How to Cite This Chapter: Chagla Z. Neurocysticercosis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 22, 2024.
Last Updated: September 29, 2018
Last Reviewed: May 1, 2019
Chapter Information

Definition, Etiology, PathogenesisTop

Neurocysticercosis is a parasitic infection leading to cyst formation in the central nervous system (CNS). It most commonly presents as seizures and is likely the main global cause of seizures. Neurocysticercosis is probably the most common CNS infection in the world.

Etiology: Taenia solium, a tapeworm (cestode), is the causative agent. While the infection is classically acquired through the ingestion of contaminated pork, this leads only to shedding of proglottid segments (eggs) in the stool of the infected individuals. Ingestion of contaminated human stool, either by autoinoculation or fecal-oral contamination of food or water, results in oncosphere hatching and eventual cyst formation in end-organ tissue. This can occur in the CNS, eyes, subcutaneous tissues, and muscle.

Clinical Features and Natural HistoryTop

The typical presentation is generalized tonic-clonic seizures, which are a consequence of the cyst itself or the patient’s immunologic response to the cyst. As cysts degenerate, the subsequent edema and calcification can also be a nidus. In patients with a high cyst burden, encephalitis may be the initial presentation. Involvement of the ventricles may lead to obstructive hydrocephalus. Involvement of the retinas may result in visual loss.


1. Laboratory tests: Taking a detailed history of potential exposure is paramount to diagnosis. Serologic studies that detect cysticercosis can be helpful, with sensitivity decreasing with 1 to 2 cysts and increasing with >2 cysts. Treatment is typically initiated based on a relevant history and radiologic findings. In treatment-refractory patients, brain biopsy for pathology may be considered to confirm the diagnosis.

2. Computed tomography (CT) and magnetic resonance imaging (MRI): Characteristic features include a single or multiple ring-enhancing lesions, occasionally with a live scolex inside. Cerebral edema is typically associated with neurocysticercosis. When cysts degenerate, the ring-enhancing lesions may look atypical and eventually form a calcification, which signifies a noninfectious process. Obstructive hydrocephalus may occur with infection of the ventricles.


1. Antiseizure therapy: The mainstay of therapy includes antiseizure drugs, as the lesions may become a focus for recurrent seizures. Specific medications should follow local practice for epilepsy.

2. Glucocorticoids/anthelmintic therapy: Anthelmintic therapy may be considered when cysts are viable (ie, they have a visible scolex or are not calcified). Glucocorticoids should be initiated in all patients with cerebral edema, and this should be done before anthelmintic drugs. Our practice is to use dexamethasone 0.1 mg/kg/d started 24 hours before anthelmintic therapy and tapered off after completion of therapy.

Anthelmintic therapy should be offered to patients with single or multiple viable lesions, but it is contraindicated in the setting of intraventricular disease, encephalopathy, or severe subarachnoid disease, until surgical and glucocorticoid therapy is initiated. Typical treatment is oral albendazole 400 mg bid used for 10 to 14 days. In patients with ≥3 lesions, praziquantel 50 mg/kg/d tid in divided doses for 10 to 14 days should be considered. Also see Anthelmintic Agents.

3. Surgery: Surgery is reserved for patients with intraventricular disease. In patients with a high burden or signs of hydrocephalus prior to or during treatment, a ventriculoperitoneal shunt may be considered.

4. Monitoring: Imaging studies should be repeated in 4 to 6 weeks or earlier if there is clinical deterioration. Ocular lesions should be followed by fundoscopy.


Worsening cerebral edema, encephalopathy, or hydrocephalus may result from degeneration of the cysts secondary to anthelmintic therapy. In such cases patients should be managed aggressively for intracranial pressure and glucocorticoids should be reinitiated. Seizures may occur at any point during the infection or resolution. The patient should be monitored for response to antiepileptic therapy.

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