persistence of the associated neurological sequelae and mortality has prompted intense investigation over the past two decades into the pathophysiology of this disease. Indeed. recent clinical studies have employed adjunctive agents (e.g .. dexamethasone) in an attempt to reduce mortality and alleviate neurological sequelae [1][2][3][4]. These studies and the resulting recommendations regarding the use of adjunctive dexamethasone have recently been reviewed [5.6].In line with the current emphasis on the pathogenesis and pathophysiology of bacterial meningitis. two workshops were held in California in the 1980s [7]. Recognizing that many advances have been made in this field in the several years since those meetings. the Department of Neurology at the University of Munich organized a similar workshop, which was held in Eibsce. Germanv. on 25 and 26 June 1993. As IS evident from its title-"Bacterial Meningitis: Mechanisms...

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“…[11][12][13]27) Indeed, reduced regional cerebral flood flow is a frequent finding in adult patients with bacterial infection. 10,32) The angiographic findings of intracranial infection include arterial narrowing and occlusion caused by vasospasm, retrograde flow, slowing of circulation, venous dilation, massive shifting of the vessels, and extravasation of contrast medium. 5,8,13,15,18,19,23) Such angiographic changes are also influenced by vasculitis with involvement of the intima.…”

Section: Discussionmentioning

confidence: 99%

Supra- and Infratentorial Subdural Empyema Secondary to Septicemia in a Patient With Liver Abscess-Case Report-

Kojima

Yamaguchi

Okui

2004

Neurol. Med. Chir.(Tokyo)

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An 81-year-old man presented with subdural empyema in the left parietotemporal convexity 2 months after treatment under diagnoses of liver abscess and septicemia. Systemic investigation found no evidence of otorhinological or other focal infection except for liver abscess. Emergency drainage of pus was performed via a single burr hole and additional intravenous antibiotics were administered. Six weeks later, magnetic resonance imaging revealed subdural empyema in the right cerebellopontine angle in addition to recurrence of pus in the left parietotemporal subdural space. Ischemic changes were also shown in the right cerebellar hemisphere and brainstem. Although subdural empyema secondary to septicemia is rare, the possibility of this type of intracranial infection must be kept in mind, especially in compromised patients with septicemia.

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Abnormalities of cerebral blood flow in the acute phase of bacterial meningitis in adults

Cited by 38 publications

References 39 publications

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Supra- and Infratentorial Subdural Empyema Secondary to Septicemia in a Patient With Liver Abscess-Case Report-

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