Cervical Artery Dissection.11

REVIEW ARTICLE
Cervical Artery
Dissection

C O N T I N UU M A UD I O
I NT E R V I E W A V AI L A B L E
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ONLINE
By Setareh Salehi Omran, MD
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ABSTRACT
OBJECTIVE: Cervical artery dissection is a common cause of stroke in young
adults. This article reviews the pathophysiology, etiology and risk factors,
evaluation, management, and outcomes of spontaneous cervical artery
dissection.
HidtNoQlXU1rbbojjYeTlxuc= on 04/15/2023
LATEST DEVELOPMENTS: Cervical artery dissection is believed to be a

multifactorial disease, with environmental factors serving as possible
triggers in patients who have a genetic predisposition to dissection
formation. Cervical artery dissection can cause local symptoms or
ischemic events, such as ischemic stroke or transient ischemic attack.
Neuroimaging is used to confirm the diagnosis; classic findings include a
long tapered arterial stenosis or occlusion, dissecting aneurysm, intimal
flap, double lumen, or intramural hematoma. Patients with cervical artery
dissection who present with an acute ischemic stroke should be evaluated
for IV thrombolysis, endovascular therapy eligibility, or both.
Antithrombotic therapy with either anticoagulation or antiplatelet
treatment is used to prevent stroke from cervical artery dissection. The
risk of recurrent ischemia appears low and is mostly limited to the first two
weeks after symptom onset.
Cervical artery dissection is a known cause of ischemic

ESSENTIAL POINTS:
strokes. Current data show no difference between the benefits and risks of
CITE AS: anticoagulation versus antiplatelet therapy in the acute phase of
CONTINUUM (MINNEAP MINN) symptomatic extracranial cervical artery dissection, thereby supporting
2023;29(2, CEREBROVASCULAR
the recommendation that clinicians can prescribe either treatment.
DISEASE):540–565.
Further research is warranted to better understand the pathophysiology
Address correspondence to and long-term outcomes of cervical artery dissection.
Dr Setareh Salehi Omran, 12401
East 17th Ave, MS L950, Aurora,
CO 80045, setareh.
salehiomran@cuanschutz.edu.
RELATIONSHIP DISCLOSURE: INTRODUCTION
D
Dr Salehi Omran reports no
issections are defined by blood collection and intramural hematoma
disclosure.
formation in the arterial wall layers. Cervical artery dissection is a
UNLABELED USE OF dissection in the carotid artery, vertebral artery, or both, and most
PRODUCTS/INVESTIGATIONAL
USE DISCLOSURE:
commonly involves the extracranial portions of these arteries.
Dr Salehi Omran reports no Dissections can occur spontaneously or as a direct result of
disclosure. significant trauma. About 15% to 24% of cases of ischemic stroke in young adults
© 2023 American Academy are due to cervical artery dissection, making it a common cause of stroke in
of Neurology. this population.1,2
540 APRIL 2023
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

This article reviews the epidemiology, pathophysiology, risk factors, clinical KEY POINTS
presentations, evaluation, management, and outcomes of cervical artery
● The overall incidence of
dissection. In particular, recent insights on risk factors and treatment, including cervical artery dissection is
acute ischemic stroke management and secondary stroke prevention, are low at 2.6 to 3.0 per 100,000
highlighted. Spontaneous cervical artery dissections are the main focus, as these people per year.
are more commonly encountered by neurologists, whereas cervical artery
● Dissections result from

dissection from major trauma is typically managed by surgeons. Purely
the separation of the arterial

intracranial dissections are not discussed and intracranial extension of wall layers causing the
extracranial cervical artery dissection is discussed briefly. formation of a false lumen
that allows blood to enter
EPIDEMIOLOGY the vessel wall.
The overall incidence of cervical artery dissection is low in the general ● Dissections can cause
population, at an estimated 2.6 to 3.0 per 100,000 people per year.3,4 Internal subintimal or subadventitial
carotid artery (ICA) dissections are more common than vertebral artery hematomas. Subintimal
dissections (1.72 per 100,000 people per year; 95% confidence interval, 1.1 to 2.3 hematomas may lead to
intraluminal stenosis or
versus 0.97 per 100,000 people per year; 95% confidence interval, 0.5 to 1.4).3 occlusion. Subadventitial
The overall incidence of cervical artery dissection is probably underestimated, as hematomas can cause
cases with few or no clinical signs are likely to remain undiagnosed or eccentric hematoma growth
misdiagnosed. and aneurysm formation.
Most epidemiologic studies on cervical artery dissection are from North
America and Europe, and it is unclear whether the findings generalize to other
populations. Based on these studies, the average age of cervical artery
dissection occurrence is 43 to 54 years.3,5,6 Data are inconsistent regarding any
sex-based differences, with North American studies showing a higher
incidence in women3,7 and European studies showing a greater occurrence
in men.5,6
ANATOMY OF CERVICAL ARTERY DISSECTION

The exact mechanism of hematoma formation in cervical artery dissection is
incompletely understood. Dissections result from separation of the arterial wall
layers causing a false lumen to form and allowing blood to enter the vessel wall
(FIGURE 8-18). These separations are thought to be from an intimal tear or direct
bleeding from ruptured vasa vasorum. Dissections can be either subintimal or
subadventitial. Subintimal dissections may cause intraluminal stenosis or
occlusion. Subadventitial dissections more commonly cause eccentric hematoma
growth, which can result in dissecting aneurysm formation.9 Intramural
hematomas can cause vessel dilatation and compression of adjacent nerves,
which can lead to local symptoms of headache and neck pain (from stimulation
of pain-sensitive receptors10), Horner syndrome, and cranial and cervical
neuropathies.
Carotid dissections occur a few centimeters above the bifurcation and
typically involve the distal two-thirds of the extracranial ICA near the skull
base.11 Spontaneous cervical artery dissections are more likely to be in the
proximal ICA whereas traumatic cervical artery dissections are typically in the
distal extracranial ICA.12 Vertebral artery dissections typically involve the V2
(cervical transverse process of C6 through C2) and V3 segments (extracranial
segment between transverse process of C2 and foramen magnum of the skull) of
the vertebral artery.13 Traumatic vertebral artery dissections more commonly
affect the V3 segment.12 Multiple simultaneous cervical artery dissections can be
seen in 13% to 22% of cases.3,5,6,14 Most cases of multiple simultaneous dissections
CONTINUUMJOURNAL.COM 541

CERVICAL ARTERY DISSECTION
FIGURE 8-1
Manifestations of cervical artery dissection. A, During initiation of the arterial dissection
blood dissects into the subintimal space to create a false lumen. B, The formation of true and
false lumina can lead to artery-to-artery embolism. This can occur from either an intraluminal
thrombus formed at the site of intraluminal stenosis or distal embolization from the
intramural hematoma through an exit site from the dissection. C, Intramural hematoma can
lead to narrowing of the true lumen and occlusion of the dissected artery. D, Subadventitial
dissections can result in dissecting aneurysm formation.
Reprinted with permission from Bond KM, et al, J Neuroradiol.8 © 2020 Elsevier Masson SAS.
occur after minor trauma or infection,15 although some data suggest a possible
association with fibromuscular dysplasia.14
ETIOLOGY AND PREDISPOSING FACTORS

The pathophysiology of cervical artery dissection is incompletely understood.
The leading theory is that cervical artery dissection is a multifactorial disease, and
that environmental factors serve as potential triggers in patients who have a
genetic predisposition to dissections (TABLE 8-116-33).
Genetic Factors
Cervical artery dissection has been linked to a few connective tissue disorders and
vascular diseases. Fibromuscular dysplasia is perhaps the most common, with one
study identifying the presence of fibromuscular dysplasia in 40% of cervical artery
dissection cases.34 A small portion of cervical artery dissection cases (nearly 2%)
have been linked to monogenic connective tissue diseases, such as vascular
Ehlers-Danlos syndrome (also known as Ehlers-Danlos syndrome type IV).35
Although the prevalence of vascular Ehlers-Danlos syndrome among all patients
with cervical artery dissection is low, there is a strong association between the
two conditions. A study found that more than half (55%) of patients with
vascular Ehlers-Danlos syndrome had supraaortic trunk lesions, the majority
being cervical artery dissections.36 Therefore, screening patients with cervical
artery dissection for clinical signs of connective tissue diseases such as vascular
Ehlers-Danlos syndrome is important, as it may lead to further genetic
542 APRIL 2023

counseling and preventive measures. Reports of cervical artery dissection in KEY POINTS
patients with other connective tissue and vascular disorders such as Marfan
● A small portion of cervical
syndrome, osteogenesis imperfecta, and alpha-1 antitrypsin deficiency occur; artery dissection cases
however, the majority of these conditions are rare, and it is unclear whether (nearly 2%) have been linked
concomitant occurrence is higher than would be expected by chance alone.37 to monogenic connective
Apart from monogenic connective tissue diseases, which encompass a small tissue diseases, such as
vascular Ehlers-Danlos
group of cervical artery dissection cases, genetic factors may play a role in a more
syndrome.
multifactorial process leading to cervical artery dissection. The role of a genetic
predisposition is supported by familial cervical artery dissection cases,38 ● Apart from monogenic
dissections in other arterial beds in the absence of an established connective disorders, which encompass
tissue disorder,39 the presence of ultrastructural connective tissue alterations that a small group of cervical
artery dissection cases,
follow an autosomal dominant inheritance pattern,40 and the occurrence of genetic factors may play a
concomitant arterial abnormalities suggesting a more systemic arteriopathy.41-43 role in a more multifactorial
Connective tissue alterations seen in cervical artery dissection include elastic process leading to cervical
fiber fragmentation and the presence of composite fibrils within collagen artery dissection.
bundles, and suggest a defect in the biosynthesis of the extracellular matrix.44,45 ● Minor cervical trauma
In contrast to the rare co-occurrence between cervical artery dissection and precedes nearly 41% of
hereditary connective tissue diseases, nearly all patients with cervical artery identified spontaneous
dissection have clinical signs suggestive of connective tissue abnormalities.46 cervical artery dissection
cases. These minor traumas
These include skeletal, skin, and ocular abnormalities and craniofacial
can be subtle and involve
dysmorphisms.46 The presence of clinically detectable signs of connective tissue hyperextension,
anomalies in patients with cervical artery dissection in the absence of an lateroversion, or rotation of
established hereditary connective tissue disease suggests that systemic the neck.
aberrations of connective tissue may be implicated in disease pathogenesis.46
Despite the evidence suggesting a genetic predisposition, no established genetic
markers for cervical artery dissection are currently established. A systematic
review of 15 genetic association studies revealed a possible association with
polymorphisms in ICAM1 and COL3A1 and the MTHFR 677TT genotype47;
however, the findings were severely underpowered and require confirmation in
larger genetic association studies.
Environmental Factors
Environmental factors, such as significant and minor trauma, play an important
role in cervical artery dissection development. Significant trauma causing
penetrating or nonpenetrating injuries (including blunt trauma) can lead to
traumatic cervical artery dissection, while minor cervical trauma or mechanical
events are linked to spontaneous cervical artery dissection. Minor cervical
trauma precedes nearly 41% of spontaneous cervical artery dissection cases.48
These minor traumas can be subtle and involve hyperextension, lateroversion, or
rotation of the neck, which can lead to intimal injury of the cervical arteries and
result in dissection, as illustrated in CASE 8-1. Minor traumas include commonly
occurring mechanical events, such as severe coughing or sneezing, violent
vomiting, sports activities, whiplash injury, or cervical manipulative therapy
(TABLE 8-1). The observation that common minor traumatic and mechanical
events cause dissections in only select individuals further supports the hypothesis
that environmental factors may lead to cervical artery dissection development in
patients already genetically predisposed to dissections.
Epidemiologic studies suggest an association between cervical manipulative
therapy and cervical artery dissection, in particular vertebral artery dissection.21,49
While an association may exist, the absolute incidence is unknown, and causality

is difficult to establish. It is unclear whether patients with dissection-related

local symptoms seek cervical manipulative therapy before they develop a stroke,
or if trauma from cervical manipulative therapy leads to cervical artery
dissection. Therefore, the American Heart Association/American Stroke
Association (AHA/ASA) recommends professionals who perform cervical
manipulative therapy, such as chiropractors, to consider the possibility of
cervical artery dissection and inform patients of the association between cervical
artery dissection and cervical manipulative therapy prior to manipulation of the

cervical spine.32
Several other predisposing factors have been associated with spontaneous
cervical artery dissection, including pregnancy and the postpartum period,28 oral
contraceptive use,31 migraine,30 recent infection,17 and atherosclerotic vascular
risk factors. The association between recent infection and cervical artery
dissection is supported by several studies.17,50,51 In a case-control study of
43 patients with cervical artery dissection and 58 young adults with non–cervical
TABLE 8-1 Common Triggers and Risk Factors for Cervical Artery Dissection
Minor trauma and other mechanical events

◆ Cervical manipulative therapy (also referred to as chiropractic manipulation)16
◆ Severe coughing or sneezing17
◆ Sports-related injuries,18 from activities such as
◇ Combat sports (eg, taekwondo, boxing, wrestling)
◇ Dancing
◇ Extreme sports (eg, bungee jumping, skydiving)
◇ Golf
◇ Gymnastics
◇ Horse riding
◇ Scuba diving
◇ Skating
◇ Swimming
◇ Tennis
◇ Trampoline use
◇ Volleyball
◇ Weightlifting
◇ Yoga
◆ Sudden neck movements (such as on roller coaster rides)19
◆ Whiplash injury20
Connective tissue or vascular diseases, including arteriopathies21
◆ α1-antitrypsin deficiency
◆ Aortic root dilation22
CONTINUED ON PAGE 545
544 APRIL 2023

artery dissection ischemic stroke, recent infection was associated with cervical
artery dissection–related ischemic stroke, although the mechanical factors
occurring in upper respiratory infections (ie, coughing, sneezing, vomiting) did
not seem to account for this association.17 Another case-control study of 47
patients with cervical artery dissection–related ischemic stroke showed that
nearly 32% of patients with spontaneous cervical artery dissection had an
infection within the preceding month, compared to 14% of the patients with
non–cervical artery dissection ischemic stroke.50 The association was stronger

among patients with multiple cervical artery dissections.50 Infections may
predispose individuals to cervical artery dissection via an indirect inflammatory
response or a prothrombotic mechanism. A seasonal pattern in cervical artery
dissection incidence has also been observed regardless of geographic location,
with cervical artery dissections occurring more often in autumn or winter.52 This
seasonal pattern may be due to increased occurrence of infection and
weather-related changes in blood pressure and physical activity.
CONTINUED FROM PAGE 544
◆ Autosomal dominant polycystic kidney disease

◆ Cerebral aneurysms23
◆ Cervical artery tortuosity24 and vessel redundancy
◆ Cystic medial necrosis of intracranial vessels
◆ Fibromuscular dysplasia
◆ Hereditary hemochromatosis
◆ Hyperhomocysteinemia
◆ Osteogenesis imperfecta type I
◆ Marfan syndrome
◆ Moyamoya disease
◆ Reticular fiber deficiency25
◆ Reversible cerebral vasoconstriction syndrome26
◆ Segmental mediolytic arteriopathy27
◆ Turner syndrome
◆ Vascular Ehlers-Danlos syndrome (Ehlers-Danlos syndrome type IV)
◆ Williams syndrome
Other risk factors
◆ Current use of oral contraceptives28
◆ Hypertension29
◆ Infection30
◆ Migraine31
◆ Pregnancy and postpartum period32
◆ Longer styloid process33

CASE 8-1 A 30-year-old previously healthy woman presented to the emergency

department with severe vertigo, nausea, and gait impairment causing her
to lean to the left side. Her last time known well was 12 hours prior to
presentation. Her symptoms occurred in the setting of 4 days of
left-sided neck pain that started after hyperextending her neck during a
yoga session. Her only medication was an estrogen-containing oral

contraceptive. Neurologic examination was notable for left-sided

dysmetria and gait instability with leaning to the left.
CT angiography (CTA) of the head and neck revealed a left vertebral
artery dissection in the V2 segment at the level of C3, with thrombus
filling the false lumen and causing severe stenosis of the true lumen
(FIGURES 8-2A and 8-2B). The vertebral artery regained normal caliber distal
to the dissection before fully occluding in the intracranial V4 segment
with nonopacification of the left posterior inferior cerebellar artery
(PICA). Brain MRI confirmed a large PICA-territory infarct (FIGURE 8-2C).

The patient was admitted to the neurologic intensive care unit and
closely monitored for malignant cerebellar edema. Her brain imaging
appeared stable for several days and suboccipital craniectomy was not
necessary. She was started on treatment dose anticoagulation with
apixaban 7 days after presentation. Repeat CTA 4 months after initial
presentation showed interval recanalization of the previously occluded
left PICA and intracranial vertebral artery, with no residual dissection flap
(FIGURE 8-2D). She underwent genetic testing with gene sequencing and
deletion/duplication studies that showed no known disease-causing
genetic mutations.
COMMENT This case illustrates the importance of identifying possible risk factors and
providing a tailored treatment approach. This woman was taking an
estrogen-containing oral contraceptive, which is a risk factor for cervical
artery dissection and ischemic stroke. Additionally, she most likely suffered
from minor neck trauma while hyperextending her neck during yoga. She
was advised to discontinue the estrogen-containing oral contraceptive and
avoid yoga and other sports that can cause neck trauma. This case also
highlights the importance of managing acute stroke from cervical artery
dissection with the same approach used in all patients with stroke. In this
case, the patient was monitored for malignant cerebellar edema and
started on treatment dose anticoagulation after the risk of hemorrhagic
conversion from the stroke was decreased. While direct oral
anticoagulants have not been used to treat cervical artery dissection in
randomized controlled trials, experts believe these oral agents can be
safely used in place of vitamin K antagonists.
546 APRIL 2023

FIGURE 8-2
Imaging of the patient in CASE 8-1. A, Left vertebral artery stenosis from dissection on axial CT
angiography (CTA) of the head and neck. Vessel measurements indicate that the artery is
narrowed to only 0.9 mm. B, Redemonstration on CTA of the left vertebral artery dissection
in the V2 segment at the level of C3, with severe luminal stenosis on sagittal imaging (arrow).
C, Diffusion restriction on axial diffusion-weighted brain MRI in the distribution of the left
posterior inferior cerebellar artery, distal to the left vertebral artery dissection, consistent
with an acute infarct. D, Repeat sagittal CTA performed 4 months after initial presentation
(and treatment with oral anticoagulation) showing interval resolution of the dissection with
no residual stenosis or dissection flap (arrow).

Several vascular risk factors have also been linked to cervical artery dissection.
Patients with cervical artery dissection are more likely to have hypertension,
lower body weight, and lower body mass index than matched healthy
controls.52-54 Other studies found no association or an inverse association
between hypercholesterolemia and cervical artery dissection.52,54
CLINICAL PRESENTATION
Common local signs and symptoms of cervical artery dissection include

new-onset head pain, neck pain, or both, cranial and cervical neuropathies,
Horner syndrome, and pulsatile tinnitus. Cervical artery dissection can cause
ischemic stroke, transient ischemic attack, and rarely subarachnoid hemorrhage.
Local Symptoms and Signs

Headache and neck pain are the most common local symptoms and are seen in
roughly 57% to 69% of cervical artery dissection cases.55-57 Patients with ICA
dissection are more likely to present with headache, whereas patients with
vertebral artery dissections are more likely to have cervical neck pain.56 Headaches
are typically on the ipsilateral side of the dissection, and are anterior in ICA
dissections and occipital in vertebral artery dissections.57 The characteristics of
cervical artery dissection–related headache are not specific and can mimic
migraine symptoms. A large series of patients with cervical artery dissection
showed variable headache presentations ranging from steady and pulsating to
thunderclap in nature.57 Isolated orbital pain is a rare presentation of
ICA dissections.58
ICA dissections can also cause Horner syndrome and cranial neuropathies.
Horner syndrome is seen in 25% to 39% of cases,3,59 and results from distention of
the third-order sympathetic fibers that span the external surface of an enlarged
and dissected ICA. The Horner syndrome seen in ICA dissections is partial and
consists of ptosis and miosis without anhidrosis. Cranial nerve palsies may result
from compression of the nerves adjacent to the ICA and along its cervical
trajectory.6 The hypoglossal nerve is most commonly involved, followed by the
glossopharyngeal and vagus nerves. In rare cases, vertebral artery dissection can
cause cervical nerve root injury.60 Pulsatile tinnitus can result from turbulent
blood flow at the site of dissection and is seen in roughly 8% of cervical artery
dissection cases.61
Ischemic and Hemorrhagic Events

Ischemic stroke and transient ischemic attack are the most feared complications
of cervical artery dissection. Nearly 67% of patients with cervical artery
dissection develop symptoms of cerebral ischemia, the majority being ischemic
stroke.3 Ischemic strokes from cervical artery dissection are usually due to artery-
to-artery embolism of intraluminal thrombus formed at the site of intraluminal
stenosis. Less commonly, ischemia may occur from hypoperfusion distal to a
high-grade intraluminal stenosis or occlusion.62
Ischemic events typically accompany local signs and symptoms. Stroke
symptoms from cervical artery dissection depend on the involved vascular
territory. Carotid artery dissections can result in anterior circulation syndromes
or retinal ischemia, and vertebral artery dissection may lead to posterior
circulation strokes including brainstem or cerebellar infarcts. Rarely, vertebral
artery dissections can cause spinal cord infarcts.
548 APRIL 2023

Subarachnoid hemorrhage is a less common complication seen in 1% of KEY POINTS
cervical artery dissection cases.6 Subarachnoid hemorrhage results from
● Pregnancy and the
intracranial extension of the dissection, or from an intracranial artery dissection. postpartum period, oral
Intracranial arteries lack external elastic lamina and have a thinner media and contraceptive use, migraine,
adventitia compared with extracranial arteries. These differences allow recent infection, and
intracranial dissections to be more prone to aneurysm formation and vascular risk factors have all
been associated with

subsequent rupture.63
cervical artery dissection.
Time from Local Symptom Onset to Neurologic Event ● Common local signs and
Ischemic stroke or transient ischemic attack can be the presenting symptom in symptoms of cervical artery
cervical artery dissection; however, patients may develop local symptoms dissection include
new-onset headache, neck
without associated ischemic events. The overall incidence of local symptoms pain, cranial and cervical
without ischemia may be underestimated due to delays or failures in neuropathies, Horner
presentation. Additionally, some nonspecific cervical artery dissection syndrome, and pulsatile
symptoms, such as headache and neck pain, may lead to misdiagnosis. A tinnitus.
retrospective cohort study of 7090 patients diagnosed with cervical artery ● Ischemic strokes from
dissection found that 1 in 30 patients had a probable emergency department cervical artery dissection
misdiagnosis in the 2 weeks before their eventual cervical artery dissection are usually due to artery-to-
diagnosis.64 Around 6% of cervical artery dissection cases are completely artery embolism of
intraluminal thrombus
asymptomatic and discovered only on routine examination.3
formed at the site of
Local symptoms typically precede the ischemic event; this delay can range intraluminal stenosis. Less
from minutes to weeks. The majority of ischemic events occur within the first commonly, ischemia may
week after local symptom onset.65 A large, retrospective study of nearly 2800 result from hypoperfusion
distal to a high-grade
patients with cervical artery dissection without ischemia found an increased risk
intraluminal stenosis or
of stroke only in the first 2 weeks after diagnosis.66 ICA dissections are less likely occlusion.
to present with ischemia compared to vertebral artery dissections.56 This may be
due to the proximity of cranial nerves and sympathetic fibers to the ICA, causing ● Subarachnoid
carotid artery dissections to manifest with more local signs and symptoms from hemorrhage may result from
intracranial extension of a
compression of these adjacent structures. dissection. Intracranial
arteries lack external elastic
EVALUATION AND DIAGNOSIS lamina and have a thinner
The diagnosis of cervical artery dissection should be suspected in patients with media, making them more
prone to aneurysm
acute onset of local symptoms of headache or neck pain and Horner syndrome, formation and subsequent
particularly if these are associated with an ipsilateral ischemic stroke. A history of rupture.
recent mechanical events, including minor trauma or sports-related injuries, or a
personal or family history of connective tissue or vascular diseases should also ● The majority of ischemic
events from cervical artery
increase suspicion for cervical artery dissection. Cervical artery dissection in
dissection occur within the
older adults (≥60 years) is more likely to be painless with few mechanical first 1 to 2 weeks after
triggers; in such cases, imaging should be carefully reviewed for any signs symptom onset.
of dissection.67
Neuroimaging should be used to confirm a clinical diagnosis of cervical artery ● The diagnosis of cervical
artery dissection should be
dissection. Characteristic neuroimaging findings include the presence of a suspected in patients with
long-tapered arterial stenosis or occlusion, dissecting aneurysm, intimal flap, acute onset of local
double lumen, or intramural hematoma. Tapered stenosis is the most common symptoms of headache,
neuroimaging finding (48%), followed by tapered occlusion (35%) and neck pain, Horner
syndrome, or any
dissecting aneurysm (17%).3 The presence of a long-tapered stenosis is combination of the three,
suggestive of cervical artery dissection when located at common sites of particularly if they are
dissection (more than 2 cm after the carotid bifurcation, and the V2 and V3 associated with an
segments of the vertebral artery), and in the absence of signs of large ipsilateral ischemic stroke.
artery atherosclerosis.

The most commonly used imaging modalities include head CT and CT

angiography (CTA), or MRI of the brain and magnetic resonance angiography
(MRA) of the head and neck. Ultimately, the choice of imaging modality
depends on availability and physician preference.
MRI evaluation includes the standard axial T1-weighted, T2-weighted, and
fluid-attenuated inversion recovery (FLAIR) axial MRI imaging. MRA can be
performed using two-dimensional time of flight, three-dimensional time of

flight, or phase contrast techniques. The use of contrast for MRA can yield
higher-quality images. Characteristic MRI findings supporting cervical artery
dissection include a decrease or absence of signal flow void and a crescent sign
resulting from narrowing of the vessel by an intramural hematoma.68 This
pathognomonic crescent sign is formed by an eccentric rim of hyperintensity,
corresponding to intramural hematoma, surrounding a hypointense arterial
lumen on axial cross-sectional T1-weighted sequences (FIGURE 8-3).68 The age of
the dissection can be determined based on the methemoglobin content and signal
intensity on T1-weighted and T2-weighted MR imaging. The combination of

MRA with T1-weighted axial cervical MRI imaging with fat suppression
(sometimes referred to as T1-weighted fat sat) allows for better visualization of
intramural hematomas, in particular smaller ones.68 Intimal flaps separating the
true lumen from the false lumen may be seen on T2-weighted images. Brain MRI
performed alongside MRA can help diagnose acute ischemic strokes resulting
from a dissection. Typically, the pattern of infarct is embolic, although
borderzone infarcts may also be seen in cases of hypoperfusion.62
CTA evaluation with axial source images and three-dimensional
reconstructions can detect arterial dissections, intimal tears, intramural
hematomas, and dissecting
aneurysms.68 Common CTA findings
include an irregular and asymmetric
vessel, narrowed lumen, and a
crescentic hyperdensity (intramural
hematoma) with thickened vessel
wall.68 The sensitivity (100%),
specificity (98%), positive predictive
value (95%), and negative predictive
value (100%) of CTA for the detection
of vertebral artery dissection compares
favorably with digital subtraction
angiography,69,70 although it may be
lower for ICA dissections.71 CTA is
superior to MRA in identifying
pseudoaneurysms, intimal flaps, and
high-grade stenosis.71 Vertebral artery
dissections may also be better visualized FIGURE 8-3
71 Axial T1-weighted cervical MR
on CTA than MRA. While CTA is a angiography (MRA) with fat suppression
quick and efficient tool to diagnose showing a right vertebral artery
cervical artery dissection, image dissection. MRA demonstrates intrinsic
interpretation may be limited due to T1 hyperintensity involving the right
vertebral artery with some adjacent
inaccurate contrast bolus timing or crescent-shaped T1 hyperintensity
streak artifacts from implants or within the vessel wall caused by an
beam-hardening artifacts. Additionally, intramural hematoma (arrow).
550 APRIL 2023

CTA involves exposure to radiation and iodinated contrast, which may be an issue KEY POINTS
in pregnant patients or those with contrast allergy or renal dysfunction.
● The most commonly used
Carotid ultrasound and transcranial Doppler are inexpensive and readily imaging modalities include
available tests that may be used to diagnose cervical artery dissection. Cervical CT and CT angiography
artery dissection often demonstrates a “double lumen” on B-mode ultrasound (CTA), or MRI and magnetic
imaging, consisting of the true and false lumina; however, ultrasound has several resonance angiography
(MRA) of the head and neck.

limitations, including its highly operator-dependent nature, low diagnostic
utility for detecting dissections near the skull base or within transverse foramina, ● MRI in cervical artery
and poor ability to detect carotid dissections with isolated Horner syndrome.9,72 dissection may show a
Confirmation with MRA or CTA should be done in patients with normal pathognomonic crescent
ultrasound findings but high clinical suspicion for cervical artery dissection. sign. The crescent sign is
formed by an eccentric rim
Occasionally, noninvasive neuroimaging can be negative in suspected cases of of hyperintensity,
cervical artery dissection. When using MRA, dissection involving the horizontal corresponding to intramural
course of the V3 segment of the vertebral artery may be missed due to the hematoma, surrounding a
orientation of the vessel causing difficulty in visualizing the classic crescent sign on hypointense arterial lumen
on axial cross-sectional T1-

axial images.73 Neuroimaging may also be negative if it is performed long after weighted sequences. The
symptom onset, as early recanalization can occur (16% at 1 month and 50% combination of MRA with
at 3 months).74 T1-weighted axial cervical
Digital subtraction angiography continues to be the gold standard for MRI imaging with fat
suppression allows for
identifying cervical artery dissection; however, given the accuracy (high better visualization of
sensitivity and specificity) and ability to detect intramural hematoma on intramural hematomas.
noninvasive neuroimaging, digital subtraction angiography is rarely used in the
diagnosis of cervical artery dissection, unless the clinical suspicion for a ● CTA is an efficient tool
with high sensitivity and
dissection continues to remain high despite negative noninvasive imaging.
specificity for diagnosing
Classic cervical artery dissection findings include the presence of focal stenosis cervical artery dissection.
(“string sign”), flame-shaped tapering with occlusion, pseudolumen and true However, image
lumen, intimal flap, and dissecting aneurysm.68 interpretation may be
limited due to inaccurate
contrast bolus timing or
TREATMENT streak artifacts from
Patients with cervical artery dissection who present with acute ischemic stroke or implants or beam-hardening
transient ischemic attack should be managed with the same guideline-based artifacts.
approach used in all acute stroke patients. All patients with acute ischemic stroke
● Diagnostic cerebral
should be evaluated for eligibility for IV thrombolysis, endovascular therapy, or angiography continues to be
both, as illustrated in CASE 8-2. the gold standard for
identifying cervical artery
Acute Stroke Treatment dissection. However, given
the high sensitivity and
IV thrombolysis, either with alteplase or tenecteplase, is indicated for eligible
specificity of noninvasive
patients with acute ischemic stroke, including those with extracranial cervical imaging methods, digital
artery dissection. The landmark trials of IV thrombolysis did not exclude patients subtraction angiography is
with cervical artery dissection, and subsequent observational studies have shown rarely needed, unless the
clinical suspicion for a
a similar effectiveness and safety profile compared to stroke from other causes75;
dissection continues to
however, data are limited on the safety of IV thrombolysis in patients with remain high despite negative
isolated intracranial dissections and those with intracranial extension of an noninvasive imaging.
extracranial dissection.76 In particular, concern exists for an increased risk of
subarachnoid and intracerebral hemorrhage after thrombolysis in patients with ● All patients with acute
ischemic stroke from
intracranial dissections. Further studies should examine the safety of acute cervical artery dissection
stroke treatments in such cases. Importantly, IV thrombolysis should be avoided should be evaluated to
in patients with aortic dissections. determine eligibility for IV
Endovascular therapy should be considered in select patients with cervical thrombolysis and
endovascular therapy.
artery dissection with acute ischemic stroke from a large vessel occlusion. This

includes cases of tandem occlusions (ie, extracranial carotid dissection with

proximal intracranial artery occlusion), although the optimal treatment method is
still being explored. A prospective, multicenter observational study compared the
safety and efficacy of stenting versus no stenting in 136 patients with tandem
occlusion from carotid dissection. Patients who underwent emergent carotid
artery stenting experienced higher rates of successful reperfusion (89% versus
68%) but similar rates of 90-day favorable outcome (54% versus 61%) as those
who did not undergo stenting.77 No differences in safety outcomes were seen
between the two groups. Therefore, emergent carotid artery stenting can be
considered in cases of persistent, high-grade stenosis from dissection after
intracranial reperfusion is achieved.
Antithrombotic Agents for Stroke Prevention

Strokes from cervical artery dissection are most commonly due to artery-to-
artery embolism from an intraluminal thrombus, as illustrated in CASE 8-3.
CASE 8-2 A 63-year-old man with history of hypertension and tobacco use
presented with left arm weakness that developed 35 minutes prior to
arrival at the emergency department. His examination was notable for
normal speech, left-sided homonymous hemianopia, left-sided visual
and sensory neglect, left face and arm weakness, and left-sided
hemisensory loss (a National Institutes of Health Stroke Scale score of 7).
Head CT was negative for hemorrhage and showed no signs of early
ischemic changes. Head and neck CT angiography showed complete
occlusion of the right internal carotid artery from the level of the
bifurcation to the proximal cavernous carotid with subsequent
reconstitution, and occlusion of the right midinferior M2 branch of the
middle cerebral artery, with decreased collateralization along the sylvian
fissure, right lateral temporal lobe, and right parietal lobe. He had no
known contraindications to IV alteplase and received thrombolysis within
1 hour of symptom onset. Endovascular therapy was pursued for acute
ischemic stroke, and angiography showed tapering of the internal carotid
artery with complete occlusion just distal to a dilated carotid bifurcation,
consistent with a dissection (FIGURE 8-4A). Complete recanalization of the
intracranial middle cerebral artery occlusion was achieved, after which
emergent carotid artery stenting was performed (FIGURES 8-4B and 8-4C).
The patient was started on aspirin and clopidogrel to prevent acute stent
thrombosis and further ischemic events. Subsequent MRI showed
extensive areas of restricted diffusion throughout the right cerebral
hemisphere (FIGURE 8-4D). Despite the significant radiographic stroke
burden, he had minimal remaining neurologic deficits, with only mild left
arm weakness and pronator drift at the time of discharge.
552 APRIL 2023

Antithrombotic therapy, either with anticoagulation or antiplatelet agents, is
often used to minimize the risk of embolism and prevent either a new or
recurrent stroke from cervical artery dissection.
Current data suggest that no significant difference exists between
anticoagulation and antiplatelet therapy for preventing either new or recurrent
ischemic strokes in patients with extracranial cervical artery dissection. Two
large, randomized trials compared anticoagulation to antiplatelets for cervical

artery dissection (TABLE 8-278,79).78,79

CADISS (Cervical Artery Dissection in Stroke Study) was the first randomized
controlled trial of cervical artery dissection treatment. CADISS was an open-
label, assessor-blind study of 250 patients with extracranial cervical artery
dissection between 2006 and 2013 who were randomly assigned to either
antiplatelet or anticoagulant therapy for 3 months.78 Treatment was initiated
within 7 days of symptom onset. Importantly, the specific antiplatelet or
anticoagulant drug used was left at the discretion of the treating physician; in the
FIGURE 8-4
Imaging of the patient in CASE 8-2. Panels A, B, and C are all coronal view cerebral digital
subtraction angiograms showing injection of the carotid artery. Tapering of the internal
carotid artery with complete occlusion just distal to a dilated carotid bifurcation (A, arrow),
consistent with carotid artery dissection. Post-thrombectomy angiogram demonstrating the
recanalization of the dissected internal carotid artery using a stent (B) and recanalization of
the occluded middle cerebral artery (C). Diffusion-weighted axial MRI (D) demonstrating
diffusion restriction in the right middle cerebral artery distribution indicating an acute infarct
from the dissection.
This case illustrates the importance of acute, timely intervention for an COMMENT
ischemic stroke from cervical artery dissection. The patient presented soon
after symptom onset and was able to receive IV thrombolysis within the
golden hour. Given the presence of a tandem occlusion (extracranial carotid
artery disease and intracranial occlusion), the decision was made to proceed
with endovascular therapy with intracranial revascularization followed by
emergent carotid artery stenting.

antiplatelet arm, 22% were on aspirin monotherapy, 33% on clopidogrel

monotherapy, 28% on aspirin and clopidogrel, and 16% on aspirin and
dipyridamole. In the anticoagulant arm, all patients received warfarin. At
3 months, no significant difference was found in ischemic stroke and death
between the two treatment groups. Ischemic stroke occurred in 3 out of 126
patients (2%) in the antiplatelet group and 1 out of 124 patients (1%) in the
anticoagulation group (odds ratio 0.34, 95% confidence interval, 0.01 to 4.23). No
deaths occurred in either group. The risk of recurrent stroke continued to be low
at 12 months follow-up; although twice as many strokes occurred in the
antiplatelet group versus the anticoagulant group (4 versus 2), no statistically
significant difference in outcomes was shown (odds ratio 0.56; 95% confidence
interval, 0.10 to 3.21).78 The majority of strokes occurred within the first
3 months. One major bleeding event occurred in the anticoagulation group,
in a patient who had intracranial extension of a VA dissection. No differences in
the 3-month angiographic recanalization rate were found between the two
CASE 8-3 A 43-year-old woman with no past medical history presented to the
emergency department with 5 days of left-sided neck pain and a
transient 15-minute episode of right face and arm numbness. She denied
any accompanying weakness, slurred or nonsensical speech, or gait
abnormalities. She recently suffered from an upper respiratory viral
illness that was accompanied by a significant cough. Neurologic
examination was notable for a left-sided ptosis and miosis.
Brain MRI showed no signs of acute infarct. Head and neck CT
angiography (CTA) showed 50% stenosis of the left internal carotid artery
at the level of the carotid bulb, thought to be from nonocclusive
thrombus with a possible underlying dissection (FIGURES 8-5A and 8-5B).
Magnetic resonance angiography (MRA) of the neck with and without
contrast, with T1-weighted fat saturation imaging protocol, revealed an
intraluminal clot along the posterior wall of the left proximal internal
carotid artery. The left internal carotid artery was also 50% stenotic and
displayed internal T1 hyperintensity on T1-weighted fat saturation imaging
reflecting intramural hematoma from an underlying dissection.
The presence of an intraluminal thrombus led to the decision to start
the patient on warfarin to prevent a recurrent ischemic event. Repeat
CTA of the neck performed 3 months after initial diagnosis showed near
complete resolution of the intraluminal thrombus, and full resolution of
dissection and stenosis. Given the resolution of the intraluminal
thrombus, she was switched from warfarin to lifelong aspirin for
secondary stroke prevention.
554 APRIL 2023

groups. CADISS was a landmark trial that had several noteworthy limitations.
Because of the low stroke rate and rarity of outcome events, CADISS was unable
to determine which antithrombotic treatment was superior. The results
questioned the feasibility of a randomized controlled trial based only on clinical
endpoints, as a large sample size (>10,000 participants) would have been
required to detect a meaningful result. Additionally, 20% of CADISS participants
did not have a dissection confirmed by central adjudication, either due to an

alternative cause being identified or because of low image quality; however, the
results remained unchanged in a per-protocol analysis that excluded
these participants.78
The TREAT-CAD (Biomarkers and Antithrombotic Treatment in Cervical
Artery Dissection) trial was an open-label, assessor-blind, noninferiority trial
of 194 adult patients with symptomatic cervical artery dissection within
2 weeks of enrollment who were randomly assigned to aspirin monotherapy
(300 mg daily) or anticoagulation (vitamin K antagonist with an international
FIGURE 8-5
Imaging of the patient in CASE 8-3. CT angiography
of the head and neck (A, axial; B, coronal) showing
50% stenosis of the left internal carotid artery at
the level of the carotid bulb, thought to be due to
nonocclusive thrombus from underlying
dissection (arrows). No signs of atherosclerosis
are seen in intracranial or extracranial arteries.
This case illustrates the typical time course from clinical symptom onset to COMMENT
ischemic event (in this case, a transient ischemic attack). The majority of
patients with cervical artery dissection without ischemia have an increased
risk of stroke in the first 2 weeks after symptom onset. In this patient, the
dissection caused carotid artery stenosis with an intraluminal thrombus,
and the transient ischemic attack was most likely a result of artery-to-
artery embolism from the thrombus. While equipoise exists for the best
antithrombotic therapy after cervical artery dissection, the presence of an
intraluminal thrombus put her at high risk for another ischemic event and
led to the preference for anticoagulation over antiplatelet therapy.

TABLE 8-2 Randomized Controlled Trials of Stroke Prevention in Cervical Artery

Dissection
Study design Baseline

Study name Aim and population characteristics

CADISS (Cervical Artery Compare antiplatelet and Multicenter, open-label, N = 250; 118 (47%) carotid, 132
Dissection in Stroke anticoagulant treatment for randomized controlled trial; (53%) vertebral; mean time to
Study)78 stroke prevention in extracranial cervical artery randomization, 3.7 days; 224
cervical artery dissection dissection within the prior (90%) patients presented with
7 days; randomized to stroke or transient ischemic
antiplatelet or anticoagulant, attack and 26 (10%) with only
with specific treatment local symptoms
decided by the local clinician
TREAT-CAD (Biomarkers Test the noninferiority of Multicenter, open-label, N = 194; 130 (67%) carotid, 67
and Antithrombotic aspirin to vitamin K randomized noninferiority trial; (35%) vertebral, 14 (7%)
Treatment in Cervical antagonist treatment in symptomatic, MRI-verified multivessel dissection; mean
Artery Dissection) trial79 patients with cervical artery extracranial cervical artery time to randomization,
dissection dissection within the prior 2.9 days; 138 (71%) presented
14 days, randomized to aspirin with stroke or transient
300 mg daily or vitamin K ischemic attack and 56 (29%)
antagonists; noninferiority with only local symptoms
margin: 12%
CONTINUED ON PAGE 557
556 APRIL 2023

CONTINUED FROM PAGE 556
Primary outcome Follow-up Results Limitations

Ipsilateral stroke or death in intention- 3 months; Intention-to-treat analysis: 126 (50.4%) (1) Time to enrollment, may
to-treat population at 90 days 1 year in antiplatelet group and 124 (49.6%) in have missed outcomes early
anticoagulant group in disease course;
Primary outcome at 3 months: 3 (2.4%) (2) central imaging review
in antiplatelet group and 1 (0.8%) in failed to confirm dissection
anticoagulant group (odds ratio, in 20% of patients;
0.335; 95% confidence interval, 0.006
(3) heterogeneity of
to 4.233). All events were strokes, no
antiplatelet treatment;
deaths. No significant differences in
treatment groups (4) use of clinical endpoints
resulted in few recurrences;

Primary outcome at 1 year in intention-
study underpowered
to-treat analysis: 4 (3.2%) in
antiplatelet group and 2 (1.6%) in
anticoagulant group (odds ratio, 0.56;
95% confidence interval, 0.10-3.21)
Primary outcome at 1 year in per-
protocol analysisa: 4 (4.0%) in
antiplatelet group and 1 (1.0%) in
anticoagulant group (odds ratio, 0.32;
95% confidence interval, 0.03-3.04)
Composite of clinical (stroke, major 3 months Per-protocol analysis: 173 patients, 91 (1) Time to enrollment, may
hemorrhage, or death) or MRI outcomes (53%) in aspirin group and 82 (47%) in have missed outcomes early
(new ischemic or hemorrhagic brain vitamin K antagonist group in disease course;
lesions) in per protocol population at
Primary outcome: 21 (23%) in aspirin (2) not powered to establish
14 days (clinical and MRI outcomes) and
group and 12 (15%) in vitamin K superiority of either
90 days (clinical outcomes only) after
antagonists group (absolute treatment
treatment
difference 8% [95% confidence
interval, -4 to 21]). Noninferiority of
aspirin was not shown
Ischemic stroke: 7 (8%) in aspirin group
and 0 (0%) in vitamin K antagonists
group
Major extracranial hemorrhage: 0 (0%)
in aspirin group and 1 (1%) in vitamin K
antagonists group
No intracranial hemorrhage or deaths
in either group
MRI = magnetic resonance imaging

a
Per-protocol analysis was performed in patients meeting the inclusion criteria following central review of imaging to confirm the diagnosis of
dissection (n = 197).

normalized ratio [INR] goal of 2.0 to 3.0) for 90 days.79 Based on the low rate
of clinical events limiting the findings of the CADISS trial, the investigators
aimed to improve the feasibility of TREAT-CAD by including both clinical and
MRI outcomes, thereby reducing their sample size. The primary outcome
was a composite of clinical (ie, stroke, major hemorrhage, or death) and
MRI (ie, new ischemic or hemorrhagic brain lesions) outcomes in the per-
protocol analysis of 173 patients who completed the assessment period, with a
noninferiority margin of 12%. The composite endpoint occurred more often in the
aspirin group compared with the vitamin K antagonist group (23% versus 15%,
absolute difference 8%; 95% confidence interval, -4% to 21%). No symptomatic
intracranial hemorrhages occurred in either group, and one major extracranial
hemorrhage (a gastrointestinal bleed) occurred in a patient in the vitamin K
antagonist group. Based on the findings, aspirin failed to meet noninferiority
criteria. These findings do not indicate that aspirin is worse than vitamin K
antagonists, or that vitamin K antagonists are superior to aspirin, either; however,
all the ischemic strokes occurred in the aspirin group (n = 7), and five of the
seven strokes occurred on day 1 after treatment onset (the remaining two occurred
on day 7). The early recurrence rate further suggests that the heightened risk of
stroke is within the immediate period and supports the early initiation of
antithrombotic treatment.
Given the inconclusive evidence, the most recent 2021 AHA/ASA
guidelines on secondary stroke prevention recommend either warfarin or
aspirin in patients with recent ischemic stroke or transient ischemic attack
(TIA) from extracranial cervical artery dissection.80 Factors such as severe
stenosis, occlusion, accompanying aneurysm, the presence of intraluminal
thrombus, and infarct size may all impact a clinician’s decision on whether to
use an antiplatelet or anticoagulant agent. Antithrombotic agents should be
delayed for 24 hours after IV thrombolytic therapy. In patients considered for
antiplatelet therapy (rather than anticoagulation), aspirin monotherapy can
be considered in those with low-risk TIA or moderate to large ischemic
strokes. No consensus exists on the best dose of aspirin (TREAT-CAD used
aspirin 300 mg daily, while local physicians decided the type and dose of
antiplatelet in CADISS); treatment with aspirin 81 mg to 325 mg daily is
reasonable. A 21-day course of dual antiplatelet therapy with aspirin and
clopidogrel can be considered in patients meeting CHANCE (Clopidogrel in
High-risk Patients With Acute Non-disabling Cerebrovascular Events) or
POINT (Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke)
trial criteria (either high-risk TIA with ABCD2 [age, blood pressure, clinical
features, duration of TIA, presence of diabetes] score ≥4 or minor ischemic
stroke with a National Institutes of Health Stroke Scale [NIHSS] score ≤5, and
within 12 [POINT] or 24 hours [CHANCE] of symptom onset) before
switching to aspirin monotherapy.81 In patients considered for anticoagulant
therapy, the size of the infarct may play a role in determining the optimal time
for anticoagulation initiation. While direct oral anticoagulants were not used
in CADISS or TREAT-CAD, observational data suggests that they are safe and
effective, and experts believe direct oral anticoagulants can be used in place
of warfarin.82
No randomized controlled trials have addressed the management of
intracranial artery dissections. Antiplatelet therapy may be preferred over
anticoagulation given the increased risk of subarachnoid hemorrhage with
558 APRIL 2023

intracranial dissections; however, a single-center study of 81 patients suggested KEY POINTS
the safety and efficacy of oral anticoagulants in patients with nonaneurysmal
● Endovascular therapy
intracranial artery dissections who presented without subarachnoid should be considered in
hemorrhage.83 Further studies are needed to determine the best antithrombotic select patients with cervical
agent for such cases. artery dissection with acute
Endovascular intervention is occasionally considered in cases of extracranial ischemic stroke from a large
vessel occlusion. This

cervical artery dissection that result in recurrent thromboembolism, enlarging
includes patients with

pseudoaneurysm, and flow-limiting dissections; however, the safety and efficacy tandem occlusions,
data are mostly from small studies, and randomized trials to support the benefit although the optimal
of endovascular interventions are lacking.84 Current AHA/ASA guidelines treatment method is still
being explored.
suggest consideration of endovascular procedures in patients with extracranial
cervical artery dissection who have recurrent ischemic events despite ● The most recent
antithrombotic therapy.80 American Heart Association
The optimal duration of antithrombotic therapy is unclear. AHA recommends (AHA) guidelines
at least 3 months of antithrombotic therapy in patients with recent ischemic stroke recommend either warfarin
or aspirin in patients with

or transient ischemic attack from cervical artery dissection.80 Anticoagulants are recent ischemic stroke or
typically discontinued after the first 6 months of treatment, and patients are transient ischemic attack
usually switched to antiplatelet therapy; only 38% of patients in the anticoagulant from extracranial cervical
arm of CADISS were still on warfarin at 6 months, and the number dropped to 13% artery dissection.
at 12 months.78 Patients on antiplatelet therapy in the acute phase are generally
● The AHA recommends at
continued on long-term antiplatelet therapy, although discontinuation can be least 3 months of
considered in patients with full recanalization of the dissected vessel81; however, antithrombotic therapy in
further studies are needed to determine optimal duration of antithrombotic patients with recent stroke
or transient ischemic attack
therapy and whether follow-up imaging may be helpful to guide treatment
from cervical artery
duration. Improving the understanding of the pathophysiology of cervical artery dissection, but the optimal
dissection may help better tailor long-term secondary stroke prevention duration of treatment is
recommendations, such as the need for long-term antithrombotic agents. unclear.
● Most cases of vessel

OUTCOME recanalization after cervical
Most cases of vessel recanalization occur within the first few months after artery dissection occur
the initial event. The rate of recurrent stroke is highest within the acute period. within the first few months
This section covers the time to vessel recanalization, risk of recurrent stroke and after the initial event (16% at
1 month, 50% at 3 months,
dissection, and overall prognosis after cervical artery dissection. and 60% at 6 and 12 months).
Initial occlusion reduces the
Resolution of Arterial Abnormalities likelihood of complete
Vessel healing can result in complete recanalization or stable residual luminal recanalization, whereas the
presence of only local signs
irregularity. Occlusions may lead to residual stenosis over time, while stenotic and
and symptoms increases the
irregular arteries can undergo more thorough recanalization and healing.85 A odds of complete
prospective study of nearly 250 patients with spontaneous carotid artery dissection recanalization.
showed a rate of complete recanalization of 16% at 1 month, 50% at 3 months, and
60% at 6 and 12 months.74 Initial occlusion reduces the likelihood of complete ● Repeat neurovascular
imaging is typically done 3 to
recanalization, whereas the presence of only local signs and symptoms increases 6 months after symptom
the odds of complete recanalization.74 Vertebral artery dissections have similar onset or diagnosis with the
rates of early recanalization.86 Another population-based study showed that goal of assessing
82% of instances of vessel healing occurred within the first year.3 Dissecting recanalization status of
affected arteries and
aneurysms can develop at various time points; some aneurysms resolve within guiding ongoing
3 months of the initial event, while others are noted for the first time on follow- antithrombotic treatment in
up imaging.87 cervical artery dissection.
Repeat neurovascular imaging is typically done 3 to 6 months after symptom
onset or diagnosis with the goal of assessing the recanalization status of affected

arteries and guiding ongoing antithrombotic treatment. This is typically done

with noninvasive imaging modalities such as MRA and CTA.
Recurrent Stroke and Dissection

The rate of recurrent ischemic events after cervical artery dissection ranges from
0% to 13% at 1 year in published studies.9 The recurrence rate is probably on the
lower end of this spectrum when accounting for events that occurred only after
cervical artery dissection diagnosis was confirmed and appropriate treatment

was started. The rate of recurrent ischemic stroke after cervical artery dissection
is low at around 2% to 4% at 3 months and 2.5% at 12 months in the two large,
randomized trials (CADISS and TREAT-CAD).78,79 The greatest risk of recurrent
ischemic stroke was within the first 2 weeks of randomization, suggesting that
the risk of recurrent events beyond the acute period is low. Dissecting aneurysms
do not appear to be associated with an increased risk of recurrent stroke.87
The rate of cervical artery dissection recurrence is inconsistent among studies.
The CADISP (Cervical Artery Dissection and Ischemic Stroke Patients) registry
showed a recurrence rate of 2% at 3 months.56 Another single-center study found
a 16% rate of recurrence at 1 year, with the majority of events (22 out of 39)
occurring within a month of the initial dissection.88 Risk factors that may be
associated with recurrent cervical artery dissection include younger age at initial
diagnosis, family history of cervical artery dissection, vascular Ehlers-Danlos
syndrome, and fibromuscular dysplasia.9 Limited data exist regarding methods
that may prevent cervical artery dissection recurrence; however, most clinicians
discuss avoiding contact sports, cervical manipulative therapy, and mechanical
events that may lead to minor trauma. Continued surveillance for recurrent
dissections may be reasonable in patients with an underlying connective tissue
disorder or fibromuscular dysplasia, as these patients may be at an increased risk
of recurrent arteriopathies.
Long-term Functional Outcome

Functional outcome and mortality after cervical artery dissection are largely
dependent on the severity of the associated ischemic stroke or subarachnoid
hemorrhage. Overall, outcome appears to be favorable (modified Rankin Scale
score of 0 or 1) in 75% to 82% of patients with cervical artery dissection, with
mortality rates of less than 5%9,13; however, nearly two out of five patients with
cervical artery dissection report impaired quality of life at 6 months despite good
functional outcome, with posttraumatic stress syndrome playing a large role in
their quality of life.89-91 A low NIHSS score at onset of symptoms and younger age
are predictors of favorable outcome,13 whereas ICA dissection and artery
occlusion predict less favorable outcome.56,91 The vast majority of patients
experience resolution of headache and pain within the first few days, although a
small subset of patients may develop prolonged residual headaches.57
CONCLUSION
Cervical artery dissection is an important cause of ischemic stroke, particularly in
young adults. Early recognition and management of cervical artery dissection
may lead to earlier initiation of antithrombotic agents, thereby reducing the risk
of ischemic events. Although the pathophysiology is incompletely understood,
cervical artery dissection is thought to be a multifactorial disease, with
560 APRIL 2023

environmental factors serving as potential triggers in patients who have genetic KEY POINTS
predispositions to dissections. Patients can develop local symptoms and signs
● The rate of recurrent
prior to or accompanying an ischemic event; sudden-onset Horner syndrome ischemic stroke after
with headache or neck pain or with an ipsilateral ischemic stroke is highly cervical artery dissection is
suggestive of cervical artery dissection and warrants further vessel imaging. low at around 2% to 4% at
Neuroimaging studies are necessary to confirm a clinical suspicion of cervical 3 months and 2.5% at
12 months. The greatest risk

artery dissection, with MRA or CTA being the most commonly performed
of recurrent ischemic stroke

noninvasive imaging modalities. Typical imaging findings include a long-tapered is within the first 2 weeks of
arterial stenosis, a tapered occlusion (“flame-shaped” occlusion), dissecting diagnosis. Dissecting
aneurysm, intimal flap, double lumen, or intramural hematoma. Equipoise exists aneurysms do not appear to
be associated with an
for the best antithrombotic agent for primary or secondary stroke prevention
increased risk of recurrent
from cervical artery dissection, with AHA/ASA guidelines recommending either stroke.
aspirin or warfarin for secondary stroke prevention. The highest risk of recurrent
ischemic events appears to be within the first 2 weeks after diagnosis, further ● The rate of cervical artery
supporting the importance of early recognition and treatment. The risk of dissection recurrence is
uncertain, ranging from 2%

recurrent dissections is low. Future studies should aim to improve our to 9.2% within the first 1 to
understanding of the influence of environmental and genetic factors on 3 months. The highest risk of
predisposing patients to cervical artery dissection and the long-term outcomes of cervical artery dissection
this disease. Ultimately, improving the understanding of the pathophysiology of recurrence is within the first
month of the initial
cervical artery dissection would help better tailor long-term secondary stroke dissection.
prevention recommendations (eg, the need for long-term antithrombotic
therapy) for patients with cervical artery dissection.
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LATEST DEVELOPMENTS: Cervical artery dissection is believed to be a

Cervical artery dissection is a known cause of ischemic

RELATIONSHIP DISCLOSURE: INTRODUCTION

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● Dissections result from

the separation of the arterial

ANATOMY OF CERVICAL ARTERY DISSECTION

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ETIOLOGY AND PREDISPOSING FACTORS

542 APRIL 2023

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Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

is difficult to establish. It is unclear whether patients with dissection-related

artery dissection and cervical manipulative therapy prior to manipulation of the

Minor trauma and other mechanical events

CONTINUED ON PAGE 545

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non–cervical artery dissection ischemic stroke.50 The association was stronger

CONTINUED FROM PAGE 544

◆ Autosomal dominant polycystic kidney disease

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CASE 8-1 A 30-year-old previously healthy woman presented to the emergency

yoga session. Her only medication was an estrogen-containing oral

contraceptive. Neurologic examination was notable for left-sided

(PICA). Brain MRI confirmed a large PICA-territory infarct (FIGURE 8-2C).

546 APRIL 2023

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Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Common local signs and symptoms of cervical artery dissection include

Local Symptoms and Signs

Ischemic and Hemorrhagic Events

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been associated with