Differential diagnoses: Pyogenic abscesses, tuberculomas, metastases, tuberous sclerosis, and toxoplasmosis.
The images show several round, ring-enhancing lesions at the gray
matter-white matter interface measuring approximately 1 cm in diameter.
Each is associated with vasogenic edema, but there is no midline shift
or subfalcine or transtentorial herniation.
Neurocysticercosis results when encysted larval forms of Taenia solium (pork tapeworm) invade the central nervous system.2 It is the most common parasitic disorder of the CNS,5
occurring in 4% of autopsy series from endemic countries of the world
(in Latin America, Asia, Africa, and some European countries).
is one of the 8 cestode species that infect man (Table 1). Humans are
the definitive host for the parasite (harboring the adult worm), while
omnivorous or herbivorous vertebrates (like pigs) host its larval form
(intermediate host). Although the adult forms of the cestodes that
humans host rarely cause harm, the larval forms cause variable degrees
of illnesses in humans. In the former case the parasites often reside
harmlessly in the bowels, while in the latter they invade the tissues.
example, in the pork tapeworm’s normal life cycle, humans harbor the
parasite and shed its eggs (either individually or in proglot tides
impregnated with eggs) in our feces. The pig, an omnivore and its
natural intermediate host, consumes the eggs of the parasite, which
hatch into larval forms in its alimentary tract and invade its tissues.
Consumption of undercooked meat from infected pork by humans completes
the cycle, freeing the encysted larvae when they encounter gastric acid
and bile salts.
In contrast, humans act as the intermediate host
of the parasite when they ingest the tapeworm eggs by eating food
infected with them (the mother in this case may have infected her child
this way). Their larvae invade the bowel walls and invade human tissues
as far afield as the brain, eyes, muscles, heart, and others, wreaking
havoc along the way.4
In the CNS, the cysticerci (the
larvae) may lodge in the brain parenchyma, the spinal cord, the
subarachnoid space, or the ventricles, lying dormant for years or
causing various categories of clinical disease (Table 2).5
However, 2 to 10 years after CNS invasion, the dormant cysts may die,
lose osmoregulation, absorb fluid and disintegrate, releasing antigens
that set up variable degrees of inflammation. The clinical conundrum
that results from CNS larval invasion depends upon the size of the
invasion, and the location and degree of the inflammation.
certain diagnosis of neurocysticercosis can be made by analyzing
infected tissue microscopically. But a presumptive diagnosis of the
disease can be made if the patient is from or resides in an endemic area
(as in this case) and, if laboratory analysis of their CSF specimen,
including an immunoblot test, and their CNS imaging results are positive
for markers of the disease (Table 3).5,6
For cysts that cause symptoms outside the CNS, surgical resection achieves a cure.
treatment of symptomatic neurocysticercosis, which carries 50%
mortality rate, is more problematic. Two drugs, albendazole and
praziquantel, control symptoms and cause regression in the size and
number of cysts in patients with viable (nonenhancing) cysts in the
brain parenchyma. However, they provide limited improvement in patients
with arachnoiditis and no improvement in patients with intraventricular
cysts. These latter patients should be treated with surgery or palliated
with ventricular shunting, anticonvulsants, and anti-inflammatory
drugs. According to our case’s physician, the patient did not receive
antiparasitic medication because the imaging features suggested that the
parasites were dying (vasogenic edema and ring enhancement).7
cautionary injunctions about treatment: First, 20% of patients with
parenchymal cysticercosis worsen symptomatically following institution
of drug treatment as the parasites die and release their antigens.
Concomitant administration of antiinflammatory drugs subdues this
phenomenon. Second, because anti-inflammatory agents alter the CNS
pharmakokinetics of the anti-parasitic agents, their routine use is
Patients should be rescanned 3 months after therapy to judge their response to treatment; an alternative drug to the one used ab initio can be used if there is no response.
patients with ocular cysticercosis (remember, 20%), it is preferable to
hold off drug treatment until resection of their lesions because they
do not respond well to medication.
MRI is an effective examination for evaluating neurocysticercosis and
other similar conditions. Utilizing techniques, such as axial T1W image
after IV gadolinium administration, axial T2W image, and coronal FLAIR
images, effectively depicts enhanced views of the lesions at the gray
matter-white matter interface.
- Shandera WX, White AC Jr, Chen JC, et al. Neurocysticercosis in Houston, Texas. A report of 112 cases. Medicine (Baltimore). 1994;73:37-52.
- Domenici R, Matteucci L, Meossi C, Stefani G, Frugoli G. Neurocysticercosis: A rare cause of convulsive crises. Pediatr Med Chir. 1995;17(6):577-581. [in Italian]
- Caparros-Lefebvre D, Lannuzel A, Alexis C, et al. Cerebral cysticercosis: Why it should be treated. Presse Med. 1997;26:1574-1577. [in French]
- Ruiz-Garcia M, González-Astiazaran A, Rueda-Franco F. Neurocysticercosis in children. Clinical experience in 122 patients. Childs Nerv Syst. 1997;13:608-612.
- Grill J, Pillet P, Rakotomalala W, et al. Neurocysticercosis: Pediatric aspects. Arch Pediatr. 1996;3(4):360-368. [in French]
- Riley T, White AC Jr. Management of neurocysticercosis. CNS Drugs. 2003;17):577-591.
- Rahalkar MD, Shetty DD, Kelkar AB, et al. The many faces of cysticercosis. Clin Radiol. 2000;55:668-674.