Acta Neurol Scand., 1988:77:220-223
Key words: aneurysms, dissecting; cerebral infarction,
etiology; accidents, traffic; insurance

Closed cervicocranial trauma, “false aneurysm”
of the internal carotid artery and brain infarction
S. Keikkala, H. Somer, L. Valanne
Department of Neurology and t h e Institute of
Diagnostic Radiology, University of Helsinki,
Finland

ABSTRACT - A 17-year-old man developed acute hemiparesis 6 months after a
motor cycle accident. In the accident he had a closed trauma on the contralateral side
of the head and the neck, with multiple bone fractures. Aortocervical angiography,
performed after the infarction, revealed a 2.5 crn long aneurysmatic dilatation in the
internal carotid artery, the presumably source of embolic infarction. This and the 24
other cases gathered from the literature support the notion that closed neck trauma
may create “false aneurysm” which again may cause neurological deficits.
Accepted f o r publication September 27, 1987

Aneurysms are relatively rare in the internal carotid artery (1-5) but somewhat more frequent in
the common carotid and external carotid artery
(3). Lancering neck trauma appears to be a logical and rather frequent cause of carotid artery
aneurysm (2, 6, 7), whereas a closed cervicocranial trauma is only seldom recognized in the
previous history (6-8).
We describe a case where a cerebral infarct
developed in a 17-year-old man, 6 months after
a road accident. Similar cases with the association of closed trauma and internal carotid artery
aneurysms are reviewed from the literature.

Case report
A healthy 17-year-old man crashed his motorcycle off the road in May 1985. During the
accident he wore a helmet strapped under his
chin. He was conscious when found and had
no neurological deficit on examination. He had
a dislocated fracture of the mandible with one
tooth injured and 6 teeth injured in the maxilla,
a dislocated fracture of the left humerus, a
distension of the left acromioclavicular ligament

and a contusion of the left lung. H e made a
good recovery and was discharged from the
hospital after 2 weeks.
Six months later he was admitted to the hospital with an acute leftsided hemiparesis. CTscan showed an infarction (Fig. la-b). Aortocervical angiography revealed a 2.5 cm long
aneurysmatic dilatation of the right internal
carotid artery about 5 cm beyond the bifurcation (Fig. 2). Other branches of the aortic arch
were normal.
Investigations of risk factors and other
etiologies were unrewarding. There were no cerebral infarcts in the family history. The patient
had smoked about 10 cigarettes per day, but for
a period of 3 years only. His blood pressure,
blood sugar, serum cholesterol and triglyceride
values were normal. ECG, M-mode and 2-dimensional echocardiography and continuous monitoring of the heart rhythm gave normal results.
Physical examination, radiological and laboratory investigations excluded Marfan’s syndrome,
Takayasu arteritis, homocystinuria, generalized
infection including endocarditis, and other predisposing causes.

CLOSED CERVICOCRANIAL TRAUMA

Fig. l a . CT-scan on the day of arrival shows a slightly
hypodense area of infarct at the territory of the right
middle cerebral artery.

Surgery was not considered possible and the
patient was placed immediately on permanent
anticoagulant therapy. His condition improved
to some extent. One year after the infarction he
still has a spastic hemiparesis. He is able to walk
without support, but can use his left hand for
grasping only.

221

Fig. Zb. Two days later the infarcted area has become
more hypodense and expansive.

Discussion
A dissecting aneurysm of the internal carotid
artery was an obvious origin for an embolus that
caused a cerebral infarct in our patient. To evaluate the possible association of the aneurysm and
the previous trauma we reviewed the literature

Table 1
Clinical findings in 24 cases of traumatic carotid artery aneurysms
Sex
Age
Type of the trauma
Localization of the lesions
Time latency between the
trauma and the symptoms
Primary symptoms and signs
Angiographic findings
Therapy
Outcome
Follow-up time

men 19, women 5
mean 31.2 y r s (range 15-65 yrs)
traffic accident 16 (hyperextension in at least 7) hyperextension of the neck 4, fall 3, direct
blow to the neck 1
head and neck 17, head and chest 1, head and trunk 3, trunk and extremities 3
immediate 11, hours 2, days 3, weeks 2, months 3, years 3
unconscious or stuporous 9, amnestic, desorientated, confused 3, local signs (pain in the
neck, a pulsatile mass, a Horner’s syndrome, epistaxis) 8, signs of carotid ischemia 8
aneurysm in the left carotid artery 15, in the right carotid artery 7. aneurysm bilaterally 2;
extracranially 22, intracranially 2
operation 14. anticoagulant therapy 6, antiaggregative therapy 2
dead 4, severe neurological deficit 2, minor neurological deficit 4, symptomfree 14
mean 2.5 y r s (n = 14)

Clinical information obtained from the

222

KEIKKALA ET AL

Fig. 2. An irregular aneurysmatic
dilatation can be seen in the distal
part of the right internal carotid
artery (arrows). The lesion extends
to the base of the skull
(arrowhead) but the upper limit
can not be depicted.

and found 24 cases where a closed trauma to the
craniocervical region preceded the finding of an
aneurysm in the internal carotid artery (1, 4-12)
(Table 1). The pathogenesis is probably a stretch
injury the vessels being compressed over the
bony prominences of the atlas and the axis as
well as over the styloid process during hyperextension and rotation of the head ( 5 , 6, 8, 10-14).
This type of stretch injury may be more likely in
younger individuals, since the carotid artery
becomes more tortuous with advancing age (14).
Another suggested mechanism is impingement of
the carotid artery between the angle of the mandible and the upper cervical transverse process.
This may lead to a transmural crush damage (7).
It may have been a contributing factor causing
extra compression during the trauma. One previous case had a somewhat similar mechanism
(1).

Most traumatic aneurysms are apparently
"false aneurysms", where the aneurysm is not
made up of the 3 layers of the normal vessel
wall, but only of the lining endothelium and
organized clot giving rise to occlusion or
thrombosis of the carotid artery (1, 2, 9, 13).
In some cases the aneurysms have a saccular
appearance. It is presumed that the pathogenetic mechanism in these particular cases might be
an acute crush damage with subsequent rupture
and hemorrhage or vasospasm. The onset of
clinical symptoms appears to be more acute in
these cases (6, 7). It is, however, difficult to
divide the traumatic aneurysms into definite
subgroups since information on vascular pathology is available from a few cases only, and
they may not be so representative for the whole
clinical spectrum. We therefore gathered information from all the traumatic aneurysms

CLOSED CERVICOCRANIAL TRAUMA

appearing in the extracranial portion of carotid
arteries (Table 1).
In most cases local neurological signs or symptoms from the corresponding carotid territory
develop within a few days from the trauma, but
occasionally the time interval may be months or
even years (7, 9-11, 13). Pain associated with a
pulsatile mass in the neck and Horner’s syndrome are suggestive local signs. Carotid bruit,
however, is present only infrequently (7). We were
unable to find any data of the value of Doppler
ultrasound technique in the diagnosis. Aortocervical angiography therefore remains as a decisive
diagnostic method. Traumatic aneurysms are
actually difficult to distinguish from other
aneurysms by angiography (6) except that they
are usually located distally in the extracranial
portion.
Recognition of a traumatic aneurysm is of
considerable importance for several reasons. Surgery should always be considered and its long
term results are usually excellent (4-6, 14). Some
cases, like ours, was beyond surgical therapy
because of the size and location of the aneurysm.
These cases might benefit from long term anticoagulant therapy. The diagnosis of traumatic
carotid artery aneurysm also carries a great significance from the medicolegal point of view.

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223

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Address

Dr. H . Somer
Department of Neurology
University of Helsinki
Haartmaninkatu 4
00290 Helsinki
Finland