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Ş. O. Dörtkol and E. Ekizoğlu
follow-up within less than 1 month. All these features fullled third edition of the
International Classication of Headache Disorders (ICHD-3) diagnostic criteria for
acute headache or facial or neck pain attributed to cervical carotid or vertebral
artery dissection.
22.7 Clinical Characteristics
The third edition of the International Classication of Headache Disorders (ICHD-3)
established specic criteria to make the diagnosis of headache or facial or neck pain
associated with cervical artery or vertebral artery dissection. These diagnostic criteria were given in Table22.1 [19].
Factors inuencing the development of headaches associated with CAD were
reported to be female gender, dissection affecting posterior circulation, prior history
of headaches, and low-density lipoprotein levels [20]. Acute onset headache was
observed in 53% of the patients, and 35% of these patients experienced headache as
the initial symptom. Therefore, artery dissections should also be assessed in the differential diagnosis of thunderclap headache [21].
The pain was reported to be throbbing pain in one third (35%) of the patients and
localized usually on one side of the head or neck (71.7%) [22]. In carotid artery dissections, pain was most frequently localized in the temporal region (46%), followed
by the frontal region (19.2%). In contrast, in vertebrobasilar artery dissections, the
Table 22.1 ICHD-3 diagnostic criteria for acute headache or facial or neck pain attributed to
cervical carotid or vertebral artery dissection
A.Any new headache and/or facial or neck pain fullling criteria C and D
B.Cervical carotid or vertebral dissection has been diagnosed
C.Evidence of causation demonstrated by at least two of the following:
1. Pain has developed in close temporal relation to other local signs of the cervical artery
dissection, or has led to its diagnosis
2. Either or both of the following:
(a) Pain has signicantly worsened in parallel with other signs of the cervical artery
dissection
(b) Pain has signicantly improved or resolved within 1month of its onset
3. Either or both of the following
(a) Pain is severe and continuous for days or longer
(b) Pain precedes signs of acute retinal and/or cerebral ischemia
4. Pain is unilateral and ipsilateral to the affected cervical artery
D.Either of the following:
1. The headache has revolved within 3months
2. The headache has not yet resolved, but 3months have not yet passed
E.Not better accounted for by another ICHD-3 diagnosis
22 Headache or Facial or Neck Pain Attributed to Cervical Carotid or Vertebral…
213
occipital region and the nape of the neck stood out as the locations where the pain
was most frequently observed (79.7%) [22]. The severity of the headache may vary
depending on age. A previous study compared the clinical features of dissections in
the young population and the elderly and observed that both neck pain and headaches were more frequently experienced by young people than the elderly [23].
In a recently published review that evaluates the clinical characteristics of
patients with CAD, it has been reported that headache was a more prevalent symptom in cases of vertebral artery dissection than in those of carotid artery dissection
[22]. Furthermore, Uludüz etal. observed that patients with vertebral artery dissection experienced more frequent headaches with higher rates of photophobia and
phonophobia in comparison to patients with carotid artery dissection [24]. Another
report has also described a case of vertebral artery dissection with migraine-like
headache accompanied by photophobia and nausea [25]. The higher rates of headache, photophobia, and phonophobia in patients with vertebral artery dissection are
thought to be associated with trigeminovascular system activation [26]. However,
another study evaluating 51 patients with vertebral artery dissection reported that
only 4% of the patients reported photophobia at the time of diagnosis [27]. In a
survey conducted by Mayer-Suess etal., headaches occurred frequently with a sudden onset in patients with arterial dissection. The character of the pain in vertebral
artery dissection was often described as a pulling sensation, whereas in carotid
artery dissection, it was typically characterized as dull and throbbing. Furthermore,
among patients with vertebral artery dissection, it was noted that the duration of
headaches was signicantly longer than in carotid artery dissection [28]. A recent
study reported that headaches associated with CAD were more severe, more often
unilateral, and more frequent than those associated with large artery occlusion. It
was also found that headaches were frequently throbbing in patients with dissection,
but pulsating in those with occlusion [29].
The relationship between migraine and CAD has also been reported in some
reports, although the sample sizes were usually limited to small groups. While an
association between migraine with aura and CAD has been reported [29], a cohort
study investigating 2485 ischemic stroke patients showed that the prevalence of
CAD was higher in patients with migraine without aura compared with migraine
with aura [19].
It should also be noted that clinical presentations in CAD may vary depending on
the localization and the surrounding structures of the dissected segment as well.
Horner’s syndrome is mostly seen in carotid dissections because pericarotid sympathetic bers are frequently affected. However, vertebrobasilar dissections cause
symptoms associated with brainstem ischemia, such as vertigo, ataxia, and nausea
[30, 31]. One of the most common presentations in patients is cerebral ischemia,
which occurs in two-thirds of patients [4]. Symptoms are consistent with the ischemic area in these patients. Rarely seen presentations include retinal infarctions
leading to monocular vision loss or ischemic optic neuropathy [32, 33].
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22.8 Diagnostic Workup
Several neuroimaging tests are helpful in the diagnosis of arterial dissection.
Computed tomographic angiography (CTA) has half the spatial resolution of digital
subtraction angiography (DSA) and twice the spatial resolution of magnetic resonance angiography (MRA) [34]. Rapid image acquisition and widespread availability make CTA the most frequently preferred diagnostic method. The specicity
(67–100%), sensitivity (64–100%), negative (70–100%), and positive predictive
(65–100%) values of CTA for the detection of cervical or cephalic arterial dissection are comparable to those of DSA [35–37]. An asymmetrical and irregular vessel
wall appearance is the most common nding. Intramural hematoma is seen as a
crescent-shaped hyperdensity in addition to the thickening of the vessel wall [38].
CTA can also easily demonstrate intimal aps and pseudoaneurysms, which is a
common consequence of extracranial dissection and occur in 13–49% of patients
with CAD [39]. Although well-tolerated and relatively safe and less invasive than
DSA, CTA involves exposure to iodinated contrast and radiation, which may be
harmful for patients with impaired renal function or allergies to contrast material.
CTA is a neuroimaging test that is relatively contraindicated during pregnancy and
in childhood [40].
The combination of axial T1-weighted cervical MRI examination with fat suppression is used for a noninvasive imaging modality to detect dissection. It is more
sensitive to detect small intramural hematomas than CT imaging [41]. The characteristic MRI nding is the hyperintense crescent sign observed on T1-weighted and
FLAIR sequences that results from intramural leaking of the blood, causing the
intramural hematoma that appears in the shape of a half-moon spiral [41–43].
Recent studies have also demonstrated the effectiveness and reliability of
susceptibility- weighted imaging (SWI) in detecting intramural hematoma [44].
Other abnormalities that can be identied through magnetic resonance imaging
(MRI) include vessel diameter enlargement and hyperintense signal abnormality on
the entire vessel, compromise of the vessel lumen by the adjacent tissue with an
abnormally increased signal, and poor to no visualization of the vessel [45].
Digital subtraction angiography is accepted as the gold standard test to identify and reveal the features of dissected segments. This procedure allows dynamic
characterization of the blood ow across the lesion. However, it carries risks of
stroke, retroperitoneal hemorrhage, vascular perforation, and contrast-induced
nephropathy [46].
22.9 Treatment
Although there is a limited number of studies on the treatment of dissections, the
most important treatment step is the acute treatment to prevent possible complications such as ischemic stroke or subarachnoid hemorrhage. The primary therapeutic
22 Headache or Facial or Neck Pain Attributed to Cervical Carotid or Vertebral…
215
management strategy is therefore to start antiplatelets or anticoagulants as soon as
possible for stroke prevention in CAD [47]. Acute treatment with intravenous
thrombolysis and/or mechanical thrombectomy is also recommended in selected
cases [41]. However, other symptoms, such as headaches, may also require treatment. It has been observed that headaches secondary to dissections may improve
with antimigraine medications [41]. Medical management is based on both empirical and clinical observations. Nevertheless, a previous study showed that headaches
associated with CAD had a better prognosis than headaches caused by other vascular causes [48].
22.10 Prognosis
There are very few studies evaluating the long-term prognosis of headaches associated with CAD.Evaluations of the clinical course of internal carotid artery dissections have noted that headaches resolved within a short time frame in a
signicant portion of patients [49]. As headaches improve typically shortly after
the diagnosis, prolonged headaches are rarely reported in the literature. Analgesics
are administered to the majority of patients and are benecial in the majority of
the reported cases. Only one case has been documented in which the headache
resolved after a short course of steroid treatment [50]. Infrequently, arterial dissections with dissecting aneurysms can lead to subarachnoid hemorrhage. A
poorer prognosis was observed in these cases where dissecting aneurysms occur
[51]. Recurrence of dissections has a low rate of approximately 1% during at least
1 year of follow-up [9].
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Chapter 23
Post-endarterectomy Headache
PauloSergioFaroSantos
23.1 Introduction
Endarterectomy is the treatment of choice for the prevention of stroke in patients
with symptomatic carotid stenosis [1]. Although this procedure is generally safe and
effective, postoperative headache is a recognized but often underestimated complication [1–4]. The objective of this chapter is to present and analyze in depth a clinical case of post-endarterectomy headache with its characteristics and management.
23.2 Pathophysiology
The pathophysiology of post-endarterectomy headache is not yet fully understood,
but some hypotheses may help in understanding the mechanism of this headache, namely:
• Oculosympathetic autonomic dysfunction: In a case series of post- endarterectomy
headache, a group of patients who developed cluster headache phenotype had
signicantly decreased oculosympathetic activity compared with the control
group without headache. The authors suggest that damage to the sympathetic
plexus resulting from the surgical procedure may be involved in the development
of postoperative headache.
• Cerebral hemodynamic abnormalities: Björne et al. described the case of a
patient with chronic cluster headache who had been in remission for over
20years and who, the day after carotid endarterectomy, returned to experience
attacks identical to his previous headache. It is known that pharmacologically
P. S. FaroSantos (*)
Faro Institute, Curitiba, PR, 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_23
221© The Author(s), under exclusive license to Springer Nature
222
P. S. FaroSantos
induced vasodilation can trigger an attack in a susceptible individual during a
period of cluster headache. This knowledge led them to suspect that the state of
cerebral hyperperfusion caused by the restoration of blood ow after the surgical
procedure had reactivated the headache in this patient [5, 6]. In addition, cerebral
hyperperfusion syndrome, a rare complication characterized by headache, focal
neurological decits and seizures in the absence of cerebral ischemia, is well
described and is also believed to be related to failure of cerebral blood autoregulation [7].
• Activation of the Trigeminovascular System: Surgical manipulation of vascular
and nervous structures during the procedure can activate the trigeminovascular
system and cause the release of several chemical mediators, including calcitonin
gene related peptide (CGRP) and substance P, leading to vasodilation and sensitization of pain pathways, contributing to the manifestation of headache [5, 8].
23.3 Case Presentation
A 64-year-old man was diagnosed with a transient ischemic attack due to recurrent
episodes of left hemiparesis lasting up to 30min. The patient had a past medical
history of hypercholesterolemia and a sedentary lifestyle. He denied any history of
recurrent headaches. Neurological examination revealed no focal decits. Brain
magnetic resonance imaging (MRI) showed no signs of acute ischemia, but only
white matter hyperintensities on uid-attenuated inversion recovery (FLAIR)
(Fazekas 2), with no other signicant changes. Cervical arterial computed tomography (CT) angiography revealed substantial carotid stenosis (>70%) of the right
internal carotid artery, for which he underwent carotid endarterectomy.
From the fth postoperative day onwards, he developed a moderate-intensity
right-sided fronto-orbitotemporal headache, which occurred in attacks lasting
between 20 and 40min, once a day, and was associated with conjunctival hyperemia, lacrimation, and rhinorrhea ipsilateral to the pain. His blood pressure was
within normal limits.
Due to the pattern of symptoms, the patient was treated acutely with oxygen,
obtaining a good therapeutic response. A new cervical arterial magnetic resonance
imaging and angioresonance were performed, but they did not show ischemic or
hemorrhagic lesions, nor arterial stenosis or dissection. As the headache attacks
continued daily for more than 1week, verapamil was started, and the headache
regressed approximately 40days later.