A 59-year-old man sought evaluation at our hospital due to perioral paresthesias and dysarthria on 25 April 2009. In 1997, he was admitted to our hospital due to headaches and seizures of 1 week duration. He had experienced intermittent seizures since 1991. On the brain magnetic resonance imaging (MRI), there were multiple dark signal intensity lesions that were suggestive of calcifications in both cerebral hemispheres and peripheral-enhancing cystic lesions in both frontal lobes. A dot-like, high signal intensity on the T1-weighted image and a low signal intensity on T2-weighted image were noted in the right frontal lobe, suggesting a scolex of cysticercosis (images not shown). Positive results were reported on the serum and cerebrospinal fluid (CSF) cysticercosis enzyme-linked immunosorbant assay (ELISA) tests (0.32 and 0.68, respectively). He was diagnosed with neurocysticercosis and treated with an anti-helminthic (biltricide). He recovered completely and was discharged.

In 2001, the patient had complaints of headaches, dizziness and numbness in both arm and legs. On brain CT, there were multiple nodular calcifications in both cerebral hemispheres and no abnormal enhancing lesions (Figs. 1A, B), and this was all compatible with endstage neurocysticercosis. He was hospitalized for several days and he improved. In 2002, he was admitted to our hospital with dysarthria and focal seizures of the lip several times during 1 day. There were no significant results on the serum and CSF cysticercosis ELISA tests. Thick bands of peripheral enhancement of multiple nodular calcified lesions and surrounding edema were noted on the brain MRI (Figs. 1C, D). The patient appeared to have reactivated neurocysticercosis and he was treated with the anti-helmintic praziquantel. His symptoms improved after treatment and he was prescribed carbamazepine for controlling his seizures. He was healthy without any neurologic symptoms for 7 years, except for the present admission (Figs. 1E, F). He had no other primary symptoms and no remarkable findings on the physical examination. The laboratory findings, including the blood cell count, electrolytes and serum glucose level, were within the normal limits. He then underwent brain MRI with gadolinium-enhancement. On brain MRI, there were several dark signal intensity lesions suggestive of calcifications in both cerebral hemispheres, which were unchanged since the previous brain MRI in 2004. There was edema around the calcified lesions on the axial T1- and T2-weight images, and this looked like the previous reactivation of neurocysticercosis in 2002 (Fig. 1G). On the gadolinium-enhancement T1-weighted image, there were no changes in the diffuse thin bands of enhancement in the peripheral portion of the lesions (Fig. 1H). On a CSF study, he was negative for cysticercus IgG. It was thought that there was a second reactivation of neurocysticercosis and so he was treated with albendazole. The symptoms were resolved and the patient was discharged.

Neurocysticercosis is an infection of the human central nervous system with Taenia solium, the pork tapeworm. Neurocysticercosis is a common parasitic disease in Latin America, South Africa, China, India and the United States (1). The seropositive rate for neurocysticercosis is 4.0% in epilepsy patients and 2.1% in otherwise healthy persons in Korea (2). Neurocysticercosis is a common cause of epilepsy in these endemic areas. Brain imaging modalities, such as CT and MRI, are necessary for detecting or differentiating neurocysticercosis in epilepsy patients.

The natural course of neurocysticercosis is divided into four pathologic stages according to the Escobar classification (3). The typical image findings on CT and MRI at each of the stages are vesicular, colloid vesicular, granular nodular and nodular calcified lesions, respectively (45). Neurocysticercosis appears as cystic lesions without enhancement or peripheral edema in the vesicular stage, but in the colloid vesicular stage, surrounding edema and ring enhancement are noted as aggravated immune reactions. In the granular nodular stage, the cystic fluid is absorbed and the lesions are seen as solid nodules. Calcifications are detected in the nodular calcified stage, which is the terminal stage of neurocysticercosis, and this indicates that the larvae are dead. In our case, there were multiple cysts and calcifications on MRI (image not shown) when the patient was initially admitted and diagnosed with neurocysticercosis in 1997; this appeared to be a mixture of the colloid vesicular, granular nodular and nodular calcified stages. There were multiple calcified nodules without enhancement and no cystic lesions on the brain CT performed in 2001 (Figs. 1A, B), which appeared to be the nodular calcified stage of neurocysticercosis and accordingly death of the larvae. On the brain MRI performed in 2004, a persistent thin ring of enhancement was shown in the calcified nodules, which did not represent reactivation of neurocysticercosis, but rather, inflammation in the vicinity of the lesion (Figs. 1E, F) (6).

Peripheral thick bands of enhancement and peripheral edema were detected twice on the follow-up brain MRIs in 2002 and 2009 (Figs. 1C, H), which were considered to be reactivation of neurocysticercosis.

Unlike tuberculosis, neurocysticercosis is thought not to reactivate. One case has been reported by Sheth et al. (7) on the reactivation of neurocysticercosis in which there were thick bands of peripheral enhancement of multiple calcified nodules with surrounding edema on the brain MRI, as in our case. The authors suggested that antigens released from dead larvae or other causes of immunologic reactions triggered an intense immune response. However, there were neither underlying diseases nor clinical symptoms of induced immune reactions in our patient, and pathologic confirmation was not performed other than the serum and CSF ELISA tests. Thus, the basis for neurocysticercosis reactivation was not demonstrated.

This is the first case report of twice-reactivated neurocysticercosis. Immunologic and pathologic studies are necessary for demonstrating the mechanism of reactivation of neurocysticercosis. Radiologists and clinicians should keep the possibility of reactivation of neurocysticercosis in mind, despite observing findings that are consistent with the nodular calcified stage.