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Journal of Clinical Neuroscience 16 (2009) 867–876
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience
journal homepage: www.elsevier.com/locate/jocn
Review
Neurocysticercosis: A review of current status and management
Sumit Sinha *, B.S. Sharma
Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, Ansari Nagar, Aurobindo Marg, New Delhi 110 029, India
a r t i c l e
i n f o
Article history:
Received 14 September 2008
Accepted 31 October 2008
Keywords:
Neurocysticercosis
Cysticidal therapy
Surgical management
Endoscopy
a b s t r a c t
Neurocysticercosis (NCC) is an infection of the brain and its coverings by the larval stage of the tapeworm
Taenia solium. It is the most common helminthic infestation of the central nervous system and a leading
cause of acquired epilepsy worldwide. NCC induces neurological syndromes that vary from an asymptomatic infection to sudden death. Neuroimaging is the mainstay of diagnosis. The diagnosis is suggested
in patients living in endemic areas with typical CT scan findings and a compatible clinical picture. Since
the late 1980s, successful medical treatment has been established with relatively short courses of either
albendazole or praziquantel. The selection of cases for medical or surgical treatments has improved and
these two forms of therapy are complementary. In general, indications of surgery are: cysts that compress
the brain and cranial nerves locally, intracranial hypertension or edema refractory to medical treatment,
intraventricular NCC, spinal NCC with cord or root compression and ocular cysts. Recently, endoscopic
approaches for ventricular NCC have been developed, which are now the treatment of choice for ventricular NCC with hydrocephalus.
Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction
3. Clinical presentation
Neurocysticercosis (NCC) is an infection of the brain and its coverings by the larval stage of the tapeworm Taenia solium. It is the
most common helminthic infestation of the central nervous system
(CNS) and a leading cause of acquired epilepsy worldwide.1–6 NCC
results from ingestion of the eggs of T. solium. The oncospheres
hatch in the intestine, penetrate the intestinal wall and disseminate to several body tissues, showing strong tropism to the CNS.
The clinical manifestations of NCC are non-specific and varied
and depend on the number of lesions and the developmental stage
of the cysticercus. Seizures are the commonest manifestation,
occurring in 50% to 80% of patients.3,4 NCC has been classified
depending on the location of cysts, its clinical presentation, prognosis and cyst viability.7–10
NCC induces neurological syndromes that vary from an asymptomatic infection to sudden death. Differences in the clinical picture depend on the number, size, stage and localization of cysts
and the patient’s immune response. Patients commonly present
with seizures or headaches.5,6 The clinical manifestations of NCC
are listed in Table 1.
2. Pathogenesis and life cycle
T. solium has a complex life cycle, requiring two hosts (Fig. 1).
Humans are the definitive host whereas pigs are the intermediate
host.3,4 Humans can also act as intermediate hosts after ingestion
of Taenia eggs. The disease manifests itself as two distinct clinical
entitites: taeniasis and cysticercosis.
* Corresponding author. Tel.: +91 11 26731172/+91 9868398244; fax: +91 11
26106803.
E-mail addresses: sumitaiims@yahoo.com, sumitneuro@gmail.com (S. Sinha).
0967-5868/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jocn.2008.10.030
3.1. Parenchymatous form (Figs. 2-6)
In the parenchymatous form, the parasite lodges in the brain
parenchyma as single (Fig. 2) or multiple cysts forming clumps.
Epilepsy is the most common clinical manifestation. Pericystic
inflammation results in a granuloma formation, which is the cause
of epilepsy in most patients (Fig. 2). The cysts may continue to
grow and produce a tumor-like syndrome. In India, the single small
enhancing lesion (SSEL) is the commonest form of parenchymatous
NCC.11–13 It commonly presents with simple partial seizures, partial complex seizures, simple partial seizures with secondary generalization or generalized seizures. Tuberculous granuloma,
microabscess, focal meningo-encephalitis, neoplasms and vascular
lesions should be considered in the differential diagnosis.14–16
Chandy et al. reported that 12 out of 15 patients with SSELs were
shown to have cysticercosis.17
In disseminated or miliary NCC, there are multiple cysts in varying stages of development (i.e. living, dying and calcified cysts)
(Fig. 3). There may be associated extracranial (i.e. conjunctival,
subcutaneous or muscle) cysts. This variety is uncommon but
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S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
Ingestion raw
pork
HUMAN
Cysticerci in
small
intestine
HUMAN
Cysticerci in
brain, muscle,
eyes
Cross GIT
PIG
Cysticerci in
brain, muscle,
eyes, other
organs
Cross GIT
HUMAN
Oncospheres
in stomach
HUMAN
Cestode in
small
intestine
Feco-oral contamination
PIG
Oncospheres
in stomach
Ingestion of human feces
Proglottids and eggs
excreted in feces
Fig. 1. Life cycle of Taenia solium. Cysticerci are the larval cyst of the parasite, oncospheres are the embryonic form and the cestode is the adult form of the tapeworm.
Proglottids are the segments of the tapeworm, which can detach and reproduce independently. Taeniasis is intestinal infection with the adult tapeworm (gray shaded boxes)
while cysticercosis is systemic infection with larval cysts (unshaded boxes). GIT = gastrointestinal tract.
Table 1
Clinical manifestations of neurocysticercosis (after91)
Clinical manifestation
Pathology
Epilepsy
Raised intracranial pressure
Pericyst inflammation, granuloma formation
Hydrocephalus (arachnoiditis, ependymitis,
ventricular cysts), pseudotumor (edema), giant
cysts, cysticercal encephalitis
Direct compression by large or multiple cysts
Widespread subarachnoid inflammation
Inflammation, local mass effect, vasculitis
Focal deficits
Meningitis
Myelo radiculopathy
Others
Mental changes (dementia)
Encephalitis
SAH
Trigeminal neuralgia
Subdural hematoma
Stroke/TIA
Dizziness
Endocrinological or
ophthalmic symptoms
CSF = cerebrospinal
ischaemic attack.
fluid,
Multiple parenchymatous cysts
Intense inflammation and edema
Inflammatory aneurysm27
Arachnoiditis28
Collection of multiple cysts29
Angiitis30,31
Intermittent CSF obstruction
Sellar/intraocular cysts
SAH = subarachnoid
haemorrhage,
TIA = transient
may have a malignant course with unfavourable prognosis. It is
most frequently seen in children and adolescents and presents like
an acute or subacute allergic or viral encephalitis.18
There are four stages of development of a parenchymal larval
cyst: vesicular, colloidal, nodular and calcified. The vesicular cyst
is viable, where the scolex exists as an eccentric nodule within
the cyst, and there is little or no enhancement due to a minimal
host immune response (Figs. 4–6). As the scolex dies after cysticidal treatment or an effective immune response, the transparent
vesicular fluid is replaced by a viscous and turbid fluid, which is
readily identifiable on MRI.19 The fluid migrates from the degenerating cyst into the surrounding parenchyma and incites a strong
Fig. 2. Contrast enhanced axial CT Scan of a patient with neurocysticercosis
showing a single dying parenchymal cyst (solitary cerebral cysticercal granuloma)
(arrow) with a scolex of Taenia solium and surrounding perilesional edema.
immune response, characterized by strong enhancement on contrast CT scans or MRI. This is the colloidal cyst, which has contrast
enhancement but lacks a well-defined scolex. As the cyst further
degenerates, it develops into a nodular cyst, which still shows some
contrast enhancement. Finally, the degenerated cyst calcifies and is
recognized as a punctuate calcification on CT scan (Fig. 3).
S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
869
3.3. Intraventricular and subarachnoid (cisternal) forms (Figs. 7–12)
The intraventricular and subarachnoid (cisternal) forms of NCC
are seen in 15% to 54% of patients and present clinically in a more
aggressive manner as compared to the parenchymatous form.21–23
The oncosphere reaches the ventricular cavity via the choroid
plexus. The parasite migrates through the ventricular system,
occluding CSF communication corridors, causing acute episodes of
ventriculomegaly with sudden death, or mass effect with focal
compression. About 38% of patients present with rapid clinical
deterioration. Larval death initiates ependymitis and occlusion of
ventricular outlets, producing hydrocephalus.21,24 Patients commonly present with raised intracranial pressure caused by large
cyst size or load, occlusion of CSF pathways, associated ependymitis
and basal arachnoiditis.22 Ventricular entrapment may occur secondary to ependymitis and cause double compartment syndrome.21
The intraventricular form has a rapidly progressive clinical
course and demands prompt action. It tends to occur in isolation
in most patients; however, parenchymatous disease may be associated in 24% of patients.23 The fourth ventricle is the commonest
site (53%) (Figs. 8–10), followed by the third ventricle (27%), lateral
ventricle (11%) and the aqueduct (9%) (Fig. 7). Isolated cystic lesions within the lateral ventricle are mobile (migratory); transventricular migration is towards the fourth ventricle due to the effects
of gravity. This results in entrapment of the cyst in the fourth ventricle because of the size of the foraminae of Luschka and
Magendie.
3.4. Spinal form
Fig. 3. Noncontrast axial CT Scan of a patient with neurocysticercosis showing
multiple (arrows) punctate calcified lesions in the disseminated variety of
neurocysticercosis.
3.2. Meningeal form
The meningeal form commonly presents with raised intracranial pressure secondary to widespread subarachnoiditis, arachnoiditis and adhesions resulting in cerebrospinal fluid (CSF)
obstruction and hydrocephalus. It may also manifest as focal deficits due to vasculitis and fibrous entrapment of cranial nerves.7,20
The spinal form occurs in 1.6% to 13% of patients with NCC. The
clinical features depend on the lodgment site of the parasite. Two
forms of spinal NCC are recognized: (i) leptomeningeal (extramedullary) and (ii) intramedullary. The leptomeningeal (extramedullary) form is 6 to 8 times more common than the intramedullary
form. This form occurs as a consequence of downward migration
of larvae from the cerebral to the spinal subarachnoid space. The
intramedullary form is uncommon. It occurs through hematogenous or ventriculoependymal migration. The parasite commonly
lodges in the thoracic spinal cord according to percentage distribution of blood flow to the spinal cord.25,26
Figs. 4–6. (left to right) 4: Viable parenchymal cyst. Fluid attenuated inversion recovery (FLAIR) axial MRI showing a viable parenchymal cyst. 5: T2-weighted coronal MRI
showing a cyst with the scolex seen as a central low density lesion. 6: Contrast enhanced axial T1-weighted MRI showing a viable cyst (vesicular cyst) with the scolex seen as
an eccentric nodule within the cyst. Note the minimal contrast enhancement due to a weak host immune response.
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Fig. 7. Noncontrast axial CT Scan showing a cyst in the aqueduct (arrow) causing
obstructive hydrocephalus.
Fig. 8. Noncontrast axial CT Scan showing a fourth ventricular cyst with obstructive
hydrocephalus. Note the deformation of the shape of the ventricular cavity and the
same density of the cyst and cerebrospinal fluid, making them indistinguishable.
4. Diagnosis of NCC
The diagnosis of NCC is suspected in patients living in endemic
areas presenting with a compatible clinical picture and lesions suggestive of NCC on CT scans. Neuroimaging is the mainstay of diagnosis of NCC. Table 2 shows proposed objective diagnostic
criteria.32 These criteria are complex and need validation in population or hospital-based studies. The major drawback of these criteria is that they do not differentiate between NCC and
tuberculoma, which is of utmost importance in endemic countries,
such as India.33–35 Moreover, access to enzyme-linked immunoelectrotransfer blot assay (EITB) is limited in India and consequently the usefulness of these criteria has been questioned.36,37
4.1. Radiological investigations
4.1.1. Plain X-ray
Plain X-rays of muscles and the skull may show cigar-shaped
calcifications.
4.1.2. CT scan of the head
CT scans have a sensitivity and specificity of over 95% in the
diagnosis of NCC,38,39 but it is much lower for diagnosing ventricular or cisternal forms of the disease. CT scans are optimal for
detecting calcifications, which occur in about 50% of patients.
On a CT scan, cysts may appear as single or multiple, rounded
lesions of variable size and low density, with a small, hyperdense,
eccentric mural nodule representing the scolex. This gives a ‘‘starry
night” effect in the parenchyma (Fig. 3). Ring enhancement occurs
with an inflammatory reaction or a granuloma formation. Perilesional edema is seen around dying cysts (Fig. 2). The ventricles
may be either small or there may be hydrocephalus. In fourth ventricular cysts, there may be deformation or rounded enlargement
of the ventricular cavity (Fig. 8). Ventricular or periventricular
enhancement suggests ependymitis. The encephalitic variety
shows extensive edema. Degenerative cysts are seen as single or
multiple pinhead-sized calcified dots without preferential localization (Fig. 3). A ‘‘honeycomb appearance” may be due to additional
Table 2
Diagnostic criteria for definitive or probable diagnosis of neurocysticercosis (after32)
Level of
criteria
Findings
Absolute
Major
Pathologic demonstration of the parasite; CT scans or MRI showing a cystic lesion with scolex; direct funduscopic visualization of parasite
Lesions highly suggestive of neurocysticercosis on neuroimaging; positive serum enzyme-linked immunoblot assay for cysticercal antibodies; resolution of
cysts after antiparasitic therapy; spontaneous resolution of a small solitary enhancing lesion
Lesions compatible with neurocysticercosis on neuroimaging; clinical manifestations suggestive of neurocysticercosis; positive cerebrospinal fluid enzymelinked immunosorbent assay for anticysticercal antibodies or cysticercal antigens; cysticercosis outside of the central nervous system
Household contact with Taenia solium infection; immigrants from or living in an endemic area; history of frequent travel to disease-endemic areas
Minor
Epidemiologic
Diagnosis: definitive – one absolute criterion or two major + one minor + one epidemiologic criterion; probable – one major + two minor criteria, or one major + one
minor + one epidemiologic criterion, or three minor + three epidemiologic criteria.
S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
871
extracranial cysts in temporalis or nuchal muscles.38 On positive
contrast ventriculography, the presence of a regular, rounded filling defect similar to an inverted cup suggests the presence of a cyst
and defines its extent, contour and mobility,40 whereas a cul-desac suggests inflammatory obstruction. A cyst within the third ventricle may mimic a colloidal cyst.41,42
The patients with epilepsy frequently have SSELs. SSELs are the
commonest cause of partial seizures in children in India.35,37,38
Most of these lesions represent solitary cerebral cysticercus granuloma (SCCG). SCCG is the granulonodular form of the parenchymal
cyst and accounts for nearly 60% to 70% of all forms of NCC seen in
patients in India.38
The differential diagnosis of SSEL includes tuberculoma, pyogenic brain abscesses, fungal abscess, toxoplasmosis, a primary or
metastatic brain tumor and infectious vasculitis. The diagnosis relies on associated features, especially in those with uncertain imaging. Serology is also often negative in patients with SCCG, because
the parasite is already dead or because a sole parasite does not elicit a strong antibody response. However, many patients with
tuberculoma do not have detectable tuberculosis in the lungs or
in any other location to confirm the diagnosis. Rajshekhar et al.16
described CT scan criteria for differentiating NCC and tuberculoma.
An enhancing ring lesion that is <20 mm in size, regular in outline
and not producing a midline shift is likely to be NCC. However, the
authors themselves believe that these criteria are not absolute and
it may be difficult to differentiate a small tuberculoma from NCC
on a CT scan alone. MRI has better sensitivity to differentiate tuberculomas from NCC. Preliminary experience with proton magnetic
resonance spectroscopy has shown promise in differentiating
tuberculoma from NCC.43
4.1.3. MRI of the brain
MRI is the most accurate technique to assess degree of infection,
location and evolutionary stage of the parasite. MRI is able to detect perilesional edema and degenerative changes of the parasite
and is suitable for small cysts or those located in the ventricles,
brainstem, cerebellum, base of the brain, eye and spine.44 The main
disadvantages of MRI are its high cost and limited availability.
Thus, in our Indian center, a CT scan may be the first investigation,
reserving MRI for patients with inconclusive CT findings.
It is possible to differentiate the various cyst stages on MRI.45
The intensity of fluid in live cysts is similar to CSF. The scolex appears as a mural nodule of high signal intensity on T1-weighted
MRI and of low signal intensity on T2-weighted MRI (like a hole
with a dot, or a pea in a pod) (Fig. 5). There is no perilesional edema
at this stage.46 In a degenerated cyst, the fluid becomes turbid (colloid vesicular stage), appearing as high intensity on a T1-weighted
MRI. In the granulonodular stage, ring enhancement occurs on gadolinium injection (isointense on T1-weighted and hypointense on
T2-weighted MRI) and there is variable perilesional edema. However, calcified cysts are better delineated on CT scans. The racemose type of cyst is a large lobulated cyst without a scolex
whereas the cellulose type contains a scolex inside a vesicle. Intraventricular cysts (Figs. 9–12) are well delineated with a small
metacystode inside the cyst.47 Abnormal enhancement after gadolinium suggests ependymitis or ventricular entrapment (Fig. 12).48
MRI is useful in follow-up to assess reduction in the number or size
of cysts with treatment.
Fig. 9. T1-weighted Axial MRI showing a well-delineated fourth ventricular cyst.
4.2. Serology
Fig. 10. T1-weighted sagittal MRI showing a well-delineated fourth ventricular cyst
with obstructive hydrocephalus.
The available serological tests are of little value in clinical practice. These have a sensitivity of 65% to 98% and a specificity of 67%
to 100%, depending on the specific test used, and the cyst burden,
location, and phase of infection.49–51 The most commonly used enzyme-linked immunosorbent assay is neither sensitive nor spe-
cific.49 EITB is reported to have a sensitivity of 98% and
specificity of 100%, and it is the test of choice as a major diagnostic
criterion.50 However, its sensitivity in a patient with a single
enhancing or calcified lesion is much lower.51
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Dilated ophthalmologic examination is sensitive for the detection of ocular cysts and is necessary for anyone diagnosed with
cysticercosis to rule out ocular involvement.54
5. Treatment
The treatment modalities available to patients with NCC
include:
1. cysticidal agents – to kill larvae
2. corticosteroids – to decrease or prevent the inflammatory
reaction.
3. anti-epileptic drugs (AEDs) – to prevent or decrease the severity
and number of seizures
4. surgery – to remove the cyst or insert a shunt for hydrocephalus. Garcia et al. analyzed the current evidence and reported
consensus guidelines for the management of NCC56 (Table 3).
5.1. Cysticidal agents
Fig. 11. A,B. T2-weighted coronal (A) and sagittal (B) MRI showing a rounded welldefined cyst in the fourth ventricular cavity with a hyperintense scolex.
5.1.1. Is cysticidal therapy needed?
There are three major arguments against the use of cysticidal
therapy in NCC: (i) immediate risks due to acute inflammation
from the death of cysts; (ii) worsening of long-term prognosis of
seizures with increased scarring due to acute inflammation,57
and (iii) treatment may be unnecessary due to natural death of
the parasites within a short period.58 According to a Cochrane
Database Systematic Review, there is insufficient evidence to assess the beneficial effects of cysticidal drugs in NCC.59 However,
in a double-blind, placebo-controlled study in patients with seizures resulting from viable parenchymal cysts, cysticidal therapy
decreased the burden of parasites and was effective in reducing
the number of generalized seizures.60 A recent meta-analysis
showed that there is a reduced seizure rate and increased resolution of parenchymal lesions with cysticidal therapy.61
The clinical benefit from cysticidal therapy in the treatment of
SSELs is also controversial. A few trials from India have assessed
the efficacy of cysticidal therapy for SSEL in adults and children.15,62–64 More complete resolution on imaging and fewer seizures during follow-up were reported in an albendazole group in
two of these trials.63,64 In contrast, Gogia et al.65 did not show
any benefit of albendazole in hastening resolution of CT lesions.
Table 3
Guidelines for the treatment of neurocysticercosis (after56)
Type of neurocysticercosis
Fig. 12. Gadolinium-enhanced sagittal MRI of a patient showing an inflammatory
cyst with enhancement of the cyst wall and surroundings.
Serology should be used together with clinical and neuroimaging data. Antigen detection assays are also available, which perform well in comparison with other available tests on CSF
samples.52 Antibodies can persist after cysts die; therefore, serology should always be reviewed in light of the presenting clinical
picture and imaging studies.36
4.3. Other tests
Biopsy of brain, skin or muscle can provide a definitive diagnosis in an otherwise ambiguous clinical situation and may be the
diagnostic method of choice for ocular, extraocular muscle, or
painful muscular or subcutaneous cysts.5,53–55
Parenchymal
neurocysticercosis
Viable cysts
Calcified
Enhancing lesions
Cysticercotic encephalitis
Extraparenchymal
neurocysticercosis
Intraventricular cyst
Subarachnoid cyst
Hydrocephalus with no
viable cyst
Hydrocephalus + intracranial
cyst
Ocular cysticercosis
Spinal cysticercosis
Treatment
Cysticidal treatment + steroids
AED – no cysticidal therapy
Single – AED, cysticidal drugs if persistent
Multiple – AED, cysticidal drugs + steroids
High dose steroids + osmotic diuretic or
immunosuppressive therapy + cysticidal therapy
Neuroendoscopic removal
Cysticidal treatment + steroids; VP shunt if
required
VP shunt, no cysticidal treatment
Shunt before cysticidal therapy
Surgery (cysticides avoided)
Surgical treatment
AED = antiepileptic drugs, VP = ventriculoperitoneal.
S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
However, some authors would not recommend leaving a live
parasite untreated in the brain.60 Thus, although there is controversy regarding the routine use of cysticidal drugs in SSELs, cysticidal drugs are generally considered helpful in the management
of some patients (such as those with persisting lesions) as they
hasten the resolution of the lesion, and thus, may avoid diagnostic
pitfalls.
5.1.2. Cysticides
Cysticidal drugs, albendazole and praziquantel, are effective in
all forms of NCC.1,7,61,66,67
Praziquantel (an isoquinolone) produces spastic paralysis of the
parasite and destroys the scolex. About 60% to 70% of parenchymal
cysticerci disappear after a 15-day treatment at doses of 50 mg/kg
per day.68–70 Recently, ultrashort single-day therapy with praziquantel has been introduced, and the reduction in cyst number
has been the same as for longer courses of treatment.71–74
Albendazole (an imidazole) acts by inhibiting glucose uptake by
parasitic membranes thereby causing energy depletion. About 75%
to 90% of parenchymal cysts disappear, and albendazole is considered superior to praziquantel in several trials.75–77 Other points
favoring albendazole are its efficacy against meningeal, subarachnoid and ventricular cysticerci, and its lower cost. Albendazole
does not interact with corticosteroids or antiepileptic drugs.78 It
was initially recommended to be administered at a dosage of
15 mg/kg per day for 1 month, but later studies showed that a 1
week course of albendazole is equally effective and is probably
more effective than praziquantel.60,79,80 Infections with more than
a few lesions may require longer courses of anti-parasitic medication.61 The optimal duration of cysticidal therapy for other less
common forms such as giant cysts or subarachnoid forms is unknown but should perhaps be longer than for parenchymal NCC.56
An additional course of praziquantel can be given if cystic lesions remain unchanged on repeat MRI after 1 month to 2 months
of therapy. However, with a partial response to one cysticidal drug,
administration of the other cysticide (such as albendazole 15 mg/
kg per day in 2 divided doses for 8 days) is probably better than
repetition of the same drug course.66
Intraventricular cysts have generally been excised, but many
authors have reported disappearance of intraventricular and subarachnoid cysts with cysticidal therapy.48 A recent trial suggests
that a high dose of albendazole (30 mg/kg per day) increases clearance of subarachnoid and intraventricular cysts, as compared with
usual dosing.81 However, regardless of the treatment chosen, a
ventriculoperitoneal shunt should be placed in all patients with
evidence of significant obstructive hydrocephalus. Steroids should
be commenced prior to cysticidal treatment to reduce the risk of
shunt obstruction. There are concerns of catastrophic complications with cysticidal treatment due to ventriculitis and recurrent
obstruction of the ventricular drainage system.42
Corral et al.26 successfully treated intramedullary spinal cysticercosis with cysticidal therapy. In the meningeal form, cysticidal
treatment may give only marginal benefit and the prognosis is
poor due to hydrocephalus, meningeal fibrosis and multiple brain
infarcts secondary to vasculitis. In these patients administration
of 50 mg prednisolone 3 times per week may be useful to prevent
or diminish chronic inflammation.66,67
5.2. Corticosteroids
Corticosteroids are used as adjuncts to cysticidal therapy to
alleviate symptoms due to the inflammatory reaction caused by
the death of larvae, which occurs from 2 days to 5 days after initiating therapy. There is conflicting evidence to support corticosteroid use as the primary treatment in SSELs;82,83 however, high
dose corticosteroids are the primary therapy for cysticercotic
873
encephalitis. Steroids should be given with cysticidal drugs for patients with subarachnoid cysts, chronic meningitis or multiple viable cysts. Oral prednisolone is preferred and should be commenced
2 days to 3 days before cysticidal therapy and continued for 7 days
to 10 days, since maximum exacerbation occurs during this period.
Long-term steroid therapy depends on the parasite load and
inflammation. All trials to evaluate cysticidal therapy have used
steroids for a variable period of time.64,82
5.3. Anti-epileptic drugs
A single agent first-line AED such as phenytoin or carbamazepine usually results in adequate seizure control. The optimal duration of AED therapy has been debated and is estimated by
identifying the parasite stage at the time of the seizure.84 Patients
with degenerating cysticerci develop acute symptomatic seizures
because of the inflammatory response of the brain. Therefore, these
patients may be treated for the duration of the acute condition
only, perhaps several months, during the active inflammatory response. There are, however, no guidelines for how long AEDs
should be continued after an acute episode. For patients with SCCG,
it is most appropriate to monitor cyst activity with neuroimaging
and to continue AEDs until resolution of the acute lesion. Most
physicians repeat MRI or CT scans after 6 months in patients with
parenchymal cysticercosis (earlier if the patient is symptomatic).
Once the lesion has resolved on neuroimaging, the AED may be tapered off over the next 12 weeks. However, seizures in a patient
with inactive or calcified parasites may be categorized as unprovoked seizures. The treatment should last until the patient has
experienced a seizure-free period of 2 years. Treatment in patients
with multiple lesions or extraparenchymal NCC should be tailored
to the individual.
5.3.1. Future research
More studies are needed to study the prevention of disease
spread and to further elucidate treatment regimes. The Center for
Disease Control and Prevention Working Group on Parasitic Diseases has classified cysticercosis as a potentially eradicable disease.85 Recent studies have demonstrated the potential utility of
various vaccines against Taenia solium for use in pigs, but their
widespread use is not yet a reality.86,87
5.4. Surgery
In general, indications for surgery are:
1.
2.
3.
4.
5.
6.
7.
cysts exhibiting local compression of brain and cranial nerves.
pseudotumor (edema) refractory to medical treatment.
hydrocephalus.
intraventricular cysticercosis.
intracranial hypertension.
spinal cysticercosis with cord/ root compression.
ocular cysts.54
5.4.1. Extraparenchymal forms
5.4.1.1. Cisternal forms. Patients with the cisternal form of NCC usually have racemose cysts in the basal cisterns and are prone to
symptoms that result from local compression. Direct excision of
these cysts is not recommended and can be dangerous due to severe adhesions. However, excising individual cysts that cause local
compression can be beneficial for local compressive symptoms, but
is not helpful to reduce the inflammatory reaction.
5.4.1.2. Ventricular forms. The indications for excision of a viable
ventricular cyst are: (i) mass effect, (ii) CSF obstruction, (iii) uncertain diagnosis, and (iv) fourth ventricular cysts, as they may cause
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brainstem compression even after shunt placement. The treatment
options for ventricular NCC include medical therapy, CSF diversion
and surgical resection by microsurgery and/or endoscopy. Repeat
imaging should be performed immediately before surgical intervention, to exclude cyst migration between the time of diagnosis
and surgery.
The development of acute hydrocephalus requires an emergency ventriculostomy, especially if the patient has an altered level
of consciousness, followed by definitive resection of cysts. A ventriculoperitoneal shunt may be required thereafter, once the cysts
have been resected, especially in the presence of ependymitis.41
Due to the frequency of ventriculitis, shunt failure rates have been
reported as high as 30% to 67%. Therefore, multiple shunt revisions
may be required in these patients, with a high mortality rate (50%
in 2 years).88–91
Direct microsurgical excision via a posterior fossa exploration is
invasive and carries a high risk of morbidity and mortality. Sharma
et al. reported posterior fossa craniotomy for fourth ventricle cysts
and supratentorial open or stereotactic craniotomy for third or lateral ventricular cysts.91
Endoscopic approaches for ventricular NCC have been described92–102 and have become the treatment of choice for ventricular NCC with hydrocephalus. The neuroendoscopic approaches to
treatment of NCC have many advantages including the avoidance
of a shunt with its attendant complications,89,92,94,96,97,99 quick
and easy navigation within the ventricles and excision of multiple
ventricular cysts with minimal postoperative complications.
Proano et al. reported endoscopic exploration of the fourth ventricle entrapped secondary to vasculitis.48 Later, Bergsnaider et al.
reported a transvalecular exploration of fourth ventricular NCC
with removal of cysts in 5 patients.96,97 The transfrontal transaqueductal approach was first described by Schroeder and Gaab for the
treatment of aqueductal stenosis.103 The use of this approach for
the removal of ventricular NCC was reported by Anandh et al.
(using a flexible endoscope)99 and Zymberg et al. (using a rigid
endoscope).102 Hussain et al. recommend a transventricular transforaminal approach to remove a third or even a fourth ventricular
cyst and to perform an endoscopic third ventriculostomy at the
same time, through a single burr hole. They used a 5 Fr. angiographic catheter and passed it through the rigid endoscope to
negotiate through the aqueduct. In their series, minimal periaqueductal contusions developed in 3 patients due to catheter negotiation, although none had any sequelae.92–94 In their series of 13
patients, Suri et al. used a flexible endoscope and passed it through
a rigid scope to negotiate the catheter through the aqueduct under
direct vision. A long flexible biopsy forceps was then used to excise
the fourth ventricular NCC. This avoided the chance of periqueductal injury and all their patients had normal extra-ocular movements postoperatively.104,105
Many series have reported aspiration of the contents of the cyst
prior to its removal, as a collapsed cyst is easier to handle and retrieve.92,94,101 Although there are some concerns regarding ventriculitis after perioperative cyst rupture, techniques such as
preoperative continuous irrigation with Ringer’s solution and postoperative lumbar drainage can clear debris and maintain ventricular patency.
However, despite advantages, neuroendoscopic procedures
have some potential drawbacks and limitations.48,97,99,101 Firstly,
endoscopic excision may be hazardous in presence of ependymitis
and dense adhesions. Therefore, patients in whom MRI demonstrates significant ependymal enhancement are considered poor
candidates for this procedure and should probably undergo shunt
placement. Secondly, intraventricular bleeding can be problematic.
5.4.1.3. Encephalitic forms. Patients with the encephalitic form of
NCC have diffuse cerebral edema due to multiple cysticerci in the
brain parenchyma. Treatment of this form is primarily medical in
order to reduce the raised intracranial pressure. However, decompressive craniotomy has been recommended for these patients
with only transient benefits; now, with more effective means to
control raised intracranial pressure, most authors would not advise
this.106
5.4.1.4. Parenchymal forms. For parenchymatous NCC, the following
surgical approaches are recommended:1,21,24,88,107–109
1. Stereotactic excisonal biopsy or open craniotomy and cyst
removal is recommended for a single giant cortical cyst or large
clumps exhibiting tumor-like behavior, provided that the lesion
is surgically accessible, is producing progressive deficits or is
not responding to cysticidal treatment. This approach may also
be used when diagnosis is uncertain (e.g. a SSEL is not responding to cysticides) or multiple lesions. Supratentorial decompressive craniotomy, craniectomy or lobectomy is undertaken when
the psuedotumor-type edema is refractory to medical treatment, particularly in the disseminated variety.
2. For spinal cysticercosis, excision needs to be undertaken. Intramedullary and clumped leptomeningeal cysts producing symptoms by mass effect and not responding to cysticidal drugs can
be removed via laminectomy. When diagnosis is in doubt, surgery helps in getting a histopathological diagnosis.108
References
1. Del Brutto OH, Santibanez R, Noboa CA, et al. Epilepsy due to
neurocysticercosis: analysis of 203 patients. Neurology 1992;42:389–92.
2. Commission on Tropical Diseases of the International League against
Epilepsy. Relationship between epilepsy and tropical diseases. Epilepsia
1994;35:89–93.
3. Medina MT, DeGiorgio C. Introduction to neurocysticercosis: a worldwide
epidemic. Neurosurg Focus 2002;12:6.
4. Flisser A. Taeniasis and cysticercosis due to Taenia solium. Prog Clin Parasitol
1994;4:77–116.
5. Garcı´a HH, Gonzalez AE, Evans CA, et al. Cysticercosis working group in Peru.
Taenia solium cysticercosis. Lancet 2003;362:547–56.
6. Carpio A. Neurocysticercosis: an update. Lancet Infect Dis 2002;2:751–62.
7. Sotelo J, Marine C. Hydrocephalus secondary to cysticercotic arachnoiditis. A
long term follow up review of 92 cases. J Neurosurg 1987;66:686–9.
8. Venkataraman S. Neurocysticercosis scene in India. Prog Clin
Neurosci:297–314.
9. Estanol B, Corona T, Abad P. A prognostic classification of cerebral cysticercosis:
therapeutic implications. J Neurol Neurosurg Psychiatry 1986;49:1131–4.
10. Carpio A, Placencia M, Santillan F, et al. A proposal for classification of
neurocysticercosis. Can J Neurol Sci 1994;21:43–7.
11. Murthy JM, Yangala R. Etiological spectrum of localization-related epilepsies
in childhood and the need for CT scan in children with partial seizures with no
obvious causation-a study from South India. J Trop Pediatr 2000;46:202–6.
12. Aggarwal A, Aneja S, Taluja V, et al. Etiology of partial epilepsy. Indian Pediatr
1998;35:49–52.
13. Singhal BS, Ladiwala U, Singhal P. Neurocysticercosis in Indian context (with
special reference to solitary parenchymatous cyst). Neurol India
1997;45:211–7.
14. Rajshekhar V. Etiology and management of single small CT lesions in patients
with seizures: understanding a controversy. Acta Neurol Scand
1991;84:465–70.
15. Rajshekhar V. Albendazole therapy for persistant solitary cysticercous
granulomas in patients with seizures. Neurology 1993;43:1238–40.
16. Rajshekhar V, Prakash S, Chandy MJ. Differentiating solitary small cysticercous
granuloma and tuberculomas in patients with epilepsy. J Neurosurg
1993;78:402–7.
17. Chandy MJ, Rajshekhar V, Ghosh S, et al. Single small enhancing CT lesions in
Indian patients with epilepsy: clinical, radiological and pathologic
considerations. J Neurol Neurosurg Psychiatry 1991;54:702–5.
18. Kalra V, Paul VK, Marwah RK, et al. Neurocysticercosis in childhood. Royal Soc
Trop Med Hyg 1987;81:371–3.
19. Salgado P, Rojas R, Sotelo J. Cysticercosis. Clinical classification based on
imaging studies. Arch Intern Med 1997;157:1991–7.
20. Joubert J. Cysticercal meningitis. A pernicious form of neurocysticercal
meningitis which responds poorly to praziquantel. S Afr Med J
1990;77:528–30.
21. Apuzzo MLJ, Dobkin WR, Zee CS, et al. Surgical considerations in the treatment
of intraventricular neurocysticercosis: an analysis of 45 cases. J Neurosurg
1984;60:400–7.
S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
22. Lobato RD, Lamas E, Portillo JM. Hydrocephlus in cerebral cysticercosis.
Pathogenic and therapeutic considerations. J Neurosurg 1981;55:786–93.
23. Zee CS, Segall HD, Destian S, et al. MRI of intraventricular cysticercosis:
surgical implications. J Comput Assist Tomogr 1993;17:932–9.
24. Stern WE. Neurological considerations of cysticercosis of the central nervous
system. J Neurosurg 1981;55:382–9.
25. Sharma BS, Banerjee AK, Kak VK. Intramedullary cysticercosis – case report
and review of literature. Clin Neurol Neurosurg 1987;89:111–6.
26. Corral I, Quereda C, Moreno A, et al. Intramedullary cysticercosis cured with
drug treatment. A case report. Spine 1996;21:2284–7.
27. Soto-Hernandez JL, Andrade SG, Rojas-Echeverri LA, et al. Subarachnoid
hemorrhage secondary to a ruptured inflammatory aneurysm. A possible
manifestation of neurocysticercosis: case report. Neurosurg 1996;38:
197–200.
28. Revuelta R, Juambeiz P, Baiderrama J, et al. Contralateral trigeminal neuralgia:
a new clinical manifestation of neurocysticercosis: case report. Neurosurg
1995;37:138–40.
29. Feinberg WM, Valdivia FR. Cysticercosis presenting as a subdural hematoma.
Neurology 1984;34:1112–3.
30. Rodriguez-Carvajal J, Del Brutto OH, Penagos P, et al. Occlusion of middle
cerebral artery due to cysticercotic angiitis. Stroke 1989;20:1095–9.
31. Sawhney IMS, Singh G, Lekhra OP, et al. Uncommon presentations of
neurocysticercosis. J Neurol Sci 1998;154:94–100.
32. Del Brutto OH, Wadia NH, Dumas M, et al. Proposal of diagnostic criteria for
human cysticercosis and neurocysticercosis. J Neurol Sci 1996;142:1–6.
33. Shah GV. Central nervous system tuberculosis. Neuroimaging Clin N Am
2000;10:355–74.
34. Case records of the Massachusetts General Hospital, Case 39-1996. N Engl J
Med 1996;335:1906–14.
35. Garg RK. Proposed diagnostic criteria for neurocysticercosis. Neurology
2002;58:1315.
36. Singh G. Neurocysticercosis in South-Central America and the Indian
subcontinent. A comparative evaluation. Arq Neuropsiquiatr 1997;55:349–56.
37. Garg RK. Diagnostic criteria for neurocysticercosis: some modifications are
needed for Indian patients. Neurol India 2004;52:171–7.
38. Wadia RS, Makhale CN, Kelkar AN, et al. Focal epilepsy in India with special
reference to lesions showing ring or disc like enhancement on contrast
computed tomography. J Neurol Neurosurg Psychiatry 1987;50:1298–301.
39. Nash TE, Neva FA. Recent advances in the diagnosis and treatment of cerebral
cysticercosis. N Engl J Med 1984;311:1492–6.
40. Salazar A, Sotelo J, Martinez H, et al. Differential diagnosis between
ventriculitis and fourth ventricle cyst in neurocysticercosis. J Neurosurg
1983;59:660–3.
41. Couldwell WT, Chandrasoma P, Apuzzo MLJ, et al. Third ventricular cysticercal
cyst mimicking a colloid cyst: case report. Neurosurg 1995;37:1200–3.
42. Meneses MS, Arruda WO, Ramina R. Third ventricular cysticercal cyst
mimicking a colloid cyst: case report. Neurosurg 1996;39:623.
43. Jayasundar R, Singh VP, Raghunathan P, et al. Inflammatory-granulomas:
evaluation with proton MRS. NMR Biomed 1999;12:139–44.
44. Martinez HR, Rangel-Guerra R, Elizondo G, et al. MR imaging in
neurocysticercosis: a study of 56 cases. Am J Neuroradiol 1989;10:1011–9.
45. Jena A, Sanchatee PC, Gupta RK, et al. Cysticercosis of the brain shown by
magnetic resonance imaging. Clin Radiol 1998;39:542–6.
46. Suss RA, Maravilla KR, Thompson J. MR imaging of intracranial cysticercosis:
comparison with CT and anatomopathologic features. Am J Neuroradiol
1986;7:235–42.
47. Ginier BL, Poirier VC. MR imaging of intraventricular cysticercosis. Am J
Neuroradiol 1992;13:1247–8.
48. Proano JV, Madrazo I, Garcia L, et al. Albendazole and praziquantel treatment
in neurocysticercosis of fourth ventricle. J Neurosurg 1997;87:33.
49. Rosas N, Sotelo J, Nieto D. ELISA in the diagnosis of neurocysticercosis. Arch
Neurol 1986;43:353–6.
50. Tsang VC, Brand JA, Boyer AE. An enzyme-linked immunoelectrotransfer blot
assay and glycoprotein antigens for diagnosing human cysticercosis (Taenia
solium). J Infect Dis 1989;159:50–9.
51. Wilson M, Bryan RT, Fried JA, et al. Clinical evaluation of the cysticercosis
enzyme-linked
immunoelectrotransfer
blot
in
patients
with
neurocysticercosis. J Infect Dis 1991;164:1007–9.
52. Garcia HH, Parkhouse RM, Gilman RH, et al. Cysticercosis working group in
Peru. Serum antigen detection in the diagnosis, treatment, and follow-up of
neurocysticercosis patients. Trans R Soc Trop Med Hyg 2000;94:673–6.
53. Hawk MW, Shahlaie K, Kim KD, et al. Neurocysticercosis: a review. Surg Neurol
2005;63:123–32.
54. Sharma T, Sinha S, Shah N, et al. Intraocular cysticercosis: clinical
characteristics and visual outcome after vitreoretinal surgery. Ophthalmology
2003;110:996–1004.
55. Del Brutto OH, Rajshekhar V, White Jr AC, et al. Proposed diagnostic criteria for
neurocysticercosis. Neurology 2001;57:177–83.
56. Garcia HH, Evans CA, Nash TE, et al. Current consensus guidelines for
treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747–56.
57. Kramer LD. Medical treatment of cysticercosis – ineffective. Arch Neurol
1995;52:101–210.
58. Carpio A, Santillan F, Leon P, et al. Is the course of neurocysticercosis modified
by treatment with antihelminthic agents? Arch Intern Med 1995;155:1982–8.
59. Salinas R, Prasad K. Drugs for treating neurocysticercosis (tapeworm infection
of the brain). Cochrane Database Syst Rev:CDOO0215.
875
60. Garcia HH, Pretell EJ, Gilman RH, et al. Cysticercosis Working Group in Peru. A
trial of antiparasitic treatment to reduce the rate of seizures due to cerebral
cysticercosis. N Engl J Med 2004;350:249–58.
61. Del Brutto OH, Roos KL, Coffey CS, et al. Meta-analysis: cysticidal drugs for
neurocysticercosis:
albendazole
and praziquantel.
Ann Int
Med
2006;145:43–51.
62. Padma MV, Behari M, Misra NK, et al. Albendazole in single CT ring lesions in
epilepsy. Neurology 1994;44:1344–6.
63. Baranwal AK, Singhi PD, Khandelwal N, et al. Albendazole therapy in children
with focal seizures and single small enhancing computerized tomographic
lesions: a randomized, placebo-controlled, double blind trial. Pediatr Infect Dis
J 1998;17:696–700.
64. Kalra V, Dua T, Kumar V. Efficacy of albendazole and short-course
dexamethasone treatment in children with 1 or 2 ring-enhancing lesions of
neurocysticercosis: a randomized controlled trial. J Pediatr 2003;143:111–4.
65. Gogia S, Talukdar B, Choudhury V, et al. Neurocysticercosis in children: clinical
findings and response to albendazole therapy in a randomized, double-blind,
placebo controlled trial in newly diagnosed cases. Trans R Soc Trop Med Hyg
2003;97:416–21.
66. Sotelo J, Del Brutto OH. Review of neurocysticercosis. Neurosurg Focus
2002;12:e1.
67. Sotelo J, Del Brutto OH, Penagos P, et al. Comparison of therapeutic regimen of
anticysticercal drugs for parenchymal brain cysticercosis. J Neurol
1990;237:69–72.
68. Nash TE. Human case management and treatment of cysticercosis. Acta Trop
2003;87:61–9.
69. Sotelo J, Escobedo F, Rodriguez-Carbajal J, et al. Therapy of parenchymal brain
cysticercosis with praziquantel. N Engl J Med 1984;310:1001–7.
70. Sotelo J, Torres B, Rubio-Donnadieu F, et al. Praziquantel in the treatment of
neurocysticercosis: a long-term follow-up. Neurology 1985;35:752–5.
71. Corona T, Lugo R, Medina R, et al. Single-day praziquantel therapy for
neurocysticercosis. N Engl J Med 1996;334:125.
72. Del Brutto OH, Campos X, Sánchez J, et al. Single-day praziquantel versus 1week albendazole for neurocysticercosis. Neurology 1999;52:1079–81.
73. López-Gómez M, Castro N, Jung H, et al. Optimization of the single-day
praziquantel therapy for neurocysticercosis. Neurology 2001;57:1929–30.
74. Pretell EJ, García HH, Custodio N, et al. Short regimen of praziquantel in the
treatment of single brain enhancing lesions. Clin Neurol Neurosurg
2000;102:215–8.
75. Cruz M, Cruz I, Horton J. Albendazole vs praziquantel in the treatment of
cerebral cysticercosis: clinical evaluation. Trans R Soc Trop Med Hyg
1991;85:244–7.
76. Sotelo J, Escobedo F, Penagos P. Albendazole vs praziquantel therapy for
neurocysticercosis. A controlled trial. Arch Neurol 1988;45:532–4.
77. Takayanagui OM, Jardim E. Therapy for neurocysticercosis. Comparison
between albendazole and praziquantel. Arch Neurol 1992;49:290–4.
78. Bittencourt PR, Gracia CM, Martins R, et al. Phenytoin and carbamazepine
decreased oral bioavailability of praziquantel. Neurology 1992;42:492–6.
79. García HH, Gilman RH, Horton J, et al. Albendazole therapy for
neurocysticercosis: a prospective double-blind trial comparing 7 versus 14
days of treatment. Cysticercosis Working Group in Peru. Neurology
1997;48:1421–7.
80. Sotelo J, Penagos P, Escobedo F, et al. Short course of albendazole therapy for
neurocysticercosis. Arch Neurol 1988;45:1130–3.
81. Gongora-Rivera F, Soto-Hernandez JL, Gonzalez Esquivel D, et al. Albendazole
trial at 15 or 30 mg/kg/day for subarachnoid and intraventricular
cysticercosis. Neurology 2006;66:436–8.
82. Singhi PD, Jain V, Khandelwal N. Corticosteroids versus albendazole for
treatment of single small enhancing computed tomographic lesions in
children with neurocysticercosis. J Child Neurol 2004;19:323–7.
83. Mall RK, Agarwal A, Garg RK, et al. Short course of prednisolone in Indian
patients with solitary cysticercus granuloma and new-onset seizures. Epilepsia
2003;44:1397–401.
84. Singhi PD, Dinakaran J, Khandelwal N, et al. One vs. two years of anti-epileptic
therapy in children with single small enhancing CT lesions. J Trop Pediatr
2003;49:274–8.
85. Figueroa JP. Report of the Workgroup on Parasitic Diseases. MMWR Morb
Mortal Weekly Rep 1999;48:118–25. Accessed January 31, 2007, at: http://
www.cdc.gov/mmwr/preview/mmwrhtml/su48a21.htm.
86. Guo A, Jin Z, Zheng Y, et al. Induction of protection against porcine
cysticercosis in growing pigs by DNA vaccination. Vaccine 2007;25:170–5.
87. Yancey LS, Diaz-Marchan PJ, White AC. Cysticercosis: recent advances in
diagnosis and management of neurocysticercosis. Curr Infect Dis Rep
2005;7:39–47.
88. Colli BO, Martelli N, Assirati Jr JA, et al. Results of surgical treatment of
neurocysticercosis in 69 cases. J Neurosurg 1986;65:309–15.
89. Cuetter AC, Andrews RJ. Intraventricular neurocysticercosis: 18 consecutive
patients and review of the literature. Neurosurg Focus 2002;12:e5.
90. Kelley R, Duong DH, Locke GE. Characteristics of ventricular shunt
malfunctions
among
patients
with
neurocysticercosis.
Neurosurg
2002;50:757–62.
91. Sharma BS, Gupta SK, Khosla VK. Neurocysticercosis: surgical considerations.
Neurol India 1998;46:177–82.
92. Husain M, Jha D, Vatsal DK, et al. Neuro-endoscopic surgery – experience and
outcome analysis of 102 consecutive procedures in a busy neurosurgical
centre of India. Acta Neurochir (Wien) 2003;145:369–76.
876
S. Sinha, B.S. Sharma / Journal of Clinical Neuroscience 16 (2009) 867–876
93. Husain M, Rastogi M, Jha D, et al. Endoscopic transaqueductal removal of
fourth ventricular neurocysticercosis with an angiographic catheter.
Neurosurg 2007;60:249–54.
94. Husain M, Jha DK, Rastogi M, et al. Neuro-endoscopic management of
intraventricular
neurocysticercosis
(NCC).
Acta
Neurochir
(Wien)
2007;149:341–6.
95. Madrazo I, Garcia-Renteria JA, Sandoval M, et al. Intraventricular cysticercosis.
Neurosurg 1983;12:148–52.
96. Bergsneider M. Endoscopic removal of cysticercal cysts within the fourth
ventricle: technical note. J Neurosurg 1999;91:340–5.
97. Bergsneider M, Langston TH, Lee HJ, et al. Endoscopic management of
cysticercal cysts within the lateral and third ventricles. J Neurosurg
2000;92:14–23.
98. Neal JH. An endoscopic approach to cysticercosis cysts of the posterior third
ventricle. Neurosurg 1995;36:1040–3.
99. Anandh B, Mohanty A, Sampath S, et al. Endoscopic approach to
intraventricular cysticercal lesions. Minim Invas Neurosurg 2001;44:194–6.
100. Cudlip SA, Wilkins PR, Marsh HT. Endoscopic removal of a third ventricular
cysticercal cyst. Br J Neurosurg 1998;12:452–4.
101. Psarros TG, Krumerman J, Coimbra C. Endoscopic management of
supratentorial ventricular neurocysticercosis: case series and review of the
literature. Minim Invas Neurosurg 2003;46:331–4.
102. Zymberg ST, Paiva Neto MA, Gorgulho AA, et al. Endoscopic approach to fourth
ventricle cysticercosis. Arq Neuropsiquiatr 2003;61:204–7.
103. Schroeder HWS, Gaab MR. Endoscopic aqueductoplasty: technique and
results. Neurosurg 1999;45:508–18.
104. Suri A, Goel RK, Ahmad FU, et al. Transventricular, transaqueductal scope-inscope endoscopic excision of fourth ventricular neurocysticercosis: a series of
13 cases and a review. J Neurosurg Pediatrics 2008;1:35–9.
105. Suri A, Goel RK, Ahmad FU, et al. Endoscopic excision of intraventricular
neurocysticercosis in children: a series of six cases and review. Childs Nerv Syst
2008;24:281–5.
106. Colli BO, Carlotti Jr CG, Assirati Jr JA, et al. Surgical treatment of cerebral
cysticercosis: long-term results and prognostic factors. Neurosurg Focus
2002;12:eq.
107. Ramina R, Hunhevicz SC. Cerebral cysticercosis presenting as mass lesion. Surg
Neurol 1986;25:89–93.
108. Ahmad FU, Sharma BS. Treatment of intramedullary spinal cysticercosis:
report of 2 cases and review of literature. Surg Neurol 2007;67:74–7.
109. Colli BO, Martelli N, Assirati Júnior JA, et al. Cysticercosis of the central
nervous system. I. Surgical treatment of cerebral cysticercosis: a 23 years
experience in the Hospital das Clínicas of Ribeirão Preto Medical School. Arq
Neuropsiquiatr 1994;52:166–86.