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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5526_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Contents
- •1.1 Introduction
- •1.2 Pathophysiology
- •1.3 Case Presentation
- •1.4 Case Discussion
- •1.5 Clinical Characteristics
- •1.6 Diagnostic Algorithm
- •1.8 Management
- •1.9 Conclusion
- •References
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Case Presentation
- •2.4 Case Discussion
- •2.5 Clinical Characteristics
- •1.7 Differential Diagnosis
- •2.6 Diagnostic Algorithm
- •2.7 Management
- •2.8 Conclusion
- •References
- •3.1 Introduction
- •3.2 Pathophysiology
- •3.3 Case Presentation
- •3.4 Case Discussion
- •3.5 Clinical Characteristics
- •3.6 Diagnostic Algorithm
- •3.7 Management
- •3.8 Conclusion
- •References
- •4.1 Introduction
- •4.2 Pathophysiology
- •4.3 Case Presentation
- •4.4 Case Discussion
- •4.6 Diagnostic Algorithm
- •4.7 Management
- •4.8 Conclusion
- •References
- •5.1 Introduction
- •5.2 Pathophysiology
- •5.3 Case Presentation
- •5.4 Case Discussion
- •5.5 Diagnostic Algorithm
- •5.6 Management
- •5.7 Conclusion
- •References
- •6.1 Introduction
- •6.2 Pathogenesis
- •6.3 Case Presentation
- •6.4 Case Discussion
- •6.5 Diagnostic Algorithm
- •6.6 Management
- •6.7 Conclusion
- •References
- •7.1 Introduction
- •7.2 Pathophysiology
- •7.3 Case Presentation
- •7.5 Differential Diagnosis
- •7.7 The Following Strategies Are Essential
- •7.7.1 Acute Symptom Relief
- •7.7.1.1 Pharmacological Treatment
- •7.7.2.1 Pharmacologic Prophylaxis
- •7.8 Conclusion
- •References
- •8.1 Introduction
- •8.3 Case Study
- •8.4 Case Discussion
- •8.5 Clinical Management
- •8.7 Diagnosis
- •8.8 Treatment
- •8.9 Conclusion
- •References
- •9.1 Introduction
- •9.2 Case Presentation
- •9.4 Diagnosis Algorithm
- •9.5 Secondary SUNCT
- •9.6 Management
- •9.8 Conclusion
- •References
- •10.1 Introduction
- •10.2 Pathophysiology
- •10.3 Case Presentation
- •10.4 Case Discussion
- •10.5 Clinical Characteristics
- •10.6 Diagnostic Algorithm
- •10.7 Management
- •10.8 Conclusion
- •References
- •11.1 Introduction
- •11.2 Pathophysiology
- •11.3 Case Presentation
- •11.4 Case Discussion
- •11.5 Clinical Characteristics
- •11.6 Diagnostic Algorithm
- •11.6.1 Step 1: Detailed Patient History
- •11.8 Management
- •11.9 Conclusions
- •12.2 Pathophysiology
- •12.3 Case Presentation
- •12.4 Case Discussion
- •12.6 Treatment
- •12.7 Conclusion
- •References
- •References
- •12.1 Introduction
- •13.1 Introduction
- •13.2 Pathophysiology
- •13.3 Case Presentation
- •13.4 Case Discussion
- •13.5 Clinical Characteristics
- •13.6 Diagnostic Algorithm
- •13.7 Management
- •13.8 Conclusion
- •References
- •14.1 Introduction
- •14.2 Pathophysiology
- •14.3 Case Presentation
- •14.3.1 Clinical Case 1
- •14.3.2 Clinical Case 2
- •14.4 Case Discussion
- •14.5 Clinical Characteristics
- •14.7 Treatment/Management
- •14.8 Conclusion
- •References
- •15.1 Introduction
- •15.2 Case Presentation
- •15.3 Case Discussion
- •15.4 Diagnostic Algorithm
- •15.5 Pathophysiology
- •15.6 Clinical Presentation
- •15.6.1 External-Compression Headache (ECH)
- •15.6.2 External-Traction Headache (ETH)
- •15.7 Management
- •15.7.1 Nonpharmacological Strategies
- •15.7.2 Pharmacological Strategies
- •15.7.3 Patient Education and Awareness
- •15.8 Conclusion
- •References
- •16.1 Introduction
- •16.2 Pathophysiology
- •16.3 Case Presentation
- •16.4 Case Discussion
- •16.6 Diagnostic Algorithm
- •16.7 Management
- •16.8 Conclusion
- •References
- •17.1 Introduction
- •17.2 Pathophysiology
- •17.3 Case Presentation
- •17.4 Case Discussion
- •17.5 Clinical Characteristics
- •17.6 Diagnosis
- •17.7 Differential Diagnosis
- •17.8 Treatment
- •17.9 Conclusion
- •References
- •18.1 Introduction
- •18.2 Pathophysiology
- •18.3 Case Presentation
- •18.4 Case Discussion
- •18.5 Clinical Presentation
- •18.6 Diagnosis
- •18.7 Differential Diagnosis
- •18.8 Treatment
- •18.9 Conclusion
- •References
- •19.1 Introduction
- •19.2 Pathophysiology
- •19.3 Case Presentation
- •19.4 Case Discussion
- •19.5 Diagnostic Approach
- •19.6 Management
- •19.7 Conclusion
- •References
- •20.1 Introduction
- •20.3 Case Report
- •20.4 Case Discussion
- •20.6 Clinical Presentation
- •20.7 Diagnostic Algorithm
- •20.8 Conclusion
- •References
- •21.1 Introduction
- •21.2 Case Presentation
- •21.3 Clinical Characteristics
- •21.4 Diagnosis
- •21.5 Treatment
- •References
- •22.1 Introduction
- •22.3 Case Presentation 1
- •22.4 Case Discussion
- •22.5 Case Presentation 2
- •22.6 Case Discussion 2
- •22.7 Clinical Characteristics
- •22.8 Diagnostic Workup
- •22.9 Treatment
- •22.10 Prognosis
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Case Presentation
- •23.4 Case Discussion
- •23.6 Diagnostic Algorithm
- •23.7 Management
- •23.8 Conclusion
- •References
- •24.1 Introduction
- •24.2 Case Presentation
- •24.3 Case Discussion
- •24.4 Pathophysiology
- •24.6 Clinical Characteristics
- •24.8 Treatment Approaches
- •24.10 Conclusion
- •References
- •25.1 Introduction
- •25.2 Case Presentation
- •25.3 Case Discussion
- •25.4 Conclusion
- •References
- •26.1 Introduction
- •26.2 Pathophysiology
- •26.3 Case Presentation
- •26.4 Case Discussion
- •26.5 Clinical Characteristics
- •26.6 Diagnostic Algorithm
- •26.7 Management
- •26.8 Conclusion
- •References
- •27.1 Introduction
- •27.2 Case Presentations
- •27.3 Clinical Characteristics
- •27.4 Discussion
- •27.5 Conclusion
- •References
- •28.1 Introduction
- •28.2 Case Presentation
- •28.3 Case Discussion
- •28.4 Clinical Characteristics
- •28.5 Diagnosis
- •28.6 Conclusion
- •28.7 Key Messages
- •References
- •29.1 Introduction
- •29.2 Pathophysiology
- •29.3 Case Presentation
- •29.4 Clinical Presentation
- •29.5 Diagnosis
- •29.6 Treatment
- •29.7 Conclusion
- •References
- •30.1 Introduction
- •30.2 Clinical Case
- •30.3 Clinical Presentation
- •30.4 Differential Diagnosis
- •30.5 Diagnosis
- •30.6 Treatment
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.2 Pathophysiology
- •31.3 Case Presentation
- •31.4 Case Discussion
- •31.5 Clinical Presentation
- •31.7 Conclusion
- •References
- •32.1 Introduction
- •32.2 Pathophysiology
- •32.3 Case Presentation
- •32.4 Case Discussion
- •32.6 Diagnosis
- •32.7 Additional Diagnostic Evaluations
- •32.8 Apply ICHD-3 Diagnostic Criteria [9]
- •32.10 Management
- •32.11 Conclusion
- •References
- •33.1 Introduction
- •33.2 Pathophysiology
- •33.3 Case Presentation
- •33.4 Clinical Characteristics
- •33.5 Diagnostic Algorithm
- •33.6 Treatment
- •33.7 Conclusion
- •References
- •34.1 Introduction
- •34.2 Pathophysiology
- •34.3 Case Presentation
- •34.4 Case Discussion
- •34.6 Diagnostic Algorithm
- •34.7 Treatment
- •34.8 Conclusion
- •References
- •35.1 Introduction
- •35.3 Case Presentation
- •35.4 Case Discussion
- •35.7 Treatment
- •35.7.1 Oxygen Therapy (100% Oxygen)
- •35.8 Conclusion
- •References
- •36.1 Introduction
- •36.2 Pathophysiology
- •36.3 Case Presentation
- •36.5 Diagnostic Algorithm
- •36.6 Treatment
- •36.7 Conclusion
- •References
- •37.1 Introduction
- •37.2 Pathophysiology
- •37.3 Case Presentation
- •37.4 Headache Characteristics
- •37.5 Case Discussion
- •37.6 Treatment
- •37.7 Conclusion
- •References
- •38.1 Introduction
- •38.2 Pathophysiology
- •38.3 Case Presentation
- •38.4 Clinical Presentation
- •38.5 Diagnostic Algorithm
- •38.6 Treatment
- •38.7 Conclusion
- •References
- •39.1 Introduction
- •39.3 Case Presentation
- •39.4 Case Discussion
- •39.6 ICHD-3 Diagnostic Criteria [28]
- •39.6.1 Diagnostic Criteria
- •39.7 Diagnostic Algorithm
- •39.9 Conclusion
- •References
- •40.1 Introduction
- •40.3 Case Presentation
- •40.4 Case Discussion
- •40.5.1 Diagnostic Algorithm
- •40.6 Treatment
- •40.7 Conclusion
- •References
- •41.1 Introduction
- •41.3 Case Presentation
- •41.4 Clinical Presentation
- •41.5 Differential Diagnosis
- •41.6 Conclusion
- •41.7 Key Messages
- •References
- •42.1 Introduction
- •42.2 Pathophysiology
- •42.3 Case Presentation
- •42.5 Case Discussion
- •42.6 Clinical Presentation
- •42.7 Diagnostic Algorithm [9]
- •42.8 Preeclampsia
- •42.9 Eclampsia
- •42.10 Fetal Assessment
- •42.11 Treatment
- •42.12 Antihypertensive Management [8]
- •42.14 Conclusion
- •References
- •43.1 Introduction
- •43.2 Pathophysiology
- •43.3 Case Presentation
- •43.4 Case Discussion
- •43.5 Clinical Manifestations
- •43.6 Diagnosis
- •43.7 Treatment
- •43.8 Conclusion
- •References
- •44.1 Introduction
- •44.2 Pathophysiology
- •44.3 Case Presentation
- •44.4 Case Discussion
- •44.6 Diagnostic Approach
- •44.7 Management
- •44.8 Conclusion
- •References
- •45.1 Introduction
- •45.2 Pathophysiology
- •45.3 Case Presentation
- •45.6 Treatment
- •45.7 Conclusion
- •References
- •46.1 Introduction
- •46.2 Pathophysiology
- •46.3 Case Presentation
- •46.4 Clinical Characteristics
- •46.5 Differential Diagnosis
- •46.6 Treatment
- •46.7 Conclusion
- •References
- •47.1 Introduction
- •47.2 Pathophysiology
- •47.3 Case Presentation
- •47.4 Case Discussion
- •47.5 Clinical Presentations
- •47.6 Diagnostic Algorithm
- •47.7 Differential Diagnosis
- •47.8 Treatment
- •47.9 Conclusion
- •References
- •48.1 Introduction
- •48.2 Pathophysiology
- •48.3 Case Presentation
- •48.4 Case Discussion
- •48.5 Clinical Characteristics
- •48.7 Treatment
- •48.8 Conclusion
- •References
- •49.1 Introduction
- •49.2 Pathophysiology
- •49.3 Case Presentation
- •49.4 Clinical Presentation
- •49.5 Diagnosis
- •49.6 Treatment
- •49.7 Conclusion
- •References
- •50.1 Introduction
- •50.2 Pathophysiology
- •50.3 Case Presentation
- •50.4 Case Discussion
- •50.5 Clinical Characteristics
- •50.6 Diagnosis
- •50.7 Treatment
- •50.8 Conclusion
- •References
- •51.1 Introduction
- •51.2 Case Presentation
- •51.3 Clinical Characteristics
- •51.4 Diagnosis
- •51.5 Treatment
- •51.6 Conclusion
- •References
- •52.1 Introduction
- •52.2 Pathophysiology
- •52.3 Case Presentation
- •52.4 Case Discussion
- •52.5 Clinical Characteristics
- •52.6 Diagnosis
- •52.6.1 Cervicogenic Headache
- •52.6.2 Migraine
- •52.6.3 Neck Pain
- •52.6.4 Demyelinating Lesions
- •52.6.5 Cervical Myelitis
- •52.6.6 Occipital Allodynia
- •52.6.7 Cervical Muscle Spasms
- •52.7 Treatment
- •52.7.2 Acupuncture
- •52.7.3 Transcutaneous Electrical Nerve Stimulations (TENS)
- •52.8 Minimally Invasive Treatment
- •52.8.1 Nerve Blocks
- •52.8.2 Botulinum Toxin A
- •52.8.3 Radio Frequency
- •52.8.4 Occipital Nerve Stimulation
- •52.9 Surgical Treatments
- •52.10 Conclusions
- •References
- •53.1 Introduction
- •53.2 Pathophysiology
- •53.3 Characteristics of Pain
- •53.4 Case Presentation
- •53.5 Case Discussion
- •53.6 Clinical Characteristics
- •53.8 Treatment
- •53.9 Conclusion
- •References
- •54.1 Introduction
- •54.2 Pathophysiology
- •54.3 Case Presentation
- •54.4 Case Discussion
- •54.5 Clinical Characteristics
- •54.6 Diagnostic Algorithm
- •54.7 Management
- •54.8 Conclusion
- •References
- •55.1 Introduction
- •55.2 Pathophysiology
- •55.3 Case Presentation

15 External-Pressure Headache
147
headache (EPH). This condition became even more evident when she began waterbased exercise, which required the use of a swim cap. Studies indicate that patients
with pre-existing headache disorders are three times more likely to develop de novo
accessory-associated headaches [2].
Her experience with two different cap materials provides valuable insights and
supports the diagnosis of external-pressure headache. When using a fabric swim cap
with an elastic band, her pain was localized to the contact points with the elastic,
without diffuse holocranial involvement, and resolved entirely upon removal. In
contrast, the silicone swim cap, which applied more intense and diffuse compression, triggered holocranial pain. This pain persisted for more than an hour after
removing the cap and was accompanied by migrainous features such as photophobia, phonophobia, difculty concentrating, and an inability to continue exercising.
Prolonged exposure to compressive stimuli can lead to sensitization, exacerbating
migrainous headaches in predisposed individuals [3].
This case underscores the importance of patient education on selecting appropriate headgear and implementing strategies to minimize pericranial pressure. For
healthcare providers, recognizing EPH as a distinct headache subtype is essential
for tailoring management plans and improving patients’ quality of life. Beyond
encouraging physical activity, these observations can also benet individuals in
occupational settings, such as healthcare professionals using personal protective
equipment (PPE), who may experience similar headaches. Addressing these issues
has the potential to enhance both comfort and productivity in such environments.
15.4 Diagnostic Algorithm
In the ICHD-3, this headache type is classied under Group 4: Other primary headaches. This category includes headache disorders considered primary because they
result from physiological, non-damaging stimuli [1].
The classication of EPH encompasses headache disorders caused by external
forces applied to the scalp, either through compression or traction, without signicant underlying tissue damage. The International Classication of Headache
Disorders (ICHD-3) denes three subtypes within this group: 4.6.1 Externalcompression headache, 4.6.2 External-traction headache, and 4.6.3 Probable external pressure headache (Table 15.1). These subtypes are distinguished by their
causative mechanisms. The diagnostic criteria emphasize the transient and reversible nature of these headaches. The onset of pain is directly linked to the application
of external force, and the resolution occurs rapidly after the removal of the trigger
[1]. These features distinguish these headaches from conditions such as occipital
neuralgia, which involves neuropathic pain, and tension-type headache, which is
diffuse and unrelated to external stimuli.
The ECH subtype is typically associated with prolonged pressure on the scalp or
forehead caused by external objects such as helmets, goggles, or tight headbands.
These headaches are often seen in occupational or recreational settings [1]. The

148
E. R. R. dos Santos et al.
Table 15.1
ICHD-3 [1]
Headache type Diagnostic criteria
External-pressure
headache (4.6)
External-compression
headache (4.6.1)
External-traction
headache (4.6.2)
Probable externalcompression headache
(4.6.3)
Diagnostic criteria for external-pressure headache subtypes according to the
Headache resulting from sustained compression of or traction upon
pericranial soft tissues.
Comment: 4.6 External-pressure headache is a primary headache
disorder because compression and traction are too subtle to cause
damage to the scalp; in other words, they are physiological stimuli.
A.At least two episodes fullling criteria B–D
B.Provoked by and occurring within one hour of sustained external
compression
C.Maximal pain at the site of compression
D.Resolves within 1h after compression relief
E.Not better explained by another ICHD-3 diagnosis.
A.At least two episodes fullling criteria B–D
B.Provoked by and occurring during sustained external traction
C.Maximal pain at the site of traction
D.Resolves within 1h after traction relief
E.Not better explained by another ICHD-3 diagnosis.
A.Either of the following:
1. A single episode of headache fullling criteria B and D
2. At least two episodes of headache fullling criterion B and either
but not both of criteria C and D
B.Brought on by and occurring only during sustained external
compression of or traction on the forehead and/or scalp
C.Maximal at the compression or traction site
D.Resolving within 1h after compression or traction is relieved
E.Not fullling ICHD-3 criteria for any other headache disorder
F.Not better accounted for by another ICHD-3 diagnosis.
Comment: Codable subforms are 4.6.3.1 Probable externalcompression headache and 4.6.3.2 Probable external traction headache.
COVID-19 pandemic signicantly increased the prevalence of this subtype due to
the widespread and prolonged use of personal protective equipment (PPE), such as
N95 masks and face shields, among healthcare workers. The repetitive pressure on
the pericranial soft tissues, especially from tight-tting PPE, has been cited in
numerous studies as a signicant trigger for this condition [4].
In contrast, ETH results from continuous pulling forces exerted on the scalp.
Common triggers include hairstyles such as tight ponytails, braids, or hijabs [5, 6].
This subtype is more likely to occur in individuals with pre-existing scalp sensitivity
or tenderness. The pain is typically localized to the area of traction, but may radiate
if the force persists for a prolonged period [1].

15 External-Pressure Headache
149
15.5 Pathophysiology
The distinction between intracranial and extracranial headache origins is crucial for
understanding and managing EPH.Intracranial headaches, such as those caused by
meningitis, subarachnoid hemorrhage, or migraine, arise from internal brain structures. In contrast, extracranial headaches, including ECH and ETH, originate from
supercial tissues such as the skin, subcutaneous layers, muscle fascia, and cutaneous nerves, particularly branches of the trigeminal and occipital nerves [5].
The ECH are believed to result from the compression of cutaneous nerves, especially branches of the trigeminal and occipital nerves [3]. Bands or accessories
applied around the head, such as goggles (e.g., swimming goggles), tight hats, professional helmets, or PPE like face shields, masks, and goggles, can exert pressure
on areas such as the occipitofrontal and temporalis muscles (Fig.15.1) [3, 7]. This
localized mechanical stress may irritate supercial sensory nerves, induce peripheral sensitization, and activate the trigeminocervical complex, potentially triggering
headaches. Additionally, compression-induced neuralgia and cervical tension can
further contribute to headache development [8]. During the COVID-19 pandemic,
prolonged PPE use was frequently reported to trigger or exacerbate headaches, particularly in healthcare workers with pre-existing headache disorders [7]. Similarly,
Fig 15.1 Relationship
between the straps of the
PPE and the cutaneous
nerves of the head,
branches of the trigeminal
nerve, and cervical spinal
nerve. The black arrow
indicates the overlap of
straps and rods in regions
innervated by branches of
the cervical spinal nerves.
The red arrow points to the
upper nasal region affected
by the adjustment of the
N95 mask’s metal clip and
the bridge of the glasses

150
the traction caused by tightly tied ponytails, headbands, or similar accessories demonstrates how mechanical forces can produce extracranial headache symptoms,
with relief achieved by loosening or removing the source of pressure [5].
The inuence of prolonged external stimuli is particularly signicant in individuals predisposed to headaches, such as those with migraines or tension-type headaches. Compression of supercial sensory nerves—whether caused by PPE or other
external sources—increases the likelihood of headache onset or intensies preexisting headache disorders. The literature highlights that these effects are especially pronounced in individuals with underlying headache risk factors, emphasizing
the need for tailored preventive strategies and further investigation into these mechanisms [2, 9].
E. R. R. dos Santos et al.
15.6 Clinical Presentation
15.6.1 External-Compression Headache (ECH)
The ECH is characterized by moderate pain that does not typically impede routine
activities. The pain often intensies gradually over minutes and is described as mild
to moderate on the visual analog scale (VAS), with an average intensity of 4/10 [3, 10].
The pain is usually constant and non-pulsatile, localized to the area under pressure [3]. It is commonly reported as a sensation of pressure or heaviness, present in
87.5% of cases, while throbbing or pulling pain was noted in 11.7% of participants
[2]. In healthcare workers using PPE, headaches were bilateral and occurred at
points of contact with masks, goggles, or elastic straps [2]. Similarly, helmetinduced headaches were diffuse, with a pressing pain reported as the predominant
type, alongside pulsating and sharp pain in fewer cases [11].
The source of compression strongly inuences the location of pain. The frontal
region is most frequently affected, although headaches related to helmets often
extend diffusely to other areas of the head [11]. Pain onset typically occurs within
60 min of applying the compressive source and resolves spontaneously within
30min to 1h after its removal [10]. However, in some cases, continued use could
lead to habituation and eventual remission of symptoms [11].
While ECH is generally not accompanied by associated symptoms [3], 23.4% of
healthcare workers reported mild symptoms, including nausea, photophobia, phonophobia, neck discomfort, or movement sensitivity [2]. However, these symptoms
were more likely in individuals with pre-existing primary headache disorders, such
as migraines or tension-type headaches [2]. Notably, prolonged use of N95 masks
and protective eyewear, especially when exceeding four hours per day, signicantly
increases the risk of headaches [2]. Rigid helmets with non-distensible materials
and poorly adjustable bands were also identied as primary triggers [10].
In some cases, the persistence of the compressive stimulus exacerbated headache
severity, particularly in individuals predisposed to migraines. Among affected

15 External-Pressure Headache
151
individuals, 13.4% reported progression to unilateral, pulsating headaches with
nausea and photophobia. For these individuals, removing the compressive accessory was insufcient to alleviate the pain, requiring symptomatic treatment with
medications and rest. Interestingly, medications effective for their previous headache types were not consistently effective for ECH [10].
Prolonged exposure to compressive stimuli can lead to sensitization, causing
more severe migrainous headaches in predisposed individuals [3]. Healthcare work-
ers with pre-existing headache disorders were three times more likely to develop de
novo PPE-associated headaches, particularly those working in high-stress environments such as emergency departments. Despite this, 68.8% of participants with
PPE-related headaches did not require analgesics, and most who did used over-thecounter medications like paracetamol or non-steroidal anti-inammatory drugs [2].
15.6.2 External-Traction Headache (ETH)
The ETH have a clinical presentation that is often inuenced by the specic external
stimulus. Ponytail headache, for example, is a well-recognized extracranial headache associated with hair being tied tightly in a ponytail. In a previous study, 50 out
of 93 women reported experiencing headaches caused by this hairstyle. Pain was
localized to the site of the hair tie in some cases, while in others it extended to areas
such as the vertex, forehead, parietal region, or neck. The onset of pain occurred
during or shortly after tying the hair, and loosening the ponytail provided immediate
or gradual relief, typically within an hour. The headache was described as mild to
moderate and purely extracranial, without accompanying autonomic or migrainous
symptoms [5].
Similarly, hijab headache has been identied as an extracranial headache syndrome among women wearing a hijab. In another study, ve cases involving women
aged 20–63years. All reported experiencing headaches directly related to donning
the hijab. Four of these women had no prior history of headaches, while the fth
noted an increase in the severity and frequency of pre-existing tension-type headaches. The pain was typically mild or moderate, bilateral, and throbbing, localized
to the vertex or parietal areas, with one individual describing pain involving the
entire head. Symptom onset occurred within 30min to 4h of wearing the hijab, and
relief was achieved within an hour of removing it. Notably, modications to the
hijab style, such as repositioning pins or using different fabrics, provided some
relief for a subset of these women. One patient reported reduced symptoms during
a two-year hiatus from wearing the hijab, further supporting the direct link between
the headscarf and headache onset [6].
Both syndromes highlight the predictable clinical pattern of external-pressure
headaches: pain localized to areas under mechanical stress, a clear temporal relationship between the application of the stimulus and the onset of symptoms, and
rapid resolution upon removing or loosening the source of pressure. Although mild
and self-limiting, these headaches can signicantly impact individuals’ daily

152
comfort and activities, particularly when external pressure is prolonged or unavoidable due to cultural or occupational practices.
E. R. R. dos Santos et al.
15.7 Management
Management and prevention of EPH primarily focus on addressing the underlying
mechanical triggers and minimizing the impact of prolonged external pressure.
Strategies include non-pharmacological approaches, pharmacological treatments,
and patient education, tailored to individual cases and occupational needs.
15.7.1 Nonpharmacological Strategies
The cornerstone of managing EPH is the removal or adjustment of pressure-causing
devices. Patients are advised to either avoid headgear or ensure it ts properly and
comfortably. Trying different sizes or styles of helmets or adjusting internal components, such as leather bands, can help alleviate discomfort [3]. Frequent removal of
the headgear during use to relieve pressure can also prevent the progression of
pain [10].
Ergonomic modications are particularly effective for individuals who cannot
avoid wearing headgear, such as healthcare workers or military personnel.
Suggestions include loosening ponytails or adopting alternative hijab styles to
reduce tension and pressure on sensitive areas. When PPE is required, ensuring a
proper t and alternating between different designs may reduce the risk of EPH [3].
15.7.2 Pharmacological Strategies
Most EPH cases do not require pharmacological treatment. Studies show that up to
68.8% of participants with PPE-associated headaches did not use analgesics during
episodes. When necessary, over-the-counter medications such as paracetamol or
non-steroidal anti-inammatory drugs are the most commonly used options for
acute pain relief [2]. Similarly, among military personnel experiencing helmetinduced headaches, 28% occasionally used over-the-counter analgesics to alleviate
symptoms [11].
For patients with underlying migraine or other primary headache disorders, prolonged exposure to external compression can trigger severe migrainous episodes. In
these cases, removing the causative stimulus alone is insufcient, and standard
migraine-specic medications, such as triptans or preventive treatments, may be
necessary to control the symptoms [10]. However, the efcacy of these treatments
for compression-related headaches remains inconsistent and often requires further
individualized management strategies.

15 External-Pressure Headache
153
15.7.3 Patient Education and Awareness
Raising awareness about EPH among at-risk populations is crucial for prevention.
Educational materials can inform patients and workers about the importance of
proper headgear t and the potential risks associated with prolonged compression.
Emphasizing the importance of trying different headgear designs to nd the most
comfortable options and taking regular breaks to relieve pressure can help reduce
the frequency and intensity of headaches [3]. For healthcare workers, awareness
programs about the risk of PPE-associated headaches and practical strategies for
minimizing their occurrence can enhance comfort and productivity, particularly in
high-stress environments such as emergency departments [2].
15.8 Conclusion
The EPH represent a distinct group of primary headache disorders, often triggered
by mechanical forces such as compression or traction applied to the scalp. These
headaches, while typically mild and transient, can signicantly affect individuals’
quality of life, particularly in occupational or cultural contexts where the use of
headgear or specic hairstyles is unavoidable. This chapter has explored the classication, pathophysiology, clinical presentation, and management strategies for
EPH, emphasizing its growing relevance during the COVID-19 pandemic and in
high-risk occupational settings.
The pathophysiology of EPH involves localized mechanical stress on cutaneous
nerves, leading to peripheral sensitization and activation of pain pathways. Accurate
diagnosis relies on recognizing the characteristic temporal relationship between
symptom onset and the application of external pressure, as well as the rapid resolution of symptoms upon removing the stimulus. Effective management focuses on
non-pharmacological strategies, including ergonomic modications and patient
education, while pharmacological interventions are reserved for more severe or persistent cases, particularly in individuals with a predisposition.
Despite advances in understanding EPH, signicant knowledge gaps remain.
Future research should address the long-term impact of repetitive external compression, the role of individual susceptibility factors, and the development of optimized
prevention and management strategies. Increased awareness and tailored interventions can mitigate the burden of EPH, enhancing comfort and functionality in both
occupational and daily settings.
References
1. Headache Classication Committee of the International Headache Society (IHS). The
International Classication of Headache Disorders, 3rd edition. Cephalalgia, 2018. 38(1):
p. 1–211.

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2. Ong JJY, et al. Headaches associated with personal protective equipment – a cross-sectional
study among frontline healthcare workers during COVID-19. Headache. 2020;60(5):864–77.
3. Krymchantowski AV. Headaches due to external compression. Curr Pain Headache Rep.
2010;14(4):321–4.
4. Ribeiro ERR, Lal A, Tardieux FM, Ribeiro ECO, Fortes HMS, Valença MM. Cefaleia por
pressão externa: uma entidade frequente e menos reconhecida. In: Valença MM, editor.
Cefaleia, vol. 1. Advances in Science; 2022. p. 223–33.
5. Blau JN.Ponytail headache: a pure extracranial headache. Headache. 2004;44(5):411–3.
6. Ansari HN, Solomon GD.Hijab (headscarf) headache. Headache. 2015;55(3):437–8.
7. Ong JJY, et al. Headache Related to PPE Use during the COVID-19 Pandemic. Curr Pain
Headache Rep. 2021;25(8):53.
8. Barmherzig R, Kingston W.Occipital neuralgia and Cervicogenic headache: diagnosis and
management. Curr Neurol Neurosci Rep. 2019;19(5):20.
9. dos Santos ERR, Lal A, Tardieux FM, Fortes HMS, Valença MM.External compression head-
ache during Covid-19 pandemic: a neglected entity. Headache Medicine. 2023;14(2):77–82.
10. Krymchantowski A, et al. Helmet-related, external compression headache among police of-
cers in Rio de Janeiro. MedGenMed. 2004;6(2):45.
11. Rahmani Z, et al. Helmet-induced headache among Danish military personnel. Scand J Public
Health. 2017;45(8):818–23.
E. R. R. dos Santos et al.

Chapter 16
Epicrania Fugax
GonçaloDinizPinho andRaquelGilGouveia
16.1 Introduction
Epicrania Fugax (EF) is a rare primary headache disorder characterized by brief,
intense paroxysms of stabbing or shock-like unilateral pain localized to the scalp
that start in specic points and follow a fast trajectory usually in postero-anterior
direction, though antero-posterior, coronal, diagonal, or multidirectional patterns of
radiation have also been reported [1–5]. These trajectories do not conform to specic nerve territories and may even involve the face [6]. At the end of attacks, ipsilateral autonomic signs such as lacrimation, conjunctival injection, and/or rhinorrhea
may occur [7].
Epicrania Fugax is listed in the appendix of the International Classication of
Headache Disorders (ICHD) [7]. Still, shares features with other epicranial pain
syndromes categorized under primary headaches, such as nummular headache and
primary stabbing headache. Similar to nummular headache, EF typically originates
from a well-dened circular area or a broader linear band located in the frontal,
temporal, parietal, or occipital regions of the scalp. However, unlike nummular
headache, EF is distinguished by the rapid and transient migration of pain to other
neurocranial areas. Primary stabbing headache is characterized by brief, sharp, unilateral pain typically lasting around one second and occurring in diverse sites on the
cranial surface, including extra-trigeminal areas. However, it may be xed in up to
a third of patients. Attacks may be associated with sudden head or body movements
G. D. Pinho
Neurology Department, Hospital da Luz Lisboa, Lisboa, Portugal
R. G. Gouveia (
Neurology Department, Hospital da Luz Lisboa, Lisboa, Portugal
Center for Interdisciplinary Research in Health, Universidade Católica Portuguesa,
Lisboa, Portugal
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_16
*)
155© The Author(s), under exclusive license to Springer Nature

156
G. D. Pinho and R. G. Gouveia
(jolts), and their frequency can vary widely, ranging from a single attack per year to
up to 50 attacks per day, with no consistent temporal pattern.
These epicranial primary headaches can be mistaken for headaches secondary to
pericranial neuralgias, particularly those involving the trigeminal nerve, most notably the rst branch (V1), auriculotemporal neuralgia [8] as well as the intermediate
branch of the facial nerve (cranial nerve VII), the glossopharyngeal nerve (cranial
nerve IX), or cervical nerve root compression. The key distinguishing feature lies in
their variable onset and radiation patterns, which often do not follow classical dermatomal distribution [9–11]. Additionally, the differential diagnosis may include
trigeminal autonomic cephalalgias, such as Short-lasting Unilateral Neuralgiform
Headache with Conjuntival Injection and Tearing (SUNCT) or Short- lasting
Unilateral Neuralgiform Headache attacks with Cranial Autonomic Symptoms
(SUNA), especially when mild autonomic symptoms are present [9].
Secondary forms of EF have been described in association with ipsilateral structural lesions, most notably involving the posterior fossa, such as intracranial tumors,
abscesses, or ischemic stroke, as well as peripheral abnormalities, including postsurgical or traumatic scalp scars [12–15], thus justifying a broad etiological assessment, particularly in older patients.
Most reported cases involve female patients, with a female-to-male ratio of
approximately 1.6:1 and a mean age of 45years. However, the age at onset varies
widely, ranging from 19 to 84years. The time from symptom onset to diagnosis is
also highly variable, spanning from 2days to 38years. Some studies have suggested
a possible association with specic personality traits and the presence of anxiety or
depressive symptoms [16, 17]. No pediatric cases have been documented to date [9].
Given the absence of population-based studies and the fact that all reported cases
originate from headache clinics, the available epidemiological data are likely subject to selection bias. The frequent comorbidity with other primary headache disorders, such as migraine, tension-type headache, trigeminal neuralgia, cluster
headache, and auriculotemporal neuralgia, further supports this. It is plausible that
patients presenting with EF were identied primarily due to these associated headache conditions, which brought them to medical care and increased the likelihood
of referral to specialized neurological attention [9].
16.2 Pathophysiology
The pathophysiology of EF remains incompletely understood but is believed to
involve both peripheral and central mechanisms. This dual involvement is supported
by reports of secondary EF-like cases linked to lesions at either level, including
surgical epicranial scars, trigeminal root lesions, and brainstem infarctions [9].
Current hypotheses propose a multifactorial interplay involving focal neuropathy
of terminal cranial sensory bers, anomalous or redundant anastomoses between
these bers, either congenital or acquired (e.g., via aberrant reinnervation), and
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