Brief Reports

Delayed Hemiparesis Following Nonpenetrating
Carotid Artery Trauma
ROBERT P. MOONEY, MD, HOWARD A. BESSEN, MD
A 21-year-old
man developed
transient, recurring right arm and
leg weakness 2 weeks after a motorcycle accident. He utimateiy
proved to have an intimai tear and thrombosis of the left internal
carotid artery with transient cerebral ischemia due to distal emboli. Neuroiogic
deficits eventually resolved after anticoagulation
and balloon occlusion of the vessel. The differential diagnosis of
the patient’s presentation
is discussed,
and the topic of nonpenetrating trauma of the carotid artery is reviewed, with special
attention to mechanism
of injury and clinical presentation.
(Am J
Emerg Med 1988;6:341-346.0
1988 by W.8. Saunders Company.)

Nonpenetrating
trauma of the carotid artery is an
unusual injury. We present a case of delayed thrombosis of the internal carotid artery in a young man who

developed
symptoms of focal cerebral ischema 2
weeks after a motorcyle accident. This type of vascular injury is associated with significant morbidity and
mortality, and patients who sustain such an injury are
likely to be seen in an emergency department.
CASE REPORT
A 21-year-old white man was involved in a desert motorcycle accident 2 weeks before presentation. He was thrown
from this cycle and landed on his head and shoulder. He was
wearing a helmet and suffered no loss of consciousness. Minor headache and neck stiffness resolved over 2 days. On the
day of admission, the patient noted a sudden onset of weakness and numbness in his right arm and leg while walking.
The symptoms resolved gradually over 1 hour, but then returned, prompting him to visit an emergency department.
The neurologic examination was reported as normal except
for slight weakness of the right hand. Results of cervical

From the Department
of Emergency
Medical Center, Torrance, California.
Manuscript
1987.

received

April

Medicine,

23, 1987; revision

Harbor-UCLA

accepted

July 13,

Address reprint requests to Dr Mooney: Associated Emergency
Physicians, Inc, Medical Group of Northern California, 1625 The
Alameda, Suite 201, San Jose, CA 951262277.
Key Words:

Carotid

artery,

0 1988 by W.B. Saunders

trauma.
Company.

0735-6757/88/0604-0007$5.00/O

spine radiographs and head computed tomography (CT) scan
with contrast were normal. The patient was transferred to
Harbor-UCLA
Medical Center for further evaluation. While
waiting for consultation in the emergency department, he
reported a recurring sensation of weakness and numbness in
his right arm and leg. He denied headache, neck pain, chest
pain, and fever. There was no prior history of migraines,
collagen vascular disease, valvular heart disease, seizures,
or intravenous drug use.
Physical examination revealed a temperature of 97.7”C, a
heart rate of 60 beats/min, a blood pressure of 140/90 mmHg,
and respirations of 16/min. The patient was a well developed
male in no distress. Scattered healing abrasions were noted
on the face and extremities. No blood was seen behind the
typanic membranes. Pupils were equal and reactive to light
and the fundi were benign. The neck was slightly tender in
the left occipital region but otherwise supple without masses
or bruits. The left carotid pulse was absent. The chest was
clear to ascultation and heart sounds were regular without
murmur, gallop, or rub. The abdomen was soft and nontender. Rectal examination revealed normal sphincter tone;
the prostate was nondisplaced and the stool contained no
blood. The extremities were without rash, cyanosis, and
edema. Radial and dorsalis pedis pulses were full and palpable.
On neurologic examination the patient was alert and fully
oriented. Cranial nerves II through XII were intact. The face
was symmetric and speech was clear. Sensation was intact
to light touch and proprioception.
Diffuse 415 motor weakness was found in the right upper and lower extremities.
Left-sided strength testing was normal. Finger to nose and
rapid alternating movements were intact. Deep tendon reflexes were normal and symmetric.
Because the patient’s symptoms and signs were consistent
with transient ischemic attacks involving the left carotid territory, carotid-cerebral
contrast
angiography
was performed. The study revealed an intimal flap obstructing the
left internal carotid artery (Fig. 1). A carotid duplex scan
revealed a 50% diameter reduction of the left proximal internal carotid artery (ICA) with a long intimal flap extending
to the base of the skull.
The patient was heparinized and placed at bed rest on the
neurology service. He continued to complain of right-sided
weakness and numbness,
and transient focal deficits recurred. Embolization was thought to be the etiology of the
transient ischemic attacks. The distal extension of the intima1 flap precluded surgical revascularization
with resection
and grafting or anastamosis. In lieu of surgical ligation, a
341

AMERICAN

JOURNAL

OF EMERGENCY

MEDICINE

n Volume 6, Number 4 H July 1988

FIGURE 1. Obstruction of the left internal carotid artery due to an
intimal flap.
balloon was passed under fluoroscopic guidance into the left
distal ICA, occluding flow but causing no neurologic deficit.
The balloon was filled with silicon and left in place. The

patient’s focal deficits resolved within 24 hours, but rightsided weakness recurred when heparin was discontinued.
The deficits again resolved when heparinization was resumed. The patient was placed on warfarin therapy and
has been asymptomatic

as an outpatient

for 5 months.

DIFFERENTIAL DIAGNOSIS
This patient presented with a focal neurologic deficit
that was transient and recurrent. Because his motorcyle accident had occurred 2 weeks earlier, it was initially unclear whether his symptoms were related to
the trauma. Several etiologies could have explained
the clinical presentation.
(The differential diagnosis
will be limited to conditions likely to be seen in young
patients).
Intracranial mass lesions such as hemorrhage, neoplasm, or abscess must be ruled out in a patient presenting with a focal deficit. However, these entities
usually do not cause transient and recurrent neurologic findings, and they were essentially ruled out by the
normal CT scan.
Patients with focal seizures may have a postictal
paralysis (Todd’s paralysis) that sometimes persists
for days. ’ Without a history of witnessed seizures, this
can be a difficult diagnosis to establish. In our patient,
the fluctuating neurologic course made this diagnosis
unlikely.
A variety of focal neurologic abnormalities can be
seen in patients with migraines. In classic migraines,
342

visual, sensory, and/or motor disturbances occur before or during the headache. Hemiparesis can outlast
the headache and persist for days or weeks after the
headache has resolved (hemiplegic migraine). Neurologic deficits ultimately attributed to migraine can occur in the absence of headache; these symptoms (migraine equivalents)
can be the sole expression
of
migraine.’ This was a possibility in our patient, but an
unlikely one, especially with no prior history of similar
episodes.
Some CNS infections, such as herpes encephalitis,
commonly present with focal findings3; others, such as
bacterial meningitis, can cause focal changes due to
cerebral arteritis or thrombophlebitis.4
However, this
patient did not have fever, headache, or other symptoms suggesting CNS infection.
Impairment of cerebral blood flow caused by abnormalities of intracranial or extracranial vessels could
also have accounted for the patient’s symptoms. Possible diagnoses included the many types of vasculitis,
and extrinsic vessel compression (for example, by a
tumor or hematoma). Arterial or venous thrombosis
affecting cerebral perfusion can be caused by hypercoagulable states, which may be seen in association
with hemoglobinopathies.
the use of oral contraceptives, and other disorders.
Aortic dissections can extend into the carotid arteries and cause cerebral ischemia; vascular obstruction
in this condition may be transitory and recurrent.’
Spontaneous or traumatic aortic dissections can certainly occur in young patients; chest pain usually, but
not invariably, dominates the clinical picture.6
Intracranial aneurysms usually cause no symptoms
and are unrecognized until they rupture, but unruptured aneurysms occasionally cause transient ischemic
episodes. Transient ischemic attacks due to unruptured aneurysms have been attributed to emboli originating in the aneurysmal sac, or to compression of the
parent artery or adjacent brain by the aneurysm
itself.7.8
The most likely etiology of our patient’s symptoms
was cerebral ischemia due to embolism to the brain.
After they occlude a vessel, emboli may fragment and
then migrate or lyseg-“; symptoms may thus be transient or fluctuating. Recurrent emboli can cause recurrent symptoms, which may be identical or vary from
one attack to the next, depending on the site where the
embolus lodges. The middle cerebral artery and its
branches are the vessels usually affected.‘,’ ’ The diagnosis of cerebral embolism must be strongly considered in young patients with cerebral ischemia, since
other etiologies are much less common.iO*”
The source of cerebral emboli is usually the left
heart. lo Atria1 fibrillation is an important risk factor
because of the formation of mural thrombi in the noncontracting left atrium. Cardiac valves can be the

MOONEY AND BESSEN n HEMIPARESIS FOLLOWING CAROTID TRAUMA

source of embolic material in patients with rheumatic
valvular disease (especially mitral stenosis), prosthetic
valves, or endocarditis. Mitral valve prolapse has been
implicated as the cause of cerebral thromboembolism
in up to one third of patients aged ~45 years with
cerebral ischemia. ‘*,I3 Atria1 myxomas and mural
thrombi which occur in patients with cardiomyopathies are also potential sources of emboli.
In this young patient, with no history or evidence of
cardiac disease, emboli from the heart were still possible, but other sources needed to be ruled out. Paradoxical embolization
via right-to-left
intracardiac
shunts (clinically inapparent interatrial shunts) has recently been suggested as a common cause of cerebral
ischemia in young patients.14 In the proper clinical setting, emboli consisting of tumor cells, air, fat, or clots
from pulmonary veins should be considered; these
were highly unlikely in our patients.
Finally, intracranial and extracranial vessels can be
the source of cerebral emboli. In older patients with
atherosclerosis,
transient ischemic attacks are often
caused by emboli from an atherosclerotic lesion in the
internal carotid artery.’ In young patients, thrombi
may form in an uninjured or diseased vessel and embolize distally, as was the case in our patient. Angiography revealed a dissection and thrombosis of the internal carotid artery, attributable to the trauma sustained 2 weeks before. The fact that complete balloon
occlusion of the internal carotid artery did not produce
neurologic symptoms provides evidence that distal
emboli, rather than the thrombus itself, caused the patient’s focal deficits.

NONPENETRATING CAROTID ARTERY TRAUMA
Carotid trauma accounts for approximately 10% of
all arterial injuries. Only 3% to 5% of these are
nonpenetrating. 15,16The first reported case of internal
carotid artery thrombosis following nonpenetrating
neck trauma occurred in 1872.” Yamada et al reviewed 52 cases of carotid artery occlusion caused by
nonpenetrating neck trauma before 1967.” No more
than 130 cases of blunt carotid artery injury and 40
cases of blunt vertebral artery injury were reported
between 1952 and 1980.19 While these cases are infrequent, a review of 96 cases of nonpenetrating carotid
artery injury by Krajewski and Hertzer in 1980 revealed significant rates of mortality and morbidity.
Thirty percent of the patients died, and 42% of the
survivors were left with severe permanent neurologic
deficits.*’
Approximately 60% of cases of carotid artery stenosis following nonpenetrating head or neck trauma
have been attributed to an intimal tear and subsequent
thrombosis. I* Autopsy in v es ti ga ti o n s have shown that

the vessel intima and media are often tom, while the
elastic adventitia remains intact.** Other lesions have
included spasms, contusions, intramural hematomas,
mural fibros, and aneurysms.22-t5 Crissey and Bemstein have speculated that delayed symptoms are
caused by gradual development of thrombosis after an
intimal tear. Emboli may then create sudden neurologic deficits despite adequate collateral circulation.22
Gonzalez has suggested that delayed symptoms may
also be attributed to enlarging hematomas or progressive intimal dissection.23 Angiographic studies have
shown that 85% of nonpenetrating carotid injuries involve the extracranial ICA or carotid bifurcation.26
Most of the affected vessels are only partially occluded, as only three of 52 cases reviewed by Yamada
et al showed complete occlusion by angiography or
surgery. l8
Four types of craniocervical
injury may produce
traumatic thrombosis of the interal carotid artery**:

(1) Direct blows to the anterior neck account for
50% of the cases. These cause thrombosis
more commonly in the elderly, caused by
fracture of an atheromatous plaque at the carotid bifurcation.
A
(2) blow to the side of the head, with hyperextension and rotation or lateral flexion, may
stretch the ICA across the third cervical vertebra. This occurs more commonly in young
patients who are victims of violent assault or
motorcycle accidents.
(3) Blunt intraoral trauma is most common in
children, usually caused by falling on objects
with an open mouth.21
(4) Finally, a basilar skull fracture may lead to
thrombosis of the intrapetrous portion of the
ICA.
However, neither mechanism of injury nor associated injuries can accurately predict carotid vascular
injury following craniocervical
trauma. Jemigan and
Garner reported that ~50% of nonpenetrating carotid
artery injuries are associated
with motor vehicle
accidents.*’ 75% of the 52 cases reviewed by Yamada
were associated with head injury, but these injuries
were not further classified according
to level of
consciousness.18 Zelenock et al found no consistent
pattern of associated bony injuries. In fact, fractures
of the skull, face, first rib, and thorax are unusual.16
The diagnosis of blunt carotid artery injury is
fraught with pitfalls. Twenty-five percent to 50% of the
patients have no sign of cervical trauma.18*** Delayed
neurologic deficits are the rule rather than the exception. Only 10% of patients have symptoms of transient
ischemic attacks or stroke on admission.18 Most develop symptoms within the first 24 hours, but 17%
have no symptoms for days or weeks after the injury.18
343

AMERICAN JOURNAL OF EMERGENCY MEDICINE n Volume 6, Number 4 n July 1988

Before the advent of CT scanning, many cases of carotid injury were fortuitously diagnosed by angiography in unconscious patients with head injuries. Now
that CAT scans are the standard method of evaluating
serious head injury, carotid injuries are more easily
missed.
The early clinical features of nonpenetrating carotid
artery injury have included the followingz7:

(1) A lucid interval is common.
(2) 50% of patients demonstrate

a lateral neck
hematoma, particularly in the anterior triangle.
(3) Horner’s syndrome has often been reported
before other neurologic deficits. This is probably because of stretching or compression of
the sympathetic ganglia which accompany
the ICA.
(4 Transient ischemic attacks involving the middle cerebral artery distribution usually represent emboli.
(5) Hemiplegia or hemiparesis in the alert patient
or in the unconscious trauma patient with a
normal head CT are hallmarks of carotid obstruction.
The definitive

diagnosis can be made by contrast
angiography and
magnetic resonance imaging have not been extensively
studied in these patients.
The prognosis for patients who have developed carotid artery thrombosis
following nonpenetrating
trauma is often poor, and management is controversial. Although some authors suggest that conservative
management with anticoagulants prevents propagation
of thrombosis and embolism,‘6,21 larger studies have
shown that surgical revascularization
is often
curative. 18,20 Ligation or balloon occlusion are reserved for high lesions in young patients with good
collateral flo~.~’
The patient described in this report probably sustained a hyperextension-rotation
injury during his motorcycle accident. This type of injury is more likely to
produce extensive intimal dissection than is direct
trauma.22 His delayed presentation with transient ischemit attacks was a sign of emboli dislodging from a
carotid thrombus. There was no evident hematoma,
but lesions of the high ICA usually show no palpable
mass.28 Heparinization
may have halted thrombus
propagation, but did not prevent recurrent emboli.
Balloon occlusion of the ICA was necessary to block
embolization, and was relatively safe in this healthy
young patient with a patent Circle of Willis. A recent
report of successful surgical access to high ICA lesions
via mastoid bone resection2’ may change the way patients with such an injury will be managed in the future.

angiography .26 Digital subtraction

344

SUMMARY
We have presented a case of delayed hemiparesis in
a young man following nonpenetrating trauma to the
carotid artery. Traumatic dissection of the internal carotid artery is an unusual lesion, frequently presenting
in a delayed fashion that makes diagnosis difficult. The
emergency physician should consider this diagnosis in
any young patient with symptoms of focal cerebral
ischemia, particularly when the patient is alert and
when results of head CT scan are normal.
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