Brain edema after aneurysmal subarachnoid hemorrhage

• The role of the PDGF-BB/PDGFR-beta signaling pathway in microcirculatory disturbances and BBB destruction after experimental subarachnoid hemorrhage in mice
• Icariin attenuates oxidative stress via SIRT1/PGC-1α pathway in SAH mice
• The effect of Fibulin-5 on early brain injury after subarachnoid hemorrhage in mice
• Tremella fuciformis Polysaccharides Alleviate Early Brain Injury in Experimental Subarachnoid Hemorrhage by Inhibiting the KDR-Mediated P38 MAPK/NF-kappaB Pathway
• Shikonin attenuates blood-brain barrier injury and oxidative stress in rats with subarachnoid hemorrhage by activating Sirt1/Nrf2/HO-1 signaling
• Effectiveness of Continuous Intra-Arterial Nimodipine Infusion for the Treatment of Refractory Vasospasm after Aneurysmal Subarachnoid Hemorrhage
• Donepezil Improves PSD95 Expression, Mitigates Neuroinflammation via PI3K/Akt/NF-kappaB and Mitochondrial Dysfunction in a Rodent Model of Subarachnoid Haemorrhage
• Localized pulmonary vascular changes in a mouse model of subarachnoid hemorrhage created by combining filament perforation and blood injection

Primary brain swelling increases brain volume after aSAH.

Given the importance of edema to the outcome of patients with aSAH and its status as a highly modifiable pathological process, a better understanding of cerebral edema in aSAH promises to hasten the development of medical therapies to improve outcomes in this frequently devastating disease ¹⁾

Brain edema after aneurysmal subarachnoid hemorrhage diagnosis.

Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal circulatory brain arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome ²⁾.