CASE REPORT
cerebellar hemorrhage, cysticercosis, central nervoussystem
cysticercosis, central nervous system, cerebellar hemorrhage

Central Nervous System Cysticercosis
Simulating an Acute Cerebellar Hemorrhage
We report the case of a Mexican man who suddenly developed severe occipital headache, vomiting, vertigo, and ataxia. Neurologic examination
showed nystagmus and cerebellar findings. Computed tomography of the
brain demonstrated a large left cerebellar cystic lesion consistent with the
diagnosis of cysticercosis. The patient was treated with dexarnethasone and
praziquantel and required surgical removal of the lesion to prevent herniation. He recovered without neurologic sequelae. The abrupt onset of cerebellar findings is an unusual presentation of this disease. Central nervous
system cysticercosis is being recognized with increasing frequency in the
United States, where it is found primarily in Hispanic and Asian immigrants. The literature of central nervous system cysticercosis is reviewed and
the pathogenesis, clinical presentation, and therapy are discussed. [Catapano MS, Marx JA: Central nervous system cysticercosis simulating an
acute cerebellar hemorrhage. Ann Emerg Med July 1986;15:847-849.]
INTRODUCTION
Infestation of the central nervous system with Cysticercus cellulosae, the
larval form of the pork tapeworm, Taenia solium, is a prevalent worldwide
disease. ~-5 CNS cysticercosis presents with seizures, symptoms of increased
intracranial pressure, focal neurologic deficits, neuropsychiatric disorders, or
visual difficulties. The disease generally follows a chronic course but may
present with the sudden onset of symptoms, s-lo
In this report we present a patient who abruptly developed the signs and
symptoms of a cerebellar mass.

Michael S Catapano, MD*
John A Marx, MDt
Denver, Colorado
From the Denver General Hospital
Residency* and the Department of
Emergency Medicine,l- Denver General
Hospital, Denver, Colorado.
Received for publication September 3,
1985. Revision received December 12,
1985. Accepted for publication January 7,
1986.
Address for reprints: John A Marx, MD,
Department of Emergency Medicine,
Denver General Hospital, 777 Bannock
Street, Denver, Colorado 80204.

CASE REPORT
A 58-year-old Hispanic man presented with a three-hour history of severe
occipital headache, nausea, vomiting, vertigo, and difficulty walking because
of loss of balance. He had a ten-year history of mild occipital headaches, but
these never were associated with other symptoms and did not require medical attention. He had a four-year history of hypertension and was treated
with a diuretic. There was no history of intestinal tapeworm infestation. He
was born in Mexico and immigrated to Colorado 13 years prior to admission.
Physical examination showed a well-developed Hispanic man. The vital
signs were as follows: blood pressure, 130/88 m m Fig; pulse, 84; respiratory
rate, 20; and oral temperature, 36.7 C. There were no palpable subcutaneous
nodules. The mental status was normal. Cranial nerves were normal.
Strength was normal; deep tendon reflexes were 2 + and symmetric; and the
plantar responses were flexor. Sensory examination was normal. There was
left horizontal nystagmus with leftward gaze. Truncal ataxia was present and
there was mild abnormality on left finger to nose testing. The patient had an
ataxic gait with tendency to fall to the left. The remainder of the examination was normal.
The hemoglobin was 16 mg/dL, hematocrit was 48%, and the white blood
cell count was 13,000/ram3 with 96% polymorphonuclear cells, 4% lymphocytes, and no eosinophils. The urinalysis was normal. The electrolytes, BUN,
and glucose were normal. Examination of the stools showed no ova or parasites. Radiographic examination of the thighs showed no soft tissue calcification. Computed tomography of the brain demonstrated a large, left cerebe!lar
cystic lesion with calcification internally and ring enhancement. In addition,
15:7 July 1986

Annals of Emergency Medicine

847/119

CNS CYSTICERCOSIS
Catapano & Marx

FIGURE. Note large ring-enhancing
cystic mass in left cerebellum (with
central marker) and two smaller nonenhancing cystic lesions in the left
temporal cortex.
there were two small cystic lesions in
the left t e m p o r a l c o r t e x (Figure).
There was mass effect and obliteration
of the fourth ventricle. Plain films of
the skull and thighs revealed no calcification.
The patient was treated with highdose dexamethasone 40 mg/day and
praziquantel 1,200 mg orally every
eight hours. He exhibited m i n i m a l
improvement and surgery was deemed
necessary to avoid herniation. On the
fourth hospital day, a posterior fossa
craniotomy was performed and the
left cerebellar lesion was removed.
Pathologic examination demonstrated
the larval form of the pork tapeworm,
Taenia solium. The hospital course
was complicated by a pulmonary embolism, which resolved without sequelae. The patient improved steadily
and was discharged on the 18th hospital day with no neurologic deficits and
on no medications. The patient was
doing well at followup one m o n t h
later.

DISCUSSION
Human beings can serve as both the
definitive and intermediate host for
the pork tapeworm Taenia solium, tl
Intestinal infestation is acquired by
ingesting undercooked pork containing the larval form, Cysticercus cellulosae. The larvae attaches to the intestine and develops into the adult
tapeworm. The adult tapeworm consists of numerous segments, or proglottids. The terminal, egg-bearing
proglottids occasionally separate and
are discharged in the feces. Under the
poor hygiene conditions existing in
developing countries, both pigs and
human beings can ingest ova in contaminated food and water. Embryos
are released in the gastrointestinal
tract, penetrate the intestines, and are
eventually deposited in tissues, with a
preference for muscle, subcutaneous
tissue, and brain. Within 60 to 70 days
e m b r y o s d e v e l o p i n t o larvae, or
cysticerci, thus completing the life
cycle.
Most patients with CNS cysticercosis are between the ages of 20 and
50, although no age is exempt.3,4,
9,1o,124s No significant differences ap120/848

pear to exist among races or the sexes.
CNS cysticerci cause illness
through three major pathophysiologic
mechanisms. Occasionally, a single
cyst is large enough to cause signs and
symptoms of a cerebral tumor.a,s,z, gAo
More often, the parasites obstruct the
flow of cerebrospinal fluid (CSF) and
cause either a communicating hydrocephalus from chronic meningitis or
an obstructive hydrocephalus from
ventricular involvement.3,s, Lg,10 In
the third, or parenchymatous form,
the cysts are numerous and produce
diffuse cerebral swelling. A patient
may exhibit a combination of these
three types.a,s, 16
The clinical presentation of CNS
cysticercosis is nonspecific and varied
and d e p e n d s on t h e n u m b e r of
cysticerci p r e s e n t and their location.a-10A5,17 Seizures, both focal and
generalized, are common and occur in
30% to 92% of patients.2,5,8, 9 Symptoms of increased intracranial pressure
occur frequently and include nausea,
vomiting, altered mental status, and
headache. Psychosis, dementia, and
impaired memory also have been reported, s A wide variety of focal neurologic deficits, sometimes mimicking
stroke or tumor, have been described.
Invasion of the eye with cysts can produce visual abnormalities.2,s,s,9 CNS
cysticercosis may be accompanied by
painless nodules in striated muscle
and subcutaneous tissue. The time
from exposure to the first symptoms
can be less than one year or as many
as 30 years w i t h 83% e x h i b i t i n g
symptoms within seven years.S ManAnnals of Emergency Medicine

ffestations can develop insidiously but
frequently present suddenly.5-1o
Cerebellar cysts occur in up to 18%
of autopsy cases s but s y m p t o m a t i c
cerebellar cysts are uncommon.9 Patients w i t h s y m p t o m s of headache,
vomiting, ataxia, vertigo, and nystagm u s h a v e been r e p o r t e d b u t the
etiology u s u a l l y has been hydrocephalus caused by disruption of the
flow of CSF.a,s,z, to, 18"21 D i x o n and
Lipscomb describe nine patients with
this symptomatology.S The causes
were basilar meningeal involvement
or obstruction of the fourth ventricle.
Cerebellar pathology was not found.
T h e r e was no evidence of hydrocephalus or basal meningitis in our
patient.
Laboratory evaluation provides limited diagnostic information. A mild
peripheral leukocytosis can be seen in
as many as one-third of patients.8, 9 Peripheral eosinophilia has been reported to occur in 3% to 35% of
cases.a, 8-1o Examination of the stool
rarely reveals ova or parasites.9, lo The
CSF frequently is abnormal. Elevated
protein, depressed glucose, or pleocytosis occur in approximately 80% of
patients wih CNS cysticercosis.3,4, 8-1o
When Wright stains are performed on
the CSF, eosinophilia is more evident,
and in one report had an incidence of
29%. 3 Serologic testing of the serum
and CSF, using the indirect hemagglutination test, is positive in 60% to
100% of patients and frequently is the
m o s t i m p o r t a n t diagnostic information.S4O, lS
Radiographic e x a m i n a t i o n often
15:7 July 1986

will demonstrate evidence of cysticercosis a n d f r e q u e n t l y w i l l be diagn o s t i c . C a l c i f i e d c y s t i c e r c i in soft
tissue have been discovered on plain
films in as m a n y as 98% of patients, S
a l t h o u g h m o r e r e c e n t s t u d i e s have
found a lower incidence of soft tissue
c a l c i f i c a t i o n s . g A o I n t r a c r a n i a l calcifications seen on skull radiographs
strongly suggest the diagnosis of cerebral cysticercosis and occur in about
24% of patients, s
C o m p u t e d tomography of the brain
in patients w i t h CNS cysticercosis exh i b i t s s e v e r a l p a t t e m s and o f t e n is
m o s t helpful in achieving a diagnosis.
T h e m o s t frequent, and diagnostic, appearance on C T is multiple, small intraparenchymal calcifications.9, lO,13A4
T h e second m o s t c o m m o n finding is
circular, c y s t i c l e s i o n s in t h e b r a i n
parenchyma.9,1o,13,14 Other pathology
on C T includes hydrocephalus, vent r i c u l a r cysts, r i n g e n h a n c e m e n t of
c y s t i c l e s i o n s w h e n IV c o n t r a s t is
given, solid lesions, and lesions seen
only w i t h contrast enhancement. The
C T m a y be normal.9,1o,13,14 Air contrast studies will assist in the surgical
m a n a g e m e n t of selected p a t i e n t s by
defining the intraventricular and subarachnoid spaces.lOA3,22
Treatment consists of therapy w i t h
praziquantel and dexamethasone, seizure control w i t h c o n v e n t i o n a l anticonvulsants, and surgery. Praziquantel
is a b r o a d - s p e c t r u m a n t i h e l m i n t i c
agent, and, when combined with
steroid t r e a t m e n t , appears to reduce
the m o r b i d i t y and m o r t a l i t y associated w i t h C N S cysticercosis. 23-2s Surgery should be reserved for p a t i e n t s
with hydrocephalus (decompressive
procedures) a n d large s y m p t o m a t i c
cysts. Operative m o r t a l i t y has been
reported to be as high as 32%3, 4 but
m o r e r e c e n t studies report no operative mortality.9, lo
SUMMARY
CNS cysticercosis has not been re-

15:7 July 1986

p o r t e d p r e v i o u s l y in t h e e m e r g e n c y
medicine literature. If immigration to
the U n i t e d States increases, however,
CNS cysticercosis m a y become m o r e
prevalent. This disorder should be
considered in H i s p a n i c or A s i a n i m migrants w h o p r e s e n t w i t h seizures,
focal neurologic deficits, s y m p t o m s of
increased intracranial pressure, neuropsychiatric disorders, or visual abnormalities.
REFERENCES

1. Nash TE, Neva FA: Recent advances in
the diagnosis and treatment of cerebral
cysticercosis. N EngI J Med 1984;34:
1492-1496.
2. Olive JI, Angulo-Rivero P: Cysticercosis of the nervous system. I. Introduction and general aspects. ] Neurosurg
1962; 19:632-634.
3. Stepien L: Cerebral cysticercosis in Poland. J Neurosurg 1962;19:505-513.

12. Goni PB: Cysticercosis of the nervous
system. III Clinical findings and treatment. l Neurosurg 1962;19:641-643.
13. Byrd SE, Locke GE, Biggers S, et al:
The computed tomographic appearance of
cerebral cysticercosis in adults and children. Radiology 1982;144:819-823.
14. Carbajal JR, Palacios E, Azar-Kia B, et
al: Radiology of cysticercosis of the central nervous system including computed
tomography. Radiology 1977;125:127-131.
15. Sotelo l, Guerro V, Rubio F, et al: Neur o c y s t i c e r c o s i s : A new c l a s s i f i c a t i o n
based on active and inactive forms. Arch
Intern Med 1985;145:442-445.
16. Cardenas ]C: Cysticercosis of the nervous system II. Pathologic and radiologic
findings. Neurosurgery 1962;19:635-640.
17. Dixon HBE Hargreaves WH: Cysticercosis - - A further ten years clinical study,
covering 284 cases. Q J Med 1944;13:
107-121.

4. Lombardo L, Mateos HJ: Cerebral
cysticercosis in Mexico. 196l; Neurol
11:824-828.

18. Nieto D: Cysticercosis of the nervous
system: Diagnosis by means of the spinal
fluid c o m p l e m e n t fixation test. Neurology 1956;6:725-737.

5. Dixon HBF, Lipscomb FM: Cysticercosis: An analysis and follow-up of 450
cases. M e d Res Counc Spec Rep Ser
1961;299:1-57.

19. Bickerstaff ER, Cloake PCP, Hughes B,
et al: The racemose form of cerebral
cysticercosis. Brain 1952;75:1-18.

6. Latovitshi N, Abrams G, Clark C, et
al: Cerebral cysticercosis. Neurology
1978;28:838-842.
7. Shanley JD, Jordan MC: Clinical aspects of CNS cysticercosis. Arch Intern
Med 1980;140:1309-1313.
8. G r i s o l i a JS, W i e d e r h o l t WC: CNS
c y s t i c e r c o s i s . Arch Neurol 1982;39:
540-544.
9. M c C o r m i c k GF, C h i - S h i n g Zee,
Heiden J, et ah Cysticercosis cerebri. Review of 127 cases. Arch Neurol 1982;
39:534-539.
10. Leo L, Braude A: Cerebral cysticercosis in San Diego. Medicine 1982;61:
341-359.
11. Mandel E (ed): Principles and Practice
of Infectious Disease. New York, John
Wiley and Sons, 1979, pp 1283-1287.

Annals of Emergency Medicine

20. Arseni C, Samitca DC: Cysticercosis
of the brain. Br Med J 1957;2:494-497.
21. Bickerstaff ER: Cerebral cysticercosis
-common but unfamiliar manifestations. Br Med J 1955;1:1055-1058.
22. Stern WE: Neurosurgical consideration of cerebral cysticercosis. J Neurosurg
1981;55:382-389.
23. Pearson RD, G u e r a n t RL: Praziquanteh A major advance in anthelmintic
therapy. Ann Intern Med 1983;99:195-198.
24. de Ghetaldi LD, Norman RM, Douville AW, et al: Cerebral cysticercosis
treated biphasically with dexamethasone
and p r a z i q u a n t e l . A n n I n t e r n M e d
1983;99:179-181.
25. Sotelo J, Escobedo F, Carbajal JR, et al:
Therapy of parenchymal brain cysticercosis with praziquantel. N Engl J Med
1984;310:1001-1007.

849/121