Incidence of cerebral infarction associated with ruptured intracranial aneurysms

Birse, Sheila H.; Tom, Mary I.

doi:10.1212/wnl.10.2.101

Cited by 63 publications

(24 citation statements)

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“…7,9 Spreading ischemia induces laminar cortical necrosis, a lesion pattern also characteristic of DINDs after SAH. 10,11 The clinical relevance of this concept is supported by recent findings of a status of recurrent prolonged spreading depolarizations in SAH patients developing DINDs. 4 It has remained undetermined why the brains of these patients are more susceptible to CSDs.…”

Section: Discussionmentioning

confidence: 76%

“…7 Because hemoglobin can be replaced by nitric oxide synthase (NOS) inhibitors, hemoglobin likely acts as an NO scavenger. 8 Spreading ischemia appears to be pathophysiologically linked to DINDs, because (1) it is triggered by products of hemolysis 7 in clinically relevant concentrations, 5,6 (2) spreading ischemia 9,10 and DINDs 11 share similar infarct morphologies, (3) extracellular NO is reduced after clinical and experimental SAH, 12,13 and (4) nimodipine and hemodilution inhibit spreading ischemia 14 and DINDs. 15 These data indicate that prevention of CSDs in SAH may be useful in the treatment of DINDs.…”

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confidence: 99%

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Nitric Oxide Modulates Spreading Depolarization Threshold in the Human and Rodent Cortex

Petzold

Haack

Halbach

et al. 2008

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Background and Purpose-Recent clinical data have suggested that prolonged cortical spreading depolarizations (CSDs) contribute to the pathogenesis of delayed ischemic neurologic deficits after subarachnoid hemorrhage. Elevated extracellular potassium concentrations and lowered nitric oxide (NO) levels have been detected in experimental and clinical subarachnoid hemorrhage. We investigated whether a similar extracellular composition renders the brain more susceptible to CSDs. Methods-Electrophysiologic and blood flow changes were studied in vivo in rats. Intrinsic optical signals, alterations of NO level, and electrophysiologic changes were investigated in rodent and human brain slices. Results-Elevation of subarachnoid extracellular potassium in rats in vivo triggered CSDs. Using NO-sensitive dyes, we found that CSDs induce NO synthesis in neurons and endothelial cells. When we blocked NO synthesis in vivo, CSDs occurred at a significantly lower threshold and propagated with a wave of ischemia. This increased susceptibility for CSDs by a low NO level was confirmed in rat and human neocortical slices and depended on P/Q-type calcium channels and N-methyl-D-aspartate receptors, but not on guanylate cyclase. Mice deficient in endothelial NO synthase, in contrast to mice deficient in neuronal NO synthase, had an inherently lower threshold. Conclusions-Basal NO production determined CSD threshold. The threshold effect depended predominantly on endothelial NO synthase. Reduced NO levels, as in patients with subarachnoid hemorrhage, may render the brain more susceptible to CSDs. Because CSDs have been linked to the pathogenesis of delayed ischemic neurologic deficits, raising its threshold by increasing NO availability may prove therapeutically beneficial in patients with subarachnoid hemorrhage.

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Section: Discussionmentioning

confidence: 76%

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confidence: 99%

Nitric Oxide Modulates Spreading Depolarization Threshold in the Human and Rodent Cortex

Petzold

Haack

Halbach

et al. 2008

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“…The arteriographic demonstration of vasospasm 93 and the analysis of several cerebral infarcts in aneurysm patients cemented the relationship between the two [94][95][96][97] . Based on these observations, a series of quite reasonable assumptions was made, on which the understanding of vasospasm pathogenesis still rests.…”

Section: Proximately 30% Of Patients Develop Signs Of Cerebral Ischemiamentioning

confidence: 99%

Brain Ischemia in Patients with Intracranial Hemorrhage: Pathophysiological Reasoning for Aggressive Diagnostic Management

et al. 2013

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“…He hypothesized the infarctions were caused by temporary arterial spasm because the arteries did not contain thrombi or emboli. Subsequent autopsy series by Birse and Tom 29 identified focal, diffuse, patchy cortical necrosis in some cases that can now be observed radiologically. In 1964, Crompton 30 associated cerebral infarctions at autopsy with the location of subarachnoid blood and with angiographic vasospasm.…”

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confidence: 95%

“…Birse и M.I. Tom [29] выявили очаговый, диффузный, островковый кортикаль-ный некроз, который в некоторых случаях в настоящее время можно обнаружить методами нейровизуализации. В 1964 г. M.R.…”

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Origins of the Concept of Vasospasm

Macdonald

2016

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Incidence of cerebral infarction associated with ruptured intracranial aneurysms

Cited by 63 publications

References 0 publications

Nitric Oxide Modulates Spreading Depolarization Threshold in the Human and Rodent Cortex

Nitric Oxide Modulates Spreading Depolarization Threshold in the Human and Rodent Cortex

Brain Ischemia in Patients with Intracranial Hemorrhage: Pathophysiological Reasoning for Aggressive Diagnostic Management

Origins of the Concept of Vasospasm

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