Transcript SPONTANEOUS DISSECTION OF THE CAROTID AND …

SPONTANEOUS DISSECTION
OF THE CAROTID AND
VERTEBRAL ARTERIES
N Engl J Med, Vol. 344, No. 12. March 22, 2001
950518
張維傑
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Mr. Jou, 42 yrs Male, sudden onset of blindness
and recovery 2 years ago. Headache and
tinnitus for one month
Introduction
Till the late 1970s, when Fisher et al. and
Mokri et al. described dissections of
carotid and vertebral arteries
 Blood entered the wall of the artery and
split its layers, either stenosis or
aneurysmal dilatation
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EPIDEMIOLOGIC FEATURES
2.5-3 /100000, 2 % of all ischemic stroke,
10-15% young and middle-aged ischemic
stroke patients
 all age groups, including children, but
there is a distinct peak in the fifth decade
of life
 Female average about five years younger
than men at the time of the dissection.
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PATHOLOGICAL FEATURES
Extracranial segments, the greater mobility,
contact with bony structures
 arise from an intimal tear >> intramural
hematoma:
subintimal dissection >stenosis;
subadventitial dissection >aneurysmal
formation
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PATHOGENESIS
Genetic Factors
1. Connective-tissue disorder: (1-5%)
Ehlers–Danlos syndrome type IV. Marfan’s
syndrome, autosomal dominant polycystic
kidney disease, and osteogenesis
imperfecta type I.
2. The arterial media of the aorta
melanocytes, and the aortic valvular cusps
derived from neural-crest cells,
3. Fibromuscular dysplasia(15%)
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Environmental Factors
1. Hyperextension or rotation of the neck:
yoga, painting a ceiling, coughing,
vomiting, sneezing, the act of resuscitation
2. Chiropractic manipulation of the neck: 1 in
20,000 spinal manipulations
3. Respiratory tract infection: with a peak
incidence in the fall.
4. Vascular disease: tobacco use,
hypertension,
5. migraine as a risk factor for dissection.
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CLINICAL MANIFESTATIONS
Dissection of the Internal Carotid Artery
1. Pain on one side of the ipsilateral headache
(frontotemporal, “thunderclap”), face, or neck
accompanied by a partial Horner’s syndrome
2. Oculosympathetic palsy: miosis, ptosis, (No facial
anhidrosis: ECA sympathetic plexus)
3. Cranial-nerve palsies(12%):the most commonly
the hypoglossal nerve, Impairment of taste, ¼
Pulsatile tinnitus
4. Cerebral or retinal ischemic symptoms (50-90%),
Permanent blindness as a result of ischemic optic
neuropathy or occlusion of the retinal artery: rare
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Vertebral-Artery Dissection
Pain in the back of the neck (1/2),
occipital area headache(2/3)
Ischemic symptoms(90%), brain stem,
particularly the lateral medulla
(Wallenberg’s syndrome),
Transient ischemic attacks are less
frequent after vertebral-artery dissections
than after carotid-artery dissections.
DIAGNOSTIC TESTS
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Conventional angiography: gold standard
Starts about 2 to 3 cm distal to the carotid bulb,
not past its entry into the petrous portion
Flame-like appearance in acute phase
Aneurysmal type: most commonly in distal
subcranial segment
Both stenotic and aneurysmal lesions of
vertebral arteries are most common in distal
segment of the artery at the level of the first and
second cervical vertebrae
The vertebral artery enters the skull through
the foramen magnum: 10 % vertebral-artery
dissections extend intracranially.
 Magnetic resonance techniques are
replacing the gold standard
 Ultrasonographic techniques are useful in
the initial: an abnormal pattern of flow is
identified in more than 90 percent
 Helical computed tomographic angiography
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PROGNOSIS
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The rate of death from dissections of the carotid and
vertebral arteries <5%, ¾ recovery well
The radiographic appearance may worsen during the
acute phase of dissection, about 90 percent of stenoses
eventually resolve, two thirds of occlusions are
recanalized, and one third of aneurysms decrease in
size within the first two to three months, thromboembolic
complications years after the dissection but they never
rupture.
2% recurrent dissection in initially unaffected vessels in
first month, then decreased rate 1% per year
TREATMENT
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To prevent thromboembolic complications: intravenous
heparin >> oral warfarin recommended for all patients
Because 90 percent of infarcts due to are
thromboembolic rather than hemodynamic (i.e., caused
by insufficient flow)
Anticoagulation with a target PTINR: 2.0 to 3.0 for 3-6
months, MRA in 3 months, if luminal irregularities
medication for another 3 months
Recanalization within the first three months after the
dissection symptoms occasionally recur within three to
six months after the onset of dissection rarely after six
months.
no symptoms of ischemia: antiplatelet therapy alone,
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Surgical or endovascular treatment should be
reserved for patients who have persistent
symptoms of ischemia despite adequate
anticoagulation.
Ligation of the carotid or vertebral artery,
combined with an in extracranial-to-intracranial
bypass.
Balloon angioplasty placement of one or more
metallic stents,
The long-term results of carotid stenting are
unknown