883

Delayed Traumatic Cerebral Aneurysm After Brain Injury
David O'Brien, Jr., MD, Michael W. O'Dell, MD, Amy Eversol, BA
ABSTRACT. O'Brien D Jr, O'Dell MW, Eversol A. Delayed traumatic cerebral aneurysm after brain injury. Arch Phys
Med Rehabil 1997;78:883-5.
Traumatic aneurysms (TAs) are an unusual etiology for late
neurological deterioration after traumatic brain injury (TBI) and
represent less than 1% of all cerebral aneurysms. TAs most
often are diagnosed acutely but may be delayed in presentation.
To increase awareness of this serious but treatable condition
when diagnosed early, we report a delayed TA after a motor
vehicle accident. The patient experienced a seizure on day 46
postinjury while in rehabilitation and demonstrated persistent
lethargy and hemiparesis. Neuroimaging revealed a large, ruptured left pericallosal artery TA, which was surgically clipped.
The patient completed his rehabilitation course and was eventually discharged home with family. Among TBIs, TAs are associated with penetrating injuries and skull base or anterior cranial
fossa fractures. Associated mortality is high, especially if rupture has occurred. Although TAs are rare, the clinician should
be vigilant in the at-risk patient.

© 1997 by the American Congress of Rehabilitation Medicine
and the American Academy of Physical Medicine and Rehabilitation
HERE ARE SEVERAL causes for late neurological deterioration in persons with traumatic brain injury (TBI), including the development of intracranial post-traumatic aneurysms
(TAs). TAs are uncommon, representing less than 1% of all
intracranial aneurysms.l'2 TAs appear to be relatively more common in children than adults. 3'4 Approximately 250 cases of TAs
have been reported in the literature, 23% in children 18 years
old or younger.5 They are seen three times more often in males
than females, reflecting the increased incidence of head trauma
in males. 6
TAs usually present acutely associated with intracranial hemorrhage but may present weeks to years after head trauma. 7-9
They can potentially occur with any type of traumatic head
injury and manifest in a variety of ways. To increase awareness
of this serious but treatable condition, we present an indisputable case of a delayed TA and outline associated clinical findings and likely risk factors involved.

T

CASE REPORT
A previously healthy 23-year-old man was riding on the roof
of a car ("car surfing") which was involved in a collision; he
was thrown onto the pavement. His initial Glasgow Coma Score
was 3. Initial computed tomography (CT) of the brain showed
From the Departmentof PhysicalMedicineand Rehabilitation,Universityof
Cincinnati College of Medicine, and Brain Injury RehabilitationPrograms,
DrakeCenter, Inc.,Cincinnati,OH.
Submittedfor publicationMarch 18, 1996. Acceptedin revisedform January
2, 1997.
A commercialparty with a direct or indirectinterestin the subjectmatter of
this articlehas conferredor will confer a financialbenefitupon one or more or
the authors.
Reprintsrequests to MichaelW, O'Dell,MD, 5161 MedicalScienceBuilding,
Mail Location530, 231 BethesdaAvenue,Cincinnati,OH 45267-0530.
© 1997by the AmericanCongressof RehabilitationMedicineandthe American
Academyof PhysicalMedicineand Rehabilitation
0003-9993/97/7808-394853.00/0

a right frontal contusion and possible subarachnoid hemorrhage
(SAH). The presence of subarachnoid blood prompted a subsequent cerebral angiogram, which indicated no signs of an aneurysm or any causes for the SAH other than trauma (fig 1). On
day 4 after injury, repeat CT showed worsening cerebral edema
with midline shift. Because of elevated intracranial pressures,
the patient underwent a right frontotemporal lobectomy.
On day 7 postinjury, he was transferred to our rehabilitation
unit at Rancho Los Amigos Level of Cognitive Function IV
(agitated). He continued to show progressive functional improvement until day 46 postinjury, when he experienced a seizure with persistent lethargy and hemiparesis. CT of the brain
showed a large intraventricular hemorrhage with midline shift
(fig 2). Subsequent cerebral angiogram revealed a large, left
pericallosal artery aneurysm not shown by the initial angiogram
(fig 3). He underwent successful neurosurgical clipping and
returned to rehabilitation, where he progressed well (fig 4). He
was discharged home with his family 76 days after injury.
DISCUSSION
Histologically, TAs can be classified as true, false, mixed, and
dissecting. False types are the most common6'7'1° and involve
complete laceration of the arterial wall. A subsequent perivascular hematoma undergoes cavitation and a false lumen develops.
True aneurysms develop secondary to intimal disruption, which
produces local vessel wall weakening with subsequent aneurysm formation. Mixed aneurysms are true aneurysms that rupture and form a false aneurysm outside the true one. Dissecting
aneurysms result from intimal injury with subsequent hemorrhage into the vessel wall.
The development of a TA in most cases is related to direct
arterial wall injury against an adjacent skull fracture. Penetrating
injuries, especially knife wounds at the base of the neck or
through the orbit, can result in direct arterial damage and subsequent TA formation. Unlike stab wounds, high velocity missile
injuries infrequently result in T A s . 6-9'1I
A majority of TAs are of the false type and associated with
basilar skull fractures and fractures involving the anterior cranial fossa] '11 Unlike congenital aneurysms, most TAs are not
related to arterial branching points but are usually located in
the superficial circulation and often involve the internal carotid
artery (ICA). Of 94 cases of TAs reviewed by Yokota and
colleagues, ~ 46% were located on distal middle cerebral artery
branches, 38% on anterior cerebral artery branches (most distal
to the anterior communicating artery), and 7% involved the
ICA. Other authors, however, have shown the ICA to be involved in as many as 48% of cases, most often involving the
intracavernous segment.9'13 TAs involving the ICA sometimes
result in fistula formation with sphenoid sinus extension which
can present as massive epistaxis appearing months to years
after injury. This type of TA is usually nonfatal, but recurrent
epistaxis is expected, with mortality reaching 30% to 50% if
diagnosis and treatment is not undertaken.6'7'9'14'15
In contrast to the location of most TAs, our case illustrates
the delayed development of a pericallosal artery TA (PCTA).
PCTAs are usually false aneurysms that occur infrequently and
often go unrecognized. They arise with high-velocity, rapiddeceleration head injuries, occur near the falcine edge unrelated

Arch Phys Med Rehabil Vol 78, August 1997

884

TRAUMATIC CEREBRAL ANEURYSM, O'Brien

Fig 1. Initial angiogram on day of injury showing no evidence of aneurysm or hemorrhage (IC, internal carotid artery; AC, anterior cerebral
artery; PC, pericallosal artery).

to arterial branching points, and often present as delayed, acute
intracerebral bleeding. 6'7 Presumably, sudden brain and arterial
movement results in vessel wall injury against the stationary
edge of the falx, thus creating a nidus for aneurysm development. ~6'17As our case demonstrates, PCTAs are not necessarily
associated with skull fractures, in contrast to most TAs.

Fig 3. Presurgical angiogram showing a large left pericallosal artery traumatic aneurysm (TA) as the etiology of the patient's clinical deterioration
(IC, internal carotid artery; AC, anterior cerebral artery; PC, pericallosal
artery).

In general, TAs manifest in numerous ways. Presenting signs
and symptoms result from the expanding aneurysm with associated mass effect, hemodynamic changes, or hemorrhage (table
1.) Unlike the PCTA in this case, Maurer's triad of unilateral
blindness, orbital fracture, and massive epistaxis should alert
the physician to the possibility of an intracavernous TA of the
ICA with sphenoid sinus extension. 18
Although TAs are rare, they are potentially devastating lesions with overall mortality rates ranging from 20% to
30%. 12.15,19After overt hemorrhage, the mortality rate is approximately 50%, compared with 16% when the TA is found incidentally before rupture. 7'12'~5 The mortality rate in operatively
treated patients is between 10% to 20%, compared with approximately 40% for those treated nonoperatively, underscoring the
need for early identification and appropriate referral. 7't2,t5
In summary, we report an indisputable case of TA, confirmed
by pre- and post-aneurysm angiography, as a cause of late neurological deterioration during rehabilitation of a TBI. TAs can
Table 1: Presenting Signs and Symptoms for Traumatic
Cerebral Aneurysms

Fig 2. CT of the brain on day 46 postinjury after new onset seizures and
hemiparesis showing a large intraventricular hemorrhage (A). The arrow
at B indicates area of the aneurysm.

Arch Phys Med Rehabil Vol 78, August 1997

Progressive cranial nerve palsy
Enlarging or bulging skull fracture
Recurrent, massive epistaxis
Unilateral visual loss
Progressive exophthalmos and chemosis
Cranial bruits
Headache
Delayed neurologic deterioration leg, new onset seizures, change in
mental status, progressive hemiparesis, etc)
Delayed intracerebral bleeding
Extensive intracerebral blood after minor head injury
Unusual distribution of blood on initial CT of the brain
Unexplained, major arterial bleeding during evacuation of a cerebral
hematoma
Discrepancy between amount of subarachnoid or intraventricular blood
and severity of brain injury on CT

TRAUMATIC CEREBRAL ANEURYSM, O'Brien

885

120

100

o

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

8o

o~
6O
Acute Hospital Transfer 1/10 - 2/2

"~
jO 40

.I
o
Injury11/25

II ~Rehab

j

ReadmJssion

Rehab
Admission

20
Fig 4. Functional Independence
Measure scores for our patient.
Data are presented for inpatient
rehabilitation admissions and
outpatient follow-up.

0
NOV.

Dec.

Jan.

occur in mild to severe brain injury and open or closed head
injuries. They tend to be associated with nonmissile penetrating
injuries, fractures across the anterior cranial fossa or skull base,
and acceleration-deceleration head injuries. As a T A enlarges,
various signs and symptoms m a y present, such as recurrent
epistaxis, seizures, progressive cranial nerve deficits, and an
enlarging skull fracture. Radiographic evidence of intracerebral
and subarachnoid bleeding should particularly alert the physician to the possibility of a TA. For patients with head trauma
demonstrating characteristic signs and symptoms and in w h o m
a high index of suspicion is held, angiography should be considered. TAs can result in delayed deterioration after head trauma,
with a high rate of associated morbidity and mortality.

Acknowledgment: The authors thank Mario Zuccarello, MD, University of Cincinnati College of Medicine, Department of Neurological
Surgery, for reviewing the manuscript.
References
1. Benoit BG, Wortzman G. Traumatic cerebral aneurysms: clinical
features and natural history. J Neurol Neurosurg Psychiatry 1973;
36:127-38.
2. Laun A. Traumatic aneurysms. In: Pia HW, Langmain C, Zierski
J, editors. Cerebral aneurysms: advances in diagnosis and therapy.
Berlin: Springer-Verlag; 1979. p. 364-74.
3. Patel AN, Richardson AE. Ruptured intracranial aneurysms in the
first two decades of life: a study of 58 patients. J Neurosurg 1971;
35:571-6.
4. Almeida GM, Pindaro J, Plese P, Bianco E, Shibata MK. Intracranial arterial aneurysm in infancy and childhood. Childs Brain 1977;
3:193-9.
5. Fox JL. Intracranial aneurysms, Vol III. New York: Springer-Vetlag; 1983.
6. Takakura K, Snito I, Sasaki T. Special problems associated with

Feb.

Mar.

Apr.

J~Aug.

Se~t.

subarachnoid hemorrhage. In: Youmans JR, editor. Neurological
surgery. 3rd ed. Philadelphia: Saunders; 1990. p. 1864-85.
7. Buckingham MJ, Crone KR, Ball WS, Tomsick TA, Berger TS,
Tew JM. Traumatic intracranial aneurysms in childhood: two cases
and a review of the literature, Neurosurgery 1988;22:398-408.
8. Haddad FS, Haddad GF, Taha J. Traumatic intracranial aneurysms
caused by missiles: their presentation and management. Neurosurgery 1991;28:1-7.
9. Steinmetz H, Heiss E, Mironov A. Traumatic giant aneurysms of
the intracranial carotid artery presenting long after head injury. Surg
Neurol 1988;30:305-10.
10. Jungueira LC, Carneiro J, Long JA. Basic histology. 5th Ed. Norwalk (CT): Appleton-Century-Crofts; 1986.
11. Becket DP, Gade GF, Young HF, Feverman TF. Diagnosis and
treatment of head injury in adults. In: Youmans JR, editor. Neurological surgery. 3rd ed. Philadelphia: Saunders; 1990. p. 2105-6.
12. Yokota H, Tazaki T, Murayama K. Traumatic cerebral aneurysm:
94 cases from the literature and 5 cases observed by the authors.
No Shiaki Geka (Tokyo) 1983; 11:521-9.
13. Fox JL. Intracranial aneurysms. New York: Springer-Verlag, 1983.
14. Burton C, Velasco F, Dorman J. Traumatic aneurysm of a peripheral
cerebral artery: review and case report. J Neurosurg 1968;28:46874.
15. Fleisher AS, Patton JM, Tindall GT. Cerebral aneurysms of traumatic origin, Surg Neurot 1975;4:223-39.
16. Lanrent JP, Check WR, Mims T, McCluggage CW. Traumatic intracranial aneurysm in an infant: case report and review of the literature. Neurosurgery 198l;9:303-6.
17. Smith KL, Bardenheier JA. Aneurysm of the pericaltosal artery
caused by closed cranial trauma: case report. J Neurosurg 1968; 29:
551-4.
18. Manrer TJ, Mills M, German WJ. Triad of unilateral blindness,
orbital fractures and massive epistaxis after head injury. J Neurosurg
1961; 18:837-49.
19. Asari S, Nakamura S, Yamada O, Beck H, Sugantani H, Higashi
T. Traumatic aneurysm of peripheral cerebral arteries: report of two
cases. J Neurosurg 1977;46:795-803.

Arch Phys Med Rehabil Vol 78, August 1997