Imaging Findings in Neurocysticercosis

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Radiología. 2013;55(2):130---141

www.elsevier.es/rx

UPDATE IN RADIOLOGY

ଝ

Imaging ﬁndings in neurocysticercosis

∗

S. Sarria Estrada , L. Frascheri Verzelli, S. Siurana Montilva,

C. Auger Acosta, A. Rovira Canellas˜

Unitat de Ressonància Magnètica (IDI), Servei de Radiologia, Hospital Universitari Vall d’Hebron, Barcelona, Spain

Received 2 September 2011; accepted 23 November 2011

KEYWORDS Abstract Neurocysticercosis, caused by the larvae of Taenia solium, is the parasitic infec-

Taenia solium; tion that most commonly involves the central nervous system in humans. Neurocysticercosis is

Cysticercosis; endemic in practically all developing countries, and owing to globalization and immigration it

Neurocysticercosis; is becoming more common in developed countries like those in western Europe.

Computed The most common clinical manifestations are epilepsy, focal neurologic signs, and intracranial

tomography; hypertension.

Magnetic resonance The imaging ﬁndings depend on the larval stage of Taenia solium, on the number and loca-

imaging tion of the parasites (parenchymal, subarachnoid, or intraventricular), as well as on the host’s

immune response (edema, gliosis, and arachnoiditis) and on the development of secondary

lesions (arteritis, infarcts, or hydrocephalus).

The diagnosis of this parasitosis must be established on the basis of the clinical and radiologi-

cal ﬁndings, especially in the appropriate epidemiological context, with the help of serological

tests.

PALABRAS CLAVE

Neurocisticercosis. Hallazgos radiológicos

Taenia solium;

Cisticercosis; Resumen La neurocisticercosis es una parasitosis humana causada por las larvas de la Taenia

Neurocisticercosis; solium, que es la que con mayor frecuencia afecta el sistema nervioso central. Esta infección es

Tomografía endémica en prácticamente todos los países en vías de desarrollo, pero debido a la globalización

computarizada; y a las migraciones humanas su frecuencia ha aumentado en países desarrollados como los de

Imagen por Europa Occidental.

resonancia magnética Las manifestaciones clínicas más frecuentes son la epilepsia, signos neurológicos focales e

hipertensión intracraneal.

ଝ

Please cite this article: Sarria Estrada S, et al. Neurocisticercosis. Hallazgos radiológicos. Radiología. 2013;55:130-41. ∗

Corresponding author.

E-mail address: [email protected] (S. Sarria Estrada).

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 131

Los hallazgos radiológicos dependen del estadio larvario de la Taenia solium, número y loca-

lización de los parásitos (parenquimatosa, subaracnoidea e intraventricular), así como de la

respuesta inmune del huésped (edema, gliosis, aracnoiditis) y del desarrollo de lesiones secun-

darias (arteritis, infartos o hidrocefalia).

El diagnóstico de esta parasitosis debe establecerse en función de los hallazgos clínicos y ra-

diológicos, especialmente en un contexto epidemiológico adecuado, con apoyo de la serología.

Introduction Etiopathogenesis

Cysticercosis is a parasitic disease caused by the larva of Tae- Taenia solium is one of the eight species of cestodes that

nia solium. Human cysticercosis occurs after a person ingests infect humans. T. solium has a scolex and a body with

eggs that are passed in the feces of a T. solium carrier (fecal- several hundreds of proglottids. Its life cycle includes the

1 --- 3 1

oral contamination). Although infection may develop in egg and larval stage and the adult stage. The hexacanth

any organ, the central nervous system (parenchyma, sub- embryo (thin-walled larval cysts) measures 10---20 mm in

arachnoid spaces, ventricles and spinal cord), eyes and length and contains an invaginated scolex (larval head). The

muscles are the most commonly involved. cyst, whose wall is rich in glycoproteins, is ﬁlled with a

Cysticercosis is endemic in virtually all developing clear ﬂuid during this phase, but it becomes cloudy after

countries (Latin America, South-East Asia and Africa), with the parasite dies.

the exception of Muslim countries, where pork is not The adult Taenia is 2 --- 4 m long and inhabits the small

1 --- 3

consumed (Fig. 1). In recent years, the incidence of cysticer- intestine of humans, attached by the scolex. Proglotidds

cosis has risen in developed countries due to immigration containing thousands of eggs detach daily and are passed

2,3 2

from endemic areas. in the feces, contaminating water and soil. The eggs are

Neurocysticercosis is the most common parasitic disease eaten by pigs, and once in the pig’s intestine, they transform

of the human central nervous system, being the main cause into oncosphere that enter the bloodstream and disseminate

of acquired epilepsy in endemic areas and a major public to target organs where the larvae develop. In humans, the

1 --- 4

health problem worldwide. In 1993, the International Task larvae reaches the small intestine after the ingestion of con-

Force for Disease Eradication declared that cysticercosis is taminated pork, raw or undercooked, the scolex attaches to

potentially eradicable, and proposed to declare neurocys- the intestinal wall and begins to form proglotidds. Lastly,

5,6

ticercosis a reportable disease. cysticercosis occurs when humans become intermediate

1,2

The objective of this paper is to update the most impor- hosts by ingesting Taenia solium eggs (Fig. 2).

tant radiologic features of neurocysticercosis and describe Humans acquire the infection through fecal-oral contami-

the etiopathogenesis of the disease, clinical presentation, nation by infected individuals hosting the parasite. Humans

and differential diagnosis. A brief description of the recom- are the only deﬁnitive hosts of Taenia solium, while both

1 --- 3

mended treatment is also provided. humans and pigs are intermediate hosts.

High prevalence Moderate prevalence Low prevalence

No information available

Figure 1 Epidemiology. Cysticercosis is endemic to Africa, Asia and South America and particularly favored by poor socio-economic

conditions. Source: modiﬁed from Román et al.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

132 S. Sarria Estrada et al.

Ingestion of eggs of T. solium 2. Inﬂammatory response (edema).

(human cysticercosis)

3. Presence of sequelae (ﬁbrosis, granuloma, and calciﬁca- Eyes tions). Brain

Lungs

Muscles

Ingestion of Clinical presentation of neurocysticercosis infected pork

(taeniasis)

Neurocysticercosis is a pleomorphic disease whose mani-

festations depend on individual variation in the number,

location, size, stage of parasites, and degree of the host 1,2,7,9 Eggs and inﬂammatory response.

proglotidds

Most symptomatic patients are 15---40 year old, and the

Neurocysticercosis 1

disease shows no predilection for sex or race.

The most common clinical ﬁndings include epilepsy,

Ingestion of eggs of T.solium or

proglotidds (swine cysticercosis) intracranial hypertension, encephalitis and meningitis.

Epilepsy is the most common clinical manifestation, seen

in more than 70% of patients. In endemic areas, neuro-

Figure 2 Life cycle of Taenia solium. The cycle starts with

cysticercosis is the leading cause of late-onset epilepsy.

the ingestion of raw or undercooked meat containing larvae.

Seizures are secondary to perilesional inﬂammation in

The larvae reach the small intestine and attach to the intesti-

degenerating cysts, although infarction and vasculitis may

nal wall. The proglotidds containing thousands of eggs detach

also act as predisposing factors. Calciﬁed granulomas may

daily, are passed with the feces, contaminating water and soil.

1,8,10,11

also cause epilepsy.

Animals like pigs become infected by ingesting food contam-

Clinical manifestations usually have a slowly progres-

inated with eggs that develop in their intestine. They enter

sive onset; however, an acute presentation such as cerebral

the bloodstream and spread to muscle where larvae develop.

2,12

infarction secondary to vasculitis, may also occur.

When humans ingest this undercooked or raw meat containing

Tw o mechanisms can cause intracranial hypertension:

the cysticerci, the life cycle starts over again. Lastly, cysticerco-

(1) obstructive hydrocephalus secondary to intraventricular

sis occurs when humans become intermediate hosts by ingesting

cysts, arachnoiditis or granular ependymitis; and (2) mass

the eggs of Taenia solium.

1,2,13

effect in cases of very large cysts. Patients with neu-

rocysticercosis of the fourth ventricle may have transient

obstruction of the Sylvian aqueduct, whose symptoms and

Forms of infection with the cysticercus

signs are known as Bruns’ syndrome. This syndrome is caused

by an intraventricular mobile lesion, which leads to episodic

Humans may develop two types of disease, taeniasis and

obstructive hydrocephalus. This syndrome is characterized

cysticercosis. Taeniasis is acquired by eating pork meat

by headache, papilledema and loss of consciousness with

infected with cysts, while cysticercosis occurs by ingestion

rapid recovery induced by rotational movements of the

of T. solium eggs present in the feces of a human tapeworm head.9

carrier.

Cysticercotic encephalitis results from intense inﬂamma-

In taeniasis, the ingestion of tissues infected with larvae

tory response of the host to massive cysticercal infection

allows the development of the adult form of the parasite

of the brain parenchyma. Encephalitis is most common in

in the intestinal tract of the deﬁnitive host (i.e., humans),

young women and children, who present with altered con-

where eggs are produced and discharged, thus, perpetuating

sciousness, seizures, visual anomalies, headache, vomiting, 1

the cycle. 1,13

and papilledema.

In contrast, cysticercosis develops by means of fecal-oral

Invasion of subarachnoid spaces may result in thicken-

contamination. The embryos, hatched from the ingested

ing of the leptomeninges, but without signs of meningeal

eggs, reach the systemic circulation after actively cross- 1

irritation. Thickening along the base of the skull and the

ing the intestinal mucosa, although some are cleared by the

ventral aspect of the brainstem may entrap the optic chiasm

liver.1

and the cranial nerves, leading to nerve palsy or dysfunction.

Cysts lodge in capillaries, mostly in muscle and brain tis-

Up to 3---4% of cases of neurocysticercosis manifest as

sue, where they develop into immature cysts and, up to 14

brain strokes, with a prevalence of 3.4%. They include

three months later, into larval cysts. These cysts are pro-

lacunar or cortical infarct, transient ischemic attacks and

tected from the host’s immune response by the blood-brain

brain hemorrhage. Cerebrovascular complications are the

barrier and, as long as the cyst wall remains intact, there is

result of different mechanisms, including luminal narrow-

no inﬂammatory response.

ing due to subintimal thickening, vasospasm due to arteritis

When the parasite dies, from natural causes or therapy,

in perforating and midsized vessels, inﬂammatory pseudoa-

an inﬂammatory response with edema ensues, followed by 1,14---16

neurysms and thrombi.

calciﬁcation.1,7

The progressive midbrain syndrome is the result of mul-

Thereby, Taenia solium can cause the disease by the fol-

tiple infarctions in the midbrain and thalamus secondary to 1,8

lowing mechanisms :

occlusion of the perforating arteries that arise from the

basilar artery. These patients typically have a history of

1. Presence of the parasite itself (mass effect or obstruc-

shunted hydrocephalus secondary to diffuse leptomeningi-

tion).

tis, with neurological impairment, somnolence, paraparesis,

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 133

impaired vertical gaze, ﬁxed and dilated pupils, and urinary ventricular and spinal. Based on the stage, they are clas-

1,12

incontinence. siﬁed as non-cystic, vesicular, colloidal-vesicular, granular-

Spinal involvement is seen in only 1.5% of cases. Less nodular, and calciﬁed nodular.

frequently, spinal leptomeningitis can manifest as radicular

pain associated with muscle weakness. The most common

form is intradural-extramedullary spinal cysticercosis, which Classiﬁcation according to the location

17,18

usually manifests as spinal cord section syndrome.

Subarachnoid cysticerci

The subarachnoid location is the most common. The par-

Classiﬁcation asite reaches the basal cisterns, subarachnoid spaces and

meninges by hematogenous spread, eliciting an intense per-

The cysticercus enters the central nervous system through ilesional inﬂammatory reaction. This reaction involves the

the bloodstream, initially invading the subarachnoid space, leptomeninges at the base of the skull and may extend to

and then the cortex and the cortical---juxtacortical junction. the foramen magnum, resulting in basilar leptomeningitis

The macroscopic appearance of cysticerci varies according that can lead to entrapment of cranial nerves and arter-

to their location within the nervous system and stage of the ies. Involvement of the foramina of Luschka and Magendie

disease. Different stages of the disease and locations may may result in hydrocephalus. While subarachnoid cysticerci

coexist in the same patient. in the depth of cortical sulci are small, lesions located in

Neurocysticercosis may be classiﬁed according to the the Sylvian ﬁssure or in the basal cisterns may reach 5 cm

location and stage of the disease. According to the loca- in size (Fig. 3). This location facilitates hydropic degen-

tion, cysticerci are classiﬁed as subarachnoid, parenchymal, eration caused by continuous adsorption of cerebrospinal

Figure 3 Subarachnoid cysticerci. FLAIR MRI in the transverse plane (A) shows small cysts in the depth of the sulci of both parietal

lobes. Cystic lesions in the basal cisterns. Contrast-enhanced CT (B) and T2-weighted MRI (C), both in transverse planes, show the

basal cisterns occupied by cystic lesions with content similar to the cerebrospinal ﬂuid.

Figure 4 Parenchymal cysticerci. Contrast-enhanced CT (A), T2-weighted (B) and T1-weighted gadolinium-enhanced MRI

sequences in the transverse plane (C) show small cysts in the right frontal cortex, with minimal perilesional edema, ring enhancement

and scolex visible in the interior (arrow).

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

134 S. Sarria Estrada et al.

ﬂuid to the vesicle. In this situation, cysticerci do not in diameter, because their growth is limited by the pres-

develop a protoscolex or the scolex degenerates (racemose sure exerted by the brain parenchyma. Parenchymal forms

4,19

cysticercosis). include different stages, from viable cysts (cysts with scolex)

to degeneration that ends in calciﬁcations.

Parenchymal cysticerci

Parenchymal neurocysticercosis is the second most common Ventricular cysticerci

form of neurocysticercosis after the arachnoid form. Cysts Intraventricular cysticerci account for less than 33% of all

are usually located in the cerebral cortex and basal gan- cases of neurocysticercosis. Cysts vary in size and are usu-

glia, areas that get more blood supply (Fig. 4). Parenchymal ally solitary. The fourth ventricle is the most common site

cysts are usually small, and are rarely larger than 10 mm (50%), followed by the lateral ventricles (35%) and, less

Figure 5 Intraventricular cysticercus. Unenhanced CT (A) image shows a cyst in the fourth ventricle. T1-weighted gadolinium-

enhanced (B) and T2-weighted (C) MRI sequences in the axial plane, and high-resolution T2-weighted (D) and T1-weighted

gadolinium-enhanced (E) sequences in the sagittal planes show one intraventricular cysts obstructing the fourth ventricle, with

a lower mural nodule that enhances with gadolinium (arrow). Follow-up MRI after anticestodal drugs (F and G) shows a decrease

in size of intraventricular lesion, with persistence of minimal gadolinium enhancement in the lower margin of the fourth ventricle

(arrow). Courtesy of Dr. Antoni Rovira, Corporació Sanitària Parc Taulí, Sabadell.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 135

Figure 5 (Continued ).

frequently, the third ventricle (10%) and the Sylvian in the cortical---juxtacortical junction or in the basal gan-

1,20---22

aqueduct (5%) (Fig. 5). Parasites may adhere to glia, cerebellum, midbrain, cisterns or ventricular system

the ependymal layer, leading to ventriculitis (granular (Fig. 7).

ependymitis and subependymal gliosis), or may ﬂoat freely

within the ventricular cavities, leading to obstruction

Colloidal-vesicular stage

of cerebrospinal ﬂuid. Persistent obstruction leads to

In this stage, the larva dies and an inﬂammatory response

hydrocephalus and intermittent obstruction causes Bruns’

starts due to the release of metabolites. This causes intense syndrome.

Spinal cysticerci

Spinal cysticerci are very rare (1---3% of cases). The cysts

are located in the subarachnoid space that surrounds the

spine as a result of the spread of the larva throughout the

cerebrospinal ﬂuid (Fig. 6). Intramedullary cysticerci are

even rarer (<1%), most cases occurring in the dorsal spine.

Macroscopic appearance of spinal cysticerci is similar to

that of brain cysts. Leptomeningeal cysts may move freely

within the subarachnoid space and change their position

according to the movements of the patient during exami-

nation.

Stages of neurocysticercosis

Based on the stage and radiologic ﬁndings, neurocysticer-

cosis is divided into ﬁve stages: non-cystic, vesicular,

colloidal-vesicular, granular-nodular, and calciﬁed-nodular

(Table 1).

Non-cystic stage

The lesions correspond to tissue invasion by the cysticerci.

This stage is usually asymptomatic and therefore no imaging

studies are normally performed, but if performed, images

show focal areas of edema that may be associated with

nodular enhancement after contrast administration, on both

CT and MRI.

Vesicular stage

The host shows immune tolerance, as a result, there is only

minimal inﬂammatory reaction. The cysticercus appears as Figure 6 Spinal cysticercosis. Sagittal T2-weighted MRI of

a rounded cyst, a thin capsule surrounds the viable larva and dorsal spine (A), axial T2-weighted MRI of the lumbar spine(B),

the ﬂuid-ﬁlled vesicle. A cyst cavity that is isointense rela- and sagittal T1-weighted gadolinium-enhanced sequence of

tive to the cerebrospinal ﬂuid is seen on MR images. The cyst the lumbar spine (C) show intradural, intramedullary and

is 5---20 mm in diameter and has a 2 --- 4 mm mural nodule that extramedullary cysts of various sizes (arrows), located along

corresponds to the scolex. The scolex is isointense relative the spinal canal at the dorsal-lumbar segment, with associated

to the brain parenchyma on all sequences, enhancing after inﬂammatory reaction (arrow). Courtesy of Dr. Piedad Uruena,˜

IV contrast administration. The cyst is commonly located Instituto Neurológico de Antioquia, Medellín, Colombia.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

136 S. Sarria Estrada et al.

Table 1 Stages of neurocysticercosis.

Stage Pathophysiology MRI features

Non-cystic Tissue invasion by the cysticercus - Local focus of edema

- There might be nodular contrast

enhancement

- Usually no imaging studies are performed

Vesicular Minimal inﬂammatory reaction - Cyst: hypointense T1/hyperintense T2.

Cyst with scolex CSF-like signal.

- Scolex: isointense to parenchyma on T1

and T2, hypointense onT2* sequences,

hyperintense on FLAIR

Colloidal-vesicular Death of the parasite - Vasogenic edema surrounding the cyst.

Intense inﬂammatory response - Cyst: formation of capsule, hypointense on

T2 sequences. Increased signal in the cyst ﬂuid

- Ring-like contrast enhancement

- Formation of ﬂuid-ﬂuid level

Granular-nodular Absorption and cyst retraction - Residual cyst is smaller in size, thickening of

the capsule. Isointense to the parenchyma on

T1-/iso-hypointense on T2-weighted sequences

- Calciﬁed scolex (target appearance)

- Minimal vasogenic edema might persist

- Nodular or micronodular

contrast-enhancement

Calciﬁed-nodular Complete cyst involution - Calciﬁed nodule without

Mineralization contrast-enhancement

- Hypointense nodule on T2* sequences

CSF: cerebrospinal ﬂuid.

perilesional edema and formation of a capsule. This capsule both T2- and T2*-weighted sequences (Fig. 10). Cavernomas

1 --- 7

is hypointense on T2-weighted Images. Ring-like enhance- should be included in the differential diagnosis in this stage.

ment of the wall is seen in two-thirds of cases after contrast Patients with neurocysticercosis will frequently present

administration. As a result of the parasite’s death, there is with cysts in varying stages and in multiple locations.

hyperattenuation on CT images, and increased signal on MR

images. A ﬂuid-ﬂuid level can also be observed. In the stage,

the cyst begins to contract (Fig. 8). Diagnosis

Granular-nodular stage

Diagnosis of neurocysticercosis may be difﬁcult because

In this stage, absorption of the cyst ﬂuid results in

in many cases the infection with Taenia solium cannot

cyst contraction, with capsule thickening and scolex

be demonstrated. Therefore, the diagnosis is based on a

calciﬁcation. CT reveals an isoattenuating cyst with a

combination of epidemiological, clinical, radiological and

hyperattenuating calciﬁed scolex. Peripheral edema and

immunological (serological tests for the detection of anti-

enhancement after contrast administration persist. The

cysticercal antibodies in blood and cerebrospinal ﬂuid)

residual cyst is isointense on T1-weighted sequences rel-

criteria.

ative to the parenchyma and iso- to hypointense on T2

In 2000, a group of experts proposed a series of diagnostic

sequences. Nodular or micronodular enhancement is com- 25

criteria based on four categories :

monly observed in this stage, which suggests granuloma. A

target or bull’s-eye appearance is seen with the calciﬁed

scolex in the center of the lesion (Fig. 9).

1. Absolute criteria allow unequivocal diagnosis of neuro-

cysticercosis:

Calciﬁed-nodular stage --- Histologic demonstration of the parasite in brain or

In this stage, the cyst involutes completely. The granulo- spinal biopsy.

matous lesion has shrunk to a fraction of its initial size --- Scolex within a cystic lesion on CT or MRI.

and it is completely calciﬁed. Typically, CT shows a calci- --- Direct visualization of subretinal parasites by fundo-

ﬁed nodule without mass effect or contrast enhancement. scopic examination.

However, persistent enhancement can be identiﬁed in some 2. Major criteria are suggestive of neurocysticercosis, but

calciﬁed nodules. It has been suggested that the presence of do not conﬁrm the disease:

these lesions represents a risk factor for seizures after ther- --- Neuroimaging studies highly suggestive of neurocys-

apy. These lesions appear as small hypointense nodules on ticercosis.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 137

Figure 7 Vesicular stage. Unenhanced CT (A) shows a non-calciﬁed scolex (white arrow) and a small parenchymal calciﬁcation

adjacent to the cyst (nodular-calciﬁed stage) (black arrow). Axial T1-weighted gadolinium-enhanced (B), T2-weighted (C) and proton

density (D) MRI sequences. The cysts have similar signal and intensity to those of the cerebrospinal ﬂuid. On the proton-density

sequence, the scolex is hyperintense (white arrow) and shows no enhancement after IV contrast administration. No inﬂammatory

reaction is observed.

--- Identiﬁcation of anticysticercal antibodies by EITB The interpretation of these criteria permits two levels of

(Enzyme-linked immunoelectrotransfer blot assay) diagnostic certainty:

using puriﬁed antigens of Taenia solium.

--- Resolution of cysts after therapy with albendazole or

1. Deﬁnitive diagnosis, in patients with one absolute crite-

praziquantel.

rion or in those with two major criteria, one minor and

--- Spontaneous resolution of small ring-like enhancing

one epidemiological criteria.

lesions (<20 mm) in patients with seizures, without

2. Probable diagnosis, in patients with one major and two

other symptoms.

minor criteria, in those who have one major, one minor

3. Minor criteria are common but not speciﬁc of the disease:

and one epidemiological criteria, and in those who have

--- Neuroimaging studies demonstrating lesions compati-

three minor and one epidemiological criteria.

ble with neurocysticercosis.

--- Clinical features suggestive of neurocysticercosis,

such as epileptic seizures, focal neurological signs, Neuroimaging studies

intracranial hypertension and dementia.

--- Positive CSF ELISA (enzyme-linked immunosorbent

CT findings are based on the identification of a well-defined

assay) for the detection of anticysticercal antibodies

cystic lesion in the cortical---juxtacortical junction, basal

or antigens.

ganglia, cerebellum, midbrain, cisterns or ventricular sys-

--- Cysticercosis outside the CNS.

tem. The lesion may show minimal contrast enhancement,

4. Epidemiologic criteria refer to circumstantial evidence

and an enhancing mural nodule, corresponding to the scolex.

supporting the diagnosis of neurocysticercosis:

Chronic lesions of neurocysticercosis appear as calciﬁca-

--- Evidence of household contact with Taenia solium.

tions, readily visible on CT images.

--- Individuals living or coming from endemic countries.

Generally, MRI is more sensitive than CT for the diag-

--- History of frequent visits to endemic areas.

nosis of the disease, since it allows us to identify a larger

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

138 S. Sarria Estrada et al.

Figure 8 Colloidal-vesicular stage. Unenhanced (A and B) and post-contrast (C) CT images showing two extraparenchymal lesions

in the left frontal lobe with ring-like enhancement after IV contrast administration (white arrow). Calciﬁed nodules in the convexity

(black arrows). T2-weighted (D) and T-1 weighted gadolinium-enhanced (E) sequences in the transverse plane show two lesions.

The anterior one is in the colloidal-vesicular stage and the posterior in the vesicular stage. The former shows a peripheral halo with

hypointensity on T2 sequences and perilesional edema. Ring-like enhancement is visible after contrast administration.

number of lesions, classify the stage of the disease, and detection of the scolex, which appears as a hyperintense

determine the degree of inﬂammatory response (perile- eccentric nodule within the cyst.

sional edema and blood---brain barrier disruption). T1- and The low sensitivity and speciﬁcity of MRI in comparison

T2-weighted MRI sequences depict the cyst, which shows to CT for the determination of the presence of calcium has

similar signal to that of the cerebrospinal ﬂuid in the vesic- been traditionally considered a limitation. The detection of

ular stage. Diffusion MRI sequences demonstrate the fluid small parenchymal calcifications is a finding suggestive of

behavior within the lesions and help differentiate them from neurocysticercosis (calciﬁed-nodular stage). Currently, the

abscess. At the colloidal-vesicular stage (death of the par- use of higher magnetic ﬁelds and new sequences like mag-

asite), the protein content of the cyst increases and so netic susceptibility MRI help to overcome this limitation.

does the signal intensity of basic MRI sequences. In addi- Signal recording in magnetic susceptibility sequences allows

tion, during this stage there is formation of a capsule that reconstruction of phase and magnitude images from the

is hypointense on T2-weighted sequences. This hypointen- raw data. Magnitude images clearly depict lesions with

sity is due to the presence of free radicals produced by magnetic susceptibility, but cannot differentiate microhe-

macrophages; however, this finding is not specific since it can morrhage from calcification, unlike phase images, which

also be found during the early encapsulation of parenchymal can be used for their differentiation. The processed

abscesses. phase images show a negative phase (hypointense) for

Among the multiple imaging ﬁndings of neurocysticerco- paramagnetic substances and a positive phase (hyper-

sis, the presence of the scolex within the cyst is considered intense) for diamagnetic substances. Calciﬁcations are

patognomonic. The identiﬁcation of the scolex on the dif- considered diamagnetic substances and thus they appear

ferent sequences becomes therefore a primary goal. The with the opposite signal intensity in ﬁltered phase images

scolex is depicted on T1- and T2-weighted sequences as (hyperintense). Comparison of ﬁltered phase images with

an isointense nodule relative to brain parenchyma, and as magnitude images helps identify calciﬁcations and differen-

mildly to moderately hypointense on T2* sequences. Proton- tiate them from chronic microhemorrhages. This sequence

density and FLAIR sequences are more sensitive for the may demonstrate small, markedly hypointense nodules

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 139

Figure 9 Granular-nodular stage. Axial T1-weighted gadolinium-enhanced MRI sequences (A and B) and FLAIR sequences (C and

D) show small lesions with nodular and ring-like hyperenhancement located in left basal ganglia, left posterior temporal lobe and

both occipital lobes (black arrows) with associated vasogenic edema (white arrows).

in the brain parenchyma, often indistinguishable from calciﬁed-nodular stage the differential diagnosis should be

cavernomas. made with cavernomas and amyloid microangiopathy.

The use of a contrast agent permits identiﬁcation of Atypical presentations of neurocysticercosis may simu-

lesions with nodular enhancement in non-cystic and gran- late other neurological diseases. Basal arachnoiditis should

ular stages, and ring-like enhancement of the cystic wall be differentiated from carcinomatous meningitis, granulo-

in the colloidal-vesicular stage. Acquisition of T1-weighted matous diseases like sarcoidosis, tuberculosis and fungal

sequences in delayed phases after contrast administration meningitis. In spinal neurocysticercosis, the differential

increases the sensitivity for identiﬁcation of lesions. diagnosis should include ependymomas, cystic astrocy-

tomas, syringomyelic cavities, hydatid cysts and congenital

cysts (arachnoid and dermoid).

Differential diagnosis

Treatment

Differential diagnosis of neurocysticercosis in endemic areas

may be extremely difﬁcult due to the coexistence of tuber- Treatment of neurocysticercosis is controversial and

culosis and other parasitic infections. Ring-like lesions depends on the number, location and viability of cysts,

(solitary or multiple) in the parenchyma of the central and the presence of complications. Medical therapy is con-

nervous system are not speciﬁc for neurocysticercosis and sidered the ﬁrst choice, except in cases of intracranial

represent a diagnostic problem, since serological tests are hypertension requiring surgery. The use of cysticidal drugs

often negative. In colloidal-vesicular neurocysticercosis, the is based more on the geographic area and the clinician

differential diagnosis should include tuberculomas, pyo- experience than on consensus protocols. Cysticidal therapy

genic abscesses, toxoplasmosis, neurosyphilis, hydatidosis, itself initiates a host inﬂammatory response that increases

as well as primary and secondary neoplasms, while in the brain edema and may result in intracranial hypertension.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

140 S. Sarria Estrada et al.

Conﬂict of interest

The authors declare that they do not have any conﬂict of interests.

References

1. Kimura-Hayama ET, Higuera JA, Corona-Cedillo R, Chávez-

Macías L, Perochena A, Quiroz-Rojas LY, et al. Neurocys-

ticercosis: radiologic---pathologic correlation. Radiographics.

2010;30:1705---19.

2. Del Brutto OH. Neurocisticercosis: actualización en diagnóstico

y tratamiento. Neurología. 2005;20:412---8.

3. Saavedra H, Gonzales I, Alvarado MA, Porras MA, Vargas V, Cjuno

RA, et al. Diagnóstico y manejo de la neurocisticercosis en el

Perú. Rev Peru Med Exp Salud Pública. 2010;27:586---91.

4. Del Brutto OH. Neurocisticercosis. Rev Neurol. 1999;29:456---66.

5. Recommendations of the international task force for disease

eradication. MMWR Recomm Rep. 1993;42:1---38.

Figure 10 Calciﬁed-nodular stage. T2-weighted gradient- 6. Román G, Sotelo J, Del Brutto O, Flisser A, Dumas M, Wadia

echo MRI sequence in the transverse plane shows multiple N, et al. A proposal to declare neurocysticercosis a interna-

tional reportable disease. Bull World Health Organ. 2000;78:

nodular lesion markedly hypointense. Differential diagnosis

399---406.

should be made with cavernomas.

7. García HH, González AE, Tsang VCW, Gilman RH. Neurocysticer-

cosis: some of the essentials. Pract Neurol. 2006;6:288---97.

8. Sotelo J, Guerrero V, Rubio F. Neurocysticercosis: a new classiﬁ-

In general, treatment includes antiepileptic and cysticidal cation based on active and inactive forms. A study of 753 cases.

drugs (e.g., albendazole and praziquantel), corticosteroids Arch Internal Med. 1985;145:442---5.

and other anti-inﬂammatory agents used to control the 9. Coyle CM, Tanowitz HB. Diagnosis and treatment of neurocys-

1 --- 4

ticercosis. Interdiscip Perspect Infect Dis. 2009;2009:180742.

severe host inﬂammatory response.

10. Nash TE, Pretell J, García HH. Calciﬁed cysticerci provoke per-

ilesional edema and seizures. Clin Infect Dis. 2001;33:1649---53.

11. Relationship between epilepsy and tropical diseases. Commis-

Conclusion

sion on tropical diseases of the international league against

epilepsy. Epilepsia. 1994;35:89---93.

Due to the migration phenomenon that has taken place 12. Del Brutto OH. Cysticercosis and cerebrovascular disease: a

over the last decade, neurocysticercosis is no longer a rare review. J Neurol Neurosurg Psychiatry. 1992;55:252---4.

13. Rangel R, Torres B, Del Bruto O, Sotelo J. Cysticercotic

infection in Spain. As neurocysticercosis is the most com-

encephalitis: a severe form in young females. Am J Trop Med

mon parasitic disease of the central nervous system and

Hyg. 1987;36:387---92.

the most common cause of acquired epilepsy in developing

14. Rodríguez-Carbajal J, Del Brutto OH, Penagos P, Huebe J,

countries, radiologists should be familiar with the radio-

Escobar A. Occlusion of the middle cerebral artery due to cys-

logic ﬁndings of the disease and include it in the differential

ticercotic angiitis. Stroke. 1989;20:1095---9.

diagnosis of intracranial lesions, especially in patients from

15. Sawhney IM, Singh G, Lekhra OP, Mathuriya SN, Parihar PS,

endemic areas. Prabhakar S. Uncommon presentations of neurocysticercosis. J

Neurol Sci. 1998;154:94---100.

16. Kim IY, Kim TS, Lee JH, Lee MC, Lee JK, Jung S. Inﬂam-

Authorship matory aneurysm due to neurocysticercosis. J Clin Neurosci.

2005;12:585---8.

17. Shin DA, Shin HC. A case of extensive spinal cysticercosis involv-

1. Responsible for the integrity of the study: SSE, LFV and

ing the whole spinal canal in a patient with a history of cerebral

ARC.

cysticercosis. Yonsei Med J. 2009;50:582---4.

2. Conception of the study: SSE, LFV and ARC. 18. Collister RE, Dire DJ. Neurocysticercosis presenting to the emer-

3. Design of the study: SSE and ARC. gency department as a pure motor hemiparesis. J Emerg Med.

4. Acquisition of data: SSE, SSM and CAA. 1991;9:425---9.

19. Hawk MW, Shahlaie K, Kim KD, Theis JH. Neurocysticercosis:

5. Analysis and interpretation of data: SSE.

a review. Surg Neurol. 2005;63:123---32.

6. Bibliographic search: SSE, LFV and ARC.

20. Castillo M, Quencer RM, Post MJ. MR of intramedullary spinal

7. Writing of the paper: SSE, LFV and ARC.

cysticercosis. Am J Neuroradiol. 1988;9:393---5.

8. Critical review with intellectually relevant contrib-

21. Cuetter AC, García-Bobadilla J, Guerra LG, Martínez FM, Kaim

utions: SSM, CAA and LFV.

B. Neurocysticercosis: focus on intraventricular disease. Clin

9. Approval of the ﬁnal version: SSE, ARC, LFV, CAA and

Infect Dis. 1997;24:157---64.

SSM.

22. Sánchez L, Abad L, Lozano E, Maldonado G. Neurocisticercosis

10. All the authors have read and approved the ﬁnal version intraventricular. Presentación de un caso localizado en el tercer

of the manuscript. ventrículo. Radiología. 2002;44:309---13.

Document downloaded from http://www.elsevier.es, day 09/07/2015. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited.

Imaging ﬁndings in neurocysticercosis 141

23. Palacios E, Salgado Lujambio P, Rojas Jasso R. Computed tomo- 27. Lucato LT, Guedes MS, Sato JR, Bacheschi LA, Machado LR,

graphy and magnetic resonance imaging of neurocysticercosis. Leite CC. The role of conventional MR imaging sequences in

Semin Roentgenol. 1997;32:325---34. the evaluation of neurocysticercosis: impact on characteriza-

24. Teitelbaum GP, Otto RJ, Lin M, Watanabe AT, Stull MA, Manz tion of the scolex and lesion burden. Am J Neuroradiol. 2007;28:

HJ, et al. MR imaging of neurocysticercosis. Am J Roentgenol. 1501---4.

1989;153:857---66. 28. Haddar D, Haacke E, Sehgal V, Delproposto Z, Salamon G,

25. Del Brutto OH, Rajshekhar V, White Jr AC, Tsang VC, Nash TE, Seror O, et al. Susceptibility weighted imaging. J Radiol.

Takayanagui OM, et al. Proposed diagnostic criteria for neuro- 2004;85:1901---8.

cysticercosis. Neurology. 2001;57:177---83. 29. Wu Z, Mittal S, Kish K, Yu Y, Hu J, Haacke EM. Identiﬁcation of

26. García HH, Del Brutto OH. Taenia solium cysticercosis. Infect calciﬁcation with MRI using susceptibility-weighted imaging: a

Dis Clin N Am. 2000;14:97---119. case study. J Magn Reson Imaging. 2009;29:177---82.