Limitations
After describing the aforementioned inflammatory pathways in response to SAH and their impact on EBI, it’s crucial to point out the review’s shortcomings. The majority of the evidence included in this study regarding the inflammatory pathways following SAH was based only on in vitro and animal research. When it comes to experimental SAH, several methods have been used to simulate SAH for research aims. Two of the most commonly used models are blood injection and endovascular perforation. The blood injection model is less accurate than the endovascular perforation model in simulating SAH because it does not involve perforation of the cerebral artery. As a result, there may be discrepancies in experimental outcomes due to the different models, which we failed to account for in this review. When establishing the pathways, there was no distinction made between the molecular expression components of the pathways and the neurologic effects. Secondary brain injury may emerge from the activation of several different inflammatory pathways following SAH, although the severity of each pathway’s ability to control inflammation has not been studied in detail in this review. After SAH, there was no distinction made in the inflammatory response time since it may be critical in the development of SAH problems in individuals who survive the first bleed. We highlight the majority of inflammatory pathways, however we understand that there may be more inflammatory pathways after SAH. The majority of the pathways included in the research did not take into account the different grades of SAH severity.