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.