J Neurol (1985) 232 : 314-3t7

Journal of

Neurology
© Springer-Verlag t985

Short communications

Bilateral traumatic extracranial aneurysms of the internal carotid artery
with delayed brain infarction
J .-P. Matin 1*, H. Becker 2, and J. Abicht 1

1Neurology Clinic and
2Neuroradiology Department, Medizinische Hochschule Hannover, Konstanty-Gutschow-Str. 8, D-3000 Hannover 61,
Federal Republic of Germany

S u m m a r y . A 24-year-old woman with a left-sided cerebral
infarction presented with hemiplegia and aphasia. Five
months earlier she had had a closed head injury. Angiography
revealed bilateral extracranial post-traumatic aneurysms of
the internal carotid artery at the atlanto-axial level. There was
full recovery without operative treatment within a week.
Key words: H e a d injury, closed - Carotid artery, internal -

Aneurysm, bilateral extracranial - Cerebral infarction

Injuries to the internal carotid artery following head trauma
are well known. Traumatic thrombosis of the internal carotid
artery, arteriovenous fistulas of the cavernous sinus, and
traumatic aneurysms of the intracranial arteries have been
reported as a complication of head injury [2, 3]. Aneurysms of
the cervical segments of the carotid arteries resulting from
non-penetrating injuries are, however, quite rare. Schmidt [7]
reported six cases of unilateral extracranial aneurysms. Further
cases have been reported by several authors [4-6, 9]. Fleisher
et al. [2] summarized 41 cases of intracerebral traumatic
aneurysms, collected from the world literature. However, we
could not find a case report of a bilateral traumatic extracranial
aneurysm of the internal carotid artery at the atlanto-axial
level, secondary to closed head injury. We describe, therefore, a 24-year-old woman who was examined because of cerebral infarction in the left hemisphere in the territory of the
middle cerebral artery.

Case report

A 24-year-old woman had an accident on 20 March 1984.
During a climbing tour in Spain she fell from a rock, from a
height of about 8m, Immediately after the fall she was
unconscious; 2 - 3 h later she was observed to be in a semicomatose state, unable to give any information about the
accident. On admission to hospital the following injuries were
noted: fracture of the left floor of the orbit and left zygoma,
pelvic fracture with involvement of the hip, fracture of the
right radius, splenic rupture, kidney trauma and pulmonary
* Corresponding author

contusion. The patients was discharged in April 1984. During
the hospital stay no neurological disturbances were noted. She
became conscious and alert within a few days after the accident. After discharge, she continued studying veterinary
medicine and preparing for an examination. On the morning
of 17 August 1984 a right-sided hemiplegia and aphasia
suddenly occurred.

Neurological evaluation on 17 August. The woman was
conscious and well orientated. A right-sided hemiplegia with
central facial nerve paresis was noted. She had severe aphasia,
agraphia and dyslexia. Examination revealed no other abnormafities; in particular, cardiac auscultation and auscultation of
the carotid arteries were normal. Blood pressure was 120/
80 mm Hg on both sides. Doppler sonography of both internal
carodid arteries was normal. The electrocardiogramm and
echocardiography revealed no abnormalities. Further laboratory investigations, including blood and plasma viscosity, showed no abnormality. There was no diabetes. The patient did
not smoke or use oral contraceptives.

X-ray examination. Cranial computed tomography (CT) on
17 August, 6h after onset of hemiplegia, revealed an old
encephalomalacia ( l c m in diameter) on the right side, i.e.
ipsilateral to the hemiplegia (Fig. l a). Eleven days later the
CT scan showed an infarction of 3 cm in diameter, located in
the left insula. In the plain CT the infarct area was hypodense
and isodense ("fogging effect"; [1]; Fig. l b , c ) . After intravenous injection of contrast medium marked enhancement
appeared. A further CT on the 21st day showed the whole
infarction area to be hypodense in the plain CT scan with
marked enhancement following contrast medium injection.
Magnetic resonance (MR) examination revealed an extensive
area of increased signal intensity in the left insula and a smaller
area in the right parietal lobe (Fig.2a,b). The examination
was done by spin-echo and inversion recovery technique. Left
carotid angiography revealed an aneurysm i cm in diameter at
the atlanto-axial level. The lumen of the internal carotid
artery was narrowed near to the aneurysm. Occlusion of
vessels in the region of the insula was not shown. Right carotid
angiography revealed a nearly identical aneurysm of the right
internal carotid artery (Fig. 3 a, b).
The patient recovered very quickly: hemiplegia and aphasia
disappeared within the 1st week after onset. On 13 September

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Fig.1. a CT scan: small old infarction in the right parietal lobe. b CT:
unenhanced scan shows a small hypodense infarcted area only in the
left insula 11 days after the acute onset. ¢ CT: after injection of contrast medium the whole area of infarction is visible
%

in the tests for aphasia (Aachen Aphasia Test) no disturbances
could be detected. The patient left hospital to take an examination at the university and passed. T r e a t m e n t was restricted
to physiotherapy in the acute phase, together with speech
therapy. Operation was refused. A t a follow-up examination
in D e c e m b e r 1984 the patient was completely normal.

Discussion
A n e u r y s m s of the internal carotid artery secondary to nonpenetrating head injuries are typically located at the atlantoaxial level [4, 7, 8], n e a r the base of the skull. Such extra-

b
Fig.2. a MR (SE, TR 1600, TE 68): increased signal intensity in the left
insuta,, for comparison with Fig. l b and c. b MR (SE, TR 1600, TE
68): small area of increased signal intensity in the right parietal lobe,
for comparison with Fig. 1 a.

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Fig.3. a Right carotid angiography: aneurysm of the internal carotid artery at the atlanto-axial level, b Left carotid angiography: nearly identical

aneurysm at the same level

cranial aneurysms are not c o m m o n . In the literature we were
not able to find a case of bilateral extracranial aneurysm.
T h e mechanism of d e v e l o p m e n t is the same as in unilateral
aneurysms. W e assume that an acute, severe "hyperextension"

of the carotid artery occurred at the atlanto-axial level. H e r e ,
the transverse process of the first cervical vertebra acted as a
hypomochlion [6, 8]. Fractures of the upper part of the cervical
spine are not u n c o m m o n in such cases [4, 5]. The primary

317
vascular lesion is a tear in the vessel wall, leading to occlusion
of the vessel lumen or to an aneurysm [8, 9]. The clinical
symptomatology of traumatic aneurysms of the cervical internal
carotid artery varies. Traumatic aneurysms can develop
without clinical symptoms. However, neurological disturbances, such as hemiplegia, hemiparesis and aphasia, may be the
initial symptoms [5]. Following neck trauma, aneurysms
commonly present as a mass in the neck. In such cases dysphagia, dyspnoea, vertigo or tinnitus occur. The symptomfree interval between trauma and onset of neurological disturbances is very variable, intervals between a few weeks and 2
years being recorded. In our case the interval between trauma
and cerebral infarction was 5 months. The right-sided parietal
infarction [Fig. 1 a) obviously occurred asymptomatically.
Repeated angiographic examinations have demonstrated
an increase in size of the aneurysm in addition to spontaneous
thrombosis [7]. Undoubtedly, such an aneurysm is a considerable risk for the (commonly young) patient. Only exceptionally is cerebral angiography with visualization of the cervical vessels performed in the early stage of a closed head
injury. Therefore, if there has been appropriate trauma (e.g.
fractures of te upper cervical spine), the possibility of an
extracranial aneurysm should be considered. In patients with
cerebral infarction without clear risk, but with an appropriate
history of trauma in the past, late infarction from post-traumatic
extracranial aneurysm should be considered in differential
diagnosis.
Therapy may initially be surgical and eventually a by-pass
operation may be necessary. With an aneurysm on both sides

the difficulties involved in operating are considerable, and the
decision regarding operative treatment is problematic.

References

1. Becker H, Desch H, Hacker H, Pencz A (1979) CT fogging effect
with ischemic cerebral infarcts. Neuroradiology 18 : 185-192
2. Fleisher AS, Patton JM, Tindall GT (1975) Cerebral aneurysms of
traumatic origin. Surg Neurol 4: 233-239
3. Huber P (1977) Angiographie beim Sch~idel-Hirntrauma. Aktuel
Neurol 4: 41-60
4. Lai MD, Hofflnan HB, AdamkiewiczJJ (1966) Dissecting aneurysm
of internal carotid artery after non-penetrating neck injury. Acta
Radiol [Diagn] (Stockh) 5:290-295
5. Margolis MT, Stein RL, Newton TH (1972) Extracranial aneurysms
of the internal carotid artery. Neuroradiology 4 : 78-89
6. New PF, Momose KJ (1969) Traumatic dissection of the internal
carotid artery at the atlanto-axial level, secondary to non-penetrating
injury. Radiology 93 : 41-49
7. Schmidt RC (1978) Extrakranielle Aneurysmen der A. carotis
interna bei stumpfen Schfidelhirntraumen. Neurochirurgia 21:
139-145
8. Simon RS, Schramm J, Bradac GB (1976) Carotis-Lasion bei
stumpfem Halstrauma. Aktuel Neurol 3 : 191-196
9. Teal JS, Bergeron RT,, Rumbaugh CL, Segall HD (1972) Aneurysms
of the cervical portion of the internal carotid artery associated with
non-penetratingneck trauma. Radiology 105 : 353-358

Received March 8, 1985/Accepted May 13, 1985