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The most important extrapulmonary site for paragonimiasis is the brain (Fig. 22.10), first recognized in Japan in 1887. The worms probably reach the brain by migration through the soft tissues of the neck along the sheaths of the jugular veins, internal carotid arteries, or nerve trunks. In different series, 1 to 24% of patients with clinical pulmonary paragonimiasis have shown cerebral involvement. The highest incidence of cerebral paragonimiasis is seen in Asian countries, particularly Korea, were P. westermani is the predominant species; in African countries, where P. africanus and P. uterobilateralis are the principal species, brain involvement is a rare occurrence.

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Fig. 22.10A,B. Cerebral paragonimiasis, gross specimens. (A) Everted capsule of a Paragonimus cyst of the brain reveals a dead fluke attached to the wall of the cyst. (B) Two flukes are seen in the bridging veins (arrows), the upper worm entering the longitudinal sinus and the lower worm lying in a cortical vein. (A and B courtesy of Dr. S.K. Kim and reproduced from R.A. Marcial-Rojas: Pathology of Protozoal and Helminthic Diseases. Robert Krieger, Huntington, NY, 1975).

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Fig. 22.11A,B. Paragonimiasis involving the brain. (A) An early Paragonimus cyst of the cerebellum. X4-1/8 (AFIP 55-4742.) (B) Multiple eggs of P. westermani are seen within a cerebral abscess. There is an inflammatory reaction. The small round or oval spaces surrounded by bifringent substances are the remnants of eggs trapped in the tissue.

As the fluke migrates through the brain, it leaves a necrotic eosinophilic track and parasitic lesions of different sizes and shapes containing various numbers of eggs (Fig. 22.11). The parasite elaborates toxins which cause venous stasis and anoxia of brain tissue, resulting in infarction. There is then liquefaction and a pseudocavity is formed. The parasite itself is lysed so that is unusual to find an actual fluke within the brain, although the residual cysts and ova may be numerous. These reactions cause diffuse adhesions between the meninges, mainly an arachnoiditis. The cystic masses may lie as deep as 8 cm or more within the cerebral substance and measure up to 10 cm in diameter. Some will shell out at surgery. They are often bilateral, may involve any part of the brain (although the frontal lobes and cerebellum are rarely involved), and may block the circulation of cerebrospinal fluid. Many authorities regard the process in the brain as being continuous, the granulomas developing into encapsulating abscesses progressing to the cystic lesions which may eventually calcify (Figs. 22.41 thru 22.48 ).

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