Department of Neurology and Algology, Neuropsychiatry Center, Neuroscience and Neurotechnology Center (NÖROM), Gazi University Hospital, Medical Faculty, Besevler, 06510, Ankara, Turkey.
Neurology Department, University of Health Science, Gülhane School of Medicine, Ankara, Turkey.
J Headache Pain. 2021 Aug 12;22(1):94. doi: 10.1186/s10194-021-01306-7.
Pathogenesis of COVID-19 -related headache is unknown, though the induction of the trigeminal neurons through inflammation is proposed. We aimed to investigate key systemic circulating inflammatory molecules and their clinical relations in COVID-19 patients with headache.
This cross-sectional study enrolled 88 COVID-19 patients, hospitalized on a regular ward during the second wave of the pandemic. Clinical characteristics of COVID-19 patients were recorded, and laboratory tests were studied.
The mean ages of 48 COVID-19 patients with headache (47.71 ± 10.8) and 40 COVID-19 patients without headache (45.70 ± 12.72) were comparable. COVID-19 patients suffered from headache had significantly higher serum levels of HMGB1, NLRP3, ACE2, and IL-6 than COVID-19 patients without headache, whereas CGRP and IL-10 levels were similar in the groups. Angiotensin II level was significantly decreased in the headache group. COVID-19 patients with headache showed an increased frequency of pulmonary involvement and increased D- dimer levels. Furthermore, COVID-19 was more frequently associated with weight loss, nausea, and diarrhea in patients with headache. Serum NLRP3 levels were correlated with headache duration and hospital stay, while headache response to paracetamol was negatively correlated with HMGB1 and positively associated with IL-10 levels.
Stronger inflammatory response is associated with headache in hospitalized COVID-19 patients with moderate disease severity. Increased levels of the circulating inflammatory and/or nociceptive molecules like HMGB1, NLRP3, and IL-6 may play a role in the potential induction of the trigeminal system and manifestation of headache secondary to SARS-CoV-2 infection.
COVID-19 相关头痛的发病机制尚不清楚，尽管有人提出炎症会诱发三叉神经神经元。我们旨在研究 COVID-19 头痛患者中关键的循环系统炎症分子及其与临床的关系。
本横断面研究纳入了 88 名在大流行第二波期间住院的 COVID-19 患者。记录 COVID-19 患者的临床特征，并进行实验室检查。
48 例 COVID-19 头痛患者（47.71±10.8）和 40 例 COVID-19 无头痛患者（45.70±12.72）的平均年龄相当。与 COVID-19 无头痛患者相比，COVID-19 头痛患者的血清 HMGB1、NLRP3、ACE2 和 IL-6 水平显著升高，而 CGRP 和 IL-10 水平在两组间相似。头痛组的血管紧张素 II 水平显著降低。头痛组的肺部受累频率更高，D-二聚体水平也更高。此外，头痛患者 COVID-19 更常伴有体重减轻、恶心和腹泻。血清 NLRP3 水平与头痛持续时间和住院时间相关，而头痛对扑热息痛的反应与 HMGB1 呈负相关，与 IL-10 呈正相关。
在疾病严重程度中等的住院 COVID-19 患者中，更强的炎症反应与头痛相关。循环炎症和/或伤害性分子（如 HMGB1、NLRP3 和 IL-6）水平升高可能在 SARS-CoV-2 感染引起的三叉神经系统潜在诱导和头痛表现中发挥作用。
