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Simulated Airplane Headache: A Proxy Towards Identification of Underlying Mechanisms

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Simulated Airplane Headache: A Proxy Towards Identification of Underlying Mechanisms

Sebastian Bao Dinh Bui et al. J Headache Pain.

Abstract

Background: Airplane Headache (AH) occurs during flights and often appears as an intense, short lasting headache during take-off or landing. Reports are limited on pathological mechanisms underlying the occurrence of this headache. Proper diagnosis and treatments would benefit from identification of potential pathways involved in AH pathogenesis. This study aimed at providing a simulated airplane headache condition as a proxy towards identification of its underlying mechanisms.

Methods: Fourteen participants including 7 volunteers suffering from AH and 7 healthy matched controls were recruited after meeting the diagnostic and safety criteria based on an approved study protocol. Simulation of AH was achieved by entering a pressure chamber with similar characteristics of an airplane flight. Selected potential biomarkers including salivary prostaglandin E2 (PGE2), cortisol, facial thermo-images, blood pressure, pulse, and saturation pulse oxygen (SPO) were defined and values were collected before, during and after flight simulation in the pressure chamber. Salivary samples were analyzed with ELISA techniques, while data analysis and statistical tests were handled with SPSS version 22.0.

Results: All participants in the AH-group experienced a headache attack similar to AH experience during flight. The non-AH-group did not experience any headaches. Our data showed that the values for PGE2, cortisol and SPO were significantly different in the AH-group in comparison with the non-AH-group during the flight simulation in the pressure chamber.

Conclusion: The pressure chamber proved useful not only to provoke AH-like attack but also to study potential biomarkers for AH in this study. PGE2, and cortisol levels together with SPO presented dysregulation during the simulated AH-attack in affected individuals compared with healthy controls. Based on these findings we propose to use pressure chamber as a model to induce AH, and thus assess new potential biomarkers for AH in future studies.

Keywords: Airplane headache; Biomarker; Blood pressure; Cortisol; Pressure chamber; Prostaglandin E2; Pulse; Saturation pulse oxygen; Simulated airplane flight; Thermo imagining.

Figures

Fig. 1
Fig. 1
Between and within group comparisons for cortisol (a), PGE2 (b) and SPO (c). SF: Simulated flight. Bars indicate SD. *: p < 0.05. **: p < 0.001
Fig. 2
Fig. 2
Between and within group comparisons for pulse rate (a), SBP (b), DBP (c) and facial skin temperature (FST) (d). SF: Simulated flight. Bars indicate SD.*: p < 0.05
Fig. 3
Fig. 3
Proposed mechanisms underlying development of AH. Berilgen et al. [7] suggest that AH results from local inflammation caused by sinus barotrauma due to changes in the atmospheric pressure during the landing. The first degree of sinus barotrauma [41] is a short lasting discomfort with almost no anatomical changes in the sinuses and can be considered as a potential player in AH. Most passengers sense pressure changes during landing and gas trapping in the sinuses often occurs that can contribute in sinus barotrauma and a transient local inflammation. Since we identified that PGE2, an inflammation mediator, was higher in AH-group and SPO was lower, we suggest that a mild hypoxia may occur during a flight travel that may lead to reflective but perhaps mild hyperventilation. Hyperventilation can result in decreasing levels of carbon dioxide (CO2) and elevated blood pH [42]. As a response to the decreased CO2, vasodilation may occur [42]. Vasodilation in the cerebral arteries as a reaction to local inflammation or hypoxia can theoretically lead to development of AH. This hypothesis should be examined. Furthermore, interrelationship between anxiety, stress and other environmental and internal subjective factors linked with AH should also be investigated thoroughly to approve or falsify the theoretical model presented here

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References

    1. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition (beta version) Cephalalgia. 2013;33:629–808. doi: 10.1177/0333102413485658. - DOI - PubMed
    1. Bui SB, Petersen T, Poulsen JN, Gazerani P (2016) Headaches attributed to airplane travel: a Danish survey. J Headache Pain 17:33 - PMC - PubMed
    1. Mainardi F, Maggioni F, Lisotto C, Zanchin G (2013) Diagnosis and management of headache attributed to airplane travel. Curr Neurol Neurosci Rep 13:335 - PubMed
    1. Potasman I, Rofe O, Weller B. Flight-associated headaches-prevalence and characteristics. Cephalalgia. 2008;28:863–867. doi: 10.1111/j.1468-2982.2008.01601.x. - DOI - PubMed
    1. Mainardi F, Lisotto C, Palestini C, Sarchielli P, Maggioni F, Zanchin G. Headache attributed to airplane travel (“airplane headache’): first Italian case. J Headache Pain. 2007;8:196–199. doi: 10.1007/s10194-007-0390-y. - DOI - PMC - PubMed
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