The frequency of cerebral involvement has been reported in 20 to 45% of patients with erratic paragonimiasis [
6]. In a recently reported case, 3.5% of patients with food-borne parasitic encephalopathy were due to cerebral paragonimiasis. In hospital-based studies, 0.8% of the positive reactions in intradermal tests for
Paragonimus are compatible with a cerebral paragonimiasis [
7]. Cerebral paragonimiasis is diagnosed by radiological findings, as well as by immunologic and parasitology methods. Nomura
et al. reported four pathological stages of the cerebral parasite. Briefly, stage I consisted of apparently viable cysts surrounded by a thin layer of collagen type I. In stage II, a mononuclear-rich inflammatory infiltrate became evident around the parasite. At stage III, granulomas with associated inflammatory infiltrates and fibrosis were formed, and an abundant number of eosinophils had migrated to the center of the lesion, to be located between the parasite and granuloma. By stage IV the same cell types were evident, but the center of the lesion contained the disintegrated parasite and amorphous material reminiscent of necrosis [
8]. This granulomatous response in swine resembled previous findings in humans, but differed in the abundance of eosinophils, the presence of fewer plasma cells and discrete deposition of collagen. These variations may be partly attributed to an immune response that is detected earlier in swine, but at a more chronic stage in humans. The CT and MRI findings for chronic cerebral paragonimiasis have been generally recorded as conglomerates of multiple ring-shaped shadows or enhancements of ‘grape cluster’ or ‘soap bubble’ forms in one hemisphere [
3,
4,
8,
9]. The present case showed typical radiology findings of chronic paragonimiasis such as multiple conglomerated round calcified nodules in the brainstem, which has not been reported. An enzyme-linked immunosorbent assay (ELISA) is recommended as a complementary tool for diagnosing cerebral paragonimiasis, and the serum and ELISA antibody levels are generally positive in 48% and 31% of chronic cases, respectively [
3]. In our case, the ELISA results for the diagnosis of paragonimiasis were positive and there were many
P. Westermani eggs in the worm capsules resected from the patients’ brain. Numerous
P. Westermani eggs were well preserved and were also present in the tunnel sign, which showed the track of the adult worm. In addition, most of the eggs in the worm capsules retained a shell without a yolk. This indicates that the worm capsules in the brain had been established a long time ago, as adult worms die within 10 to 20 years, even without treatment [
9]. In addition, the worm capsules remain as multiple nodules with a low-density cavity containing the
Paragonimus eggs in cases of cerebral paragonimiasis that persist for more than 20 years [
1,
9].