AUTHOR(S): Levy, A. Stewart, M.D.;
Lillehei, Kevin O., M.D.; Rubinstein, David, M.D.;
Stears, John C., M.D.
Department of Surgery, Division of Neurosurgery
(ASL, KOL), Department of Radiology, Division of
Neuroradiology (DR, JCS), University of Colorado
Health Sciences Center, Denver, Colorado
Neurosurgery 36; 183-188, 1995
ABSTRACT: CYSTICERCOSIS IS THE most
common parasitic disease affecting the central
nervous system. Stroke is a recognized complication
of neurocysticercosis, occurring in 2 to 12% of cases,
mostly in the form of small lacunar infarcts. We
report a case of hemiparesis and aphasia in a 51-yearold Hispanic woman, which was secondary to
complete occlusion of the left internal carotid and
bilateral anterior cerebral arteries. Magnetic
resonance imaging demonstrated the presence of
enhancing subarachnoid material surrounding these
occluded cerebral arteries, providing antemortem,
noninvasive documentation of the inflammatory
meningeal cysticercotic reaction that was presumably
responsible for the occlusive arteritis causing the
cerebral infarction. This represents the third reported
case of internal carotid artery occlusion and the first
reported case of anterior cerebral artery occlusion
secondary to neurocysticercosis.
KEY WORDS: Cysticercosis; Hydrocephalus;
Stroke
Cysticercosis is the most common parasitic disease
affecting the central nervous system. Seizures,
hydrocephalus, and stroke are the usual presenting
complications, with stroke or focal neurological
deficit as the primary manifestation of
neurocysticercosis (NCC) in 2-12% of cases (5,7-9,12,
14,15,17)
. Most instances of cerebral infarction
associated with NCC involve occlusive arteritis in
small perforating vessels, resulting in lacunar infarcts
(1,4-8,15)
. Only six cases of cerebral infarction from the
occlusion of a major intracranial artery in patients
with NCC have been reported--four cases of middle
cerebral artery (MCA) occlusion (13,16) and two cases
of internal carotid artery (ICA) occlusion (11,17).
We report the third case of complete occlusion of
the ICA resulting from inflammatory arteritis of
subarachnoid cysticercosis. In the same patient, we
demonstrate, for the first time, bilateral occlusion of
the A2 segments of the anterior cerebral arteries
(ACA) from an adjacent inflammatory subarachnoid
lesion in the interhemispheric fissure. The magnetic
resonance imaging (MRI) characteristics of these
NCC inflammatory cysts surrounding the arteries in

the subarachnoid space are detailed.
CASE REPORT
A 51-year-old right-handed Hispanic woman
presented to the emergency room at our institution
with a history of increasing weakness on the right
side and difficulty with speech occurring over several
days. She had recently moved from Guadalajara,
Mexico, where she had been diagnosed with NCC 6
weeks before admission to our facility. At the time of
the initial diagnosis, she was observed to have a mild
right hemiparesis. A computed tomographic (CT)
scan revealed mild-to-moderate hydrocephalus, but
no evidence of cerebral infarction (Fig. 1A). She was
treated with albendazole, and her hemiparesis
improved.
At admission to our institution, she reported a 4day history of an increased right hemiparesis and a
new aphasia. She denied any headache, nausea, or
emesis, but did report a fever that reached 101°F 4
days before admission. Her medical history was
negative for hypertension, cardiac disease, or
diabetes, and there was no significant family history
of ischemic cerebrovascular disease.
At admission, her temperature was 37.0°C, her
heart rate was 72, her blood pressure was 100/60, and
her respiratory rate was 16. Her general physical
examination was normal, including bilateral normal
carotid pulses without bruits.
A neurological examination revealed an alert
Hispanic woman with a nonfluent aphasia. She was
unable to name objects or repeat words and could
only follow simple one-step commands. Her pupils
measured 3 mm and were reactive; her visual fields
were full; and her ocular movements were intact. She
was observed to have lower right facial weakness,
consistent with a left hemispheric central facial palsy.
Her motor power was 5/5 on the left, 2 to 3/5 in the
right arm and 3 to 4/5 in the right leg. Her deep
tendon reflexes were slightly increased on the right,
and the patient exhibited a right Babinski reflex. Her
sensation to light touch and pin prick was intact
bilaterally. Her electrolyte, glucose, and cholesterol
levels were normal, as was her complete blood count;
her erythrocyte sedimentation rate was 30, and the
cerebrospinal fluid cysticercosis immunoblot assay
was positive.
A CT scan on the day of admission (Fig. 1B)
demonstrated increased hydrocephalus, compared
with the CT scan from Mexico obtained 1 month
earlier (Fig. 1A). Scattered small calcified lesions
were seen throughout the cerebral parenchyma. There
were enhancing hypodensities in the left MCA
distribution (Fig. 1B and C), consistent with subacute
infarcts, and nonenhancing low density in the left
frontal white matter. Enhancing material in the region
of the subarachnoid ICA and the proximal ACAs was
also noted (Fig. 1D).
The patient was admitted to the surgical intensive
care unit and began receiving dexamethasone
intravenously, 10 mg every 6 hours; gentle volume
expansion with intravenous administration of 25%
albumin, 25 gm every 8 hours, was initiated. She also
began receiving praziquantel, 900 mg orally, three

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Neurosurgery 1992-98
January 1995, Volume 36, Number 1
183 Subarachnoid Neurocysticercosis with
Occlusion of the Major Intracranial Arteries: Case
Report
Case Report

DISCUSSION
With the increasing numbers of immigrants to the
United States from regions in which cysticercosis is
endemic, it is imperative that we familiarize ourselves
with the diverse clinical syndromes of NCC. Most
physicians with an interest in neurological disorders,
especially those in the West and Southwest, readily
recognize the classic aspects of CT scans in patients
with NCC and are quite familiar with the presentation
and management of patients with hydrocephalus or
seizures associated with NCC. However, in patients
with ischemic cerebrovascular events, NCC is seldom
considered in the differential diagnosis; concern for
patients developing a stroke during the course of
treatment for NCC, as occurred in this case, rarely
arises.
In large series of patients with NCC, the reported
incidence of stroke ranges from 2 to 12% (5,7-9,12,14,15,
17)
. Conversely, in endemic regions, cysticercosis has
been considered as the cause of stroke in 2 to 7% of

cases in large stroke series (1,3). Alarcon et al. (2) found
cerebral cysticercosis to be an independent risk factor
for stroke in a group of patients under the age of 65 in
Ecuador. However, with stroke defined simply as the
sudden onset of focal neurological deficit, some
patients have been diagnosed with an NCCassociated stroke without any evidence of anatomical
cerebral infarction by radiographic studies or autopsy
(1,3,12)
. In some patients, a focal neurological deficit
may be explained by the presence of a large
intraparenchymal NCC cyst and the resulting mass
effect, with no indication of true cerebral infarction
(12,15,17)
. Of the cases with clear documentation of
cerebral infarction, small lacunar infarcts are
decidedly the most common cerebrovascular
complication of NCC (1,4-8,15).
Only six cases of stroke associated with occlusion
of a major intracranial artery in a patient with NCC
have been reported (Table 1); four involved the MCA
(13,16)
, and two involved the ICA (11,17). We report the
third case of complete occlusion of the ICA from
cysticercotic arteritis. This is the first such case
involving the ACA. Presumably, occlusion of these
arteries has occurred as a result of the intense
inflammatory reaction associated with the adjacent
cysticerci in the subarachnoid space. A dense
inflammatory exudate is believed to surround the
arteries of the circle of Willis in patients with basilar
meningitis secondary to cysticercosis. The vessel
walls are then invaded by inflammatory cells,
resulting in an occlusive endarteritis, with thickening
of the adventitia, fibrosis of the media, and
endothelial hyperplasia (7,10,13,17).
Recently, it has been recognized that patients with
meningeal NCC may develop a cerebral infarction
during a course of anticysticercal drug therapy. In at
least two reported cases of stroke associated with
NCC, the cerebral infarction occurred while the
patient was receiving praziquantel (5,7). In our case,
the stroke occurred while the patient was undergoing
therapy with albendazole. It is possible that the
meningeal inflammatory reaction, leading to
occlusive endarteritis, is intensified by the
anticysticercal drug as a result of acute destruction of
the parasites in the subarachnoid space and the
subsequent host inflammatory reaction. It would
seem prudent, as has been suggested by others (5,7,9),
to administer corticosteroids during antibiotic
treatment for meningeal cysticercosis. Some authors
have recommended using steroids in conjunction
with anticysticercal drugs only after patients have
demonstrated clinical signs and symptoms of an
increased inflammatory reaction, such as fever,
headache, nausea/vomiting, seizures, or increased
neurological deficit (8,9). We think it is appropriate to
await these clinical signs and symptoms before
adding steroids when treating parenchymal
cycticercosis, because, in this setting, local
parenchymal inflammation and edema is the likely
cause of patient deterioration, and this is usually
readily reversible with steroid treatment. However, in
cases of subarachnoid NCC, we think that the
significant risk of neurological deterioration from
inflammatory arteritis, with subsequent stroke during

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

times a day. The morning after admission, a cerebral
angiogram was performed that revealed complete
occlusion of the left ICA at the level of the anterior
choroidal artery (Fig. 2A-C). Bilateral occlusion of
the A2 segments of the ACAs was noted on the right
ICA injection (Fig. 2D), and on late arterial phase
films, the right ACA distribution demonstrated
retrograde filling from the right MCA collaterals.
After the angiogram, a ventriculoperitoneal shunt was
placed for treatment of the hydrocephalus. After
ventriculoperitoneal shunt placement, more
aggressive volume expansion was performed and the
patient demonstrated improvement with respect to her
hemiparesis and aphasia. An echocardiogram was
normal.
After the ventriculoperitoneal shunt placement, an
MRI scan with gadolinium was obtained that revealed
enhancing subarachnoid material surrounding the left
ICA from its entry into the subarachnoid space to its
bifurcation. The expected flow void of the ICA was
diminished in diameter proximally and absent
throughout the remainder of its course in the
subarachnoid space (Fig. 3A-D). Enhancing material
was also seen in the interhemispheric fissure in the
region of the A2 segments of the ACAs (Fig. 4). The
left MCA distribution infarcts enhanced as they did
on the CT scan. The ventricles were slightly
decreased in size, compared with the CT scan
obtained before the placement of the
ventriculoperitoneal shunt. During the ensuing
weeks, the treatment with dexamethasone was tapered
slowly and changed to prednisone; the patient was
then weaned from the prednisone after the completion
of a 4-week course of praziquantel.
At a 2-month follow-up, the patient demonstrated
significant neurological improvement and was able to
name objects and to follow three-step commands. Her
right hemiparesis had improved significantly, with
her gait now normal, but she continued to
demonstrate a moderate weakness in her right hand.
A follow-up MRI scan revealed a normal ventricular
size and persistent signal change in the region of the
left MCA infarct.

with neurocysticercosis.
Received, March 21, 1994.
Accepted, July 28, 1994.
Reprint requests: A. Stewart Levy, M.D., Division
of Neurosurgery, University of Colorado Health
Sciences Center, 4200 E. Ninth Avenue, C-307,
Denver, CO 80262.
REFERENCES: (1-17)
1.
2.

3.
4.
5.
6.
7.
8.
9.

10.

11.
12.
13.

14.
15.

16.

Alarcon F, Hidalgo F, Moncayo J, Vinan I,
Duenas G: Cerebral cysticercosis and stroke.
Stroke 23:224-228, 1992.
Alarcon F, Vanormelingen K, Moncayo J,
Vinan I: Cerebral cysticercosis as a risk factor
for stroke in young and middle-aged people.
Stroke 23:1563-1565, 1992.
Barinagarrementeria F, Cantu C:
Neurocysticercosis as a cause of stroke.
Stroke 23:1180-1181, 1992 (letter).
Barinagarrementeria F, Del Brutto OH:
Neurocysticercosis and pure motor
hemiparesis. Stroke 19:1156-1158, 1988.
Barinagarrementeria F, Del Brutto OH:
Lacunar syndrome due to neurocysticercosis.
Arch Neurol 46:415-417, 1989.
Barinagarrementeria F, Del Brutto OH, Otero
E: Ataxic hemiparesis from cysticercosis.
Arch Neurol 45:246, 1988 (letter).
Del Brutto OH: Cysticercosis and
cerebrovascular disease: Review. J Neurol
Neurosurg Psychiatry 55:252-254, 1992.
Del Brutto OH, Sotelo J: Neuroscysticercosis:
An update. Rev Infect Dis 10:1075-1087,
1988.
Ernest MP, Reller LB, Filley CM, Grek AJ:
Cysticercosis in the United States: 35 cases
and a review. Rev Infect Dis 9:961-979,
1987.
Escobar A: The pathology of
neurocysticercosis, in Palacios E, RodriguezCarbajal J, Taveras JM (eds:) Cysticercosis of
the Central Nervous System. Springfield,
Charles C Thomas, 1983, pp 27-54.
McCormick GF, Giannotta SL, Zee C-S,
Fisher M: Carotid occlusion in cysticercosis.
Neurology 33:1078-1080, 1983.
McCormick GF, Zee C-S, Heiden J:
Cysticercosis cerebri: Review of 127 cases.
Arch Neurol 39:534-539, 1982.
Rodriguez-Carbajal J, Del Brutto OH,
Penagos P, Huebe J, Escobar A: Occlusion of
the middle cerebral artery due to cysticercotic
angiitis. Stroke 20:1095-1098, 1989.
Scharf D: Neurocysticerosis: Two hundred
thirty-eight cases from a California hospital:
Arch Neurol 45:777-780 1988.
Sotelo J, Guerrero V, Rubio F:
Neurocysticercosis: A new classification
based on active and inactive forms. Arch
Intern Med 145:442-445, 1985.
terPenning B, Litchman CD, Heier L: Bilateral
middle cerebral artery occlusions in

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

antibiotic therapy, warrants the routine use of
corticosteroids in patients demonstrated to have
extensive disease in the basilar subarachnoid space.
In such patients, waiting for clinical signs of
neurological deterioration before administering
steroids may result in an irreversible deficit or even
death from cerebral infarction. Therefore, our
preference in the management of subarachnoid NCC
has been the use of anticysticercal drugs along with
dexamethasone at the onset of therapy.
We have reserved surgical intervention for patients
in whom there is an acute obstruction to the flow of
cerebrospinal fluid caused by a focal cysticercotic
lesion or for patients with a significant focal
neurological deficit secondary to a large
subarachnoid or parenchymal cysticercus with mass
effect. In these situations, surgery is the treatment of
choice; for patients with evidence of residual disease,
antibiotics are used, with or without the addition of
steroids, according to the factors discussed above.
The benefit of surgery to remove subarachnoid
lesions in patients at risk for vascular occlusion is
unclear. McCormick et al. (11) reported a case of
carotid artery occlusion from NCC that was managed
by direct surgical excision of a cluster of cysts from
around the right ICA in the subarachnoid space.
Despite the fact that the ICA was already occluded
and no attempt was made to reopen it, the patient did
well and recovered from the left hemiparesis,
apparently as a result of improvement in the cerebral
perfusion pressure that occurred by keeping the
patient recumbent.
Our goal in the management of patients with NCC
is to recognize those at risk for stroke before the
development of neurological deficits. We have shown
that a gadolinium enhanced MRI scan can be used to
identify patients with extensive inflammatory basilar
NCC meningitis who may be at increased risk for
stroke during therapy with anticysticercal drugs;
these patients should, therefore, be considered as
candidates for treatment with adjuvant
corticosteroids.
A review of the literature reveals only one reported
case in which MRI was employed in the evaluation of
a patient with a stroke related to the occlusion of a
major intracranial vessel from NCC meningitis (16). In
this report of a patient with bilateral MCA occlusions,
terPenning et al. (16) demonstrated the presence of a
cyst in the region of the MCA bifurcation, but no
gadolinium enhanced scans were included. In our
case, gadolinium MRI demonstrated enhancing
material in the subarachnoid space surrounding the
occluded left ICA as well as an enhancing lesion
adjacent to the proximal A2 segments of the ACAs.
This focal subarachnoid enhancement, when
correlated with the occlusion of the adjacent vessels
and a positive cerebrospinal fluid cysticercosis
immunoblot assay, is consistent with an
inflammatory exudate associated with a cluster of
NCC cysts. Thus, with enhanced MRI, we have
provided clear antemortem, noninvasive
documentation of the inflammatory meningeal
cysticerci presumably responsible for the occlusive
endarteritis causing cerebral infarction in a patient

neurocysticercosis. Stroke 23:280-283, 1992.
Torrealba G, Del Villar S, Tagle P, Arriagada
P, Kase CS: Cysticercosis of the central
nervous system: Clinical and therapeutic
considerations. J Neurol Neurosurg
Psychiatry 47:784-790, 1984.

COMMENTS
This is a report of a rare complication of
subarachnoid neurocysticercosis and stroke.
Cysticercosis, especially subarachnoid cysticercosis,
should be considered as a cause of ischemic
cerebrovascular events in areas where there is an
increasing influx of immigrants from the endemic
areas. This report provided an excellent discussion on
the treatment of subarachnoid cysticercosis. Surgery
is indicated when the cerebrospinal fluid pathway is
obstructed or when a large cyst is compressing on
vital structures such as the brain stem. From our
experience, gadolinium enhanced magnetic resonance
images may provide valuable information in
predicting whether surgery will be successful.
Enhancement of the cyst wall indicates the presence
of adhesion and reaction to adjacent tissue, and
attempts to remove these cysts surgically may not
succeed. A nonenhancing cyst disclosed by magnetic
resonance images is easily removed at surgery.
Medical treatment with anticysticercal drugs is a
controversial issue. As stated by the authors, patients
with meningeal cysticercosis may develop a cerebral
infarction during a course of anticysticercal drug
therapy. We concur with the authors that the
significant risk of neurological deterioration from
inflammatory arteritis, with subsequent stroke during
antibiotic therapy, warrants the routine administration
of corticosteroids in patients demonstrated to have
extensive disease in the basilar subarachnoid space.
We believe medical treatment merely accelerates the
degeneration of cysticercosis cysts. Whether patients
will benefit from such treatment in the long run
requires a well-controlled prospective study.
Chi-Shing Zee
Los Angeles, California
Levy et al.'s report brings up a frequent clinical
situation in which Latin American neurosurgeons are
involved everyday: circulatory complications of
subarachnoid neurocysticercosis resulting from
inflammatory and scarring reactions in major or
minor vessels. Because it is such a common situation
in our environment, we are used to living with it, so
we have scarcely felt the need of publishing such an
important issue. The relevance of this report is that it
puts in "black and white" a very common and usually
deleterious complication of this disease, with the
example of a very characteristic and well-documented
case.
Another important aspect that the authors
emphasize is the increase of neurological symptoms
and signs after the antiparasite treatment as a result of
the liberation of enzymes when the parasites die,
which should always be taken in consideration when
a patient is going to be treated with drugs. This is true

in any of the different locations of living parasites
and may increase parenchymal, cranial nerve, or
vascular signs and symptoms. This article is a good
example of how to use one clinical case to remark
upon the important clinical features of a disease.
Ignacio Madrazo
Mexico City, Mexico
REFERENCES: (1)
1.

Madrazo I, Flisser A: Cysticercosis, in
Apuzzo MLJ (ed): Brain Surgery:
Complication Avoidance and Management.
New York, Churchill Livingstone, Inc., 1993,
pp 1419-1430.

This case report makes several points that can be
emphasized. First, most centers in the United States
that treat immigrants from endemic zones would most
likely recognize the diagnosis of cysticercosis from
the computed tomographic scan showing punctate
parenchymal calcifications. However, it would not be
generally recognized by the average practitioner in
the United States, neurologically oriented or not, that
a stroke might be the result of cysticercosis. This
report admirably documents such a case, and the
images also show the extent of cysticercosis in the
subarachnoid space around the sella. There is nothing
specific in this appearance on the magnetic resonance
imaging scans, computed tomographic scans, or
angiograms, which could be attributable to other
lesions, e.g., tuberculosis, sarcoidosis, or other
inflammatory problems. One of the beauties of
magnetic resonance scanning is that it not only lays
out the symptom-causing abnormality, such as the
deep and superficial brain enhancements secondary to
the vascular occlusion, but it also goes more deeply
than that, when it is appropriate, to outline the
character and extension of meningeal or subarachnoid
space disease. This is a major contribution, as is the
better analysis of other meningoencephalitides.
It is easy to see how this patient could have
developed endarteritis, which we know can be caused
by other granulomatous processes, and it is just as
easy to see from the images how something such as
an orbital apex syndrome, for instance, could be due
to this disease process.
There are a couple of interesting features, one of
which is that this patient began receiving steroids
concomitant with the institution of specific therapy,
and, despite the steroids, worsened somewhat.
However, it might be that the steroids protected
against even more worsening, by virtue of the fact
that the left internal carotid artery looks a great deal
worse on the angiogram performed at the start of
therapy than it did on the magnetic resonance
imaging scan performed some months later.
A final point is the importance of simultaneously
administering steroids as definitive therapy is started
and especially making the distinction between
parenchymal lesions and subarachnoid space lesions.

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

17.

The authors' reasoning is lucid and, I think,
contributes to the reader's information bank. Whether
others are correct in stating that parenchymal
neurocysticercosis should not be treated until
symptoms appear is not resolved, but that is another
story.

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

David O. Davis
Washington, District of Columbia

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Figure 1. A, CT scan from Guadalajara, Mexico,
demonstrates moderate hydrocephalus and
calcification (arrowhead). B, CT scan at the time of
admission to our facility, performed 6 weeks after the
CT scan from Mexico, demonstrates progression of
hydrocephalus and a new region of hypodensity
involving the caudate, internal capsule, and lentiform
nuclei (straight arrow). Also noted are scattered
parenchymal calcifications (arrowheads). C,
intravenous administration of contrast medium
reveals enhancement around the hypodensity in the
left basal ganglia (curved arrow), consistent with
subacute infarction. D, diffuse enhancement of the
subarachnoid space surrounding the left ICA and
both ACAs is also demonstrated (small arrowheads).

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Figure 2. Anteroposterior (A) and lateral (B and C)
radiographic views of the left carotid arteriogram
demonstrating complete occlusion of the ICA at the
level of the anterior choroidal artery (arrows) and a
normal bulb. Anteroposterior projection of the right
carotid arteriogram (D) reveals bilateral occlusion of
the A2 segments of the ACAs (arrowheads) and
stenosis of the right A1 segment.

Redistribution of this article permitted only in accordance with the publisher’s copyright provisions.

Figure 3. Axial (A and B) and coronal (C and D)
MRI scans with gadolinium enhancement
demonstrate diffuse enhancing subarachnoid material
(arrowheads) surrounding the left ICA from its entry
into the subarachnoid space to its bifurcation.
Narrowing of the ICA flow void is seen proximally
(A), with complete absence of the expected ICA flow
void more distally (B-D). Note also the enhancing
MCA distribution infarctions (straight arrows).

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Figure 4. Axial gadolinium enhanced MRI scan
reveals densely ring-enhancing structure in the
anterior interhemispheric fissure (curved arrow) in
the region of the occluded A2 segments of the ACAs.

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Table 1. Summary of Major Intracranial Artery
Occlusions Secondary to Neurocysticercosisa