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37 Headache Attributed toAirplane Travel
18. Nierenburg H, Jackfert K.Headache attributed to airplane travel: a review of literature. Curr
Pain Headache Rep. 2018;22(7):48.
19. Koçer A. Airplane headache and its management with oxymetazoline nasal spray: a case
report. J Headache Pain. 2020;21(1):151.
PMID: 33302898; PMCID: PMC7731784.
https://doi.org/10.1007/s11916- 018- 0701- 9.
https://doi.org/10.1186/s10194- 020- 01211- 8.
363
Chapter 38
Diving Headache
JulianaRamosde Andrade , MarcosAntônioInáciode OliveiraFilho,
andMarceloValença
38.1 Introduction
Headache attributed to disorders of homeostasis, as classied by the International
Classication of Headache Disorders, 3rd edition (ICHD-3), encompasses a group
of secondary headaches triggered by physiological imbalances such as hypoxia,
hypercapnia, and pressure changes [1]. Within this category, diving headache (DH)
represents a rare but clinically relevant phenomenon associated with the specic
environmental and metabolic challenges encountered during scuba diving.
Although often considered benign, diving headaches (DH) may reect a range of
underlying mechanisms, including carbon dioxide retention (hypercapnia) due to
inadequate ventilation of compressed gases, barotrauma involving the sinuses or
middle ear, decompression illness, arterial gas embolism, or the exacerbation of preexisting primary headache disorders such as migraine [2–4].
Among these, hypercapnia is the most consistently implicated etiology, typically
presenting as a bilateral, pulsatile headache during or shortly after a dive. Rapid
symptom resolution with the administration of 100% oxygen has been documented,
reinforcing its metabolic origin [3]. In other cases, headache may result from mask
compression, cervical muscle strain, or psychological tension, especially in novice
divers with anxiety or fear of marine life [5].
A retrospective review of incident reports published by Divers Alert Network
(DAN) International between 2001 and 2009 revealed that the absolute number and
J. R. de Andrade · M. A. I. de OliveiraFilho
Federal University of Pernambuco, Recife, Pernambuco, Brazil
M. Valença (
Federal University of Pernambuco, Recife, Pernambuco, Brazil
Center of Excellence in the Treatment of Migraine and Other Headache Disorders, Hospital
Esperança, Recife, Pernambuco, 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_38
*)
365© The Author(s), under exclusive license to Springer Nature
366
J. R. de Andrade et al.
relative percentage of headaches reported as the primary complaint in diving-related
incidents were consistently low. In 2001, 64 out of 1480 incidents (4.3%) involved
headache. This proportion peaked in 2002, with 57 cases among 573 incidents
(10%), and gradually declined over subsequent years. By 2008 and 2009, the number of headache-related incidents dropped signicantly, with only 12 and 17 cases
reported, respectively, representing 0.1 and 0.15% of the total incidents [2–7]. These
ndings suggest a downward trend in reported diving-related headaches, reinforcing the impression that DH is a relatively rare occurrence.
Accurate diagnosis requires a detailed clinical history and neurological examination, particularly in the presence of focal neurological signs, which may indicate
serious conditions that require urgent hyperbaric treatment [3]. Although DH is
rare, its clinical relevance lies in the need to differentiate benign headache from lifethreatening complications.
38.2 Pathophysiology
The pathophysiology of diving headache is multifactorial, involving a combination
of physiological and environmental stressors specic to the underwater setting.
These headaches can occur at various phases of the dive and are inuenced by
changes in ambient pressure, altered gas composition, cold exposure, physical exertion, and individual predispositions such as primary headache disorders. A solid
understanding of the underlying mechanisms is essential for accurate diagnosis,
effective management, and the development of preventive strategies, especially for
recreational or occupational divers at higher risk.
Hypercapnia, or elevated carbon dioxide levels, is one of the most wellestablished causes of diving headache. It results from inadequate ventilation of
compressed gases, often due to shallow breathing or poorly adjusted equipment,
leading to CO₂ accumulation. The consequent cerebral vasodilation increases intracranial pressure, triggering headache symptoms that are usually diffuse, throbbing,
and accompanied by confusion or malaise. Oxygen administration is the treatment
of choice in such cases, as it helps lower carbon dioxide levels and rapidly alleviates
symptoms [2, 4].
Barotrauma is another frequent cause, particularly involving the middle ear or
paranasal sinuses. Failure to properly equalize pressure during descent can create a
vacuum effect, resulting in mucosal stretching, localized pain, and headache, often
in the frontal or temporal regions. In more severe cases, such as barotrauma affecting the sphenoid sinus, vital adjacent neurovascular structures may be involved,
leading to vertigo, nausea, or even neurological decits [3, 8, 9]. On ascent, expand-
ing gas trapped in these cavities may exert mechanical pressure, further intensifying
the headache.
Additional contributors to diving headache include external compression from
tight-tting equipment, cold-water exposure, and physical exertion. Cold-stimulus
headaches and exertional headaches are typically benign and self-limiting but can
38 Diving Headache
367
be distressing for divers [2, 10]. Furthermore, individuals with a history of primary
headache disorders such as migraine or tension-type headache may experience
exacerbations triggered by the diving environment [11]. While most diving headaches are benign, serious conditions like decompression sickness or arterial gas
embolism must always be ruled out, particularly in the presence of neurological
symptoms [3, 4, 8]. A comprehensive understanding of these mechanisms is crucial
for clinicians to distinguish between benign and potentially life-threatening causes
and to ensure safe diving practices.
Diving headache does not follow a single, well-dened clinical phenotype.
Reported cases typically involve pain that begins during or shortly after diving, with
locations ranging from frontal and occipital to diffuse. The quality of the pain varies—pulsatile or pressing in nature—and its intensity ranges from mild to severe,
often lasting from a few minutes to several hours. In some cases, the headache is
aggravated by equipment use, pre-dive anxiety, or equalization maneuvers.
The multifactorial origin of DH includes potential triggers such as:
• CO₂ retention due to hypoventilation
• Sinus or middle ear barotrauma
• Cervical muscle tension
• Psychological stress
• Environmental conditions (cold water, depth, physical exertion)
Cases attributed to hypercapnia often respond quickly to 100% oxygen therapy,
reinforcing the metabolic nature of some DH subtypes.
Most frequently, DH is observed in individuals with a history of primary headache disorders—particularly migraine—suggesting that diving may act as a trigger
rather than an independent cause.
38.3 Case Presentation
A representative case report is not presented in this chapter due to the absence of a
typical clinical pattern and the heterogeneous nature of DH.Instead, we present a
clinical observation based on prospective eld data.
In 2013, a cohort of 50 recreational divers without a prior history of migraine
was prospectively assessed for headache occurrence within 24hours post-dive. The
sample consisted predominantly of males (90%), with a mean age of approximately
33years. Pre-dive anxiety was commonly reported, and 52% of participants used
medications to prevent motion sickness (e.g., meclizine). All participants provided
informed consent.
None of the divers reported headache during or after the dive. This nding supports the hypothesis, also observed in retrospective DAN data, that scuba diving
under safe, controlled conditions does not induce headache in healthy, non-migraine
individuals.
368
Unfortunately, we were not able to include a case of a patient with this type of
headache. Instead, we chose to present a study involving several individuals who
had undergone professional diving. However, none of them reported experiencing
headache. There may be a selection bias, as individuals who have previously experienced this type of headache may avoid diving exposure.
J. R. de Andrade et al.
38.4 Clinical Presentation
Diving headache remains a rare secondary headache disorder, more often associated
with individual susceptibility and situational stressors than with the diving activity
itself. Retrospective data from DAN International (2001–2009) demonstrate low
absolute and relative frequencies of headache reported as a primary complaint.
These values are notably lower than the general population prevalence of headache
in Brazil (15.2%), suggesting a low burden of DH.
This discrepancy may be due to underreporting, preemptive exclusion of chronic
headache sufferers from diving, and adherence to medical advice discouraging
dives deeper than 18 meters for individuals with migraine. The absence of headache
in the 2013 prospective cohort further supports the conclusion that scuba diving is
not an independent trigger of headache in individuals without primary headache
disorders.
Nonetheless, headache occurring during or after diving should always be evaluated carefully, especially when accompanied by focal neurological symptoms, as
these may indicate serious complications such as arterial gas embolism or decompression illness. In such cases, immediate referral to a hyperbaric facility is
warranted.
38.5 Diagnostic Algorithm
The diagnosis DH is straightforward, as it refers to any headache precipitated by the
act of diving. Since it is a multifactorial condition, the associated signs and symptoms will vary depending on the underlying cause. For example, it may result from
a tight-tting mask, barotrauma-related otitis, or be triggered in individuals with a
predisposition to migraine.
A. Any headache fullling criterion C
B. Both of the following:
1. The patient is diving at a depth>10 meters
2. No evidence of decompression illness
38 Diving Headache
C. Evidence of causation demonstrated by at least one of the following:
1. Headache has developed during the dive
2. Either or both of the following:
3. (a) Headache has worsened as the dive is continued
4. (b) Either of the following:
5. Headache has spontaneously resolved within three days of completion of
the dive
6. Headache has remitted within one hour after treatment with 100% oxygen
7. At least one of the following symptoms of CO2 intoxication:
(a) Mental confusion
(b) Light-headedness
(c) Motor incoordination
(d) Dyspnoea
(e) Facial ushing
D. Not better accounted for by another ICHD-3 diagnosis.
369
38.6 Treatment
Treatment begins with immediate removal of the individual from the act of diving,
always observing the necessary protocols for a slow ascent from deeper waters to
avoid complications such as gas embolism. Depending on the underlying cause,
specic treatment will be required.
38.7 Conclusion
Diving headache is a rare and multifactorial entity, more commonly affecting individuals with pre-existing primary headache disorders such as migraine. Evidence
from both retrospective DAN reports and a prospective cohort study indicates that,
when conducted under standard safety protocols, scuba diving does not independently cause headache in healthy individuals.
The absence of a typical clinical presentation justies the decision to forgo a
standard case report in this chapter. Instead, we emphasize the need for individualized assessment and awareness of risk factors. Preventive strategies—such as proper
screening, adherence to dive safety standards, and counseling for migraineurs—
remain effective measures to minimize the occurrence of DH.
370
J. R. de Andrade et al.
References
1. Headache Classication Committee of the International Headache Society (IHS). The
International Classication of Headache Disorders, 3rd edition (beta version). Cephalalgia.
2013;33(9):629–808.
2. Cheshire WP, Ott MC.Headache in divers. Headache. 2001;41(3):235–47.
3. Cheshire WP. Headache and facial pain in scuba divers. Curr Pain Headache Rep.
2004;8(4):315–20.
4. Burkett JG, Nahas-Geiger SJ.Diving headache. Curr Pain Headache Rep. 2019;23(7):46.
5. Di Fabio R, Vanacore N, Davassi C, Serrao M, Pierelli F.Scuba diving is not associated with
high prevalence of headache: a cross-sectional study in men. Headache. 2012;52(3):385–92.
6. Durham PL, Cady R.Insights into the mechanism of OnabotulinumtoxinA in chronic Migraine.
Headache. 2011;51(10):1573–7.
7. Lantéri-Minet M.The role of general practitioners in Migraine management. Cephalalgia.
2008;28(2_suppl):1–8.
8. Newton HB. Neurologic complications of scuba diving. Am Fam Physician.
2001;63(11):2211–8.
9. Schipke JD, Cleveland S, Drees M.Sphenoid sinus barotrauma in diving: case series and
review of the literature. Res Sports Med. 2018;26(1):124–37.
10. Indo T, Takahashi A.Swimmer’s migraine. Headache. 1990;30(8):485–7.
11. Beduhn B, Roe G, Furst W, Lewno A.Head pain in the competitive aquatic athlete—an approach
to a differential diagnosis and management. Curr Sports Med Rep. 2022;21(11):398–404.
Chapter 39
Dialysis Headache
AnaLuisade LimaAntoniazzi andAndreCleristonJosedos Santos
39.1 Introduction
Chronic kidney disease (CKD) is a signicant public health concern, with a high
global prevalence (850 million people in 2022, 7–12%) [1, 2]. A considerable proportion of these patients progress to end-stage renal disease (ESRD), requiring renal
replacement therapy (hemodialysis, peritoneal dialysis, or kidney transplantation).
Among these, hemodialysis remains the most widely available and commonly used
treatment, having saved millions of lives since its implementation in the 1940s [3].
Patients undergoing hemodialysis often experience a range of systemic and neurological symptoms, with headache being the most frequently reported [4]. Studies
dating back to the 1970s have characterized a distinct type of headache associated
with hemodialysis [5]. This chapter provides a concise review of hemodialysisrelated headache, discussing its clinical implications and future research directions.
39.2 Pathophysiology ofDialysis Headache
The pathophysiology of hemodialysis-related headache is multifactorial, with several mechanisms proposed to explain its occurrence [6]. Patients with CKD are
predisposed to neurological symptoms due to endothelial dysfunction, neurotoxin
accumulation, and electrolyte imbalances [7, 8]. Additionally, those undergoing
A. L. de LimaAntoniazzi (*)
Member of Brazilian Headache Society, Ribeirão Preto, Brazil
A. C. J. dos Santos
Department of Neurology at the Hospital das Clínicas, Ribeirão Preto Medical School–
University of São Paulo, Ribeirão Preto, 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_39
371© The Author(s), under exclusive license to Springer Nature
372
A. L. de LimaAntoniazzi and A. C. J. Santos
hemodialysis experience acute homeostatic alterations, which may contribute to
headache development.
In a seminal 1972 study, Bana etal. suggested that hemodialysis-related headaches might be linked to “dialysis disequilibrium syndrome” [5]. This syndrome is
characterized by mental confusion, nausea, and headache occurring during or after
dialysis. The rapid removal of urea and the production of idiogenic osmoles in the
brain create a gradient between the blood and brain, resulting in water inux into
brain tissue, leading to edema and increased intracranial pressure [9]. However,
Bana also hypothesized that additional mechanisms were involved, as headache frequently occurred in isolation and often resembled other primary headache disorders, such as migraine and tension-type headache. Subsequent research has
conrmed his hypothesis, revealing multiple contributing factors.
Several elements have been implicated in dialysis headache, including dialysate
composition, electrolyte imbalances, vasoactive substances, cerebrovascular regulation, hemodynamic changes, and variations in uid balance [10].
One study reported that patients undergoing bicarbonate dialysis experienced
fewer headaches compared to those receiving acetate dialysis [11]. However, a more
recent study found no signicant difference related to dialysate composition [4].
Regarding the hemodialysis technique, evidence suggests that online hemodialtration offers substantial protection against headache development when compared to
conventional methods [12].
Electrolyte disturbances, such as low pre-dialysis sodium levels, magnesium
uctuations, and urea and renin concentrations, have been identied as risk factors
for dialysis headache [6, 13–15]. The ultraltration rate also appears to be a contributing factor, with slower rates tending to cause fewer headaches [10, 16]. Blood
pressure (BP) variability, both pre-dialysis hypertension and intradialytic hypotension, has also been linked to headache occurrence [4, 6, 17].
Vasoactive substances, such as nitric oxide and bradykinin, exhibit elevated levels during hemodialysis and have been implicated in other primary headaches [18].
These substances alter cerebrovascular regulation, as demonstrated by a transcranial
Doppler ultrasound study by Sousa Melo et al., which revealed reduced middle
cerebral artery pulsatility in patients experiencing dialysis headache compared to
those without headache [19]. Additionally, increased levels of substance P and calcitonin gene-related peptide (CGRP) have been associated with headache onset
before or after dialysis [20]. The role of CGRP was conrmed in a recent study that
evaluated patients with hemodialysis-induced headaches without a history of primary headaches, also demonstrating higher levels in those experiencing headaches [21].
39 Dialysis Headache
373
39.3 Case Presentation
A 51-year-old female teacher with a history of hypertension, type 2 diabetes mellitus, and generalized anxiety disorder, had no prior history of headaches. She also
had no family history of migraine or other primary headaches. Due to end- stage
renal disease, she initiated hemodialysis three times per week, with each session
lasting 4 hours.
She reported a unilateral frontal headache (without a preferential side), pulsating
in nature, and of severe intensity (8/10 on the Visual Analog Scale—VAS), typically
beginning 2–3 hours after the start of the dialysis session. The headache was not
associated with photophobia or phonophobia and tended to persist for 6–8 hours
after the session in the absence of treatment. It signicantly impacted her quality of
life to the extent that she described it as the most bothersome symptom during
hemodialysis sessions.
No signicant changes in blood pressure were observed before, during, or after
hemodialysis. Additionally, sodium, potassium, magnesium, urea, calcium, and
other electrolyte levels remained within normal limits. Neurological examination
was unremarkable. However, given the recent onset of headache and her concern
about secondary causes, a brain magnetic resonance imaging (MRI) was performed,
revealing only mild microangiopathy (Fazekas 2).
During dialysis sessions, the pain improved, though usually incompletely, with
intravenous dipyrone (2g). The patient also noted that when the headache persisted
for several hours after dialysis, she occasionally used an over-the-counter analgesic
(Dorex®: dipyrone 300mg, caffeine 50mg, and orphenadrine 35mg), which provided relief in some instances.
39.4 Case Discussion
This case illustrates a common presentation of hemodialysis headache. A clear temporal relationship was observed, with the pain beginning during dialysis sessions
and typically resolving within a few hours after their completion. The headache
intensity ranged from moderate to severe, signicantly affecting the patient’s quality of life.
Although the headache was unilateral and pulsatile, it lacked additional features
characteristic of migraine or tension-type headache. Notably, the pain pattern did
not follow a specic characteristic and could even mimic other primary headache
disorders.
Blood pressure remained controlled and did not show signicant uctuations
during dialysis sessions, ruling out hypertensive crisis as a potential cause. The
patient reported symptom relief with a common analgesic and a caffeine-containing
medication but did not exhibit excessive caffeine consumption, limiting her intake