(neurocysticercosis)

Virtually zero prevalence in Western Europe, but imported cases (migrations, vacations in endemic countries) are possible. Infection caused by the larva of Taenia solium, the pig tenia. Cerebral involvement is the most frequent cerebral parasitosis.

Figure: endemic areas for cysticercosis

Two routes of contamination by T.solium larvae are described (figure):

1)        consumption of undercooked, infested pork meat (in red). This leads to the presence of tenia in the digestive tract (teniasis), followed by the expulsion of eggs and proglotids in the feces.

2)        ingestion of food or water contaminated with human feces containing eggs (in blue). This leads to the development of cysticerci containing larval forms of T.solium (cysticercosis). Once in the patient's intestine, these larvae explode and can migrate to any organ in the body. In most cases, cysts develop in the eyes, CNS, muscles or subcutaneous tissues.

Many patients are asymptomatic. Clinical presentation is delayed compared to the time of infection (a few months) and varies according to the number of lesions, their location in the central nervous system, the stage of evolution of the parasite and the perilesional inflammatory reaction it provokes:

-        epileptic seizures

-        unusual, atypical headaches

-        focal neurological deficits, visual disturbances

-        signs of intracranial hypertension.

Diagnosis: imaging (CT or MRI). The specificity of serology is variable.  The absence of eggs in the patient's stool does not exclude the diagnosis. Look for asymptomatic forms in close contacts (family, school).

Treatment: adult worms can be eliminated with praziquantel (50 mg/kg/day for 10 days). Treatment of symptomatic neurocysticercosis is complicated, and includes corticosteroids, antiepileptics and, in certain situations, albendazole (15 mg/kg/day for 10 days to 1 month, depending on location) or praziquantel. Surgery may be required. Risk of acute deterioration in the days following the start of medical treatment, due to the inflammatory reaction caused by the death of the parasite. Calcified lesions contain only dead cysts.

Anesthetic implications:

depending on cerebral involvement; risk of acute intracranial hypertension at the start of treatment.

References :

-        Garcia HH, Nash TE, Del Brutto OH.
Clinical symptoms, diagnosis, and treatment of neurocysticercosis. 
Lancet Neurol. 2014 13(12): 1202-15. doi:10.1016/S1474-4422(14)70094-8.

-        Salavracos  M.
Diagnostic and therapeutic approaches in case of neurocysticercosis in Belgium.
Louvain Médical 2019 ; 138 : 239-45

-        Vanden Driessche K, Dermauw V, Schoonjans A-S, Gabriël S, Theeten H, on behalf of the Cysticercosis Outbreak Team.
Neurocysticercosis school outbreak in Belgium.
The Lancet 2024 ; 404 : 2415-6 doi.org/10.1016/ S0140-6736(24)02432-2

Updated: December 2024