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Chapter 37
Headache Attributed toAirplane Travel
HiltonMarianoda SilvaJúnior andLeticiaBragaliaPassarella
37.1 Introduction
Aeroplane headache (AH), or headache attributed to aeroplane travel, is a distinct
and fascinating type of head pain that occurs exclusively during air travel. First
described in 2004 by Atkinson and Lee [1], AH has since gained recognition as a
specic clinical condition, characterized by sudden, severe headaches triggered by
changes in cabin pressure. Although air travel is now one of the safest and most
widely used forms of transportation, moving millions of people worldwide daily,
these debilitating headaches during certain ight phases remain underrecognized
and often misunderstood. Initially, AH caught the medical community’s attention
through isolated case reports and small-scale clinical studies [2], providing a limited
understanding of its causes, symptoms, and potential treatments. Only after larger
studies were conducted was AH ofcially acknowledged as a distinct medical condition. This milestone led to its inclusion in the International Classication of
Headache Disorders, third edition (ICHD-3) [3], providing standardized diagnostic
criteria that have guided further research and clinical identication. Before this classication, the absence of clear diagnostic guidelines made it difcult to distinguish
AH from other types of headaches, like migraines, tension headaches, or sinusrelated pain, which can present with comparable symptoms. Growing awareness of
AH has opened up new investigation paths into its epidemiology, underlying mechanisms, and management strategies, underscoring its importance in clinical practice
and public health. Research shows that AH most often occurs during aircraft descent,
strongly linked to rapid shifts in cabin and atmospheric pressure. The pain is characteristically described as sharp, pulsating, or stabbing, often affecting just one side
of the head, especially around the forehead and eye.
H. M. da SilvaJúnior (*) · L. B. Passarella
Pontical Catholic University of Campinas, School of Medicine, Sao Paulo, Brazil
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_37
353© The Author(s), under exclusive license to Springer Nature
354
H. M. da SilvaJúnior and L. B. Passarella
Yet, despite these advances, much remains unknown about the precise mechanisms behind AH.Possible factors include sinus barotrauma, cerebral blood vessel
dilation, and individual anatomical differences. Managing AH is still a challenge,
with treatments based mainly on case reports and clinical observations rather than
solid randomized controlled trials (RCTs). Some medications, like non-steroidal
anti-inammatory drugs (NSAIDs), triptans, and nasal decongestants, have shown
promise, particularly when taken before a ight, but standardized treatment protocols are still lacking. There is a strong need for further research to better understand
and manage this condition.
This chapter aims to present a comprehensive and updated review of AH, encompassing its epidemiology, pathophysiological theories, diagnostic criteria, and current therapeutic strategies. The goal is to provide healthcare professionals with
practical tools to identify, diagnose, and manage AH effectively, ultimately improving the quality of life and travel experience for affected patients. The potential
impact of this research on patient care is signicant and should not be
underestimated.
37.2 Pathophysiology
The exact pathophysiology of aeroplane headache (AH) remains incompletely
understood. However, several mechanisms have been proposed to explain its origin,
with most hypotheses emphasizing the interaction between cabin pressure changes
and individual anatomical or physiological predisposition.
1. Sinus Barotrauma Due to Cabin Pressure Changes
One of the most broadly accepted mechanisms is sinus barotrauma resulting
from rapid cabin pressure uctuations during takeoff and landing. These pressure
shifts may provoke an imbalance between the atmospheric pressure and the pressure
within the paranasal sinuses, leading to nasal mucosal damage, local inammation,
and activation of pain pathways [9, 14]. Berligen and Mungen [5] proposed that AH
commonly results from the temporary local inammation caused by hypoxia or dryness in the sinus mucosa or sinus barotrauma. They advocate that their treatment
ndings in patients support this hypothesis. According to them, AH did not occur in
95% of the patients in their subsequent ights when they received naproxen sodium
(550mg) one hour before takeoff. In a person who suffers from AH, it was proposed
that there are possible anatomical variations, particularly in the ethmoidal sinuses,
causing reduced patency of the nasal pathways and making it difcult to equalize
pressure during ascent or descent. The ethmoidal air cells and arteries, innervated
by the ethmoidal nerve (a branch of the ophthalmic division of the trigeminal nerve),
may become sensitized due to barotrauma, triggering inammatory responses and
activating both the trigeminovascular system and trigeminocervical complex, leading to the typical fronto-orbital pain seen in AH.Additionally, negative pressure
within the sinuses may contribute to tissue inammation and a “vacuum effect,”
37 Headache Attributed toAirplane Travel
355
thereby further intensifying pain. Although many AH patients consistently show
normal ndings on ENT (ear, nose, and throat) workup, this may reect mild (rstdegree) barotrauma not detectable through routine diagnostics [8, 12].
2. Cerebral Vasodilation and Prostaglandin E2 (PGE2) Release
Cerebral vasodilation is at the core of an additional proposed mechanism for
AH.Fluctuations in atmospheric pressure may induce vasodilation of cerebral arteries, possibly mediated by prostaglandin E2 (PGE2), a powerful vasodilator produced by mast cells and cerebral endothelial cells. In the experimental study by Bui
etal. [15], 14 participants were evaluated using a pressure chamber to simulate
(AH) conditions. The study included seven individuals with a history of AH and
seven healthy controls, with a mean age of 24years (±1.6), comprising four males
and 10 females. All participants in the AH group developed headache attacks during
the simulated ight, while none of the control group experienced symptoms. The
AH attacks were mostly fronto-orbital, unilateral, and described as stabbing or pulsating, with severe or moderate intensity. Biomarker analysis showed that cortisol
and prostaglandin E2 (PGE2) levels were signicantly elevated in AH patients compared to controls, and oxygen saturation (SPO) was markedly lower in the AH group
during the simulated ight. These ndings suggest that AH predominantly affects
young adults and is associated with physiological changes during pressure alterations, supporting the use of pressure chamber models to study AH mechanisms and
potential therapeutic targets. PGE2 may induce vasodilation and activate perivascular sensory afferents, contributing to headache generation. Furthermore, local sinus
inammation during AH episodes could stimulate PGE2 release, supporting its
potential role as a biomarker and mediator in AH pathophysiology [14].
3. Cerebral Vasoconstriction (Controversial Hypothesis)
Although less supported, some evidence suggests cerebral vasoconstriction may
contribute to AH.Hiraga etal. [16] reported the case of a 74-year-old woman who
presented with thunderclap headache during aeroplane descent. A magnetic resonance angiography showed segmental vasoconstriction of cerebral vessels that
improved 9days after onset. Nevertheless, this hypothesis remains controversial, as
AH clinical features differ from those of reversible cerebral vasoconstriction syndrome (RCVS), particularly concerning shorter attack duration (typically <30minutes) and absence of postictal headache [17].
4. Psychological Factors (Anxiety and Stress)
Anxiety and mental stress have been found at higher rates in patients with AH
attacks, hence making these potential inuencing factors to the development of
AH.Psychological stress and anxiety are also recognized as possible contributing
factors. Anticipatory anxiety, notably in individuals with prior painful episodes,
may exacerbate AH symptoms or even act as a trigger. The fear of ying and associated somatic responses may amplify pain perception in susceptible individuals [18].
Besides, Bui etal. [15] demonstrated that cortisol a primary stress hormone released
by the hypothalamic–pituitary–adrenal (HPA) axis was signicantly elevated in AH
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H. M. da SilvaJúnior and L. B. Passarella
patients when subjected to barometric pressure changes mimicking aeroplane ascent
and descent.
5. Hypoxia
Although hypoxia is not prominently featured in recent AH pathophysiological
models, cabin pressure changes may indirectly reduce oxygen availability, potentially affecting individuals who are sensitive to hypoxia. While not a primary mechanism, hypoxia may act synergistically with other factors in some cases [2, 5].
6. Anatomical and Environmental Factors
Structural abnormalities, such as nasal septum deviation, frontal sinus polyps, or
mucosal edema, may impede normal sinus ventilation and pressure equalization,
predisposing to AH.Furthermore, environmental factors including aircraft type,
speed, angle of ascent/descent, and cabin pressurization systems may inuence the
occurrence and severity of AH episodes [5].
7. Differential Diagnosis and Secondary Causes
According to ICHD-3, AH is classied as a primary headache. However, it is
crucial to exclude secondary causes, particularly acute and chronic sinusitis, nasal
or sinus masses, and RCVS.Serial imaging studies (e.g., magnetic resonance imaging [MRI], MRA) may be required when clinical suspicion persists [8].
8. Inammatory Processes
An inammatory component is also suspected in AH pathogenesis, supported by
the observed benet of NSAIDs (e.g., ibuprofen, naproxen) in some cases [8]. The
role of local inammation, whether initiated by barotrauma, vascular changes, or
both, remains a subject of ongoing investigation.
In summary, the pathophysiology of AH appears to be multifactorial, possibly
involving sinus barotrauma triggered by rapid changes in cabin pressure. This leads
to local inammation, trigeminal nerve activation, and potential vasodilation of
cerebral arteries. The imbalance between intrasinus and external cabin pressure is
believed to be a key factor. Nevertheless, further research is needed to elucidate the
underlying mechanisms of this condition fully.
37.3 Case Presentation
A 45-year-old woman presented to our private clinic with a history of headache
attacks that occur during aeroplane ights. Such attacks started six months previously and never came outside of plane ights. The patient regularly ies from Brazil
to the USA for family reasons every two weeks. The attacks began during takeoff
and before landing. The headache was left-sided, orbitofrontal, sometimes also
placed in the vertex, was pulsatile in quality, had moderate-to-severe intensity, and
was associated with nausea, photophobia, and phonophobia. The attacks usually last
37 Headache Attributed toAirplane Travel
357
45minutes. Headache spontaneously improved within 30minutes after the ascent
or descent of the aeroplane. The patient tried over-the-counter medications, such as
paracetamol, dipyrone, ibuprofen, and acetylsalicylic acid (isolated or in combination), to take before and during the ight, with a slight response. She has a previous
history of systemic arterial hypertension. The neurological examination showed no
abnormalities. An extensive neurological and otolaryngological workup was unremarkable. The patient’s clinical picture fullls the International Classication of
Headache Disorders-3 criteria for AH.Naratriptan 2.5mg was prescribed 30minutes before the ight and landing. The patient reported no more headaches during
takeoff and landing. She had tried this therapeutic approach at least 10 times until
our last communication.
Some studies have investigated the epidemiology of AH, although clear epidemiological data are still limited. It is critical to consider that much of the initial
epidemiological data on aeroplane headache was derived from case series and small
cohort studies. Chronologically, the epidemiologic landmarks of headache attributed to aeroplane travel are as follows:
• 2004: A 28-year-old man experienced severe jabbing headaches over the fore-
head and between the eyes during aeroplane ascent and descent, resolving at
cruising altitude. It was the rst description of “headache associated with aero-
plane travel” in the literature [1].
• 2006: Six cases of AH were reported [2]. All patients were male, with a mean age
of 37.3years (ranging from 33 to 42years), and the mean age of headache onset
was 35.4 years. The average disease duration was 2.1 years, varying from
7months to 4years.
• 2008: A cohort study by Potasman etal. [4] found that approximately 5.7% of
906 air travelers attending a travel clinic for a wide range of other complaints
were affected by AH.The mean age was 33.3±14.2years (range 18–91years).
It is a noteworthy clinical condition among individuals who frequently travel by
air. A signicant female predominance was observed, and 19.2% of individuals
with AH also had a formal diagnosis of migraine.
• 2011: Berilgen and Müngen [5] studied 33 patients with AH, of whom 28 were
men (85%) and 5 were women (15%). The mean age of the patients was
33.1± 8.2years, and headaches typically began suddenly during the descent
phase of ights, although some occurred during the ascent phase. The authors
proposed preliminary diagnostic criteria and possible mechanisms of etiopatho-
genesis for headaches associated with aeroplane travel.
• 2011: İpekdal etal. [6] reported ve patients (three women and two men) suffer-
ing from AH, the mean age was approximately 30years (from 27 to 32). All
patients experienced headaches exclusively during aeroplane ascent or descent.
• 2012: Mainardi etal. [7] evaluated 75 patients with AH, with a male predomi-
nance (61.3%) and a mean age of 36.5years. Most patients (88%) developed
headaches after their rst ight, and over half (54.6%) had coexisting primary
headaches, mainly tension-type and migraine without aura.
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H. M. da SilvaJúnior and L. B. Passarella
• 2013: The third edition of the International Classication of Headache Disorders
(ICHD-3) recognized headache attributed to aeroplane travel as a distinct type of
secondary headache [2].
• 2016: Bui etal.’s Danish survey [8] included 21 patients (9 males, 12 females)
with a mean age of 39±14years among 254 Scandinavian air travelers. The 21
participants (8.3%) fullled the aeroplane headache (AH) diagnostic criteria
dened by ICHD-3.
• 2017: Bui etal. [9] analyzed 39 scientic papers representing 275 patients. This
review highlights the initially reported male predominance; however, as more
case reports emerged, no signicant gender predominance was observed. The
median age at diagnosis was 28.7±4.8years.
• 2018: The third edition of the International Classication of Headache Disorders
(ICHD-3) was published [10].
• 2018: In the rst multicentric survey on aeroplane headache (AH) in a pediatric
population, De Carlo etal. [11] evaluated 320 children with primary headaches
who had travelled by aeroplane, identifying 15 cases (4.7%) of AH.The mean
age at headache onset was 7.2 years, and the mean age at recruitment was
12.4years, with a marked female predominance (80%).
• 2020: Lima etal. [12] conducted a prospective, cross-sectional study involving
Brazilian medical students who had traveled by aeroplane at least three times.
The study included 155 participants, among whom 14.2% (22/155) reported
experiencing headache attributed to aeroplane travel (AH), corresponding to
7.5% of all ights (80/1070 trips). Among those affected, 63.6% (14/22) were
men and 36.4% (8/22) were women, indicating a slight male predominance,
although this difference did not reach statistical signicance. The mean age of
individuals with AH was 22.4years for those experiencing headaches during
takeoff or landing, and 23years for those reporting headaches during the cruise
phase, consistent with the overall young demographic of the medical student
population. Notably, most headaches (77.3%) occurred during takeoff and land-
ing, highlighting these ight phases as primary triggers for AH.
• 2022: In an extensive cross-sectional study, Konrad etal. [13] assessed 50,000
airline passengers and found a 0.2% prevalence of aeroplane headache (AH),
much lower than previous reports. The mean age of affected individuals was
41.8years, with no signicant difference in gender. Most headaches began dur-
ing periods of pressure change (79.2%) and were short-lived (lasting ≤30min-
utes in 82.2%).
The prevalence of headache attributed to aeroplane travel varies between studies,
possibly due to the different populations studied and data acquisition methodologies. While initially thought to affect adult males more, more recent data suggest
there might not be a signicant gender predominance in adults. In children with
primary headaches, it is more prevalent in females and presents distinct characteristics. More population-based studies are needed to determine the exact prevalence in
the general population and to better understand the risk factors and clinical features
of this condition.
37 Headache Attributed toAirplane Travel
359
37.4 Headache Characteristics
The typical clinical picture of AH is a sudden, severe, and strictly unilateral pain,
typically located in the frontal, orbital, or fronto-orbital regions, and closely linked
to aeroplane travel, particularly during takeoff and landing [4, 5, 7–9]. It lasts a few
to 30minutes, sometimes accompanied by ipsilateral nasal congestion or lacrimation. The pain is frequently described as sharp, stabbing, jabbing, or pulsating, with
moderate-to-severe intensity, and usually resolves spontaneously within 5–30minutes after pressure stabilization. Seldom are migraine-like symptoms like nausea,
photophobia, and phonophobia present. AH primarily affects young to middle-aged
adults, with some studies suggesting a slight male predominance, though more
recent data indicate no signicant gender difference. Its hallmark is the exclusive
occurrence during ights, without headache episodes outside air travel. Aeroplane
headache is a primary headache under the International Classication of Headache
Disorders (ICHD-3):
10.1.2 Headache Attributed to Aeroplane Travel
Description:
Headache, often severe, usually unilateral and periocular and without autonomic
symptoms, occurring during and caused by aeroplane travel. It remits after landing.
Diagnostic criteria:
A. At least two episodes of headache fullling criterion C
B. The patient is traveling by aeroplane
C. Evidence of causation demonstrated by at least two of the following:
1. Headache has developed during the aeroplane ight
2. Either or both of the following:
(a) Headache has worsened in temporal relation to ascent following takeoff
and/or descent before landing of the aeroplane
(b) Headache has spontaneously improved within 30 minutes after the
ascent or descent of the aeroplane is completed
3. Headache is severe, with at least two of the following three characteristics:
(a) Unilateral location
(b) Orbitofrontal location
(c) Jabbing or stabbing quality
1
2
3
D. Not better accounted for by another ICHD-3 diagnosis4.
Notes:
1. Side-shift between different ights occurs in around 10% of cases.
2. Parietal spread may occur.
3. Pulsation (throbbing) may also be noted.
4. In particular, sinus disorder should be excluded.
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H. M. da SilvaJúnior and L. B. Passarella
37.5 Case Discussion
Our case demonstrates various distinctive features supporting the diagnosis of aeroplane headache (AH), by the International Classication of Headache Disorders,
third edition (ICHD-3, code 10.1.2). The headache presents an exclusive temporal
relationship with aeroplane travel, specically during takeoff and landing, directly
correlating with cabin pressure changes. The pain is strictly unilateral, localized to
the orbitofrontal and vertex regions, which aligns with the typical distribution
described in AH.The headache is characterized by a pulsatile quality, with moderateto- severe intensity, and demonstrates spontaneous resolution shortly after cabin
pressure stabilizes. The absence of headache attacks outside of ights reinforces the
situational and mechanically triggered nature of this condition. Although associated
migrainous symptoms, including nausea, photophobia, and phonophobia, are not
universally reported in AH, their presence in this case may reect individual variation in pain processing. Additionally, neurological, otolaryngological, and imaging
evaluations were unremarkable, ruling out other structural or sinus-related causes.
37.6 Treatment
Many medications have been used to treat and prevent aeroplane headache (AH),
with variable degrees of reported efcacy according to different sources [7, 14, 18,
19]. These pharmacological approaches include non-steroidal anti-inammatory
drugs (NSAIDs), triptans, and nasal decongestants. However, it is essential to
emphasize that most of the available evidence regarding the effectiveness and use of
these medications is derived from case reports, small case series, and retrospective
studies. While these sources offer valuable insights into possible treatment options,
they are limited by their observational nature and small sample sizes, which prevent
broader generalizations. Therefore, randomized controlled trials (RCTs) are critically needed to establish more denitive and evidence-based treatment guidelines
for managing aeroplane headache. Robust clinical studies would help determine the
most effective medications, appropriate dosing regimens, and preventive strategies,
ultimately improving the care and quality of life for individuals affected by this
condition. Until such data are available, therapeutic approaches to AH will remain
based on empirical evidence and individual patient responses as observed in clinical
practice. The pharmacological and non-pharmacological approaches to treat AH are
shown in Tables 37.1, 37.2 and 37.3:
37 Headache Attributed toAirplane Travel
361
Table 37.1
Class Examples How to use Evidence/Comments
Triptans Naratriptan 2.5mg,
NSAIDs Ibuprofen 400–600mg,
Combination
(triptan +
NSAID)
Nasal
decongestants
Table 37.2
Class Examples Evidence/Comments
Analgesics Paracetamol 1g, dipyrone
NSAIDs Ibuprofen, naproxen It may offer partial relief but is less effective
Triptans Sumatriptan 50mg oral or 6mg
Preventive treatment
sumatriptan 50–100mg,
zolmitriptan 2.5mg
naproxen 500mg
Naratriptan + ibuprofen,
etc.
Pseudoephedrine
60–120mg,
oxymetazoline nasal
spray
Acute treatment
(Metamizole)
subcutaneous
Take 30–60minutes
before takeoff and/or
landing
Take 1hour before
ight
Take before ight Anecdotal reports suggest
Use 30–60minutes
before ight
Often insufcient alone but may help in mild
cases
than prophylactic triptans
If not used preventively, may be attempted as
rescue
According to case reports,
the most effective
prophylaxis is long-acting
triptans, which are
preferred
Variable efcacy; may help
in milder cases
possible additive effect
It may help if sinus
barotrauma is suspected;
there is limited evidence
Table 37.3
Approach Description
Pressure equalization
techniques
Nasal saline sprays To improve sinus drainage before/during ight
Behavioral strategies Stress/anxiety management for psychological components
Avoidance of known triggers Choosing seats near the wing, avoiding ights during respiratory
Non-pharmacological approaches
Yawning, swallowing, chewing gum, and using the Valsalva
maneuver
infections
37.7 Conclusion
Aeroplane headache (AH) is a unique, under-recognized condition that can cause
signicant distress during air travel. Recognizing AH as a distinct headache entity
has advanced understanding, classication, and therapeutic approaches. Prophylactic
measures with NSAIDs and triptans, possibly combined with nasal decongestants,
are currently the most effective strategies. More controlled studies are needed to
conrm optimal treatments and elucidate the underlying mechanisms of AH, to
improve patient outcomes and comfort during ights.
362
H. M. da SilvaJúnior and L. B. Passarella
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