Neuroscience & Medicine, 2013, 4, 189-193
Published Online December 2013 (
Open Access NM
Neurocysticercosis in Iran: An Unexpected Case and
Literature Review
Zeinab Kishani Farahani, Afshin Moradi, Amirsaiid Sedighi, Mohammadmehdi Soleimani
Shahid Beheshti University of Medical Sience, Shohada Hospital, Tehran, Iran.
Received April 6th, 2013; revised May 8th, 2013; accepted June 4th, 2013
Copyright © 2013 Zeinab Kishani Farahani et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Neurocysticercosis is a significant public health issue worldwide. Even though cysticercosis was once thought to have
been eradicated in the United States, it is currently a growing public health problem in the United States, and immi-
grants from endemic areas are at the highest risk of acquiring this disease. In Iran, there was no report from this worri-
some infection. The clinical presentation of neurocysticercosis is variable and vague. In this article, we will explain a
case of neurocysticercosis encountered in the Shohada Hospital pathology department, and then we will review neu-
rologic and radiologic symptoms, laboratory and pathologic findings, as well as medication for treatment, briefly.
Keywords: Neurocysticercosis; Epilepsy; Racemose; Scolex
1. Introduction
Neurocysticercosis is the most common helminth infec-
tion of the central nervous system, and accounts for
ab out 50 ,00 0 deaths per ye ar worldwide, and many time s,
this number of people are with active epilepsy [1,2].
It is endemic in Mexico, Central and South America,
Asia, India, Africa, and Indonesia [3].
With increased travel to disease-endemic areas and
the migration of tapeworm carriers or people infected
with the disease, neurocysticercosis is becoming in-
creasingly prevalent even in industrialized countries
2. Case Presentation
A 63 years old man presented to Shohada Hospital emer-
gency department with headache and nausea for 2
months with unconsciousness worsened during 14 days.
He had history of ischemic heart disease, diabetes melli-
tus and cardiac bypass surgery. His brain CT scans re-
vealed multiple cystic deep parieto occipital lesions,
which induced midline shifting and moderate hydro-
cephalus. The patient admitted in ICU and went under
insertion of external ventricular drainage that improved
the level of consciousness. The patient was candidate for
stereotactic biopsy which diagnosed as neurocysticerco-
sis in our pathology department. Our case radiologic and
pathologic findings will be represented in forthcoming
relevant sessions. Due to definite pathologic diagnosis,
albendazole 400 mg twice daily, dexamethasone 8 mg
3 times daily administered for the patient, but showed
no marked response unfortunately. He gradually dete-
riorated and was intubated for airway protection,
placed on a mechanical ventilator but during next days
the patient expired due to septicemia secondary to pneu-
2.1. Life Cycle
Neurocysticercosis is an infestation of the brain by Tae-
nia solium, the tissue-invading larval form of the pork
tapeworm. The larvae are introduced into the body by the
accidental ingestion of fertile T. solium eggs in fecally
contaminated vegetable or water. The eggs of T. solium
can remain viable for up to 2 months in water, soil or
vegetation. Once the eggs are in the intestinal tract, the
actions of bile and pancreatic enzymes dissolve their
protective coatings. Liberated from their coats, they be-
come embryos (oncospheres), penetrate the intestinal
wall and enter the bloodstream. There they are carried to
the tissues of the host, where they eventually localize as
cysts within the brain, the skeletal muscles, and the eyes
and become established as cystic larvae or cysticerci [5].
The former described infection differs from taeniosis.
Neurocysticercosis in Iran: An Unexpected Case and Literature Review
Taeniosis in humans results from consumption of im-
properly cooked meat from swine that are infected by
cysticerci (viable larvae) [6]. Taeniosis is usually benign,
although it may produce abdominal discomfort and pe-
ripheral eosinophilia.
2.2. Clinical Presentation
From the moment a cysticercus invades the brain tissue,
for example, it is exposed to a hostile environment.
When the host’s immune system recognizes the parasite
as foreign, it usually mounts an appropriate inflammatory
reaction to overcome the inf ection. In many cases , how-
ever, such a vigorous response does not occur, and the
host reaches a state of immunologic tolerance to the
parasite, leaving it almost undisturbed for many years.
No clear explanation exists for the individual differ-
ences observed in the severity of immunologic response
against infection of the central nervous system by cysti-
cerci [6].
Clinical manifestations of neurocysticercosis depend
on the number, size, and location of CNS lesions and on
the intensity of the host immune response [7,8].
Neurocysticercosis can cause many neurologic symp-
toms. Late-onset epilepsy is the most common clinical
symptom; neurocysticercosis is the leading cause of epi-
lepsy worldwide [9].
Patients with neurocysticercosis may also present with
headache associated with intracranial hypertension (an-
other common presentation in disease-endemic coun-
tries), focal signs or dementia. Intracranial hypertension
is most commonly caused by hydrocephalus related to
granular ependymitis, arachnoiditis or ventricular cysts.
Other causes include giant cysts or cysticercotic en-
The course of disease may remain sub acute or chronic
for many years, then present with focal signs of a cere-
brovascular event secondary to an acute inflammatory
response to the parasites. Cysticerci can also invade the
spinal cord, the eyes and the subcutaneous and muscular
tissues of the body. Muscular pseudo hypertrophy is seen
more frequently in patients from Asia who has cysticer-
cosis; it accounts for 0.6% of cases in China, but is ex-
tremely rare in America [6].
2.3. Diagnosis
2.3.1. Path ol o gic Ex ami n ation
Detection of the parasite in a biopsy of a brain or spinal
cord lesion is one of the proposed abso lute criteria for the
diagnosis of neurocysticercosis [10-12].
Grossly, the lesion shows a fibrous capsule, easily
demarcate from adjacent brain tissue, when sectioned is
cystic; the cyst contents may be grumous and nondescript,
but occasionally have recognizable organism-like shapes.
Histologically, cysticerci manifest 4 distinct stages in
addition to the racemose form; vesicular, colloidal, gra-
nular and calcified [20,18]. The vesicular stage consists
of vesicles with viable organisms. Each viable organism
is composed of a larva containing an invaginated scolex
(head) and is surrounded by translucent fluid that is lined
by a thin membranous wall [18,20,23]. The reactive in-
flammatory response and associated changes, which are
more likely to correlate with clinical symptoms, are usu-
ally not elicited with viable cysticerci but instead are
found with degenerating cysts [19,23]. Depending on the
inflammatory process, cysticerci have been documented
to survive in the brain for up to several years.
The inflammatory response induced by degenerating
cysticerci consists predominantly of lymphocytes and
plasma cells, with variable edema, gliosis, fibrosis, and
necrosis [7,9,18]. The degeneration process begins with
the colloidal stage. 7 The vesicle fluid becomes more
turbid and the larvae become hyalinized. The inflamma-
tory infiltrate becomes more intense, extending to sur-
rounding structures, and includes lymphocytes, some
neutrophils and eosinophils, and the formation of multi-
nucleated histiocytic giant cells [9,22]. The reactive in-
flammatory process can cause arteritis, arachnoid itis, and
ependymitis [7]. The granular-nodular stage involves
progressive degenerative changes with increased larval
decay, vesicle involution, and thickening of the vesicle
wall [7,19]. The larvae in this stage begin to mineralize
with calcium [18]. The degenerative process ends with
the nodular-calcified stage. In this stage, cysticerci are
replaced by collagen and calcify [18,19]. Although this
stage is associated with decreased inflammation, foreign
body giant cells and gliosis may persist [7,18].
The racemose form of neurocysticercosis most likely
represents cysticercal decay with cyst enlargement and
hydropic changes [20,22]. Racemose cysticerci usually
do not contain scolices and are considered nonviable
encysted organisms. The degenerated vesicle wall is
characteristically convoluted with external bulbous pro-
jections and evokes an inflammatory response [18,22].
The associated reactive process elicited by the racemose
form can also cause meningitis [20,22].
2.3.2. Imaging Studies
Apart from histologic examination the diagnosis of neu-
rocysticercosis is based on results of neuroimaging stud-
ies. Computed tomography is the most commonly used
neuroimaging test for the disease and maintains relatively
good diagnostic sensitivity when used in disease-en-
demic areas. Viable cysts are non-enhancing, either in
leptomeninges or parenchyma. After several (3 - 30)
years, the organism dies and the cyst starts to degenerate
and enhance. The cyst wall thickness due to inflamma-
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Neurocysticercosis in Iran: An Unexpected Case and Literature Review 191
tion forms a fibrous capsule and the cyst fluid become
denser. Eventual cyst shrinkage can take months to years
with replacement by a small calcification. Calcifications
in the brain parenchyma are the most commo n finding in
computed tomography studies and, in many cases, the
only radiologic evidence of the disease. For that reason,
computed tomography remains the best screening tool for
assessing patients with suspected neurocysticercosis.
Figures 1(a) and (b), representing our case CT imaging,
show small cystic lesion in parietal and occipital region.
Figure 1. CT scan imaging of cystic neurocystisercosis le-
Small lesions, especially those situated close to bone
or within ventricles, may be missed on computed tomo-
graphy scans. A magnetic resonance imaging scan is
therefore often added for increased diagnostic sensitivity
and accuracy. Magnetic resonance imaging is also the
modality of choice when evaluating patients with intra-
ventricular cysticercosis and when assessing brainstem
cysts and small cysts located over the convexity of the
cerebral hemispheres. The main shortcoming of magnetic
resonance imaging is its failure to detect small calcifica-
The appearance of cysticerci in brain parenchyma on
neuroimaging scans depends on their stage of develop-
ment. Vesicular cysts appear as rounded lesions with
signal properties similar to those of cerebrospinal fluid in
both T1- and T2-weighted images. The scolex may be
seen within the cyst as a high-intensity no dule, giving the
lesion a pathognomonic “hole-with-dot” appearance.
When the parasite begins to degenerate, the lesion be-
comes heterogeneous, and its appearance varies depend-
ing on the degree of degeneration. Cysticercotic en-
cephalitis involves multiple cysts in the brain paren-
chyma associated with severe, diffuse inflammation.
Cysticercosis may present with a single intraparen-
chymal brain lesion with nodular or ring enhancement
detected with the use of contrast in neuroimaging studies.
The differential diagnosis for this type of lesion includes
brain tumors, hydatidosis, multiple sclerosis and tuber-
T. solium larvae occasionally are deposited in ven-
tricular spaces or in the sub arachnoid space. There, free
from surrounding solid tissues, the cyst walls, which de-
velop are often more delicate, and also can grow larger
and into more complex shapes. This behavior is de-
scribed by the term “racemose” cysticercosis.
2.3.3. Other Fi ndi ngs
Hematologic abnormalities in patients with neurocysti-
cercosis include mild leukocytosis an d eosinophilia in up
to 30% of patients. Stool examination for T. solium eggs
is positive in on ly 5% - 10% o f patients. In a similar pro-
portion of cases, a T. solium carrier can be found in the
patient’s close environment. Because analysis of cere-
brospinal fluid shows abnormalities in 50% or less of
patients with neurocysticercosis, a normal finding on
examination of cerebrospinal fluid does not ru le out neu-
Serologic assays, mainly enzyme-linked immunoelec-
tron transfer blot, are also commonly used to detect spe-
cific antibodies.
Epidemiologic factors that may lead to a diagnosis of
neurocysticercosis include evidence of household contact
with T. solium, immigration from an area where the dis-
ease is endemic and a history of repeated travel to dis-
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Neurocysticercosis in Iran: An Unexpected Case and Literature Review
ease-endemic regions. An accurate and complete patient
history is crucial for neurocysticercosis identification.
Patients should be questioned about recent travel. Immi-
grants are in high risk for bringing this condition with
them from less-developed countries. However, with the
increase in world travel, persons who would previously
not have been exposed to parasitic illnesses such as neu-
rocysticercosis are now susceptible [12] .The use of epi-
demiologic information together with clinical suspicion
and laboratory tests is essential in making the final diag-
nosis and starting treatment.
However, the combination of epidemiologic, clinical
and laboratory information may lead to an accurate di-
agnosis and avoid an invasive diagnostic procedure.
Neurocysticercosis should be included in the differen-
tial diagnosis of neurologic infections in HIV patients in
endemic populations. Consideration of the patient’s im-
mune status should alert the clinician to poten tial atypical
presentations. Despite the wide en demicity of cysticerco-
sis and HIV infection, less than 30 cases of neurocysti-
cercosis have been reported in HIV infected patients
2.4. Treatment and Prognosis
Pharmaceutical treatments for symptoms include analge-
sics, corticosteroids, and anti seizure medications [17].
Anti parasitic medications are generally effective but
there have been rare treatment-related deaths (1% - 4%)
in cases with hydrocephalus, intracranial hypertension,
and massive parasitic loads [7,24].
Placement of a ventriculoperitoneal shunt is indicated
in cases of intracranial hypertension before the use of
antiparasitic drugs, and surgical removal may be appro-
priate for large or intraventricular cysts [7,19,24]. Shunt
dysfunction rate is also high (30% - 67%) [14]. Surgery
eliminates the inflammatory nidus, potentially obviating
the need for a complication prone shunt. Treatment of
intraventricular cysticercosis is a contentious issue. Me-
dical management is less favored because of poor cysti-
cidal CSF penetration, delay in resp onse and, lysis of the
cyst leading to ependymitis with resultant acute compli-
cations and chronic sequelae [13].
Open surgery was the only available modality previ-
ously but now neuro endoscopy has beco me the treatment
of choice [15,16].
The prognosis of is multifactorial and ultimately de-
pends on the host immune response, disease duration,
and parasite location, load, size, and stage [7,21,25].
Intraventricular and basal subarachnoid neurocysticer-
cosis have a worse prognosis due to obstruction of cere-
brospinal fluid outflow leading to hydrocephalus and
increased intracranial pressure [19,23]. In addition, the
racemose form of neurocysticercosis has a high mor-
tality rate [23].
3. Discussion
In our case, the inflamed fibrous wall encircles the con-
tents and as are not wholly necrotic and degenerated, are
readily recognizable as non-human tissue. The outer wall
of these invertebrate multi cellular parasites is an acellu-
lar exoskeleton of chitin. Under th at wall, there is a layer
of small round cells; deep to, th at is the gut of the organ-
ism with atypical glandular ep ithelium thrown into many
folds (Figures 2( a) and (b)).
This appearance is typical for cysticerci but is not di-
agnostic for T. solium as compared to other types of
metazoan parasites. Correct species identification de-
pends on characterization of the scolices of the larva, but
these are rarely completely or even partially visualized in
tissue sections, so that precise identification may require
other studies like DNA analysis and immunoassays. As
treatment and prognosis are independent of species iden-
tification, this is not generally done. Other parasites
which may be encountered include Sparganosis, Tri-
Figure 2. Low and high power view of the parasites (H & E
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Neurocysticercosis in Iran: An Unexpected Case and Literature Review
Open Access NM
chionosis, and Echinococcus cysts.
[1] M. Gemmell, Z. Matyas, Z. Pawlowsky and E. J. L.
Soulsby, “Guidelines for Surveillance and Control of
Taeniasis/Cysticercosis, Vol. 83,” World Health Organi-
zation, Switzerland, 1983, p. 49.
[2] G. Roman, J. Sotelo, O. Del Brutto, et al., “A Proposal to
Declare Neurocysticercosis an International Reportable
Disease,” Bulletin of the World Health Organization, Vol.
78, No. 3, 2000, pp. 399-406
[3] K. Hutcheson III, M. Kalafian, I. Taylor, J. Sagel and B.
Clyburn, “Neurocysticercosis,” Southern Medical Journal,
Vol. 7, 2000, pp. 666-668.
[4] M. T. Wallin and J. F. Kurtzke, “Neurocysticercosis in
the United States: Review of an Important Emerging In-
fection,” Neurology, Vol. 63, No. 9, 2004, pp. 1559-1564.
[5] O. H. Del Brutto, J. Sotelo, “Neurocysticercosis: An Up-
date,” Clinical Infectious Disease, Vol. 10, No. 6, 1988,
pp. 1075-1087.
[6] J. G. Burneo, I. Plener and H. H. Garcia, “Neurocysticer-
cosis in a Patient in Canada,” CMAJ, Vol. 180, No. 6,
2009, pp. 639-642.
[7] H. H. Garcia and O. H. Del Brutto “Neurocysticercosis:
Updated Concepts about an Old Disease,” The Lancet
Neurology, Vol. 4, No. 10, 2005, pp. 653-661.
[8] J. A. Serpa, L. S. Yancey and A. C. White Jr., “Advances
in the Diagnosis and Management of Neurocysticercosis,”
Expert Review of Anti-infective Therapy, Vol. 4, No. 6,
2006, pp. 1051-1061.
[9] H. H. Garcia, R. Gilman, M. Martinez, et al., “Cysticer-
cosis as a Major Cause of Epilepsy in Peru. The Cysti-
cercosis Working Group in Peru (CWG),” Lancet, Vol.
341, No. 8839, 1993, pp. 197-200.
[10] O. H. Del Brutto, V. Rajshekhar, A. C. White Jr., et al.,
“Proposed Diagnostic Criteria for Neurocysticercosis,”
Neurology, Vol. 57, No. 2, 2001, pp. 177-183.
[11] J. A. Serpa, A. Moran, J. C. Goodman, T. P. Giordano,
and A. C. White Jr, “Neurocysticercosis in the HIV Era:
A Case Report and Review of the Literature,” American
Journal of Tropical Medicine and Hygiene, Vol. 77, No.
1, 2007, pp. 113-117.
[12] S. Remy, MSN, RN, CEN and Vineland, “A 44-Year-Old
Man with Neurocysticercosis,” Journal of Emergency
Nursing, Vol. 35, No. 4, 2009, pp. 348-349.
[13] S. A. Cudlip, P. R. Wilkins and H. T. Marsh, “Endo-
scopic Removal of a Third Ventricular Cysticercal Cyst,”
British Journal of Neurosurgery, Vol. 12, No. 5, 1998, pp.
[14] R. Kelley, D. H. Duong and G. E. Locke, “Characteristics
of Ventricular Shunt Malfunctions among Patients with
Neurocysticercosis,” Neurosurgery, Vol. 50, No. 4, 2002,
pp. 757-762.
[15] M. Bergsneider, L. T. Holly, J. H. Lee, W. A. King and J.
G. Frazee, “Endoscopic Management of Cysticercal cysts
within the Lateral and Third Ventricles,” Journal of Neu-
rosurgery, Vol. 92, No. 1, 2000, pp. 14-23.
[16] V. Kalra, D. Mishra, A.Suri, R. Seth and A. Garg, “Intra-
ventricular Neurocysticercosis,” The Indian Journal of
Pediatrics, Vol. 76, No. 4, 2009, pp. 420-423.
[17] H. H. García, C. A. Evans, T. E. Nash, O. M. Takayana-
gui, A. C. White, D. Botero, V. Rajshekhar, V. C.Tsang,
et al., “Current Consensus Guidelines for Treatment of
Neurocysticercosis,” Clinical Microbiology Reviews, Vol.
15, No. 4, 2002, pp. 747-756.
[18] A. Escobar and K. M. Weidenheim, “The Pathology of
Neurocysticercosis,” In: G. Singh and S. Prabhakar, Eds.,
Taenia solium Cysticercosis: From Basic to Clinical Sci-
ence, United Kingdom CABI Publishing, Wallingford,
2002, pp. 289-305.
[19] A. C. White Jr., “Neurocysticercosis: Updates on Epide-
miology, Pathogenesis, Diagnosis, and Management,”
Annual Review of Medicine, Vol. 51, 2000, pp. 187-206.
[20] A. Carpio, “Neurocysticercosis: An Update,” The Lancet
Infectious Diseases, Vol. 2, No. 12, 2002, pp. 751-762.
[21] M. P. Earnest, L. B. Reller, C. M. Filley and A. J. Grek,
“Neurocysticercosis in the United States: 35 Cases and a
Review,” Reviews of Infectious Diseases, Vol. 9, No. 5,
1987, pp. 961-979.
[22] J. E. Pittella, “Neurocysticercosis,” Brain Pathology, Vol.
7, No. 1, 1997, pp. 681-693.
[23] H. H. García, A. E. Gonzalez, C. A. Evans and R. H.
Gilman, “Cysticercosis Working Group in Peru. Taenia
solium Cysticercosis,” Lancet, Vol. 362, No. 9383, 2003,
pp. 547-556.
[24] C. M. DeGio rgio, M. T. Me di na , R. Dur ón , C. Zee a nd S.
P. Escueta, “Neurocysticerc osis,” Epilepsy Currents, Vol.
4, No. 3, 2004, pp. 107-111.
[25] D. Scharf, “Neurocysticercosis: Two Hundred Thirty-
Eight Cases from a Ca lifornia Hospit al,” Archives of Neu-
rology, Vol. 45, No. 7, 1988, pp. 777-780.