0148-396X/84/1504-0572$02.00/0
NEUROSURGERY
Copyright © 1984 by the Congress of Neurological Surgeons

Vol. 15, No. 4, 1984
Printed in U.S.A.

Giant Intracranial Aneurysms Presenting with Massive
Cerebral Edema

Roberto C. Heros, M.D., and Sastry Kolluri, M.D.

Neurosurgical Service, Massachusetts General Hospital, Boston, Massachusetts

Two cases of giant left middle cerebral artery aneurysm presenting with rapidly progressing hemiparesis and aphasia are
presented. In both, the computed tomographic scan showed recent intraaneurysmal thrombosis and massive edema and
swelling of the cerebral hemisphere. There was no evidence of recent hemorrhage in either case. In both patients, surgical
resection of the aneurysm was accomplished, but the outcome was disastrous. The literature is reviewed and the possible
mechanisms responsible for brain swelling in these cases are discussed. (Neurosurgery 15:572-577, 1984)

Key words: Aneurysmal thrombosis, Brain swelling, Cerebral edema, Giant intracranial aneurysm

The clinical presentation and problems in management of
patients with giant intracranial aneurysms have been amply
discussed (2, 6, 10-13, 16, 18, 27, 28, 30). A small number
of these aneurysms reach truly massive proportions and may
present with a distinctive clinical picture of accelerated neu-
rological deterioration secondary to mass effect from the
aneurysm itself as well as from surrounding brain edema. We
present two such patients with massive middle cerebral artery
(MCA) aneurysms. Surgical intervention had disastrous con-
sequences in both patients.

CASE REPORTS

Case 1

This 54-year-old right-handed woman first came to neuro-
surgical attention in 1979 with a 1-year history of complex
partial seizures. The findings of neurological examination

were normal. A computed tomographic (CT) scan showed a
homogenously enhancing lesion in the left frontotemporal
region. There was no evidence of brain swelling or edema.
Angiography showed a giant left MCA aneurysm. She under-
went an extracranial to intracranial (EC-IC) bypass in prepa-
ration for aneurysmal exploration and possible ligation of the
MCA. A postoperative arteriogram showed occlusion of the
graft (Fig. 1). In view of this, the aneurysm was not explored
and she was treated by ligation of the left internal carotid
artery (ICA), which she tolerated well. Except for occasional
seizures, she remained asymptomatic until July 16, 1982,
when she had a sudden headache with nausea and vomiting.
On the next day, she was found to be unresponsive and was
taken to a local hospital where she was treated with mannitol,
steroids, and hyperventilation. With this she improved and
became responsive, but had a right hemiparesis and moderate
dysphasia. At this time, she was transferred to our service.

Fic. 1. Case |. Lateral (4) and anteroposterior (AP) (B) left common carotid injection. This angiogram was done after the initial EC-IC
bypass procedure and before carotid ligation. The aneurysm is clearly demonstrated. The bypass is not visualized.
572

October 1984

FiG. 2. Case 1. Enhanced CT scan at two different levels shows
the large, partially thrombosed aneurysm and massive cerebral edema
with midline shift.

The admission CT scan showed evidence of recent, partial
intraaneurysmal thrombosis. The overall size of the aneurysm
was about twice what it had been originally. In addition, there
was prominent left hemispheric edema and midline shift (Fig.
2). There was no evidence of subarachnoid hemorrhage (SAH)
or intracerebral hemorrhage. Angiography confirmed the
large mass effect and partial thrombosis of the aneurysm. The
MCA was supplied by a very large left posterior communi-
cating artery (Fig. 3). The level of consciousness fluctuated
over the following days. On July 19, 1982. the patient sud-
denly deteriorated into a comatose state with a dilated left
pupil and decerebrate posture on the right side. She was
immediately intubated, and mannitol was given. A repeat CT

GIANT ANEURYSMS AND BRAIN SWELLING $73

scan showed no change. With mannitol and hyperventilation,
the left pupil returned to a normal size and she became
decorticate rather than decerebrate on the right side. She did
not improve further. Therefore, on August 6, 1982, under
barbiturate coma and hypothermia, the aneurysm was excised
after thrombectomy. An aneurysmorrhaphy was necessary
because the main divisions took origin from the base of the
aneurysm. The MCA was temporarily occluded for about 40
minutes. Flow through the MCA trunk and its divisions
appeared to be adequate at the completion of the aneurys-
morrhaphy. Postoperatively, the patient was unconscious with
decerebrate posture. A CT scan showed massive hemispheric
edema on the left side with marked midline shift. The patient
did not recover and died on August 11, 1982. Autopsy showed
generalized left hemispheric infarction and swelling. There
was marked downward herniation of the brain stem, which
produced occlusion of the posterior communicating artery at
the petroclinoid ligament. The entire left MCA trunk was
thrombosed.

The final surgical attempt in this patient was rather desper-
ate and, not surprisingly, it failed. It is possible that the MCA
thrombosed spontaneously during the postoperative period
and that this in turn led to hemispheric infarction, more
edema, and death. More likely, however, is that this very
compromised hemisphere did not tolerate the period of tem-
porary MCA occlusion in spite of barbiturates and moderate
hypothermia. Hemispheric infarction then led to exacerbation
of the already existing massive edema with herniation. Occlu-
sion of the posterior communicating artery and the MCA,
which was supplied exclusively by the posterior communicat-
ing artery, was in all likelihood an epiphenomenon of cerebral
herniation rather than its cause.

In retrospect, the time to have treated the aneurysm aggres-
sively was upon initial presentation. At that time, the aneu-
rysm was already very large and almost certainly could not
have been clipped without aneurysmorrhaphy, but the patient
may have tolerated the latter procedure well because there
was no hemispheric edema at that time and the mass effect
from the aneurysm was much smaller. A direct attack was
contemplated by the initial neurosurgeon, but this plan was
abandoned when the bypass was found to be occluded. The
bypass became occluded probably because of the “lack of
demand” for flow in the MCA territory in view of the excellent
flow provided by the large posterior communicating artery.
The patient was then treated by ICA ligation. This procedure,
however, had little chance of affecting the natural history of
an MCA aneurysm (9).

Case 2

This 56-year-old hypertensive woman had had left-sided
headaches since September 1980. The headaches gradually
became worse, and the patient began to have episodes of
speech impairment. She was investigated in another hospital
in March 1981. Neurological examination was normal. A CT
scan revealed a large lesion in the left frontotemporal area
that enhanced with contrast medium. Moderate cerebral
edema was associated with the lesion, which was thought to
be a brain tumor. The patient was taken to the operating
room on March 18. 1981. At operation. the mass was sus-
pected to be an aneurysm, and this was confirmed by intra-
operative angiography. The operation was abandoned and a
Selverstone clamp was applied to the left common carotid
artery (CCA), which was gradually occluded without any
untoward effects. The patient developed infection of the cra-
niotomy wound and the bone flap was removed.

In January 1983, the patient was reassessed for recurrence

574 HEROS AND KOLLURI

of speech difficulty. On neurological examination, there was
evidence of expressive dysphasia and some confusion. There
was no motor, sensory, or reflex abnormality. An angiogram
showed that the CCA was still patent, although it was mod-
erately narrowed at the site of the clamp. The aneurysm had
enlarged considerably from the time of the previous angio-
gram. On January 14, 1983, a cranioplasty was performed.
On June 8, 1983, the patient was referred to our service
because of rapidly progressing right hemiparesis and dys-
phasia. A CT scan showed a giant left MCA aneurysm with
evidence of recent partial intraaneurysmal thrombosis. There
was massive hemispheric edema (Fig. 4). Angiography con-
firmed the presence of a partially thrombosed aneurysm with
considerable mass effect (Fig. 5). After angiography, she de-
teriorated further and her aphasia and right hemiparesis be-
came severe. On June 20, 1983, an EC-IC bypass was at-
tempted. The cortex was found to be quite swollen and no
cortical vessel of adequate size was available for an anasto-
mosis in spite of a very large craniotomy exposure. Thus, the
efforts to do a bypass were abandoned. We then planned to
resect the aneurysm under cardiopulmonary arrest and deep
hypothermia. She underwent coronary angiography to estab-
lish that there was good coronary circulation and cardiac
function. On June 29, 1983, under complete cardiac standstill
and profound hypothermia, the aneurysm could be com-
pletely resected but, because of calcification at the neck of the
aneurysm, it was impossible to oversew the proximal pouch
of the aneurysm from where the divisions took origin. An
attempt to overcome this difficulty by endarterectomy re-
sulted in a tear at the base of the aneurysm between the
takeoff of the two divisions. The distal MCA had to be
sacrificed. A saphenous vein bypass graft from the external
carotid artery to the largest division was accomplished after
the patient was warmed enough to be taken off cardiopul-

Neurosurgery, Vol. 15, No. 4

5°

. Case 1. Lateral (4) and AP (B) left vertebral injections show excellent filling of the left MCA by a large posterior communicating
he partially thrombosed aneurysm and the temporal mass effect are well demonstrated.

monary bypass. Postoperatively, the patient was aphasic and
hemiplegic. She had made no significant recovery by the time
of transfer to a chronic care hospital several weeks after the
operation.

Drake commented on the difficulty in finding an appropri-
ately sized cortical vessel for anastomosis in a case of giant
MCA aneurysm with hemispheric edema (6). He thought,
retrospectively, that in his case the sylvian fissure should have
been opened to find a more proximal branch to receive the
anastomosis. We also believe that, in our case, by resecting
the small cap of temporal lobe covering the aneurysm, we
could have found the two major divisions and done a double
bypass graft to each division before attempting to resect the
aneurysm. In fact, at the time of aneurysmal resection we did
easily identify and dissect the divisions off the wall of the
aneurysm. A vein graft to each division, even at that time,
may have prevented disaster.

We have not seen any comments in the literature about
unusual friability of cerebral vessels under profound hypo-
thermia and circulatory arrest. It seemed to us that the base
of the aneurysm and the distal MCA were unusually friable
under these conditions in this patient. Nevertheless, it is clear
that the technical error in this case consisted of overaggressive
endarterectomy at the calcified base of the aneurysm.

DISCUSSION

About one-third of patients with giant aneurysm present
clinically because of SAH: the rest usually present with symp-
toms of compression of either brain or the visual apparatus
(6, 10. 11, 13. 16, 27, 28, 30). The compressive symptoms are
usually thought to result from direct pressure of the aneurysm
on surrounding structures. Our two patients are unusual in
that, at the end, their clinical deterioration was due not to

October 1984

Fic. 4. Case 2. Enhanced CT scan at two different levels shows
the large, partially thrombosed aneurysm and massive cerebral edema
with midline shift.

direct pressure from the aneurysmal mass, but rather to
generalized hemispheric edema and midline shift. There are
a few similar cases mentioned in the literature, mostly within
reports of larger series. Nadjmi and colleagues mentioned a
patient who presented with abrupt clinical deterioration. CT
scanning showed a freshly thrombosed giant MCA aneurysm
with massive cerebral edema and displacement of the median
structures (14), Terao and Muraoka reported a patient with
“an enormous globoid aneurysm” of the right MCA who
presented with rapidly progressing left hemiparesis and stupor
and died after the aneurysm was explored, but not resected.
At autopsy, the right hemisphere was edematous and swollen
with evidence of uncal herniation (29). Sadik et al. reported
a patient with a “globoid” MCA aneurysm that presented
with papilledema and acute neurological deterioration. At
operation, massive swelling of the brain was found. and there
was no evidence of bleeding. The patient died postoperatively

GIANT ANEURYSMS AND BRAIN SWELLING 575

in spite of a frontal lobectomy done for decompression. At
autopsy, the aneurysm was partially thrombosed and there
was massive hemispheric edema and uncal herniation (21).
One of the patients reported by Bull presented with rapidly
progressing dementia, papilledema, and eventually stupor. At
operation, a giant right MCA aneurysm was excised. The
patient died 24 hours later. At autopsy, massive right hemi-
spheric swelling with subfalcial herniation was evident (2).
Within his large series of giant aneurysms, Drake mentions a
patient with a giant MCA aneurysm who developed “devas-
tating postoperative cerebral swelling with hemiplegia, aphasia
and stupor” after simple exploration with evacuation of
thrombus from the sac of a partially thrombosed aneurysm
(6).

The mechanism whereby these aneurysms produce massive
hemispheric edema is unclear. Certainly, most giant aneuryms
are not associated with significant brain edema. Indeed, sev-
eral recent reports concerning the differential diagnosis be-
tween giant aneurysms and tumors by CT scan emphasize
that aneurysms are not associated with edema and that this is
an important point in differentiating aneurysms from tumors
(3, 5, 8, 15, 19). Whittle et al., however, noted that in 2 of
their 25 patients with giant aneurysms the CT scan showed
contiguous cerebral edema not related to aneurysmal rupture
(30). Shubiger and colleagues also noted the presence of
“perifocal lucency with finger-like extensions into the white
matter” in 3 of their 10 cases of giant aneurysm studied by
CT scan (23). They postulated that the low density areas
probably represented local atrophy or ischemia because in |
patient steroids did not change the appearance of the CT
scan. Segal and McLaurin, however, reported a patient with
a giant serpentine aneurysm in whom the presenting symp-
toms improved with steroid treatment, which led them to
infer that the symptoms were due to surrounding brain edema
(25). In our 2 cases, as well as in the others briefly alluded to
earlier in the discussion, the presence of a mass effect much
larger than could be attributed to the size of the aneurysm per
se indicated that indeed the problem was brain swelling and
not atrophy. In each of these cases, the aneurysm was massive,
usually in the range of 5 to 7 cm in diameter. It seems that,
at least in aneurysms, size is an important factor in determin-
ing the presence and degree of cerebral edema. In brain
tumors, size is also, of course, an important determinant of
the amount of surrounding edema. However, other factors
such as rate of growth and histology seem to be more impor-
tant (4, 26).

All of the aneurysms that presented with massive cerebral
edema were partially thrombosed. Whether intraluminal
thrombosis is a causal factor in the edema in these cases is
not certain. It seems clear that aneurysms can swell acutely
and produce abrupt symptoms and signs of compression as
they thrombose (7, 10, 17, 18, 20, 31). It may be that, in these
cases, as implied by Drake in his comment on the case of a
giant MCA aneurysm, “the brain must have been at the limits
of acceptable compression” (6). Under these circumstances,
even a slight further abrupt increase in size as a result of
thrombosis may result in a breakdown of autoregulation, with
cerebral vasodilation and swelling. Whether ischemia also
plays a role remains speculative, Certainly, in some of these
cases (see Fig. 5B) the branches of the MCA seem to be
stretched and compressed by the aneurysm. Ischemia could
lead to a breakdown of the blood-brain barrier with subse-
quent edema. Acute thrombosis secondary to compression of
one of the major divisions or embolism from an intraaneu-
rysmal clot are other mechanisms that could lead to acute
ischemia and explain the rather abrupt deterioration in some
of these cases (1, 22, 24).

576 HEROS AND KOLLURI

_—_——_,

gITT S.C

a y ~
the stretching of the MCA divisions around the aneurysm (B).

We are not in a position to comment about the treatment
of these massive aneurysms. One of our patients died and the
second is neurologically devastated as a result of our surgical
intervention. Preoperatively, one of the patients had signs of
uncal herniation in spite of maximal medical therapy and the
second was deteriorating rapidly. Therefore, we think that
both would have done poorly without a surgical attempt.
Furthermore, in each case the mass effect of the aneurysm
was the problem and simple hunterian ligation without aneu-
rysmal excision, even if tolerated, would not have been likely
to reverse the neurological deficits. Retrospectively, we think
a functional bypass, preferably a saphenous vein interposition
graft, to each main division of the MCA before the aneurysm
was tackled directly could have made a difference. However,
in each of the other similar reported cases, the outcome,
regardless of treatment, was bad. It is possible that, at this
stage of massive brain swelling, these patients were doomed
and no surgical intervention could have helped. Clearly, our
message in reporting these two cases is the need to treat these
aneurysms definitively before they reach such a stage. Both
of our patients were initially seen when there was no signifi-
cant brain swelling and when it was possible that the aneu-
rysms could have been dealt with satisfactorily.

ACKNOWLEDGMENTS

The authors thank Doctor R. G. Ojemann for his generous
advice and assistance in the management of these two difficult
patients,

Received for publication, March 6, 1984: accepted, May 23, 1984.
Reprint requests: Roberto C. Heros, M.D.. Neurosurgical Service,
Massachusetts General Hospital, Boston, Massachusetts 02114.

REFERENCES

1, Antunes JL. Correll JW: Cerebral emboli from intracranial aneu-
rysms. Surg Neurol 6:7-10, 1976.

2. Bull J: Massive aneurysms at the base of the brain. Brain 92:535-
570, 1969.

Neurosurgery, Vol. 15, No. 4

Fic. 5. Case 2. Lateral (4) and AP (B) left carotid injection shows the partially thrombosed MCA aneurysm and a large mass effect. Note

. Byrd SE, Bentson JR, Winter J, Wilson GH, Joyce PW, O’Con-

nor L: Giant intracranial aneurysms simulating brain neoplasms
on computed tomography. J Comput Assist Tomogr 2:303-307,
1978.

. Challa VR, Moody DM, Marshall RB, Kelly DL Jr: The vascular

component in meningiomas associated with severe cerebral
edema. Neurosurgery 7:363-368, 1980.

. Cohen AR, Aleksic S, Budzilovich GN, Pinto RS, Flamm ES:

Giant intracranial aneurysm presenting as a posterior fossa mass.
Surg Neurol 20:160-164, 1983.

. Drake CG: Giant intracranial aneurysms: Experience with sur-

gical treatment in 174 patients. Clin Neurosurg 26:12-95, 1979.

. Ferguson GG, Drake CG: Carotid-ophthalmic aneurysms: Visual

abnormalities in 32 patients and the results of treatment. Surg
Neurol 16:1-8, 1981.

. Golding R, Peatfield RC, Shawdon HH, Edwards JMR: Com-

puter tomographic features of giant intracranial aneurysms. Clin
Radiol 31:41-48, 1980.

. Heiskanen O, Nikki P: Large intracranial aneurysms. Acta Neu-

rol Scand 38:195-208, 1962.

. Heros RC, Nelson PB, Ojemann RG, Crowell RM, DeBrun G:

Large and giant paraclinoid aneurysms: Surgical techniques,
complications, and results. Neurosurgery 12:153-163, 1983.

. Hosobuchi Y: Direct surgical treatment of giant intracranial

aneurysms. J Neurosurg 51:743-756, 1979.

. Maxwell RE, Chou SN: Aneurysmal tumors of the basifrontal

region. J Neurosurg 46:438-445, 1977.

. Morley TP, Barr HWK: Giant intracranial] aneurysms: Diagnosis,

course, and management. Clin Neurosurg 16:73-94, 1969.

. Nadjmi M, Ratzka M, Wodarz M: Giant aneurysms in CT and

angiography. Neuroradiology 16:284-286, 1978.

. O'Neill M, Hope T, Thomson G: Giant intracranial aneurysms:

Diagnosis with special reference to computerised tomography.
Clin Radiol 31:27-39, 1980.

. Onuma T, Suzuki J: Surgical treatment of giant intracranial

aneurysms. J Neurosurg 51;33-36, 1979.

. Peerless SJ. Durward QJ: Comment on Heros et al (Ref. 10).
. Pia HW, Zierski J: Giant cerebral aneurysms: Problems in treat-

ment, in Pia HW, Langmaid C, Zierski J (eds): Cerebral Aneu-
ryyms: Advances in Diagnosis and Therapy. Berlin, Springer-
Verlag. 1979, pp 336-342.

. Pinto RS. Kricheff II, Butler AR, Murali R: Correlation of

computed tomographic, angiographic, and neuropathological
5-92, 1979,

changes in giant cerebral aneurysms. Radiology 132:

October 1984

20. Pozzati E, Nuzzo G, Gaist G: Giant aneurysm of the pericallosal
artery: Case report. J Neurosurg 57:566-569, 1982.

21. Sadik AR, Budzilovich GN. Shulman K: Giant aneurysm of
middle cerebral artery: A case report. J Neurosurg 22:177-181,
1965.

22. Sakaki T, Kinugawa K. Tanigake T. Miyamoto S, Kyoi K.
Utsumi S: Embolism from intracranial aneurysms. J Neurosurg
53:300-304, 1980.

23. Schubiger O, Valavanis A, Hayek J: Computed tomography in
cerebral aneurysms with special emphasis on giant intracranial
aneurysms. J Comput Assist Tomogr 4:24-32. 1980.

24. Scott RM, Ballantine HT Jr: Spontaneous thrombosis in a giant
middle cerebral aneurysm: Case report. J Neurosurg 37:36 |-362,
1972.

25. Segal HD, McLaurin RL: Giant serpentine aneurysm: Report of
two cases. J Neurosurg 46:1 15-120, 1977.

26. Smith HP, Challa VR, Moody DM, Kelly DL Jr: Biological
features of meningiomas that determine the production of cere-
bral edema. Neurosurgery 8:428-433, 1981.

27. Sonntag VKH, Yuan RH, Stein BM: Giant intracranial aneu-
rysms: A review of 13 cases. Surg Neurol 8:81-84, 1977.

28. Sundt TM Jr, Piepgras DG: Surgical approach to giant intracra-
nial aneurysms: Operative experience with 80 cases. J Neurosurg
51:731-742, 1979,

29, Terao H, Muraoka I: Giant aneurysm of the middle cerebral
artery containing an important blood channel: Case report. J
Neurosurg 37:352-356, 1972.

30. Whittle IR, Dorsch NW, Besser M: Giant intracranial aneurysms:
Diagnosis, management and outcome. Surg Neurol 21:218-230,
1984,

31. Whittle IR, Dorsch NW, Besser M: Spontaneous thrombosis in
giant intracranial aneurysms. J Neurol Neurosurg Psychiatry
45:1040-1047, 1982.

COMMENT

Drs. Heros and Kolluri have reported in detail two cases
which typify the problems encountered with the management
of giant aneurysms arising at the bifurcation of the middle
cerebral artery. They also comment about the CT finding of
edema surrounding the mass lesion and appropriately indicate
that, in the past, edema around giant aneurysms has not been
considered to be a typical finding.

Both of the patients underwent carotid ligation and, in
these particular cases, the ligation had little effect and prob-
ably was ill-advised. We reserve internal carotid artery ligation
for giant aneurysms of the internal carotid artery that cannot
be repaired primarily. In 210 giant aneurysms, we have used
internal carotid ligation alone or in combination with a bypass
in 59 cases. The others have been repaired primarily. Thus,
we strongly advise that internal carotid ligation be considered
only for certain aneurysms from the internal carotid artery
itself and that it not be used for aneurysms elsewhere in the
system.

GIANT ANEURYSMS AND BRAIN SWELLING 577

We agree with Dr. Heros that the approach of choice in
these cases would have been a direct approach to the aneurysm
when it first presented. In our experience, when giant aneu-
rysms become symptomatic they continue to expand and
increase in size. Unless the patient is elderly or for other
reasons is not a good candidate, these aneurysms should be
operated. A prophylactic bypass before the operation is fea-
sible in some cases. In fact, we treated one patient in whom
the giant aneurysm thrombosed along with the main trunk of
the middle cerebral artery after a double-barreled temporal
artery to middle cerebral artery bypass. The aneurysm was
thereafter resected and the patient returned to full employ-
ment. In most cases, however, we have explored the aneu-
rysm, temporarily occluded the middle cerebral artery, per-
formed a thrombectomy in the aneurysm, and converted the
base for a channel for blood. In some cases, because of the
location of the branches of the middle cerebral artery, it is
not possible to convert the base of the aneurysm to a channel
for blood because of the distance between the inflow from the
main trunk of the middle cerebral artery and the outflow to
its two major branches. In one patient, we were successful in
converting this situation to a good result by anastomosing the
main trunk of the middle cerebral artery to one of the major
limbs of the middle cerebral artery complemented with an
end-to-side anastomosis between the second limb and the first
limb.

Unfortunately, however, we have had our share of disap-
pointment and grief with aneurysms in this location. A recent
case very similar to the ones described by Dr. Heros comes
to mind. This patient had undergone carotid ligation for a
giant middle cerebral artery aneurysm a number of years
earlier and had had a failed bypass procedure several months
before referral. The aneurysm appeared very similar to the
aneurysm illustrated in Figure 4. Although we were successful
in resecting the aneurysm, we could not find an adequate
recipient vessel and we were not successful in reconstructing
the major vessels at the base of the aneurysm. The patient
had a severe preoperative right hemiparesis but good speech
function. She improved for 3 days and then rapidly deterio-
rated, dying approximately | week after operation from mas-
sive edema of the entire hemisphere.

Our recent experience suggests that these giant aneurysms
are prone to be associated with a considerable amount of
edema and that the presence or absence of edema cannot
therefore be used to distinguish these mass lesions from a
tumor. In fact, a number of the middle cerebral artery aneu-
rysms that we have seen have been referred to us as sphenoid
wing meningiomas because of the surrounding edema.

Thoralf M. Sundt, Jr.. M.D.
Rochester, Minnesota