Detection of Delayed Cerebral Vasospasm, after Rupture of Intracranial Aneurysms, by Magnetic Resonance Angiography

Tamatani, Shinichi; Sasaki, Osamu; Takeuchi, Shigekazu; Fujii, Yukihiko; Koike, Tetsuo; Tanaka, Ryuichi

doi:10.1097/00006123-199704000-00017

Cited by 37 publications

(28 citation statements)

References 28 publications

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“…45 Noninvasive angiography with computed tomography (CT) or magnetic resonance imaging (MRI) is less sensitive for detecting vasospasm. [46][47][48] Small prospective studies indicate that CT angiography (CTA) had a sensitivity of 86% to 91.6% 46,47 CTA is most sensitive for vasospasm of proximal arterial segments and for severe vasospasm and has a high negative predictive value (95%). CTA is limited by artifact from metallic aneurysm clips and coils.…”

Section: Detectionmentioning

confidence: 99%

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How Should Aneurysmal Subarachnoid Hemorrhage Be Managed?

Wendell¹,

Levine²

2010

Evidence-Based Practice of Critical Care

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Section: Detectionmentioning

confidence: 99%

“…MRA has a sensitivity for vasospasm detection of 45.6% compared with conventional angiography. 48 Transcranial Doppler ultrasonography (TCD) detects increased cerebral blood flow velocities (CBFVs) associated with vasospasm. TCD is noninvasive, may be performed daily at the bedside, and is less expensive than many other monitoring tests.…”

Section: Detectionmentioning

confidence: 99%

How Should Aneurysmal Subarachnoid Hemorrhage Be Managed?

Wendell¹,

Levine²

2010

Evidence-Based Practice of Critical Care

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“…Noninvasive angiography (CT and MRI) may have utility in some patients but is less sensitive for vasospasm than conventional angiography [46,47]. CT angiography (CTA) is noninvasive, quick, and may be performed at the bedside with a portable CT scanner.…”

Section: Cerebral Angiographymentioning

confidence: 99%

“…Magnetic resonance angiography (MRA) is less useful for vasospasm detection. It takes longer to perform, is subject to more artifact from aneurysm clips and coils and from metallic intracranial monitoring devices, and has a lower sensitivity for vasospasm than conventional angiography and, likely, CTA [46].…”

Section: Cerebral Angiographymentioning

confidence: 99%

Critical care management of subarachnoid hemorrhage

Levine

2009

Curr Treat Options Neurol

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Successful critical care management of patients with aneurysmal subarachnoid hemorrhage (SAH) requires a thorough understanding of the disease and its complications and a familiarity with modern multimodality neuromonitoring technology. This article reviews the natural history of aneurysmal SAH and strategies for disease management in the acute setting, including available tools for monitoring brain function. Intensive care management of patients with SAH focuses on prevention of further neurologic injury. Aneurysmal rebleeding, hydrocephalus, seizures, and delayed ischemic injury represent major threats. There is increasing awareness of extracerebral complications, including electrolyte disturbances (eg, cerebral salt wasting) and cardiac dysfunction. Prompt recognition and treatment of these disorders maximizes the odds of a good functional outcome. Technologic advances hold the promise of improved detection and treatment of secondary neurologic insults.

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“…Measuring certain factors, such as endothelin-1 or TNF-␣, in cerebrospinal fluid might provide an indication of their production in the CNS, 24 although local production may be missed with these measurements. Assessment of vasospasm may be aided by imaging technologies such as magnetic resonance angiography, 25 but such technologies are rarely available in malaria endemic countries. Microarray analysis of gene expression in peripheral mononuclear cells could give a picture of the systemic response to P. falciparum infection that leads to CM, but gene expression in the brain may be very different from that in other tissues such as the liver or spleen, as Lovegrove and colleagues 26 have demonstrated in an earlier murine CM study.…”

Section: Learning About Human CM From Murine Cm Microarray Analysismentioning

confidence: 99%

Cerebral Malaria Pathogenesis

John

2007

The American Journal of Pathology

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Cerebral malaria (CM) attributable to Plasmodium falciparum infection is estimated to affect 575,000 children in sub-Saharan Africa every year 1 and is among the deadliest forms of malaria, with an average estimated mortality rate of 18.6%. 2 Although extensive studies have been conducted in murine models of CM and in human populations with CM, the pathogenesis of CM is still incompletely understood. Studies to date suggest that CM is attributable to a combination of local brain tissue damage from microvascular ischemia and hypoxia and more global brain injury caused by the host immune response to the parasite. 3 A deficiency of most murine and human CM studies is that assessment has been restricted to specific predefined factors hypothesized to be of importance. These studies address specific hypotheses but cannot provide a systemic evaluation of the potential factors in the pathogenesis of CM.Systems biology, in particular the decoding of the human and murine genome, development of microarray analysis, and application of more sophisticated computational technology to assess the results of this analysis, has moved us ahead in our understanding of numerous diseases. In an elegant and carefully designed series of experiments in this issue of The American Journal of Pathology, Lovegrove and colleagues 4 use microarray analysis of whole brain tissue gene expression in CM-susceptible and CM-resistant mice to define potential pathways involved in murine CM pathogenesis. Their microarray analysis and confirmatory quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry studies demonstrate that interferon (IFN)-regulated processes and neuronal apoptosis appear to be important in murine CM pathogenesis. These findings, particularly the findings about neuronal apoptosis, are novel and add significantly to our understanding of murine CM pathogenesis. Although there are important differences between murine CM models and human CM, these findings may also provide clues about human CM pathogenesis and, in particular, suggest potential mechanisms for the long-term cognitive sequelae that occur in children with CM. 5,6 Differences between Murine CM Models and Human CM As is the case for many diseases affecting the brain, far more is known about the pathogenesis of murine CM than human CM. The most obvious reason for this is that sizeable numbers of murine brains can be studied at different phases of the illness, but human brain studies of CM are limited to those done at autopsy. Another reason for the paucity of information on human CM pathogenesis is that human CM occurs almost exclusively in low-and middle-income countries. The resources in these countries for investigating CM pathogenesis are severely limited, and the resources provided by wealthier countries for such studies in malaria endemic areas have to date been relatively meager. Despite these limitations, in addition to cultural problems with acceptance of autopsies in children who die of CM, remarkable human brain autopsy studies have been con...

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Detection of Delayed Cerebral Vasospasm, after Rupture of Intracranial Aneurysms, by Magnetic Resonance Angiography

Abstract: MRA could be useful for management of cerebral vasospasm, although it cannot become a practical alternative to conventional angiography.

Cited by 37 publications

References 28 publications

How Should Aneurysmal Subarachnoid Hemorrhage Be Managed?

How Should Aneurysmal Subarachnoid Hemorrhage Be Managed?

Critical care management of subarachnoid hemorrhage

Cerebral Malaria Pathogenesis

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