J. Neurosurg. / Volume 32 / April 1970

Carotid Aneurysm and Contralateral Carotid Stenosis with
Successful Surgical Treatment of Both Lesions
Case Report
HAROLDD. PORTNOY,M.D., ANDANTHONYAVELLANOSA,M.D.
Department of Surgery (Neurosurgery), Pontiac General Hospital, Pontiac, Michigan,
and the Department o] Neurosurgery, Wayne State University School oJ Medicine,
Detroit, Michigan

N the geriatric population the occurrence
of carotid stenosis or occlusion is relatively common, as is that of intracranial
saccula aneurysm. The combination of extracranial carotid stenosis or occlusion and intracranial aneurysm, however, appears to be
rare. In review of the English literature, we
could find only nine previously recorded
cases2 ,1~,~5,~1 In only two cases were both
lesions symptomatic. In one case the patient
died following rupture of the aneurysm, no
surgical treatment having been instituted for
either lesion. 15 In the other instance, the patient died after a successful endarterectomy,
because of recurrent hemorrhage from the
aneurysm.25
The following case report is of an elderly
woman who had a right internal carotid artery aneurysm and a left internal carotid artery stenosis, both lesions producing symptoms and both lesions successfully treated
surgically. The association in this patient of
atherosclerosis, the "hydraulic" effect of a
contralateral "tight" carotid stenosis, and
congenitally anomalous circle of Willis introduces the question of the relative significance
of these factors in the formation of saccular
aneurysm.

so!idation in both lungs. The diagnosis was
viral pneumonia with meningitis; she was
treated with wide spectrum antibiotics, improved, and was discharged on November 6.
The patient was admitted to another local
hospital on November 17, with headache,
meningismus, slight paresis of the right medial rectus, paresis of upward gaze, slight bilateral deafness, right ptosis, and a right
pupil larger than the left but reactive to light
and accommodation. Grossly bloody cerebrospinal fluid obtained at lumbar puncture
was xanthochromic on centrifugation; it contained 16,100 red blood cells (RBC) and 79
white blood cells (WBC) per cu mm (64
lymphocytes and 15 polymorphonuclear
cells); the protein content was 161 rag%
and sugar content, 63 mg%. Electroencephalography on November 20 indicated
"the presence of a deep level or subcortical
disturbance with right-sided preponderance."
Blood pressures at this time varied from 140
to 180 systolic, and the patient was placed
on reserpine and phenobarbital. Bilateral carotid angiography on November 21 demonstrated a right internal carotid artery aneurysm (Fig. 1 lelt) and a left internal carotid
artery stenosis of 90% (Fig. 1 right). In addition,
there was partial stenosis of the right
Case Report
internal carotid artery best seen on a subseA 69-year-old white woman was in good quent brachial angiogram (Fig. 2 left), hyhealth until mid-October, 1968, when she poplasia of the left anterior cerebral artery,
experienced fever, generalized weakness, and evidence that the right posterior cerebral
shortness of breath, right-sided neck stiff- artery originated from the internal carotid
ness, anorexia, epigastric distress, and re- artery (Fig. 1 left). The following day the
peated episodes of vomiting. She was admit- patient suddenly developed right-sided weakted to another hospital on October 21, ness and dysphasia while walking. The blood
where no abnormality of the nervous system pressure was 130 systolic when she was rewas noted. Three days later she had a tem- turned to bed but prior to this, the blood
perature of 101~
meningismus, positive pressure had not been recorded lower than
Kernig's sign, and clinical evidence of con- 140 systolic. She improved following discontinuation of the reserpine and phenobarbital
Received for publication April 15, 1969.
476

I

Carotid Stenosis and Aneurysm

477

FIG. 1. Le]t: Right lateral carotid angiogram showing a bilobed aneurysm of the internal carotid artery
at the origin of the posterior cerebral artery. The posterior communicating artery takes origin from the
internal carotid artery. Right: Left lateral carotid angiogram showing the 90% stenosis at the origin
of the internal carotid artery.

and restoration of blood pressure, but had a
residual nocturnal confusion and disorientation.
Examination. On November 27, the patient was transferred to Pontiac General
Hospital for definitive therapy. Normal
values for the following laboratory tests were
noted on admission: hemoglobin, RBC,
WBC, urinalysis, syphilis ( V D R L ) , serum
cholesterol, calcium, inorganic phosphorus,
total bilirubin, albumin, total protein, uric
acid, blood urea nitrogen (BUN), lactate
dehydrogenase ( L D H ) , alkaline phosphatase, serum glutamic oxaloacetic transaminase (SGOT), prothrombin time, and
bleeding time. Fasting blood sugar was 125
mg% (slightly elevated). The electroencephalogram showed "evidence of generalized superficial and deep level disturbance
without focal abnormality." The electrocardiogram revealed a normal sinus rhythm and
suggested left ventricular hypertrophy. When
left carotid compression was carried out for
1 minute on November 29, the patient complained only of a slight amount of giddiness.
First Operation. On December 12, bilateral brachiovertebral angiography followed by the left carotid endarterectomy was
carried out under general anesthesia. Following angiography, which demonstrated a
hypoplastic right divisional branch of the
basilar artery, the right brachial arterial can-

nula was connected to a blood pressure transducer for continuous measurement during
surgery. Technical difficulties precluded measurement of pressures above and below the
stenosis. Jugular bulb venous pH and gas
studies were carried out. Initial studies disclosed a pH of 7.35; a pCO~ of 50 mm Hg;
and a pO2 of 39 mm Hg. Following occlusion of the internal carotid artery for 1 minute, the pH was 7.35; the pCO2 was 55 mm
Hg; and the pO2 was 36 mm Hg. Since there
had been no significant change in pO2, it was
felt that the patient could tolerate temporary
occlusion of the vessel during endarterectomy. This was done. On restoration of circulation after removal of the plaque, the pH
was 7.38; the pCO2 was 54 mm Hg; and the
pO~ was 34 mm Hg.
First Postoperative Course. Immediately
postoperatively the patient was fully awake
and responsive with no evidence of weakness. Right carotid compression was carried
out 2 days later and syncope associated with
a slight cardiac slowing ensued after 15 sec.
Carotid compression on subsequent days
yielded similar results. Following atropine
block and right carotid compression, the patient did not lose consciousness but did become confused and disoriented after 20 to
25 sec. During these several days the ptosis
improved. Because of failure to tolerate right
carotid compression, it was decided to

478

Harold D. Portnoy and Anthony Avellanosa

Fro. 2. Left: Right brachiovertebral angiogram demonstrating stenosis of the carotid bulb and adjacent
internal carotid artery. A hypoplastic right vertebral artery is also present. Right: Left carotid angiogram
obtained following left carotid endarterectomy. Note restoration of the lumen at the origin of the internal carotid artery.
reinvestigate the carotid circulation by angiography on December 12. Left carotid angiography demonstrated that the lumen had
been restored (Fig. 2 right). In addition, on
left carotid angiography with right carotid
compression, the contrast medium crossed
into the right anterior cerebral artery. It was
felt that complete occlusion of the right internal carotid artery would probably result
in hemiplegia2; therefore, following the angiogram, the blood pressure was slowly
dropped to 88/66 by use of Arfonad to determine if hypotension could be tolerated.
The state of consciousness and motor function of the patient was continuously determined during the hypotensive episode. The
patient tolerated the procedure well. During
the night of December 14 the patient became confused and developed increased

right ptosis and it was felt that the aneurysm
had leaked again.
Second Operation. A right frontotemporal craniotomy was carried out on December 17 using Mannitol and hypothermia to
31.5~ After opening the dura the frontal
and temporal lobes were elevated, and the
chiasmatic cistern was opened and allowed
to drain. The internal carotid artery was
brought into view; filaments of arachnoid
and adhesions about the internal carotid artery were freed and the aneurysm identified.
The fundus of the aneurysm was beneath the
edge of the tentorium. An atheromatous
plaque was clearly seen involving the first
millimeter of the neck of the aneurysm as it
emerged from the internal carotid artery.
The posterior communicating artery could
be easily delineated from the neck of the an-

Carotid Stenosis and Aneurysm
eurysm. A Scoville clip was then eased about
the neck of the aneurysm and slowly closed
in such a manner as to be placed inferior to
the tip of the atheromatous area. As the clip
closed, the aneurysm ruptured and bled transiently. At the time of the approach and
clipping of the aneurysm, the blood pressure
was between 90 and 100 mm Hg systolic,
but immediately after, the blood pressure
jumped to 140 m m Hg systolic, but there
was no further bleeding. The craniotomy
was closed in the usual manner with care
being taken to tent the dura and leave an adequate temporal craniectomy. An epidural
drain was left in for 24 hours even though
there was no unusual bleeding.
Second Postoperative Course. On the following day the patient was quite drowsy and
confused. No weakness was noted, but there
was a complete right third nerve palsy. The
next day the right pupil returned to normal
as did extraocular muscle function. The ptosis persisted. During the postoperative period the patient remained quite drowsy and
confused but moved both sides well. Right
carotid angiogram on December 26 showed
that about 1 to 2 m m of the neck of the aneurysm were still present (Fig. 3). There
was also a small epidural hematoma in the
temporal area limited by the tenting sutures.
On December 31 the patient became stuporous. The right temporal area was slightly
fluctuant. Following aspiration of 10 cc of
old blood, the patient became more alert and
was generally improved. Right carotid angiogram on January 8, 1969, showed the epidural hematoma was smaller.
Progress thereafter was rapid and the patient was discharged on January 15. At the
time of discharge she was alert and oriented
except at night, when she became slightly
confused and occasionally would have nocturnal enuresis. At the time of her last outpatient visit on April 3, 1969, she was no
longer confused at night and was taking care
of her grandchildren. Her neurological examination was normal except that she had
considerable giddiness on compression of either carotid artery for 10 to 15 sec.
Discussion
Atherosclerotic cerebrovascular disease is
present in a high percentage of individuals
over the age of 60,12,2~ and the incidence
of saccular aneurysm is certainly not rare.

479

Fro. 3. Right carotid angiograrn. A Scoville clip
occludes all by 1 to 2 mm of the aneurysrn neck.
McCormick and Nofzinger ~1 in an autopsy
study of 7650 adults found that 32% of the
151 aneurysms discovered were in individuals over 60 years old. It is of particular interest, therefore, that the combination of
saccular aneurysm and carotid artery stenosis is rare, especially when atherosclerosis
has been suggested as one of the etiological
factors in the development of saccular
aneurysm.~,~-8,30,~,35
Six of the nine previously reported cases
of aneurysm associated with carotid artery
stenosis or occlusion are mentioned in a
paper by Gurdjian, et. al.) in a table of concomitant angiographic findings in 205 cases
of carotid artery stenosis. Follow-up ~1 shows
that five patients have done well while the
sixth had a fatal rupture of the aneurysm.
Gurdjian, et aI., also reported a 65-year-old
man with a right internal carotid artery stenosis at the bifurcation, and right middle cerebral artery aneurysm, no further clinical
data were presented. TM
A case of Jaffe and McHenry 1~ was reported in detail and involved a 79-year-old
Negro woman who, 10 years prior to an episode of subarachnoid hemorrhage, had developed an occlusion of the left internal carotid artery with contralateral weakness. At
the time of investigation for the episode of
subarachnoid hemorrhage, a right internal
carotid artery aneurysm was demonstrated.
No surgical intervention was carried out and
the patient died from a subsequent hemorrhage.

480

Harold D. Portnoy and Anthony Avellanosa

Pool and Potts 25 describe a patient of
Mount's with a left internal carotid artery
aneurysm and contralateral internal carotid
artery stenosis at the bifurcation. An endarterectomy was carried out successfully on
the stenotic vessel, but the patient died subsequent to recurrent hemorrhage before
planned surgical intervention for the aneu-

rysm.
Somach and Shenkin 31 briefly mention a
patient with aneurysm who also had a concomitant narrowing of the left carotid artery.
Complete angiographic studies after right carotid ligation were abandoned when introduction of a needle into the narrowed vessel
produced transient aphasia and hemiplegia.
One other case of intracranial aneurysm
and carotid stenosis has been seen by one of
us (H.D.P.). This was a 69-year-old white
man who was admitted for subarachnoid
hemorrhage and left hemiparesis. Angiography demonstrated a right internal carotid
artery aneurysm and 70% stenosis of the
right internal carotid artery at the bifurcation. He was treated with bedrest over a period of 8 weeks, gradually improved, and at
present is alive, well, and active. The neurological deficit appeared to be due to the ruptured aneurysm, although possibly the carotid stenosis was of significance.
The patient reported here is the only one
to our knowledge who has been successfully
treated surgically for both lesions.
While extracranial carotid artery disease
is infrequently associated with aneurysm, it
is not unusual for aneurysms to be grossly
arteriosclerotic. 1~ Stehbens 3'-' has been able to
demonstrate arteriosclerotic defects in the
media of cerebral arteries, primarily at bifurcations. Based on these findings and the altered dynamic flows found in patients with
arteriosclerosis, he suggested that aneurysms
may be formed from degenerative changes in
the arterial wall. This theory could be applied to the development of the aneurysm reported in this case since an arteriosclerotic
plaque was clearly seen in the neck of the
aneurysm at surgery. In addition, altered
flow dynamics were evident both angiographically and by the Matas (carotid compression) test.
The development of an aneurysm secondary to altered cerebral circulation due to
occlusion of a carotid artery has been exper-

imentally demonstrated in rabbits by
Hassler? 3 This "hydraulic" theory has a
clinical correlate in the cases reporting the
development or enlargement of a second aneurysm following carotid ligation for the first
ruptured aneurysm. 7,9,af,17,22-24,27,31,3a One
case of Somach and Shenkin 31 and the case
of Gurdjian, e t a l . , 9 had carotid angiography
demonstrating a previously normal vascular
pattern. In all other instances, either there
was no note as to whether complete angiography had been carried out at the time of the
initial ligation, or it was specifically mentioned that only the vessel which had been
subsequently ligated was studied. Because of
the high incidence of multiple and frequently
symmetrical aneurysms, ~,'~,~s,19,21,2~,:~G it cannot be supposed that all of these cases represent the development of a new aneurysm
subsequent to carotid ligation. The findings
of only two verified cases of aneurysms developing subsequent to carotid ligation suggest that Hassler's experimental work on the
rabbit is seen infrequently in clinical counterpart in man. This is further supported by
the fact that only one case has been reported
of an aneurysm developing subsequent to
spontaneous contralateral carotid occlusion? ~
Although the case presented here can be
used as an example of the development of an
acquired aneurysm on the basis of concomitant atherosclerosis and altered blood flow,
support for the congenital theory of origin
can likewise be raised by noting the associated congenital abnormalities of the circle
of Willis? ,2'-',3~,3~ In this patient there was hypoplasia of the left anterior cerebral artery
and right divisional branch of the basilar artery, and the right posterior cerebral artery
originated from the internal carotid artery. It
is not unreasonable to assume, therefore,
that the aneurysm found at the junction of
the right internal carotid and posterior cerebral arteries had a congenitally defective
media5 A possible explanation for the development and eventual rupture of the aneurysm could be as follows. The bifurcation of
the internal carotid artery and posterior cerebral arteries had a congenitally defective
media. With age and development of atherosclerosis the elastic fibers of the intima
gradually disintegrated, allowing ballooning
of the arterial wall and aneurysm formation.
As the stenosis of the contralateral internal

Carotid Stenosis and Aneurysm
carotid artery progressed, a compensatory
increase in blood flow through the ipsilateral
carotid artery occurred, causing further ballooning and rupture of the aneurysm.
As pointed out by Pool and Putts, 2~ in this
rare combination of carotid artery aneurysm
associated with a c o n t r a l a t e r a l c a r o t i d stenosis, the t r e a t m e n t of choice is first to relieve
the stenotic vessel b y e n d a r t e r e c t o m y , a n d
s u b s e q u e n t l y to t r e a t the a n e u r y s m . I n our
case, carotid c o m p r e s s i o n testing a n d angio g r a p h y with c a r o t i d c o m p r e s s i o n suggested
that the patient w o u l d n o t have tolerated
right carotid ligation, ~ thus l e a v i n g i n t r a c r a nial clipping of the a n e u r y s m as the only
logical alternative.

Summary
We have reported the case of a 69-yearold woman who had a subarachnoid hemorrhage associated with right third nerve involvement. Angiography demonstrated a
right internal carotid artery aneurysm, left
carotid stenosis, fetal origin of the right posterior cerebral artery, and hypoplastic left
anterior cerebral artery. Following a hypotensive episode in the hospital, the patient
developed a transient right hemiparesis. She
was successfully treated by left carotid endarterectomy and subsequent intracranial
clipping of the aneurysm. The contributions
of coexisting atherosclerosis, congenital abnormalities of the circle of Willis, and the
"hydraulic" effect of the carotid stenosis to
the development of the aneurysm have been
discussed.
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