The Relation of Cerebral Vasospasm to the Extent and Location of Subarachnoid Blood Visualized by Ct Scan

Kistler, J P; Crowell, R. M.; Davis, K R; Heros, Roberto C.; Ojemann, R. G.; Zervas, T.; Fisher, C. M.

doi:10.1097/00004728-198312000-00053

Cited by 73 publications

(93 citation statements)

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“…12,13 Aneurysm location, maximal diameter, and immediate final angiographic treatment results were studied by using the classification of Roy et al, 14 in which class 1 is complete aneurysm occlusion, class 2 is residual neck filling, and class 3 is residual aneurysm filling. The lengths of both HydroCoil and bare platinum coils were documented.…”

Section: Clinical and Angiographic Featuresmentioning

confidence: 99%

Angiographic and Clinical Outcomes in 200 Consecutive Patients with Cerebral Aneurysm Treated with Hydrogel-Coated Coils

Gunnarsson¹,

Tong²,

Klurfan³

et al. 2009

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:Denser coil packing in intracranial aneurysms is believed to result in lower recanalization rates. Hydrogel-coated expandable coils (HydroCoil) improve volumetric packing of aneurysms in animal models and clinical studies, but data from large clinical series are limited. The objective of this retrospective analysis was to analyze immediate and follow-up angiographic results as well as complications in a large consecutive series of patients treated with HydroCoils at a single institution.

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Section: Clinical and Angiographic Featuresmentioning

confidence: 99%

Angiographic and Clinical Outcomes in 200 Consecutive Patients with Cerebral Aneurysm Treated with Hydrogel-Coated Coils

Gunnarsson¹,

Tong²,

Klurfan³

et al. 2009

AJNR Am J Neuroradiol

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“…Examples of compounds in the first class would be hemoglobin (Hb)and BOXes, and examples in the second class of compounds would be endothelin or nitric oxide (Figure 2), which could be directly or indirectly induced by the BOXes. The rationale that blood itself or some metabolite of components of blood cause vasospasm is compelling since this helps explain why vasospasm tends to occur where large blood clots occur around vessels at the base of the brain (Harrod et al, 2005;Kistler et al, 1983).…”

Section: Two Classes Of Compounds That Could Cause Vasospasmmentioning

confidence: 99%

BilirubinOxidation Products (BOXes) and Their Role in Cerebral Vasospasm after Subarachnoid Hemorrhage

Clark

Sharp

2006

J Cereb Blood Flow Metab

113

110

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Many factors have been postulated to cause delayed subarachnoid hemorrhage (SAH)-induced vasospasm, including hemoglobin, nitric oxide, endothelin, and free radicals. We propose that free radicals (because of the high levels that are produced in the blood clots surrounding blood vessels after SAH) act on bilirubin, biliverdin, and possibly heme to produce BOXes (Bilirubin OXidized Products). Bilirubin oxidation products act on vascular smooth muscle cells to produce chronic vasoconstriction and vasospasm combined with a vasculopathy because of smooth muscle cell injury. This review summarizes recent evidence that BOXes play a role in SAH-induced vasospasm. The data supporting a role for BOXes includes (1) identification of molecules in cerebrospinal fluid (CSF) of patients with vasospasm after SAH that have structures consistent with BOXes; (2) BOXes are vasoactive in vitro and mimic the biochemical actions of CSF of patients with vasospasm; (3) BOXes are vasoactive in vivo, constricting rat cerebral vessels; and (4) there is a correlation between clinical occurrence of vasospasm and BOXes concentration in our preliminary study of patients with SAH. Since oxidation of bilirubin, biliverdin, and perhaps heme is proposed to produce BOXes that contribute to vasospasm, either blocking bilirubin formation, inactivating bilirubin or BOXes, or removing all of the blood clot before vasospasm are potential treatment targets.

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“…Delayed cerebral ischemia has classically been associated with vasospasm and with the amount of blood present in the subarachnoid space [21,22]. However, the changes in intracranial pressure, autoregulation, cortical spreading depolarization, blood-brain barrier opening and neuronal apoptosis that exist in the first 72 h after rupture lead to early brain injury and also contribute to the occurrence of DCI [23].…”

Section: Discussionmentioning

confidence: 99%

Evolution of diffusion tensor imaging parameters after acute subarachnoid haemorrhage: a prospective cohort study

et al. 2016

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Introduction Few studies assessed diffusion tensor imaging (DTI) changes in the acute phase of subarachnoid haemorrhage (SAH). We prospectively evaluated DTI parameters in the acute phase of SAH and 8-10 days after and analysed whether changes could be related to SAH severity or to the development of delayed cerebral ischemia (DCI). Methods Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) changes over time were assessed in a prospective cohort of patients with acute SAH. Two MRI studies were performed at <72 h (MRI-1) and 8-10 days (MRI-2). DTI parameters were recorded in 15 ROIs. Linear mixed regression models were used.

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The Relation of Cerebral Vasospasm to the Extent and Location of Subarachnoid Blood Visualized by Ct Scan

Cited by 73 publications

References 0 publications

Angiographic and Clinical Outcomes in 200 Consecutive Patients with Cerebral Aneurysm Treated with Hydrogel-Coated Coils

Angiographic and Clinical Outcomes in 200 Consecutive Patients with Cerebral Aneurysm Treated with Hydrogel-Coated Coils

BilirubinOxidation Products (BOXes) and Their Role in Cerebral Vasospasm after Subarachnoid Hemorrhage

Evolution of diffusion tensor imaging parameters after acute subarachnoid haemorrhage: a prospective cohort study

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