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14 Cold-Stimulus Headache
137
activation is transmitted to the trigeminal nucleus in the brainstem, resulting in a
referred pain sensation in the head. It is speculated that the participation of Transient
Receptor Potential Melastatin 8 (TRPM8) is crucial in this process, as this coldsensitive receptor, expressed in primary afferent neurons of the trigeminal ganglia
or dorsal root, plays a role in neuronal sensitization, mediating responses to thermal
stimuli and contributing to pain transmission [19, 20].
Additionally, cold can trigger a rapid vascular response in the cranial region,
starting with vasoconstriction followed by compensatory dilation of the blood vessels [12]. These uctuations can exacerbate the onset of pain, especially in individuals with migraine, as the underlying mechanism of transitioning from vasoconstriction
to vasodilation of cranial arteries, often associated with the pathophysiology of
migraine, can be observed in cold-stimulus headache attributed to ingestion or inhalation of cold stimuli [17, 18]. It is possible that TRPM8, by regulating the activation of cold-related nerve bers, plays a crucial role in these vascular responses,
directly inuencing the perception of pain by increasing sensitivity to cold stimuli [21].
Finally, the trigeminovascular reex plays a key role in various primary headaches, including cold-stimulus headache, which is attributed to the ingestion or
inhalation of cold stimuli. Activation of this system can lead to the release of
inammatory neuropeptides, such as calcitonin gene-related peptide (CGRP),
which amplies pain perception. Moreover, cold sensitivity is inuenced by
genetic and neurophysiological factors, with individuals who have a history of
migraine showing a greater predisposition to respond intensely to cold stimuli
[18, 19].
14.3 Case Presentation
We will describe the clinical case of two volunteers who experienced a migraine
headache after being stimulated with ice. To induce pain, a standardized ice cube
measuring 15×20mm was placed on the palate. The volunteers were instructed to
close their mouths and keep the lower jaw immobile during the test. The ice contact
time on the palate was set at 90s. Both volunteers reported a prior history of headache attributed to the ingestion or inhalation of cold stimuli and were able to tolerate
the ice stimulation for the full 90s. They also stated that they avoided consuming
cold foods to prevent the unpleasant sensation, and when consuming, they preferred
to eat in a slower, more gradual manner at lower temperatures as alternatives to
avoid triggering the pain.
The study was approved by the Ethics in Research Committee of the Health
Science Center of the Federal University in Pernambuco, Brazil, under protocol
number 089/2008 in accordance with resolution 196/96 of the National Health
Council and in line with the principles of the Declaration of Helsinki.
138
D. A. de Oliveira and M. Valença
14.3.1 Clinical Case 1
A 19-year-old healthy woman with a diagnosis of migraine for approximately
10 years. The frequency of migraine attacks was, on average, two episodes per
week, with a pain intensity of 8 on the numeric visual scale. She reported not using
any prophylactic treatment for headaches, relying instead on analgesics to abort the
attacks. During ice stimulation, the pain was described as an intense stabbing sensation of short duration (13s), with a pain intensity of 9 on the numeric visual scale,
occurring bilaterally in the temporal region, spontaneously resolving within 2min
after removal of the cold stimulus. Approximately one hour after ice stimulation, the
patient experienced a migraine attack lasting an average of six hours, accompanied
by other associated symptoms such as nausea and photophobia.
14.3.2 Clinical Case 2
A 38-year-old healthy woman with a diagnosis of migraine for ve years. She
reported frequent migraine attacks, approximately three episodes per week, with a
pain intensity of 10 on the numeric visual scale. She had not been under specialized
medical care for headache management for the past three years and relied on analgesics to abort attacks. During ice stimulation, the pain was described as an intense
stabbing sensation, short in duration (25s), with an intensity of 8 on the numeric
visual scale, occurring unilaterally in the temporal region (the side associated with
her habitual migraine). The pain spontaneously resolved within 2min after removal
of the cold stimulus. The volunteer then began a migraine episode approximately
three hours after the ice test, lasting an average of twelve hours, accompanied by
nausea, vomiting, osmophobia, photophobia, and phonophobia. In both cases, the
volunteers reported using medication for pain relief but did not achieve success.
14.4 Case Discussion
These cases demonstrate the complexity of cold-stimulus headache in patients with
a previous diagnosis of migraine. Both patients experienced a cold-induced headache during the ice stimulation protocol, characterized by a short-lasting, intense
stabbing pain localized to the temporal region. Notably, the pain resolved spontaneously within two minutes after removal of the cold stimulus in both cases.
In the rst case, a 19-year-old woman with a long-standing history of migraine
experienced an attack approximately one hour after cold exposure, accompanied by
classic migrainous symptoms. In the second case, a 38-year-old woman developed
a migraine episode about three hours after the ice stimulation, which lasted for
approximately twelve hours.
14 Cold-Stimulus Headache
139
The temporal relationship between the cold stimulus and the onset of migraine
episodes in both patients raises the possibility of a triggering role of cold exposure
in susceptible individuals. Neither patient had been under prophylactic treatment,
and both relied solely on abortive analgesics, which proved insufcient in managing
their symptoms. This highlights the importance of considering preventive strategies,
particularly in patients with frequent and disabling attacks, and in whom cold exposure may act as a potential trigger.
Although CSH typically presents as a brief, self-limited pain, its ability to trigger
full-blown migraine attacks in individuals with migraine predisposition suggests a
potential pathophysiological overlap or sensitization. Further, the variable latency
between the stimulus and the onset of migraine, as well as the different proles of
associated symptoms, reects the heterogeneity of responses in migraine patients.
14.5 Clinical Characteristics
Headache attributed to ingestion or inhalation of cold stimuli is characterized by
sharp, short-lasting pain, typically described as pulsating or stabbing, occurring
after the consumption of cold food or beverages or inhalation of cold air. It is commonly referred to as the frontal or temporal region, and more frequently bilateral
(though it can be lateralized to the side of habitual migrainosus headache in individuals experiencing unilateral headache). The pain spontaneously resolves upon
removal of the cold stimulus. Although not incapacitating, its presentation can be
uncomfortable, with intensity ranging from moderate-to-intense but transient [1].
Rarely do individuals with this condition seek medical attention, as it is an avoidable condition.
The primary trigger of headache attributed to ingestion or inhalation of cold
stimuli is the consumption of icy foods or beverages, such as ice cream or cold
water [1]. For this reason, individuals with this type of headache often avoid consuming such foods [22]. Studies indicate that about half of migraine patients take
specic precautions when consuming cold foods, aiming to minimize the risk of
triggering painful episodes [2, 11].
Individuals with a history of migraine are more predisposed to headache attributed to ingestion or inhalation of cold stimulus, likely due to hyperexcitability of the
trigeminovascular system [2, 4, 5, 7, 8, 10, 17]. This heightened sensitivity to cold
stimuli suggests a shared pathophysiological link between the two conditions,
involving the amplication of pain perception mediated by inammatory neuropeptides and sensory neural pathways [18]. These factors highlight the importance of
considering a migraine history in the evaluation of patients with headache induced
by cold stimuli.
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D. A. de Oliveira and M. Valença
14.6 Diagnostic Algorithm forCold-Stimulus Headache
The diagnosis of headache attributed to ingestion or inhalation of cold stimulus is
predominantly clinical, based on a detailed patient history and the identication of
typical triggers, according to the criteria proposed by the International Classication
of Headache Disorders [1].
Step 1: Clinical Suspicion
• Identify Key Symptoms:
– Sudden-onset, sharp or stabbing head pain triggered by direct exposure to
cold stimuli (e.g., ice packs, cold wind, swimming in cold water, ingestion
of cold food or drinks).
– Pain is typically short in duration (seconds to minutes), localized to the
forehead, temples, or occipital region.
– In some cases, particularly in individuals with migraine, the cold stimulus
may trigger a delayed migraine attack (minutes to hours later).
– No underlying structural abnormalities on neuroimaging.
Step 2: Rule Out Secondary Causes
• Clinical History and Examination:
– Exclude other causes of cold-induced pain, such as trigeminal neuralgia,
sinus pathology, or Raynaud’s phenomenon.
– Evaluate for signs of systemic illness or neurological decit.
Step 3: Evaluate for Comorbid Migraine
• Assess Headache History:
– Determine the presence of an underlying primary headache disorder, espe-
cially migraine.
– Identify if cold-stimulus acts as a consistent trigger for migraine episodes;
– Consider the frequency, intensity, and duration of subsequent migraine
attacks.
Step 4: Apply ICHD-3 Diagnostic Criteria (Table 14.1)
• Use the criteria from ICHD-3 (2018) to classify:
– 4.5.1: External application of cold stimulus.
– 4.5.2: Ingestion or inhalation of cold stimulus.
– 4.5.3: Probable Cold-stimulus Headache (when criteria are almost, but not
fully, met).
14 Cold-Stimulus Headache
141
Table 14.1
Classication of Headache Disorders [1]
4.5 Cold-stimulus headache
Description: Headache brought on by a cold stimulus applied externally to the head or ingested
or inhaled.
4.5.1 Headache attributed to the external application of a cold stimulus
Description: Headache following exposure of the unprotected head to a very low environmental
temperature.
Diagnostic criteria:
A.At least two acute headache episodes fullling criteria B and C
B.Brought on by and occurring only during application of an external cold stimulus to the
C.Resolving within 30min after removal of the cold stimulus
D.Not better accounted for by another ICHD-3 diagnosis.
4.5.2 Headache attributed to ingestion or inhalation of a cold stimulus
Description: Short-lasting frontal or temporal pain, which may be intense, is induced in
susceptible people by the passage of cold material (solid, liquid, or gaseous) over the palate and/
or posterior pharyngeal wall.
Diagnostic criteria:
A.At least two episodes of acute frontal or temporal headache fullling criteria B and C
B.Brought on by and occurring immediately after a cold stimulus to the palate and/or
C.Resolving within 10min after removal of the cold stimulus
D.Not better accounted for by another ICHD-3 diagnosis.
4.5.3 Probable cold-stimulus headache
Diagnostic criteria:
A.A single headache episode fullling criteria B and C
B.Brought on by and occurring only during or immediately after a cold stimulus applied
C.Resolving within 10min after removal of the
cold stimulus
D.Not fullling ICHD-3 criteria for any other headache disorder.
E.Not better accounted for by another ICHD-3
Diagnosis
Comment: Codable subforms are 4.5.3.1 Headache, probably attributed to external application
of a cold stimulus, and 4.5.3.2 Headache, probably attributed to ingestion or inhalation of a
cold stimulus.
Diagnostic criteria for headaches according to the third edition of the International
head.
posterior pharyngeal wall from ingestion of cold food or drink or inhalation of cold air
externally to the head or ingested or inhaled.
14.7 Treatment/Management
Management of cold-stimulus headache primarily involves educating patients about
potential triggers, such as exposure to low ambient temperatures or the consumption
of cold foods and beverages. Preventive strategies are limited to the avoidance of
these stimuli, as there is currently no evidence-based prophylactic treatment recommended for this type of headache.
142
D. A. de Oliveira and M. Valença
• Avoidance Strategies:
Educate the patient to avoid known cold triggers (e.g., sudden cold drinks, unpro-
tected exposure to cold air or water).
• Immediate Removal of the Cold Stimulus:
Patients should be instructed to stop or terminate exposure to the triggering cold
stimulus immediately. This may involve avoiding cold foods or beverages, staying
out of cold environments, or covering exposed skin when in contact with cold temperatures. Immediate cessation of the stimulus is usually sufcient to quickly relieve
symptoms, as the headache typically resolves within seconds to minutes after the
trigger is removed.
14.8 Conclusion
The report of these two cases, in which an ice stimulus applied to the oral cavity
triggered not only immediate pain (i.e., cold-stimulus headache) but also pain
occurring one and three hours after the cold stimulus, a full-blown migraine attack
lasting for hours, demonstrates that ice-induced headache can act as a trigger for a
migraine episode. This observation highlights another connection between these
two types of headaches, not only in their occurrence in susceptible migraine patients
but also in the potential role of cold-stimulus headache as a trigger for a migraine
episode a few hours after the cold stimulus.
Although not debilitating, a headache attributed to ingestion or inhalation of cold
stimulus raises important questions about the underlying mechanisms of coldinduced pain and its interactions with other primary headaches, such as migraine. It
is speculated that these two conditions share similar pathophysiological mechanisms, such as neuronal hyperexcitability and the activation of the trigeminovascular system [18].
In this context, it is speculated that the TRPM8 receptor, a cold-sensitive ion
channel activated by low temperatures (<28°C) and cooling compounds like menthol, may have implications as a central mediator in cold-stimulus headache. Its
activation, located in peripheral thermoreceptors, particularly in the oral cavity and
pharynx, triggers a cascade of neural signals that propagate through the trigeminal
nerve to the central nervous system [19, 21]. Thus, it is possible that TRPM8 acts as
a modulator of neuronal excitation in cold conditions, contributing to the perception
of pain. Increased expression or heightened sensitivity may explain why some individuals are more susceptible to headache attributed to the ingestion or inhalation of
cold stimuli [20, 21].
Furthermore, the fundamental role of the trigeminovascular reex in the observed
pathophysiology is highlighted [17]. In the two clinical cases presented, the activation of this system likely led to the release of inammatory neuropeptides, such as
CGRP (calcitonin gene-related peptide). This release may have played a key role in
14 Cold-Stimulus Headache
143
sensitizing the trigeminovascular neurons, contributing to the onset of the migraine
attacks observed in the volunteers [3, 18].
The headache attributed to ingestion or inhalation of cold stimulus is a common
clinical condition that clearly illustrates the complex interplay between environmental, physiological, and neurological factors in the genesis of pain. Despite its
non-disabling nature, understanding its mechanisms, such as possible activation of
the trigeminal nerve, cerebral vasoconstriction, vasodilation, the trigeminovascular
reex, and the role of the TRPM8 receptor, not only improves clinical management
but also paves the way for new research in primary headaches and the mechanisms
of pain in general.
The typical presentation, characterized by acute, short-duration pain triggered by
cold stimuli, facilitates the clinical diagnosis but requires careful consideration to
rule out secondary conditions in atypical presentations. Simple preventive strategies, combined with patient education, are often sufcient to manage most cases,
while advancements in molecular neuroscience, such as the study of TRPM8, offer
promising prospects for future treatments. By recognizing and exploring this condition, healthcare professionals and researchers can not only alleviate patient discomfort but also contribute to a broader understanding of headache mechanisms.
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D. A. de Oliveira and M. Valença
Chapter 15
External-Pressure Headache
ErleneRobertaRibeirodos Santos , JulianaRamosde Andrade ,
andWelberSousaOliveira
15.1 Introduction
External-pressure headaches (EPH) are a distinct group of primary headache disorders caused by sustained mechanical forces applied to the scalp [1]. Previously
classied as cranial neuralgias in the International Classication of Headache
Disorders, second edition (ICHD-2), they have been redened as primary headaches
in ICHD-3, reecting a better understanding of their pathophysiology. EPH includes
three subtypes: external-compression headaches (ECH), typically caused by tight
headgear such as helmets or personal protective equipment (PPE), and externaltraction headaches (ETH), associated with hairstyles or accessories exerting pulling
forces. These subtypes are distinguished by their causative mechanisms, with diagnostic criteria emphasizing the transient and reversible nature of these headaches.
The onset of pain is directly linked to the application of external force, and resolution occurs rapidly after the removal of the trigger [1].
The signicance of EPH has been highlighted in specic occupational and environmental contexts. During the coronavirus disease 2019 (COVID-19) pandemic,
healthcare workers reported bilateral headaches linked to the prolonged use of N95
masks and goggles, underscoring the condition’s prevalence in high-stress settings
E. R. R. dos Santos (*)
Department of Physical Education, Federal University of Pernambuco, Recife, PE, Brazil
Coordinator of the Public Policy and Advocacy Committee of the Brazilian Headache
Society, Recife, PE, Brazil
J. R. de Andrade
Danish Headache Center, Translational Research Centre, Rigshospitalet, Copenhagen of
University, Denmark Brazilian Headache Society– Experimental and Clinical Research
Committee, Copenhagen, Denmark
W. S. Oliveira
Centro Especializado em Hipermobilidade e Dor, Brasília, Federal District, 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_15
145© The Author(s), under exclusive license to Springer Nature
146
[2]. Similar patterns have been observed in military and occupational settings where
helmets and other equipment are mandatory.
Although typically mild and transient, EPH can become severe and persist in
individuals with pre-existing headache disorders, affecting their quality of life and
productivity. Understanding its denition, classication, and epidemiology is essential for accurate diagnosis and management. This includes ergonomic adaptations,
preventive strategies, and prompt symptom relief to minimize its impact, particularly in settings where headgear or similar accessories are unavoidable.
E. R. R. dos Santos et al.
15.2 Case Presentation
A 53-year-old woman presented with a long-standing history of headaches that
began at menarche, predominantly occurring during perimenstrual periods. These
headaches were described as frontal, constant, and moderate to severe in intensity,
often accompanied by photophobia and phonophobia, though she denied nausea or
osmophobia. The headaches were aggravated by routine physical activity and
occurred approximately two to three days per month. More recently, following the
onset of amenorrhea, the intensity of her headaches diminished. The episodes were
often preceded by cervical pain, and she reported no auras. Over-the-counter analgesics were typically effective in managing her symptoms.
The patient also noted sensitivity to other headgear, such as glasses and headbands, which needed to be lightweight and soft to avoid triggering headaches.
Approximately one year ago (in 2024), she began participating in water-based
exercise (hydro-gymnastics) and experienced headaches directly related to the use
of a swim cap. When wearing a fabric swim cap with an elastic band, she experienced mild, localized discomfort at the points of contact with the elastic. This discomfort resolved immediately upon removing the cap and did not require the use of
analgesics. However, after switching to a silicone swim cap, her headaches became
more severe and diffuse, described as holocranial with a pressing quality. These
headaches were accompanied by photophobia and phonophobia, signicantly
affecting her ability to concentrate during exercise sessions. Unlike the headaches
caused by the fabric swim cap, these episodes persisted even after removing the silicone cap and occasionally required the use of common analgesics. Due to the worsening of her symptoms, she eventually discontinued hydro-gymnastics.
15.3 Case Discussion
This case presents a female patient with a pre-existing history of headaches that
meet the criteria for episodic migraine without aura and menstrual related migraine
without aura. Her history of avoiding head accessories, such as glasses and headbands, due to pain, already suggested a previous diagnosis of external-pressure