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L. P. Queiroz and A. M. Soares
frequently missed due to the paucity of clinical manifestations, but it can be present
in up to 65% of GCA patients at the time of diagnosis [4].
21.2 Case Presentation
This is a 72-year-old female patient, Heloisa. She was referred to rheumatology by
her neurologist due to a new daily persistent headache, which started 2 months
before. She reported intense throbbing pain in the temporoparietal region, sometimes on the right and sometimes on the left. The pain was constant and progressive,
with no relieving or worsening factors. She had no nausea, no phonophobia or photophobia. In addition to the pain, she reported signicant sensitivity in her scalp,
which made it difcult for her to comb her hair. According to her report, the sensitivity seemed to be worsening in the last few weeks, causing allodynia, which was
preventing her from sleeping. Her neurologist requested initial tests that indicated
inammatory changes, prompting the referral. The patient denied any visual disturbances, jaw claudication, pain, or stiffness in the pelvic and shoulder girdles.
In the rst evaluation, the patient brought a magnetic resonance imaging (MRI)
scan of the brain that showed only minimal foci of gliosis and a slight diffuse reduction in volume, compatible with the patient’s age. Rheumatoid factor and antinuclear factor were negative, C-reactive protein (CRP) was 50.08mg/L, and erythrocyte
sedimentation rate (ESR) was 109mm/hr. Suspicion of giant cell arteritis (GCA)
was then raised, and Doppler ultrasound of the temporal, carotid, and vertebral
arteries was requested, in addition to magnetic resonance angiography of the thoracic and abdominal aorta and their main branches.
None of the requested tests showed images suggestive of GCA.Meanwhile, the
patient complained of progression of allodynia and, in addition to the imaging tests,
had a new CRP of 57mg/L and ESR of 117mm/hr. Procalcitonin was negative.
It was decided to request an
(18F-FDG-PET) of the whole body, due to high suspicion of GCA and the result is
shown in Fig.21.1a and b. After diagnosis, treatment with prednisone was started at
a dose of 60mg for 15days, followed by 40mg thereafter. Methotrexate was also
started at a dose of 15mg per week, combined with folic acid (5mg) on the day
after taking methotrexate. Tocilizumab 162 mg subcutaneous (SC) was requested
weekly. After 30 days, the patient returned reporting resolution of the headache and
scalp allo dynia. She also reported a signicant reduction in fatigue, which she had
not previously associated with the case. She brought tests, now with a CRP of 7.43
mg/L and ESR of 39 mm/hr.
A few weeks later, the patient had access to tocilizumab, which was initiated.
Methotrexate was then suspended, and the dose of prednisone was reduced until it
was discontinued. The patient achieved complete remission on tocilizumab monotherapy, as perceived both clinically and laboratory and by imaging (Fig.21.1c and d).
18
F-uorodeoxyglucose positron tomography
ab
cd
21 Headache Attributed toAngiitis oftheCentral Nervous System: Giant Cell Arteritis
Fig. 21.1 18F-FDG-
PET-CT performed
longitudinally in a patient
with large vessel giant cell
arteritis. (a and b) scan at
diagnosis (October 2021)
showing pathological
18
F-FDG uptake (higher
than the liver) in the walls
of the abdominal aorta,
thoracic aorta, supra-aortic
branches, femoral arteries,
popliteal arteries, and
tibiobular trunk. (c and d)
Scan during clinical
remission after starting
Tocilizumab (July 2021)
showing reduction in
18
F-FDG uptake (lower
than the liver)
203
21.3 Clinical Characteristics
The most common premonitory and cardinal symptom of GCA is a new-onset headache or an uncommon headache (a change in the characteristics of a previous headache) in a patient over 50years of age. It is a complaint in more than 70% of the
cases [8]. Headache can be the only symptom of GCA, but this is only a modest
discriminator when trying to predict the likelihood of GCA.The report of a temporal headache, however, does not signicantly increase the probability of a diagnosis
of GCA [2, 4]. Headaches are also common when there is a relapse.
Although the headache is usually described as temporal, it may be frontal, occipital, hemicranial, or holocranial (generalized). It can be continuous (occurring daily
or almost daily in 60%) or paroxysmal (occurring in 40% of cases). The intensity
can be from mild to severe, with uctuations in severity [4]. Occasionally, the headache can mimic the characteristics of a migraine, with pulsating pain, nausea, phonophobia, and/or photophobia [9].
Most patients complain of unilateral headaches, but Moudrous etal. [5] reported
that bilateral headaches were a positive predictive factor for a positive temporal
artery biopsy (TAB), especially when associated with weight loss, thrombocytosis,
and a positive halo sign on color Doppler ultrasound.
The diagnostic criteria of the International Classication of Headache
Disorders—third edition (ICHD-3) [10] for headache attributed to GCA are:
204
L. P. Queiroz and A. M. Soares
A. Any new headache fullling criterion C.
B. Giant cell arteritis (GCA) has been diagnosed.
C. Evidence of causation demonstrated by at least two of the following:
1. A headache has developed in close temporal relation to other symptoms and/
or clinical or biological signs of onset of GCA, or has led to the diagnosis of GCA.
2. Either or both of the following:
(a) The headache has signicantly worsened in parallel with the worsen-
ing of GCA.
(b) The headache has signicantly improved or resolved within 3 days of
high-dose steroid treatment.
3. Headache is associated with scalp tenderness and/or jaw claudication.
D. Not better accounted for by another ICHD-3 diagnosis.
In general, there is no association between headache characteristics and the presence of GCA [11]. The headache phenotype in these patients in terms of frequency,
severity, and other associated symptoms is not yet well characterized.
Other cranial signs and symptoms (Fig.21.2): Temporal cutaneous hyperalgesia,
jaw claudication (up to 50% of cases), abnormalities of the temporal artery on
examination (prominent, beaded or irregular artery, with a decreased pulse), tongue
claudication, scalp or tongue necrosis, and rarely ischemic stroke. Tongue pain is
rare, but if present, it increases the chance of a GCA [4].
Between 20% and 30% of patients develop ophthalmic signs and symptoms:
transient monocular visual loss (Amaurosis fugax) or permanent loss of vision (5%)
[2, 7]. Amaurosis fugax usually occurs within 8.5days before permanent visual
loss. It is the initial symptom of GCA in about 18% of the cases [7]. Of those with
permanent visual loss or blurred vision at the time of the diagnosis, 44% had an
amaurosis fugax previously. Some patients may present with Charles Bonnet syndrome [1].
These permanent losses of vision are due to arteritic anterior ischemic optic neuropathy (AAION), central retinal artery occlusion, branch retinal artery occlusion,
posterior ischemic optic neuropathy, or choroidal infarction.
Other visual symptoms include transient or permanent diplopia, secondary to
extraocular muscle ischemia or ocular cranial nerve palsies. Systemic symptoms are
fever, myalgia, fatigue, night sweats, anorexia, unintentional weight loss, mood
changes, arthralgias, stiffness of shoulders, and pelvic joints [1, 12]. Large vessel
manifestations include aortitis, limb claudication, thoracic and abdominal aortic
aneurysms, and myocardial infarction [12]. Pain and stiffness in the shoulders and
the pelvic girdle, predominantly in the morning, may mean the associated presence
of polymyalgia rheumatica [13].
21 Headache Attributed toAngiitis oftheCentral Nervous System: Giant Cell Arteritis
Fig. 21.2 Clinical
manifestations in GCA
205
21.4 Diagnosis
The diagnosis of GCA will depend on an extensive clinical history that generates
suspicion through characteristic symptoms and a detailed physical examination.
This should be associated with inammatory laboratory changes and the presence
of vasculitis in imaging tests or biopsy [12].
Criteria for diagnosing GCA were established in 1990 by the American College
of Rheumatology (ACR) [14], and a revision was proposed in 2021 [15]. In 2022,
the ACR and the European Alliance of Associations for Rheumatology (EULAR)
released guidelines for the classication of GCA, which is more useful for research
purposes [16].
There are no currently specic blood biomarkers that can diagnose GCA.Elevated
acute phase reactants: Erythrocyte sedimentation rate (ESR)—≥50mm/h; C-reactive
protein (CRP)—>10 or 20mg/L; thrombocytosis—platelets >300,000; increased
brinogen. Only 4% of GCA patients have normal ESR and CRP.CRP is a more
sensitive marker for inammation, as ESR levels can increase with age, anemia,
chronic kidney disease, and hypergammaglobulinemia [1].
206
L. P. Queiroz and A. M. Soares
Other laboratory ndings are normochromic normocytic anemia, hypoalbuminemia, and increased transaminases (liver enzymes).
Biopsy of the supercial temporal artery is still considered the gold standard for
the diagnosis of GCA.It is positive in 50–80% of cases. A negative TAB does not
exclude the diagnosis of GCA.
Moudrous etal. [5] found that the predictive factors for positive TAB were, after
multivariate logistic regression: weight loss, halos on color Doppler ultrasound,
thrombocytosis, and bilateral headache (sensitivity of 89% and specicity of 91%).
With the presence of only one of these four factors, the chance of a positive TAB
was less than 35%; when three or four were present, the chance of a positive biopsy
increased to 97.9–99.9%.
Limitations of the TAB include the delay in results, its invasive nature, and
imperfect sensitivity. The biopsy should be done as soon as possible after starting
glucocorticoid therapy, to avoid false-negative results. The ideal is within 14days,
but some authors found positive TAB up to 42days.
Color Doppler ultrasound of the temporal arteries and supra-aortic branches
(head, neck, and upper extremities) is nowadays considered as the rst-line examination in cases of suspected GCA, because it is less invasive, less expensive, and has
a lower rate of false negative than TBA [7].
The halo sign is the hallmark of vasculitis (extensive, circumferential, homogeneous, and hypoechoic thickening of the arterial wall), visible on longitudinal and
transverse planes. It has a sensitivity of 68% and a specicity of 81%. When the
halo sign is bilateral, the specicity is very high. The halo sign disappears approximately 5 days after the appropriate equipment.
18
F-uorodeoxyglucose positron emission tomography (18F-FDG-PET) of the
whole body is used to be indicated only for large vessel GCA.Still, recently, with
new technology and protocols, it has been helpful also for the diagnosis of cranial
disease [6, 12].
Computed tomography (CT) angiography and MRI angiography of aorta and its
branches are both used to look for vasculitis mainly in aorta and its branches. The
presence of circumferential and homogeneous arterial wall thickening and/or contrast enhancement of the arterial wall is suggestive of vasculitis [3, 12].
For typical presentations of GCA, there are almost no differential diagnoses.
For atypical cranial GCA, there are a few: Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis, temporal arteritis due to varicella zoster virus,
atherosclerotic disease, uremic calcifying arteriopathy, posttraumatic arteriovenous stulas or pseudoaneurysms, nonarteritic anterior ischemic optic neuropathy, and immunoglobulin 4 (IgG4)-related disease [12, 17].
21 Headache Attributed toAngiitis oftheCentral Nervous System: Giant Cell Arteritis
207
21.5 Treatment
Whenever there is a high clinical suspicion of GCA, a high dose of glucocorticoid
(40–60mg/day) should be immediately started [18].
For patients with visual symptoms, pulses of IV methylprednisolone
(250–1000mg/day, for 3days) may be considered, followed by oral prednisone, but
its benet has not been proven [12, 18, 19].
Currently, both the ACR and PANLAR (Pan American League of Associations for
Rheumatology) recommend starting an immunosuppressant together with the use of
corticosteroids at the diagnosis of GCA [18, 19]. Thanks to the giant cell arteritis
actemra trial (GiACTA) study [20] that produced evidence in favor of the use of
tocilizumab (a humanized monoclonal antibody to the interleukin-6 [IL-6] receptor)
in GCA, this has been the recommended rst-line immunosuppressant [18, 19]. If
there is difculty in accessing the use of this medication or contraindication, the use
of methotrexate associated with glucocorticoid may be an alternative [19].
The isolated use of glucocorticoids is associated with high rates of relapse and
complications related to the drug itself [18]. The duration of glucocorticoid therapy,
when associated with immunosuppressants, is not well established, but it is suggested to progressively reduce the dose until its withdrawal, when possible, in 6
months. The duration of treatment with immunosuppressants is also not well established in the literature [12, 18, 19].
In patients with severe carotid and vertebral involvement, the use of aspirin associated with immunosuppressive treatment has been conditionally recommended
[18, 19].
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3. Van der Geest KSM, Sandovici M, Brouwer E, etal. Large vessel giant cell arteritis. Lancet
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17, 2020. ISSN 1129-2369
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Janssen PM, J B Janssen J, L Rensma P, J F Brekelmans G.A new prediction model for giant cell
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6. Wang D, Liu Z, Guo H, Yang L, Zhang X, Peng L, Cheng M, Jiang H. Headache attributed to giant cell arteritis complicated with rheumatic polymyalgia diagnosed with F18uorodeoxyglucose positron emission tomography and computed tomography: a case report.
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7. Dinkin M, Johnson E.One giant step for giant cell arteritis: updates in diagnosis and treatment.
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9. Devi S, Dash A, Purkait S, Sahoo B.Giant cell arteritis masquerading as migraine: a case
report. Cureus. 2023;15(8):e44107. https://doi.org/10.7759/cureus.44107.
10. Headache Classication Committee of the International Headache Society (IHS). The international classication of headache disorders, 3rd edition. Cephalalgia. 2018;38(1):1–211. https://
doi.org/10.1177/0333102417738202.
11. Shimohama S, Imai N, Tsubata T, Shinohara K, Moriya A, Yagi N, Konishi T, Serizawa
M, Tashiro K.Headache-related characteristics of biopsy-conrmed giant cell arteritis and
the relationship of transmural inammation with artery tenderness and chordal thickening.
Cureus. 2024;16(3):e56843. https://doi.org/10.7759/cureus.56843.
12. de Boysson H, Devauchelle-Pensec V, Agard C, André M, Bienvenu B, Bonnotte B, Carvajal
Alegria G, Espitia O, Hachulla E, Heron E, Lambert M, Lega JC, Ly KH, Mekinian A,
Morel J, Regent A, Richez C, Sailler L, Seror R, Tournadre A, Samson M, Collaborators.
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Campbell SM, Abeles M, Clark P, etal. The American College of Rheumatology 1990 criteria
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diseases. J Clin Med. 2022;11(1):275. https://doi.org/10.3390/jcm11010275.
18. Scolnik M, Brance ML, Fernández-Ávila DG, Inoue Sato E, de Souza AWS, Magri SJ,
Saldarriaga-Rivera LM, Ugarte-Gil MF, Flores-Suarez LF, Babini A, Zamora NV, Acosta
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Full KA, Grayson PC, Ibarra MF, Imundo LF, Kim S, Merkel PA, Rhee RL, Seo P, Stone
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20. Stone JH, Tuckwell K, Dimonaco S, Klearman M, Aringer M, Blockmans D, Brouwer E, Cid
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Collinson N.Trial of Tocilizumab in giant-cell arteritis. N Engl J Med. 2017;377(4):317–28.
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L. P. Queiroz and A. M. Soares
Chapter 22
Headache or Facial or Neck Pain
Attributed toCervical Carotid or Vertebral
Artery Dissection
Ş.OzanDörtkol andEsmeEkizoğlu
22.1 Introduction
C.Miller Fisher rst described arterial dissection. It refers to the tear of the arterial
wall and is classied according to the location of the dissection [1]. Cervical artery
dissections (CAD), which refer to cervical carotid and vertebral artery dissections,
are not uncommon and constitute the etiology behind a variety of neurological
symptoms. The most common symptoms of dissections on the cervical segments of
carotid or vertebral arteries are headache, facial, or neck pain [2]. Other common
symptoms result from ischemia related to an ischemic stroke or to a transient ischemic attack. Cervicocerebral artery dissection is one of the important causes of
stroke seen in the young population [3]. Dissections may also be complicated with
dissecting aneurysms or subarachnoid hemorrhage (SAH).
The recorded incidence of CAD has been estimated to be 2.6–2.9 per 100,000
per year based on previous studies in the United States and France [4, 5]. Cervical
artery dissection is likely underestimated in routine practice because cases with few
or no clinical signs may be underdiagnosed or misdiagnosed [6]. However, CAD is
the cause of approximately 24% of the strokes in young patients [7]. North American
studies have found a higher incidence in women [4, 8], and European studies have
found a higher incidence in men [9, 10]. One study reported that CAD occurred
more frequently in cold months in association with increased brachial pulse pressure [11, 12]. Headache is reported as the most common symptom and also the most
common initial symptom. Although isolated headache is rarely experienced, this
may also occur as a symptom of extracranial dissection [13].
Ş. O. Dörtkol
Neurology Clinic, Istanbul Physical Medicine and Rehabilitation Training and Research
Hospital, Istanbul, Turkey
E. Ekizoğlu (
Department of Neurology, Istanbul Faculty of Medicine, Istanbul University, 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_22
*)
209© The Author(s), under exclusive license to Springer Nature
210
Ş. O. Dörtkol and E. Ekizoğlu
22.2 Pathophysiology andRisk Factors
Arterial dissections develop as a result of a tear in the media and intima layers of
the arterial wall. This condition becomes complex when blood enters the vascular
wall, which leads to the formation of a thrombus [14]. Dissections are called
“spontaneous” when there is no traumatic event, since they may result from major
or minor trauma. A headache or neck congestion is likely due to the rupture in the
vessel wall. The tear in the vessel wall likely leads to a cascade of events that also
result in the release of several pro-inammatory neurotransmitters from the blood
vessels near nerve terminals. This may result in the onset of pain in the regions of
dissection [15].
The genetic predisposition in the development of cervical dissections has been
shown in patients with collagen vascular disorders [16]. Some studies reported that
this condition was associated with a mutation in MTHFR C677T and deciency of
alpha-1 antitrypsin as genetic factors predisposing this condition [4].
However, most of the CADs occur as a result of minor neck trauma or manipulation, indicating the role of environmental factors [17]. Previous studies have also
reported an association between CAD and acute or subacute infections [17]. No
denitive data have been reported on CAD occurrence and vascular risk factors.
However, low body mass index, hypertension, and low cholesterol level appear to
increase the risk of arterial dissection. Furthermore, some previous studies have
reported a possible association between CAD and migraine [18].
22.3 Case Presentation 1
A 34-year-old woman was admitted to the emergency department with a sudden
onset of headache on the left side spreading to the forehead while cleaning the upper
surface of a tall cabinet with neck hyperextension. She described that the pain was
throbbing, accompanied by nausea, without any symptoms such as photophobia,
phonophobia, and osmophobia. She also experienced blurred vision, which began at
the same time as a headache and lasted for 15min. She beneted from a painkiller,
and her headache entirely resolved in 3 h. The same headache recurred 2 days later
when carrying a heavy object and lasted for 15min.
She was diagnosed with episodic migraine for 20years, reporting two to three
attacks per month. Her physical and neurological examinations were unremarkable.
She was neither a smoker nor an alcohol user.
Brain magnetic resonance imaging (MRI) showed small acute infarcts in the left
cerebellum. MRA revealed a left vertebral artery (VA) dissection leading to a 2cm
stenosis in the distal part of the V3 segment. Other etiological workup for stroke
was normal. She was started on dual antiplatelet therapy and did not need further
painkiller use during her hospital stay.
22 Headache or Facial or Neck Pain Attributed to Cervical Carotid or Vertebral…
211
22.4 Case Discussion
This case illustrates that secondary headaches should be considered in a patient with
a prior primary headache condition when the patient describes a sudden onset of a
new headache. Detailed history taking may provide clues for diagnosis. This patient
reported that the headache started while hyperextending her neck, which is a typical
posture causing minor neck trauma. This case also highlights the importance of
MRA (or computed tomography angiography [CTA]) in addition to brain imaging
in patients suspected of having an arterial dissection-related headache.
22.5 Case Presentation 2
A 60-year-old male patient presented with a severe progressive headache on the left
temporal region of his head that started 5 days before admission. He described the
pain as throbbing and not accompanied by nausea and vomiting. He had no history
of previous headaches or other diseases and did not report a recent head trauma or
other suspicious condition. He found some relief from painkillers without complete
recovery. Neurological examination was notable for miosis and ptosis on the left
eye (Horner’s syndrome), and mild right hemiparesis.
Brain MRI revealed an acute infarct in the left putamen and hyperintense ow
void in the distal cervical and petrosal segments of the left internal carotid artery
(ICA) on uid-attenuated inversion recovery (FLAIR) sequences. CTA disclosed a
left ICA dissection causing severe stenosis and intramural thrombus. The patient
started on dual antiplatelet therapy, and analgesic drugs were administered. His
headache resolved during hospital admission in 4 days, and the neurological ndings recovered. Repeated CTAs showed complete resolution of the thrombus and
stenosis; the patient reported being headache-free since discharge at the 3-month
follow-up visit.
22.6 Case Discussion 2
This case illustrates the importance of a detailed, systematic, and neurological
examination when evaluating patients admitted with headache to exclude secondary
headaches. In this case, the headache was progressive and experienced for the rst
time. These are important clinical features that suggest a secondary headache disorder and require further diagnostic investigations. Moreover, neurological examination revealed Horner’s syndrome on the left, suggesting carotid dissection in the
differential diagnosis, together with the presence of headache. The pain was severe
and unilateral to the affected cervical artery, lasted several days and resolved during