The vasodilatory calcitonin gene-related peptide (CGRP) is excessively released after spontaneous subarachnoid hemorrhage (sSAH) and modulates psycho-behavioral function. In this pilot study, we prospectively analyzed the treatment-specific differences in the secretion of endogenous CGRP into cerebrospinal fluid (CSF) during the acute stage after good-grade sSAH and its impact on self-reported health-related quality of life (hrQoL). Twenty-six consecutive patients (f:m = 13:8; mean age 50.6 years) with good-grade sSAH were enrolled (drop out 19% (n = 5)): 35% (n = 9) underwent endovascular aneurysm occlusion, 23% (n = 6) microsurgery, and 23% (n = 6) of the patients with perimesencephalic SAH received standardized intensive medical care. An external ventricular drain was inserted within 72 h after the onset of bleeding. CSF was drawn daily from day 1–10. CGRP levels were determined via competitive enzyme immunoassay and calculated as “area under the curve” (AUC). All patients underwent a hrQoL self-report assessment (36-Item Short Form Health Survey (SF-36), ICD-10-Symptom-Rating questionnaire (ISR)) after the onset of sSAH (t₁: day 11–35) and at the 6-month follow-up (t₂). AUC CGRP (total mean ± SD, 5.7 ± 1.8 ng/ml/24 h) was excessively released into CSF after sSAH. AUC CGRP levels did not differ significantly when dichotomizing the aSAH (5.63 ± 1.77) and pSAH group (5.68 ± 2.08). aSAH patients revealed a higher symptom burden in the ISR supplementary item score (p = 0.021). Multiple logistic regression analyses corroborated increased mean levels of AUC CGRP in CSF at t₁ as an independent prognostic factor for a significantly higher symptom burden in most ISR scores (compulsive-obsessive syndrome (OR 5.741, p = 0.018), anxiety (OR 7.748, p = 0.021), depression (OR 2.740, p = 0.005), the supplementary items (OR 2.392, p = 0.004)) and for a poorer performance in the SF-36 physical component summary score (OR 0.177, p = 0.001). In contrast, at t₂, CSF AUC CGRP concentrations no longer correlated with hrQoL. To the best of our knowledge, this study is the first to correlate the levels of endogenous CSF CGRP with hrQoL outcome in good-grade sSAH patients. Excessive CGRP release into CSF may have a negative short-term impact on hrQoL and emotional health like anxiety and depression. While subacutely after sSAH, higher CSF levels of the vasodilator CGRP are supposed to be protective against vasospasm-associated cerebral ischemia, from a psychopathological point of view, our results suggest an involvement of CSF CGRP in the dysregulation of higher integrated behavior.

血管舒张降钙素基因相关肽 (CGRP) 在自发性蛛网膜下腔出血 (sSAH) 后过度释放并调节心理行为功能。在这项初步研究中，我们前瞻性地分析了在高级别 sSAH 后急性期内源性 CGRP 分泌到脑脊液 (CSF) 中的治疗特异性差异及其对自我报告的健康相关生活质量 (hrQoL) 的影响. 连续招募了 26 名具有良好级别 sSAH 的患者（f:m = 13:8；平均年龄 50.6 岁）（退出率为 19% ( n  = 5)）：35% ( n  = 9) 接受了血管内动脉瘤封堵术， 23% ( n  = 6) 显微外科手术，23% ( n = 6) 的中脑周围 SAH 患者接受了标准化的重症监护。出血后 72 小时内插入心室外引流管。从第 1-10 天每天抽取 CSF。CGRP 水平通过竞争性酶免疫测定法测定并计算为“曲线下面积”（AUC）。所有患者在 sSAH 发作后（t ₁：第 11-35 天）都接受了 hrQoL 自我报告评估（36 项简表健康调查（SF-36）、ICD-10-症状评分问卷（ISR））和在 6 个月的随访中（t ₂）。AUC CGRP（总平均值 ± SD，5.7 ± 1.8 ng/ml/24 小时）在 sSAH 后过度释放到 CSF 中。将 aSAH (5.63 ± 1.77) 和 pSAH 组 (5.68 ± 2.08) 分为两部分时，AUC CGRP 水平没有显着差异。aSAH 患者在 ISR 补充项目评分中表现出更高的症状负担（p  = 0.021）。多元逻辑回归分析证实 t ₁时脑脊液中 AUC CGRP 的平均水平增加是大多数 ISR 评分（强迫性强迫综合征（OR 5.741，p  = 0.018）、焦虑（OR 7.748，p  = 0.021），抑郁症（OR 2.740，p  = 0.005），补充项目（OR 2.392，p = 0.004)) 和 SF-36 物理组件总分的较差表现（OR 0.177，p  = 0.001）。相反，在 t _{2 时}，CSF AUC CGRP 浓度不再与 hrQoL 相关。据我们所知，这项研究是第一个将内源性脑脊液 CGRP 水平与 sSAH 患者的 hrQoL 结果相关联的研究。过多的 CGRP 释放到脑脊液中可能会对 hrQoL 和情绪健康（如焦虑和抑郁）产生短期的负面影响。虽然在 sSAH 后亚急性期，血管扩张剂 CGRP 的较高 CSF 水平被认为可以预防血管痉挛相关的脑缺血，但从精神病理学的角度来看，我们的结果表明 CSF CGRP 参与了更高整合行为的失调。