Child's Nervous System

, Volume 34, Issue 10, pp 1957–1965 | Cite as

Pediatric neurocysticercosis

  • Ricardo Santos de Oliveira
  • Dinark Conceição Viana
  • Benedicto Oscar Colli
  • Vedantam Rajshekhar
  • José Francisco Manganelli Salomão
Special Annual Issue



Neurocysticercosis (NCC) is an infestation of the nervous system caused by encysted larvae of Taenia solium. NCC is an important acquired cause of epilepsy and other neurological manifestations especially in endemic areas. NCC in children has pleomorphic manifestations depending on the location, number, viability of the cysts, and host response. Even with advancing knowledge of the disease manifestations, many aspects related to diagnosis and treatment, particularly in children, still remain controversial and pose challenges to clinical practice. There is no gold standard test to diagnose NCC and the management recommendations are still emerging. This review provides an overview of diagnosis of NCC in children and its management with special focus on current challenges and future prospects.


In developing countries, NCC is important not only because of its frequency but also because of high morbidity and mortality rates associated, especially in cases in which it progresses to increased intracranial pressure. Because of its pleomorphic presentation, NCC should be considered in the differential diagnosis of a number of neurological conditions. Treatment with cysticidal therapy leads to reduction in seizure frequency and a faster resolution of lesions.


We have summarized the current approaches to diagnosis and treatment of NCC, recent advances in understanding the biology of NCC, and how one can take advantage of these new insights to formulate the next generation of clinical trials.


Brain Cysticercosis Epilepsy Hydrocephalus Intracranial hypertension Parasitic disease Parenchymal cyst 

Introduction and background

Human neurocysticercosis (NCC), an infestation caused by the larval stage (cysticercus) of the pork tapeworm Taenia solium, is the most common parasitic disease of the central nervous system worldwide [2]. Though it affects adults commonly, pediatric infestation is also well-recognized. NCC is endemic in most developing countries, particularly Latin America, the Indian subcontinent, Southeast Asian region, and sub-Saharan Africa. Globalization and travel have increased the incidence of NCC in many nonendemic countries including USA, UK, and Australia [8]. The rise in the number of cases of NCC in developed countries, especially in the USA, has largely been driven by the influx of immigrants from endemic to non-endemic regions and the widespread access to neuroimaging [31]. A recent systematic review on cysticercosis and T. solium teniasis in Europe showed an increasing trend; nearly 75% of imported cases were diagnosed in migrants and 18% in European travelers [40]. Among the symptomatic population, more than 5 million cases of preventable epilepsy worldwide are caused by NCC. In a recent systematic review, the pooled estimate of NCC among people with epilepsy was as high as 29% from Latin America, sub-Saharan Africa, and Southeast Asia [17]. In a community-based study of over 50,000 individuals in south India, 34% of patients with active epilepsy had a diagnosis of NCC based on contrast-enhanced CT imaging and enzyme-linked immunotransfer blot (EITB) [30]. Among patients with active epilepsy in North India, 25% of the cases tested positive for antibodies against T. solium [32]. The point prevalence of 4.5 per 1000 population has been noted in rural Northwest India [22]. Among children with partial seizures, NCC accounted for 50% of the cases in hospital-based series from India [35].

The parasite and its lifecycle

T. solium is a tapeworm belonging to cestoda class in the family Taeniida. The adult worm is found in the small intestine of humans. It is white in color and measures 2 to 3 m in length. Its head, the scolex, contains suckers and a protruding part with hooks, or rostellum, which attaches to the host intestinal wall. The body consists of several segments known as proglottids and each one acts as an independent reproductive unit containing both male and female reproductive organs.

The life cycle of T. solium involves two hosts: humans and pigs. Humans are usually the definitive host of T. solium with the adult worm residing in the small intestine (taeniasis) and pigs are the usual intermediate hosts harboring the larvae of the parasite (cysticercosis). The proglottids are shed in the human feces and break open outside the human body, releasing a large number of eggs into the environment. In places with poor sanitation and free-roaming pigs, pigs ingest human feces potentially containing T. solium eggs. After ingestion by the pigs, the eggs lose their coat, releasing embryos (hexacanthus or oncospheres) in the pig intestines. These actively cross the intestinal mucosa to the bloodstream, which carries them to the peripheral tissues, including the CNS, where they develop into the larval form or cysticerci. This disease in pigs is termed porcine cysticercosis. Cysticerci are cystic organisms composed of a complex wall surrounding a cavity that contains vesicular fluid and a scolex. The same process occurs when food or water contaminated with taenia eggs are accidentally consumed by humans. This disease in humans is termed cysticercosis, and when it involves the central nervous system, it is termed NCC. Humans who consume raw or undercooked pork infected with cysticerci (“measly pork”) can get taeniasis. In the digestive tract, the metacestode finds suitable conditions to evaginate and develop into the adult tapeworm, thus completing its natural evolutionary cycle. Hence, in humans, T. solium can cause two diseases—taeniasis, which occurs only in those who consume pork; cysticercosis, which can occur in any human being, whether vegetarian, pork consumer, or not. Human cysticercosis may also occur by self-infestation (eggs eliminated with stools of the individual himself) [4, 13] (Fig. 1).
Fig. 1

Illustration of the life cycle of NCC. The life cycle of Taenia solium (adult tapeworm) involves two hosts: humans and pigs. Humans are the definitive hosts and acquire intestinal infection (teniasis) from pigs, the intermediate hosts, by ingestion of undercooked pork infected with live cysticerci (encysted larvae). Humans acquire cysticercosis via consumption of food or water contaminated with T. solium eggs or by autoinfection. Neurocysticercosis (NCC) results when the larval stages lodge in the brain

Cysticercosis and central nervous system

The hexacanth embryo reaches the CNS, through the bloodstream, lodging in the brain parenchyma by occluding capillary vessels usually at the gray-white junction. After actively crossing the capillary wall, the embryo reaches the interstitial space where it evolves to the cystic form, transforming into cysticercus [11]. There are two basic forms of NCC: isolated cysts or cysticercus cellulosae (CC) and racemose cysts or cysticercus racemosus (CR). CC are usually intraparenchymal and pass through a sequence of four morphological stages: vesicular, colloidal, granular nodular, and nodular calcified stage. CR are extraparenchymal (ventricles, subarachnoid space, cisterns); they tend to grow irregularly according to the available space and can elicit a strong inflammatory response especially in the sub-arachnoid spaces. This racemose form may reach enormous size without scolices and has peculiar appearances and mass effects. Intraventricular cysts may cause acute hydrocephalus due to direct or inflammatory obstruction [15].

Pathological anatomy

The cysticerci in the brain and other tissues undergo a natural process of involution or degeneration within a variable period of ranging from a few weeks to several years. This process starts after the transformation of the hexacanth embryo into the cysticercus. The initial stage is a live or active cyst (vesicular stage) followed by a stage in which the cyst begins to undergo degenerative changes with thickening of the membrane and replacement of the clear fluid with a whitish gel (colloidal stage). With the progression of this process, the wall becomes thicker and the gel undergoes calcium deposition (granular stage), and finally, the cyst becomes completely calcified, being reduced to one third or one fourth of its original size (calcified nodular stage) [4]. Microscopically, the demonstration of the parasite is diagnostic. A variable inflammatory process and edema are seen in the surrounding tissues and in part depend on the stage of the process. Severe inflammatory reaction can also be seen in the leptomeninges and ependyma when the cysts are in the subarachnoid spaces or the ventricles. Occlusion of small vessels in the subarachnoid spaces may result in brain infarction.

Clinical presentation

The clinical manifestations in children are pleomorphic depending on the burden of cysts, their location, and size. Clinical manifestations can vary from completely asymptomatic infestation to severe disease and death. NCC should be suspected clinically in any normally developing child with sudden-onset seizures, headache, vomiting, or focal motor deficits where there is no other evidence of an underlying neurological disorder. Seizures are a very frequent manifestation in patients with degenerating parenchymal cysts. In Indian children, the commonest presentation of NCC is in the form of a single degenerating parenchymal cyst, the solitary cysticercus granuloma (SCG) [26]. This presentation is seen in nearly 60 to 70% of all Indian patients with NCC [32]. Mechanisms of epileptogenesis in neurocysticercosis are the subject of debate, and likely include local inflammation and the formation of reactive gliotic scars [6].

However, in endemic areas, physicians should be aware of the atypical presentations of NCC such as communicating hydrocephalus, vasculitis, strokes, dorsal midbrain syndrome, brain stem dysfunction, ptosis, amaurosis fugax, dystonia, neurocognitive deficits, and psychiatric disturbs. Due to the lack of specific neurological symptoms, diagnosis on clinical grounds alone is impossible and needs to be substantiated with neuroimaging and serology [34]. The interaction of several factors, including variations in native versus acquired immune responses and age or sex-related differences in reactivity of the immune system, could be responsible for the the patterns of disease expression [12].


Histological confirmation of the parasite is not possible in most cases; therefore, diagnosis is usually based on neuroimaging and confirmed by serology. Despite modern neuroimaging methods and reliable immune diagnostic tests, diagnosis of neurocysticercosis can still be a challenge because of the low specificity of clinical and neuroimaging findings and low sensitivity and specificity of immunodiagnostic tests, particularly in endemic settings [36]. Hence, clinicians are forced to rely on diagnostic criteria. Diagnostic criteria for SCG have been defined and validated in prospective studies [25]. These diagnostic criteria have a high sensitivity and specificity (> 99%) in endemic settings. Diagnostic criteria have also been evolved for NCC in general [3, 9]. The sensitivity and specificity of these criteria are less than those for SCG and only one has undergone some degree of validation.

The most reliable serological test, presently available, is the enzyme-linked immunoelectrotransfer blot (EITB) assay (developed by Centers for Disease Control, Atlanta, USA in 1989), which uses lentil lectin-purified glycoprotein antigens (LLGP) to detect antibodies to T. solium in serum [37]. For the EITB, testing of serum rather than CSF is recommended. EITB sensitivity is around 98% for patients with two or more live parasites in the nervous system; thus, people with more than one viable parenchymal cyst, ventricular or subarachnoid disease at the time of testing will have a positive serology. EITB does not cross-react with heterologous infections [37]. A major weakness of EITB is its low sensitivity (50–60%) in patients with SCG [20, 28, 29] and even lower sensitivity in those with calcific lesions; therefore, a negative test cannot exclude NCC. Another major limitation of the EITB is that a positive test only indicates exposure to the larval antigen and does not necessarily indicate disease. EITB also remains positive for up to a year after the disease has been treated. Detection of anticysticercal antibodies in the CSF by ELISA is 89% sensitive and 93% specific in patients with viable neurocysticercosis infections and is still used when EITB is not available [18]. Parasite DNA detection by PCR has also been used for diagnosis from CSF and fecal samples [16]. Real-time CSF PCR has been shown to confirm the diagnosis of NCC in cases suggested by clinical, imaging, immunologic, and epidemiologic features. Comparison of immunodiagnostic assays (antibody detection by ELISA and EITB and HP10 antigen detection by ELISA) with PCR-based detection of parasite DNA from CSF suggests the role of PCR primarily in NCC cases not diagnosed by the available radiological or immunological tests [16, 39].

CT and MRI show the morphology and localisation of cysts, burden of infection, stage of the cysts, and the presence of surrounding inflammation (Fig. 2). The imaging characteristics of typical parenchymal NCC vary according to the pathological staging of the cyst [14]: (a) vesicular stage: characterized by small cyst with fluid similar to cerebrospinal fluid (CSF), thin wall, and an eccentrically located scolex, showing no contrast enhancement of the cyst’s wall and no surrounding tissue edema; (b) colloidal vesicular stage: density and signal intensity of the cystic fluid are different from that of CSF and show a thicker cyst wall, ill-defined shrunken scolex, and ring-like enhancement with perilesional edema; (c) granular nodular stage: characterized by small enhancing cyst or nodule, with mild surrounding edema and little mass effect; (d) nodular calcified stage: characterized by small calcified nodule with no edema and is best seen on CT.
Fig. 2

Neuroradiological imaging of human neurocysticercosis. a Viable cysts in lateral ventricle in axial flair MR scan. b Fourth ventricle cyst in posterior fossa in T1-weighted sagittal MR scan. c Solitary cysticercus granuloma in the left posterior temporoparietal region. d Solitary cysticercus granuloma with spontaneous resolution after 6 months. e, f Solitary cysticercus granuloma resolving with a calcific residue after 1 year. g, h Massive parenchymal neurocysticercosis. i Intraparenchymal cysticercosis with a huge racemose cysticercus compressing the left brain hemisphere. j CT scan showing many brain calcifications suggestive of NCC

Disease management

Therapeutic approaches might include symptomatic therapy (anti-epileptic drugs (AEDs) in most patients), antiparasitic treatment, or surgery (lesion resection or shunt placement), and often more than one of these options are needed. In the vast majority of patients, surgery is not required.

Children with SCG can be managed with AEDs alone as spontaneous resolution of the granuloma is expected (Fig. 2c–f) [23]. However, cysticidal drugs such as albendazole may hasten the resolution, and some evidence suggests that it might lead to possible better seizure outcome.

Medical treatment

In the definitive therapy, for cyst destruction, antihelminthic drug albendazole has been used in a dose of 15 mg/kg/day in two or three divided doses for 28 days, although shorter courses of 14 to 8 days have also been used [12, 13]. Resolution of the lesion on CT scans at 3 months was seen in 68.3 and 68.8% in the 1- and 4-week treatment groups, respectively. Although resolution of the active lesions on CT was observed after 3 months of the treatment, cured patients remain seropositive even after 1 year of the treatment. It indicates that persistent seropositivity does not necessarily indicate active infection [1]. Praziquantel is the older cysticidal drug and is used in a dose of 50 mg/kg/day for 15 days. A single-day praziquantel therapy (25 mg/kg/dose every 2 h × 3 doses) has been reported to be as effective as 7-day treatment with albendazole. Side effects of praziquantel include abdominal pain, dizziness, headache, and allergic reactions in rare cases [36]. Cysticidal therapy at the outset is contraindicated in children with markedly elevated intracranial pressure and ophthalmic cysticercosis due to the risk of inducing an inflammatory response and clinical worsening. Corticosteroids alone are preferred in such cases. Cysticidal therapy has no effect on calcified lesions [32].

Surgical treatment

Surgery is infrequently needed in children with NCC [24]. One of the commonest indications for surgery in these children is for the excision of intraventricular cysts [24]. Cisternal Forms Causing Local Compression-Patients with cisternal cysts usually harbor racemose cysticerci in the basal cisterns; the lesions are varied in size and cause symptoms of local compression independent of signs of hydrocephalus or mass effect-induced intracranial hypertension. Among cranial nerves most affected by cysticerci or arachnoiditis-induced local compression are the optic nerve and the chiasm, the oculomotor, the trigeminal, and the facial nerves (Fig. 3a, b). Direct excision of the cysticerci in the basal cisterns is not a safe and effective procedure. Only in rare cases can all cysts be removed because they are usually multiple and are frequently degenerated in part and adherent to the cranial nerves, vessels, and brain parenchyma due to arachnoiditis [4]. Forms Progressing to Intracranial Hypertension-The incidence of increased ICP in patients with cerebral cysticercosis ranges from 25 to 65.9% [15]. These patients could be classified in three groups according to the pathophysiological mechanism of the hypertension: (1) hypertension caused by space-occupying cysticerci (tumoral form), (2) hypertension caused by diffuse cerebral edema (pseudotumoral form), and (3) hypertension secondary to hydrocephalus caused by obstruction of CSF circulation. Complete resection of giant cysts is usually relatively easy when the cyst is located within the parenchyma or cisterns, as well as when they are in the active phase because they are only loosely adherent to the parenchyma. Degenerating cysts may adhere firmly to the nervous tissue and to blood vessels due to inflammatory reaction, especially those located in the cisterns. Resection of these cysts, especially those close to eloquent areas of the brain, is usually associated with a considerable risk of additional lesions [4].
Fig. 3

Basal subarachnoid neurocysticercosis. Axial (a) contrast-enhanced T1-weighted MR images of the brain revealing several cysts in the parenchyma, cisterns (interhemispheric, left-sylvian fissure, and peri-mesencephalic). Control coronal (b) contrast-enhanced T1-weighted MR images showing progressive hydrocephalus due to increase in the size of the interhemispheric cyst occluding the foramen of Monro. This cyst was endoscopically removed. Intraoperative photograph of the posterior fossa obtained with the patient in the sitting position. c A degenerating racemose cysticercus was observed in the cerebellopontine angle compressing and distorting the VII-VIII cranial nerves. d After surgical opening of the cyst, multiple adherences were observed involving cranial nerves with associated arachnoiditis

Pseudotumoral or Encephalitic Form-This form is characterized by increased ICP secondary to a diffuse inflammatory reaction of the brain parenchyma due to massive infestation with cysticerci, and it is more frequent in the pediatric population. Treatment of this form is primarily medical to reduce the intracranial hypertension. Osmotic diuretics and steroid agents are effective in most cases. Decompressive craniectomy can be considered for patients refractory to medical therapy.

Hydrocephalus is the most frequent mechanism of intracranial hypertension in NCC and may be caused by mechanical obstruction of the CSF pathways. Obstruction results from either cysts themselves, inflammatory reaction (ependymitis, arachnoiditis), or both. It may also be caused by reduced absorption of CSF due to parasagittal arachnoiditis, with involvement of arachnoid villi. Endoscopic removal of cysts may be required in cases of intraventricular and subarachnoid NCC as well ventriculoperitoneal (VP) shunting for hydrocephalus. Free cysts located inside the lateral ventricles or third ventricle can also be reached by endoscopy. Access to the fourth ventricle is obtained by posterior fossa craniotomy, and the free cysts can spontaneously protrude through the foramen of Magendie toward the cistern magna and be removed without or with minimal traction (Fig. 4). The placement of a VP shunt has been considered the best treatment for patients with hydrocephalus due to inflammatory obstruction caused by cysticercosis and/or arachnoiditis, allowing for resolution of increased ICP in 50 to 90% of cases. However, VP shunt malfunction is frequent and shunt revisions are required in more than half of the patients, mainly during the first postoperative year [4].
Fig. 4

Intraoperative photograph of the posterior fossa obtained with the patient in sitting position. Surgical removal of a free cysticercus in the fourth ventricle. After gentle lateral displacement of the cerebellar tonsils, the cyst is spontaneously protruding from the ventricle leading to “delivery” of the cysticercus (asterisk). Note that the cyst membrane is transparent (arrow), its fluid content is colorless and that there is no arachnoiditis in the posterior fossa

Spinal cord cysticercosis

Intradural spinal cysticercosis can be subdivided in leptomeningeal (subarachnoid) or intramedullary (parenchymal) forms, the former being the most prevalent type of spinal parasitic infestation. There are several possible routes by which the parasite reaches the spinal cord parenchyma or CSF. (1) One is the hematogenous (venous) route, through retrograde blood flow via the inner vertebral venous plexus and the intervertebral veins. (2) A second possibility is the ventriculoependymal route: during intraventricular hypertension, the central canal of the spinal cord could dilate, allowing the cysticercus to migrate from the fourth ventricle into the spinal cord. Additionally, the ependymal canal is usually open until the 12th year of age, providing the small embryos a natural pathway into the spinal cord, before they transform into the 5- to 18-mm cysticerci. (3) A third possible route is through the subarachnoid space, followed by transpial migration into the spinal cord, a phenomenon that would explain the intramedullary form (although it is unlikely, if at all possible) [5]. Although some patients may be best treated with anticysticidal agents, surgical treatment with laminectomy and excision of the cysticerci is still indicated in cases of spinal cord or radicular compression by free cysts. In symptomatic patients with intramedullary cysts, surgery is commonly indicated for decompression of the spinal cord as well as to provide a diagnosis (Fig. 5).
Fig. 5

Spinal cord cysticercosis. a, b Sagittal and axial T1-weighted MR images of the spinal cord showing an intramedullary dorsal cyst (arrow). ce Intraoperative photograph of the spinal cord demonstrating the presence of an intramedullary cyst and microsurgical ressection. f Degenerating cyst

Prognosis and outcome

The follow-up of children with NCC needs to be individualized. In children with persistent lesions, an additional course of cysticidal therapy is usually given. The outcome depends upon the type of NCC, cyst location (parenchymal better than extraparenchymal), and numbers (single lesions better than multiple). SCG has a good prognosis with lesion disappearing within 6 months in more than 60% of the cases allowing early withdrawal of AEDs in those in whom the lesion has resolved [23, 27]. The seizures are usually well controlled with just one AED. Recurrence of seizures in children with single lesions varies from 10 to 20%, whereas multiple and calcified lesions have frequent seizure recurrences [7]. Children with a single ventricular cyst also have a good outcome following excision of the cyst. The prognosis is poor in children with cysticercotic encephalitis and racemose NCC [13, 34].

Future directions

In order to improve the management of children with NCC, it is important to develop validated criteria for diagnosis, since the current available criteria have not been validated conclusively. Newer insights into the immune mechanisms underlying symptomatic human cysticercosis and helminth-induced immune suppression are being obtained through recent studies. Toll-like receptor-4 and soluble intercellular adhesion molecule K469E polymorphisms have been suggested to predispose to symptomatic infection [33, 38]. The understanding of these immune and genetic mechanisms will help develop newer drugs such as tamoxifen and newer drug delivery systems such as lactic acid conjugated solid lipid nanoparticles bearing albendazole and prednisolone, for effective management of NCC [10, 19]. Recent studies showing up regulation of certain genes in patients with NCC associated seizures/epilepsy might lead to better understanding the biology of the disease and also contribute to the development of simple serological tests for the disease [21].


NCC is an important acquired cause of epilepsy and other neurological manifestations especially in endemic areas. Because of its pleomorphic presentation, NCC should be considered in the differential diagnosis of a number of neurological conditions. NCC can also be conceptualized as a human model for development of seizures and epilepsy, and properly designed studies should yield valuable information about genetic predisposition, pathological mechanisms, and potential therapeutic targets for chronic epilepsy. Finally, if local elimination of transmission is confirmed and replicated, this will open the door to cysticercosis eradication efforts worldwide. Children with single or few lesions have a good outcome. Development of newer cysticidal drugs and drug delivery systems for both human and swine population are the potential areas of research.


Compliance with ethical standards

Conflict of interest

There was no financial support nor industry affiliations involved in this work. None of the authors has any personal or institutional financial interest in drugs, materials, or devices.


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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Division of Neurosurgery and Pediatric Neurosurgery, Department of Surgery and Anatomy, University Hospital of Ribeirão Preto Medical SchoolUniversity of São PauloSão PauloBrazil
  2. 2.Department of Neurological SciencesChristian Medical College HospitalVelloreIndia
  3. 3.Division of Pediatric Neurosurgery, National Institute of WomenChildren and Adolescents Health Fernandes Figueira - Oswaldo Cruz Foundation (IFF - Fiocruz)Rio de JaneiroBrazil

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