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Neurocysticercosis.

CASE SUMMARY

An 18-month-old child born to a Mexican immigrant mother resident in Texas presented with a convulsive crisis in the emergency room. (1) Her pregnancy and his birth history were unremarkable. A magnetic resonance imaging (MRI) examination of the child's brain was performed (Figure 1).

DIAGNOSIS

Neurocysticercosis

Differential diagnoses: Pyogenic abscesses, tuberculomas, metastases, tuberous sclerosis, and toxoplasmosis.

IMAGING FINDINGS

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.

DISCUSSION

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).

Taenia solium 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.

For example, in the pork tapeworm's normal life cycle, humans harbor the parasite and shed its eggs (either individually or in proglottides 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 sub-arachnoid 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.

A 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.

The 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)

Two 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 discouraged.

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.

For 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.

CONCLUSION

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.

REFERENCES

(1.) Shandera WX, White AC Jr, Chen JC, et al. Neurocysticercosis in Houston, Texas. A report of 112 cases. Medicine (Baltimore). 1994;73:37-52.

(2.) 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]

(3.) Caparros-Lefebvre D, Lannuzel A, Alexis C, et al. Cerebral cysticercosis: Why it should be treated. Presse Med. 1997;26:1574-1577. [in French]

(4.) Ruiz-Garcia M, Gonzalez-Astiazaran A, RuedaFranco F. Neurocysticercosis in children. Clinical experience in 122 patients. Childs Nerv Syst. 1997;13:608-612.

(5.) Grill J, Pillet P, Rakotomalala W, et al. Neurocysticercosis: Pediatric aspects. Arch Pediatr. 1996;3(4):360-368. [in French]

(6.) Riley T, White AC Jr. Management of neurocysticercosis. CNS Drugs. 2003;17):577-591.

(7.) Rahalkar MD, Shetty DD, Kelkar AB, et al. The many faces of cysticercosis. Clin Radiol. 2000;55:668-674.

Obidike A. Nwakudu, MD, and Kenneth U. Ekechukwu, MD, MPH, FACP

Prepared by Dr. Nwakudu while in the Department of Family Medicine, and Dr. Ekechukwu while Section Chief, Division of Interventional Radiology, Department of Radiology, at Mount Sinai Hospital in Chicago, IL.


Table 1. Human cestode infections

                    Stage seen
Species             In man       Common name      Disease

Taenia saginata     Adult        Beef tapeworm    Rarely symptomatic
Taenia solium       Adult        Pork tapeworm    Rarely symptomatic
                    Larva        Cysticercosis    Brain and tissue
                                                  cysts
Taenia multiceps    Larva        Bladderworm,     Brain and eye cysts
                                 coenurosis
E. granulosus       Larva        Hydatid cyst     Solitary tissue
                                 disease          cysts
E. multilocularis   Larva        Alveolar cyst    Multilocular cysts
                                 disease
Diphyllobothrium    Adult        Fish tapeworm    Pernicious anemia
latum
Hymenolepis nana    Adult        Dwarf tapeworm   Rarely symptomati
Spirometra          Larva        Sparganosis      Subcutaneous larva
mansonoides

Table 2. Clinical categories of Neurocysticercosis

Syndrome               Clinical features

Acute invasive stage   Most common in children; mortality, 10%.
                       Occurs immediately after the infection with
                       fevers, head-aches, and myalgias. Heavy
                       infection may result in coma with rapid
                       deterioration (cysticercal encephalitis).
                       Treat aggressively with anti-para-sitic and
                       anti-inflammatory agents.

Parenchymal CNS        50% of cases; there is established
cysticercosis          parenchymal disease with seizures, focal
                       deficits, intellectual impairment,
                       personality changes and signs of raised ICP
                       when severe.

Subarachnoid           30% of cases; there is larval invasion of the
cysticercosis          sub arachnoid space including the cisterns
                       causing disturbed CSF flow, sensorial changes
                       and, as in other chronic basal meningitis,
                       signs of vasculitis and parenchymal
                       infarctions.

Intraventricular       15% of cases; there are cysts in the
the cysticercosis      ventricles, 4th most frequently involved,
                       causing intermittent obstruction to CSF flow
                       with head movements. The aggressive form is
                       racemose cysticercosis in which sheets of
                       parasites spill out into the sub-arachnoid
                       space severely impairing CSF drain-age. It is
                       most common in young women

Spinal cysticercosis   Cord compression with radiculopathy,
                       transverse myelitis, and signs of meningitis.

Ocular cysticercosis   Eye pain with scotomata, iridocyclitis,
                       clouding of the vitreous and retinal
                       inflammation or detachment.

Table 3. Diagnosis of neurocysticercosis

CSF
analysis   * Hypoglycorrhachia.

           * Elevated CSF protein.

           * Lymphocytosis and eosinophylic pleocytosis (5-500 cells/
           microliter).

           * ELISA and Western blot testing for specific IgM and
           IgG anticysticercal antibodies in the CSF (75 to
           100% sensitivity).

CT         * A variable appearance including multiple, low-density
           lesions, 0.5 to 2.0 cm in diameter. In acute disease, they
           enhance after contrast administration, surrounded by
           vasogenic edema with or without mass effects. Dead
           parasites (not dying parasites) show as non-enhancing
           calcified 5-mm bodies.

MRI        * Live forms have a characteristic appearance: fluid-filled
           lesions containing an inverted scoleces, surrounded by
           thin low-signal capsule. They do not stimulate
           inflam-mation and do not enhance; dying forms do. In the
           less common racemose type, the cysts may be hard to see
           because they have similar imaging features as the CSF.
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Title Annotation:RADIOLOGICAL CASE
Author:Nwakudu, Obidike A.; Ekechukwu, Kenneth U.
Publication:Applied Radiology
Article Type:Case study
Geographic Code:1USA
Date:Jan 1, 2013
Words:1386
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