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Chapter 13
Primary Headache Associated withSexual
Activity
FüsunMaydaDomaç
13.1 Introduction
Primary headache associated with sexual activity (HAS) is classied within the
fourth group of primary headaches in International Classication of Headache
Disorders-3 [1]. HAS, being a benign headache, has been previously named as
coital, preorgasmic, orgasmic, intercourse or sexual headache or cephalalgia, and
nomenclature has changed to primary headache associated with sexual activity
[2–4]. In International Classication of Headache Disorders, 1st edition (ICHD-1),
three subtypes were identied: 1-dull and intensifying, 2-explosive at orgasm and
3-postural and post-coital [5], whereas in ICHD-2, two subtypes have remained: 1.
pre-orgasmic and 2. orgasmic headache [6]. Subtypes have been removed in ICHD-3
beta and ICHD-3 classications. Still, in diagnostic criteria, characteristics of pain
have been remarked either as progressively increasing with sexual excitement or as
suddenly appearing during or before orgasm [1, 7]. In ICHD-3, HAS has been
regarded as a single entity with variable presentation [1]. An underlying intracranial
pathology may also be present with headache during sexual activity; therefore,
detailed examination for differential diagnosis must be applied before the diagnosis
of this benign primary headache [8]. In this chapter, the clinical features, diagnosis
and management strategies of HAS will be discussed to increase awareness of HAS
among specialists.
Although the exact lifetime prevalence of HAS is not known [9], research has
indicated that it ranges from 0.9% to 1.6% [10–12]. According to our previously
published article, HAS was identied in 2% of the patients who were followed up
at our headache outpatient clinic. We have suggested that the low ratio of HAS
F. M. Domaç (*)
University of Health Sciences, Hamidiye Medical Faculty, Neurology Department, Erenköy
Mental Health and Nervous Diseases Training and Research Hospital, İstanbul, Türkiye
e-mail: fusundomac@yahoo.cım.tr
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_13
127© The Author(s), under exclusive license to Springer Nature
128
diagnosis may be due to patients’ unwillingness or embarrassment in describing the
occurrence of their headaches [13].
HAS can occur at any sexually active age, but is mostly seen in the third or fourth
decades in both females and males. Male to female ratio ranges from 1.2 to 3:1, and
in males with obesity and hypertension, the ratio can be higher [1, 9, 14]. In our
published case series, the mean age of the patients was 37.07±7 67 with a male
predominance [13].
F. M. Domaç
13.2 Pathophysiology
Although several mechanisms have been proposed, the exact mechanism of HAS
remains unknown. Headaches occurring during the preorgasmic phase have been
linked to excessively contracted jaw and neck muscles during sexual activity. Evers
etal. have reported that a sudden increase in both heart rate and blood pressure
might cause headaches during orgasm [15]. Vasospasm was also considered a potential factor in the pathophysiology, but it does not appear to be a reasonable explanation [4, 16]. HAS has also been regarded as a variant of migrainous headache, as
many patients have a history of migraine; therefore, the cause of HAS was suggested to result from haemodynamic changes during orgasm [2, 17]. Calcitonin
gene-related peptide (CGRP) was also thought to be an essential mediator facilitating HAS attacks [18]. Genetic inheritance was also suspected, as HAS has been
identied among members of families [3, 19].
13.3 Case Presentation
EA, a 30-year-old newlywed woman, presented with a severe throbbing headache
that commenced during orgasm. In the previous week, she had two attacks of headache during sexual intercourse, which developed abruptly during orgasm with high
intensity (8 out of 10 on the visual analogue scale). The headaches were bilateral
and localised at the occipital areas, gradually diminishing within half an hour but
lasting for approximately two hours. Neither photophobia nor phonophobia, nausea
or vomiting accompanied the headaches. After the third headache attack associated
with sexual activity the night before, she was admitted to the neurology outpatient clinic.
Additionally, she has had a history of migraine without aura for three years. The
frequency of unilateral migraine headaches was two or three times a month, localised at the frontotemporal region. The intensity of attacks was moderate and mainly
responded to analgesic treatment. Triggers included hunger and stress, and during
these attacks, she also experienced photophobia, phonophobia and nausea. She did
not report any other illnesses or a history of drug treatment, smoking or alcohol
consumption.
13 Primary Headache Associated withSexual Activity
On her physical examination, her temperature was 36.5°C, and her systolic and
diastolic blood pressures were 120/78mm Hg, with a heart rate of 82 per minute.
Her body mass index was 23.2. Electrocardiography showed sinus rhythm.
Neurological examination and fundoscopy were unremarkable. A cranial computed
tomography (CT) was performed, revealing no intracranial or subarachnoid haemorrhage. Routine blood tests also fell within normal ranges. To assess for reversible
vasoconstriction syndrome, cerebral arteriopathies, dissection, aneurysm, cranial
venous sinus thrombosis, mass, or other intracranial pathologies, cranial magnetic
resonance imaging (MRI), MR angiography and MR venography were conducted.
None of these investigations revealed pathological ndings related to HAS.She was
started on indomethacin and advised to take it 30min before sexual activity. During
follow-up, she reported two additional attacks during orgasm in a month, with moderate intensity (5 out of 10 on the visual analogue scale) and lasting half an hour.
She also experienced two migraine attacks unrelated to HAS.Propranolol was prescribed, and at her follow-up after two months, it was found to be effective for both
migraine and sexual activity-related headaches.
129
13.4 Case Discussion
Headache during sexual activity may result from a life-threatening condition; early
diagnosis is crucial for appropriate treatment. EA’s headaches highlight the importance of ruling out intracranial pathologies and vascular abnormalities. Her headache characteristics, being associated with orgasm during sexual intercourse, and
the exclusion of secondary headache causes, were key in considering a primary
headache related to sexual activity.
13.5 Clinical Characteristics
Headache occurring during sexual excitement is usually dull and increases with rising excitement. The occurrence of a headache is unpredictable [20]. Although headaches are mainly associated with intercourse, they can also be related to masturbation
[21]. Severe headaches mostly occur during orgasm, and the intensity diminishes
within 5–15min [15]. The duration of mild headaches can last from 24 to 72h,
while severe headaches may last from minutes up to 24h. Headaches may be throbbing, pressing, explosive or stabbing; they may be unilateral or bilateral (at least
60%) and are mainly located in the occipital area or can be diffuse [1, 13, 22, 23].
Nausea, vomiting, photophobia or phonophobia is rare, and autonomic symptoms
are not typically present [4, 24].
For the accurate diagnosis of HAS, at least two attacks that are not better
explained by another diagnosis are required. If there is only one attack, the diagnosis remains as probable HAS [1]. Lin etal. have suggested an algorithm to identify
130
F. M. Domaç
the causes of headaches associated with sexual activity [20, 23]. To exclude most
common underlying causes such as subarachnoid or intracranial haemorrhage,
reversible vasoconstriction syndrome, arterial dissection, cerebral venous sinus
thrombosis or space-occupying lesions, initial assessment with non-contrast cranial
CT is recommended, followed by cranial MRI, CT or MR angiography and venography [4, 8, 20, 23]. Frese etal. proposed that episodic and chronic forms of HAS
exist, based on their follow-up of patients for at least 12months. They identied
episodic HAS in 75% of their patients, the chronic form in 25% [25]. Lin etal. have
reported that patients with HAS had a greater chance of evolving to a chronic type
in ≥1year [23].
In several months, remissions may occur, but in some patients, attacks may recur
or transform into a chronic form [8]. Frese etal. have reported that even in patients
with chronic HAS, the outcome seems to be favourable. After three years of follow up, 69% of patients experienced remissions [25]. In our reported case series, we
have followed up with our patients for two years, and none of them experienced
recurrence or progression to a chronic course [13]. In some studies, it was observed
that patients with HAS also experience migraine headaches [12, 13]. Frese etal.
investigated cognitive processing in HAS patients by visual event-related potentials.
They did not observe a loss of cognitive habituation and concluded that this nding
was similar to those observed in migrainous patients in previous studies [26]. In a
case report, after orgasm, a female patient with a history of migraine with aura experienced a visual aura followed by a throbbing unilateral headache [27]. In another
case report, two patients experienced auras (one with brainstem aura, one with
visual aura and vertigo) associated with orgasm without accompanying headaches
and with evidence of underlying cranial pathologies [28]. Tension-type headache,
hypnic headache and primary exercise headache may also co-occur in patients with
HAS [4].
13.6 Diagnostic Algorithm
Step 1: Clinical Suspicion
• Identify Key Symptoms:
– Bilateral, sudden onset, throbbing pain associated with orgasm and gradu-
ally diminished, lasting for 3h
Step 2: Initial Diagnostic Workup
• Perform
Cranial CT
– Evaluate for intracranial or subarachnoid haemorrhage
Cranial MRI
13 Primary Headache Associated withSexual Activity
131
– Assess for mass or other intracranial pathologies
Cranial and MR Angiography
– Assess for reversible vasoconstriction syndrome
– Assess for cerebral arteriopathies, dissection or aneurysm
Step 3: Additional Diagnostic Evaluations
MR Venography
– Assess for cerebral sinus thrombosis
Electrocardiography
– Exclude referred pain of cardiac ischaemia
Step 4: Apply ICHD-3 Diagnostic Criteria [1]
A. At least two episodes of pain in the head and/or neck fullling criteria B–D
B. Brought on by and occurring only during sexual activity
C. Either or both of the following:
1. Increasing in intensity with increasing sexual excitement
2. Abrupt explosive intensity just before or with orgasm
D. Lasting from 1min to 24h with severe intensity and/or up to 72h with mild
intensity
E. Not better accounted for by another ICHD-3 diagnosis
Step 5: Conrm Diagnosis
The diagnosis of primary headache associated with sexual activity is based on dif-
ferential diagnosis and excluding underlying vascular and structural cranial
pathologies and pharmacological causes of abrupt, severe and throbbing
headaches.
13.7 Management
Nonpharmacological treatments include patient education about the existing headache. Abstaining from sexual activity if the beginnings of a headache develop or
taking a more passive role in sexual activity can also be advised. Still, these may not
be acceptable for all patients [4]. Pharmacological treatment of HAS is based on
case series and experience. Being an infrequent headache disorder, there are no
randomised controlled studies for both acute and prophylactic treatments [22].
Symptomatic acute treatment includes triptans, nonsteroidal anti-inammatory
drugs (NSAIDs) and antiemetic drugs (whether in combination or alone). Naproxen
(500 mg orally), metoclopramide (10 mg intravenous [IV]), prochlorperazine
132
F. M. Domaç
(10mg IV or intramuscular [IM]), zolmitriptan intranasal spray (5mg) and sumatriptan (3, 4 and 6mg subcutaneous injections) can be therapeutic options [29].
Preventive therapies can be either pre-emptive (before sexual activity) or daily
treatments. Diclofenac, acetaminophen, acetylsalicylic acid, ergotamine and benzodiazepines have been used before sexual activity, but their benecial effects seem to
be limited [17]. Indomethacin, taken 30min before sexual activity, appeared to be
successful in most patients [13, 25, 30, 31]. Naratriptan (2.5mg) has been noted to
be of value before sexual intercourse [32], but Frese etal. have observed that only
half of the patients responded to triptans [33].
If headaches recur, contraindications exist or symptoms persist, daily preventive
therapy may be recommended. Oral indomethacin (25mg/day up to 225mg/day) or
beta-blockers such as propranolol (40mg daily up to 240mg daily) [13, 25], as well
as metoprolol, nadolol, bisoprolol and nebivolol [18, 25], have been reported to be
effective. Calcium channel blockers, including nimodipine [23, 34] and diltiazem
[35, 36], have shown benets in case reports. Propranolol and indomethacin are
benecial in 80–90% of patients in case series [2, 3, 13, 20, 25, 29, 33, 37, 38].
If there are contraindications to these treatments or symptoms persist, antiseizure
drugs such as topiramate (50–100mg/day) [23, 32, 39–41] or CGRP-targeted thera-
pies can be considered [18, 31]. Erenumab (70mg) is effective in a patient experiencing frequent HAS and migraine attacks [18]. The greater occipital nerve blockade
procedure was applied to a patient with HAS, using a local anaesthetic and steroid
combination at the symptomatic site, resulting in a complete resolution of the
pain [42].
13.8 Conclusion
Headache during sexual activity may develop due to life-threatening conditions, and
early diagnosis is essential for adequate treatment. Excluding aetiologies for secondary headaches is pivotal in considering HAS.Understanding the pathophysiological mechanism of HAS will lead to new therapeutic targets and the utilisation of
new treatment options. Awareness about headaches associated with sexual activity
should be raised among specialists, and patients must be educated about their existing headaches and encouraged to seek treatment.
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F. M. Domaç
Chapter 14
Cold-Stimulus Headache
DaniellaAraújode Oliveira andMarceloValença
14.1 Introduction
The cold-stimulus headache is described as a headache induced by a cold stimulus
applied externally to the head, ingested, or inhaled [1]. When triggered by exposure
to cold environments, such as immersion in icy water or exposure to low outdoor
temperatures, it is classied as subtype 4.5.1: Headache attributed to the external
application of a cold stimulus. The other subtype, commonly known as “brain
freeze” or ice cream headache (4.5.2: Headache attributed to ingestion or inhalation
of a cold stimulus), is a benign condition characterized by sudden and transient head
pain induced by the consumption of cold foods or beverages [1].
In the latest international classication of headaches, a new subtype, 4.5.3
Probable Cold-stimulus Headache, was described. Its diagnostic criteria differ from
those of other subtypes, as it considers only a single episode of headache that occurs
exclusively during or immediately after exposure to a cold stimulus applied externally to the head, or ingested or inhaled. Unlike other headaches, cold-stimulus
headaches are not disabling and appear to occur in susceptible individuals
(International Classication of Headache Disorders, 3rd edition [ICHD-3]) [1].
In the clinical context, understanding the underlying mechanisms of the coldstimulus headache deepens the comprehension of the activation of the trigeminovascular pathway and the role of cold in the pathogenesis of migraine. This chapter
D. A. de Oliveira (*)
Federal University of Pernambuco, Recife, Pernambuco, Brazil
e-mail: daniella.aoliveira@ufpe.br
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_14
135© The Author(s), under exclusive license to Springer Nature
136
D. A. de Oliveira and M. Valença
focuses on the clinical, diagnostic, and therapeutic aspects of this condition, integrating scientic evidence and case examples to provide practical insights for its
management. The primary goal is to explore in detail the headache attributed to
ingestion or inhalation of cold stimuli, expanding knowledge about its pathophysiology and association with migraine.
Regarding headache attributed to ingestion or inhalation of a cold stimulus, the
prevalence varies widely, ranging from 8% to 79%, even when using the criteria
established by the International Headache Society [2–12]. This variation is likely
inuenced by the methods used to evaluate or induce pain, as well as by the age
range of the studied population. Several studies have assessed the prevalence of this
headache using questionnaires [2, 4, 7, 9, 11]. In contrast, others employ experimental stimulation [3, 5, 6, 8, 10, 13], which may include the ingestion of cold
water, ice cream, or even palate stimulation with ice cubes.
When analyzing prevalence by age group, it is evident that in adult populations,
prevalence was 8 [5, 9], 15 [14], 37 [12], and 60% [8]. In adolescent populations,
prevalence rates ranged from 23 [4], 41 [6], 60% [11], to as high as 79% [7].
Considering studies conducted experimentally, the prevalence of headache attributed to ingestion or inhalation of a cold stimulus was 41% [6] among adolescents,
while in adults, the prevalence was 60 [8], 37 [5, 10], and 44% [3].
Studies have shown a higher incidence of headache attributed to ingestion or
inhalation of a cold stimulus in individuals with a history of migraine, suggesting a
possible interaction between cold sensitivity and a predisposition to migraine. Both
experimental studies and questionnaire-based studies indicate that individuals with
migraines reported cold-stimulus headaches more frequently than those with other
types of headaches or no headaches at all [2, 4, 5, 7, 8, 10].
In questionnaire-based studies, the prevalence of headache attributed to ingestion or inhalation of a cold stimulus ranged from 33 [4] to 55.2% [7] and up to 93%
[2] in patients with migraine.
14.2 Pathophysiology
Although the exact pathophysiology of headache attributed to the ingestion or inhalation of a cold stimulus is not fully understood, several factors are believed to play
important roles, including the activation of the trigeminal nerve, cerebral vasoconstriction and vasodilation, the trigeminovascular reex, and individual sensitivity to
cold [12, 15–17].
It is suggested that transient activation of sensory mechanisms in the trigeminal
region, frequently triggered by cold exposure, partially contributes to the onset of
pain. Additionally, the pain threshold may be a signicant factor, as well as possible
local vasoconstriction, reduced blood ow, or stimulation of nociceptors [12,
17, 18].
Exposure to cold, especially in areas like the palate or pharynx, activates local
thermoreceptors that stimulate the afferent bers of the trigeminal nerve. This