Abstract
Endogenous Calcitonin Gene-Related Peptide (CGRP) stored in perivascular nerve fibers around the cerebral arteries mediates vasodilation and regulates cerebral blood flow under physiological conditions. Increased levels of CGRP have been continually reported in patients with migraine, but the role of CGRP in the pathophysiology of Subarachnoid Hemorrhage (SAH) has not yet been sufficiently evaluated. Over 10 days, serum was prospectively collected from 33 consecutive patients (17 women, 16 men; mean age 52.8 years) with spontaneous non-traumatic SAH. All patients were graded III or IV according to the Fisher Score. CGRP levels were determined by means of an Enzyme-Immunosorbent Assay (EIA). CGRP concentrations were correlated to (1) the anatomical localization of the aneurysm (anterior circulation or posterior circulation), (2) the treatment modality (clipped group, coiled group, or untreated group) and (3) the rate of ischemia determined by computed tomography (ischemia group, non-ischemia group, or iatrogenic ischemia group). (1) Anatomical localization: CGRP levels were significantly higher in patients with a ruptured aneurysm of the anterior circulation (p<0.001). (2) Treatment modality: CGRP levels differed significantly between the groups (coil group, clip group, or untreated group; p<0.001). The highest levels of CGRP were detected in the coil group and the lowest levels in the untreated group. About (3) Ischemia: CGRP levels differed significantly between the three groups (ischemia group, non-ischemia group, or iatrogenic ischemia group; p = 0.038). The highest levels of CGRP were found in the ischemia group. The maximum levels of CGRP in serum were found for patients with a ruptured aneurysm of the anterior circulation and subsequent ischemia treated by endovascular coiling. These findings support the theory that CGRP is produced and excessively released to counteract cerebral vasospasm and subsequent ischemia. Presumably, the serum levels of CGRP are affected by the anatomical localization of the aneurysm and can be stimulated by any endoluminal manipulation of the parent artery.
Highlights
The peptidergic regulation of the cerebral vasculature under normal conditions is well established (Edvinsson et al, 1994; McCulloch et al, 1986; Hokfelt et al, 1992), its role in pathophysiology after spontaneous Subarachnoid Hemorrhage (SAH), arterial vasospasm and Cerebral Ischemia (CI) remains unclear (Kokkoris et al, 2012)
The maximum levels of Calcitonin Gene-Related Peptide (CGRP) in serum were found for patients with a ruptured aneurysm of the anterior circulation and subsequent ischemia treated by endovascular coiling
This study showed that CGRP levels in Cerebrospinal Fluid (CSF) were markedly increased whereas the corresponding CGRP levels of a control group were not measurable
Summary
The peptidergic regulation of the cerebral vasculature under normal conditions is well established (Edvinsson et al, 1994; McCulloch et al, 1986; Hokfelt et al, 1992), its role in pathophysiology after spontaneous Subarachnoid Hemorrhage (SAH), arterial vasospasm and Cerebral Ischemia (CI) remains unclear (Kokkoris et al, 2012). Described the functional antagonism of NPY and the vasodilator Calcitonin Gene-Related Peptide (CGRP) in mesenteric resistance arteries (De Mey et al, 2008). This antagonism had been proposed to be present in the central nervous system and some research groups have evaluated the possible role of CGRP in SAH (Kokkoris et al, 2012; Juul et al, 1990; 1995; Schebesch et al, 2013b). The vascular tone is increased by the intrinsic release of vasoconstrictive neuropeptides, such as NPY, Vasointestinal Peptide (VIP) and Substance P (SP). To the best of our knowledge, no data are yet available on the influence of the anatomical localization of the ruptured aneurysm and the effect of endovascular or surgical occlusion on the intrinsic release and dynamics of CGRP in serum
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