Secondary Brain Injury by Oxidative Stress After Cerebral Hemorrhage: Recent Advances

Abstract

Intracerebral hemorrhage (ICH) is a clinical syndrome in which blood accumulates in the brain parenchyma because of a nontraumatic rupture of a blood vessel. Because of its high morbidity and mortality rate and the lack of effective therapy, the treatment of ICH has become a hot research topic. Meanwhile, Oxidative stress is one of the main causes of secondary brain injury(SBI) after ICH. Therefore, there is a need for an in-depth study of oxidative stress after ICH. This review will discuss the pathway and effects of oxidative stress after ICH and its relationship with inflammation and autophagy, as well as the current antioxidant therapy for ICH with a view to deriving better therapeutic tools or targets for ICH.

Early Fever in Patients with Primary Intracerebral Hemorrhage is Associated with Worse Long-Term Functional Outcomes: A Prospective Study

“…(1) ICH can lead to primary or secondary brain injury. Primary brain injury involves initial damage to the parenchyma induced by the blood clot, and secondary brain injury involves damage to blood vessels caused by various mechanisms, including oxidative stress, excitotoxicity, in ammatory response, mitochondrial dysfunction, and cell death (1,2). Excessive production of reactive oxygen species (ROS) leads to excessive oxidative stress, which aggravates secondary brain injury.…”

“…Excessive production of reactive oxygen species (ROS) leads to excessive oxidative stress, which aggravates secondary brain injury. (2) The aforementioned processes may be accelerated by fever. Therefore, fever is considered a potential contributor to secondary brain injury after ICH.…”

Cerebro-spinal fluid glucose and lactate concentrations changes in response to therapies in patIents with primary brain injury: the START-TRIP study

“…The complex pathophysiology responsible for secondary brain injury involves both systemic complications (i.e., hypoxemia, hypocapnia, fever, anemia, hyponatremia, hyperglycemia, etc.) [ 4 – 6 ], as well as cerebral complications, such as reduced cerebral perfusion pressure (CPP), cerebral edema, and blood–brain barrier dysfunction, tissue hypoxia, microvascular abnormalities, seizures and oxidative stress [ 7 – 9 ], all being associated with in an increased probability of poor prognosis.…”