Anesthetic Approach of Pregnant Woman with Cerebral Arteriovenous Malformation and Subarachnoid Hemorrhage during Pregnancy: Case Report

Carvalho, Catarina Santos; Resende, Filipa; Centeno, Maria João; Ribeiro, Ícaro José Santos; Moreira, João

doi:10.1016/s0034-7094(13)70220-4

Cited by 16 publications

(1 citation statement)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The normal angiographic findings in these instances are consistent with a venous origin of the bleeding, which can occur due to the rupture of a prepontine or interpeduncular vein (Hashimoto et al, 2000). Approximately 5% of SAH are associated with other medical conditions such as arteriovenous malformation, intracranial artery dissections, mycotic aneurysms, bleeding disorders, reversible cerebral vasoconstriction syndrome, vasculitis, moyamoya disease, cerebral amyloid angiopathy, or drug abuse (Cabral et al, 2013; Cuvinciuc et al, 2010; Rinkel et al, 1993; Santos Carvalho et al, 2013; Venti, 2012; Viswanathan et al, 2012). This review focuses only on current neurobiological knowledge of aneurysmal SAH.…”

Section: Sah Backgroundmentioning

confidence: 99%

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Chen

Feng

Sherchan

et al. 2014

Progress in Neurobiology

314

264

View full text Add to dashboard Cite

Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms “early brain injury” and “delayed brain injury” are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications.

show abstract