The Importance of Early Intervention in Ruptured Cerebral Aneurysm: Biochemical and Pathophysiological Foundations Within the First 24 Hours
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Background: Severe vasospasm in cases of subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms accounts for a high mortality rate ranging from 36% to 67%, as well as permanent neurological deficits. Biochemical changes involving neuropeptides such as Neuropeptide Y (NPY) and Calcitonin Gene-Related Peptide (CGRP) have been studied as regulators of vascular tone and protectors of cerebral perfusion. These peptides may become imbalanced during subarachnoid hemorrhage (SAH). Methods: This is an analytical descriptive case-control study with a 1:1 ratio, comparing patients diagnosed with subarachnoid hemorrhage secondary to ruptured aneurysms to those with incidental, unruptured aneurysms. A total of 46 patients were included, distributed equally into two groups: 23 in the case group and 23 in the control group. Cerebrospinal fluid (CSF) samples were collected from all participants during surgery, directly from the cerebral cisterns, ventricles, and through spinal catheters. The objective of this study was to analyze and correlate the levels of NPY and CGRP between patients with aneurysmal SAH and those with unruptured aneurysms. Results: A similarity in mean age was observed between both groups: cases = 57 ± 13.4 years vs. controls = 56.3 ± 12.4 years. Regarding NPY and CGRP values, the control group showed a median NPY level of 796 (P25 = 94, P75 = 903) versus 210 (P25 = 49, P75 = 901) in the aneurysmal rupture group. Although there was a trend toward increased NPY levels in the rupture group, the difference was not statistically significant (p = 0.62). For CGRP, the median level was 35.5 (P25 = 38.8, P75 = 61.9) in the control group versus 66.5 (P25 = 11.4, P75 = 88) in the case group, also without statistical significance (p = 0.39). In the control group, a negative correlation was found between NPY and CGRP levels, with a strong inverse relationship and statistical significance (Rho = –0.6; p = 0.001). Conclusions: In this study, we analyzed the levels of neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) in cerebrospinal fluid (CSF) collected from the basal cisterns, ventricles, and a spinal catheter in patients with subarachnoid hemorrhage (SAH) secondary to aneurysmal rupture, comparing them to patients without rupture. Although we observed a trend toward higher NPY levels in the rupture group, supporting the notion of early aneurysm intervention within the first 24 hours to prevent the development of vasospasm, and also noted differences in CGRP levels, these findings were not statistically significant. These results suggest that while these neuropeptides may play a role in vascular tone regulation and the pathophysiology of cerebral vasospasm, their specific function appears to be disrupted, representing one of the mechanisms of SAH that remains incompletely understood. Further studies with larger sample sizes and designs better suited to assessing the causal relationship between these biomarkers and clinical outcomes are required.