Introduction
Neurocysticercosis (NCC) is the most common parasitic infection of the central nervous system worldwide, representing a leading cause of adult-onset seizures, particularly in endemic regions of Latin America, Sub-Saharan Africa, and Southeast Asia. With increasing globalization, immigration, and international travel, NCC has become a significant diagnostic consideration even in non-endemic developed countries.
Despite being preventable, NCC continues to pose major diagnostic and therapeutic challenges due to its protean clinical manifestations, variable radiologic appearances, and complex host–parasite interactions. Advances in neuroimaging—especially MRI—have dramatically improved diagnostic accuracy, allowing earlier detection and targeted treatment strategies.
This column provides an in-depth, expert-level review of neurocysticercosis, integrating pathophysiology, epidemiology, clinical manifestations, advanced imaging features, differential diagnosis, management strategies, and prognosis.
Pathophysiology of Neurocysticercosis
Neurocysticercosis is caused by infection with the larval stage (cysticercus) of Taenia solium. Humans become accidental intermediate hosts through ingestion of T. solium eggs, typically via fecal–oral transmission.
Life Cycle and CNS Involvement
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Ingested eggs release oncospheres in the intestine.
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Oncospheres penetrate the intestinal wall.
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Hematogenous dissemination allows larvae to lodge in the brain, spinal cord, eyes, or subcutaneous tissues.
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Larvae evolve through four histopathological stages:
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Vesicular stage (viable cyst, minimal inflammation)
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Colloidal vesicular stage (degenerating cyst with inflammatory response)
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Granular-nodular stage
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Calcified nodular stage (inactive disease)
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The host immune response, rather than the parasite itself, is primarily responsible for neurological symptoms.
Epidemiology
Neurocysticercosis accounts for:
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~30% of epilepsy cases worldwide
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Up to 50% of adult-onset seizures in endemic regions
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Increasing prevalence in North America and Europe due to migration
High-risk populations include:
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Immigrants from endemic regions
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Individuals with poor sanitation
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Household contacts of tapeworm carriers
Clinical Presentation
Clinical manifestations depend on:
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Number of lesions
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Location
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Stage of parasite evolution
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Host immune response
Common Presentations
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Seizures (most common)
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Chronic headaches
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Focal neurological deficits
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Hydrocephalus
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Cognitive decline
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Raised intracranial pressure
Special Forms
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Intraventricular NCC → obstructive hydrocephalus
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Subarachnoid (racemose) NCC → high mortality
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Spinal NCC → radiculopathy, myelopathy
Imaging Features (Radiologic Diagnosis)
Figure 1. MRI Brain – Vesicular Stage
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Thin-walled cyst
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CSF intensity on T1/T2
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Eccentric scolex (“hole-with-dot” sign)
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No surrounding edema
Figure 2. Colloidal Vesicular Stage
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Hyperintense lesion on T2
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Ring enhancement post-contrast
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Prominent perilesional edema
Figure 3. Granular-Nodular Stage
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Nodular lesion with decreasing edema
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Partial calcification
Figure 4. Calcified Stage
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Small hyperdense foci on CT
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No enhancement
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Epileptogenic potential remains
MRI with contrast remains the imaging modality of choice, while CT is superior for detecting calcified lesions.
Differential Diagnosis
| Condition | Key Differentiating Features |
|---|---|
| Tuberculoma | MR spectroscopy lipid peak, basal meningitis |
| Brain metastasis | Multiple lesions with edema, known primary cancer |
| Toxoplasmosis | Immunocompromised patients, basal ganglia involvement |
| Pyogenic abscess | Restricted diffusion, thick wall |
| Glioma | Progressive mass effect, infiltrative margins |
Diagnosis
Diagnosis is based on Del Brutto’s diagnostic criteria, incorporating:
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Neuroimaging findings
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Serology (EITB)
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Clinical manifestations
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Epidemiological exposure
Definitive diagnosis includes visualization of the scolex on imaging or histopathology.
Treatment
Medical Therapy
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Albendazole (15 mg/kg/day for 7–28 days)
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Praziquantel (alternative or adjunct)
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Corticosteroids to control inflammation
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Antiepileptic drugs for seizure control
Surgical Management
Indicated in:
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Obstructive hydrocephalus
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Intraventricular cysts
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Large cysts causing mass effect
Prognosis
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Excellent prognosis in parenchymal NCC with appropriate therapy
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Calcified lesions may cause chronic epilepsy
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Intraventricular and subarachnoid forms carry higher morbidity
Early diagnosis and imaging-based staging are critical determinants of outcome.
Quiz
Question 1
A 32-year-old man presents with new-onset seizures. MRI shows a cystic lesion with an eccentric mural nodule and minimal edema. What is the most likely diagnosis?
A. Glioblastoma
B. Tuberculoma
C. Neurocysticercosis
D. Brain abscess
✅ Answer: C
Explanation: The eccentric scolex (“hole-with-dot sign”) is pathognomonic for neurocysticercosis.
Question 2
Which imaging modality is most sensitive for detecting calcified neurocysticercosis?
A. MRI T1
B. MRI FLAIR
C. CT scan
D. PET-CT
✅ Answer: C
Question 3
Which stage of neurocysticercosis is associated with maximal inflammation?
A. Vesicular
B. Colloidal vesicular
C. Granular nodular
D. Calcified
✅ Answer: B
Conclusion
Neurocysticercosis remains a global neurological challenge requiring multidisciplinary management. Advances in neuroimaging have transformed diagnosis, enabling precise staging and targeted therapy. Awareness of its imaging spectrum is critical for clinicians, radiologists, and neurologists worldwide.
References (IEEE Style)
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Del Brutto OH et al., Clinical Microbiology Reviews, 2017.
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Garcia HH et al., Lancet Neurology, 2020.
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White AC Jr., New England Journal of Medicine, 2021.
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Carpio A., The Lancet Infectious Diseases, 2019.
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Garcia HH, Nash TE. New England Journal of Medicine, 2014.
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Wallin MT et al., Neurology, 2004.
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Nash TE et al., Clinical Infectious Diseases, 2018.
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