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Aim of Study: This study aimed to compare headache and facial pain prevalence and headache phenotype among people with common upper respiratory tract infections (URTIs)., Clinical Rationale for Study: Headache is a common symptom in viral URTI, but its phenotyping has so far been limited to coronavirus disease 2019 (COVID-19) and influenza. Additionally, the prevalence of facial pain in URTIs has only rarely been discussed in scientific publications., Material and Methods: Patients with acute URTI symptoms were evaluated for headache phenotype using a semi-structured questionnaire. Antigen swab tests were performed in all participants., Results: The analysis included 276 URTI/APVRS (acute post-viral rhinosinusitis) episodes in 223 patients (136 women, 60.1%) aged 18-73 [mean 41.3 / median (25th, 75th) 40 / standard deviation 15.1]. Participants were diagnosed with: COVID-19 - 107/276 (38.8%); 'common cold' - 103/276 (37.3%); influenza - 36/276 (13.0%); or APVRS - 30/276 (10.9%). Headache was present in 183/276 (66.3%) and URTIs and facial pain in 107/276 (38.8%). Predictors of headache in URTIs included sinonasal symptoms (odds ratio (OR) 10.70, p < 0.001) and fever (OR 2.9, p = 0.004). Headache more often (p = 0.030) had a migraine-like phenotype in COVID-19 (27.4% (20/73) vs. 9.1% (10/110) and tension-type headache (TTH)-like phenotype in 'common cold' (75.4%, 49/64 vs. 61.3%, 73/119). Previous COVID-19 immunisation (vaccination or infection) was associated (p = 0.004) with a lower prevalence of migraine-like headache [6.3% (1/16) vs. 32.8% (19/58)]., Conclusions and Clinical Implications: Headache and facial pain are prevalent during URTIs, and are associated with general and sinonasal immune response rather than virus type. Headache phenotype may depend on the causative microorganism, but it can evolve in response to previous immunisation. Our study supports vaccination against COVID-19, as people with prior immunisation are probably less likely to experience migraine-like headache.

Headache is one of the most prevalent, although often underreported, symptoms of coronavirus disease 2019 (COVID-19). It is generally accepted that this symptom is a form of secondary headache due to systemic viral infection. There are several hypotheses that try to explain its aetiopathogenesis. One of the most compelling is related to innate immune response to viral infection. This rationale is supported by similarities to other viral infections and the temporal overlap between immunological reactions and headache. Moreover, several key factors in innate immunity have been shown to facilitate headache e.g. interferons, interleukin (IL) -1-β, IL-6, and tumour necrosis factor. There is also a possibility that the virus causes headache by the direct activation of afferents through pattern recognition receptors (i.e. Toll-like receptor 7). Moreover, some data on post-COVID-19 headache and after vaccination against SARS-CoV-2 infection suggests a similar cytokine-mediated pathomechanism in these clinical situations. Future research should look for evidence of causality between particular immune response factors and headache. Identifying key molecules responsible for headache during acute viral infection would be an important step towards managing one of the most prevalent secondary headache disorders.