ABSTRACT
Despite breakthroughs in care and treatment, the consequences of a subarachnoid hemorrhage (SAH) are still associated with morbidity and mortality. Early brain injury is still a major source of clinical deterioration in people with SAH.
When a patient suffers a SAH, they are more likely to develop long-term neurological problems, which can be life-threatening. According to recent research, the management and remission of SAH are dependent on inflammatory mechanisms. The development of problems after SAH has recently been linked to inflammation. Many investigations have failed to show how inflammatory mechanisms affect SAH patients’ prognosis and outcome. SAH procedures and management will be improved by better understanding the various inflammatory pathways that occur after SAH. It was the goal of this review to outline some of the most important inflammatory pathways that emerge after SAH and to provide a general understanding of SAH.
Keywords : inflammation, EBI (early brain injury), cerebral vasospasm, subarachnoid hemorrhage, secondary brain injury.
INTRODUCTION : Acute subarachnoid hemorrhage (SAH) is a dangerous illness that affects many organ systems in addition to the brain (Cardentey-Pereda & Pérez-Falero, 2002).
Subarachnoid hemorrhage (SAH) accounts for around 5% of all strokes (Hong, Tosun, Kurland, Gerzanich, Schreibman & Simard, 2014), with more than 30% of patients dying as a result of the first or subsequent bleeding (Ostrowski, Colohan & Zhang, 2006). Brain injury that occurs immediately after bleeding is well understood and occurs as a result of a rise in intracranial pressure and a subsequent fall in cerebral perfusion. Brain injury that occurs later has a variety of causes and may necessitate a variety of treatment options because of the different time windows of varying duration (Schneider, Xu & Vajkoczy, 2018).  The fact that some SAH patients improve while others continue to deteriorate after their initial spasm is also puzzling (Miller, Turan, Chau & Pradilla, 2014). Early brain injury (EBI) is primarily responsible for the poor outcome of subarachnoid hemorrhage (SAH), which is intimately linked to inflammation (Sun, Duan, Jing, Wang, Hou & Zhang, 2019). In individuals with subarachnoid hemorrhage (SAH), neuroinflammation is directly linked to functional prognosis. Microglia are myeloid cells that make up the CNS’s innate immune system. In response to damage or disease processes in the CNS, they become highly engaged. The use of brain injury biomarkers could be useful not only for diagnosing and identifying intracranial lesions, but also for assessing severity, prognosis, and therapeutic efficacy (Mrozek, Dumurgier, Citerio, Mebazaa & Geeraerts, 2014).
SAH-related brain injury has been shown to be protected by inflammation as a defensive mechanism. In the event of a stroke, blood components such as red blood cells (RBCs), leukocytes (including macrophages), and plasma proteins (including Endothelin-1) enter the brain instantly. There is an inflammatory response as soon as there is blood present in the parenchyma. Inflammatory cells are mobilized and activated during this time period. The early inflammatory cells in reaction to the extravascular blood component are believed to be microglia and astrocytes.
Inflammatory mechanisms following SAH :
Following SAH, researchers began to look for probable links between cerebral vasospasm and inflammatory alterations in the CSF, because at the time, this condition was considered to be the primary, if not the only, cause of secondary brain injury. SAH-related secondary brain injury can result from a variety of factors, including traumatic brain injury (TBI) and SAH. It has been established in both human and animal research that inflammatory processes can occur in the central nervous system in conjunction with, contribute to, or even initiate programmed cell death (Minami, Tani, Maeda, Yamaura & Fukami, 1992). The first findings on systemic inflammation appeared around the end of the 1990s and the beginning of the 2000s, and they outlined a peripheral immune modulation after SAH (Yoshimoto, Tanaka & Hoya, 2001)
Inflammation was merely accounted to occur alongside, or aggravate cerebral vasospasm, rather than being comprehended as an unique pathomechanism, when cerebral vasospasm was thought to be the only-or at least biggest-contributor to subsequent brain injury following SAH (Schneider, Xu & Vajkoczy, 2018). With more recent studies, it is believed that not only cerebral vasospasm is a main interest when talking about secondary brain injury but also, early brain injury is an important condition. Around this same time, in early 2000, many mechanisms were studied to show effects of many substances on SAH (Fassbender et al., 2000).
Although cellular components reach the subarachnoid region from within the blood arteries, both cellular and molecular factors operate on the vascular walls, raising the question of whether CSF inflammation is an outside-in or inside-out event (Schneider, Xu & Vajkoczy, 2018).