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Spontaneous Internal Carotid Artery Dissection

Spontaneous Internal Carotid Artery Dissection

A 36-year-old man who had collapsed
and sustained a bruised right shoulder
was brought to the emergency department
with acute emesis, cephalgia,
blurred vision, aphasia, and right
hemiparesis. He was confused but able
to follow simple commands.

The patient was right-handed and
worked as a computer programmer.
He denied alcohol, tobacco, and illicit
drug use. The history included migraine,
asthma, and a single incident
of spontaneous pneumothorax about
10 years earlier. There was no personal
history of stroke; however, family members
had been treated for hypertension
and stroke.

Blood pressure was normal.
Pupils were equal (2.5 mm bilaterally)
and reactive to light. The patient preferred
the left gaze visual field. No
papilledema, exudates, or hemorrhage
was noted.

Right facial droop was apparent,
but there was no tongue deviation.
The patient complained of numbness in
his tongue, which he was unable to
protrude. No facial numbness or tingling
sensation was found.

A decreased carotid upstroke and
bruit in the left carotid artery near the
angle of the mandible were noted; a
good pulsating left carotid pulse was
detected 2 cm above the left clavicle.
Right-sided strength was 0/5 in both
upper and lower extremities with spasticity;
left-sided strength was 5/5
throughout. Sensory response to pinprick,
light touch, and temperature
was significantly decreased on the right
side. Withdrawal from painful stimuli
was less pronounced on the right
side than the left. Bilateral Babinski,
Oppenheimer, and Chaddock reflexes
were intact; clonus was absent.

An ECG showed sinus tachycardia
with normal sinus rhythm. The
creatine kinase level was 102 U/L;
creatine kinase MB isoenzyme,
1.8 ng/mL; creatine kinase MB isoenzyme
index, 2; troponin T, less
than 0.10 ng/mL; aspartate aminotransferase,
22 U/L; alanine aminotransferase,
16 U/L; and lactate
dehydrogenase, 181 U/L. Cholesterol
level was 98 mg/dL; triglycerides,
59 mg/dL; high-density lipoprotein
cholesterol, 34 mg/dL; low-density
lipoprotein cholesterol, 52 mg/dL;
very-low-density lipoprotein cholesterol,
12 mg/dL; total bilirubin,
0.5 mg/dL; thyrotropin, 1.15 μIU/mL;
blood urea nitrogen, 12 mg/dL; and
creatinine, 0.9 mg/dL. White blood
cell count was 11,300/μL; hemoglobin,
12.2 g/dL; hematocrit, 35.7%;
platelets, 190,000/μL; prothrombin
time, 11.4 seconds; international normalized
ratio (INR), 0.99; and partial
thromboplastin time (PTT),
26 seconds. Neither alcohol nor acetaminophen
was found in the serum.
The urine drug screen was negative
for cocaine and other drugs.

Figure 1
Figure 1

The initial CT scan of the brain
showed a linear hyperdensity in the
region of the left middle cerebral artery,
which indicated thrombus formation
(Figure 1). An area of cerebral edema
was noted in the region with a small
effacement from left to right. A cerebral
angiogram performed 6 hours after the
CT scan revealed a complete dissection
of the left internal carotid artery (ICA)
from the second cervical segment
craniad (Figure 2). A follow-up CT
brain scan 24 hours later demonstrated
a large, left middle cerebral artery
ischemic infarction with midline shifting
and evidence of left uncal herniation
(Figure 3).

Figure 2
Figure 2
Figure A
Figure A
Figure B
Figure B

Anticoagulants were initiated.
Although the patient was awake and
aware of the environment, aphasia and
right hemiparesis persisted. No evidence
of Horner syndrome (miosis, ptosis, and
enophthalmos) was noted. A 2-dimensional
echocardiogram demonstrated no
cardiac anomalies. Rehabilitation and
speech, physical, and occupational therapies were begun. The patient's vital signs
remained unchanged.

After 1 month of rehabilitation,
the patient's functional status returned
to baseline. He is now able to perform
activities of daily living without significant

Internal carotid artery dissection
(ICAD) can be traumatic or
spontaneous.1 Spontaneous ICAD is
the cause of cerebral infarction in
22% of otherwise healthy stroke patients
younger than 30.1-4 One study
found that about 40% of patients with
spontaneous ICAD have a history of

Carotid dissection is associated
with cystic medial necrosis; syphilitic
arteritis; α1-antitrypsin deficiency;
and several heritable collagen disor-
ders, including Marfan syndrome,
Ehlers-Danlos syndrome, and type III
collagen deficiency.3,4,6,7 No gender differences
have been reported.4,8 ICAD
and chronic and recurrent arterial dissection
are more likely to occur in patients
with fibromuscular dysplasia--
particularly women.3,4

Hyperextension of the neck may
precipitate a stretch injury to the ICA.
However, a possible clinical correlation
between carotid artery dissection
and cervical spine manipulation has
not been proved.4

Figure 3
Figure 3
Figure 3b
Figure 3b

The pathogenesis of spontaneous
ICAD is unknown. Dissecting
aneurysm causes an intramural hemorrhage
into the subintimal layer of
the artery. The fragility and distensibility
of the arterial wall is related to
an extracellular defect9; the media
and subadventitial layers are involved
less frequently.4

A pseudoaneurysm forms when
a dissection occurs between the
media and adventia layers. Generally,
a pseudoaneurysm is caused by
trauma and is not demonstrated on
a radiograph until several days after
the injury. Typically found in the
cervical portion of C1 and the skull
base, a pseudoaneurysm may become
enlarged or remain stable, but
it does not completely resolve

The cephalad extension of
ICAD usually begins approximately
2 cm distal to the carotid bulb and
stops at the skull base region (a
petrous portion), where the ICA begins
to enter the foramen lacerum
to resume its normal caliber. The
dissection force courses in the longitudinal
cephalad direction, sparing
the siphon.3,5


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