Article first published online: 28 JUN 2008
Volume 7, Issue 1, pages 681–693, January 1997
How to Cite
Pittella, J. E. H. (1997), Neurocysticercosis. Brain Pathology, 7: 681–693. doi: 10.1111/j.1750-3639.1997.tb01083.x
- Issue published online: 28 JUN 2008
- Article first published online: 28 JUN 2008
Cysticercosis is an infection caused by Taenia solium larvae (cysticerci). When the cysticercus is lodged in the central nervous system (CNS), the disease is known as neurocysticercosis (NCC). NCC is the most frequent and most widely disseminated human neuroparasitosis. It is endemic in many parts of the world, particularly Latin America, Africa, and Asia, and still relatively frequent in Portugal, Spain and Eastern European countries. It is also endemic in developed countries with high rates of immigration from endemic areas. Man may act as an intermediate host after ingestion of mature, viable T. solium eggs via the fecal-oral route. The development of lesions in the brain and leptomeninges, and the consequent onset of symptoms associated with NCC are mainly due to the host immune-inflammatory response. As long as the cysticercus remains viable, there is relative host immune tolerance. It is only when the parasite dies that massive antigen exposure occurs, with intensification of the immune response/inflammatory reaction and the appearance or worsening of symptoms. NCC can be asymptomatic or cause widely varied clinical manifestations, such as seizures, increased intracranial pressure, ischemic cerebrovascular disease, dementia, and signs of compression of the spinal roots/cord. The combination of two or more symptoms is common. Such clinical polymorphism is determined by 1) the number of lesions (single or multiple cysticerci); 2) the location of CNS lesions (subarachnoid, intracerebral, intraventricular, intramedullary); 3) the type of cysticercus (Cysticercus cellulosae, Cysticercus racemosus); 4) the stage of development and involution of the parasite (vesicular or viable, necrotic, fibrocalcified nodule); and 5) the intensity of the host immune-inflammatory response (no inflammatory reaction, leptomeningitis, encephalitis, granular ependymitis, arteritis).