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16 Epicrania Fugax
157
central trigeminal sensitization, which may occur independently or in the context of
a central nervous system lesion [5, 18].
The pain’s non-dermatomal distribution and directional propagation suggest
mechanisms such as ephaptic transmission between neighboring nerve endings or
trans diploic signal conduction [19, 20]. A potential role for pathology affecting the
proximal cervical nerve roots (before their distal branching) has also been proposed
[3]; in such cases, however, coexisting cervical or other headache syndromes should
be carefully ruled out.
Involvement of the trigemino-cervical complex is likely, as it integrates nociceptive input from both the trigeminal and upper cervical spinal nerves. This convergence may underlie the characteristic linear, strictly unilateral trajectory of pain in
EF, which can be accompanied by ipsilateral autonomic symptoms [9]. Additional
central subcortical mechanisms in the brainstem or spinal cord may contribute to the
extracranial radiation patterns observed in some patients [21]. However, unlike
migraine or other primary headache disorders, EF pain is typically dynamic and
sharply localized, rather than static or diffuse.
This challenges the extent to which higher-order central sensitization (such as
thalamo-cortical involvement) contributes to its clinical presentation, and suggests
a distinct pathophysiological prole compared to other central pain syndromes,
such as migraine or other primary headache disorders with allodynia [9].
The observation that anxiety and depressive symptoms are more frequently
reported in EF patients than in those with other headache disorders [9] could also
suggest a more prominent central component to pain processing. However, paradoxically, patients with low-frequency EF episodes have been found to exhibit
higher levels of anxiety, which argues against a direct correlation with central modulation of pain. This inconsistency may be better explained by referral biasasindividuals with higher levels of anxiety may be more likely to seek medical care [22].
16.3 Case Presentation
A 61-year-old woman presented to the neurology clinic with a two-year history of
brief, recurring episodes of dull pain, occasionally accompanied by tenderness,
localized to the right scalp. Her past medical history included low-frequency episodic tension-type headache starting back in her 40s, as well as arterial hypertension
and anxiety. She recalled a previous episode of blunt parietal trauma in her youth,
requiring observation in the hospital for a few hours. Yet, she denied posttraumatic
headache and did not relate the site of pain origin to the trauma location. She also
denied having had any precipitating event of skin lesions at the time of symptom
onset. Her daily medication included escitalopram 10mg id and losartan 100mg id.
She described a sharp, intense (8/10 VAS) pain as occurring in a horizontal barlike area extending from the occipital to frontal scalp regions, moving rapidly in a
linear fashion. Each episode lasted fewer than 10s and occurred 10–20 times per
day, sometimes persisting daily, for up to two weeks, without seasonal
158
predominance. Sometimes, a dull discomfort persisted in the same area, between
paroxysms. There were periods of pain freedom that lasted days, up to one month.
There were no identiable triggers, nor were there associated migraine or cranial
autonomic symptoms during attacks.
General and neurological examinations were unremarkable. Notably, cranial
artery palpation was normal, with no trophic skin changes or sensory abnormalities
in trigeminal or cervical dermatomes. There was no craniofacial or cervical tenderness on palpation or maneuvering, and deep tendon reexes were preserved.
Laboratory investigations, including erythrocyte sedimentation rate, C-reactive
protein, serum electrolytes, calcium, albumin, magnesium, phosphorus, lactate dehydrogenase, alkaline phosphatase, Herpes Zoster serology, and vitamin B complex,
were all within normal limits. Cranial magnetic resonance imaging (MRI) and Doppler
ultrasound of the supercial temporal arteries revealed no abnormalities. Cervical
spine MRI showed uncovertebral arthrosis from C5 to C7, with mild bilateral foraminal stenosis but no signicant spinal canal narrowing or cord compression.
Rescue treatment with paracetamol and ibuprofen provided only occasional mild
relief and was used less than once per week. A therapeutic trial with indomethacin
was ineffective. Switching escitalopram with duloxetine yielded modest improvement at two months. She was subsequently referred to the headache clinic, where
gabapentin was started and titrated to 1200mg/day, resulting in a good and sustained clinical response at the six-month follow-up.
G. D. Pinho and R. G. Gouveia
16.4 Case Discussion
This case raised several red ags, including the new onset of headache after the age
of 60, with a phenotype consistent with a rare primary headache disorder. The differential diagnosis of secondary headaches in this patient included posterior fossa
structural lesions, giant cell arteritis, zoster sine herpete, and high cervical nerve root
compression, all of which were ruled out through an extensive diagnostic workup.
Initial treatment strategies, including nonsteroidal anti-inammatory drugs, indomethacin, and duloxetine, were ineffective. However, initiation of antiepileptic therapy resulted in signicant and sustained symptom relief, supporting a neuropathic pain.
16.5 Characteristics ofEpicrania Fugax
andDifferential Diagnosis
EF is most commonly perceived in the sensory territories of the upper trigeminal
(particularly V1) and occipital nerves. However, the pain does not strictly follow
anatomical boundaries and is almost invariably unilateral [3, 21, 23]. Notably, in a
few reported cases, the pain trajectory has crossed the sagittal plane [4, 9].
Patients typically describe EF as brief, sharply localized paroxysms lasting less than
10 seconds. These episodes are characterized by a rapid, linear (occasionally irregular
16 Epicrania Fugax
159
and zigzagging) pain that travels across the scalp on one side of the head, a presentation considered pathognomonic for this condition [24]. Although one or both hemicrania may be affected, the pain projection pattern is nearly always ipsilateral to its point
of origin. The pain typically moves in a postero-anterior (forward) direction, while
retrograde (backwards) radiation is less frequently reported. In very rare cases, pain
has been observed to alternate sides between episodes or radiate beyond the head to
other regions such as the lower face, thorax, abdomen, or limbs [6, 9, 11, 25, 26], main-
taining the same fast, progressive, and orderly propagation pattern characteristic of EF.
The pain in EF is typically neuralgic in nature (commonly described as electric
shock-like or stabbing) but may also present as burning, sharp, or oppressive, and is
generally of moderate to severe intensity. In up to one-third of patients, EF may be
accompanied by ipsilateral autonomic symptoms such as conjunctival injection,
tearing, or rhinorrhea, suggesting activation of the trigemino-autonomic reex [3,
24]. The headache’s topography and the temporal pattern of attacks are useful to
differentiate it from trigeminal autonomic cephalalgias (TACs).
EF episodes are characteristically very brief, usually lasting less than 15s and
never exceeding one minute. Unlike TACs, EF does not follow a consistent circadian
or seasonal pattern. The frequency of attacks varies widely; episodes may occur
sporadically, only a few times per year, or several times daily. Attacks can appear as
isolated events, in clusters of pain paroxysms, or both. Notably, EF attacks have not
been reported during sleep. While most patients experience daily attacks for prolonged periods, others may report more infrequent episodes with spontaneous or
treatment-induced remissions. No seasonal predominance has been observed [9].
Paroxysms may be triggered by pressure or touch at the site of pain onset, neck
movements, stress, eye movements, or Valsalva maneuvers [9]. Persistent local allodynia may persist after attacks [20], requiring differentiation from trigeminal or
other cranial neuralgias.
The brief, stabbing nature of EF also necessitates differentiation from primary
stabbing (ice-pick) headache. In some patients, a longer-lasting, duller pain may
persist at the site of origin between paroxysms, mimicking nummular headache [19,
21, 27]. Additionally, EF may resemble linear headache (a variant of nummular
headache) where the painful and dysesthetic area is linear rather than round or coinshaped. In both conditions, the affected area may cross several terminal nerve territories. However, a key distinction is that EF pain is migratory, traveling across the
scalp, whereas linear headache pain typically remains stationary [9].
16.6 Diagnostic Algorithm
Step 1: Clinical Suspicion
• Identify Key Symptoms:
Clinical Presentation: Recurrent, short-lasting, unilateral, supercial,
shock-like pain with a dynamic trajectory, most commonly posteroanterior, but occasionally antero-posterior, coronal, or diagonal in direction.
160
G. D. Pinho and R. G. Gouveia
The pain typically follows a linear, zigzag, or back-and-forth path across
mixed trigeminal and occipital sensory nerve distributions.
Clinical Evaluation: Assessment should include careful documentation of
associated symptoms (e.g., autonomic features) and the temporal pattern
of pain paroxysms, including frequency, duration, and triggering factors.
Physical Examination: Thorough evaluation should focus on the area of
pain onset, with detailed inspection and palpation of the cranium, epicranial skin, muscles, and arteries. A complete neurological examination is
essential, along with general physical assessment, to exclude secondary
causes and identify possible contributing factors.
Step 2: Diagnostic Workup
• Blood Tests:
– Exclude systemic inammation or vasculitis, particularly giant cell arteri-
tis, depending on the patient’s age.
– Screen for nutritional or metabolic causes of neuropathy (e.g., vitamin
deciencies, diabetes).
– Assess for potential inammatory or toxic neuropathies; include zoster
serology if clinical suspicion exists.
– Evaluate for metabolic bone diseases, such as Paget’s disease.
• Neuroimaging: Brain and cervical spine MRI to investigate:
– Lesions affecting the trigeminal sensory nerve root, brainstem, or cervical
spinal cord.
– Mass-occupying lesions or compressive abnormalities (e.g., pontocerebel-
lar angle tumors, aneurysms).
– Structural changes due to bone remodeling (e.g., Paget’s disease).
– Trophic or inltrative lesions affecting supercial sensory nerve bers or
overlying skin.
• Additional Diagnostic Workup (age-dependent and based on clinical
suspicion):
– Temporal artery Doppler ultrasound to rule out giant cell arteritis.
– Electroneuromyography (ENMG) for evaluation of peripheral nerve
dysfunction.
– Somatosensory evoked potentials (SSEPs) to assess central sensory path-
ways, including the brainstem and cervical spinal cord.
– Electroencephalography (EEG) in cases with possible sensory focal sei-
zures presenting as paroxysmal pain [21].
Step 3: Apply ICHD-3 Diagnostic Criteria [24]
A. Recurrent stabbing head pain attacks lasting 1–10 s and fullling
criterion B
16 Epicrania Fugax
B. Pain moving with a linear or zigzag trajectory across the surface of one
hemicranium, commencing and terminating in the distributions of different nerves
C. Not better accounted by another ICHD-3 diagnosis
161
16.7 Management
Management of EF primarily focuses on symptomatic relief and patient reassurance. Preventive daily anticonvulsant medications are considered the most effective
treatment, with gabapentin and lamotrigine being the most commonly used.
However, other options such as pregabalin, carbamazepine, oxcarbazepine, eslicarbazepine, lacosamide, levetiracetam, and valproic acid are also utilized, titrated to
the most effective non-toxic doses [5, 9, 28].
Other medications such as amitriptyline, duloxetine, and indomethacin have
shown some success in some instances. For patients with limited response or poor
tolerability to these agents, local anesthetics (e.g., lidocaine, bupivacaine) with or
without corticosteroids, and subcutaneous onabotulinum toxin A injections have
been tried with favorable outcomes [9, 29, 30].
The prognosis for most patients is generally good, with many experiencing
improvements with treatment or spontaneous remission. In patients who respond
well to treatment, a gradual withdrawal of medication may be considered, although
there is no established consensus or protocol for this approach. Some patients with
infrequent attacks may choose not to initiate treatment, as symptom exacerbation
without intervention is rare.
16.8 Conclusion
Epicrania Fugax was rst dened in 2008 [20], and to date, over 100 cases have
been described in the literature, making it a rare headache disorder. However, given
the brief nature of the attacks, it is likely that many more patients exist who remain
undiagnosed. These individuals may not seek medical attention due to the transient
nature of the pain, or primary care physicians may not be aware of the condition,
leading to missed diagnoses and a lack of referrals. Even within neurology clinics,
this rare primary headache may be underdiagnosed due to the overlap of some of its
characteristics with other primary headache disorders. The atypical pain patterns,
such as the zigzag trajectory, shifts in direction, and radiation to other parts of the
body, are often mistakenly attributed to anxiety, depression, or functional neurological disorders. While EF is frequently comorbid with mental health conditions, the
increasing recognition of its unique manifestations and pathophysiological mechanisms has improved patient care and treatment options. A correct diagnosis is critical for encouraging patients and promoting better outcomes.
162
G. D. Pinho and R. G. Gouveia
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163
Chapter 17
Nummular Headache
TülayYılmaz andBetülBaykan
17.1 Introduction
First described in 2002 by Pareja etal. [1] and previously referred to as “coinshaped headache”, nummular headache (NH) is recognized as a primary headache
disorder in the International Classication of Headache Disorders-3 (ICHD-3) [2].
It is characterized by persistent, intermittent, or chronic pain conned to a specic,
circumscribed region of the scalp, in the absence of any underlying structural or
lesional cause. The painful region can be located anywhere on the scalp, but it is
most commonly found in the parietal area. In rare instances, NH may present as bior multifocal complaints, with each affected region maintaining all the dening
features of the condition. Pain intensity is typically mild to moderate, but it can
occasionally become severe. In addition to the baseline discomfort, spontaneous or
triggered exacerbations may occur. The duration is highly variable; up to 75% of the
reported cases have shown a chronic pattern (lasting longer than three months),
though episodes lasting seconds, minutes, hours, or days have also been reported
[2]. Symptoms such as allodynia, dysesthesia, paresthesia, or hypoesthesia may
accompany episodes of pain [3].
Although large-scale epidemiological studies are lacking, the annual incidence
rate is estimated to be approximately 9 cases per 100,000 individuals. NH is more
common in women (1.8:1) and typically begins in the fourth decade of life, although
it has a wide age range of onset (4-79 years) [4]. In a recent hospital-based,
T. Y ılmaz
Ümraniye Training and Research Hospital, University of Health Sciences, Istanbul, Turkey
B. Baykan (
Neurology and Clinical Neurophysiology, EMAR Medical Center, Istanbul, Turkey
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_17
*)
165© The Author(s), under exclusive license to Springer Nature
166
T. Yılmaz and B. Baykan
multicenter study, Head-MENA-A (Middle East, North Africa, Asia), which
included a large cohort from Türkiye, the prevalence of NH among patients presenting with headaches was reported to be 0.3% [5].
17.2 Pathophysiology
The pathogenesis of NH remains unclear and has yet to be fully elucidated. Two
primary theories have been proposed: one emphasizing a peripheral origin and the
other focusing on central mechanisms. Initially, NH was described as a form of
localized neuralgia arising from epicranial structures, particularly the terminal
branches of cutaneous nerves. This hypothesis is supported by the fact that the pain
is conned to a specic area and by the presence of sensory alterations, such as
hypoesthesia, hyperesthesia, or paresthesia, in some patients. Additionally, some
cases have reported trophic changes, such as hair heterochromia, within the affected
area [6]. As stated, the origin of NH may involve a local lesion or dysfunction in the
terminal branches of the pericranial nerves. Still, it may also be associated with a
deeper level of localization. The presence of nerve bers traversing the skull through
emissary channels and ssures has been identied using uorescence microscopy
and electron microscopy [7]. The diffuse hypersensitivity of pericranial structures,
characteristic of migraine and tension-type headaches, appears to be absent in NH
[8]. Pressure algometry has revealed that pain thresholds are reduced specically at
the symptomatic site, while the remainder of the scalp shows no signicant change,
which is intriguing [7, 9]. On the other hand, NH does not align precisely with the
distribution of peripheral innervation territories and does not consistently respond
to local anesthetic injections [6]. Some patients exhibit triggers and symptoms
resembling those seen in migraine, suggesting that central mechanisms may play a
prominent role [10, 11]. In some cases, algometric assessments have revealed a
generally reduced pain threshold, which supports the hypothesis of central sensitization [11]. Some patients with NH experience pain that crosses the midline of the
scalp or occurs in multiple areas, which also suggests a central mechanism [6].
Although NH is classied as a primary headache, cases with secondary etiologies have also been reported. These cases are associated with underlying structural
lesions or other causes such as meningioma, arachnoid cysts, fusiform aneurysms,
prior local neurosurgery, varicella-zoster rash, cranial bone pathologies, or some
benign cranial lesions. Almost all the cases described showed a close anatomical
relationship between the pain and the underlying lesion. There are also reported
cases following head trauma and cranial surgery. These observations suggest the
existence of a secondary form of NH.Therefore, secondary causes should be carefully considered and excluded during the differential diagnosis [6, 12]. In some
patients with NH, autoimmune markers have been detected, and it has been suggested that immunological mechanisms may trigger the pain in these patients. The
presence of antinuclear antibodies (ANA) was the most frequently observed nding
in the blood tests of these patients [13].
17 Nummular Headache
167
17.3 Case Presentation
This case report presents a 47-year-old female patient, S*, who has been experiencing unilateral, throbbing headache attacks for approximately 10years. These headaches, which occur alternately on the right and left sides, originate from the occipital
region and extend to one half of the head, often involving the eye. The attacks are
accompanied by photophobia, phonophobia, nausea, and occasionally vomiting,
typically lasting around eight hours. The frequency of the attacks has been reported
as one to two times per month. The patient was previously diagnosed with migraine
without aura. It was noted that her symptoms subsided with the use of eletriptan
40mg during attack periods. However, in the past three months, the patient became
concerned about a newly developed pain pattern that was distinct from her typical
migraine attacks. She described a burning, numbness, and tingling sensation localized to a circular area of approximately 6cm in diameter in the right parietal region.
She stated that these new symptoms developed independently of her migraine episodes, were unrelated to stress, and lasted from one to three days. The patient noted
that her symptoms completely resolved with the use of urbiprofen.
The patient consulted her family physician due to this headache that, although
not very severe, was noticeably different from her previous side-changing migraine
attacks and consistently located at the same spot, causing concern. The family physician, sharing the patient’s concern, recommended a referral to neurology to rule
out any underlying conditions. Neurological examination revealed no abnormalities, and the pain was localized to a well-dened circular area in the right parietal
region without any associated skin lesions. Laboratory tests and brain magnetic
resonance imaging (MRI) showed no pathological ndings.
Based on these ndings, the patient was diagnosed with NH.She was informed
that NH is a benign condition, and symptomatic treatment would be sufcient unless
it signicantly affected her quality of life. The treatment plan included NSAIDs for
symptom relief on an as-needed basis, and gabapentin can be recommended in case
of persistent or chronic symptoms.
During the follow-up period, no signicant worsening of the patient’s symptoms
was observed, and the symptoms were well controlled with NSAID use.
17.4 Case Discussion
This case highlights the possibility that NH may coexist with other primary headache disorders, such as migraine [5, 14, 15], emphasizing the need for careful clinical differentiation. The key characteristic of NH is its localized circular nature,
conned to a specic area of the scalp, which helps differentiate it from other headache types [1]. However, secondary causes such as meningioma, cranial lesions,
head trauma, vascular anomalies, or infections such as varicella-zoster must be thoroughly ruled out [16, 17]. Therefore, a comprehensive medical history, neurological