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Review of Neurocysticercosis

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Review of Neurocysticercosis Neurosurg Focus 12 (6):Article 1, 2002, Click here to return to Table of Contents Review of neurocysticercosis JULIO SOTELO, M.D., AND OSCAR H. DEL BRUTTO, M.D. National Institute of Neurology and Neurosurgery, Mexico City, Mexico; and Department of Neurological Sciences, Hospital-Clínica Kennedy, Guayaquil, Ecuador In the neurosurgical services in many developing countries, treatment of neurocysticercosis (NCC) accounts for greater than 10% of brain surgical procedures and approximately 15% of neurological consultations. In these areas brain cysticercosis is the leading cause of hydrocephalus in adults and the first cause of late-onset epilepsy. During the last two decades, successful medical treatment has been established. Additionally, neuroimaging and immunological studies have clearly defined the topography, pathophysiological mechanisms, and biological status of these lesions. Thus, selection of cases for medical or surgical treatment has improved; in a significant number of cases, both inter- ventions are required. New therapies with either albendazole or praziquantel have respectively reduced to 8 days and to 1 day the course of anticysticidal therapy, which now is fast, effective, inexpensive, atoxic, and convenient, particu- larly in endemic areas where most patients belong to the lower socioeconomic groups. Additionally, the rational use of steroid agents facilitates the treatment of inflammation, a conspicuous accompaniment in cases of NCC. A major effort, however, is still required to eradicate this disease. KEY WORD • neurocysticercosis • hydrocephalus • epilepsy Neurocysticercosis is caused by the larvae of the tape- tode, whereas both pigs and humans may act as interme- worm Taenia solium in the nervous system, a disease suf- diate hosts for the larval form or cysticercus.30 The adult fered by millions of people living in the developing coun- T. solium inhabits the small intestine in humans, where it tries of Central and South America, sub-Saharan Africa, is attached to the intestinal wall by its suckers and hooks. and east and south Asia.7,9,26,47 In these areas, the disease Every day, a few pregnant proglottids are detached from accounts for up to 12% of all admissions to neurological the distal end of the body of the worm and passed with the hospitals and is the leading cause of acquired epilepsy in feces; each proglottid contains thousands of eggs, which adults.34,42 More than 50,000 new NCC-related deaths oc- are fully embryonated, infective, and resistant to adverse cur annually, and of the many more patients who suffer environments. In regions in which systems for disposal of related neurological sequelae, most are affected at pro- human feces are deficient, wandering pigs eat human fe- ductive ages.24,53 This makes NCC a large public health ces containing T. solium eggs. Once in the intestinal tract problem in developing countries. Moreover, massive emi- of the pig, the action of bile and pancreatic enzymes cause gration of people from endemic to nonendemic areas has the eggs to lose their coats, liberating oncospheres that increased its prevalence in North America and some Eu- cross the intestinal wall, enter the bloodstream, and are ropean countries, where this condition had been consid- carried to the tissues of the host where embryos evolve to 57,76 ered rare. form larvae (cysticerci). In these circumstances, pigs be- come the intermediate hosts in the life cycle of T. solium. ETIOPATHOGENESIS OF Human consumption of improperly cooked infected NEUROCYSTICERCOSIS pork results in the transmission of viable cysticerci in the small intestine, where, by the action of bile and digestive Taenia solium has a complex life cycle that requires two enzymes, the scolex of a cysticercus evaginates and at- hosts. Humans are the only known hosts for the adult ces- taches to the intestinal wall. Thereafter, proglottids begin to multiply and the parasite becomes a cestode that can be passed in the feces as mature proglottids approximately 4 Abbreviations used in this paper: CNS = central nervous system; CSF = cerebrospinal fluid; CT = computerized tomography; months after attachment. Humans can also act as interme- ELISA = enzyme-linked immunosorbent assay; EITB = enzyme- diate hosts for T. solium after ingestion of Taenia eggs. linked immunoelectrotransfer blot; MR = magnetic resonance; In these circumstances, human cysticercosis develops.24,30 NCC = neurocysticercosis. The mechanisms by which eggs cross the intestinal wall Neurosurg. Focus / Volume 12 / June, 2002 1 Unauthenticated | Downloaded 09/30/21 08:22 AM UTC J. Sotelo and O. H. Del Brutto and lodge in human tissues are the same as those in pigs. action in the subarachnoid space, forming an exudate The two main sources from which humans contact cysti- composed of collagen fibers, lymphocytes, multinucleat- cercosis are ingestion of food contaminated with T. solium ed giant cells, eosinophils, and hyalinized parasitic mem- eggs and the fecal–oral route in individuals harboring the branes leading to abnormal thickening of the leptomen- intestinal cestode. inges and difficulty in CSF absorption, which produces Cysticerci are vesicles consisting of two main parts: the hydrocephalus in a significant number of patients.3,45 The vesicular wall and the scolex. The scolex has a similar optic chiasm and cranial nerves arising from the anterior morphology to the adult T. solium, including an armed aspect of the brainstem are encased in this leptomeningeal rostellum and a rudimentary body.45 The macroscopic ap- thickening. Because the foramina of Luschka and Magen- pearance of cysticerci varies according to their location die may also be occluded by the thickened leptomeninges within the CNS. Viable cysticerci in brain parenchyma and parasitic membranes, noncommunicating hydroceph- measure approximately 10 mm. These cysts tend to lodge alus subsequently may develop.29 Small penetrating arter- in the cerebral cortex or the basal ganglia because of the ies arising from the circle of Willis are frequently affected high vascular supply in these areas. Subarachnoid cys- by the subarachnoid inflammatory reaction elicited by ticerci may be located within cortical sulci or in the CSF meningeal cysticerci, and this may cause occlusion of the cisterns at the base of the brain.3 After a long period of lumen of the vessel and the subsequent development of infection some cysticerci lose their scolices and grow to cerebral infarctions.13,43 reach 50 mm or more, which more frequently occurs in Ventricular cysticerci also cause an inflammatory re- cysts located in the subarachnoid cisterns, because their action if they are attached to the choroid plexus or the growth is not limited by the effect of pressure within the ventricular wall. The ependymal lining is disrupted, and brain parenchyma. Some of these cysts are composed of ependymal cells are replaced by proliferating subependy- several membranes attached to each other with a grapelike mal glial cells that protrude toward the ventricular cavities appearance (racemose form of cysticerci).27 Ventricular and may block the transit of CSF, particularly when the cysts are usually single lesions; they may be attached to site of protrusion is at or near the foramen of Monro or the the choroid plexus or float freely within the ventricu- cerebral aqueduct. This process is called granular ependy- lar cavities. Other locations within the CNS include the mitis and is usually associated with hydrocephalus.2 subdural space, the sellar region, the eye, and the spinal Cysticerci have several antigens that stimulate the pro- cord.1,6,20 duction of specific antibodies, which can be detected on After entering the CNS, cysticerci are viable and induce immunodiagnostic tests. Some antigens may play a role in slight inflammatory changes in the surrounding tissues. At the mechanisms by which cysticerci evade the immune this stage, called the vesicular stage, parasites have a response.24 One of them, antigen B, may be localized both transparent membrane, clear vesicular fluid, and larva or within the parasite and in the surrounding tissue. It is part- scolex. They may remain for decades in this stage or, as ly composed of collagen and may bind to C1q, inhibiting the result of a complex immunological attack from the the classic pathway of complement activation. Because host, may begin a degenerative process that may lead to destruction of cysticerci appears to be mediated by activa- the death of the parasite and its further transformation into tion of the complement cascade, antigen B could play a an inert nodule.27 After cysticidal treatment or successful role in the protection of cysticerci against the host’s im- immune response, the first sign of involution of cysticerci munological attack.77 Analysis of several studies suggests is the colloidal stage, in which the transparent vesicular the presence of cellular immune dysfunction in patients fluid is replaced by a viscous and turbid fluid, readily with NCC. This depressed immunity may be responsible identifiable by MR imaging studies,55 and the scolex dies. for the reported association of this parasitic disease with Colloidal cysticerci are surrounded by a thick collagen conditions resulting from immunological disturbances capsule, and the surrounding brain parenchyma shows an such as hematological malignancies and conditions lead- intense astrocytic gliosis associated with microglial prolif- ing to the development of cerebral tumors.18,19,38 eration, diffuse edema, neuronal degenerative changes,
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